Medicinalfirmaet Merck & Co.: De kan ikke se mig! c poj

Tirsdag kørte Politiken på forsiden en historie om at kolesterolpatienter får forkert medicin.Det gav mig anledning til et læserbrev afsendt samme dag. I gode gamle dage fik man svar, om det ville blive bragt eller ej. Da jeg har bemærket, at dette ofte svigter, og jeg her lørdag endnu ikke har set det bragt, formoder jeg, det ikke bliver trykt.

I dag lørdag bringer Information der i mod på forsiden en historie om selv samme sag. Her afsløres det, at min mistanke fra læserbrevet er korrekt: Der er et medicinalfirma med interesse i sagen, som står bag den undersøgelse, Politiken byggede sagen på. Interessant at se, hvordan Politiken vil håndtere denne vinkel!

Her er mit utrykte læserbrev fra tirsdag:

Jeg blev så vred

Overskriftlobbyen slår til igen: ”Kolesterolpatienter får forkert medicin”. (Pol. 25.9.). Hvorfor er der ikke nogen, der kan fortælle de noksagter, at der er forskel på, om nogle ikke får optimal medicin, eller om alle ikke får det? Og at der er forskel på, om en medicin ikke er optimal, eller om den er forkert? Er den forkert, har den modsat effekt af hensigten.
Det hedder nok blikfang. Pyt så med, at blikfanget er tæt på lodret løgn.
Men vi der bruger Simvastatin med godt resultat, skal absolut lige jages en kniv i maven før morgenmaden.
Eller er der igen tale om en velgennemført kampagne for en medicinalvirksomhed?

2.9.09: Det endte med at Politiken i mandags sendte sit standard nej-tak til læserbrevet. Jeg svarer: – - tak for svaret. Selvfølgelig skal der ikke svares på et indlægs indhold i og for sig, når det ikke bliver trykt – men når det gælder kritik af avisen, som i dette tilfælde af måden I den dag serverede en overskrift på, er der jo intet der forhindrer det naturlige svar: “Ja det var dumt, vi prøver at gøre det bedre næste gang”.

 I går tirsdag havde Information en god leder om emnet.

Institut for Rationel Farmakoterapi har en oplysende artikel ”Kan kolesterolpatienter behandles bedre?”.

Apopos

http://talegaver.wordpress.com/2009/09/05/pas-pa-den-journalistiske-jiu-jitsu/

http://www.dseneste.dk/index.php/medier/medierne-misinformerer/

http://www.dr.dk/P1/menneskerogmedier/Udsendelser/2009/09/03154113.htm

Statins are projected to be  the saviours of human race against the  killer atherosclerosis .Now we have reached a stage  soon ,  where every healthy individual may be administered this drug. There are consistent evidence for statins to reduce , retard , prevent progression of existing atheroscelorosis  and possibly prevent future atherosclerosis.

This  wonder drug acts by blocking the HMG COA enzyme a vital  enzyme that regulates the lipid metabolism within the cells. It is made to appear  as if ,  the  God has  created this enzyme  with the only purpose for human suffering , by blocking this   we  expect  all errors in lipid  metabolism is corrected.

This enzyme is  part of the house keeping  system  that is meant to service the human cellular lipid layers 24hrs a day. If it  is impaired intentionally one can imagine the consequences. That’s what modern science is all about. Luckily God is kind enough the side effects of  blocking this enzyme is seen only in minority. The myopathies that are classically described with statins are due to possible mitochondrial dysfunction .

As the debate still  continues to find the   optimal bottom levels  of LDL  , we have more worries ,  real world experiences have brought us a new issue  namely  the  reduction of HDL with statins. While literature search on statins and HDL  tell  us there is marginal increase in HDL up to 10% the fact is there is marginal fall or significant  fall in many of the patients .

How can this happen ? A  huge difference between real world and trial world ?

* Brands shown  not intentional

Readers are welcome to add their input on this question .

Reference

Visit HDL forum

http://www.hdlforum.org/

From Outlook:

Despite a long history of battles and a still-intact fort, dusty, small-town Chittorgarh doesn’t quite look like a place where revolutions still happen. But thanks to a project that started last July, this hilly district in south Rajasthan has quietly overthrown the prevailing regime of high-priced medicines—a key failure of India’s healthcare system. In its stead, it has introduced another that dramatically lowers the cost of drugs, making access to healthcare easier for even the very poor. The usual ‘medical shops’ that sell at maximum retail price still exist, but in 16 stores run by the Central Cooperative Bank essential medicines are being supplied as part of a ‘Generic Drugs Initiative’—prices here are 40-50, sometimes 90 per cent lower.

Chittorgarh is among the 50 worst performing districts on the human development index, with poverty widespread and access to social services dismal at best. It’s in this milieu that the cooperative stores have come forward to sell generic versions of hundreds (564 to be precise) of drugs. The stores have opened near hospitals and, no surprises, patients are flocking to them. So much so, the administration now believes there’s room for a further drop in prices.

Another round of price cuts may sound far-fetched—the popular stress relief medicine Diazepam, for instance, already sells at the cooperative store for Rs 2.48 per injection instead of the usual Rs 21. Similarly, the price of a two-day supply of the blood pressure-regulating drug, Simvastatin, has gone down from Rs 120 to less than Rs 35. The cooperatives manage the price cuts because they sell only generic versions—copies of drugs whose patents have expired. The law says once the patent expires on a medicine, any drug company can manufacture it. Without the associated R&D, marketing and advertising costs, generics can retail at far lower prices.

Como el sindrome metabólico es el mecanismo principal para el desarrollo del hígado graso , se especuló que las drogas que mejoran el perfil metabólico como el simvastatin ( Zocor MR) podrían mejorar el hígado graso.

En un estudio publicado recientemente ( mayo 2009) se administró simvastatin a un grupo de pacientes y lo que es muy importante se les realizó , aparte de los estudios de sangre , biopsia hepática antes y luego de finalizar el tratamiento a los 12 meses.

Aunque los pacientes disminuyeron los niveles de LDL colesterol no presentaron ningún cambio con respecto a los valores del hepatograma ni el grado de esteatohepatitis o fibrosis .

Como conclusión podemos decir que el simvastatin como monodroga no sirve para el tratamiento del hígado graso

After a shaky FDA advisory panel meeting last Thursday, the Danish drug maker Novo Nordisk is entertaining new doubts about whether their most promising new diabetes drug liraglutide will receive timely FDA approval.  An intense discussion about a rare form of thyroid cancer (medullary thyroid cancer) seen in mouse and rat studies seemed to unexpectedly pall the focus of the meeting, one of the first meetings to evaluate diabetes drugs under stricter new guidelines to rule out cardiovascular risk.  The panel initially believed a few cases of a common thyroid tumor found in human clinical trials was insignificant, but when considered in light of the more serious type of thyroid tumors in rats and mice, the panel could not convincingly rule out the cancer risk.

Novo Nordisk Chief Scientific Officer Mads Krogsgaard Thomsen was indeed caught off-guard: “We knew we were going to discuss the issue, but we did not know [it was going to be] the overarching dominating thing.”  The advisory panel was decidedly split (6-6 with 1 abstention) on whether the thyroid tumor risk should preclude the drug’s approval, and could not agree how to reliably assess the cancer risk.  In the vote that was supposed to make headlines regarding whether there was sufficient data to rule out “unacceptable excess” cardiovascular risk, the panel voted 8-5 that the data was sufficient (not a hopeful sign either).

Liraglutide (to be branded Victoza) belongs to the promising class of diabetes drugs called GLP-1 (glucagon-like peptide) agonists.  GLP-1 (a.k.a. incretin) is a protein hormone released by the gut (intestinal L cells) after meals, stimulating digestion and insulin production.  It increases secretion of insulin from the pancreas in a glucose-dependent manner and decreases the secretion of glucagon (a counter-hormone to insulin), thus amplifying checks on blood-sugar levels.  The fact that insulin release responds to glucose levels is a nice guard against hypoglycemia (blood-sugar level that is too low).

Another appealing effect of GLP-1 agonists is its remarkable ability to induce weight loss–it delays the emptying of food from the stomach to the small intestine, prolonging satiety (the feeling of being full).  According to a Mar. 2006 New York Times article, a clinical trial of 537 patients showed Byetta (the first GLP-1 agonist on the market) induced an average weight loss of 5 pounds after 6 months (vs. average weight gain of 4 pounds on insulin) while another trial of 146 patients showed Byetta induced an average weight loss of 12 pounds after 2 years.

The fascinating history of the GLP-1 class is detailed in an Aug. 2008 Forbes article, where the GLP-1 hormone was first discovered in the 1970’s by Harvard professor Joel Habener as he was studying monkfish.  He noticed that the hormone stimulated the pancreas to secrete just the right amount of insulin in response to blood-sugar levels, but the hormone itself was transient in vivo and rapidly degraded in the body (by the DPP-4 enzymes currently targeted by Merck’s Januvia and Bristol-Myers Squibb’s prospective drug Onglyza).

Then in the early 1990’s, John Eng, an endocrinologist at the Veterans Affairs Medical Center in Bronx, NY isolated a compound in the venomous saliva of the Gila monster that mimicked the effects of GLP-1 while exhibiting more staying power in the physiological environment.  This research was first reported at a 1996 diabetes conference and soon licensed by Amylin Pharmaceuticals who wanted to develop a synthetic version of this novel compound.  Oddly enough, a Sept. 2007 article in Diabetes Wellness News revealed that John Eng had no idea about the weight loss effects of the compound until clinical trials.  The FDA approved Byetta (compound name: exenatide) in Apr. 2005, and Amylin Pharmaceuticals partnered with Eli Lilly in promoting this twice-daily injection, first-t0-market in the GLP-1 class.  In 2008, Byetta gained sales of $751 million, a 16% increase from the year before.  Novo Nordisk is seeking to penetrate the market with Victoza, a more convenient once-a-day injection.  Not to be outdone, Eli Lilly and Amylin is working with Alkermes in developing a long-acting version of Byetta, a once-weekly injection that itself has been plagued by delays.

Byetta has been on the market for nearly 4 years and while it has been rattled by safety concerns (mainly from pancreatitis), thyroid cancer has not one of them.  In fact, a Mar. 2006 New York Times article hailing Byetta as a “ray of hope” for obese diabetics does mention initial concerns about thyroid cancer risk: “Based on tests in rats, moreover, some scientists have raised the possibility that Byetta may increase the risk of thyroid cancer, although no evidence of that link has appeared in human clinical trials.”  A Jan. 2006 article in Smart Money elaborated on the risk, explaining that Byetta stimulates the same receptor in the insulin-producing cells of the pancreas (beta cells) that is also found in the C-cells of thyroid tissue, where the insidious medullary thyroid cancer forms.  Byetta’s FDA-approved label does describe a 2-year rat study where “benign thyroid C-cell adenomas were observed in female rats at all exenatide doses” [emphasis added] with incidences between 11% to 23% (compared to 5% to 8% in control groups), but the doses that were tested were at least 5 times the doses prescribed in humans and the cancer risk was not even dose-dependent (11 micrograms/kg/day had a higher incidence than 70 micrograms/kg/day).  In a parallel 2-year study in mice, there was no evidence of tumors.  The thyroid C-cell growths “didn’t seem to affect the rats’ longevity, so the Food and Drug Administration found that the study was no cause for worry.”  As things turned out, an article this week on TheStreet.com noted that “nine cases of ’spontaneous’ thyroid cancer have been reported in the approximate 1 million diabetes patients taking Byetta, according to FDA records, but none of these tumors were fatal nor of the type under FDA scrutiny with liraglutide.”

Byetta’s initial thyroid cancer concern seems to inform liraglutide’s current predicament in suggesting that this may indeed be a GLP-1 class effect.  Peter Savage of the National Institute of Health, who voted against liraglutide, conveyed this sentiment: “It certainly sounded from what I heard today that this may be a class effect for any of the longer-acting agents.”  Amylin Pharmaceuticals vehemently sought to distance their long-acting version of Byetta from the type of thyroid cancer risk whirling around liraglutide, arguing that they are distinct molecules and that unlike Byetta (short-acting and long-acting versions), liraglutide did reveal elevated thyroid cancer risk in both rats and mice across multiple doses.  In an e-mail response to Forbes, Amylin clarified that “there is no identified association between thyroid C-cell carcinoma and [Byetta] based upon clinical trial and post-marketing data.”  But it might not matter much in defense of Byetta’s long-acting version, as the same article from TheStreet.com believes: “Amylin may have cleaner animal safety data, but it remains to be seen whether the FDA will, regardless, consider thyroid tumor risk to be a class effect of the GLP-1 agonist drugs.”

The FDA’s newfound conservative bent towards safety would ordinarily translate into more data (or studies) to rule out such a risk, but this could be developmentally impractical and prohibitively expensive particularly for cancers that are slow-developing like medullary thyroid cancer.  In a recent Forbes article describing this very debate, panel member Michael Tuttle of Sloan-Kettering Cancer Center voted to approve liraglutide given the big picture, realizing that “there was no obvious study that could be done to rule out the risk.”  Utilizing the same reasoning, committee chair Kenneth Burman of Washington Hospital Center voted against approval, and contended: “Should we expose the entire population to the potential risk even though it is probably low?”  One missing (and potentially critical) piece in answering this question is the absence of thyroid problems in a recent 2-year clinical study on liraglutide conducted in 1,500 patients (the study wrapped up recently enough to be not included in the application).  But does a 2-year window of cancer safety in humans offer enough confidence for the FDA?  Note that much of the advisory panel’s concerns are still rooted in an extrapolation of cancer results observed from rat and mice models.

It is quite a challenge to attribute cancer risk to an investigational drug based on clinical trials.  According to the Center for Disease Control, most cancers (aside from the most common ones–prostate, breast, lung, colorectal) have an incidence rate of about 20 per 100,000 people (0.02%).  Even the largest clinical trials only involve around 10,000 to 20,000 patients on a given drug, meaning we would normally expect less than 5 cancer cases according to average incidence rates.  These trials are ordinarily sized to detect significant differences in primary endpoints, but often lack the statistical power to detect significant differences in cancer risk.  Another key consideration is the duration of the clinical trials, since many cancers slowly develop over time.  Most clinical trials last no more than a couple of years, so patients aren’t tracked long enough to identify cancers that develop much later on.  The statistical exercise to ascertain cancer risk from clinical trials is still valuable, but should be cautiously viewed within the overall context of the drug’s efficacy and safety considerations. There will be cases where cancer risk is a deal-breaker, but in the grey area that liraglutide finds itself in, maybe an FDA-sanctioned risk evaluation and mitigation strategy (REMS) program is a better compromise.

An interesting statistical quarrel regarding cancer risk played out last September over Merck’s troubled drug Vytorin (a combination pill of Merck’s genericized statin Zocor and Schering-Plough’s Zetia, a drug that inhibits cholesterol absorption in the small intestine).  Vytorin’s prospects had already been deflated by the lackluster results of the ENHANCE study (released in Jan. 2008), which reported no clinical advantage of adding Zetia to the generic statin (compound name: simvastatin) in preventing heart attacks and strokes.  In fact, patients on Vytorin had more plaque buildup in the arterial walls than patients on the generic statin alone.  But the negative publicity indeed got worse in Sept. 2008 with the results from the SEAS clinical trial, which understated an observation that patients on Vytorin had 50% more cancers than placebo–there were 102 cases of cancer for Vytorin patients vs. 67 on placebo.

Statins have been extensively studied enough for over a decade in tens of thousands of patients for cancer risk to be ruled out for simvastatin, but the SEAS study represented the largest and longest study conducted on Zetia, fueling motivation to further investigate Vytorin’s purported cancer risk.  As described in a Forbes article, Sir Richard Peto of Oxford University (one of the most highly-regarded statistical minds) was recruited to evaluate this “cancer question” using unblinded data from two ongoing Vytorin studies (SHARP and IMPROVE-IT) involving 20,000 patients.  These studies showed 313 cancer cases among Vytorin patients compared with 326 cancer cases for patients on Zocor or placebo, a statistically insignificant difference in his calculation.  The number of cancer-related deaths was greater for patients on Vytorin (97 vs. 72) for a p-value of around 0.06, but for Peto, this was still close enough to 95% confidence (p-value less than 0.05).

Despite Sir Richard Peto’s reputation, his analysis to rule out Vytorin’s cancer risk has been intensely scrutinized.  Sanjay Kaul of Cedars-Sinai Medical Center in Los Angeles believed that using incomplete studies weakened Peto’s analysis because they are “notorious for being unpredictable” but James Talcott of Harvard University thought the need for independent data (apart from SEAS) was critical, and that using the incomplete studies was appropriate.  Another top statistician Thomas Fleming from the University of Washington weighed in critically against Peto’s conclusions.  Although he agrees with Peto’s approach of relying on the 2 independent trials (instead of lumping all 3 together) to examine the question of whether the cancer risk observed in SEAS appears elsewhere, Fleming argues in a New England Journal of Medicine editorial that “there are clinically important increases in the risk of cancer-related deaths that are not ruled out by this data.”  He calculates that the “approximate” hazard ratio for cancer-related deaths associated with Vytorin was 1.34 with a 95% confidence interval between 0.98 and 1.84, suggesting that one “cannot exclude a relative increase of as much as 84% in the risk of cancer-related death.”  Fleming also raises concerns about how Merck and Schering-Plough handled the matter since rushing out the results of the SEAS study may have compromised the ongoing studies’ ability to assess Vytorin’s cancer risk once they complete.

So is Vytorin’s cancer risk real?  How does one reconcile the incidence of cancer being statistically similar with cancer-related deaths being arguably different?  Does this mean that the types of cancers between the Vytorin and placebo groups are different?  If so, how come the cancer types haven’t been mentioned in this debate–shouldn’t cancer type have an impact on the credibility of the putative causality relationship?  More data is likely needed in this case.

The Angry Pharmacist already did a rant about Solodyn, so I won’t try to outdo him.  Here’s what that stupid drug is:

That’s right, they took Minocycline, made it 90mg and ER, sucked the FDA off to give it an ‘acne’ indication, and now they are selling it for $1573.82 per bottle of 100.  Thats right, 1500 bucks for minocycline.  Go look at your shelf at that $20 bottle of minocycline 100mg in generic and tell me what 10 fucking milligrams in an “Extended Release” is going to do (and is it worth the 100x price increase).

The rant continues from there, and it is awesome.  Moving on, I’ll start with the Keppra and Simcor before moving on to a huge rant about Tricor / Trilipix.

Regular Keppra is generic now, so of course they just released an extended release version with a new patent and a higher price.  It’s completely AMAZING that they just found this AMAZING breakthrough in AMAZING epileptic care right when the original version went generic.  Let me just ask a really stupid question:  if Keppra XR is really better than generic Keppra, why didn’t they release it sooner?  Does UBC (makers of Keppra) love money more than they care about epileptic human beings, or is this just a ploy for more money on a drug that’s not a significant improvement?

Simcor has been out quite awhile.  Thankfully we hardly ever see a prescription for it because IT’S STUPID.  It’s simvastatin and extended-release niacin.  Simvastatin is the generic for Zocor.  Niacin is OTC.  Both are cheap, yet Simcor is really expensive.  Well a drug rep with huge knockers must have been going around about it lately because we had a doctor write for it recently.  The patient specifically told this doctor, “I don’t have prescription coverage.  If you’re writing for a cholesterol drug I need something really cheap or I can’t afford to fill it.”  So what did the doctor do?  He told the patient he was writing for the “cheapest” cholesterol drug and wrote for Simcor.  Why do doctors listen to drug reps when they quote a (wrong) price on a drug or talk about glowing studies their own employer bought and paid for?  Skepticism would be nice, doc.  Call the pharmacist and ask them what’s really up.  At least most of our doctors around here are cynical about drug reps and are far more aware of drug costs than they used to be.  An expensive therapy is a therapy that often won’t be complied with.  Simple as that.

Anyway, the cash price on 30 Simcor for this patient would be about $175.  Per month.  Generic zocor and over-the-counter niacin?  Less than $20.  And the generic zocor can be split in halves to save money if you’re not on the highest strength. We had to play phone tag with the doctor to try to get the prescription changed.  Oddly enough, the patient didn’t want to pay almost 2 grand a year extra so he could take one pill instead of two pills.

I really dislike the fact that “me too” drugs like Simcor even exist.  The FDA doesn’t have the power to decline an NDA (new drug application) on the grounds that “this is a stupid idea”, but sometimes I wish they did.  In fact, they could hire me to be the one who gets to call up a drug company CEO and laugh, “Are you kidding me with this?  HELL NO it ain’t approved.  Now get out of my office, even though it’s really your office since we’re talking on the phone.  I said good day sir!”

Simcor is made by Abbott, by the way, and that brings me to another Abbott drug, Trilipix, which is the new Tricor, which was the old Tricor and then the old Tricor before that.  You read that right; Abbott has rebranded the same drug at least four times now.  And doctors still write for the “new” one.  ARRRRGH.  How is this even legal?  Here’s what I posted about Tricor back in 2005:

Tricor 200 was repackaged as Tricor 160 then replaced with Tricor 145. Tricor 80 became Tricor 54 then Tricor 48. Every time the patent was about to expire, they reformulated the exact same drug into pills that would dissolve better so they could package a “new” drug with a lower standard dose. Then they pulled the higher strength pill completely off the market before the patent expired (meaning no generic legally made yet). This left doctors with no choice but to either switch to the new one or switch the patient to another drug altogether. All so the bastards at the Abbott drug company could strongarm more money out of people.

Well, big surprise, the unethical taintbadgers at Abbott have done it again. There is generic Tricor 145 sitting on our shelf now, so that’s old news, baby.  The new hotness is Trilipix.  Its a delayed release capsule in 45 mg and 135 mg and it’s freaking expensive, which means it must be good.  It’s well over $1 per pill for the 45 mg and almost $4 per pill for the 135 mg.  If a doctor tries to write a prescription for Trilipix for you, do me a favor and kick him or her down an up escalator.  Doctors need to just grow a pair and say, “I’m not going to write for this drug because IT’S STUPID and it should not exist.”

There are millions of people in this country who cannot afford drug coverage because stupid rebranded drugs are driving up the prices WITHOUT IMPROVING PATIENT CARE.  This is stupid, stupid, stupid, stupid.  Did I mention it’s stupid?  Because it is.

.

.

.

Apakah benar kita tidak boleh minum obat dengan susu?

Apakah minum obat harus sesudah makan?

Bolehkah minum obat dengan air teh?

.

Menilik ilmu farmakokinetika, yakni ilmu tentang nasib obat di dalam badan. Obat masuk ke tubuh kita akan mengalami berbagai peristiwa yakni :

ADME = absorpsi/penyerapan, distribusi, metabolisme dan ekskresi.

Peristiwa yang terkait dengan cara minum obat adalah absorpsi yakni penyerapan obat dari tempat pemberiannya menembus membran biologis, masuk ke sirkulasi darah sistemik. Proses ini merupakan pintu pertama yang harus dilewati obat agar obat memberikan efeknya ke tubuh.

Cara pemberian obat yang berbeda akan mempengaruhi cepat lambatnya obat terabsorpsi, dengan kata lain juga akan mempengaruhi cepat lambatnya obat berefek. Begitu pun makanan dan minuman, sangat mempengaruhi proses absorpsi obat. Tergantung di mana obat diabsorpsi/tempat absorpsi obat, maka dengan menganalisis makanan/minuman yang masuk bersama obat, maka akan mudah memprediksi pengaruh keduanya kepada cepat lambatnya atau malah tidak terabsorpsinya obat.

Interaksi obat dengan makanan/minuman (Food drug interaction)
Sifat fisika kimia obat menentukan tempat absorpsi obat. Obat biasanya bersifat asam lemah atau basa lemah.

Obat asam lemah akan diserap di lambung (jika diberikan secara oral dengan diminum, bukan di bawah lidah atau di dinding mulut bucal), sementara yang bersifat basa lemah akan diserap di usus yang lingkungannya memang lebih basa dibandingkan lambung.

Kecepatan pengosongan lambung juga tak kalah penting untuk absorpsi obat secara oral. Semakin cepat pengosongan lambung, bagi obat bersifat asam akan merugikan karena hanya sejumlah kecil obat yang terserap, namun menguntungkan obat bersifat basa lemah karena segera mencapai tempat absorpsi di usus, segera terjadi proses penyerapan.

Selain terkait sifat obat dan tempat absorpsi, makanan/minuman akan mempengaruhi bentuk obat. Obat seharusnya berbentuk molekul kecil untuk bisa terabsorpsi dengan baik. Maka perlu dilakukan uji disolusi/pelarutan obat saat dilakukan formulasi obat. Namun, hal lain yang perlu diwaspadai adalah adanya interaksi obat dengan makanan/minuman atau nutrien tertentu, sehingga terbentuk senyawa kompleks bermolekul besar yang menghalangi obat diabsorpsi.

Contoh interaksi obat dengan makanan/minuman atau nutrient :

1. obat-obat antialergi golongan antihistamin (Benadryl, Claritin, CTM, Zyrtec, Incidal, dll)

merupakan obat bersifat asam lemah yang absorpsinya terjadi di lambung. Maka seharusnya diminum saat perut kosong (satu jam sblm makan atau 2 jam sesudah makan) atau cukup diminum dengan air putih saja. Jika diminum dengan susu, adanya pencernaan susu akan menghambat proses absorpsi di lambung, efek obat menjadi lambat.

2. Obat pain killer dan antiinflamasi (anti rematik, anti Gout/asam urat, anti bengkak).

Obat golongan ini sebagian besar bersifat asam agak tinggi (ibuprofen=Nurofen, advil, aspirin, aspilet, aspro, asam mefenamat=ponstan, mefinal) walaupun absorpsi terjadi di lambung, namun karena keasaman yang tinggi tsb akan menimbulkan efek samping nyeri lambung, maka seharusnya diminum bersama susu, atau sebentar sesudah makan. Walaupun jelas ada penundaan absorpsi, namun karena mengingat efek sampingnya yang jauh lebih berbahaya, maka lebih baik menunda absorpsi dengan makan/minum susu tsb. Begitu pula dengan obat anti inflamasi golongan non steroid (diclofenac/voltaren, difflam, cataflam) dan steroid (deksametason, metil prednisolon/meptin, medrol, prednisone/deltasone, cortisone asetat/cortef), harus diminum sesudah makan atau bersama susu. Lain lagi dengan parasetamol (panadol, tempra, lylenol), karena bersifat lebih basa lemah dan diabsorpsi di usus, maka lebih baik obat jenis ini diminum sebelum makan, diikuti makanan sehingga akan segera sampai di usus, terjadilah proses absorpsi.

3. Secara umum untuk antibiotik (penisilin=amoksisilin, ampisilin, ciproflokasasin, ofloksasin, eritromisin, azitromisin, metronidasol, cotrimoksasol) seharusnya diminum saat perut kosong.

Minum cukup dengan air putih. Karena absorpsi terjadi di lambung. Hal menarik terjadi khusus dengan golongan tetrasiklin (tetrasiklin, oksitetrasiklin, doksisiklin, minosiklin). Bila obat golongan ini diminum dengan susu atau daiyr product yang mengandung kalsium (yogurt), atau diminum bersama obat suplemen mengandung zat besi dan kalsium (multivitamin dan mineral), atau obat sakit maag (mengandung kalsium, magnesium, atau aluminium), maka mineral valensi 2 dan 3 ini akan membentuk senyawa komplaeks ermolekul besar dengan golongan tetrasiklin. Obat golongan tetrasiklin sama sekali tidak terabsorpsi sehingga tidak akan muncul efek farmakologi yang diinginkan pasien, kemungkinan besar terjadi kegagalan terapi. Obat jerawat biasanya mengandung golongan tetrasiklin ini. Hal serupa juga berlaku untuk obat antijamur (griseofulvin, ketokonazol, fluconazol). Jangan diminum bersama susu, dairy product, multivitamin dan mineral, obat antasid untuk sakit maag.

4. Obat asma yang mengandung teofilin atau aminofilin,

adanya makanan lemak tinggi atau cafein akan meningkatkan efek samping teofilin (terjadi gangguan di jantung, palpitasi). Jangan minum obat asma ini dengan kopi atau sesudah makan lemak tinggi. Makana berkadar tinggi karbohidrat seperti nasi akan menurunkan jumlah teofilin yang terabsorpsi. (Aminofilin sesudah masuk tubuh akan membentuk teofilin juga = prodrug).

5. Obat antikolesterol lovastatin, simvastatin, pravastatin,

dengan adanya susu atau makanan akan meningkatkan absorpsi obat. Maka lebih baik diminum dengan susu atau sesudah makan (kurang dari 2 jam sesudah makan).

6. Obat cacing (pirantel pamoat)

lebih baik diminum dengan susu atau sesudah makan, karena akan terjadi peningkatan absorpsi dengan makanan/susu.

7. Obat antihipertensi ACE inhibitor (captopril dan golongannya=capoten, vasotec,accupril)

jangan diminum bersama jus buah atau sayuran yang mengandung tinggi kalium/potasium (pisang, jeruk, sayuran berhijau daun), karena tingginya kalium akan meningkatkan efek obat golongan ini sehingga bisa muncul efek samping di jantung.

Jadi, sebaiknya obat diminum dengan susu, teh, air putih, jus buah, sebelum atau sesudah makan sangat bervariasi tergantung golongan obat (beserta sifat fisika kimia dan faktor lainnya yang terkait). Tidak bisa dilakukan generalisasi : tidak boleh minum obat dengan susu, minum obat harus sesudah makan, merupakan image dalam masyarakat yang harus diubah demi keberhasilan terapi obat.

—

[*] di copy paste secara liar dari milis balita-kita@yahoogroups.com

Julia Reed, to those of you who are veterans of American cable news shows, is a Vogue senior editor, and champion of all things Mississippi.

She comes from hearty stock in Greenville, the heart of the Mississippi Delta.

Greenville residents, which include her family for generations, have endured hurricanes, heat, fires, rains, tornadoes, ice storms, and a small event known as the US Civil War.

I wonder, if like Brett Favre’s family, they had to go up their attic, and wonder about Julia, who has the misfortune of having chosen to live in New Orleans.

I knew about Julia Reed anecdotally from friends in New York City.

She shares her time there and in New Orleans, but because she is such a Southerner, with her husky-voiced Southern twang which must stick out a mile in those Upper East side salons, and her much beloved charm and wit, so redolent of her home state, she must be in great demand in NYC.

What now, I wonder?

Will she go back to New Orleans, or just stick to NYC?

I think this momentous decision is one many people from the area are faced with today.

But I do know one thing.

She may well leave New Orleans, but her kinfolk will never leave Mississippi.

Some things not even a hurricane can take from you.

READ JULIA REED’S BOOK: Queen of the Turtle Derby and Other Southern Phenomena.

UPDATE WEDNESDAY 7 SEPT: Julia Reed is alive, well, and safe in her parent’s home in Greenville, MS! I noticed a hit counter referral to my site, and checked out the links. In one of them, I saw that she had been interviewed on the embattled Air America Radio’s Al Franken Show, subbed though he was last week, by Rachel Maddow. Now Julia Reed, from what I’ve heard from her previous on-air TV commentaries, is hardly a Republican. In fact, I would not hesitate to say she tilts left politically, and perhaps that’s why Air America thought they would have her on air on Friday, 2 September, being a New Orleans/Mississippi resident and all. I’m sure they thought she would tow what has become the MSM Party Line of “Blame Bush! Blame Often! Don’t Stop Blaming!”. Boy, they must’ve been livid at her for assigning blame first, foremost, and often to Governor Kathleen Blanco of Louisiana, and ESPECIALLY to Mayor Ray Nagin of New Orleans. She absolutely ripped him apart for his lackadaisical remarks before the levees broke on Tuesday. As much as Rachel Maddow tried to steer back the conversation to assign blame on the Federal response, Julia Reed would have none of it. She said she found it “terrifying” that they were in charge, and couldn’t believe Blanco was her governor, who just threw up her hands asking people to pray for Louisiana, instead of asking them to pray, which is fine, but also doing a million and one other things a governor of a State is supposed to do. And as far as Ray Nagin’s chances for re-election are concerned, she said they are nil. That’s when Rachel Maddow put on Nagin’s expletive-laden outburst which made did the rounds of all MSM outlets gleefully. Poor old Julia Reed — she didn’t get the segue, and just ripped him apart again for throwing a hissy fit AFTER his lame, lack of leadership “un-Giuliani” comments on air on Monday, when the storm first broke. Rachel Maddow desperately tried to get the conversation back to the Federal, by bringing up Speaker of the House Denny Hastert’s comments about not rebuilding New Orleans, which Reed fully agreed were ridiculous and defeatist (as do I), but the damage was done. Someone didn’t get the Blame Bush memo. She didn’t say what she did because she was being Right or Left. She said it because, using that famous Southern habit of calling it as you see it, that’s how she perceives the truth to be. Here is the mp3 clip of Reed’s lapsus lingua on ARR. Scroll to minute 77:00 until minute 88:00. Julia, on the off-chance you’re reading this one day, good on you. I just hope you get invited back to those Upper East Side salons. You might have some ’splaining to do.

Nerve Impingement and Sudden Cardiac Death?

What Happened?

In the early morning hours of 8 Aug, just a day before our National Day 2008, I was warded at the Singapore General Hospital. In fact, I checked myself into the hospital after waking up around 0230hrs and experiencing very bad numbing sensations on both my limbs; hand and legs. I took a taxi from Marsiling after weighing the pro and cons of calling for an ambulance which I felt would take much longer. Afterall, I had already popped an Alka-Selser, (an aspirin/sodium bicarbonate pill) and which had always been my trusted health panacea by my bedside to prevent sudden death. In my previous bout of heart burn (which I had attributed to over-eating and maybe nerve impingement), the Alka-Selser was provided relief within 20 minutes or so. The aspirin ingredient was to allow for better blood flow while the sodium bicarbonate was for heart burn (indigestion)

However, this time round, perhaps, the numbing sensation was pretty bad on both limbs and maybe, the aspirin was taking too long to kick in, plus my blood pressure reading taken by my good wife, measuring at a high 168 mmHg (systolic) made me panic even more. I decided to head for the hospital.

I decided to take a taxi since I had already taken an aspirin and as I stayed in Woodlands, far away from the nearest public hospitals, had assessed even before this episode, if this condition would to recur again, I would take a taxi. I had calculated if I was still conscious, could still walk 20metres to the roadside to hail a taxi, it would be faster than waiting for an ambulance which would take about half an an hour or more plus waiting time. My taxi ride took 17 twenty minutes via the via the Central Expressway to reach the Singapore General Hospital. I was relieved at least, I would be in good hands. At one point, I almost though I might pass out inside the taxi, since my blood pressure was pretty high.

At the ICU

The ICU staff were pretty efficient and took a couple of xrays including a CT scan on brain when I mentioned that my speech seemed pretty incoherent while I was in the taxi, mumbling and trying to fish out dollar notes from my wallet to pay the fare.

Was It Nerve Impingement?

Eventually when I was warded and while relating about my “heart attack” episode with the the duty doctor (maybe an Intern), it suddenly dawn on both of us that perhaps it could be the recurrent NERVE IMPINGMENT that I have been experiencing periodically following my motorcycle skidding accident in 2000. As the frequency of attacks had dwindled since 2006 after I moved to an office near to my home (lesser neck compression from my motorbike journey to work), and indeed it had slipped off my mind during this episode. Coupled with the fact that my mind was fixated on my elevated cholesterol level a week ago, before my ICU admission, when my family general physician (GP) established that I might have to be started on anti-cholesterol medications. This happened when I experienced limb numbness then.

Back at the hospital ward, The intern doctor explained that aspirin would reduce the nerve swelling, and during a nerve impingement it would provide relief. I paraphrased that aspirin had the analgesic effect, trying to let him know that I was in the know too.

In retrospect, after some thinking again, I now believe the reasons why my “heart attack” episode only occurred at night when I was sleeping.

Nerve Impingement stemmed my blood flow to the limbs

Well, you see, during daytime, my nerve impingement is still occurring without much awareness of mine other than some muscle stiffness which I probably would have shrugged off. However, due to the constant physical movement, like walking, working at my desk, or simply shuffling my feet, the voluntary muscular contractions contributed immensely to ensure circulation of blood throughout my body especially the remote corners like hands and feet that often sent out the “alarming” tingling or numbing sensation depending of the availability or stemmed blood supply. Hence during the night when I was sound asleep, the vastly reduced voluntary muscular activities could not not aid in propelling blood flow. Hence the “pinched” nerve effect would be exacerbated manifolds. It stemmed nerves signals to the involuntary muscles or gut interrupting or even stopping blood and intestinal movement that caused not only heart burnt (food indigestion) but worst still, reduced blood supply to my limbs. Hence effect not only mimic a “heart attack” but could attribute to high blood pressure since the heart would probably be pumping very heart to reach those areas stemmed by “pinched’ nerve for the supply of adequate oxygenated blood. I used the inverted commas “ “ to signify that the pinching effect could also be due to the “swelling” of the nerve rather than the continual compression of the cervical (neck) vertebrae. I noticed that whenever, I was having a sore throat or cold, my nerve would be pinched somehow. Maybe the swollen nerve (during viral infections like flu) could result in the “pinching” effect causing stemmed blood flow and indigestions. This is a casual observation of mine.

Can Nerve Impingements result in Sudden Cardiac Deaths

Well, unfortunately, I think the answer could be a YES! This is again my personal opinion basing of my experiences during such “heart attack” bouts. The MRI (Magnetic Resonance Imaging) scan result from my stay at the hospital also confirmed to pinched nerves at the fifth cervical vertebra. I should be going for some physio-therapy some to alleviate the problem soon.

Meanwhile, there should be some local researches done here to establish if any sudden deaths could have been attributed or even partly attributed to nerve impingement that cause severe heart arrhythmias or even the currently hyped “enlarged” left heart ventricles explanation being rattle-off as a plausible answer for the recent spates of sudden cardiac deaths. As I have pointed out, pinched nerves resulted in high blood pressure and palpitations, when the heart being the main pumping station, and not being assisted by the other involuntary blood transport elements like muscles, valves etc had great difficulty bring the needed oxygen to the capillaries of remote places like the hand and feet. So the tingling and numbing signals are sent out again. Hence the left heart ventricle could be enlarged from the stemmed effect. This could be validated against those with little arterial plaques to ascertain my hypothesis.

I am also very sure, it was nerve impingement I was experiencing rather than the high cholesterol effect. Three weeks ago, I started to lift heavy weights at the gymnasium when the swimming pool was closed. I was using the stationary weight stations (not free weights) and maybe some station exercises caused severe compressions against the nerves at my neck and shoulder region. I was also experiencing tight muscle contractions at my limb regions which on retrospect could be reduced blood flow to such region to bring the essential electrolytes that had been dissipated during my exercise regime in the gym. When I took my faithful potassium and magnesium combo tablet, it helped to lower my blood pressure and relax the muscles. I had been harping on the important of having adquate serum magnesium and potassium to everyone for heart maintenance for sometime. Maybe during my stay at the hospital, the blood test should also include a quantitative analysis of my magnesium serum. I noticed this “inadequacy” which my blood serum test result was out. I would also recommend it since there is indeed a correlation between heart problems and magnesium deficiency.

Maybe the intense muscle contractions during weight-lifting could have released some fragmented cholesterol plaques in my blood system, but I do not think it is major contributing factor.

Come to think of it, though it is important for to keep our muscle strong to lift our frail skeleton as we age, we should be mindful of lifting excessive weight and also the correct techniques (as Robert pointed out). I would probably focus more on those that “decompresses” the spinal column, rather than those the compresses the spine, especially my neck (cervical) vertebrae region.

Medication and Therapy

The hospital had prescribed a month dosage of anti-cholesterol pill for my elevated cholesterol-level. However, instead of taking the simvastatin pill, I am now taking my wife’s Red Yeast Rice pill (which is a natural statin pill) and of which my wife swear by it. Simultaneously, I have been doing some research in the internet, reading so many articles on both the synthetic statin drugs; Simvastatin, Lovastatin against the “natural” Red Yeast Rice which claims to be the original statin drug. In the meantime, the giant pharmaceutical companies that manufacture the synthetic or extracted statin drugs continues to mount effort against the Traditional Chinese Medicine or Herbal Therapeutic Medicine (that claimed to the original statin drugs) to gain shares in the lucrative cholesterol market.

Follow-up posting on the effect of Statin drugs

I would be writing another post on this topic later. In the meantime, I have to be wary of over-dosage of the anti-cholestorol statin pills, whether it is Simvastatin or Red Yeast Rice. The reason being that if your body detect that you have too little cholesterol, that it would start to metabolise the next available food source, that would be the muscle, and hence while some people who take very high dosage of statin drugs would have muscle weakness, and in extreme cases, blood in the urine leading to renal failure, vertigo (since cholesterol is needed for brain well being too) etc.

Right now, if I am taking my wife’s Red Yeast Rice tablets, I would definitely stay away from the Simvastatin to prevent for over-dosage of statin drug effect. I would not have done so, if I had not read out so much on it. Not many people does anyway. A word of caution to those who are trying to do a super quick cholesterol reduction like fasting, taking high dosage of synthetic statin drug plus also the herbal Red Yeast Rice (not realising that it is also a statin drug), then it is a double whammy, and highly possible that you could end up with severe muscle, renal and neural degenerations. During my stay in the hospital, I noticed a few patients next in my ward had dark coloured urine (needing assistance from nurses) plus muscle and breathing weakness. Maybe they could have over-dosing on statin drugs, intentional or unintentional without knowing it. This is just my sensing. Maybe the health authorities could make it mandatory for certain TCM product like Red Yeast Rice to be obliged to state the “contain natural statin and to consume wisely if also taking statin drugs” label since many people could be taking both product unknowingly. A questionaire survey for patients could be feasible to establish its prevalent usage here.

So please take care. I also have to take care. First I have to deal with my nerve impingement, find out other attributing factors and also to recover from my left knee’s suspected meniscus tear.

Mikey

Statins to be given to a million more over-40s

Extract from the Telegraph:

“GPs are urged to trawl the records of patients aged 40 and over to find anyone with a one in five chance of having a heart attack or stroke and call them in for advice and drugs.

Four million people already take statins, mostly after heart attacks. But the National Institute for Health and Clinical Excellence (Nice) wants healthy people deemed at high risk of an attack or a stroke within 10 years to have preventive drugs as well.

That would put 1.5 million more on medication and should prevent an extra 15,000 heart attacks, strokes and new cases of angina each year.

It will cost £28 million to implement in the first year.

Nice recommends checking the records of everyone aged between 40 and 75 to flag up those at high risk and call them in for lifestyle advice and consider prescribing 40mg of simvastatin, which costs about 4p per person each day.

That will be controversial as it will put healthy people on medication and the drug has to be taken for the rest of a patient’s life. Statins reduce the risk of a heart attack or stroke by about a quarter.”

This is absolutely disgraceful. – There is no need at all for healthy people to be put on drugs – drugs with many adverse, unpleasant side-effects – for the rest of their lives in order to reduce their risk of heart disease. – The drug-free, cost-free, totally safe and extremely effective way to reduce heart disease and stroke and to reduce high cholesterol is to avoid eating salt and salty food. – People should be told the truth about the effects of salt sensitivity and decisions made about drug recommendations should not be made in order to bring profit to the iniquitous drug companies.

Lose weight, reduce your risk of most cancers, high blood pressure, type 2 diabetes, stroke, heart disease, angina, vascular dementia, osteopenia, osteoporosis, hypercholesterolaemia, depression, liver and kidney problems, and improve your health in many other ways without drugs or expense by eating less salt! – Try it! – You will feel so much better!

See my website http://www.wildeaboutsteroids.co.uk/.html (The site does not sell anything and has no banners or sponsors or adverts – just helpful information.)

Read my Mensa article on Obesity and the Salt Connection

Children and Obesity

vulnerable groups

See Sodium in foods and

Associated health conditions

amitriptyline

prescribed steroids and HRT

advice for pregnant mothers

http://www.wildeaboutsteroids.co.uk/socio.html – social and economic considerations

My mom I can say is not the cheerful type like me. hahaha.  Most of the time i find her grumpy specially while she was getting older.  Now that she’s old and still burdened with life, I can still see tracies of sad or grumpy wrinkles outlined in her face.  I don’t hate her for that nor I count it bad against her.  That was her life and that’s the way she made her life.  I can really say — poor mom, wish she had a better way of living. 

The other day she went out for a check up on her cholesterol level and guess what? The doctor told her it’s so high as heavens.  Mom replied, “oh that’s nice, Doc. I could see Jesus then.”  The doctor laughed.  Then  she was told to have an abdominal ultrasound to check maybe a lot of stones has already formed, mom replied, “that’s fine doc, because I can then go into mining business who knows there are copper diposits in there.”  The more the doctor laughed and all of them in the clinic.  As mom was relating this to us, I was happy she still has her sense of humor but at the same time sad because I know if the cholesterol rise won’t be stopped, she’s have another attack soon or who knows when.

So beginning yesterday, I told her that we would avoid cooking foods with oil.  Instead of frying, we should boil, broil, or steam, or grill.  We can still saute’ though using water.   I’ve always been using water when am the one left in the kitchen, but mom does not know how to do it yet.  I hate thier way of plain boiled vegies too becuase the water is too much and I can see the vegies and greens swimming.  So I told her that if she liked it cooked that way, then leave ot us some steamed green vegies or some salad.  Am sure all the kids can learn how to eat that way.  There’s no problem with me.

She’s back to Simvastatin medication (to lower her bad cholesterol level) and I hope in a month’s time it will show effect. I don’t like her eating that medication coz it irritatets her stomach.   The good thing about purchasing Simvastatin now is that she is given a Pfizer card for a 30% discount for every 30 pcs Simvastatin purchase each month.  Norvasc has increased their discount, too from 50% to 60%. 

Hmmm no matter what — God is always wonderful.  I can really say those discount cards is one of the ways of God’s blessings to my mom.

Vytorin ® heißt das Medikament in Amerika, in Deutschland ist es unter dem Namen Inegy ® im Handel. Es ist eine Kombination des altbekannten Cholesterinsenkers Simvastatin und eines neuen Wirkstoffs, dem Ezitimib. Beide Wirkstoffe haben einen unterschiedlichen Angriffspunkt: Während Simvastatin die Herstellung von Cholesterin in der Leber verlangsamt, hemmt Ezitimib die Aufnahme von Cholesterin aus dem Darm.

So gesehen darf man also erwartem, dass diese beiden Wirkstoffe ideale Konbinationspartner sein sollten. Tatsächlich senkt die Kombination aus Ezitimib und Simvastatin das schädliche LDL-Cholesterin um 10 bis 15 % mehr als Simvastatin alleine. Bisher fehlen jedoch Studien, die einen Langzeitnutzen beim Menschen nachweisen konnten. Die Frage: “Verhindert diese Kombination auch mehr Herzinfarkte oder verlängert sie das Leben mehr als Simvastatin allein ? ” kann also noch nicht beantwortet werden.

Eine von den Herstellerfirmen an 720 Patienten in Amerika durchgeführte Studie sollte eigentlich Klarheit bringen, brachte jedoch nur viel Aufregung. Die Enhance – Studie (Ezetimibe and High-Dose Simvastatin vs. Simvastatin Alone on the Atherosclerotic Process in Patients with Heterozygous Familial Hypercholesterolemia Study) zeigte zwar eine stärkere Cholesterinsenkung, aber keinen besseren Schutz vor der Ateriosklerose. (Untersucht wurde die Arteriosklerose durch Ultraschall – Messung der Dicke der inneren Gefäßwandschichten in der Halsschlagader über zwei Jahre – diese Messung der Intima-Media-Dicke ist ein gängiges Verfahren zur Abschätzung der Gefäßverkalkung.)

Für Ärger sorgte die Tatsache, dass das die Studie schon 2006 beendet wurde, die Ergebnisse aber erst jetzt in einer knappen Presseerklärung bekannt gegeben wurden. Verbraucherschützer und Politiker vermuten, dass die Herstellerfirmen die Ergebnisse bewußt zurückgehalten haben. Sie konnten schließlich viel Geld damit verdienen: Die Behandlung mit der Kombination kostet mehr als 100 Dollar, Simvastatin allein ist schon für 8 Dollar im Monat zu haben. Der Staatsanwalt von New York hat ein Verfahren eingeleitet, er verweist darauf, dass alleine der Staat New York 21 Millionen Dollar im Rahmen seiner Medicaid-Hilfe für Bedürftige für die möglicherweise unwirksame Kombination ausgegeben habe.

Die amerikanischen Kardiologenverbände und die Verbraucherschutzbehörde FDA (Food and Drug Administration) haben vor einem vorzeitigen Urteil gewarnt. Der FDA scheint die Intima-Media-Dicke allein zur Beurteilung der Wirksamkeit zu dürftig, es komme schließlich auf die Zahl der Herzinfarkte und Schlaganfälle an. Dazu wird die ENHANCE-Studfie allerdings mit ihrer geringen Teilnehmerzahl und kurzen Beobachtungsdauer kaum Aufschluss geben. Eine endültige Beurteilung erhofft die Behörde sich durch das Ergebnis der Improve-It (Improved Reduction of Outcomes: Vytorin Efficacy International Trial) – Studie mit ihren 12.500 Teilnehmern. Allerdings sind diese Ergebnisse nicht vor 2011 zu erwarten.

Deutsches Ärzteblatt: Erste Nachwehen der ENHANCE-Studie – Zweifel an Cholesterinhypothese – US-Fachverbände in der Kritik

The media is great when they get the story straight but dangerous when the writer is only superficially informed about the topic. And then the title editor can totally distort the intent of the story content by jazzing up the title late at night prior to the paper going to press. I’m referring to the stories recently released about study results of 720 patients taking either Vytorin or simvastatin (brand Zocor). Unfortunately, the reported results have been misinterpreted by patients to categorically mean that the combination of Zetia and Zocor in Vytorin doesn’t work any better in reducing cholesterol than generic simvastatin alone.

What got lost in the reporting was the purpose of this study and the type of patient being treated. The objective was meant to show how well Vytorin reduced plaque buildup in neck arteries in people whose genes gave them stratospheric cholesterol. This condition medically known as Heterozygous Familial Hypercholesterolemia is not typical of patients prescribed Vytorin.

The failure of Vytorin to perform in this subpopulation should not be interpreted to mean that Vytorin doesn’t work at all or isn’t better than simvastatin alone for patients needing the drug for other reasons–called “indications”. There were earlier studies done to get FDA approval to market the drug which demonstrated Vytorin worked for the broad population in lowering cholesterol and, especially, bad LDL.

Here’s a simplified analogy. Imagine if reporters presented poor clinical results for an already marketed cancer drug in another cancer indication than that for which it was already approved and used and the cancer drug in combination with the appropriate chemotherapy showed no improvement vs the chemotherapy alone. The story shouldn’t be interpreted to mean that patients prescribed the drug for a different cancer indication should worry that it wasn’t effective for that condition.

Merck and Schering Plough pulled the direct-to-patient TV ads to ease the upset in the market. It’s not surprising that they would pull these ads to allow for changes to explain the misunderstanding to patients. Yet the media questioned if they were hiding the “truth”.

Those of us marketing ethical drugs must always remember how difficult it is to convey a complicated medical message in a short TV ad. And how important it is to educate reporters about the impact of clinical study results. The Merck press release about the results on their company website explains the results clearly but unfortunately, the language is too difficult for lay people and typical reporters to interpret correctly.

Audrey