Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0740577 (acute abdominal pain)
 1,982 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Certain of the hepatic porphyrias are classified as belonging to the acute hepatic prophyrias, namely acute intermittent porphyria (AIP), variegate porphyria (VP), hereditary coproporphyria (HCP) and ALA-dehydrase deficiency. The common feature of all acute hepatic porphyrias is the sudden onset of neurological symptoms. The whole syndrome consists of acute abdominal pain crises with autonomic dysfunction, global or focal central nervous system involvement and a predominantly motor polyneuropathy. Mono- or oligosymptomatic manifestations of acute porphyrias occur and are probably underestimated. The laboratory diagnosis of porphyria depends on the measurement of porphyrin precursors in urine, whereas the measurement of porphyrins in urine and feces is essential for evaluation of the porphyria type. Enzyme measurements are used to identify asymptomatic family members whose quantitative excretions of porphyrins are normal. At present the pathogenesis of neurological manifestations of acute porphyrias remains an unsettled question. The major hypotheses are discussed in this paper. The most important precipitating factor in acute hepatic porphyrias is drug ingestion. As many new drugs have not been in use for sufficiently long periods to assess their porphyrogenic activity, it is safer to avoid drugs in patients with porphyria. The most effective treatment of porphyria attacks is the administration of heme. Among the porphyria patients with epileptic seizures requiring antiepileptic medication, treatment with bromides should be taken into consideration.
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PMID:[Acute hepatic porphyria and its neurological syndrome]. 857 Nov 13

The long-term effects of low-level lead intoxication are not known. The sympathetic skin response (SSR) was evaluated in a group of 60 former workers of a primary lead smelter, located in Santo Amaro, BA, Brazil. The individuals participating in the study were submitted to a clinical-epidemiological evaluation including questions related to potential risk factors for intoxication, complaints related to peripheral nervous system (PNS) involvement, neurological clinical examination, and also to electromyography and nerve conduction studies and SSR evaluation. The sample consisted of 57 men and 3 women aged 34 to 69 years (mean +/- SD: 46.8 +/- 6.9). The neurophysiologic evaluation showed the presence of lumbosacral radiculopathy in one of the individuals (1.7%), axonal sensorimotor polyneuropathy in 2 (3.3%), and carpal tunnel syndrome in 6 (10%). SSR was abnormal or absent in 12 cases, representing 20% of the sample. More than half of the subjects (53.3%) reported a history of acute abdominal pain requiring hospitalization during the period of work at the plant. A history of acute palsy of radial and peroneal nerves was reported by about 16.7 and 8.3% of the individuals, respectively. Mean SSR amplitude did not differ significantly between patients presenting or not the various characteristics in the current neurological situation, except for diaphoresis. The results suggest that chronic lead intoxication induces PNS damage, particularly affecting unmyelinated small fibers. Further systematic study is needed to more precisely define the role of lead in inducing PNS injury.
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PMID:Modifications of the sympathetic skin response in workers chronically exposed to lead. 1722