Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 54-year-old woman, with no previously documented thyroid disease, treated with amiodarone (200 mg/day, five days a week for 33 months) for paroxysmal tachyarrhythmia complicating mitral stenosis, suddenly developed extremely severe thyrotoxicosis. After therapeutic failures with carbimazole and propylthyrouracil (PTU) associated with beta-blockers, she was transferred to intensive care for plasma exchange (PE). Two PE were performed, temporarily aggravating the cardiovascular status of the patient, with no secondary improvement. The quantity of T3 removed was very small, about 1,000 ng per exchange. On the 14th day PTU had to be discontinued (toxic thrombopenia) and only symptomatic treatment was maintained (assisted ventilation, digitalis, hyperalimentation). In the 4th month, while the patient had a high total serum iodine, hypothyroidism developed due to partial block of the organification of the iodine with high TSH and fixation; this state also lasted 4 months. Spontaneous recovery was observed after 8 months. In addition a severe peripheral neuropathy was observed during the hyperthyroid phase confirmed by electromyography, distinct from the signs of thyrotoxic myopathy. This gradually regressed over 7 months and may be attributed to amiodarone therapy. The association of these two successive types of thyroid disorder due to amiodarone is an exceptionally rare phenomenon. Severe thyrotoxicosis generally requires long-term symptomatic therapy, its natural course being towards spontaneous regression. PE are ineffective on the circulating hormonal levels and were dangerous because of the underlying cardiac disease. The development of hypothyroidism at the 4th month is explained by the persistent iodine overload, and therefore prolonged surveillance after withdrawal of therapy is advised. The neurological complication of amiodarone was quite distinct from the hyperthyroid myopathy.
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PMID:[Thyrotoxicosis, then hypothyroidism caused by iodine overload (amiodarone) associated with neuropathy. Failure of plasma exchange]. 630 50

A 69-year-old woman was admitted with apoplexy after operation of mitral valve stenosis and gastrectomy due to a gastric ulcer. In June 1994, her condition gradually worsened after acute pneumoniae in her right lung. Intravenous hyperalimentation with cimetidine administration was started to improve her undernourishment, because she had a history of gastric ulcer. However, after 10 days from the start of cimetidine therapy, anemia progressed rapidly. Biochemical examinations revealed that the serum indirect bilirubin and LDH levels were elevated and no serum haptoglobin was detected. These results indicated the development of hemolytic anemia, but at that time we could not clarify the reason. In October 1994, thrombocytopenia gradually progressed, and we halted the administration of cimetidine to ranitidine. Both hemolytic anemia and thrombocytopenia was dramatically improved after cessation of cimetidine administration. We then changed the drug from cimetidine, however the same phenomena have appeared again. The patient was in stable condition, after cessation of H2-blockers administration. The complication of hemolytic anemia and thrombocytopenia associated with H2-blocker administration in Japan.
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PMID:[Hemolytic anemia and thrombocytopenia induced by cimetidine: recurrence with ranitidine administration]. 905 66