Abstract
To study the pathological changes in neurophysiological examination of lower-limb peripheral nerves in patients with long-term statin treatment. Forty-two patients (23 males, 19 females, mean age 51.9 and 52.3 years) with a definitive diagnosis of combined hyperlipidemia were studied. Other metabolic disorders or chronic ethanol abuse were excluded. Initial examinations included laboratory and neurophysiological measures (peroneal and tibial nerves: MNCV, CMAP, F-wave mean latency; superficial peroneal and sural nerve: SNCV, SNAP). Subsequently, treatment with simvastatin 20mg daily was initiated. Patients were followed for 24 months with examinations at 1, 6, 12 and 24 months after statin treatment initiation. None of the patients reported subjective symptoms typical for polyneuropathy. In laboratory findings, there was no elevation of muscle enzymes. Nevertheless, electrophysiological examination of lower-limb peripheral nerves demonstrated statistically significant prolongation of F-wave mean latency on peroneal and tibial nerves (p < 0.0001, paired t-test). A control group of 50 patients with combined hyperlipidemia but no statin treatment showed no changes over the same time interval. The study demonstrated that long-term The study demonstrated that long-term treatment with statins might cause a clinically silent but still electrophysiologically definite damage to peripheral nerves.
Highlights
Classification of hyperlipidemia is established according to the European Atherosclerosis Society (EAS), which distinguishes three types: hypercholesterolemia, hypertriglyceridemia and mixed or combined hyperlipidemia
Epidemiological studies have investigated the possible association of treatment with statins and increased risk of polyneuropathy[4, 5]
In 2001, a cohort study based on data from British general practitioners, uncovered increased relative risk of idiopathic polyneuropathy in patients treated with statins
Summary
Classification of hyperlipidemia is established according to the European Atherosclerosis Society (EAS), which distinguishes three types: hypercholesterolemia, hypertriglyceridemia and mixed or combined hyperlipidemia. Statins are inhibitors of HMG-CoA reductase, cause lowering of plasma concentration of cholesterol and especially the LDL fraction by blocking intracellular synthesis of cholesterol. This results in increased expression of LDL-receptors, followed by increased LDL uptake from the plasma. Indications for treatment with statins are pure hypercholesterolemia or combined hyperlipidemia with dominant elevation of LDL-cholesterol. Statins are classified according to their physical-chemical properties into two major groups: The first group is lipophilic (simvastatin, lovastatin, atorvastatin, cerivastat), metabolized via the hepatic system of cytochrome P450 isoenzymes, especially isoenzyme CYP3A4. The second group contains hydrophilic statins (pravastatin), which are not metabolized by cytochrome P450 and s excreted by the kidney. Pravastatin metabolites do not enter liver cells and will not affect intracellular enzyme (HMG-CoA reductase)
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