Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aluminum phosphide (AlP) is an insecticide and rodenticide that produces phosphine gas when exposed to moisture. Exposure to AIP has been described as through inhalation and ingestion routes and is typically either accidental or a suicidal attempt. The result is potential multiorgan toxicity involving the heart, kidneys, lungs, and liver, with an overall mortality related to exposure reported from 30% to 77%. The initial symptoms are nonspecific and can include epigastric pain, vomiting, diarrhea, dizziness, and dyspnea. Patients rapidly experience multisystem organ failure, cardiovascular collapse, and, finally, death. We report the case of a 3 year old girl with AlP poisoning who developed cardiogenic shock, ventricular arrhythmias, respiratory failure, liver injury, and significant acute kidney injury (AKI). She was successfully supported with veno-arterial extracorporeal membrane oxygenation (ECMO) for 16 days, treated with lidocaine and magnesium sulfate for ventricular arrhythmias, and received continuous renal replacement therapy (CRRT) and hemodialysis for 24 days for metabolic acidosis secondary to AKI. Despite her severe clinical presentation, she had complete normalization of her end-organ dysfunction with no neurological sequelae. This case demonstrates the high index of suspicion required for AlP poisoning given the potential for rapid progression and severe multiorgan toxicity. The authors recommend prompt referral to a tertiary care center with ECMO and CRRT capability in cases of suspected or documented AlP poisoning.
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PMID:Aluminum phosphide poisoning: Successful recovery of multiorgan failure in a pediatric patient. 3080 53

The acute hepatic porphyrias include four disorders: acute intermittent porphyria [AIP], hereditary coproporphyria [HCP], variegate porphyria [VP], and the rare porphyria due to severe deficiency of ALA dehydratase [ADP]. In the USA, AIP is the most severe and most often symptomatic. AIP, HCP, and VP are due to autosomal dominant genetic abnormalities, in which missense, nonsense, or other mutations of genes of normal hepatic heme biosynthesis, in concert with other environmental, nutritional, hormonal and genetic factors, may lead to a critical deficiency of heme, the end-product of the pathway, in a small but critical 'regulatory pool' within hepatocytes. This deficiency leads to de-repression of the first and normally rate-controlling enzyme of the heme synthetic pathway, delta- or 5-aminolevulinic acid [ALA] synthase-1, and thus to marked up-regulation of this key enzyme and to marked hepatic overproduction of ALA. In addition, except for ADP, there is marked overproduction as well of porphobilinogen [PBG], the intermediate immediately downstream of ALA in the synthetic chain, and, especially in HCP and VP, also porphyrinogens and porphyrins farther down the pathway. The major clinical features of the acute porphyrias are attacks of severe neuropathic-type pain. Pain is felt first and foremost in the abdomen but may also occur in the back, chest, and extremities. Attacks are more common in women than in men [ratio of about 4:1], often accompanied by nausea, vomiting, constipation, tachycardia, and arterial hypertension. Hyponatremia may also occur. Some patients also describe chronic symptoms of pain, anxiety, insomnia, and others.
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PMID:Pathogenesis and clinical features of the acute hepatic porphyrias (AHPs). 3098 16