Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glucocorticoids (GCs) are among the most commonly used drugs. They have been employed to treat almost every known disease, from urticaria to leukemia. GCs are so termed because of their action to increase plasma glucose as a result of enhanced hepatic gluconeogenesis, but they play, also, key regulatory roles in a wide variety of physiologic processes. They are essential for survival under stress. GC effect is mediated through receptors localised in cytosol. Receptor-GC complexes bind to hormone response elements in nuclear DNA, affect transcription of genes, either stimulating or inhibiting mRNAs. Proteins so produced (enzymes, hormones) are responsible for the steroid response. There is one type of GC receptor and all GCs will affect all tissues in the same way. At present rational use of GCs falls into two categories: replacement therapy (in Addison's diseasse and in congenital adrenal hyperplasia) and pharmacotherapy, mostly for their anti-inflammatory and immunosuppressive properties, but also to lyse leukemic lymphocytes or to reduce brain edema. GC therapy does not cure the primary disease--it only ameliorates its manifestations and provides time for the body natural defenses to work. After the withdrawal of steroid therapy manifestations of primary process usually return. So, as a result, there is no positive effect on long-term prognosis. Most common indications for prologned high-dose GC therapy are in organ transplantation, tumour chemotherapy, collagen vascular syndromes, ulcerative colitis, nephrotic syndrome and regional enteritis. Asthma, allergic diseases, inflammatory eye diseases and blood dyscrasias are also often treated with GCs. Used in pharmacological doses GCs have a number of adverse side effects. The use of alternate 0 day therapy can decrease most GC side effects (less suppression of hypothalamic-pituitary-adrenal axis, growth inhibition, cushingoid features, infections and myopathy). Discontinuation of long-term therapy is potentially difficult ("steroid withdrawal syndrome"). It is necessary to reduce the total dose gradually, in small weekly decrements. Recent use of GCs in prenatal treatment of congenital adrenal hyperplasia is described.
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PMID:[Glucocorticoids in pediatrics]. 1819 4

Cefazolin is commonly administered before surgery as a prophylactic antibiotic. Hypersensitivity to cefazolin is not uncommon, and the symptoms mostly include urticaria, skin reaction, diarrhea, vomiting, and transient neutropenia, which are rarely life threatening. We present a rare case of fatal cefazolin hypersensitivity in a female who was diagnosed with multiple meningiomas and scheduled for craniotomy and tumor removal. Immediately after cefazolin IV administration, the patient developed acute hypertensive crisis, which resolved within 10 minutes after the treatment. This was followed by unexplained metabolic acidosis. The patient then developed severe brain edema 100 minutes later. The patient had facial edema when her face was exposed for the next 30 minutes. A computed tomography scan revealed global brain edema with herniation. She was admitted to the intensive care unit for symptomatic treatment and died 10 days after surgery from multiorgan failure. The serum IgE level was very high (734 IU/mL). Single-dose administration of cefazolin for surgical prophylaxis may lead to rare, fatal adverse reaction. The warning signs are sudden, unexplained metabolic acidosis, hypertensive crisis, tachycardia, and facial angioedema predominating with or without cutaneous symptoms like urticaria.
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PMID:A fatal adverse effect of cefazolin administration: severe brain edema in a patient with multiple meningiomas. 2692 68