Title: Organophosphate neuropathy due to methamidophos: biochemical and neurophysiological markers.
Authors: McConnell, R; Delgado-Téllez, E; Cuadra, R; Tórres, E; Keifer, M; Almendárez, J; Miranda, J; El-Fawal, H A; Wolff, M; Simpson, D; Lundberg, I
Published In Arch Toxicol, (1999 Aug)
Abstract: Neuropathy target esterase (NTE), the putative target enzyme for organophosphate induced delayed polyneuropathy (OPIDP), can be measured in lymphocytes but has rarely been assessed in acute human poisoning. Serum autoantibodies to nervous system proteins develop in hens poisoned with neuropathic insecticides and also have not been studied after human poisoning. Serial lymphocyte NTE (LNTE) was measured in a 16-year-old boy after acute poisoning with methamidophos for evaluation as a predictor of subsequent neuropathy. The profiles of serum autoantibodies to neurofilament triplet proteins, myelin basic protein, and glial fibrillary acidic protein were measured in order to characterize changes occurring as a result of OPIDP. Clinical neuropathy characterized by steppage gate and profound lower extremity weakness, decreased grip and pinch strength, and decreased ulnar and absent tibial compound muscle action potentials developed 2 weeks following poisoning. Sensory examination and nerve conduction studies were normal. On day 3 following poisoning LNTE was depressed (77% compared with subsequent baseline enzyme activity). Marked increases in serum immunoglobulin G (IgG) autoantibodies to glial fibrillary acidic protein and to neurofilament 200 were observed after the development of OPIDP. We conclude that inhibition of lymphocyte NTE is predictive of subsequent OPIDP. Serum autoantibody titers to nervous system proteins may be useful markers of neuropathy.
PubMed ID: 10447555
MeSH Terms: Adolescent; Biomarkers/analysis; Carboxylic Ester Hydrolases/antagonists & inhibitors; Humans; Insecticides/poisoning*; Lymphocytes/enzymology; Male; Nerve Tissue Proteins/immunology; Organothiophosphorus Compounds/poisoning*; Peripheral Nervous System Diseases/blood; Peripheral Nervous System Diseases/chemically induced*; Peripheral Nervous System Diseases/enzymology