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Query: UMLS:C0018099 (gout)
5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gout is a metabolic disorder that results in hyperuricemia and the deposition of positively birefringent monosodium urate crystals in various parts of the body. Intoxication of sodium bicarbonate (SBC) for 35 days in Korean native broilers was investigated. Sixty birds, aged 2 weeks, divided into 5 groups were exposed to excess SBC: 2 g/L (group A), 7.5 g/L (group B), 20 g/L (group C), 40 g/L (group D). Toxicopathological examination of all exposed birds revealed the manifestation of visceral and articular gout in group C, while birds of group D showed acute kidney damage with manifestation of excessive visceral gout. Interestingly, few birds in group D also showed signs of rare condition of acute articular gout. Dose-dependent increments in erythrocytic count, hematocrit values, and hemoglobin levels of the exposed birds were observed. Hypernatremia, hyperuricemia, hypokalemia, and hypochloremia were common findings among exposed birds. Microscopic examination of birds that manifested visceral gout revealed significant urate deposit, tubular necrosis, and tophi formation in renal interstitium. These findings provide a pathophysiological link that SBC intoxication may support hyperuricemia, which is an independent risk factor for gout and other renal dysfunctions. Further study is required to delineate the effect of lowering uric acid on progression of gout and other renal diseases.
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PMID:Gout induced by intoxication of sodium bicarbonate in Korean native broilers. 1586 64

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