Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

2 patients, who were treated with clioquinol after radical resection of carcinoma of the rectum and colostomy, developed symmetrical sensorimotor polyneuropathy, mild posterior tract ataxia, bilateral pyramidal tract lesions and optic neuropathy, a clinical picture compatible with subacute myelo-optic-neuropathy (S.M.O.N.). One patient had neurological symptoms after having received 750 g of clioquinol, 3 years after treatment started, and impairment of vision was noted after having received 1200 g. The other patient had neurological symptoms 6 weeks after clioquinol was first given, having received 65 g, the average daily dose being 1.5 g, and vision was impaired after 765 g had been administered. On examination 12 and 14 months after clioquinol had been discontinued, the first patient's vision was slightly improved, but he was otherwise unchanged, while the vision of the other patient was unchanged, but she had otherwise deteriorated slightly neurologically. Electrophysiological examinations confirmed the clinical observations. A multifactor etiology of the syndrome: neurotoxicity of clioquinol, paraneoplastic neuropathy and malabsorption, is discussed.
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PMID:[Subacute myelo-optic-neuropathy (S.M.O.N.) following treatment with clioquinol (author's transl)]. 5 Oct 51

Acquired copper deficiency has recently been recognized as a cause of myeloneuropathy mimicking subacute combined degeneration due to vitamin B-12 deficiency. A remote history of gastric surgery is frequently associated with this syndrome. However, the very limited prevalence of severe copper deficiency in patients with a history of gastric surgery suggests that additional contributing factors are likely to be involved. We describe a patient with copper deficiency and a previous Billroth II partial gastrectomy for gastric carcinoma, presenting with severe myelo-optico-neuropathy, demyelinating lesions of the brain, and subjective hyposmia. An abnormal glucose breath test also revealed small bowel bacterial overgrowth syndrome. Copper replacement therapy associated with antibiotic therapy was effective in preventing further neurological damage and in obtaining mild improvement. We propose that copper status should be evaluated in all patients presenting with unexplained noninflammatory myeloneuropathy. Small bowel bacterial overgrowth syndrome should be investigated as a cause of generalized malabsorption and a possible contributing factor to copper deficiency after gastric surgery, as should occult zinc ingestion.
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PMID:Myelo-optico-neuropathy in copper deficiency occurring after partial gastrectomy. Do small bowel bacterial overgrowth syndrome and occult zinc ingestion tip the balance? 1741 8