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)

We report on a baby food, cereal flour P (CFP), which, although guaranteed free of cow's milk protein, caused failure to thrive and diarrhea, vomiting, and coughing fits in a 22-month-old child. The purpose of this study was to identify the allergen involved. The investigation used prick tests, RAST, and the RAST inhibition method. Specific IgE was elevated to 100 kU/l for cow's milk and to 15.3 kU/l for alpha-lactalbumin (2.5 kU/l for casein, 0.7 kU/l for beta-lactoglobulin). Antibovine IgG IgEs were associated. RAST inhibition experiments demonstrated the presence of alpha-lactalbumin in "food-quality" lactose used in this flour, at a dose of 1-5 micrograms/g of CFP. The daily intake of alpha-lactalbumin was found to be less than 70 micrograms. This exquisite clinical sensitization was attributed to the intestinal hyperpermeability (IH) which favors the access of milk allergen to the blood, leading to an ever-growing state of hypersensitivity. It could have been due to egg- and mustard-associated allergies as well as to giardiasis and intestinal candidosis. This work underlines the risk of masked food allergens and the need of thoroughly informative labeling.
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PMID:Identification of a masked allergen, alpha-lactalbumin, in baby-food cereal flour guaranteed free of cow's milk protein. 890 5

One of the most frequent precipitating factors for attacks of porphyria is the administration of drugs. Use of drugs with porphyrinogenic potential often worsens the condition and often poses a therapeutic dilemma. A 23-year-old female patient presented to the casualty room with abdominal pain, chest pain and vomiting. Her past medical history was significant with episodes of generalised abdominal pain. The patient was initially treated for her abdominal pain and vomiting. She developed seizures and was treated with diazepam and phenytoin. Based on the positive investigation reports (positive urine porphyrins, elevated urine ALA and positive porphobilinogen) and symptoms, a diagnosis of acute intermittent porphyria (AIP) was done. Before the diagnosis of AIP was made, the patient was treated with drugs which are not considered to be safe in porphyric patients, such as phenytoin, metoclopramide, and diclofenac. The use of these drugs probably contributed to the initial worsening of the patient's clinical condition. After the diagnosis of AIP was made, the patient was treated with safer alternatives; gabapentin as the antiepileptic agent, promethazine as antiemetic, and propanalol as the antihypertensive agent. Withdrawal of the unsafe agents and symptomatic management with the safer alternatives contributed to the recovery of the patient. Along with the case report and the observations made on the various drugs used in the patient, the importance of the various information sources available on the safety potential of these agents is discussed. The observations with the drugs used in our case will be a useful addition to the existing information on the safety of these agents.
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PMID:Drug use in porphyria: a therapeutic dilemma. 1894 96

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