Rapid Responses to:
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Rapid Responses: Rapid Responses published:
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![[Read Rapid Response]](/icons/misc/sectionDOWN.gif)
Request for information in subsequent articles in this series.
- Stephen Fox (8 July 2006)
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fasting cholesterol or not
- Bernard Bedford, SO45 5WX (8 July 2006)
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Re: Request for information in subsequent articles in this series.
- W Stuart A Smellie (10 July 2006)
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Re: fasting cholesterol or not
- W Stuart A Smellie (10 July 2006)
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Re: Re: Request for information in subsequent articles in this series.
- Julian C Law (11 July 2006)
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Re: Re: Re: Request for information in subsequent articles in this series.
- W Stuart A Smellie (12 July 2006)
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Rhabdomyolysis 'Lite'
- Richard Bartley (17 July 2006)
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Re: Request for information in subsequent articles in this series.
- Raymond G Holder (17 July 2006)
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Re: Rhabdomyolysis 'Lite'
- W Stuart A Smellie (19 July 2006)
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Re: Re: Rhabdomyolysis 'Lite'
- Raymond G Holder (20 July 2006)
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Not clear that CoQ10 is the only problem
- Daniel R Hicks (25 July 2006)
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Re: Not clear that CoQ10 is the only problem
- W Stuart A Smellie (28 July 2006)
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Re: Re: Not clear that CoQ10 is the only problem
- Daniel R Hicks (29 July 2006)
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Re: Re: Not clear that CoQ10 is the only problem
- Raymond G Holder (2 August 2006)
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Statins should be first line in majority with hypertriglyceridaemia
- Naveed Sattar, Kevin A Deans (10 August 2006)
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Re: Statins should be first line in majority with hypertriglyceridaemia
- Eddie vo (12 August 2006)
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Re: Statins should be first line in majority with hypertriglyceridaemia
- Raymond G Holder (12 August 2006)
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Re: Statins should be first line in majority with hypertriglyceridaemia
- W Stuart A Smellie (12 August 2006)
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Re: Rhabdomyolysis 'Lite', Muscle Pain and Statins, the Role of Carnitine Deficiency
- Raymond G Holder (7 September 2006)
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Stephen Fox, General Practitioner Leigh WN7 2PE
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Can you, please, include data and advice in your subsequent articles on treating elderly patients? It has become the norm for my local District General Hospital to send everyone with abnormal lipids home on statin therapy. This includes both the fit and the doddery, even nonogenarians. My practice list of 2030 patients includes 350 in the 65-74 age group and 300 over 75's. The processing of these for QoF and monitoring of their progress is a significant workload; which is not supported by evidence. I have not been able to find the numbers needed to treat or the cost benefit versus risk in my octogenarian & nonogenarian patients. The same questions have been put to the consultants at the DGH and to the medicines management team at the Primary Care Trust. So far I have not received any response. Your input will be extremely valuable. Competing interests: None declared |
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Bernard Bedford, GP Waterside Health Centre, Hythe, SO45 5WX
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the one obvious item that this article omits, vital to primary care, is whether the cholesterol sample should be fasting or non-fasting. I've been taught that if the sample is just a cholesterol and not lipids then it doesn't matter but I know that lots of collegues insist on fasting for all samples, which puts severe strain on ealy morning venesection services. Competing interests: None declared |
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W Stuart A Smellie, Consultant CHemical PAthologist Bishop Auckland Hospital DL14 6AD
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Thank you for this request. The specific question of lipid lowering in the elderly is one which will be examined in a future review in J Clin Pathol. We do intend to link together and cross-reference answers as the nature of the questions inevitably produces overlap. The question of treatment in the very elderly is delicate, and we have found limited evidence as yet. The guidance found appears to remain rather vague as a result, and state that age should not be a bar to treatment but that those who have short life expectancy (3 years is quoted) may not benefit and treatment may be less appropriate. In addition, whilst there appears to be limited evidence to suggest that side effects occur more frequently in the very elderly, this patient group is by definition more at risk of being destabilised by any side effect, and potentially seeing their quality of life reduced, and it would appear prudent (personal opinion) to weigh any benefit against the consequences of adverse effect, and have a low threshold for discontinuation if an adverse effect occurs Competing interests: None declared |
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W Stuart A Smellie, Consultant Chemical Pathologist Bishop Auckland Hospital DL14 6AD
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Thanks for this very relevant question. It in fact forms part of a future answer not yet in press, concerning high density lipoprotein (HDL) cholesterol. As the questions originally answered are specific, related issues are often picked up in later questions, which will in time be cross -referenced to provide a joined up resource. Non-fasting results can produce higher triglycerides and lower high density lipoprotein cholesterol concentration. Our review is likely to advise that non-fasting measurements slightly overestimate CHD risk but are regarded as sufficiently accurate to use in screening and are more convenient for patients [1]. All people with an abnormal non-fasting screening lipids or at high risk should then have a fasting lipid profile [2][3]. In those patients who may justify treatment, a full risk assessment should then be performed, using a fasting value, and including triglyceride and HDL cholesterol measurement. 1. Pignone MP, Philips CJ et al. Screening and Treating Adults for Lipid Disorders. Am J Prev Med 2001;20(3S);77-89. 2. JBS 2 Joint British Societies’ guidelines on prevention of cardiovascular disease in clinical practice. Heart 2005;91:1-52 3. NSF. National service framework for coronary heart disease. London: Dept. of Health; 2000. Competing interests: None declared |
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Julian C Law, GP Kyle of Lochalsh
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Does taking an uncuffed sample make a significant difference to lipid measurements? Competing interests: None declared |
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W Stuart A Smellie, Consultant Chemical Pathologist Bishop Auckland General Hospital
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I am not aware of any significant influence of uncuffed samples on lipid measurement. Competing interests: None declared |
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Richard Bartley, Physotherapist Denbigh LL16 5BQ
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Statins appropriately prescribed according to the best available evidence are reasonably tolerated by patients and the incidence of rhabdomyolysis is extremely low. Pre-testing of CK in potentially high-risk patients reduces the risk of rhabdomyolysis within the population. You do not recommend regular testing of CK in patients prescribed statins if their initial CK levels are within 'normal' range. However, I wonder if many patients on statins do in fact suffer muscle damage over time (and do not report it). Are there sufficient on- going studies looking at the long-term effect statins have on striated muscle, in terms of both pain and function? Competing interests: None declared |
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Raymond G Holder, Retired engineer Not working
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As a patient who very nearly succumbed to statin treatment, and who has been trying to get the message across to those responsible for initiating such treatment, I deplore the continuing insistence on cholesterol reduction. everyone who prescribes or advises the use of statins should visit www.spacedoc.net and read of the thousands of patients with very real and often permanent damage from statin use. Statins reduce Coenzyme Q10 as well as cholesterol, but the attitude to this effect seems to be "So what", and the enormous importance of Q10 in all bodily functions is not known by those prescribing them. Q10 is essential for energy supply and oxygen regulation in every cell of the body, especially so in the heart liver, kidneys etc, so it is not to be wondered at that their functions are impaired by a deficit. However, as Q10 declines naturally from age 20 onwards to be only 50% of its original level at age 80, the more youthful among us may manage with a small reduction, but as the decline is an average of 8% per decade, a cholesterol reduction of 10% will give a similar Q10 reduction, i.e. an effective addition of 12 years or so to one's physical age. Body products such as carnitine, essential for muscle energy production from fat, become reduced and weakness and myopathy occur, with muscle pain due to lactic acidosis because waste products cannot be carried away. These factors have not been considered by the NICE Guidelines Committee, only a list of symptoms appears. There is considerable evidence that cholesterol is not the real culprit, in fact studies have shown that total mortality in 75 to 90 year olds is greater in those with lower cholesterol, and the trials and studies on which the saturated fat and cholesterol theories are based have been shown to be full of half truths and manipulated results. A totally independant appraisal of those insecure foundations is necessary before a generation of damaged older people becomes the legacy of this misguided "preventive " medication. I only keep alive by taking 600mg Q10 and 6grams Carnitine daily costing me £175 per month with no help from the NHS, without them my heart complains strongly and CK rises,the strength in my back disappears almost completely, certainly not a placebo effect. Cannot someone in authority research the biology and not just the statistics, then doctors would have some real knowledge available to understand the mechanisms involved, without just being instructed to toe the party line Competing interests: None declared |
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W Stuart A Smellie, Consultant Chemical Pathologist Bishop Auckland General Hospital
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This is a very fair question, which I hope will be answered more fully by someone with a more fundamental research interest in the effect of statins on striated muscle. We see patients whose CK rises on a statin, and also patients with a persistently elevated CK before receiving one. In most cases, conventional laboartory tests to exclude a macro-CK, thyroid and autoimmune disease do not reveal identifiable disease and in the routine context we do not proceed to muscle biopsy, but recheck on the assumption that these people are at theoretically increased risk of rhabdomyolysis. Our summary of the available guidance takes account of the majority of guidance that if not raised initially, further CK measurement is only recommended in symptomatic patients or those at potential risk. Within present knowledge, the largest systematic review we found [1] did not appear to identify clinically apparent chronic myopathy, other than the few cases of rhabdomyolysis, which we believe, but have no trials to support, can be reduced by identifying at risk patients. This does not exclude the possibility that myopathy could develop in cetain patients, and the clinical decision therefore becomes one of risk/benefit assessment in the context of the available evidence. 1. Law, M.R. et al. Quantifying effect of statins on low density lipoprotein cholesterol, ischaemic heart disease, and stroke: systematic review and meta-analysis. BMJ 2003; 326(7404):1423. Competing interests: None declared |
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Raymond G Holder, Retired engineer Not working BH9 3NF
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Stuart Smillie has been looking for a disease to account for muscle problems from statins. I am sure that the problem is due to effective starvation conditions in the muscle caused by the lack of carnitine to transport the fat fuel through the membrane into the mitochondria, and the demand for energy causes it to feed upon itself as in a last ditch effort at survival to fight another day. I suggest, as can be seen on my paper on the subject via www.spacedoc.net/r_holder.html, that as statins deplete the body's supply of the totally essential Coenzyme Q10, the reduced energy supply to the carnitine production mechanism means that it is no longer able to meet the body's demands. The muscle's "combustion" products are unable to get carried away because of this same deficiency, causing muscle pain by lactic acidosis. This has been verified by several affected former statin users, including myself, following successful use of carnitine by post polio sufferers for muscle wastage, and I suggested that statin damage creates a similar need, although carnitine deficiency had a different original cause in post polios. The immediate and continuing value of this supplement to many people can be seen on the spacedoc website. I have been taking it for 3 1/2 years with nothing but good results. Unfortunately, the regulators are on the scene again, withdrawing carnitine from sale in Canada for no real reason. Several hundreds have been using it regularly in Australia for several years after measured carnitine levels were found to be low in post polios, and without it I would quickly have a rise in CK and serious muscle wastage once more. Competing interests: Only as a badly damaged statin victim |
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Daniel R Hicks, Programmer Rochester MN 55901 USA
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As another person who cannot tolerate statins, I have to say that it's my impression that the suppression of CoQ10 synthesis is not the entire problem. I have experienced myopathy while taking 400mg/day CoQ10 and 4g/day l-carnitine, a protocol which would seem sufficient to compensate for the suppression of CoQ10 synthesis due to the statin. In addition, I have experienced a significant episode of rhabdomyolysis while taking niacin and the familiar symptoms of statin- induced myalgia/myopathy while taking(separately) ezetimibe and cholestyramine resin. To me this experience suggests the possibility that, in at least a small proportion of those who experience statin myopathy, the effect is directly due to the reduction in cholesterol levels, vs some side-effect of the medication. Unfortunately, in the US it's not common practice to check CK either before or during statin therapy, so it's difficult to determine how many cases in the US are associated with pre-existing CK elevation. Competing interests: None declared |
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W Stuart A Smellie, Consultant Chemical Pathologist Bishop Auckland Hospital
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There are two different and possibly overlapping issues here. One is the mechanism through which statins and other lipid lowering drugs may cause myopathy, and the other is the possibility of pre-existing myopathy acting as a risk factor for developing clinically severe myopathy if a patient is treated with a statin. It is the latter our answers try to address. It appears that some cases of rhabdomyolysis do occur in predisposed people, and that measurement of CK, whilst not sensitive enough to identify all those who might be at risk, does allow a number of people with pre-existing problems, such as hypothyroidism to be identified. This is the basis of the guidance to check CK before starting treatment. We do identify a number of people with a genuine raised CK but no apparent cause, and whilst there is limited evidence to support the policy, it would appear prudent to assume that these people are at potentially increased risk, and that more rigorous monitoring may prevent development of severe myopathy. As rhabdomyolysis remains very rare, identification of a small number of at risk people and a more cautious approach in these people, could potentially significantly reduce the incidence of this effect. More fundamental research will in time I hope identify the specific mechanisms whereby statins may contribute to this. Competing interests: None declared |
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Daniel R Hicks, Programmer Rochester, MN 55901
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Those interested in this topic might wish to look up the recent article by Dr. Panagiota Manta in Arch Intern Med 2006;166:1519-1524. I have not seen the actual article, but the Medscape summary of it ( http://www.medscape.com/viewarticle/541637 ) describes four cases of the "unmasking" of asymptomatic neuromuscular disease while under statin therapy. In my own personal case a history of occult polio and subsequent post -polio syndrome was "unmasked" by statin therapy. Competing interests: None declared |
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Raymond G Holder, Retired engineer Not working BH9 3NF
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After reading Daniel Hicks' and Stuart Smellie's responses on statin induced myopathy, I revisited Prof. Fernando Scaglia's comprehensive paper entitled Carnitine Deficiency, and it is clear that this is another case of drug induced Secondary Carnitine Deficiency, following on the heels of similar effects from valproate, pivampicillin, etc This is accompanied by and exacerbates the problems due to the known deficiency of Coenzyme Q10 due to a statin. A case of a side effect of drugs needed to improve sick patients now being inflicted upon healthy people in a vain attempt to safeguard their health. While Scaglia's paper, (which is easily accessible on http://www.emedicine.com/ped/topic321.htm), is mainly directed at pediatric problems, it does refer to later life and shows permanent supplement with L Carnitine etc may be needed. This fact has been borne out in the experience of myself and many others who have found L Carnitine effective and necessary. The other problems associated with carnitine deficiency, ie heart as well as skeletal muscle, are also of great importance. Not mentioned, but well researched by the W Australia Polio Network, is another form of Secondary Carnitine Deficiency found in Post Polio Syndrome, due to excessive demands on carnitine supplies caused by loss of Type 2 muscle and its replacement by more Type 1 in the original recovery period, needing fat as fuel, and its accompanying carnitine. Competing interests: Only as a badly damaged statin victim |
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Naveed Sattar, Professor of Metabolic Medicine Glasgow Royal Infirmary, Glasgow, G31 2ER, Kevin A Deans
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EDITOR – Smellie’s article on lipid management (1) provides a useful and welcome summary of current best practice in lipid management. We would like to make a few important comments regarding the patient with the mixed hyperlipidaemia who was eventually treated with fenofibrate (Case 2). The patient was initially treated with simvastatin 40mg daily. On finding his triglycerides and alanine aminotransferase to be elevated, he was changed to fenofibrate, and his cholesterol, triglycerides and alanine aminotransferase subsequently fell. Of the statins, simvastatin has a relatively poor triglyceride-lowering effect, and rosuvastatin and atorvastatin have a greater ability to lower triglycerides (2). We would suggest that in this patient, there would have been a strong case for stopping the simvastatin and clarifying if the elevated alanine aminotransferase was secondary to non-alcoholic steatohepatitis. Current evidence suggests that statins can be given safely in non-alcoholic steatohepatitis (3). If the cause of the elevated alanine aminotransferase was confirmed to be non-alcoholic steatohepatitis, either rosuvastatin or atorvastatin could then be cautiously introduced. In view of the incontrovertible cardiovascular endpoint evidence for the efficacy of statins (4) compared with the failure of the recent Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study to reach the primary outcome of reduced coronary events (5), there would be a strong case for not denying this patient a statin if at all possible. Similarly, while we would generally agree with the statement that persistent triglyceride concentrations above 5mmol/L justify treatment, we would like to point out that this does not necessarily mean treatment with a fibrate. Indeed, significantly more (not less) cases of pancreatitis occurred in the fenofibrate compared to placebo arm in FIELD (5). Thus there are a number of clinically important reasons to prescribe statins in those patients with modest hypertriglyceridaemia and elevated risk (>20%) risk of future cardiovascular events. 1. Smellie W. Testing pitfalls and summary of guidance in lipid management. BMJ 2006;333:83-86. 2. Jones PH, Davidson MH, Stein EA, Bays HE, McKenney JM, Miller E, et al; STELLAR Study Group. Comparison of the efficacy and safety of rosuvastatin versus atorvastatin, simvastatin, and pravastatin across doses (STELLAR* Trial). Am J Cardiol. 2003;92:152-60. 3. Kiyici M, Gulten M, Gurel S, Nak S, Dolar E, Savci G, et al. Ursodeoxycholic acid and atorvastatin in the treatment of nonalcoholic steatohepatitis. Canadian Journal of Gastroenterology 2003;17(12):713-718. 4. Baigent C, Keech A, Kearney PM, Blackwell L, Buck G, Pollicino C, et al; Cholesterol Treatment Trialists' (CTT) Collaborators. Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins. Lancet. 2005;366:1267-78. 5. The FIELD study investigators. Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): randomised controlled trial. Lancet 2005;366:1849-1861. Competing interests: None declared |
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Eddie vo, maintains health-heart.org Sutton (Qc) Canada J0E 2K0
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Prof. Sattar is evidently correct that fibrates should not be a first line treatment of hypertriglyceridaemia since the trial he cited, FIELD, ended with more deaths on drug than on placebo. Moreover, 3 trials with different fibrates also ended without mortality benefit, or with greater deaths than on placebo. Prof. Sattar then suggests statin in such patient but today's results of the SPARCL trial in NEJM are sobering when one looks at all-cause mortality (1). After over 10,000 patient-years on top dose (80 mg/d) atorvastatin [Lipitor] in high risk recent stroke patients, there are 5 more deaths than in the identical group on placebo. The failure of atorvastatin to save lives was already established in ASCOT where the mortality curves never separate over mean study duration 3.3 years. Moreover, the second statin suggested, rosuvastatin has no mortality benefit studies to its name at all. Clearly, when considering any kind of cardiovascular disease, one must consider the failure of statins to extend lives in all but very few studies [HPS, 4S], and invariably not in women, and not in those over age 70, as per PROSPER [links in (2)]. What is the point of preventing 'events', how ever they are defined in statin trials, when no lives are extended in virtually all groups in placebo controlled trials? 1. SPARCL http://content.nejm.org/cgi/content/short/355/6/549 2. http://www.cmaj.ca/cgi/content/full/173/10/1207-a Competing interests: None declared |
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Raymond G Holder, Retired engineer Nne BH9 3NF
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I get very dismayed when I see such intricate dissections of the minutia of cholesterol etc lowering, I see it as arguing about the colour of the paint on a house whose foundations are totally insecure. There now items in print entitled The Cholestrol Myths---- Con----Scam, and there is also Thincs, the Institute of cholesterol skeptics, with many professional members. These have very well researched investigations into the validity of much of the cholesterol saga, starting with Ancel Keys' very selective collection of trial results on the association of saturated fats with cholesterol level, apparently the seven countries which supported his theory are countered in his trials by seven which gave precisely the opposite result. The early cholesterol lowering by such means as absorbtion in the stomach often were counter productive, and the statin trials have been clouded by the inclusion of those sufferring from the familial form, which is not due to excess production of cholesterol, but due to a genetic defect in ability to dispose of LDL cholesterol which then accumulates in various parts of the body. It would appear that sometimes these have been included (accidentally???) in control groups and exagerrated the statin benefit. So many £ millions have spent on trials and studies carried out with insufficient discipline, or lateral thinking, for instance, the MRC/BHF trial in the 1990s assembled a cohort of 60,000, reduced to 30,000 by removing those with problems associated with reliability and clinic access, but then the trial did not commence on Day 1, but there was a 2 month run in period in which the statin was given, but no note seems to have been taken of the reasons for the quarter of those candidates who declined to carry on into the recorded part of the trial which started on the official Day 1. I suggest that many of them had the common side effects related to statins and did not wish to continue further. There was little difference in the death rate with higher cholesterol levels, and the fewer number of deaths in the treatment group was the same at all levels, leading to the amazing conclusion that levels should be further reduced. A more logical and disinterested conclusion would be that the lowering process was of benefit at all levels, but that the level itself was not important. Which brings me to the subject of Homocysteine, and by some freak, this is reduced along with cholesterol and the other essentials, Q10 etc. Prof McMully did some very informative research on homocysteine, mortality from heart attack is very strongly associated with rise in homocysteine level, the curve rises rapidly, almost following a square law. This chance effect on homocysteine appears to be the main reason why statins do save some lives, cholesterol lowering being mainly irrevelant. McMully was "drummed out of the Brownies", probably for going against the medical establishment of his day and the commercial interests of their drug company sponsors, but his assertion that Homocysteine could be countered by the use of cheap Folic acid, Vit B6 and B12 remains,(20p per tablet, not patentable), and not a great money spinner like statins. The almost universal addition of folic acid to flour and cereals makes it difficult to perform trials as an untreated control group would be hard to find. It would be far more rewarding to investigate homocysteine than wreak more havoc on a whole population with St Atins, which I consider to have been beatified without the intervention of a Devil's Advocate. Competing interests: Statin damaged patient |
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W Stuart A Smellie, Consultant Chemical Pathologist Bishop Auckland Hospital DL14 6AD
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Editor: I agree with Naveed Sattar that many patients with mild to moderate hypertriglyceridaemia may benefit statistically more from statins, at least on current evidence. I do not however think the argument applies in this case. He makes reference to points, which brevity precluded elaborating on in the original report as the main aim of the case was draw primary care laboratory users’ attention to the fact that omission of triglyceride measurement may miss significant hypertriglyceridaemia. This patient was genotyped for the Apolipoprotein E (Apo E) gene and found to be ApoE 2/2. He was assumed to have a type III hyperlipidaemia, which would be consistent with the numerically similar total cholesterol and triglyceride concentrations [1]. As we could not calculate his LDL because of the extent of his hypertriglyceridaemia (calculation threshold 400 mg/L or 4.5 mmol/L [2]) and do not quantify by ultracentrifugation, an approximation places his LDL on simvastatin at 2.0-2.5 mmol/L (assuming his VLDL concentration to be approximately 60% of his triglyceride concentration [1]), and his triglyceride concentration was very much above the exclusion limit for the FIELD trial [3](exclusion limit 5.0 mmol/L, actual baseline values: median 1.74, 1st quartile 1.34, 3rd quartile 2.34 mmol/L). This patient was therefore in a quite different risk group for pancreatitis (reviewed in the original article [4]) and extrapolation from FIELD is not valid. I referred to the frequent finding of non-alcoholic steatohepatitis with hypertriglyceridaemia in the case report. As Dr Sattar and I stated,this frequently improves when the raised triglycerides are successfully treated. I did not explicitly state however that in this case I believed the hypertriglyceridaemia and not the simvastatin to be responsible for the raised transaminase. The reason for stopping the statin was the severe hypertriglyceridaemia despite the dose of simvastatin, not the raised transaminase. Further investigation was not considered necessary as transaminase activities subsequently returned to the reference range. Whilst the more potent statins do indeed have greater triglyceride lowering properties, potency comparisons suggest (admittedly from far lower baseline triglyceride values - Astra Zeneca data on file) a maximum lowering of around 20% , representing a modest further lowering compared to that achieved on 40 mg of simvastatin. This is unlikely to have a marked additional effect in a patient with triglyceride concentrations of around 10 mmol/L on 40 mg simvastatin who is at significantly increased risk of pancreatitis. As the large scale trials have excluded patients with severe hypertriglyceridaemia, it is not possible to state the threshold when a fibrate may be used in place of a statin, although in severe mixed hyperlipidaemia, particularly type III, a fibrate may produce pronounced combined lipid lowering, [1] especially when there is marked hypertriglyceridaemia and only modest elevation of the LDL-C. Several patients nevertheless may require two classes of drug, and those with high LDL cholesterol and modest hypertriglyceridaemia will indeed be likely to benefit more from a statin. References 1. Durrington PN. Hyperlipidaemia Diagnosis and Management. 2nd Edition. Chapter 8 Type III Hyperlipidaemia 215-224 Butterworth- Heinemann1995 2. Tietz Textbook of Clinical Chemistry 3rd Edition 1999 Chapter 25 Lipids, Lipoproteins and Apolipoproteins 843-833 WB Saunders 1999. 3. The FIELD study investigators. Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): randomised controlled trial. Lancet. 2005.366:1849-1861 4. W S A Smellie, Forth J, Bareford D et al. Best Practice in primary care pathology. Review 3 Best Practice Working Group J Clin Pathol 2006;59:781- 787 Competing interests: None declared |
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Raymond G Holder, Retired Engineer BH9 3NF
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Muscle pain (and weakness) is a very common side effect of statin use, one that appears in the product literature, and so not thought worthy of a yellow card report on each case that appears, and possibly seen as a cost to be paid to avoid worse problems. However it causes considerable distress to those who suffer from it, and the website www.spacedoc.net has very many letters from those whose lives have been affected by it. Having come across the reason for this problem by diligent research of the literature available on the web, and using the results for my own benefit, I suggested to one despairing victim on the above website forum that he try some L Carnitine supplement, which he did, with very good results and now many more have now had relief from its use. However I am not altogether happy with trial and error methods like this, and I would suggest that these muscle pain patients should be given a Carnitine Level blood test to check for Secondary Carnitine Deficiency, requiring supplementation with L Carnitine (Carnitor in the BNF but rather expensive, the IV version needing to be administered slowly) Such deficiency is already recorded as a result of the use of the fairly common drugs Ampicillin and Valproic acid, although this is not mentioned in the BNF. Statins appear to cause this same problem. Not all Path. Labs will be able to perform this test locally, and referral elsewhere may be required, possibly to a paediatric unit, where some newborn may rarely inherit the deficiency, with sometimes fatal consequences. This procedure would put the subject on a proper scientific footing and permit discussion on an informed factual basis rather than the present reliance on reports of symptoms and opinions. Hundreds of Carnitine level tests have been made on Post Polio sufferers in W Australia,where Carnitine supplementation is very common and necessary, being required permanently. Competing interests: Solely as a badly damaged statin victim |
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