caa a22 4500 445810106 CHVBK 20180317145209.0 cr unu---uuuuu 170323e20110801xx s 000 0 eng 10.1007/s00415-011-5950-z doi (NATIONALLICENCE)springer-10.1007/s00415-011-5950-z Dyslipidaemia in chronic acquired distal axonal polyneuropathy [Elektronische Daten] [Yusuf Rajabally, Rahul Shah] The link between hypertriglyceridaemia (HTG) and/or hypercholesterolaemia (HCL) and neuropathy is uncertain. We retrospectively reviewed records of 100 consecutive patients investigated for acquired chronic axonal distal polyneuropathy of unknown cause. Findings were compared with those of 102 consecutive controls. Patients with idiopathic neuropathy were subsequently compared with age- and gender-matched controls. There were more neuropathy patients than controls with HCL, defined as cholesterol levels >5mmol/L (63 vs. 45.1%; p=0.011). Neuropathy patients also had higher cholesterol levels than controls (p=0.04). Cholesterol-lowering drug usage was similar in both groups. HTG (defined as >2mmol/L) and triglyceride levels were comparable in both groups. HTG ranged from 2.1-4.2mmol/L in neuropathy patients. A cause for neuropathy was identified in 59 patients. Thirty-one had impaired glucose metabolism. Forty-one had idiopathic neuropathy. No link was demonstrated between idiopathic neuropathy or painful idiopathic neuropathy, and HTG/HCL. Mean triglyceride and cholesterol levels in patients with idiopathic neuropathy were comparable to those of controls. HTG was significantly more common (p=0.027), and triglyceride levels significantly higher (p=0.005) in patients with neuropathy due to diabetes/impaired glucose tolerance (IGT)/alcoholism, than in patients with neuropathy of any other cause. These results suggest HCL >5mmol/L may represent a cofactor contributing to presence of neuropathy irrespective of the underlying cause. They on the other hand do not support mild/moderate HTG as an independent cause of neuropathy. HTG is common in patients with neuropathy associated with diabetes/IGT/chronic alcoholism, where it may play a role in peripheral nerve damage. As previously reported, IGT was in our cohort frequent, present in one case in three, in the absence of another identifiable aetiology. Springer-Verlag, 2011 Acquired nationallicence Axonal nationallicence Cholesterol nationallicence Chronic nationallicence Diabetes nationallicence Distal nationallicence Dyslipidaemia nationallicence Impaired glucose tolerance nationallicence Lipids nationallicence Neuropathy nationallicence Triglycerides nationallicence Rajabally Yusuf Neuromuscular Clinic, Department of Neurology, University Hospitals of Leicester, LE5 4PW, Leicester, UK aut Shah Rahul Neuromuscular Clinic, Department of Neurology, University Hospitals of Leicester, LE5 4PW, Leicester, UK aut Journal of Neurology Springer-Verlag 258/8(2011-08-01), 1431-1436 0340-5354 258:8<1431 2011 258 415 https://doi.org/10.1007/s00415-011-5950-z text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s00415-011-5950-z text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Rajabally Yusuf Neuromuscular Clinic, Department of Neurology, University Hospitals of Leicester, LE5 4PW, Leicester, UK aut NATIONALLICENCE 700 1- Shah Rahul Neuromuscular Clinic, Department of Neurology, University Hospitals of Leicester, LE5 4PW, Leicester, UK aut NATIONALLICENCE 773 0- Journal of Neurology Springer-Verlag 258/8(2011-08-01), 1431-1436 0340-5354 258:8<1431 2011 258 415 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer