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[Metabolic and nutritional neuropathy].
Rinsho Shinkeigaku. 2008 Nov; 48(11):1026-7.RS

Abstract

We assessed whether postgastrectomy polyneuropathy associated with thiamine deficiency is clinicopathologically identical to beriberi neuropathy, including a biochemical determination of thiamine status. The typical presentation for the two etiologies was as a symmetric sensorimotor polyneuropathy predominantly involving the lower limbs. In both groups, the main electrophysiologic findings were those of axonal neuropathy, most prominently in the lower limbs. Sural nerve biopsy specimens also indicated axonal degeneration in both groups. Subperineurial edema was commonly observed. Thiamine-deficiency neuropathies due to gastrectomy and dietary imbalance are identical despite variability in their clinicopathologic features and suggested that thiamine deficiency can be a major cause of postgastrectomy polyneuropathy. Characteristics of alcoholic neuropathy have been obscured by difficulty in isolating them from features of thiamine-deficiency neuropathy. We assessed 64 patients with alcoholic neuropathy including subgroups without and with coexisting thiamine deficiency. Thirty-two patients with nonalcoholic thiamine-deficiency neuropathy also were investigated for comparison. We concluded that pure-form of alcoholic neuropathy was distinct from pure-form of thiamine-deficiency neuropathy, supporting the view that alcoholic neuropathy can be caused by direct toxic effect of ethanol or its metabolites. However, features of alcoholic neuropathy is influenced by concomitant thiamine-deficiency state, having so far caused the obscure clinicopathological entity of alcoholic neuropathy.

Authors+Show Affiliations

Department of Neurology, Nagoya University Graduate School of Medicine.No affiliation info availableNo affiliation info available

Pub Type(s)

English Abstract
Journal Article
Review

Language

jpn

PubMed ID

19198152

Citation

Hattori, Naoki, et al. "[Metabolic and Nutritional Neuropathy]." Rinsho Shinkeigaku = Clinical Neurology, vol. 48, no. 11, 2008, pp. 1026-7.
Hattori N, Koike H, Sobue G. [Metabolic and nutritional neuropathy]. Rinsho Shinkeigaku. 2008;48(11):1026-7.
Hattori, N., Koike, H., & Sobue, G. (2008). [Metabolic and nutritional neuropathy]. Rinsho Shinkeigaku = Clinical Neurology, 48(11), 1026-7.
Hattori N, Koike H, Sobue G. [Metabolic and Nutritional Neuropathy]. Rinsho Shinkeigaku. 2008;48(11):1026-7. PubMed PMID: 19198152.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Metabolic and nutritional neuropathy]. AU - Hattori,Naoki, AU - Koike,Haruki, AU - Sobue,Gen, PY - 2009/2/10/entrez PY - 2009/2/10/pubmed PY - 2009/4/9/medline SP - 1026 EP - 7 JF - Rinsho shinkeigaku = Clinical neurology JO - Rinsho Shinkeigaku VL - 48 IS - 11 N2 - We assessed whether postgastrectomy polyneuropathy associated with thiamine deficiency is clinicopathologically identical to beriberi neuropathy, including a biochemical determination of thiamine status. The typical presentation for the two etiologies was as a symmetric sensorimotor polyneuropathy predominantly involving the lower limbs. In both groups, the main electrophysiologic findings were those of axonal neuropathy, most prominently in the lower limbs. Sural nerve biopsy specimens also indicated axonal degeneration in both groups. Subperineurial edema was commonly observed. Thiamine-deficiency neuropathies due to gastrectomy and dietary imbalance are identical despite variability in their clinicopathologic features and suggested that thiamine deficiency can be a major cause of postgastrectomy polyneuropathy. Characteristics of alcoholic neuropathy have been obscured by difficulty in isolating them from features of thiamine-deficiency neuropathy. We assessed 64 patients with alcoholic neuropathy including subgroups without and with coexisting thiamine deficiency. Thirty-two patients with nonalcoholic thiamine-deficiency neuropathy also were investigated for comparison. We concluded that pure-form of alcoholic neuropathy was distinct from pure-form of thiamine-deficiency neuropathy, supporting the view that alcoholic neuropathy can be caused by direct toxic effect of ethanol or its metabolites. However, features of alcoholic neuropathy is influenced by concomitant thiamine-deficiency state, having so far caused the obscure clinicopathological entity of alcoholic neuropathy. SN - 0009-918X UR - https://www.unboundmedicine.com/medline/citation/19198152/[Metabolic_and_nutritional_neuropathy]_ L2 - http://joi.jlc.jst.go.jp/JST.JSTAGE/clinicalneurol/48.1026?from=PubMed DB - PRIME DP - Unbound Medicine ER -