BACKGROUND Methanol is a widely used industrial short-chain aliphatic alcohol with known neurotoxic properties. Mass poisoning outbreaks due to the consumption of methanol-adulterated alcoholic drinks present a challenge to healthcare providers due to the high mortality and serious central nervous system (CNS) damage in survivors. However, the impact of methanol exposure on the peripheral nervous system is unknown. OBJECTIVES To investigate the role of acute methanol exposure in the development of peripheral polyneuropathy (PNP) during the years following discharge from the hospital. METHODS A total of 55 patients with confirmed methanol poisoning (mean age of 47.9 ± 3.6 years; 9 females) were examined 4 times within a 6-year prospective longitudinal cohort study. The program included neurological and electromyographic examinations, visual evoked potentials, ocular examinations with retinal nerve fibre layer thickness measurements, brain magnetic resonance imaging, and a series of biochemical and toxicological tests. RESULTS PNP was observed in 20/55 (36 %) patients, which, in most of the cases, was mild axonal sensorimotor neuropathy. In 8/55 (15 %) patients, worsening of electromyographic findings was registered during the follow-up period, including 5 cases with newly diagnosed PNP and 3 cases of PNP progression. In one subject, complete reversal of PNP was registered after cessation of alcohol intake. The patients with PNP were significantly older (57.3 ± 5.3 versus 42.5 ± 3.9 years; p < 0.001), with higher blood glucose (5.93 ± 0.97 versus 4.81 ± 0.32 mmol/L; p = 0.035) and lower vitamin B1 (45.5 ± 7.4 versus 57.5 ± 5.2 ug/L; p = 0.015) concentrations. The number of chronic alcohol abusers was significantly higher in the PNP group (17/20 versus 20/35; p = 0.034). No associations between PNP prevalence/ dynamics and acute parameters of poisoning severity, arterial blood pH (7.26 ± 0.07 with PNP versus 7.18 ± 0.09 without PNP; p = 0.150), or serum methanol (1320.0 ± 700.0 with PNP versus 1430.0 ± 510.0 mg/L without PNP; p = 0.813) and ethanol (460.0 ± 560.0 with PNP versus 340.0 ± 230.0 mg/L without PNP; p = 0.675) concentrations at admission were found. No difference in the number of patients with visual (9/20 with PNP versus 12/35 patients without PNP; p = 0.431) and CNS sequelae (9/20 with PNP versus 15/35 patients without PNP; p = 0.877) of poisoning was present. DISCUSSION Despite the relatively high number of PNP cases, no association was found between the severity of acute methanol poisoning and the prevalence of PNP and its dynamics during six years of observation. We did not find an association between methanol-induced visual/ brain damage and the prevalence of PNP in survivors of poisoning. A high prevalence of PNP and its progression might be attributed to other causes, mainly a history of chronic alcohol abuse and insufficiently treated diabetes mellitus. Our results highlight the importance of complete cessation of alcohol consumption and better control of glycaemia in diabetic patients in the prevention and treatment of peripheral PNP.

中文翻译：

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急性甲醇中毒后的周围性多神经病：六年前瞻性队列研究。

背景技术甲醇是具有已知神经毒性特性的广泛使用的工业短链脂族醇。由于幸存者的高死亡率和严重的中枢神经系统（CNS）损害，因食用掺甲醇的酒精饮料而引起的大规模中毒暴发给医疗保健人员带来了挑战。但是，甲醇暴露对周围神经系统的影响尚不清楚。目的探讨急性甲醇暴露在出院后几年中在周围性多发性神经病（PNP）发生中的作用。方法在为期6年的前瞻性纵向队列研究中，对55例确诊为甲醇中毒的患者（平均年龄47.9±3.6岁； 9名女性）进行了4次检查。该计划包括神经和肌电图检查，视觉诱发电位，眼底检查，视网膜神经纤维层厚度测量，脑磁共振成像以及一系列生化和毒理学测试。结果在20/55（36％）患者中观察到PNP，在大多数情况下，这是轻度的轴突感觉运动神经病。在8/55（15％）患者中，在随访期间发现肌电图检查结果恶化，包括5例新诊断的PNP和3例PNP进展。在一名受试者中，停止饮酒后发现PNP完全逆转。PNP患者年龄较大（57.3±5.3 vs 42.5±3.9岁; p <0.001），血糖较高（5.93±0.97 vs 4.81±0.32 mmol / L; p = 0.035）和较低的维生素B1（45.5±7.4）浓度为57.5±5.2 ug / L； p = 0.015）。在PNP组中，长期酗酒者的数量明显增加（17/20对20/35； p = 0.034）。PNP患病率/动力学与中毒严重程度的急性参数，动脉血pH（PNP为7.26±0.07与PNP为7.18±0.09; p = 0.150）或血清甲醇（PNP为1320.0±700.0与1430.0±510.0 mg /之间没有关联在入院时发现了L（不含PNP； p = 0.813）和乙醇（含PNP的浓度为460.0±560.0，而不含PNP的浓度为340.0±230.0 mg / L； p = 0.675）。视觉中毒患者（9/20有PNP患者与12/35无PNP患者； p = 0.431）和中枢神经系统后遗症（9/20有PNP与15/35患者无PNP； p = 0.877）无差异存在。讨论尽管PNP病例相对较多，在六年的观察中，未发现急性甲醇中毒的严重程度与PNP的患病率及其动态之间存在关联。我们没有发现甲醇诱导的视觉/脑损伤与中毒幸存者中PNP的患病率之间存在关联。PNP的高流行及其发展可能归因于其他原因，主要是慢性酒精滥用史和未充分治疗的糖尿病史。我们的结果强调了在糖尿病患者外周血PNP的预防和治疗中，完全戒酒和更好地控制糖尿病患者的血糖的重要性。PNP的高流行及其发展可能归因于其他原因，主要是慢性酒精滥用史和未充分治疗的糖尿病史。我们的结果强调了在糖尿病患者外周血PNP的预防和治疗中，完全戒酒和更好地控制糖尿病患者的血糖的重要性。PNP的高流行及其发展可能归因于其他原因，主要是慢性酒精滥用史和未充分治疗的糖尿病史。我们的结果强调了在糖尿病患者外周血PNP的预防和治疗中，完全戒酒和更好地控制糖尿病患者的血糖的重要性。