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Rapid Responses: Rapid Responses published:
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Statins therapy, every coin has two sides
- Weekitt Kittisupamongkol (13 November 2008)
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Low doses statin for primary prevention
- Plamen H Yovchevski, Nadezhda Doncheva and Zhivka Boneva (24 November 2008)
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Is statin treatment effective in familial hypercholesterolaemia?
- Uffe Ravnskov, Malcolm Kendrick , Paul J. Rosch (24 November 2008)
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Weekitt Kittisupamongkol, General Practitioner Hua Chiew Hospital, Bangkok 10100. Thailand
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I read with interest the article by Versmissen and colleagues (1). I was wondering if the authors have ever performed liver function tests in the patients during the study. Statins usages are associated with abnormal liver function tests. While the result shows the reduction in the risk of coronary heart diseases, nobody knows whether the patients develop active liver diseases. These would definitely involve the ethical issues. Liver enzymes should be checked prior to commencing statins therapy, 6–8 weeks after treatment, annually thereafter, and withdrawn statins if the transaminases rise to three times the upper limit of normal. Reference 1. Versmissen J, Oosterveer DM, Yazdanpanah M, Defesche JC, Basart DCG, Liem AH, et al. Efficacy of statins in familial hypercholesterolaemia: a long term cohort study. BMJ 2008; 337: a2423 Competing interests: None declared |
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Plamen H Yovchevski, Head of Nephrological Department Medical Institute of Ministry of Interior, 79 Skobelev blvd., 1606 Sofia, Bulgaria, Nadezhda Doncheva and Zhivka Boneva
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In a cohort study of the efficacy of statin treatment on risk of coronary heart disease in patients with familial hypercholesterolaemia, Versmissen and colleagues’ report that lower statin doses than those currently advised reduced the risk of coronary heart disease to a greater extent than anticipated in patients with familial hypercholesterolaemia (1). These results match the results from the Simvastatin vs Therapeutic Lifestyle Changes and Supplements: Randomized Primary Prevention Trial, which show a potential beneficial effect of food supplements and lifestyle changes on managing hyperlipidemia (2). In the latter study, the achieved results with red yeast rice containing monacolins equivalent of low doses of lovastatin is identical to the results from therapeutic doses of statin for primary prevention (3). The conclusions reached in the two studies are intriguing and show some potential for lowering the statin dose or starting food supplements containing monocolins instead. This will lead to the reduction of side effects of statin treatment and will improve the compliance. References 1. Versmissen J, Oosterveer DM, Yazdanpanah M, Defesche JC, Basart DCG, Liem AH, et al. Efficacy of statins in familial hypercholesterolaemia: a long term cohort study. BMJ 2008;337:a2423. (11 November.) [Full text] 2. Becker DJ, Gordon RY, Morris PB, Yorko J, Gordon YJ, Li M, et al. Simvastatin vs therapeutic lifestyle changes and supplements: randomized primary prevention trial. Mayo Clin Proc. 2008;83(7):758-764. [Full text] 3. Yovchevski PH, Doncheva NI. Low-Dose Statin Concentration in Red Yeast Rice: A Confounding Effect on Outcome? Mayo Clin Proc. 2008;83:1187. [Full text] Competing interests: None declared |
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Uffe Ravnskov, independent researcher Magle Stora Kyrkogata 9, 22350 Lund, Sweden, Malcolm Kendrick , Paul J. Rosch
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In
their cohort study of statin efficacy in familial hypercholesterolaemia (FH)
Versmissen et al claimed that such treatment was followed by a 76 % risk
reduction of coronary heart disease (CHD).1 However, they have
disregarded that heart mortality in FH is strongly and inversely associated with
age. In the Simon Broome Register Group study, relative risk of CHD for age
20-39 was 84.3, plummeted to 5.3
for age 40-59, and was only 1.2 for those age 60 or older.2 The
explanation that those with the highest cholesterol had died early is invalid,
because many studies, including that of Versmissen et al., have found no
difference in mean LDL cholesterol between those with and without cardiovascular
disease.3 That the relative risk after age 55 was close to that of the general population may therefore not have been due to treatment, but rather to the unexplained benefit of being older. A similar bias was introduced in their calculation of heart mortality in the untreated and treated periods, since the mean age before treatment was on average eight years lower than afterwards. In the Simon Broome cohort study CHD mortality decreased significantly after the introduction of statins in patients aged 20-39, but not in the older cohorts.2 The questionable benefit of statin treatment in middle-aged, and especially elderly FH patients, must therefore be balanced against potential side effects. Of particular concern is that an increased incidence of cancer has been reported in most animal experiments, in five statin trials, in one cohort and in one case-control study.4,5 Many cohort studies have found that low cholesterol is a risk factor for cancer, which might explain why cancer mortality is significantly lower in FH, even after treatment.6 But will this cardioprotection persist after lifelong statin use?
Competing interests: None declared |
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