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)

Thirty women (28 of childbearing age and 2 in the menopause), affected by acute Candida albicans vulvovaginitis were treated orally with a new antimycotic triazole derivative, itraconazole. Twenty patients were administered with 200 mg/die of itraconazole for three days. In tests carried out 7 and 30 days after the end of therapy the following results were observed. Negative cultures in 95% of patients and in 75% of patients; absence of leukorrhea in 60% of patients and in 65% of patients; disappearance of pruritus in 95% of patients and in 80% of patients. Ten patients were administered with an acute dose of itraconazole (400 mg). In the same tests, carried out 7 and 30 days after the end of therapy reported above the results were as follow. Negative culture in 80% and 60% of patients; absence of leukorrhea in 50% and 60% of patients; absence of pruritus in 70% and 50% of patients. In the first group of patients one case of slight nausea was reported whilst in the second group there were two cases of nausea, one of gastralgia and one of urticaria. No systemic side-effect was seen.
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PMID:[Preliminary clinical study of the use of itraconazole in the treatment of vulvovaginal candidiasis]. 166 25

Aspirin (ASA) and nonsteroidal anti-inflammatory drugs (NSAIDs) share common pharmacologic effects in the prevention of inflammation, at least in part through inhibition of prostaglandin formation. ASA and NSAIDs have predictable side effects such as gastric pain, ecchymosis, and tinnitus. They also cause anaphylactoid shock, urticaria/angioedema, nephropathy, and hepatitis in individuals who appear to be normal and in whom prediction of such reactions cannot be made. Two selected populations of patients are likely to experience hypersensitivity reactions to both ASA and NSAIDs. Patients with asthma have an 8% to 20% chance of experiencing asthmatic attacks after ingesting ASA and NSAID. If such patients have associated rhinosinusitis (polyps), prevalence increases to 30% to 40%. Patients with chronic urticaria/angioedema have a 21% to 30% chance of experiencing an urticarial flare after ingesting ASA and NSAIDs.
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PMID:Diagnosis, prevention, and treatment of adverse reactions to aspirin and nonsteroidal anti-inflammatory drugs. 643 54

The underlying respiratory disease is activated by unknown mechanism and results in an intense infiltration of mast cells and eosinophils into the entire respiratory mucosa. These cells synthesize leukotrienes (LTs) at a very high rate and mast cells also release histamine and tryptase and synthesize PGD(2) a vasodilator and bronchoconstrictor. Furthermore, AERD patients under synthesize from arachidonic acid (AA) a peculiar product called lipoxins, which opposes inflammation generated by leukotrienes. Finally, cysLT1 receptors are over expressed and highly responsive to LTE(4), further augmenting the underlying inflammatory disease. This inflammatory condition is partly inhibited by synthesis of PGE(2) through COX-1. PGE(2) partially inhibits 5-lipogygenase conversion of AA to LTA(4) and blocks release of histamine and tryptase from mast cells. When COX-l is inhibited by ASA or NSAIDs, PGE(2) synthesis stops and an enormous release of histamine and synthesis of LTs occurs. The upper respiratory reaction is mediated by both histamine and LTs but the bronchospastic reaction is mediated by LTs. The systemic effects of flush, gastric pain and hives are mediated by histamine. Aspirin desensitization can not be explained by disappearance of LT synthesis since urine LTE(4) levels are still elevated at acute ASA desensitization. However, mast cell products such as histamine, tryptase and PGD(2) are no longer released or synthesized at acute desensitization. It is more likely that a diminution in number or function of cysLT receptors accounts for the diminished inflammatory response found in ASA desensitization.
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PMID:Pathogenesis of aspirin-exacerbated respiratory disease. 1266 97

Strongyloidiasis, caused by Strongyloides stercoralis, is diagnosis considered as a challenge to clinician and laboratory technician. Because the auto-infective larvae are difficult to eradicate, one regimen dose may be in-sufficient and re-treatment of patients on two occasions, at 1 and 2 months after the initial treatment dose was recommended. This re-treatment regimen has yet to be proven in clinical trials. This study was performed on 24 patients who completed the study and having Strongyloides larvae in their stool obtained from Mansoura University Hospitals. Each stool sample was examined by direct saline smear, the formalin-ether sedimentation technique and agar plate culture. Patients were treated with Mirazid double course for a month to be followed up by stool examination by traditional method and agar plate culture for three consecutive months. In this study five cases out of 24 were asymptomatic (20.8%). Symptoms include abdominal manifestations as nausea and vomiting (16.7%), epi-gastric pain and nausea (12.5%), generalized abdominal pain (12.5%), chronic diarrhea (16.7%), irregular bowel habit (8.3%), and urticaria with abdominal pain (4.2%). Agar plate culture gave 100% positivity, even in cases were negative by coprological methods either direct smear and/or sedimenttation technique. All cases were cured by Mirazid given for one month except three resistant cases. Only one case responded to repeated course of Mirazid, while the other two cases still had larvae in their stool by agar culture plate. On combined therapy of both Mirazid and Mebendazole, larvae could be eliminated from their stool as approved by agar plate culture.
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PMID:New trends in diagnosis and treatment of chronic intestinal strongyloidiasis stercoralis in Egyptian patients. 1715 98

Skin testing is the diagnostic cornerstone for allergies and is considered extremely safe. It is usually performed with the prick and the prick-to-prick method. The aim of this study is to report the first two pediatric cases of systemic allergic reactions during skin prick tests (SPT) with commercial food allergens. Both patients had a history of fish allergy. A 5-year-old girl, with a history of atopic dermatitis and asthma, reported an episode of urticaria and angioedema due to ingestion of fish, which had occurred 2 years before consultation. Ten minutes after having completed SPT to fish extracts, which had resulted positive, she suffered from generalized pruritus, nausea, stomach pain, and loss of consciousness. A 9-year-old boy, with a history of asthma and two episodes of acute urticaria and angioedema upon eating fish during infancy, reported a recent episode of oropharyngeal pruritus after tasting salmon. He was evaluated for fish allergy with SPT but developed conjunctivitis and acute urticaria during the first 10 min of the test. Anaphylaxis appears to be a rare side effect of skin testing in pediatric patients. Children with a history of asthma and atopic dermatitis are more likely to react.
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PMID:Anaphylaxis during skin testing with food allergens in children. 1977 51