Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.6.5.2 (NQO1)
 6,196 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In normal erythrocytes, small quantities of methaemoglobin are formed constantly and are continuously reduced, almost entirely by the reduced nicotine adenine dinucleotide (NADH) diaphorase system, rather than the reduced nicotine adenine dinucleotide phosphate (NADPH) diaphorase system. Methaemoglobinaemias are usually the result of xenobiotics, either those that may directly oxidise haemoglobin or those that require metabolic activation to an oxidising species. The most clinically relevant direct methaemoglobin formers include local anaesthetics (such as benzocaine and, to a much lesser extent, prilocaine) as well as amyl nitrite and isobutyl nitrite, which have become drugs of abuse. Indirect, or metabolically activated, methaemoglobin formation by dapsone and primaquine may cause adverse reactions. The clinical consequences of methaemoglobinaemia are related to the blood level of methaemoglobin; dyspnoea, nausea and tachycardia occur at methaemoglobin levels of > or = 30%, while lethargy, stupor and deteriorating consciousness occur as methaemoglobin levels approach 55%. Higher levels may cause cardiac arrhythmias, circulatory failure and neurological depression, while levels of 70% are usually fatal. Cyanosis accompanied by a lack of responsiveness to 100% oxygen indicates a diagnosis of methaemoglobinaemia, which should be confirmed using a CO-oximeter. Pulse oximeters do not detect methaemoglobin and may give a misleading impression of patient oxygenation. Methaemoglobinaemia is treated with intravenous methylene blue (methyl-thioninium chloride; ;1 to 2 mg/kg of a 1% solution). If the patient does not respond, perhaps because of glucose-6-phosphate dehydrogenase (G6PD) deficiency or continued presence of toxin, admission to an intensive care unit and exchange transfusion may be required. Dapsone-mediated chronic methaemoglobin formation can be reduced by coadministration of cimetidine to aid patient tolerance. Increasing knowledge and awareness of drug-mediated acute methaemoglobinaemia among physicians should lead to prompt diagnosis and treatment of this potentially life-threatening condition.
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PMID:Drug-induced methaemoglobinaemia. Treatment issues. 882 17

Clinical assessment of the respiratory function is critical in amyotrophic lateral sclerosis (ALS). A standardized process is to monitor the respiratory subscore of the revised ALSFRS (RofALSFRS-R). We tested the utility of RofALSFRS-R and its individual questions in evaluating respiratory functionality. Three hundred and fifty-seven consecutive ALS patients were assessed at entry (T0), three and six months later (T1 and T2). ALSFRS and its subscores decayed significantly (p < 0.001) over time. Improvement in the first respiratory question (dyspnoea, QR1) was found in about 10% of the patients in each period. Between T0 and T1 a significant negative correlation was found between decrease in gait score and QR1 (p = 0.021, r = -0.395) in the subgroup of ALS patients who showed QR1 improvement (n = 34). An improvement in the other respiratory questions was noticed in about 6% of the patients, related to non-invasive ventilation. Possibly, decreased mobility and metabolic demand can cause fewer respiratory symptoms in a subset of patients. The respiratory questions included in ALSFRS-R should be re-addressed by the ALS community.
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PMID:The R of ALSFRS-R: does it really mirror functional respiratory involvement in amyotrophic lateral sclerosis? 2520 8