chiniofon and Syndrome

Topics: Adult; Child, Preschool; Clioquinol; Female; Humans; Hydroxyquinolines; Japan; Male; Middle Aged; Myelitis; Optic Neuritis; Syndrome

Topics: Acupuncture Therapy; Adolescent; Adult; Aged; Clioquinol; Female; Humans; Hydroxyquinolines; Male; Middle Aged; Moxibustion; Myelitis; Optic Neuritis; Syndrome

Topics: Adult; Clioquinol; Diarrhea; Evoked Potentials, Visual; Female; Humans; Hydroxyquinolines; Male; Middle Aged; Myelitis; Optic Neuritis; Syndrome

Topics: Clioquinol; History, 20th Century; Humans; Hydroxyquinolines; Japan; Myelitis; Optic Neuritis; Quinolines; Syndrome

Topics: Clioquinol; Humans; Hydroxyquinolines; Japan; Optic Atrophy; Peripheral Nervous System Diseases; Spinal Cord Diseases; Syndrome

Clioquinol is still consumed in India in considerable amounts but no new case reports have appeared since 1977. A review is made for a regional neurotoxicology group of an enquiry that we conducted in Bombay to gather information regarding SMON, spanning the period of 1967 to 1976. Nine patients were diagnosed with a variable degree of confidence as suffering from SMON, two from a retrospective search and seven after a prospective watch for the disease. Myelopathy with predominant more distal dysesthesia was seen more often than the full-blown picture of SMON. The peripheral neuropathy component (N) diagnosed clinically or electrophysiologically was seen only once. Pyramidal tract disturbances and resulting spasticity was as striking as posterior column disorder and sensory ataxia. Subacute myelopathy was seen in six patients, optico-myelopathy in two, and myeloneuropathy only once. It was clear that clioquinol has potential neurotoxicity, but no definitive explanation was forthcoming about the vast difference in the prevalence of SMON as reported from Japan and seen by us in Bombay.

Topics: Adult; Aged; Child; Clioquinol; Female; Humans; Hydroxyquinolines; India; Japan; Male; Middle Aged; Optic Atrophy; Peripheral Nervous System Diseases; Retrospective Studies; Spinal Cord Diseases; Syndrome

Forty Swedish victims of halogenated hydroxyquinoline neurotoxicity were claimed by Dr Hansson in 1981. He had seen only a few of these patients himself. Furthermore, in half the number of patients a neurological examination had been performed only long ago or not at all. A survey of these cases has never been presented. Therefore, extensive and, where possible, complete medical data were obtained for these 40 and one additional patient. A neurological differential diagnostic evaluation was made in each case. It was found that only one had a full-blown SMON syndrome. In all, only half of the patients in this series showed any evidence of a neurotoxic lesion due to clioquinol. The case stories were also presented in detail to the Baumgartner group, with similar diagnostic results. Detailed clinical data and differential diagnoses are presented in the communication.

Topics: Adolescent; Adult; Aged; Child; Child, Preschool; Clioquinol; Female; Humans; Hydroxyquinolines; Male; Middle Aged; Optic Atrophy; Peripheral Nervous System Diseases; Spinal Cord Diseases; Sweden; Syndrome

The disposition and metabolism of iodochlorhydroxyquin (clioquinol), an amebicidal drug with neurotoxic properties, were studied in dogs and rats with 14C-labelled drug. Pharmacokinetic studies in the dog demonstrated that the compound was well absorbed; the bioavailability was 36% of the dose of 1 mg/kg. The serum half-life was 1.3-1.8 h. In both the dog and the rat, biliary excretion was a major route of elimination. The dog excreted 27% of an intravenously administered dose (1 mg/kg) in the bile within 2 h; the rat excreted 39% of the dose (5 mg/kg i.v.) in less than 3 h. Elimination via the renal route was also substantial in both species. Urinary and biliary metabolites were separated by TLC (thin layer chromatography) and identified as sulfate and glucuronide conjugates in both species. No evidence for any other metabolites was found. A significant difference was observed between the dog and the rat in the extent of conjugation; the percentage radioactivity in the urine accounted for by the unchanged compound was six to twenty times greater for the dog than for the rat. The species differences in the disposition and metabolism of the compound might explain its greater toxicity in the dog than in the rat.

Topics: Administration, Oral; Animals; Bile; Biological Availability; Clioquinol; Dogs; Female; Hydroxyquinolines; Injections, Intravenous; Kinetics; Male; Myelitis; Optic Neuritis; Rats; Rats, Inbred Strains; Species Specificity; Syndrome

Topics: Clioquinol; Diagnosis, Differential; Humans; Hydroxyquinolines; Japan; Optic Atrophy; Spinal Cord Diseases; Syndrome

Clioquinol can increase the penetration of metallic cations through cellular membranes by forming lipophilic metal-chelates. It is suggested that the pathogenesis of SMON may involve an accumulation of injurious metals in nervous tissues due to facilitated uptake by complex formation with clioquinol. The Japanese have been more heavily exposed to metals by environmental pollution than the inhabitants of other countries, which may explain the prevalent occurrence of SMON in Japan.

Topics: Clioquinol; Drug Interactions; Environmental Pollutants; Humans; Hydroxyquinolines; Japan; Metals; Myelitis; Optic Neuritis; Syndrome

In order to explore the effects of metals upon the subsequent onset of several clinical events in SMON, a retrospective cohort study was attempted. Study subjects were 216 "exposed" patients and 149 "unexposed" patients. "Exposure" was defined as the simultaneous ingestion of metal-containing drugs with clioquinol before the onset of neurological disorders. These two cohorts were identified from 531 patients among 832 patients, collected by the nationwide survey in 1975 and 1976. Effects provoked by ingestion of five metals (alminum, calcium, magnesium, copper and bismuth) were evaluated by relative risks with and without adjustment of the total amount of clioquinol ingested. Adjusted relative risks were estimated by maximum likelihood method. Significance of relative risk was determined by its 95% confidence interval. Following major findings emerged from the present analysis. (1) Simultaneous ingestion of Al-, Ca-, Mg-, Cu- or Bi-containing drugs with clioquinol significantly reduced the risk of developing motor disturbances. (2) Risk of developing visual disturbances were favorably modified by Al-containing drugs. (3) Clinical severity was significantly reduced by ingestion of Al-, Ca-, Mg- or Bi-containing drugs. (4) About 2-fold increase in risk of unfavorable clinical course was demonstrated by Al-containing drugs. (5) Onset of both green-fur on the tongue and relapse appeared unrelated to the metal-containing drugs ingested. (6) Combined ingestion of two kinds of metal-containing drugs with clioquinol appeared to yield more favorable effects than single ingestion of metal-containing drugs. (7) Al- or Bi-containing drugs demonstrated the strongest association with clinical features of SMON, followed by the drugs containing Mg or Ca. Cu-containing drugs had little association.

Topics: Clioquinol; Drug Interactions; Female; Humans; Hydroxyquinolines; Male; Metals; Middle Aged; Motor Activity; Myelitis; Optic Neuritis; Risk; Syndrome; Tongue; Vision Disorders

A 4-year-old boy presented with consumptive coagulopathy suspected to be due to Kasabach-Merritt syndrome. Localization of homologous indium-111 platelets in the region of the right sacral ala confirmed that this was the site of disease and facilitated radiation treatment, which proved to be curative.

Topics: Blood Platelets; Child, Preschool; Hemangioma; Humans; Hydroxyquinolines; Indium; Male; Organometallic Compounds; Oxyquinoline; Radionuclide Imaging; Spinal Neoplasms; Syndrome; Thrombocytopenia

Topics: Drug Combinations; Gastrointestinal Agents; Humans; Hydroxyquinolines; Male; Middle Aged; Myelitis; Optic Neuritis; Oxyquinoline; Syndrome

Topics: Clioquinol; Diverticulum; Drug Combinations; France; Humans; Hydroxyquinolines; Male; Middle Aged; Myelitis; Optic Neuritis; Oxyquinoline; Syndrome

Topics: Humans; Hydroxyquinolines; Myelitis; Optic Neuritis; Oxyquinoline; Syndrome

Topics: Abdomen; Clioquinol; Humans; Hydroxyquinolines; Male; Middle Aged; Optic Atrophy; Pain; Spinal Cord Diseases; Syndrome

Acrodermatitis enteropathica, a heritable disease of zinc deficiency, was formerly amenable to treatment only with dihaloquinolinol drugs. A few cases of optic atrophy were reported in surviving patients and were proposed as examples of ocular drug toxicity, principally because of the association between iodochlorhydroxyquin and subacute myelo-optic neuropathy (SMON) in Japan. An alternate hypothesis is now offered: that the optic atrophy was secondary to the zinc deficiency, which is consistent with diverse evidence cited from the literature. Therefore, it would seem worthwhile to investigate zinc in cases of disk pallor described as idiopathic or drug associated, and to investigate visual function in cases of severe malnourishment.

Topics: Acrodermatitis; Clioquinol; Humans; Hydroxyquinolines; Myelitis; Optic Atrophy; Optic Neuritis; Oxyquinoline; Syndrome; Time Factors; Zinc

Topics: Humans; Hydroxyquinolines; Myelitis; Optic Neuritis; Syndrome

Topics: Adolescent; Adult; Aged; Amnesia; Amnesia, Retrograde; Child; Child, Preschool; Female; Humans; Hydroxyquinolines; Male; Middle Aged; Myelitis; Optic Neuritis; Sweden; Syndrome

Topics: Clioquinol; Humans; Hydroxyquinolines; Myelitis; Optic Neuritis; Oxyquinoline; Syndrome

Topics: Abdomen; Adult; Aged; Female; Humans; Hydroxyquinolines; Male; Middle Aged; Myelitis; Optic Neuritis; Oxyquinoline; Pain; Syndrome