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136
Film / Madagascar : Escape 2 Africa
« on: 12 January 2009, 07:42:49 PM »
Dalam bagian pertama dikisahkan bahwa Alex (Ben Stiller), Marty (Chris Rock), Melman (David Schwimmer) dan Gloria (Jada Pinkett Smith) terdampar di Madagascar. Dalam usahanya untuk kembali ke New York, tempat asal mereka, keempat penghuni kebun binatang New York ini berusaha memperbaiki pesawat yang rusak.
MADAGASCAR: ESCAPE 2 AFRICA
Celakanya, bukannya kembali ke New York, pesawat yang mereka tumpangi ini malah mendarat di benua Afrika. Di sini Alex sang singa, Marty si zebra, Melman jerapah dan Gloria si kuda nil berkesempatan untuk bertemu dengan teman-teman sejenis mereka. Di sinilah mereka akhirnya menyadari bahwa kehidupan mereka selama ini di dalam kebun binatang amatlah berbeda dengan saudara-saudara mereka yang hidup di alam bebas.
Film sekuel dari film animasi berjudul MADAGASCAR yang diluncurkan tahun 2005 lalu ini masih dipercayakan pada sutradara Eric Darnell dan Tom McGrath. Nama-nama seperti Chris Rock, Ben Stiller, Jada Pinkett Smith dan David Schwimmer pun masih tetap mengisi suara tokoh yang mereka perankan tiga tahun lalu.
MADAGASCAR: ESCAPE 2 AFRICA
Berbeda dengan film yang pertama, yang kedua ini terasa lebih digarap dengan baik terutama dari sisi naskah. Bila sebelumnya film MADAGASCAR hanya dibuat untuk konsumsi anak-anak, maka MADAGASCAR: ESCAPE 2 AFRICA ini masih bisa dinikmati orang dewasa. Humor-humor yang disajikan pun terasa cukup segar dan tak klise.
Namun tentu saja bukan cuma naskah yang diperbaiki dalam film ini. Kualitas animasi yang disajikan pun terasa jauh lebih bagus. Dreamworks agaknya tak main-main soal animasi pada film yang satu ini. Bila dibandingkan dengan bagian pertamanya, hasil animasi komputer yang disajikan di sini jelas sangat jauh berbeda. Gambar terlihat lebih halus dengan ekspresi wajah dan gerakan yang terlihat alami.
MADAGASCAR: ESCAPE 2 AFRICA
Dan soal voice over, kembalinya para pengisi suara di bagian pertama juga makin mengokohkan film yang satu ini. Ben Stiller, Chris Rock, David Schwimmer, dan Jada Pinkett-Smith mungkin sudah tak asing lagi dengan karakter yang mereka bawakan dan ini sangat berdampak pada penjiwaan yang bagus. Meski hanya animasi, namun para tokoh dalam film ini terasa memiliki emosi yang cukup kuat dan meyakinkan.
Terlepas dari bagus atau tidaknya film animasi yang satu ini, yang jelas dari biaya produksi sebesar US$150 juta, film ini berhasil mengumpulkan lebih dari US$344 juta dan sempat menduduki posisi terhormat box office.
MADAGASCAR: ESCAPE 2 AFRICA
Celakanya, bukannya kembali ke New York, pesawat yang mereka tumpangi ini malah mendarat di benua Afrika. Di sini Alex sang singa, Marty si zebra, Melman jerapah dan Gloria si kuda nil berkesempatan untuk bertemu dengan teman-teman sejenis mereka. Di sinilah mereka akhirnya menyadari bahwa kehidupan mereka selama ini di dalam kebun binatang amatlah berbeda dengan saudara-saudara mereka yang hidup di alam bebas.
Film sekuel dari film animasi berjudul MADAGASCAR yang diluncurkan tahun 2005 lalu ini masih dipercayakan pada sutradara Eric Darnell dan Tom McGrath. Nama-nama seperti Chris Rock, Ben Stiller, Jada Pinkett Smith dan David Schwimmer pun masih tetap mengisi suara tokoh yang mereka perankan tiga tahun lalu.
MADAGASCAR: ESCAPE 2 AFRICA
Berbeda dengan film yang pertama, yang kedua ini terasa lebih digarap dengan baik terutama dari sisi naskah. Bila sebelumnya film MADAGASCAR hanya dibuat untuk konsumsi anak-anak, maka MADAGASCAR: ESCAPE 2 AFRICA ini masih bisa dinikmati orang dewasa. Humor-humor yang disajikan pun terasa cukup segar dan tak klise.
Namun tentu saja bukan cuma naskah yang diperbaiki dalam film ini. Kualitas animasi yang disajikan pun terasa jauh lebih bagus. Dreamworks agaknya tak main-main soal animasi pada film yang satu ini. Bila dibandingkan dengan bagian pertamanya, hasil animasi komputer yang disajikan di sini jelas sangat jauh berbeda. Gambar terlihat lebih halus dengan ekspresi wajah dan gerakan yang terlihat alami.
MADAGASCAR: ESCAPE 2 AFRICA
Dan soal voice over, kembalinya para pengisi suara di bagian pertama juga makin mengokohkan film yang satu ini. Ben Stiller, Chris Rock, David Schwimmer, dan Jada Pinkett-Smith mungkin sudah tak asing lagi dengan karakter yang mereka bawakan dan ini sangat berdampak pada penjiwaan yang bagus. Meski hanya animasi, namun para tokoh dalam film ini terasa memiliki emosi yang cukup kuat dan meyakinkan.
Terlepas dari bagus atau tidaknya film animasi yang satu ini, yang jelas dari biaya produksi sebesar US$150 juta, film ini berhasil mengumpulkan lebih dari US$344 juta dan sempat menduduki posisi terhormat box office.
137
Pengembangan DhammaCitta / Board Anak Sekolah / Kuliah
« on: 09 January 2009, 07:12:25 PM »
Request suhu..
Saya memperhatikan cukup banyak member dc yang masih sekolah dan kuliah..
Dan kemarin di shout box Thira dan Citta minta saya ajari Kimia Dasar
Jadi saya pikir ada baiknya dibuat child board untuk bahas PR / tugas kuliah member DC bagi mereka yang kesulitan..
Mungkin board Tolong bisa di-expand dengan penambahan 1 child board lagi
Saya memperhatikan cukup banyak member dc yang masih sekolah dan kuliah..
Dan kemarin di shout box Thira dan Citta minta saya ajari Kimia Dasar
Jadi saya pikir ada baiknya dibuat child board untuk bahas PR / tugas kuliah member DC bagi mereka yang kesulitan..
Mungkin board Tolong bisa di-expand dengan penambahan 1 child board lagi
138
Kesehatan / [INFO] Ramuan Alami tidak 100% Aman
« on: 07 January 2009, 11:18:12 PM »
CEGUKAN biasa dialami semua orang, tidak terkecuali Surya. Namun, mendapati cegukannya tidak berhenti selama dua hari berturut-turut, bahkan belakangan disertai mual-mual, lelaki 56 tahun itu pun bergegas ke rumah sakit. Saat itu pertengahan September dini hari, Surya mulai dirawat di rumah sakit. Siangnya, kondisi Surya bertambah buruk, matanya membengkak dan napasnya sesak. Ia pun pindah ke ruang ICU. Malamnya, karena mengalami kejang-kejang, Surya dirujuk ke dokter saraf dan menjalani pemeriksaan CT scan otak, namun hasilnya normal.
Paginya, warga Pasar Baru, Jakarta Pusat, itu kehilangan kesadaran (koma). Karena itu, pemeriksaan MRI otak dilakukan. Namun, sama seperti hasil pemeriksaan CT scan, tidak didapati kelainan apa pun pada jaringan otak Surya. Kondisi koma terus berlanjut.
Karena hasil pemeriksaan laboratorium menunjukkan kadar kreatinin dalam darah Surya cukup tinggi, yakni 7,2 mg/dl, maka Surya direncanakan menjalani hemodialisis (cuci darah). Memang, selama ini Surya menderita komplikasi diabetes, darah tinggi, dan penyakit ginjal, tapi belum sampai tahap cuci darah.
Belum sempat rencana cuci darah dilakukan, selang empat hari kemudian kesadaran Surya mulai pulih dan kondisinya membaik. Rencana cuci darah dibatalkan. Lima hari kemudian ia pulang dengan kadar kreatinin 5,3 mg/dl. Namun, selang dua minggu kemudian, cegukan itu datang lagi. Ia pun mendatangi dokter kembali di lain rumah sakit.
Dari proses diagnosis, diketahui biang keladi cegukan, mual, dan kondisi koma yang dialami Surya adalah buah belimbing. Ia mengaku sebelum masuk rumah sakit rutin mengonsumsi belimbing karena buah itu dipercaya bisa menurunkan tekanan darahnya. Ia tidak tahu kalau konsumsi belimbing dapat berakibat fatal bagi penderita gangguan ginjal sepertinya.
"Apa yang terjadi pada Surya menunjukkan bahwa obat tradisional tidak seluruhnya aman meski berasal dari ramuan alami. Sayangnya, selama ini sebagian besar masyarakat menganggap obat atau ramuan tradisional sepenuhnya aman karena berasal dari bahan alami," ujar spesialis penyakit dalam Rumah Sakit Husada, dr Salim Lim SpPD, dalam seminar bertema Khasiat dan efek samping obat tradisional, di RS Husada, Sabtu (13/12). Salim adalah dokter konsultan ginjal yang memeriksa dan memastikan diagnosis terhadap Surya.
Belimbing, lanjut Salim, dipercaya masyarakat sebagai obat tradisional penurun tekanan darah. Namun, karena kandungan kalsium oksalatnya yang tinggi, belimbing seharusnya tidak dikonsumsi penderita gangguan ginjal seperti Surya.
Selain belimbing, menurut Salim, banyak bahan-bahan alami yang berdampak negatif bagi penderita gangguan ginjal karena tingginya kandungan oksalat. Yaitu, bayam, buah bit, jengkol, cokelat, kacang tanah, kedelai, dan ubi madu. Bahkan, konsumsi suplemen vitamin C dalam jangka panjang juga diketahui dapat menyebabkan gangguan ginjal.
"Pernah saya mendapati pasien laki-laki berumur 39 tahun menderita batu ginjal. Setelah dianalisis, batu ginjal itu terdiri dari 83% kalsium oksalat. Berdasar riwayat keseharian, ternyata sejak umur 28 tahun ia rutin mengonsumsi suplemen vitamin C satu sampai dua butir sehari," jelas dokter lulusan Jerman itu.
Salim melanjutkan, beberapa jenis obat tradisional China juga termasuk yang berefek samping menyebabkan gangguan ginjal. Bahkan ada salah satu jenis gangguan ginjal yang disebut chinese herb nephropathy, berupa terjadinya perubahan jaringan organ ginjal (fibrosis).
"Salah satu pasien saya, perempuan usia 59 tahun, rutin mengonsumsi ramuan China untuk mengatasi nyeri sendi yang dideritanya. Pada akhirnya ia harus menjalani cuci darah karena menderita chinese herb nephropathy," tutur Salim.
Tidak berkhasiat
Selain menimbulkan efek samping, kata Salim, banyak obat-obatan tradisional yang tidak terbukti berkhasiat. Kalaupun ada khasiatnya, juga tidak signifikan. Tumbuhan kumis kucing atau remujung, misalnya, ternyata belum terbukti dapat menghilangkan batu ginjal seperti yang dipercaya selama ini.
Salim menerangkan penggunaan sebagian besar obat tradisional selama ini dilakukan berdasarkan kepercayaan tanpa didasari bukti maupun uji ilmiah. Hal itu berbeda dengan obat-obatan medis modern yang harus diuji berkali-kali sebelum diluncurkan di pasaran.
Karena itulah, Salim menganjurkan agar masyarakat berhati-hati dalam mengonsumsi obat. Sebaiknya pilih obat-obatan modern yang sudah terbukti berkhasiat dan dilengkapi dengan penjelasan efek sampingnya. Kalaupun hendak mengonsumsi obat tradisional, Salim menganjurkan agar memilih obat tradisional yang sudah mengalami uji khasiat dan keamanan secara ilmiah.
"Ada bahan-bahan alami yang diakui sebagai obat medis karena setelah melalui uji ilmiah terbukti berkhasiat, efektif, dan aman digunakan," kata Salim.(S-6)
Source = http://www.mediaindonesia.com/index.php?ar_id=NTA4Mjc
Paginya, warga Pasar Baru, Jakarta Pusat, itu kehilangan kesadaran (koma). Karena itu, pemeriksaan MRI otak dilakukan. Namun, sama seperti hasil pemeriksaan CT scan, tidak didapati kelainan apa pun pada jaringan otak Surya. Kondisi koma terus berlanjut.
Karena hasil pemeriksaan laboratorium menunjukkan kadar kreatinin dalam darah Surya cukup tinggi, yakni 7,2 mg/dl, maka Surya direncanakan menjalani hemodialisis (cuci darah). Memang, selama ini Surya menderita komplikasi diabetes, darah tinggi, dan penyakit ginjal, tapi belum sampai tahap cuci darah.
Belum sempat rencana cuci darah dilakukan, selang empat hari kemudian kesadaran Surya mulai pulih dan kondisinya membaik. Rencana cuci darah dibatalkan. Lima hari kemudian ia pulang dengan kadar kreatinin 5,3 mg/dl. Namun, selang dua minggu kemudian, cegukan itu datang lagi. Ia pun mendatangi dokter kembali di lain rumah sakit.
Dari proses diagnosis, diketahui biang keladi cegukan, mual, dan kondisi koma yang dialami Surya adalah buah belimbing. Ia mengaku sebelum masuk rumah sakit rutin mengonsumsi belimbing karena buah itu dipercaya bisa menurunkan tekanan darahnya. Ia tidak tahu kalau konsumsi belimbing dapat berakibat fatal bagi penderita gangguan ginjal sepertinya.
"Apa yang terjadi pada Surya menunjukkan bahwa obat tradisional tidak seluruhnya aman meski berasal dari ramuan alami. Sayangnya, selama ini sebagian besar masyarakat menganggap obat atau ramuan tradisional sepenuhnya aman karena berasal dari bahan alami," ujar spesialis penyakit dalam Rumah Sakit Husada, dr Salim Lim SpPD, dalam seminar bertema Khasiat dan efek samping obat tradisional, di RS Husada, Sabtu (13/12). Salim adalah dokter konsultan ginjal yang memeriksa dan memastikan diagnosis terhadap Surya.
Belimbing, lanjut Salim, dipercaya masyarakat sebagai obat tradisional penurun tekanan darah. Namun, karena kandungan kalsium oksalatnya yang tinggi, belimbing seharusnya tidak dikonsumsi penderita gangguan ginjal seperti Surya.
Selain belimbing, menurut Salim, banyak bahan-bahan alami yang berdampak negatif bagi penderita gangguan ginjal karena tingginya kandungan oksalat. Yaitu, bayam, buah bit, jengkol, cokelat, kacang tanah, kedelai, dan ubi madu. Bahkan, konsumsi suplemen vitamin C dalam jangka panjang juga diketahui dapat menyebabkan gangguan ginjal.
"Pernah saya mendapati pasien laki-laki berumur 39 tahun menderita batu ginjal. Setelah dianalisis, batu ginjal itu terdiri dari 83% kalsium oksalat. Berdasar riwayat keseharian, ternyata sejak umur 28 tahun ia rutin mengonsumsi suplemen vitamin C satu sampai dua butir sehari," jelas dokter lulusan Jerman itu.
Salim melanjutkan, beberapa jenis obat tradisional China juga termasuk yang berefek samping menyebabkan gangguan ginjal. Bahkan ada salah satu jenis gangguan ginjal yang disebut chinese herb nephropathy, berupa terjadinya perubahan jaringan organ ginjal (fibrosis).
"Salah satu pasien saya, perempuan usia 59 tahun, rutin mengonsumsi ramuan China untuk mengatasi nyeri sendi yang dideritanya. Pada akhirnya ia harus menjalani cuci darah karena menderita chinese herb nephropathy," tutur Salim.
Tidak berkhasiat
Selain menimbulkan efek samping, kata Salim, banyak obat-obatan tradisional yang tidak terbukti berkhasiat. Kalaupun ada khasiatnya, juga tidak signifikan. Tumbuhan kumis kucing atau remujung, misalnya, ternyata belum terbukti dapat menghilangkan batu ginjal seperti yang dipercaya selama ini.
Salim menerangkan penggunaan sebagian besar obat tradisional selama ini dilakukan berdasarkan kepercayaan tanpa didasari bukti maupun uji ilmiah. Hal itu berbeda dengan obat-obatan medis modern yang harus diuji berkali-kali sebelum diluncurkan di pasaran.
Karena itulah, Salim menganjurkan agar masyarakat berhati-hati dalam mengonsumsi obat. Sebaiknya pilih obat-obatan modern yang sudah terbukti berkhasiat dan dilengkapi dengan penjelasan efek sampingnya. Kalaupun hendak mengonsumsi obat tradisional, Salim menganjurkan agar memilih obat tradisional yang sudah mengalami uji khasiat dan keamanan secara ilmiah.
"Ada bahan-bahan alami yang diakui sebagai obat medis karena setelah melalui uji ilmiah terbukti berkhasiat, efektif, dan aman digunakan," kata Salim.(S-6)
Source = http://www.mediaindonesia.com/index.php?ar_id=NTA4Mjc
139
Video Game / Sound / Music Game Kegemaran..
« on: 07 January 2009, 08:17:20 PM »
Main game tidak terlepas dari music / sound yang mengalun..
So sharing.. apa music kegemaranmu.. stage / game / console apa ..
Mulai dari aye..
Kebanyakan dari Rockman seh
1. Cutman stage - Rockman 1 / NES
2. Dr Wily Stage 1 - Rockman 2 / NES
3. Dr Wily Stage 3 - Rockman 3 / NES
4. Flame Mammoth - Rockman X / SNES
5. One More Time OP - Rockman X3 / PSX
6. Makenai Ai Ga Kitto Aru OP (Cinta Tak Terkalahkan yang kumiliki) - Yukie Nakama / Rockman X4 / PSX
7. Lost Painting - Michiru Yamane - Castlevania Symphony of The Night / PSX
Itu yang teringat.. kalau ingat ntar ta update lagi..
So sharing.. apa music kegemaranmu.. stage / game / console apa ..
Mulai dari aye..
Kebanyakan dari Rockman seh
1. Cutman stage - Rockman 1 / NES
2. Dr Wily Stage 1 - Rockman 2 / NES
3. Dr Wily Stage 3 - Rockman 3 / NES
4. Flame Mammoth - Rockman X / SNES
5. One More Time OP - Rockman X3 / PSX
6. Makenai Ai Ga Kitto Aru OP (Cinta Tak Terkalahkan yang kumiliki) - Yukie Nakama / Rockman X4 / PSX
7. Lost Painting - Michiru Yamane - Castlevania Symphony of The Night / PSX
Itu yang teringat.. kalau ingat ntar ta update lagi..
140
Kesehatan / [ASK] Dokter / Pengobatan Alternatif Kanker Payudara
« on: 06 January 2009, 07:41:56 PM »
Dear All,
Ada yang pernah mendengar dokter / shinshe / ahli pengobatan alternatif lainnya yang mahir dalam mengobati kanker payudara (breast cancer) di Jabotabek. Kondisi pasien, kankernya sudah besar, payudaranya sudah ada lubang dan bernanah dan sering kesakitan.
Mohon informasinya.
Ada yang pernah mendengar dokter / shinshe / ahli pengobatan alternatif lainnya yang mahir dalam mengobati kanker payudara (breast cancer) di Jabotabek. Kondisi pasien, kankernya sudah besar, payudaranya sudah ada lubang dan bernanah dan sering kesakitan.
Mohon informasinya.
141
Seremonial / Happy Birthday Mushroom Kick
« on: 26 December 2008, 08:04:53 PM »
Happy Birthday Mushroom Kick
誕生日おめでとう マッシュルーム キック
Wish all the best for you..
誕生日おめでとう マッシュルーム キック
Wish all the best for you..
142
Kesehatan / [INFO] Top Herbal Products
« on: 16 December 2008, 06:04:27 PM »
A recent survey estimated that more than 38 million adults in the United States used herbal products and dietary supplements in 2002.[1] More than half of those users said that these products were important to their health and well-being, yet only one third told a conventional healthcare provider about their use.
Other reports have estimated that 25% of patients who seek medical attention for a serious medical problem are using "unconventional" therapies, and 70% of those patients do not disclose those practices to their physician.[2,3] One survey estimated that about 18% of the US population uses herbal therapy on a regular basis.[4]
Herbal products and dietary supplements are widely available in supermarkets and other retail outlets, as well as by mail order. In fact, only a small percentage of these products (4.5%) are actually sold in pharmacies.[5] Many patients believe they derive health benefits from these herbal preparations, yet some remain skeptical and may seek advice from health professionals prior to use. Thus, it is important for all health professionals to be informed about available products and to be aware of any potential problems associated with their use.
Concerns About Herbal Products and Dietary Supplements
Unlike prescription and over-the-counter drugs, herbal products are not regulated by the US Food and Drug Administration (FDA) to determine purity or potency.[6] In fact, some products may contain contaminants, and their potency is dependent on many factors, such as the climate and soil conditions where they are grown, harvested, and stored.[7] Some herbal preparations have even been found to contain prescription drugs and heavy metals as unlabeled ingredients, and in some cases, these contaminants have resulted in toxicities.[8-17]
The labeling of herbal products is regulated by the Dietary Supplement Health and Education Act of 1994 (DSHEA).[18] Under this law, manufacturers may only make general claims about a supplement's effect on the structure or function of the human body (eg, "supports the immune system"). They must include the following statement in their labeling: "This product is not intended to diagnose, treat, cure, or prevent any disease."
The labels on herbal products are designed to promote product use and not necessarily to inform the consumer, so health professionals should be equipped with a general understanding of popular herbs and supplements, including knowledge of efficacy, common side effects, risks, and interactions. In addition, they should prospectively seek information regarding their patients' use of unconventional medicines to avoid adverse consequences.
Consumers should be advised that manufacturers of herbal supplements are not required to demonstrate safety or efficacy prior to marketing. Before the FDA can remove a product from the market, the agency must prove that the product is unsafe or ineffective. Recent examples of this include the ban on products containing ephedra due to adverse cardiovascular effects,[19] and the prohibition of kava amid concerns about hepatotoxicity.[20]
Patients with medical illness should not use herbs and dietary supplements without medical supervision. As will be discussed, some herbal products have adverse effects and may interact with prescribed medications. Furthermore, many conditions that patients try to diagnose or treat themselves may be serious, requiring a careful history and examination by a healthcare professional. For example, unsupervised use of saw palmetto for urinary symptoms may delay a diagnosis of prostate cancer.[21] Similarly, patients with symptoms such as chronic insomnia, anxiety, and depressed mood should see their health provider. Patients with cardiovascular disease, hypertension, heart failure, and hyperlipidemia should be under a healthcare professional's care and receive appropriate prescription drugs.
The following is an overview of some of the most commonly used herbal products, including important clinical considerations in the use of these products.
Echinacea for Fighting Cold Symptoms, Boosting Immunity
Echinacea is one of the most popular herbs in the United States, extracted from the purple coneflower that is native to North America. Species include Echinacea purpurea, Echinacea angustifolia, and Echinacea pallida. It has been studied as an adjunct therapy to enhance the immune system, mostly in upper respiratory tract infections, and these studies have produced mixed results.[22,23]
A recent meta-analysis concluded that standardized extracts of echinacea were effective in the prevention of common cold symptoms after clinical inoculation, when compared with placebo.[23] The authors of that study concluded that the likelihood of experiencing a cold was 55% higher with placebo than with echinacea (P < .043).
Some antiviral and bacteriostatic properties have been demonstrated in vitro, and the herb also appears to stimulate the production of cytokines (interferon, tumor necrosis factor, and interleukins).[24] Animal studies have revealed probable mechanisms of echinacea-induced immune enhancement, such as increasing the number of circulating white blood cells.[25]
Common side effects of echinacea supplements include unpleasant taste and allergic reactions. Because the flower is related to ragweed, cross allergenicity may occur in individuals allergic to ragweed.[26,27]
Echinacea is not recommended in patients with progressive or autoimmune disorders, including acquired immunodeficiency syndrome, tuberculosis, multiple sclerosis, collagen disorders, and diabetes mellitus. Theoretically, since echinacea alters the immune system, these disorders may be exacerbated.[28,29] Persistent use of echinacea has been associated with hepatotoxicity, so it should not be taken by patients who are taking other known hepatotoxins such as anabolic steroids, amiodarone, methotrexate, or ketoconazole.[30]
While not all randomized controlled trials performed to date have shown benefit for Echinacea over placebo,[22,31] a Cochrane review in 2006 concluded that the aerial parts of Echinacea purpurea might be effective for early treatment of colds in adults.[32]
Unfortunately, the optimal dose of echinacea is unknown, and multiple formulations exist, such as capsules, tinctures, teas, and extracted plant juice. Recommended dosages vary widely; for instance, capsules of Echinacea purpurea extract range from 100 to 500 mg, with manufacturers' suggested use ranging from 1 to 4 times daily for common cold prevention.
Take-home message: Clinicians should inform patients that a wide variety of Echinacea preparations and doses have been studied and results are inconsistent, making it difficult to recommend specific products. However, E. purpurea seems to be modestly effective for preventing the common cold in those at risk (eg, sick contacts). Evidence that the herb may reduce the duration of cold symptoms has been mixed. Patients allergic to ragweed, with progressive autoimmune disorders, and on hepatotoxic drugs should avoid echinacea.
Garlic: Warding Off Cardiovascular Disease?
Allium sativum, commonly known as garlic, has been used for centuries in cooking because of its flavoring properties. Today, it is used therapeutically by many consumers to prevent heart disease by controlling high cholesterol and high blood pressure. The suggested active ingredients are allicin and alliin.Numerous studies, however, have produced conflicting results regarding garlic's ability to lower lipids.[33-40] Positive findings in 3 trials exhibited a lowering of cholesterol in the range of 6.1% to 11.5%, primarily due to the lowering of low-density lipoproteins.[33-36] Other studies have yielded neutral or conflicting results.[37-39] One 12-week study tested the use of garlic powder in ambulatory patients, finding a 14% reduction of serum cholesterol.[40]
Garlic may have modest antihypertensive effects. Studies have documented either a small decline in arterial pressure (5% to 7% mm Hg) or no change at all.[41] A meta-analysis of 8 trials revealed 3 studies that concluded garlic significantly reduced systolic blood pressure, and 4 studies that found reductions in diastolic blood pressure in patients with mild hypertension.[42]
With regard to potential adverse effects, garlic has been shown to inhibit platelet aggregation in vitro[43-45] and in vivo[46]; thus, it should be used with great caution in individuals with bleeding disorders or in those who are receiving antiplatelet therapy.[47] There has been 1 report of a spontaneous epidural hematoma occurring with garlic supplementation, but this appears to be an isolated case.[48]
Garlic may also decrease warfarin concentrations.[49-51] Studies to date have not confirmed this interaction[52,53]; but particularly close monitoring of the international normalization ratio (INR) for patients taking both garlic and warfarin is prudent. Patients taking garlic supplements should discontinue use 7 to 10 days prior to having surgical procedures to avoid the potential for prolonged bleeding.[54]
The most prominent side effect of garlic supplementation is malodorous breath and garlic-like body odor.
Take-home message: Garlic should be used cautiously in individuals receiving antihypertensive medications, and blood pressure should be monitored carefully; orthostatic hypotension is a rare complication for those on antihypertensives.[55] Also, garlic should be avoided in those with a history of orthostasis or unexplained dizziness as well as in patients taking drugs that can increase bleeding, such as aspirin, warfarin and ibuprofen. A lack of standardization of garlic products and formulations makes it difficult to recommend a dose or specific product. For dyslipidemia, patients may benefit from taking 600 to 1200 mg of garlic powder daily in divided doses, or up to 4 g of raw garlic daily.
Ginkgo Biloba for Enhancing Memory, Combating Alzheimer's Disease
Ginkgo biloba is one of the oldest species of living trees, and ginkgo supplements are derived from the tree's leaves. This herbal remedy is marketed to improve memory, particularly in elderly individuals. While its mechanism of action is not fully understood, ginkgo contains flavonoids, terpenoids, and organic acids that are believed to act as free radical scavengers. These constituents have been shown to:
* Inhibit platelet activation factor (reducing thrombosis);
* Dilate arteries and capillaries; and
* Block the release of chemotactic factors and inflammatory mediators.
Studies in the United States have found that ginkgo stabilized -- and in some cases improved -- cognitive function and socialization in patients with Alzheimer's disease, although the clinical significance of the improvement was not known.[56,57] LeBars and colleagues[56] reviewed 2020 patients in an intention-to-treat analysis that resulted in a 1.4-point advantage over placebo in the Alzheimer's Disease Assessment Scale-Cognitive subscale.
In addition, studies have also demonstrated that the standardized extract of ginkgo biloba (EgB) 761, is effective in reducing symptoms of claudication, giving patients a 50% increase in pain-free walking distance.[58]
In contrast, a recent clinical trial failed to demonstrate any improvement in cognitive function or in the quality of life in cognitively intact, older individuals.[59]
Ginkgo is considered relatively safe, although the leaves have been associated with mild gastrointestinal side effects and headache. Ingestion of ginkgo seeds may result in serious neurologic and allergic reactions; therefore, they are not used for medical purposes.[60,61] Ingestion of leaf-based extracts has been associated with a spontaneous hyphema (blood in the anterior chamber of the eye) in an elderly man,[62] and with spontaneous subdural hematomas.[63] However, while some isolated adverse events such as these exist, it is considered safe when used as directed.
Ginkgolide B, an active component of ginkgo biloba, is a potent inhibitor of platelet-activating factor, which is necessary for normal platelet aggregation. As with garlic, it should be avoided in patients using anticoagulants or antiplatelet therapy, or in those who have active bleeding such as peptic ulcer disease. Based on case reports, ginkgo is not recommended in patients with seizure disorders.[64-67]
Standardization of product and recommended dosing is lacking, but a typical dose is 40 mg to 80 mg taken 3 times daily, standardized to 24% to 27% ginkgo flavone glycosides and 6% to 7% triterpines per dose. A dose of ginkgo extract EGb 761 at 160 mg daily has shown equivalent efficacy compared with donepezil 5 mg daily for the treatment of Alzheimer's disease.[68]
Take-home message: Ginkgo is a reasonable therapeutic option in patients with Alzheimer's disease who are also receiving medical care, but providers should remember that the herb has antiplatelet activity and thus may not be appropriate for patients with bleeding disorder or on antiplatelet or anticoagulation agents.
St. John's Wort Used for Depression
This yellow flowering plant (Hypericum perforatum) is named after St. John the Baptist. Extracts of the flower have been used for centuries to treat mental illnesses. The herbal product has 10 constituents, of which hypericin is believed to be the most active ingredient in treating depression.St. John's wort has a high affinity for gamma-aminobutyric acid, which, when stimulated, produces an antidepressant effect.[69] Hypericin also appears to activate dopamine receptors and inhibit serotonin receptor expression. In vitro, it has been shown to block reuptake of serotonin and norepinephrine.[70] These mechanisms may explain the lag time associated with the effectiveness of the herb.
A number of studies have examined the effectiveness of St. John's wort in depression.[71,72] A meta-analysis of 23 controlled trials concluded that it was more effective than placebo in treating mild-to-moderate depression.[72] In a 12-week study of 135 depressed patients, the herbal extract (900 mg per day) was found to be more effective than fluoxetine (20 mg per day).[73] Other investigators have confirmed the herb's efficacy over placebo in mild-to-moderate depression.[74]
Because of its pharmacology, St. John's wort should not be taken with prescription serotonin uptake inhibitors, as symptoms of serotonin syndrome have been observed with co-administration (headache, sweating, dizziness, and agitation).[75-77, 85]
In terms of other contraindications, St. John's wort should be avoided during pregnancy.[78,79] It has been associated with photosensitivity.[80] Studies have shown that the herbal product can reduce plasma concentrations of digoxin[77,81] and indinavir.[77,82,83] There have been cases of heart transplant rejection associated with the use of St. John's wort that resulted from a reduction in cyclosporine plasma concentrations.[84,85] Breakthrough bleeding and unwanted pregnancies have been reported in women on concomitant therapy of oral contraceptives and St. John's wort extract.[85,86] This is likely a result of St John's wort-induced decreases in ethinyl estradiol or metabolite concentrations due to the herb's ability to induce cytochrome P450 (CYP450)-3A4 isoenzyme.
Take-home message: Patients who are depressed should not take this herb without medical supervision. St. John's wort should be reserved for the mildly depressed patient with an aversion to prescription medication. Clinicians who recommend this botanical should be mindful of the numerous potential drug interactions arising from enzyme induction. The most commonly studied dose for depression is 300 mg taken 3 times a day, standardized to 0.3% to 0.5% hypericin per dose.
Other reports have estimated that 25% of patients who seek medical attention for a serious medical problem are using "unconventional" therapies, and 70% of those patients do not disclose those practices to their physician.[2,3] One survey estimated that about 18% of the US population uses herbal therapy on a regular basis.[4]
Herbal products and dietary supplements are widely available in supermarkets and other retail outlets, as well as by mail order. In fact, only a small percentage of these products (4.5%) are actually sold in pharmacies.[5] Many patients believe they derive health benefits from these herbal preparations, yet some remain skeptical and may seek advice from health professionals prior to use. Thus, it is important for all health professionals to be informed about available products and to be aware of any potential problems associated with their use.
Concerns About Herbal Products and Dietary Supplements
Unlike prescription and over-the-counter drugs, herbal products are not regulated by the US Food and Drug Administration (FDA) to determine purity or potency.[6] In fact, some products may contain contaminants, and their potency is dependent on many factors, such as the climate and soil conditions where they are grown, harvested, and stored.[7] Some herbal preparations have even been found to contain prescription drugs and heavy metals as unlabeled ingredients, and in some cases, these contaminants have resulted in toxicities.[8-17]
The labeling of herbal products is regulated by the Dietary Supplement Health and Education Act of 1994 (DSHEA).[18] Under this law, manufacturers may only make general claims about a supplement's effect on the structure or function of the human body (eg, "supports the immune system"). They must include the following statement in their labeling: "This product is not intended to diagnose, treat, cure, or prevent any disease."
The labels on herbal products are designed to promote product use and not necessarily to inform the consumer, so health professionals should be equipped with a general understanding of popular herbs and supplements, including knowledge of efficacy, common side effects, risks, and interactions. In addition, they should prospectively seek information regarding their patients' use of unconventional medicines to avoid adverse consequences.
Consumers should be advised that manufacturers of herbal supplements are not required to demonstrate safety or efficacy prior to marketing. Before the FDA can remove a product from the market, the agency must prove that the product is unsafe or ineffective. Recent examples of this include the ban on products containing ephedra due to adverse cardiovascular effects,[19] and the prohibition of kava amid concerns about hepatotoxicity.[20]
Patients with medical illness should not use herbs and dietary supplements without medical supervision. As will be discussed, some herbal products have adverse effects and may interact with prescribed medications. Furthermore, many conditions that patients try to diagnose or treat themselves may be serious, requiring a careful history and examination by a healthcare professional. For example, unsupervised use of saw palmetto for urinary symptoms may delay a diagnosis of prostate cancer.[21] Similarly, patients with symptoms such as chronic insomnia, anxiety, and depressed mood should see their health provider. Patients with cardiovascular disease, hypertension, heart failure, and hyperlipidemia should be under a healthcare professional's care and receive appropriate prescription drugs.
The following is an overview of some of the most commonly used herbal products, including important clinical considerations in the use of these products.
Echinacea for Fighting Cold Symptoms, Boosting Immunity
Echinacea is one of the most popular herbs in the United States, extracted from the purple coneflower that is native to North America. Species include Echinacea purpurea, Echinacea angustifolia, and Echinacea pallida. It has been studied as an adjunct therapy to enhance the immune system, mostly in upper respiratory tract infections, and these studies have produced mixed results.[22,23]
A recent meta-analysis concluded that standardized extracts of echinacea were effective in the prevention of common cold symptoms after clinical inoculation, when compared with placebo.[23] The authors of that study concluded that the likelihood of experiencing a cold was 55% higher with placebo than with echinacea (P < .043).
Some antiviral and bacteriostatic properties have been demonstrated in vitro, and the herb also appears to stimulate the production of cytokines (interferon, tumor necrosis factor, and interleukins).[24] Animal studies have revealed probable mechanisms of echinacea-induced immune enhancement, such as increasing the number of circulating white blood cells.[25]
Common side effects of echinacea supplements include unpleasant taste and allergic reactions. Because the flower is related to ragweed, cross allergenicity may occur in individuals allergic to ragweed.[26,27]
Echinacea is not recommended in patients with progressive or autoimmune disorders, including acquired immunodeficiency syndrome, tuberculosis, multiple sclerosis, collagen disorders, and diabetes mellitus. Theoretically, since echinacea alters the immune system, these disorders may be exacerbated.[28,29] Persistent use of echinacea has been associated with hepatotoxicity, so it should not be taken by patients who are taking other known hepatotoxins such as anabolic steroids, amiodarone, methotrexate, or ketoconazole.[30]
While not all randomized controlled trials performed to date have shown benefit for Echinacea over placebo,[22,31] a Cochrane review in 2006 concluded that the aerial parts of Echinacea purpurea might be effective for early treatment of colds in adults.[32]
Unfortunately, the optimal dose of echinacea is unknown, and multiple formulations exist, such as capsules, tinctures, teas, and extracted plant juice. Recommended dosages vary widely; for instance, capsules of Echinacea purpurea extract range from 100 to 500 mg, with manufacturers' suggested use ranging from 1 to 4 times daily for common cold prevention.
Take-home message: Clinicians should inform patients that a wide variety of Echinacea preparations and doses have been studied and results are inconsistent, making it difficult to recommend specific products. However, E. purpurea seems to be modestly effective for preventing the common cold in those at risk (eg, sick contacts). Evidence that the herb may reduce the duration of cold symptoms has been mixed. Patients allergic to ragweed, with progressive autoimmune disorders, and on hepatotoxic drugs should avoid echinacea.
Garlic: Warding Off Cardiovascular Disease?
Allium sativum, commonly known as garlic, has been used for centuries in cooking because of its flavoring properties. Today, it is used therapeutically by many consumers to prevent heart disease by controlling high cholesterol and high blood pressure. The suggested active ingredients are allicin and alliin.Numerous studies, however, have produced conflicting results regarding garlic's ability to lower lipids.[33-40] Positive findings in 3 trials exhibited a lowering of cholesterol in the range of 6.1% to 11.5%, primarily due to the lowering of low-density lipoproteins.[33-36] Other studies have yielded neutral or conflicting results.[37-39] One 12-week study tested the use of garlic powder in ambulatory patients, finding a 14% reduction of serum cholesterol.[40]
Garlic may have modest antihypertensive effects. Studies have documented either a small decline in arterial pressure (5% to 7% mm Hg) or no change at all.[41] A meta-analysis of 8 trials revealed 3 studies that concluded garlic significantly reduced systolic blood pressure, and 4 studies that found reductions in diastolic blood pressure in patients with mild hypertension.[42]
With regard to potential adverse effects, garlic has been shown to inhibit platelet aggregation in vitro[43-45] and in vivo[46]; thus, it should be used with great caution in individuals with bleeding disorders or in those who are receiving antiplatelet therapy.[47] There has been 1 report of a spontaneous epidural hematoma occurring with garlic supplementation, but this appears to be an isolated case.[48]
Garlic may also decrease warfarin concentrations.[49-51] Studies to date have not confirmed this interaction[52,53]; but particularly close monitoring of the international normalization ratio (INR) for patients taking both garlic and warfarin is prudent. Patients taking garlic supplements should discontinue use 7 to 10 days prior to having surgical procedures to avoid the potential for prolonged bleeding.[54]
The most prominent side effect of garlic supplementation is malodorous breath and garlic-like body odor.
Take-home message: Garlic should be used cautiously in individuals receiving antihypertensive medications, and blood pressure should be monitored carefully; orthostatic hypotension is a rare complication for those on antihypertensives.[55] Also, garlic should be avoided in those with a history of orthostasis or unexplained dizziness as well as in patients taking drugs that can increase bleeding, such as aspirin, warfarin and ibuprofen. A lack of standardization of garlic products and formulations makes it difficult to recommend a dose or specific product. For dyslipidemia, patients may benefit from taking 600 to 1200 mg of garlic powder daily in divided doses, or up to 4 g of raw garlic daily.
Ginkgo Biloba for Enhancing Memory, Combating Alzheimer's Disease
Ginkgo biloba is one of the oldest species of living trees, and ginkgo supplements are derived from the tree's leaves. This herbal remedy is marketed to improve memory, particularly in elderly individuals. While its mechanism of action is not fully understood, ginkgo contains flavonoids, terpenoids, and organic acids that are believed to act as free radical scavengers. These constituents have been shown to:
* Inhibit platelet activation factor (reducing thrombosis);
* Dilate arteries and capillaries; and
* Block the release of chemotactic factors and inflammatory mediators.
Studies in the United States have found that ginkgo stabilized -- and in some cases improved -- cognitive function and socialization in patients with Alzheimer's disease, although the clinical significance of the improvement was not known.[56,57] LeBars and colleagues[56] reviewed 2020 patients in an intention-to-treat analysis that resulted in a 1.4-point advantage over placebo in the Alzheimer's Disease Assessment Scale-Cognitive subscale.
In addition, studies have also demonstrated that the standardized extract of ginkgo biloba (EgB) 761, is effective in reducing symptoms of claudication, giving patients a 50% increase in pain-free walking distance.[58]
In contrast, a recent clinical trial failed to demonstrate any improvement in cognitive function or in the quality of life in cognitively intact, older individuals.[59]
Ginkgo is considered relatively safe, although the leaves have been associated with mild gastrointestinal side effects and headache. Ingestion of ginkgo seeds may result in serious neurologic and allergic reactions; therefore, they are not used for medical purposes.[60,61] Ingestion of leaf-based extracts has been associated with a spontaneous hyphema (blood in the anterior chamber of the eye) in an elderly man,[62] and with spontaneous subdural hematomas.[63] However, while some isolated adverse events such as these exist, it is considered safe when used as directed.
Ginkgolide B, an active component of ginkgo biloba, is a potent inhibitor of platelet-activating factor, which is necessary for normal platelet aggregation. As with garlic, it should be avoided in patients using anticoagulants or antiplatelet therapy, or in those who have active bleeding such as peptic ulcer disease. Based on case reports, ginkgo is not recommended in patients with seizure disorders.[64-67]
Standardization of product and recommended dosing is lacking, but a typical dose is 40 mg to 80 mg taken 3 times daily, standardized to 24% to 27% ginkgo flavone glycosides and 6% to 7% triterpines per dose. A dose of ginkgo extract EGb 761 at 160 mg daily has shown equivalent efficacy compared with donepezil 5 mg daily for the treatment of Alzheimer's disease.[68]
Take-home message: Ginkgo is a reasonable therapeutic option in patients with Alzheimer's disease who are also receiving medical care, but providers should remember that the herb has antiplatelet activity and thus may not be appropriate for patients with bleeding disorder or on antiplatelet or anticoagulation agents.
St. John's Wort Used for Depression
This yellow flowering plant (Hypericum perforatum) is named after St. John the Baptist. Extracts of the flower have been used for centuries to treat mental illnesses. The herbal product has 10 constituents, of which hypericin is believed to be the most active ingredient in treating depression.St. John's wort has a high affinity for gamma-aminobutyric acid, which, when stimulated, produces an antidepressant effect.[69] Hypericin also appears to activate dopamine receptors and inhibit serotonin receptor expression. In vitro, it has been shown to block reuptake of serotonin and norepinephrine.[70] These mechanisms may explain the lag time associated with the effectiveness of the herb.
A number of studies have examined the effectiveness of St. John's wort in depression.[71,72] A meta-analysis of 23 controlled trials concluded that it was more effective than placebo in treating mild-to-moderate depression.[72] In a 12-week study of 135 depressed patients, the herbal extract (900 mg per day) was found to be more effective than fluoxetine (20 mg per day).[73] Other investigators have confirmed the herb's efficacy over placebo in mild-to-moderate depression.[74]
Because of its pharmacology, St. John's wort should not be taken with prescription serotonin uptake inhibitors, as symptoms of serotonin syndrome have been observed with co-administration (headache, sweating, dizziness, and agitation).[75-77, 85]
In terms of other contraindications, St. John's wort should be avoided during pregnancy.[78,79] It has been associated with photosensitivity.[80] Studies have shown that the herbal product can reduce plasma concentrations of digoxin[77,81] and indinavir.[77,82,83] There have been cases of heart transplant rejection associated with the use of St. John's wort that resulted from a reduction in cyclosporine plasma concentrations.[84,85] Breakthrough bleeding and unwanted pregnancies have been reported in women on concomitant therapy of oral contraceptives and St. John's wort extract.[85,86] This is likely a result of St John's wort-induced decreases in ethinyl estradiol or metabolite concentrations due to the herb's ability to induce cytochrome P450 (CYP450)-3A4 isoenzyme.
Take-home message: Patients who are depressed should not take this herb without medical supervision. St. John's wort should be reserved for the mildly depressed patient with an aversion to prescription medication. Clinicians who recommend this botanical should be mindful of the numerous potential drug interactions arising from enzyme induction. The most commonly studied dose for depression is 300 mg taken 3 times a day, standardized to 0.3% to 0.5% hypericin per dose.
143
Kesehatan / [INFO] Drug Induced Hypertension
« on: 11 December 2008, 07:45:20 PM »
Introduction
Pharmacists often receive inquiries about the effects of medications on blood pressure. For example, concerns about OTC cough and cold products still arise even though some ingredients, such as phenylpropanolamine, have been removed from the U.S. market. While only a few classes of drugs cause clinically significant increases in arterial pressure, pharmacists should be aware of drugs that may interfere with effective blood pressure control. A review of drug-drug interactions with antihypertensive agents is beyond the scope of this article. However, some of the more common examples of druginduced hypertension will be discussed ( Table 1 ). Drug-induced blood pressure elevations represent an important and modifiable cause of secondary hypertension; therefore, it is imperative that pharmacists recognize this causal relationship.
Sympathomimetic Agents
It is well established that sympathomimetic amines cause dose-related increases in blood pressure.[1-4] While sympathomimetic-induced hypertension may not be clinically significant in healthy patients, it can become hazardous in others.[1-4] Sympathomimetic amines include amphetamines and similar compounds, such as pseudoephedrine, phenylpropanolamine, and ephedrine. Historically, these compounds were contained in some OTC cough and cold preparations. Because phenylpropanolamine use was correlated with hypertension and stroke, the FDA banned it from the market in November 2000.[3,4]
Pseudoephedrine
Pseudoephedrine is a bronchodilator and nasal vasoconstrictor that is generally innocuous when used in recommended doses. However, due to its potential for misuse, many retailers restrict its sale to behind the counter. Pseudoephedrine is commonly used to treat symptoms of rhinitis and rhinorrhea, but its effects on blood pressure and heart rate remain uncertain. Because of its pharmacologic similarity to ephedrine and phenylpropanolamine, use of pseudoephedrine has likewise been avoided in hypertensive patients.
Salerno et al assessed whether pseudoephedrine causes clinically meaningful elevations in blood pressure and heart rate.[5] In this meta-analysis, the primary data extracted included systolic and diastolic blood pressure and heart rate. Twenty-four clinical trials had extractable vital sign information and included a total of 1,285 patients. This analysis demonstrated that pseudoephedrine causes a small mean increase in systolic blood pressure (approximately 1 mmHg), with no significant effect on diastolic blood pressure, and a slight increase in heart rate (about 3 beats per minute). Immediate-release formulations had a greater effect than sustained-release formulations, which would be expected based on pharmacokinetics. Among immediate-release formulations, there was a dose-related increase in all three cardiovascular variables. More substantial increases in both systolic and diastolic blood pressure were noted with increasing doses of pseudoephedrine. Women seemed to be slightly less susceptible to the cardiovascular effects than men. In patients whose hypertension was stable and controlled, pseudoephedrine therapy increased systolic blood pressure but had no effect on diastolic pressure. There was no effect on heart rate in treated hypertensive patients, though this may have been because many patients were receiving beta-blockers. There was no documentation of any clinically significant adverse outcomes, such as hypertensive emergencies, stroke, or arrhythmia. Other investigators have similarly concluded that when it is used at standard doses, pseudoephedrine does not have a clinically significant effect on systolic or diastolic blood pressure in patients with controlled hypertension.[6]
Pharmacists should counsel patients that pseudoephedrine may modestly increase blood pressure and heart rate. These effects are greatest with immediaterelease formulations, higher doses, and short-term medication administration. Patients with stable, controlled hypertension do not seem to be at higher risk for blood pressure elevation compared to those without hypertension. However, one cannot predict how any individual patient will react. The risk-benefit ratio should be evaluated carefully before using any sympathomimetic agent in persons with hypertension. Pharmacists should instruct patients with cardiovascular disease to monitor their blood pressures carefully after starting pseudoephedrine- containing medications. Sustained-release products would generally be preferred to avoid increases in blood pressure. Alternatively, intranasal decongestants such as oxymetazoline could be used, since they have not been shown to induce hypertension when used at recommended doses.[7]
Amphetamine Derivates
A variety of drugs used for narcolepsy and attention-deficit/hyperactivity disorder are chemically related to amphetamine. These central nervous system (CNS) stimulants include dextroamphetamine, methamphetamine, and methylphenidate. The FDA recently issued a warning for dextroamphetamine, stating that using CNS-stimulant treatment at usual doses in children and adolescents with serious heart problems and structural cardiac abnormalities has been associated with sudden death.[8] However, adverse cardiovascular events induced by stimulants are not limited to children. Adults with known cardiac disease have also shown increased risk of sudden death with stimulant use at normal doses. As a general rule, amphetamine-related compounds (i.e., CNS stimulants) should be avoided in patients with known serious structural cardiac abnormalities, cardiomyopathy, serious heart rhythm abnormalities, or other serious cardiac problems that increase the risk of sudden death. Increases in both heart rate and blood pressure have been observed in children receiving drugs in this class.[9] Thus, this potential cardiovascular risk should be balanced against the beneficial behavioral effects of these medications.
NSAIDs and COX-2 Inhibitors
Nonsteroidal anti-inflammatory drugs (NSAIDs) have potentially adverse effects on blood pressure.[10,11] NSAIDs block both cyclooxygenase-1 (COX-1) and COX-2 enzymes, which leads to a reduction in prostaglandin formation. These drugs can have widespread beneficial and harmful effects, depending on the patient context. Drug-induced hypertension associated with NSAIDs is due to the renal effects of these drugs. Specifically, NSAIDs cause dose-related increases in sodium and water retention. This effect is also seen with COX-2 selective agents, such as celecoxib.[11]
The COX-1 and COX-2 isoforms are both expressed within the normal adult kidney, with COX-1 in the glomerulus and afferent arteriole and COX-2 in the afferent arteriole, the podocytes, and macula densa.[12] The specific location of each of these isoenzymes in the kidney translates into notably different effects on renal function. The prostaglandins produced by COX-1 primarily affect renal homeostasis by promoting vasodilation in the renal vascular bed, reducing renal vascular resistance, and consequently increasing renal perfusion. Prostaglandins produced by the COX- 2 isoenzyme have diuretic and natriuretic effects.[12,13] In patients who are hemodynamically compromised, the effects of the two isoenzymes are essential for the maintenance of renal perfusion because of their vasodilatory effects. Because NSAIDs block the production of the COX-1 and COX-2 prostaglandins, renal side effects are not uncommon, occurring in approximately 1% to 5% of NSAID users.[13]
By inhibiting COX-2's natriuretic effect, thereby increasing sodium retention, all NSAIDs carry with them the consequent risk of increased fluid retention.[14] Additionally, the inhibition of vasodilating prostaglandins and the production of vasoconstricting factors, namely endothelin-1, can contribute to the induction of hypertension in a normotensive and/or controlled hypertensive patient.[14]
In a comparison of celecoxib with diclofenac conducted in 287 patients with arthritis, cardiovascular and renal side effects were seen in 79 patients (27.8%), with hypertension being the most common (16.6%).[14] There was no statistical difference in the incidence of hypertension between the traditional NSAID and COX-2 groups. This initiation of hypertension by NSAIDs is especially important in the discussion of COX-2 safety in light of the fact that hypertensive status is a key risk factor in the progression of virtually all cardiovascular diseases including stroke, myocardial infarction, and congestive heart failure.[15]
A recent meta-analysis of COX-2 inhibitors and their effects on blood pressure was published.[16] Data were collected in 45,451 patients from 19 clinical trials. Interestingly, there appeared to be a somewhat greater blood pressure elevation with COX- 2 inhibitors compared with placebo and nonselective NSAIDs (e.g., ibuprofen and diclofenac). Rofecoxib appeared to confer a greater risk of developing clinically important elevations in both systolic and diastolic pressures in comparison to celecoxib. However, rofecoxib was voluntarily pulled from the market in 2004 due to concerns about increased risk of heart attack and stroke.[17]
Because of the widespread availability of NSAIDs without a prescription, many patients with hypertension may be at risk for aggravated blood pressure effects caused by these drugs. Pharmacists should take a careful medication history and specifically inquire about OTC use of NSAIDs. Patients with hypertension should be more closely monitored for blood pressure elevations when using NSAIDs. Patients should be counseled that this adverse effect tends to be dose related, but it is not always predictable. The adverse effect of all NSAIDs and COX-2 inhibitors on blood pressure may have the most clinical significance in the elderly, in whom the prevalence of arthritis, hypertension, and NSAID use is high.[18]
Pharmacists often receive inquiries about the effects of medications on blood pressure. For example, concerns about OTC cough and cold products still arise even though some ingredients, such as phenylpropanolamine, have been removed from the U.S. market. While only a few classes of drugs cause clinically significant increases in arterial pressure, pharmacists should be aware of drugs that may interfere with effective blood pressure control. A review of drug-drug interactions with antihypertensive agents is beyond the scope of this article. However, some of the more common examples of druginduced hypertension will be discussed ( Table 1 ). Drug-induced blood pressure elevations represent an important and modifiable cause of secondary hypertension; therefore, it is imperative that pharmacists recognize this causal relationship.
Sympathomimetic Agents
It is well established that sympathomimetic amines cause dose-related increases in blood pressure.[1-4] While sympathomimetic-induced hypertension may not be clinically significant in healthy patients, it can become hazardous in others.[1-4] Sympathomimetic amines include amphetamines and similar compounds, such as pseudoephedrine, phenylpropanolamine, and ephedrine. Historically, these compounds were contained in some OTC cough and cold preparations. Because phenylpropanolamine use was correlated with hypertension and stroke, the FDA banned it from the market in November 2000.[3,4]
Pseudoephedrine
Pseudoephedrine is a bronchodilator and nasal vasoconstrictor that is generally innocuous when used in recommended doses. However, due to its potential for misuse, many retailers restrict its sale to behind the counter. Pseudoephedrine is commonly used to treat symptoms of rhinitis and rhinorrhea, but its effects on blood pressure and heart rate remain uncertain. Because of its pharmacologic similarity to ephedrine and phenylpropanolamine, use of pseudoephedrine has likewise been avoided in hypertensive patients.
Salerno et al assessed whether pseudoephedrine causes clinically meaningful elevations in blood pressure and heart rate.[5] In this meta-analysis, the primary data extracted included systolic and diastolic blood pressure and heart rate. Twenty-four clinical trials had extractable vital sign information and included a total of 1,285 patients. This analysis demonstrated that pseudoephedrine causes a small mean increase in systolic blood pressure (approximately 1 mmHg), with no significant effect on diastolic blood pressure, and a slight increase in heart rate (about 3 beats per minute). Immediate-release formulations had a greater effect than sustained-release formulations, which would be expected based on pharmacokinetics. Among immediate-release formulations, there was a dose-related increase in all three cardiovascular variables. More substantial increases in both systolic and diastolic blood pressure were noted with increasing doses of pseudoephedrine. Women seemed to be slightly less susceptible to the cardiovascular effects than men. In patients whose hypertension was stable and controlled, pseudoephedrine therapy increased systolic blood pressure but had no effect on diastolic pressure. There was no effect on heart rate in treated hypertensive patients, though this may have been because many patients were receiving beta-blockers. There was no documentation of any clinically significant adverse outcomes, such as hypertensive emergencies, stroke, or arrhythmia. Other investigators have similarly concluded that when it is used at standard doses, pseudoephedrine does not have a clinically significant effect on systolic or diastolic blood pressure in patients with controlled hypertension.[6]
Pharmacists should counsel patients that pseudoephedrine may modestly increase blood pressure and heart rate. These effects are greatest with immediaterelease formulations, higher doses, and short-term medication administration. Patients with stable, controlled hypertension do not seem to be at higher risk for blood pressure elevation compared to those without hypertension. However, one cannot predict how any individual patient will react. The risk-benefit ratio should be evaluated carefully before using any sympathomimetic agent in persons with hypertension. Pharmacists should instruct patients with cardiovascular disease to monitor their blood pressures carefully after starting pseudoephedrine- containing medications. Sustained-release products would generally be preferred to avoid increases in blood pressure. Alternatively, intranasal decongestants such as oxymetazoline could be used, since they have not been shown to induce hypertension when used at recommended doses.[7]
Amphetamine Derivates
A variety of drugs used for narcolepsy and attention-deficit/hyperactivity disorder are chemically related to amphetamine. These central nervous system (CNS) stimulants include dextroamphetamine, methamphetamine, and methylphenidate. The FDA recently issued a warning for dextroamphetamine, stating that using CNS-stimulant treatment at usual doses in children and adolescents with serious heart problems and structural cardiac abnormalities has been associated with sudden death.[8] However, adverse cardiovascular events induced by stimulants are not limited to children. Adults with known cardiac disease have also shown increased risk of sudden death with stimulant use at normal doses. As a general rule, amphetamine-related compounds (i.e., CNS stimulants) should be avoided in patients with known serious structural cardiac abnormalities, cardiomyopathy, serious heart rhythm abnormalities, or other serious cardiac problems that increase the risk of sudden death. Increases in both heart rate and blood pressure have been observed in children receiving drugs in this class.[9] Thus, this potential cardiovascular risk should be balanced against the beneficial behavioral effects of these medications.
NSAIDs and COX-2 Inhibitors
Nonsteroidal anti-inflammatory drugs (NSAIDs) have potentially adverse effects on blood pressure.[10,11] NSAIDs block both cyclooxygenase-1 (COX-1) and COX-2 enzymes, which leads to a reduction in prostaglandin formation. These drugs can have widespread beneficial and harmful effects, depending on the patient context. Drug-induced hypertension associated with NSAIDs is due to the renal effects of these drugs. Specifically, NSAIDs cause dose-related increases in sodium and water retention. This effect is also seen with COX-2 selective agents, such as celecoxib.[11]
The COX-1 and COX-2 isoforms are both expressed within the normal adult kidney, with COX-1 in the glomerulus and afferent arteriole and COX-2 in the afferent arteriole, the podocytes, and macula densa.[12] The specific location of each of these isoenzymes in the kidney translates into notably different effects on renal function. The prostaglandins produced by COX-1 primarily affect renal homeostasis by promoting vasodilation in the renal vascular bed, reducing renal vascular resistance, and consequently increasing renal perfusion. Prostaglandins produced by the COX- 2 isoenzyme have diuretic and natriuretic effects.[12,13] In patients who are hemodynamically compromised, the effects of the two isoenzymes are essential for the maintenance of renal perfusion because of their vasodilatory effects. Because NSAIDs block the production of the COX-1 and COX-2 prostaglandins, renal side effects are not uncommon, occurring in approximately 1% to 5% of NSAID users.[13]
By inhibiting COX-2's natriuretic effect, thereby increasing sodium retention, all NSAIDs carry with them the consequent risk of increased fluid retention.[14] Additionally, the inhibition of vasodilating prostaglandins and the production of vasoconstricting factors, namely endothelin-1, can contribute to the induction of hypertension in a normotensive and/or controlled hypertensive patient.[14]
In a comparison of celecoxib with diclofenac conducted in 287 patients with arthritis, cardiovascular and renal side effects were seen in 79 patients (27.8%), with hypertension being the most common (16.6%).[14] There was no statistical difference in the incidence of hypertension between the traditional NSAID and COX-2 groups. This initiation of hypertension by NSAIDs is especially important in the discussion of COX-2 safety in light of the fact that hypertensive status is a key risk factor in the progression of virtually all cardiovascular diseases including stroke, myocardial infarction, and congestive heart failure.[15]
A recent meta-analysis of COX-2 inhibitors and their effects on blood pressure was published.[16] Data were collected in 45,451 patients from 19 clinical trials. Interestingly, there appeared to be a somewhat greater blood pressure elevation with COX- 2 inhibitors compared with placebo and nonselective NSAIDs (e.g., ibuprofen and diclofenac). Rofecoxib appeared to confer a greater risk of developing clinically important elevations in both systolic and diastolic pressures in comparison to celecoxib. However, rofecoxib was voluntarily pulled from the market in 2004 due to concerns about increased risk of heart attack and stroke.[17]
Because of the widespread availability of NSAIDs without a prescription, many patients with hypertension may be at risk for aggravated blood pressure effects caused by these drugs. Pharmacists should take a careful medication history and specifically inquire about OTC use of NSAIDs. Patients with hypertension should be more closely monitored for blood pressure elevations when using NSAIDs. Patients should be counseled that this adverse effect tends to be dose related, but it is not always predictable. The adverse effect of all NSAIDs and COX-2 inhibitors on blood pressure may have the most clinical significance in the elderly, in whom the prevalence of arthritis, hypertension, and NSAID use is high.[18]
144
Politik, ekonomi, Sosial dan budaya Umum / Bank Indonesia Mencabut dan Menarik 4 Pecahan Uang Kertas dari Peredaran
« on: 06 December 2008, 04:22:57 PM »
Sumber Data
Biro Hubungan Masyarakat
Tanggal : 26-11-2008
Contact : Biro Humas, Telp : (62-21) 381-7187 Fax : (62-21) 350-1867, E-mail : humasbi [at] bi.go. id
Lampiran
No. 10/ 61 /PSHM/Humas
Bank Indonesia terhitung mulai tanggal 31 Desember 2008, melalui Peraturan Bank Indonesia (PBI) No. 10/33/PBI/2008 secara resmi mencabut dan menarik 4 (empat) pecahan uang kertas dari peredaran. Pecahan uang kertas yang dicabut dan ditarik adalah sebagai berikut:
1. Rp10.000 Tahun Emisi (TE) 1998 (Gambar Muka: Pahlawan Nasional Cut Nyak Dhien),
2. Rp20.000 Tahun Emisi (TE) 1998 (Gambar Muka: Pahlawan Nasional Ki Hajar Dewantara),
3. Rp50.000 Tahun Emisi (TE) 1999 (Gambar Muka: Pahlawan Nasional WR. Soepratman), dan
4. Rp100.000 Tahun Emisi (TE) 1999 (Gambar Muka: Pahlawan Proklamator Dr.Ir.Soekarno dan Dr. H. Mohammad Hatta, berbahan polymer).
“Bank Indonesia secara rutin melakukan pencabutan dan penarikan uang rupiah. Hal tersebut dilakukan dengan pertimbangan antara lain masa edar yang cukup lama dan perkembangan teknologi unsur pengaman (security features) pada uang”, demikian disampaikan S. Budi Rochadi, Deputi Gubernur bidang Pengedaran Uang.
Dengan pencabutan dan penarikan uang rupiah dari peredaran maka terhitung mulai tanggal 31 Desember 2008, empat pecahan uang tersebut tidak berlaku lagi sebagai alat pembayaran yang sah (legal tender).
Namun demikian, bagi masyarakat yang masih memegang uang pecahan-pecahan tersebut dapat melakukan penukaran dengan uang rupiah pecahan yang sama atau pecahan lainnya yang masih berlaku di kantor-kantor Bank Indonesia atau bank umum terdekat. Batas waktu penukaran empat uang pecahan tersebut di bank umum adalah sampai dengan tanggal 30 Desember 2013 atau 5 (lima) tahun sejak pencabutan dan penarikan uang tersebut. Sementara itu, batas waktu penukaran di Bank Indonesia adalah sampai dengan tanggal 30 Desember 2018 atau selama 10 (sepuluh) tahun sejak tanggal pencabutan. Hak untuk menuntut penukaran empat pecahan uang rupiah yang dicabut dan ditarik tersebut tidak berlaku lagi setelah 10 (sepuluh) tahun terhitung tanggal 31 Desember 2018.
Jakarta, 26 November 2008
BIRO HUBUNGAN MASYARAKAT
Filianingsih Hendarta
Kepala Biro
Source : From forwarded mail
Biro Hubungan Masyarakat
Tanggal : 26-11-2008
Contact : Biro Humas, Telp : (62-21) 381-7187 Fax : (62-21) 350-1867, E-mail : humasbi [at] bi.go. id
Lampiran
No. 10/ 61 /PSHM/Humas
Bank Indonesia terhitung mulai tanggal 31 Desember 2008, melalui Peraturan Bank Indonesia (PBI) No. 10/33/PBI/2008 secara resmi mencabut dan menarik 4 (empat) pecahan uang kertas dari peredaran. Pecahan uang kertas yang dicabut dan ditarik adalah sebagai berikut:
1. Rp10.000 Tahun Emisi (TE) 1998 (Gambar Muka: Pahlawan Nasional Cut Nyak Dhien),
2. Rp20.000 Tahun Emisi (TE) 1998 (Gambar Muka: Pahlawan Nasional Ki Hajar Dewantara),
3. Rp50.000 Tahun Emisi (TE) 1999 (Gambar Muka: Pahlawan Nasional WR. Soepratman), dan
4. Rp100.000 Tahun Emisi (TE) 1999 (Gambar Muka: Pahlawan Proklamator Dr.Ir.Soekarno dan Dr. H. Mohammad Hatta, berbahan polymer).
“Bank Indonesia secara rutin melakukan pencabutan dan penarikan uang rupiah. Hal tersebut dilakukan dengan pertimbangan antara lain masa edar yang cukup lama dan perkembangan teknologi unsur pengaman (security features) pada uang”, demikian disampaikan S. Budi Rochadi, Deputi Gubernur bidang Pengedaran Uang.
Dengan pencabutan dan penarikan uang rupiah dari peredaran maka terhitung mulai tanggal 31 Desember 2008, empat pecahan uang tersebut tidak berlaku lagi sebagai alat pembayaran yang sah (legal tender).
Namun demikian, bagi masyarakat yang masih memegang uang pecahan-pecahan tersebut dapat melakukan penukaran dengan uang rupiah pecahan yang sama atau pecahan lainnya yang masih berlaku di kantor-kantor Bank Indonesia atau bank umum terdekat. Batas waktu penukaran empat uang pecahan tersebut di bank umum adalah sampai dengan tanggal 30 Desember 2013 atau 5 (lima) tahun sejak pencabutan dan penarikan uang tersebut. Sementara itu, batas waktu penukaran di Bank Indonesia adalah sampai dengan tanggal 30 Desember 2018 atau selama 10 (sepuluh) tahun sejak tanggal pencabutan. Hak untuk menuntut penukaran empat pecahan uang rupiah yang dicabut dan ditarik tersebut tidak berlaku lagi setelah 10 (sepuluh) tahun terhitung tanggal 31 Desember 2018.
Jakarta, 26 November 2008
BIRO HUBUNGAN MASYARAKAT
Filianingsih Hendarta
Kepala Biro
Source : From forwarded mail
145
Film / JOURNEY TO THE CENTER OF THE EARTH
« on: 06 December 2008, 11:05:17 AM »
Saat melakukan ekspedisi ke Iceland, ilmuwan Trevor Anderson (Brendan Fraser), keponakannya Sean (John Hutcherson) dan pemandu mereka yang cantik, Hannah (Anita Briem), terperangkap di sebuah gua dimana jalan keluarnya hanya membawa mereka semakin dalam menuju inti Bumi. Menyusuri dunia yang belum pernah dikunjungi orang sebelumnya, trio penjelajah itu bertemu dengan makhluk-makhluk yang tidak terbayangkan – termasuk manusia pemakan tumbuhan, piranha terbang raksasa, burung bersinar dan dinosaurus dari masa lalu. Ternyata, akan ada ledakan vulkanik dan mereka harus menemukan jalan keluar dari perut bumi tersebut sebelum terlambat.
Film yang oks banget.. ada burung unik.. yang bisa shining blue..
Film yang oks banget.. ada burung unik.. yang bisa shining blue..
146
Seremonial / Happy Birthday Eurika Winata
« on: 03 December 2008, 10:16:55 PM »
Happy Birthday Eurika Winata a.k.a calon arahat
Semoga semakin maju dalam praktek dhamma..
Semoga cepat selesai kuliah kedokterannya dan menjadi dokter yang menjaga pancasila buddhist
Mohon bantuannya selalu di board Kesehatan
Semoga semakin maju dalam praktek dhamma..
Semoga cepat selesai kuliah kedokterannya dan menjadi dokter yang menjaga pancasila buddhist
Mohon bantuannya selalu di board Kesehatan
147
Kesehatan / [PUBLIC] Ginkgo biloba & Alzheimer
« on: 29 November 2008, 01:20:43 PM »
November 20, 2008 — Results of a randomized trial show no beneficial effect of Ginkgo biloba in the prevention of Alzheimer's disease or dementia in subjects with normal cognition or in those with mild cognitive impairment.
The findings from the Ginkgo Evaluation of Memory (GEM) trial are published in the November 19 issue of the Journal of the American Medical Association.
The results of this trial are published hard on the heels of a negative trial with other supplements, vitamin E and vitamin C, in the prevention of cardiovascular disease and stroke in the Physicians' Health Study II. Results of that study were published in the November 12 issue of the Journal of the American Medical Association and were reported at the American Heart Association Scientific Sessions 2008. A second analysis looking at cancer was reported this week at the American Association on Cancer Research prevention conference and, similarly, showed no benefit of either agent in the prevention of cancer.
These outcomes underline the importance of randomized controlled clinical trials to assess the safety and efficacy of these agents, said GEM study coauthor Steven T. DeKosky, MD, from the University of Pittsburgh in Pittsburgh, Pennsylvania, and now is at the University of Virginia School of Medicine in Charlottesville.
"One of the major outcomes of this study is we proved you can actually do the study," he told Medscape Neurology & Neurosurgery. GEM is among the first trials that recruited a new cohort to look at a cognitive outcome using a supplement to actually finish and report findings. "It's disappointing," he says of their results, "but it's the way the science has to be done. The design would have been identical if it were a medication from a major pharmaceutical company, and not an over-the-counter alternative medication."
Preservation of Memory
In their study, the authors note that G biloba is prescribed in some areas of the world for the preservation of memory, although no medications are approved for the primary prevention of dementia. In the United States, worldwide sales of G biloba exceed $249 million annually.
The purported effect of G biloba is by the action of multiple antioxidants, although a recent in vitro study also suggested that has an antiamyloid aggregation effect, they note. Studies of G biloba in the setting of dementia have had mixed results, although a Cochrane Collaboration Review in 2007 found the evidence of a benefit, "not convincing," the study authors write.
The current study was a randomized, placebo-controlled clinical trial carried out at 5 academic medical centers in the United States to see whether treatment with G biloba in a dose of 120 mg 2 times/day could prevent incident dementia or Alzheimer's disease vs placebo. A total of 2587 subjects older than 75 years with normal cognition at baseline, and 482 subjects with mild cognitive impairment were included. Patients were assessed every 6 months for dementia.
After a median follow-up of 6.1 years, 523 subjects were diagnosed with dementia, 246 (16.1%) in the group taking placebo, and 277 (17.9%) in those taking G biloba. Of the total dementia cases, 92% were classified as possible or probable Alzheimer's disease or Alzheimer's disease with evidence of cerebrovascular disease.
The rate of total dementia did not differ between groups, with 3.3 vs 2.9 cases per 100 person-years with G biloba vs placebo. The rates of Alzheimer-type dementia were also similar, at 3.0 vs 2.6 cases per 100 person-years with G biloba vs placebo.
Table 1. GEM: Risk for Dementia and Alzheimer's Disease With Ginkgo Biloba vs Placebo*
Endpoint Hazard Ratio 95% CI P value
All-cause dementia 1.12 0.94 - 1.33 .21
Alzheimer's disease 1.16 0.97 - 1.39 .11
*GEM indicates Ginkgo Evaluation of Memory.
Similarly, there was no effect of treatment on the rate of progression to dementia in those with mild cognitive impairment.
Table 2. GEM: Risk for Dementia With Ginkgo Biloba vs Placebo in Patients With Mild Cognitive Impairment*
Endpoint Hazard Ratio 95% CI P value
All-cause dementia 1.13 0.85 - 1.50 .39
*GEM indicates Ginkgo Evaluation of Memory.
Adverse events were similar between groups, and there was no statistically significant difference in the rates of serious adverse events or mortality. Of note, there was no difference in the rates of major bleeding between groups or in the bleeding incidence in those taking aspirin.
Because of previous concerns about possible bleeding risk with G biloba, the protocol called for discontinuation of the study drug with the institution of warfarin therapy that resulted in the dropout of 214 subjects: 112 in the G biloba and 102 in the placebo group.
There were twice as many hemorrhagic strokes in the G biloba group vs placebo (16 vs
, but the number of cases was small and was not significant in this analysis, they note. The study authors suggest this effect should be explored in future studies.
An exploratory analysis did show a statistically significant interaction with treatment for those with a history of cardiovascular disease at baseline, with a hazard ratio (HR) of 1.56 (P = .006) with treatment vs placebo. This higher rate, they write, "is puzzling and should be viewed with caution," given the lack of evidence from basic science of a mechanism.
"What we take away from this is that it's safe, which is useful if there are other uses found for it," Dr. DeKosky said. For example, G biloba is also being investigated in the treatment of tinnitus, he noted.
They are also interested to see the results from the GuidAge trial being conducted in France, which is similar in size and scope and is using the same dose of the same standardized preparation but is not expected to report for another year. "I don't have high expectations of course that it will have something different than what we found, but it's another study looking at prevention," he said.
"Untenable" to Recommend Without Evidence
In an editorial accompanying the publication, Lon S. Schneider, MD, from the University of Southern California, Los Angeles, points out that the GEM trial is the largest and longest trial that "comprises the substantial bulk the non–industry-funded, placebo-controlled clinical database for G biloba extract" and provides no evidence that it contributes to clinically meaningful dementia risk reduction.
There was no reduction either in cardiovascular serious adverse events or in total mortality rates — 2 secondary endpoints of the trial, Dr. Schneider notes. The relationship with cardiovascular disease, though, is "potentially more complex," he adds, in that subgroup analyses showed an increased risk for dementia in those with cardiovascular disease at baseline and a nonsignificant increase in hemorrhagic stroke with treatment, although vascular dementia was lower with G biloba.
Although these observations may be the result of chance, they suggest that, "at least in patients aged 75 years or older with cardiovascular disease, G biloba may have risks and the decision to use this agent should be carefully considered," he writes.
"Users of this extract should not expect it to be helpful," Dr. Schneider concludes. "Moreover, the potential adverse effects of G biloba extract illustrate why it is untenable to recommend a drug or nutraceutical in the absence of efficacy evidence simply because it could possibly help and initially appears harmless."
Short-Term Improvements?
Dr. Schneider added that results for 2 other secondary outcomes — overall cognitive decline and functional disability — are not reported in this study, although he speculates that it is unlikely that they are positive in the setting of an overall negative trial. Nevertheless, the effects of treatment on actual cognitive test scores and daily function ratings "are important because individuals without cognitive impairment who use G biloba may expect it to noticeably improve their intellectual function over the short term but not necessarily to prevent Alzheimer disease or other dementia in the long term."
Dr. DeKosky noted that these 2 secondary endpoints will be published at a later date. The follow-up testing on these endpoints was less sensitive to small changes in cognitive function, he explains. "We are going to look at those data and see if we can find something in there that gives us a signal, but that actually turns out to be a bit more complicated an analysis, and so we knew we would not be able to put it into this study in which there were some singular outcome and safety issues that we knew everyone would want to know about," he said.
The trial was supported by the National Center for Complementary and Alternative Medicine; the Office of Dietary Supplements and National Institute on Aging; National Heart, Lung, and Blood Institute; University of Pittsburgh Alzheimer's Disease Research Center; Roena Kulynych Center for Memory and Cognition Research; Wake Forest University School of Medicine; and the National Institute of Neurological Disorders and Stroke. Schwab Pharmaceuticals, Karlsruhe, Germany, provided the G biloba tablets and placebo in identical packaging. Dr. DeKosky has received grants or research support from Elan, Myriad, Neurochem, and GlaxoSmithKline and has served on the advisory boards of, or consulting for, AstraZeneca, Abbott, Baxter, Daichi, Eisai, Forest, Genentech, GlaxoSmithKline, Lilly, Medivation, Merck, NeuroPharma, Neuroptix, Pfizer, Myriad, and Servier. The other study authors have disclosed no relevant relationships.
JAMA. 2008;300:2253-2262.
Learning Objectives for This Educational Activity
Upon completion of this activity, participants will be able to:
1. Describe the effect of Ginkgo biloba on all-cause dementia in elderly patients with and without mild cognitive impairment.
2. Describe the effect of Ginkgo biloba on Alzheimer's disease.
Clinical Context
Dementia is a chronic illness affecting more than 5 million people in the United States and is a leading cause of age-related disability. The herbal product G biloba has been proposed as an agent that may protect against cognitive decline by its multiple antioxidative actions and antiamyloid effect. However, randomized clinical trials of G biloba are needed to assess its role in the primary prevention of dementia.
This is a randomized, double-blind, placebo-controlled trial to examine the effect of G biloba supplementation on dementia, Alzheimer's disease, and cognitive decline in elderly adults.
Study Highlights
* Included were volunteers aged 75 years or older from 5 academic centers in 4 US communities with normal cognitive function or mild cognitive impairment.
* Excluded were those with a diagnosis of dementia or psychiatric disease; those taking cholinesterase inhibitors or other agents for cognitive problems or dementia; those with Parkinson's disease and other degenerative neurologic disease; and those with abnormal thyroid function, cardiovascular disease, or bleeding disorders.
* 1545 participants were randomly assigned to receive 120 mg twice daily of G biloba standardized extract (a high-potency dose) and 1524 to placebo.
* Among those randomly assigned, 2587 had normal cognition and 482 had mild cognitive impairment.
* Treatment adherence was tracked by counting pills in blister packs.
* Primary outcome was a diagnosis of dementia or Alzheimer's disease with Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, criteria.
* Secondary outcomes were overall cognitive decline and function, cardiovascular disease, and total mortality rate.
* The baseline battery of tests included memory, construction, language, attention/psychomotor speed, executive functions, and premorbid intellectual functioning.
* Participants were recruited for 2 years and were followed up for a median of 6.1 years.
* During follow-up, participants were tested every 6 months. If dementia was diagnosed, they were assigned to one of the following categories: Alzheimer's disease; Alzheimer's and vascular dementia; vascular dementia only; and dementia, other cause.
* Mean age at baseline was 79 years, 46% were women, 95% were white, one quarter had any history of cardiovascular disease, and 10% had a history of myocardial infarction.
* During the intervention period, dementia developed in 523 participants: 246 (16.1%) in the placebo group and 277 (17.9%) in the G biloba group.
* 92% were classified as having Alzheimer's disease.
* 6.3% were lost to follow-up.
* Adherence was 60.3% and did not differ between assigned groups.
* The cumulative rate of all-cause dementia was not statistically significantly different in the 2 groups: 3.3 vs 2.9 per 100 person-years (HR, 1.12 for G biloba vs placebo).
* The rate of Alzheimer's disease did not differ significantly between the 2 groups.
* There was no effect of modification by age, sex, or mild cognitive impairment.
* For a small subgroup with baseline cardiovascular disease, the HR for dementia in the G biloba group was 1.56 (P = .006), and there was no difference for those without baseline cardiovascular disease.
* There was no indication of interaction between apolipoprotein E status and treatment.
* Rates of adverse events were similar between the treatment and placebo groups.
* There were no differences in rate of coronary artery disease.
* The authors concluded that 240 mg of G biloba daily for 6 years was not effective in reducing the incidence of dementia in elderly patients with normal or mildly impaired cognition.
Pearls for Practice
* Use of 240-mg G biloba daily in elderly patients is not associated with reduced risk for all-cause dementia in those with normal or mildly impaired cognition.
* Use of 240-mg G biloba daily in elderly patients is not associated with reduced risk for Alzheimer's disease.
According to the study by DeKosky and colleagues, which of the following best describes the effect of 240 mg of G biloba daily in elderly patients?
G biloba reduces the rate of dementia in those with mild cognitive impairment
G biloba has no effect on dementia in those with normal cognition
G biloba reduces dementia rate in women only
G biloba slows dementia rate in those with dementia
According to the study by DeKosky and colleagues, G biloba may have an effect on rate of Alzheimer's disease in which of the following groups of elderly patients?
Women
Those with baseline cardiovascular disease
Those with mild cognitive impairment
Those with a positive family history of Alzheimer's disease
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This article is intended for primary care clinicians, neurologists, geriatricians, and other specialists who care for older adults at risk for dementia or Alzheimer's disease.
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CME Author
Désirée Lie, MD, MSEd
Clinical Professor, Family Medicine, University of California, Orange; Director, Division of Faculty Development, UCI Medical Center, Orange, California
Disclosure: Désirée Lie, MD, MSEd, has disclosed no relevant financial relationships.
The findings from the Ginkgo Evaluation of Memory (GEM) trial are published in the November 19 issue of the Journal of the American Medical Association.
The results of this trial are published hard on the heels of a negative trial with other supplements, vitamin E and vitamin C, in the prevention of cardiovascular disease and stroke in the Physicians' Health Study II. Results of that study were published in the November 12 issue of the Journal of the American Medical Association and were reported at the American Heart Association Scientific Sessions 2008. A second analysis looking at cancer was reported this week at the American Association on Cancer Research prevention conference and, similarly, showed no benefit of either agent in the prevention of cancer.
These outcomes underline the importance of randomized controlled clinical trials to assess the safety and efficacy of these agents, said GEM study coauthor Steven T. DeKosky, MD, from the University of Pittsburgh in Pittsburgh, Pennsylvania, and now is at the University of Virginia School of Medicine in Charlottesville.
"One of the major outcomes of this study is we proved you can actually do the study," he told Medscape Neurology & Neurosurgery. GEM is among the first trials that recruited a new cohort to look at a cognitive outcome using a supplement to actually finish and report findings. "It's disappointing," he says of their results, "but it's the way the science has to be done. The design would have been identical if it were a medication from a major pharmaceutical company, and not an over-the-counter alternative medication."
Preservation of Memory
In their study, the authors note that G biloba is prescribed in some areas of the world for the preservation of memory, although no medications are approved for the primary prevention of dementia. In the United States, worldwide sales of G biloba exceed $249 million annually.
The purported effect of G biloba is by the action of multiple antioxidants, although a recent in vitro study also suggested that has an antiamyloid aggregation effect, they note. Studies of G biloba in the setting of dementia have had mixed results, although a Cochrane Collaboration Review in 2007 found the evidence of a benefit, "not convincing," the study authors write.
The current study was a randomized, placebo-controlled clinical trial carried out at 5 academic medical centers in the United States to see whether treatment with G biloba in a dose of 120 mg 2 times/day could prevent incident dementia or Alzheimer's disease vs placebo. A total of 2587 subjects older than 75 years with normal cognition at baseline, and 482 subjects with mild cognitive impairment were included. Patients were assessed every 6 months for dementia.
After a median follow-up of 6.1 years, 523 subjects were diagnosed with dementia, 246 (16.1%) in the group taking placebo, and 277 (17.9%) in those taking G biloba. Of the total dementia cases, 92% were classified as possible or probable Alzheimer's disease or Alzheimer's disease with evidence of cerebrovascular disease.
The rate of total dementia did not differ between groups, with 3.3 vs 2.9 cases per 100 person-years with G biloba vs placebo. The rates of Alzheimer-type dementia were also similar, at 3.0 vs 2.6 cases per 100 person-years with G biloba vs placebo.
Table 1. GEM: Risk for Dementia and Alzheimer's Disease With Ginkgo Biloba vs Placebo*
Endpoint Hazard Ratio 95% CI P value
All-cause dementia 1.12 0.94 - 1.33 .21
Alzheimer's disease 1.16 0.97 - 1.39 .11
*GEM indicates Ginkgo Evaluation of Memory.
Similarly, there was no effect of treatment on the rate of progression to dementia in those with mild cognitive impairment.
Table 2. GEM: Risk for Dementia With Ginkgo Biloba vs Placebo in Patients With Mild Cognitive Impairment*
Endpoint Hazard Ratio 95% CI P value
All-cause dementia 1.13 0.85 - 1.50 .39
*GEM indicates Ginkgo Evaluation of Memory.
Adverse events were similar between groups, and there was no statistically significant difference in the rates of serious adverse events or mortality. Of note, there was no difference in the rates of major bleeding between groups or in the bleeding incidence in those taking aspirin.
Because of previous concerns about possible bleeding risk with G biloba, the protocol called for discontinuation of the study drug with the institution of warfarin therapy that resulted in the dropout of 214 subjects: 112 in the G biloba and 102 in the placebo group.
There were twice as many hemorrhagic strokes in the G biloba group vs placebo (16 vs
, but the number of cases was small and was not significant in this analysis, they note. The study authors suggest this effect should be explored in future studies.An exploratory analysis did show a statistically significant interaction with treatment for those with a history of cardiovascular disease at baseline, with a hazard ratio (HR) of 1.56 (P = .006) with treatment vs placebo. This higher rate, they write, "is puzzling and should be viewed with caution," given the lack of evidence from basic science of a mechanism.
"What we take away from this is that it's safe, which is useful if there are other uses found for it," Dr. DeKosky said. For example, G biloba is also being investigated in the treatment of tinnitus, he noted.
They are also interested to see the results from the GuidAge trial being conducted in France, which is similar in size and scope and is using the same dose of the same standardized preparation but is not expected to report for another year. "I don't have high expectations of course that it will have something different than what we found, but it's another study looking at prevention," he said.
"Untenable" to Recommend Without Evidence
In an editorial accompanying the publication, Lon S. Schneider, MD, from the University of Southern California, Los Angeles, points out that the GEM trial is the largest and longest trial that "comprises the substantial bulk the non–industry-funded, placebo-controlled clinical database for G biloba extract" and provides no evidence that it contributes to clinically meaningful dementia risk reduction.
There was no reduction either in cardiovascular serious adverse events or in total mortality rates — 2 secondary endpoints of the trial, Dr. Schneider notes. The relationship with cardiovascular disease, though, is "potentially more complex," he adds, in that subgroup analyses showed an increased risk for dementia in those with cardiovascular disease at baseline and a nonsignificant increase in hemorrhagic stroke with treatment, although vascular dementia was lower with G biloba.
Although these observations may be the result of chance, they suggest that, "at least in patients aged 75 years or older with cardiovascular disease, G biloba may have risks and the decision to use this agent should be carefully considered," he writes.
"Users of this extract should not expect it to be helpful," Dr. Schneider concludes. "Moreover, the potential adverse effects of G biloba extract illustrate why it is untenable to recommend a drug or nutraceutical in the absence of efficacy evidence simply because it could possibly help and initially appears harmless."
Short-Term Improvements?
Dr. Schneider added that results for 2 other secondary outcomes — overall cognitive decline and functional disability — are not reported in this study, although he speculates that it is unlikely that they are positive in the setting of an overall negative trial. Nevertheless, the effects of treatment on actual cognitive test scores and daily function ratings "are important because individuals without cognitive impairment who use G biloba may expect it to noticeably improve their intellectual function over the short term but not necessarily to prevent Alzheimer disease or other dementia in the long term."
Dr. DeKosky noted that these 2 secondary endpoints will be published at a later date. The follow-up testing on these endpoints was less sensitive to small changes in cognitive function, he explains. "We are going to look at those data and see if we can find something in there that gives us a signal, but that actually turns out to be a bit more complicated an analysis, and so we knew we would not be able to put it into this study in which there were some singular outcome and safety issues that we knew everyone would want to know about," he said.
The trial was supported by the National Center for Complementary and Alternative Medicine; the Office of Dietary Supplements and National Institute on Aging; National Heart, Lung, and Blood Institute; University of Pittsburgh Alzheimer's Disease Research Center; Roena Kulynych Center for Memory and Cognition Research; Wake Forest University School of Medicine; and the National Institute of Neurological Disorders and Stroke. Schwab Pharmaceuticals, Karlsruhe, Germany, provided the G biloba tablets and placebo in identical packaging. Dr. DeKosky has received grants or research support from Elan, Myriad, Neurochem, and GlaxoSmithKline and has served on the advisory boards of, or consulting for, AstraZeneca, Abbott, Baxter, Daichi, Eisai, Forest, Genentech, GlaxoSmithKline, Lilly, Medivation, Merck, NeuroPharma, Neuroptix, Pfizer, Myriad, and Servier. The other study authors have disclosed no relevant relationships.
JAMA. 2008;300:2253-2262.
Learning Objectives for This Educational Activity
Upon completion of this activity, participants will be able to:
1. Describe the effect of Ginkgo biloba on all-cause dementia in elderly patients with and without mild cognitive impairment.
2. Describe the effect of Ginkgo biloba on Alzheimer's disease.
Clinical Context
Dementia is a chronic illness affecting more than 5 million people in the United States and is a leading cause of age-related disability. The herbal product G biloba has been proposed as an agent that may protect against cognitive decline by its multiple antioxidative actions and antiamyloid effect. However, randomized clinical trials of G biloba are needed to assess its role in the primary prevention of dementia.
This is a randomized, double-blind, placebo-controlled trial to examine the effect of G biloba supplementation on dementia, Alzheimer's disease, and cognitive decline in elderly adults.
Study Highlights
* Included were volunteers aged 75 years or older from 5 academic centers in 4 US communities with normal cognitive function or mild cognitive impairment.
* Excluded were those with a diagnosis of dementia or psychiatric disease; those taking cholinesterase inhibitors or other agents for cognitive problems or dementia; those with Parkinson's disease and other degenerative neurologic disease; and those with abnormal thyroid function, cardiovascular disease, or bleeding disorders.
* 1545 participants were randomly assigned to receive 120 mg twice daily of G biloba standardized extract (a high-potency dose) and 1524 to placebo.
* Among those randomly assigned, 2587 had normal cognition and 482 had mild cognitive impairment.
* Treatment adherence was tracked by counting pills in blister packs.
* Primary outcome was a diagnosis of dementia or Alzheimer's disease with Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, criteria.
* Secondary outcomes were overall cognitive decline and function, cardiovascular disease, and total mortality rate.
* The baseline battery of tests included memory, construction, language, attention/psychomotor speed, executive functions, and premorbid intellectual functioning.
* Participants were recruited for 2 years and were followed up for a median of 6.1 years.
* During follow-up, participants were tested every 6 months. If dementia was diagnosed, they were assigned to one of the following categories: Alzheimer's disease; Alzheimer's and vascular dementia; vascular dementia only; and dementia, other cause.
* Mean age at baseline was 79 years, 46% were women, 95% were white, one quarter had any history of cardiovascular disease, and 10% had a history of myocardial infarction.
* During the intervention period, dementia developed in 523 participants: 246 (16.1%) in the placebo group and 277 (17.9%) in the G biloba group.
* 92% were classified as having Alzheimer's disease.
* 6.3% were lost to follow-up.
* Adherence was 60.3% and did not differ between assigned groups.
* The cumulative rate of all-cause dementia was not statistically significantly different in the 2 groups: 3.3 vs 2.9 per 100 person-years (HR, 1.12 for G biloba vs placebo).
* The rate of Alzheimer's disease did not differ significantly between the 2 groups.
* There was no effect of modification by age, sex, or mild cognitive impairment.
* For a small subgroup with baseline cardiovascular disease, the HR for dementia in the G biloba group was 1.56 (P = .006), and there was no difference for those without baseline cardiovascular disease.
* There was no indication of interaction between apolipoprotein E status and treatment.
* Rates of adverse events were similar between the treatment and placebo groups.
* There were no differences in rate of coronary artery disease.
* The authors concluded that 240 mg of G biloba daily for 6 years was not effective in reducing the incidence of dementia in elderly patients with normal or mildly impaired cognition.
Pearls for Practice
* Use of 240-mg G biloba daily in elderly patients is not associated with reduced risk for all-cause dementia in those with normal or mildly impaired cognition.
* Use of 240-mg G biloba daily in elderly patients is not associated with reduced risk for Alzheimer's disease.
According to the study by DeKosky and colleagues, which of the following best describes the effect of 240 mg of G biloba daily in elderly patients?
G biloba reduces the rate of dementia in those with mild cognitive impairment
G biloba has no effect on dementia in those with normal cognition
G biloba reduces dementia rate in women only
G biloba slows dementia rate in those with dementia
According to the study by DeKosky and colleagues, G biloba may have an effect on rate of Alzheimer's disease in which of the following groups of elderly patients?
Women
Those with baseline cardiovascular disease
Those with mild cognitive impairment
Those with a positive family history of Alzheimer's disease
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Disclosure: Susan Jeffrey has disclosed no relevant financial relationships.
CME Author
Désirée Lie, MD, MSEd
Clinical Professor, Family Medicine, University of California, Orange; Director, Division of Faculty Development, UCI Medical Center, Orange, California
Disclosure: Désirée Lie, MD, MSEd, has disclosed no relevant financial relationships.
148
Kesehatan / [PUBLIC] Calsium Supplementation
« on: 29 November 2008, 01:18:13 PM »
Tackling the Myths and Realities of Calcium Supplementation in CKD: An Expert Interview With Sophie A. Jamal, MD, PhD
Anne Le, PharmD, RPh
Medscape Nephrology. 2008; ©2008 Medscape
Posted 11/14/2008
Editor's Note
In patients with chronic kidney disease (CKD), disturbances of mineral metabolism are associated with significant morbidity and mortality. Unfortunately, recent evidence shows that treatment with calcium-based phosphate binders contributes to increasing coronary artery and aorta calcification compared with non-calcium-containing binders. It has also been shown that hyperphosphatemia and excess exogenous calcium administration can accelerate vascular calcification. Therefore, calcium-based phosphate binders should be avoided in many, if not most of CKD patients undergoing dialysis. Anne G. Le, PharmD, RPh, Editorial Director of Medscape Nephrology, spoke with Sophie A. Jamal, MD, PhD, Assistant Professor/Clinician Scientist at the University of Toronto and Clinical & Research Director of the Osteoporosis Program at Women's College Hospital in Toronto, about the use of calcium supplementation in CKD, the impact of high phosphorus levels, the prevalence of hypocalcemia, and the management of calcification.
Medscape: Can you tell us if there is any scientific evidence that shows that calcium has a direct impact on osteoporosis in the general population and in patients with chronic kidney disease [CKD]?
Sophie A. Jamal, MD, PhD: There are 2 parts to this question: the first concerns the relationship between calcium supplementation and osteoporosis in the general population. When we think about calcium supplementation and osteoporosis prevention in the general population, there are 2 groups to consider: young men and women acquiring peak bone mass, older men and postmenopausal women. Calcium plays an important role in enhancing the acquisition of peak bone mass. Most studies of calcium for osteoporosis prevention have included vitamin D supplementation and it is very difficult to tease out whether it is the calcium or vitamin D that influences fracture risk. There has been a meta-analysis that examined the effects of modest amounts of vitamin D 400 IU a day with calcium supplementation, and that data demonstrate that in women 45 years or older, calcium supplementation over about 2 years or so modestly prevents decreases in bone mineral density.[1] That systematic review also demonstrated a trend for fewer spinal fractures among calcium-supplemented patients; however, that didn't reach statistical significance. Indeed, there are no data that definitively demonstrate that calcium alone reduces fracture incidence. Probably a reasonable approach in healthy postmenopausal women and men would be to ensure an adequate but not excessive calcium intake.
Regarding patients with chronic kidney disease and osteoporosis, there are no data that demonstrate that giving calcium in the form of either a calcium binder or a calcium supplement, either in dietary or dairy, reduces the risk of osteoporotic fracture.
Medscape: Is there any evidence that calcium has a direct impact on arterial calcification in the CKD population?
Dr. Jamal: Yes, there have been 2 observational studies in patients with stage 5 CKD that demonstrated a positive association between calcium supplementation, calcium phosphate cross-product, and arterial calcification measured with EBCT [electron beam computed tomography] or with ultrasound.[2,3] There has also been a randomized control trial that compared calcium-based binders vs non-calcium-based binders regarding a progression in vascular calcification.[4] The trial demonstrated that patients who were randomized to the non-calcium binder, in this case, the sevelamer, did not have a progression of arterial calcification, compared to patients who were randomized to the calcium-based binder.
Medscape: For the majority of patients with CKD stages 3-4, could you tell us if there is a medical need to give calcium beyond what is found in the diet, and what about for patients with CKD stage 5?
Dr. Jamal: Generally speaking, regardless of whether you have kidney disease or not, most men and women are not particularly good at obtaining calcium from their diet. It has been estimated that we take in 1-2 dairy servings a day -- which is equivalent to about 300-600 mg of calcium, so there is likely a need to supplement with calcium. The real crux of the matter, both at stages 3-4, as well as at stage 5, is the dose of the supplement. In patients with stage 5 kidney disease, there may be a mild calcium deficit so it may be reasonable to supplement those patients with a little bit more calcium than in patients with stages 3 and 4 kidney disease. However, it should be stressed that there are no data that identify the optimum amount of calcium supplementation. I think that decisions concerning calcium supplementation need to be done on an individual basis.
Medscape: From a physiologic standpoint, what happens when patients with CKD are given calcium therapy and where does that excess calcium go?
Dr. Jamal: That is a good question but unfortunately, there is no clear answer. In otherwise healthy men and women, a large proportion of calcium is taken up by the bone during remodeling. The concern about giving calcium to patients with CKD is that the calcium therapy will not be taken up by the bone.[3] In contrast, a large number of patients with CKD have unpaired bone remodeling (low turnover or adynamic bone) and as such calcium therapy will not be taken up by the bone and theoretically may deposit in other tissues -- such as the blood vessels or skin.
Medscape: Can you tell us if there is a role for calcium in the management of mineral and bone disorder associated with CKD?
Dr. Jamal: I think the role of calcium depends on the cause of the bone mineral disorder. Patients with CKD have a variety of different causes of bone mineral disorder, some of which respond appropriately to calcium and some of which don't. So, for example, if someone has hyperparathyroid bone disease due to end-stage CKD, calcium supplementation is not necessarily going to be an appropriate treatment for them. If someone had osteomalacia and there was a vitamin D deficiency, then vitamin D replacement with calcium may be helpful. Thus, the physician who is treating these patients needs to consider the underlying cause of the bone disease or the CKD mineral disorder before recommending calcium. Unfortunately, we will not have a general prescription that will apply to all patients with CKD mineral bone disorder.
Medscape: Can you describe what the correlation is between elevated serum phosphorus and calcification?
Dr. Jamal: Elevated serum phosphorus may result in an elevated calcium/phosphate cross-product. Regarding calcification, the issue is that the calcium will precipitate out and that could lead to calcification in the skin, in internal organs, and in blood vessels.
Medscape: Do you think more could be done to educate healthcare professionals about the importance of treating elevated serum phosphorus to goal in CKD stages 3 and 4?
Dr. Jamal: Absolutely. Physicians need to be educated about the fact that abnormalities in mineral metabolism start very early in chronic kidney disease. Indeed, they occur prior to starting dialysis and physicians should be testing for abnormalities in mineral metabolism in stages 3 and 4 kidney disease. Regarding treatment of elevated serum phosphorous, we need to reconsider what level of serum phosphorous we should be aiming to achieve and how we should meet this goal. To apply a prescription of lowering the phosphorus by a certain amount with a particular product may not be the best approach. Indeed, an individualized treatment approach based on factors such as the state of renal disease and the underlying bone mineral disorder may be better.
Medscape: Do you think using a non-calcium sub-element binder like sevelamer provides added cardiovascular benefit by attenuating the degree of calcification in patients with CKD, and if so, does this apply to all stages of CKD?
Dr. Jamal: It is important when discussing cardiovascular benefit to distinguish between arterial calcification and clinical vascular endpoints. Prospective randomized control trials demonstrate that sevelamer does prevent the progression of arterial calcification. Thus, theoretically, if we can prevent the progression of arterial calcification, we may be able to prevent vascular mortality and morbidity. The underlying assumption here is that vascular calcification leads to an increase in vascular morbidity and mortality. Unfortunately this hypothesis has not been proven. We know that giving treatment with a non-calcium-based binder prevents progression of arterial calcification, but what we don't know is whether preventing that progression of arterial calcification decreases cardiovascular morbidity and mortality and while this makes physiologic sense, given the lack of data, we need to be very cautious in drawing these types of conclusions. Clearly, we need further studies in this area.
Medscape: Why do you think that calcium binders are seen as a preferred first line treatment in CKD stages 3 and 4, when in fact prevalence of hypocalcemia in these patients is as low as 5% in stage 3 patients, and only 20% in stage 4 patients?
Dr. Jamal: The majority of physicians give a calcium binder to lower phosphorous, not to correct hypocalcemia; however, it is important to remember that a calcium binder is still calcium, which may increase serum calcium.
Medscape: Does calcium supplementation put patients with kidney disease at an increased risk for adverse cardiovascular events associated with calcium overload?
Dr. Jamal: That is the crucial clinical question. Unfortunately, we don't know the answer as of yet. We know that elevated serum calcium and elevated calcium phosphate cross products lead to increased arterial calcification and increased mortality. We also know that giving a non-calcium-based binder will decrease arterial calcification, decrease serum calcium levels and theoretically will decrease calcium phosphate cross products. What we don't know is whether there is a direct link between arterial calcification, calcium phosphate cross products, and cardiovascular morbidity and mortality.
Medscape: For a long time now, it was thought that lipids are the only factor that will increase one's cardiac risk. Now is it safe to assume that we should add calcium to that list?
Dr. Jamal: Absolutely. Whether calcium in and of itself is a direct risk factor, needs further study. Patients with CKD are at an increased risk of cardiovascular disease and there are a multitude of factors that will increase that risk, some of which are related to the renal failure and those include things like anemia, hyperhomocystinuria, and perhaps -- arterial calcification.
Medscape: You touched on this a little bit before, but is there a widely held misconception in the medical community that patients with CKD stages 3-4 suffer from hypocalcemia and if so, how would you advise healthcare professionals to approach the issue of calcium supplementation in these patients?
Dr. Jamal: Some of this misconception comes from the fact that patients who have CKD do have an elevation in parathyroid hormone or PTH. Initially, it was hypothesized that this increase in PTH was due to low levels of serum calcium (which stimulates PTH secretion). However, further understanding of renal pathophysiology, particularly in early stages of CKD, has led most to agree that it is the elevated serum phosphorous that results in increased PTH and not decreased serum calcium. Hypocalcemia is very uncommon, particularly in early stages of CKD. Late in renal disease, there may be hypocalcemia related to 125 vitamin D deficiency, but this is also rare. Again, the best way to sort of deal with issues such as hypocalcemia is to treat the primary cause, so in the case of early kidney disease, a reasonable approach would be to try to lower levels of serum phosphorous, and later on it would be to replace vitamin D, as well as try to lower levels of serum phosphorus.
References
1. Shea B, Wells G, Cranney A, et al; for the Osteoporosis Methodology Group and the Osteoporosis Research Advisory Group. Meta-analysis of calcium supplementation for the prevention of postmenopausal osteoporosis. Endocr Rev. 2002;23:552-559. Abstract
2. Goodman WG, Goldin J, Kuizon BD, et al. Coronary-artery calcification in young adults with end-stage renal disease who are undergoing dialysis. N Engl J Med. 2000;342:1478-1483. Abstract
3. Mazhar AR, Johnson RJ, Gillen D, et al. Risk factors and mortality associated with calciphylaxis in end-stage renal disease. Kidney Int. 2001;60:324-332. Abstract
4. Ahmed S, O'Neill KD, Hood AF, Evan AP, Moe SM. Calciphylaxis is associated with hyperphosphatemia and increased osteopontin expression by vascular smooth muscle cells. Am J Kidney Dis. 2001;37:1267-1276. Abstract
Interviewer: Anne Le, PharmD, RPh, Editorial Director, Nephrology, Medscape, LLC, New York, NY
Interviewee: Sophie A. Jamal, MD, PhD, Assistant Professor/Clinician Scientist, Department of Medicine, University of Toronto, Toronto, Ontario, Canada; Clinical & Research Director, Osteoporosis Program, Women's College Hospital, Toronto, Ontario, Canada
Disclosure for Interviewer: Anne Le, PharmD, RPh, has disclosed no relevant financial relationships.
Disclosure for Interviewee: Sophie A. Jamal, MD, PhD, has disclosed no relevant financial relationships.
Anne Le, PharmD, RPh
Medscape Nephrology. 2008; ©2008 Medscape
Posted 11/14/2008
Editor's Note
In patients with chronic kidney disease (CKD), disturbances of mineral metabolism are associated with significant morbidity and mortality. Unfortunately, recent evidence shows that treatment with calcium-based phosphate binders contributes to increasing coronary artery and aorta calcification compared with non-calcium-containing binders. It has also been shown that hyperphosphatemia and excess exogenous calcium administration can accelerate vascular calcification. Therefore, calcium-based phosphate binders should be avoided in many, if not most of CKD patients undergoing dialysis. Anne G. Le, PharmD, RPh, Editorial Director of Medscape Nephrology, spoke with Sophie A. Jamal, MD, PhD, Assistant Professor/Clinician Scientist at the University of Toronto and Clinical & Research Director of the Osteoporosis Program at Women's College Hospital in Toronto, about the use of calcium supplementation in CKD, the impact of high phosphorus levels, the prevalence of hypocalcemia, and the management of calcification.
Medscape: Can you tell us if there is any scientific evidence that shows that calcium has a direct impact on osteoporosis in the general population and in patients with chronic kidney disease [CKD]?
Sophie A. Jamal, MD, PhD: There are 2 parts to this question: the first concerns the relationship between calcium supplementation and osteoporosis in the general population. When we think about calcium supplementation and osteoporosis prevention in the general population, there are 2 groups to consider: young men and women acquiring peak bone mass, older men and postmenopausal women. Calcium plays an important role in enhancing the acquisition of peak bone mass. Most studies of calcium for osteoporosis prevention have included vitamin D supplementation and it is very difficult to tease out whether it is the calcium or vitamin D that influences fracture risk. There has been a meta-analysis that examined the effects of modest amounts of vitamin D 400 IU a day with calcium supplementation, and that data demonstrate that in women 45 years or older, calcium supplementation over about 2 years or so modestly prevents decreases in bone mineral density.[1] That systematic review also demonstrated a trend for fewer spinal fractures among calcium-supplemented patients; however, that didn't reach statistical significance. Indeed, there are no data that definitively demonstrate that calcium alone reduces fracture incidence. Probably a reasonable approach in healthy postmenopausal women and men would be to ensure an adequate but not excessive calcium intake.
Regarding patients with chronic kidney disease and osteoporosis, there are no data that demonstrate that giving calcium in the form of either a calcium binder or a calcium supplement, either in dietary or dairy, reduces the risk of osteoporotic fracture.
Medscape: Is there any evidence that calcium has a direct impact on arterial calcification in the CKD population?
Dr. Jamal: Yes, there have been 2 observational studies in patients with stage 5 CKD that demonstrated a positive association between calcium supplementation, calcium phosphate cross-product, and arterial calcification measured with EBCT [electron beam computed tomography] or with ultrasound.[2,3] There has also been a randomized control trial that compared calcium-based binders vs non-calcium-based binders regarding a progression in vascular calcification.[4] The trial demonstrated that patients who were randomized to the non-calcium binder, in this case, the sevelamer, did not have a progression of arterial calcification, compared to patients who were randomized to the calcium-based binder.
Medscape: For the majority of patients with CKD stages 3-4, could you tell us if there is a medical need to give calcium beyond what is found in the diet, and what about for patients with CKD stage 5?
Dr. Jamal: Generally speaking, regardless of whether you have kidney disease or not, most men and women are not particularly good at obtaining calcium from their diet. It has been estimated that we take in 1-2 dairy servings a day -- which is equivalent to about 300-600 mg of calcium, so there is likely a need to supplement with calcium. The real crux of the matter, both at stages 3-4, as well as at stage 5, is the dose of the supplement. In patients with stage 5 kidney disease, there may be a mild calcium deficit so it may be reasonable to supplement those patients with a little bit more calcium than in patients with stages 3 and 4 kidney disease. However, it should be stressed that there are no data that identify the optimum amount of calcium supplementation. I think that decisions concerning calcium supplementation need to be done on an individual basis.
Medscape: From a physiologic standpoint, what happens when patients with CKD are given calcium therapy and where does that excess calcium go?
Dr. Jamal: That is a good question but unfortunately, there is no clear answer. In otherwise healthy men and women, a large proportion of calcium is taken up by the bone during remodeling. The concern about giving calcium to patients with CKD is that the calcium therapy will not be taken up by the bone.[3] In contrast, a large number of patients with CKD have unpaired bone remodeling (low turnover or adynamic bone) and as such calcium therapy will not be taken up by the bone and theoretically may deposit in other tissues -- such as the blood vessels or skin.
Medscape: Can you tell us if there is a role for calcium in the management of mineral and bone disorder associated with CKD?
Dr. Jamal: I think the role of calcium depends on the cause of the bone mineral disorder. Patients with CKD have a variety of different causes of bone mineral disorder, some of which respond appropriately to calcium and some of which don't. So, for example, if someone has hyperparathyroid bone disease due to end-stage CKD, calcium supplementation is not necessarily going to be an appropriate treatment for them. If someone had osteomalacia and there was a vitamin D deficiency, then vitamin D replacement with calcium may be helpful. Thus, the physician who is treating these patients needs to consider the underlying cause of the bone disease or the CKD mineral disorder before recommending calcium. Unfortunately, we will not have a general prescription that will apply to all patients with CKD mineral bone disorder.
Medscape: Can you describe what the correlation is between elevated serum phosphorus and calcification?
Dr. Jamal: Elevated serum phosphorus may result in an elevated calcium/phosphate cross-product. Regarding calcification, the issue is that the calcium will precipitate out and that could lead to calcification in the skin, in internal organs, and in blood vessels.
Medscape: Do you think more could be done to educate healthcare professionals about the importance of treating elevated serum phosphorus to goal in CKD stages 3 and 4?
Dr. Jamal: Absolutely. Physicians need to be educated about the fact that abnormalities in mineral metabolism start very early in chronic kidney disease. Indeed, they occur prior to starting dialysis and physicians should be testing for abnormalities in mineral metabolism in stages 3 and 4 kidney disease. Regarding treatment of elevated serum phosphorous, we need to reconsider what level of serum phosphorous we should be aiming to achieve and how we should meet this goal. To apply a prescription of lowering the phosphorus by a certain amount with a particular product may not be the best approach. Indeed, an individualized treatment approach based on factors such as the state of renal disease and the underlying bone mineral disorder may be better.
Medscape: Do you think using a non-calcium sub-element binder like sevelamer provides added cardiovascular benefit by attenuating the degree of calcification in patients with CKD, and if so, does this apply to all stages of CKD?
Dr. Jamal: It is important when discussing cardiovascular benefit to distinguish between arterial calcification and clinical vascular endpoints. Prospective randomized control trials demonstrate that sevelamer does prevent the progression of arterial calcification. Thus, theoretically, if we can prevent the progression of arterial calcification, we may be able to prevent vascular mortality and morbidity. The underlying assumption here is that vascular calcification leads to an increase in vascular morbidity and mortality. Unfortunately this hypothesis has not been proven. We know that giving treatment with a non-calcium-based binder prevents progression of arterial calcification, but what we don't know is whether preventing that progression of arterial calcification decreases cardiovascular morbidity and mortality and while this makes physiologic sense, given the lack of data, we need to be very cautious in drawing these types of conclusions. Clearly, we need further studies in this area.
Medscape: Why do you think that calcium binders are seen as a preferred first line treatment in CKD stages 3 and 4, when in fact prevalence of hypocalcemia in these patients is as low as 5% in stage 3 patients, and only 20% in stage 4 patients?
Dr. Jamal: The majority of physicians give a calcium binder to lower phosphorous, not to correct hypocalcemia; however, it is important to remember that a calcium binder is still calcium, which may increase serum calcium.
Medscape: Does calcium supplementation put patients with kidney disease at an increased risk for adverse cardiovascular events associated with calcium overload?
Dr. Jamal: That is the crucial clinical question. Unfortunately, we don't know the answer as of yet. We know that elevated serum calcium and elevated calcium phosphate cross products lead to increased arterial calcification and increased mortality. We also know that giving a non-calcium-based binder will decrease arterial calcification, decrease serum calcium levels and theoretically will decrease calcium phosphate cross products. What we don't know is whether there is a direct link between arterial calcification, calcium phosphate cross products, and cardiovascular morbidity and mortality.
Medscape: For a long time now, it was thought that lipids are the only factor that will increase one's cardiac risk. Now is it safe to assume that we should add calcium to that list?
Dr. Jamal: Absolutely. Whether calcium in and of itself is a direct risk factor, needs further study. Patients with CKD are at an increased risk of cardiovascular disease and there are a multitude of factors that will increase that risk, some of which are related to the renal failure and those include things like anemia, hyperhomocystinuria, and perhaps -- arterial calcification.
Medscape: You touched on this a little bit before, but is there a widely held misconception in the medical community that patients with CKD stages 3-4 suffer from hypocalcemia and if so, how would you advise healthcare professionals to approach the issue of calcium supplementation in these patients?
Dr. Jamal: Some of this misconception comes from the fact that patients who have CKD do have an elevation in parathyroid hormone or PTH. Initially, it was hypothesized that this increase in PTH was due to low levels of serum calcium (which stimulates PTH secretion). However, further understanding of renal pathophysiology, particularly in early stages of CKD, has led most to agree that it is the elevated serum phosphorous that results in increased PTH and not decreased serum calcium. Hypocalcemia is very uncommon, particularly in early stages of CKD. Late in renal disease, there may be hypocalcemia related to 125 vitamin D deficiency, but this is also rare. Again, the best way to sort of deal with issues such as hypocalcemia is to treat the primary cause, so in the case of early kidney disease, a reasonable approach would be to try to lower levels of serum phosphorous, and later on it would be to replace vitamin D, as well as try to lower levels of serum phosphorus.
References
1. Shea B, Wells G, Cranney A, et al; for the Osteoporosis Methodology Group and the Osteoporosis Research Advisory Group. Meta-analysis of calcium supplementation for the prevention of postmenopausal osteoporosis. Endocr Rev. 2002;23:552-559. Abstract
2. Goodman WG, Goldin J, Kuizon BD, et al. Coronary-artery calcification in young adults with end-stage renal disease who are undergoing dialysis. N Engl J Med. 2000;342:1478-1483. Abstract
3. Mazhar AR, Johnson RJ, Gillen D, et al. Risk factors and mortality associated with calciphylaxis in end-stage renal disease. Kidney Int. 2001;60:324-332. Abstract
4. Ahmed S, O'Neill KD, Hood AF, Evan AP, Moe SM. Calciphylaxis is associated with hyperphosphatemia and increased osteopontin expression by vascular smooth muscle cells. Am J Kidney Dis. 2001;37:1267-1276. Abstract
Interviewer: Anne Le, PharmD, RPh, Editorial Director, Nephrology, Medscape, LLC, New York, NY
Interviewee: Sophie A. Jamal, MD, PhD, Assistant Professor/Clinician Scientist, Department of Medicine, University of Toronto, Toronto, Ontario, Canada; Clinical & Research Director, Osteoporosis Program, Women's College Hospital, Toronto, Ontario, Canada
Disclosure for Interviewer: Anne Le, PharmD, RPh, has disclosed no relevant financial relationships.
Disclosure for Interviewee: Sophie A. Jamal, MD, PhD, has disclosed no relevant financial relationships.
149
Perkenalan / Hi.. Salam kenal dari Forte..
« on: 16 November 2008, 10:05:32 PM »
Hi.. Perkenalkan..
Aye Forte..
Mohon bimbingannya ya..
Aye Forte..
Mohon bimbingannya ya..
150
Kesehatan / [INFO] Ibuprofen Terbaik Atasi Demam Anak
« on: 13 November 2008, 09:15:27 PM »
Ibuprofen Terbaik Atasi Demam Anak
HASIL penelitian terbaru para ilmuwan Inggris menunjukkan ibuprofen terbukti lebih efektif menurunkan demam pada anak-anak daripada paracetamol. Riset yang dilakukan di kota Bristol ini menganjurkan ibuprofen sebaiknya dijadikan pilihan utama dalam pengobatan.
Untuk menguji kehandalan ibuprofen, peneliti dari Universitas Bristol dan University of the West of England melibatkan 156 anak berusia 6 bulan hingga enam tahun. Anak-anak yang diteliti adalah mereka yang temperatur tubuhnya mencapai 37,8 hingga 41 derajat akibat sakit yang ringan.
Dari hasil pantauan selama 48 jam terlihat bahwa kelompok anak yang mendapat obat ibuprofen temperaturnya rutun lebih cepat ketimbang kelompok paracetamol. Riset yang dimuat dalam British Medical Journal ini juga mengindikasikan bahwa penggunaan dua jenis obat secara bergantian dapat membantu, seperti halnya yang telah banyak direkomendasikan tenaga media di Inggris.
Namun para ahli kesehatan tidak sepakat dengan metode gabungan tersebut karena menyalahi prosedur pengobatan resmi. Yang dikhawatirkan adalah kemungkinan anak-anak akan mengalami kelebihan dosis.
Panduan yang dipublikasikan tahun oleh National Institute for Health and Clinical Excellence (NICE) mengatakan bahwa baik ibuprofen atau paracetamol dapat digunakan untuk anak-anak yang sakit atau stres karena demam. Namun dalam panduan itu juga disebutkan, karena masih minimnya bukti penelitian , kedua jenis obat ini sebaiknya tidak gunakan bersamaan atau pun diminum selang-seling.
HASIL penelitian terbaru para ilmuwan Inggris menunjukkan ibuprofen terbukti lebih efektif menurunkan demam pada anak-anak daripada paracetamol. Riset yang dilakukan di kota Bristol ini menganjurkan ibuprofen sebaiknya dijadikan pilihan utama dalam pengobatan.
Untuk menguji kehandalan ibuprofen, peneliti dari Universitas Bristol dan University of the West of England melibatkan 156 anak berusia 6 bulan hingga enam tahun. Anak-anak yang diteliti adalah mereka yang temperatur tubuhnya mencapai 37,8 hingga 41 derajat akibat sakit yang ringan.
Dari hasil pantauan selama 48 jam terlihat bahwa kelompok anak yang mendapat obat ibuprofen temperaturnya rutun lebih cepat ketimbang kelompok paracetamol. Riset yang dimuat dalam British Medical Journal ini juga mengindikasikan bahwa penggunaan dua jenis obat secara bergantian dapat membantu, seperti halnya yang telah banyak direkomendasikan tenaga media di Inggris.
Namun para ahli kesehatan tidak sepakat dengan metode gabungan tersebut karena menyalahi prosedur pengobatan resmi. Yang dikhawatirkan adalah kemungkinan anak-anak akan mengalami kelebihan dosis.
Panduan yang dipublikasikan tahun oleh National Institute for Health and Clinical Excellence (NICE) mengatakan bahwa baik ibuprofen atau paracetamol dapat digunakan untuk anak-anak yang sakit atau stres karena demam. Namun dalam panduan itu juga disebutkan, karena masih minimnya bukti penelitian , kedua jenis obat ini sebaiknya tidak gunakan bersamaan atau pun diminum selang-seling.