Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033774 (pruritus)
 14,546 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Itch, also known as pruritus, is the major symptom in skin diseases with a variety of etiologies and pathophysiologies. Significant progress has been achieved in understanding the pathophysiology of itch in the last 5 years. Neurophysiological experiments in humans and animals have revealed that itch is carried by specific C nerve fibers. Recent studies have demonstrated that peripheral mediators other than histamine are involved in induction of itch. Mast cell tryptase seems to be an important mediator in itch by its activation of proteinase activated receptor 2 in the sensory nerves. Opioids have central and peripheral itch producing activity. Neuropeptides, such as substance P, induce itch by their effect on mast cells. Based upon our improved understanding of the neurophysiology of itch a clinical classification of itch has been proposed. The classification highlights differences between peripheral pruritoceptive itch, neuropathic itch (itch related to damage to afferent nerve fibers) and neurogenic itch (itch originating in the central nervous system without any evidence of nerve damage). Emerging therapies based on these findings include topical vanilloid receptor antagonists, topical antihistamines, and topical arachidonic acid inhibitors, as well as inhibitors of non-histamine inflammatory mediators, immunomodulators and strontium salts. Systemic therapies include thalidomide, opioid antagonists, phototherapy with narrow band UVB and experimental treatments with cutaneous field stimulation and vagal nerve stimulation. With the new information it seems we will be able to better help our dermatologic patients who have itch, however we are not closer to identifying a single agent specifically targetable to this symptom.
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PMID:Itch associated with skin disease: advances in pathophysiology and emerging therapies. 1292 80

Mast cell tryptase can be an indicator of type I hypersensitivity reaction and thus may serve as a surrogate marker of anaphylaxis. A 34-year-old white male patient presented with a history of systemic lupus erythematosus. Shortly after administration of cefazolin for dialysis, he developed pruritus and shortness of breath. He expired an hour later. Autopsy excluded anatomic causes of death. There was an elevated postmortem mast cell tryptase level, 29.2 ng/mL. For mast cell tryptase level to be useful, the patient must survive long enough after exposure to an allergen for mast cells to release this enzyme. A credible allergen must be identified. In this case such, mast cell tryptase could establish anaphylaxis as the cause of death. The case suggests that in a patient with autoimmune disease, it may be prudent to test for immune reaction to a drug before administering it a second time via pinprick or other method.
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PMID:Mast cell tryptase in a case of anaphylaxis due to repeat antibiotic exposure. 1951 97