Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162275 (ketonuria)
 553 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetes in childhood is essentially represented by the type 1 or insulin-dependent diabetes mellitus (IDDM). Classical symptoms (polyuria, polydipsia, asthenia, weight loss) are usually present at the first consultation and allow an immediate diagnosis at the physician's office by performing capillary (finger-prick) blood glucose measurement (> or = 200 mg/dL) and urine-stripe test (detection of glucosuria and ketonuria). A diagnosis performed at this stage of the disease leads to the admission of the child at hospital, in order to institute the insulintherapy without delay. This attitude should permit to avoid the rapid development of diabetic keto-acidosis, which is at present too much frequent at diagnosis (50% of the cases) and which is associated with potential risks of severe complications in children. In case of incidental detection of hyperglycemia without ketonuria in childhood, the differential diagnoses of early IDDM are the rare form of familial non insulin-dependent diabetes with onset in childhood (MODY: maturity-onset diabetes of the young) and the transient hyperglycemia in childhood. Finally, diabetes could also develop in the course of an other chronic disease (i.e. cystic fibrosis) or as part of genetical syndroms.
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PMID:[Diagnosis of diabetes mellitus in children]. 881 19

Two terrorist attacks with the nerve agent Sarin affected citizens in Matsumoto and Tokyo, Japan in 1994 and 1995, killing 19 and injuring more the 6000. Sarin, a very potent organophosphate nerve agent, inhibits acetylcholinesterase (AchE) activity within the central, peripheral, and autonomic nervous systems. Acute and long-term Sarin effects upon humans were well documented in these two events. Sarin gas inhalation caused instantaneous death by respiratory arrest in 4 victims in Matsumoto. In Tokyo, two died in station yards and another ten victims died in hospitals within a few hours to 3 months after poisoning. Six victims with serum ChE below 20% of the lowest normal were resuscitated from cardiopulmonary arrest (CPA) or coma with generalized convulsion. Five recovered completely and one remained in vegetative state due to anoxic brain damage. EEG abnormalities persisted for up to 5 years. Miosis and copious secretions from the respiratory and GI tracts (muscarinic effects) were common in severely to slightly affected victims. Weakness and twitches of muscles (nicotinic effects) appeared in severely affected victims. Neuropathy and ataxia were observed in small number (less than 10%) of victims, which findings disappeared between 3 days and 3 months. Leukocytosis and high serum CK levels were common. Hyperglycemia, ketonuria, low serum triglyceride, hypopotassemia were observed in severely affected victims, which abnormalities were attributed to damage of the adrenal medulla. Oximes, atropine sulphate, diazepam and ample intravenous infusion were effective treatments. Pralidoxime iodide IV reversed cholinesterase and symptoms quickly even if administered 6 h after exposure. Post Traumatic Stress Disorder (PTSD) was less than 8% after 5 years. However, psychological symptoms continue in victims of both incidents. In summary, both potent toxicity and quick recovery from critical ill conditions were prominent features. Conventional therapies proved effective in Sarin incidents in Japan.
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PMID:Sarin experiences in Japan: acute toxicity and long-term effects. 1696 40