Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In some cases diabetes insipidus may be induced by taking medications. In this article we report the case of a 58-year-old man with manifest polyuria induced by colchicine administered because of a gout attack. Interestingly, similar symptoms were observed 6 years earlier after treatment with gentamycin. In the described state of the examined patient early detection of the disease, colchicine withdrawal and temporary amiloride (and indometacin) administration led to a full normalisation of the patient's clinical status. A similar reaction to two different drugs responsible for only a small percentage of iatrogenic diabetes insipidus suggests that some patients may exhibit a general "hypersensitivity" to the development of a drug-induced vasopressin resistance and that patients with the history of iatrogenic diabetes insipidus should not be treated or should be treated cautiously with other drugs known to induce vasopressin-resistant polyuria.
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PMID:[Nephrogenic diabetes insipidus induced by colchicine--a case report]. 1670 63

The prevalence of juvenile-onset gout has been increasing. Hereditary factors and secondary diseases should be considered in these patients. Adipsic diabetes insipidus (ADI) is characterized by arginine vasopressin (AVP) deficiency, which results in hypotonic polyuria, and dysfunction of thirst osmoreceptors, which results in failure to generate a thirst sensation in response to hypernatremia. We herein report a case of a boy with gouty arthritis, refractory hyperuricemia, prominent hypernatremia, a high creatinine concentration, and a history of surgery for a hypothalamic hamartoma. The patient was diagnosed with central diabetes insipidus after endocrine evaluation. Because he never had symptoms of thirst, the final diagnosis was corrected to ADI. This is the first report of gout due to chronic ADI in an adolescent. Volume contraction due to ADI might be one cause of hyperuricemia and renal impairment in such patients. Moreover, AVP deficiency might directly lead to low urate clearance due to the lack of vasopressin receptor 1 stimulation. Lack of polydipsia and polyuria may delay the diagnosis of ADI and lead to severe complications of a chronic hyperosmolar status. Sufficient and effective establishment of normovolemia is critical for these patients.
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PMID:Juvenile-onset gout and adipsic diabetes insipidus: A case report and literature review. 3027 Aug 4