• Title/Summary/Keyword: Hyperosmolar nonketotic coma

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A Case of Acute Renal Failure Caused by Rhabdomyolysis due to Hyperosmolar Nonketotic Coma in Children (소아의 고삼투압성 비케톤성 혼수에서 발생한 횡문근 융해증에 의한 급성 신부전 1례)

  • Kwak, Jeong Won;Oh, Jae Min;Kim, Su Yung
    • Clinical and Experimental Pediatrics
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    • v.48 no.5
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    • pp.565-568
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    • 2005
  • Hyperosmolar nonketotic coma complicated in diabetes mellitus has been a rare cause of rhabdomyolysis, although increasingly reported recently. Acute renal failure can be complicated in 15 percent of rhabdomyolysis patients, but is rare in the case of rhabdomyolysis caused by diabetic hyperosomolar nonketotic coma. We report a 14 years-old boy with acute renal failure complicated by rhabdomyolysis caused by diabetic hyperosmolar coma.

Two Cases of MELAS Syndrome Manifesting Variable Clinical Cour (다양한 임상경과를 보인 멜라스(MELAS, mitochondrial encephalopathy, lactic acidosis, and stroke-like episode) 증후군 2례)

  • Choi, Seo Yeol;Lee, Seung-Ho;Myung, Na-Hye;Lee, Young-Seok;Yu, Jeesuk
    • Journal of The Korean Society of Inherited Metabolic disease
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    • v.16 no.2
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    • pp.102-108
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    • 2016
  • Mitochondrial encephalopathy, lactic acidosis, and stroke-like episode (MELAS) syndrome is one of mitochondrial encephalopathy. As the early clinical manifestations can be variable, it is important to suspect the disease, especially in patients with multiple organ dysfunctions. A boy was diagnosed with epilepsy when he was 9 years old. Two years later, severe headache and blurred vision developed suddenly. On examination, left homonymous hemianopsia was detected with corresponding cerebral parenchymal lesions in right temporo-occipito-parietal areas. MELAS syndrome was confirmed by genetic test, which showed m.3243 A>G mitochondrial DNA mutation. Multivitamins including coenzyme Q10 were added to anticonvulsant. He experienced 4 more events of stroke-like episodes over 5 years, but he is able to perform normal daily activities. A 13-year-old boy was brought to the hospital due to suddenly developed respiratory arrest and asystole associated with pneumonia. Past medical history revealed that he had multiple medical problems such as epilepsy, failure-to-thrive, optic atrophy, and deafness. He has been on valproic acid as an anticonvulsant which was prescribed from local clinic. He recovered after the resuscitation, but his cognition and motor function were severely damaged. He became bed-ridden. He was diagnosed with MELAS syndrome by brain MRI, muscle biopsy, and clinical features. Genetic test did not reveal any mitochondrial gene mutation. Four years later, he expired due to suddenly developed severe metabolic acidosis combined with hyperglycemic hyperosmolar nonketotic coma. The clinical features of MELAS syndrome are variable. Early diagnosis before the presentation to the grave clinical course may be important for the better clinical outcome.

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