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)

Four patients with cold urticaria and six control subjects were studied. Gastric acid output was measured for 1 hr before and 1 hr after the immersion of both hands in ice cold water. The mean acid output fell in the control group by 16.3%. Acid output in the cold urticaria patients rose in each case following the cold challenge. In three cases it rose by a mean of 52.6% and in one case by 1707%. Histamine is released locally and systemically during the reaction of cold urticaria. This is the most likely cause of the increase in gastric acid secretion.
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PMID:Gastric acid secretion in cold urticaria. 738 40

Primary cold urticaria (PCU) characterized by the association of urticaria, angioedema, and sometimes a shock-like reaction after cold exposure, is usually considered to be linked with histamine and prostaglandin D2 release by mast cells. To determine the involvement of cytokines, we studied the release of tumor necrosis factor-alpha (TNF-alpha) in the blood of the efferent vein after immersion of the hand in chilled water. Five patients with PCU were compared with a control population (three patients with nonphysical urticaria and three healthy subjects). Among patients with PCU who underwent the cold immersion test, two exhibited a shock-like reaction with a large urticarial plaque (patients 1 and 2), one had only a mild cutaneous reaction, and two had no reaction. Patient 1 was reevaluated after 6 months of treatment with H1 and H2 antihistamines: he did not respond to this challenge. All controls were strictly negative. Histamine was released within the first minute after the challenge in the three patients with PCU, but at a higher level for the two patients who had a systemic reaction. TNF-alpha was undetectable in the blood of the patient with only a mild cutaneous reaction, whereas TNF-alpha release was observed for the two patients with a systemic reaction, 2 and 6 minutes after the end of the cold immersion test. The two other patients and the control subjects released neither histamine nor TNF-alpha. In parallel, pathologic and immunohistochemical (with a rabbit anti-TNF-alpha antibody) studies were performed on skin biopsy specimens collected 10 minutes after ice-cube test.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tumor necrosis factor-alpha release during systemic reaction in cold urticaria. 750 21

The aim of our investigations is to evaluate blood histamine, complement titer and cryoglobulins before and after cold stimulation (extremity water immersion test) in patients with cold urticaria and Raynaud phenomenon. In our investigations patients were put into five groups according to the following diagnoses: cold urticaria (40 patients), chronic urticaria (15 patients), Urticaria-Vasculitis Syndrome (15 patients), Raynauds Disease (16 patients), and Raynauds phenomenon (15 patients). The investigations demonstrated that the test was always positive in cold urticaria and that a high percentage of patients had a rise in blood histamine. This was found in 50% of the patients while cryoglobulins were found in one third of the patients. Consequently they can be grouped in secondary cold urticarias. A number of patients with chronic urticaria and Urticaria-Vasculitis Syndrome gave a positive history of cold sensitivity. Positive tests were accompanied by a rise in histamine, although (less frequently) there was a decrease in the complement titer and the occurence of cryoglobulins. Raynauds Disease was accompanied by a positive test in 94% of the patients, while patients with Raynauds Phenomenon (whose etiology was Thoracic Outlet Syndrome) had a negative test (60% of the patients). Significant changes were not found in the remaining groups. Positive tests were accompanied by abnormal values of cryoglobulins and of complement titer as well as an increase in histamine. The rise in histamine was not significant in Raynauds Phenomenon, while one patient had a decrease in the complement titer and the appearance of cryoglobulins.
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PMID:[Significance of monitoring histamine serum levels, cryoglobulins and complement titers during cold tests in patients with cold allergy and Raynaud's phenomenon]. 759 Apr 15

Schistosoma mansoni was introduced in the Richard Toll area (Senegal) around 1988, probably due to man-made ecological changes in the Senegal river basin. Since 1991, we investigate the community of Ndombo, close to Richard Toll. Four random population samples of approximately 400 subjects are surveyed, starting at 8 months intervals. Each cohort is examined parasitologically (Kato-Katz), clinically, serologically (circulating antigen and antibody profiles); treated with praziquantel 40 mg/kg; and followed up 6-12 weeks, 1 and 2 years after treatment. Water contact patterns and snail densities are longitudinally surveyed. In the first cohort, prevalence of infection was 91%, with 41% excreting over 1000 eggs per gram (epg); the mean egg count was 646 epg, individual counts up to 24,000 epg. Prevalences remained almost 100%, but egg counts declined strongly in adults, in spite of continued exposure and the supposed lack of acquired immunity. Antigen detection in serum and urine confirmed that the egg counts genuinely reflect variations of worm burdens. Serum circulating anodic antigen (CAA) provided intriguing epidemiological information on worm burdens, while circulating cathodic antigen (CCA) showed promise for non-invasive diagnosis and screening. So far, similar epidemiological results were found in subsequent cohorts, although some variations were observed, possibly due to seasonal transmission fluctuations. IgE levels increased with age, while IgG4 peaked in the age-group 10-19 years. IgE and IgG4-levels against adult worm antigen (AWA) and soluble egg antigen (SEA) increased between cohort 1 and cohort 3 in almost all age-groups. In all 3 cohorts examined so far a strong correlation between IgG4 and pre-treatment egg-load was observed. Further follow-up and analysis, and comparison with chronically infected populations will provide insight in the development of acquired immunity. Abdominal discomfort was reported by 61% and diarrhoea by 33% of the subjects in the first cohort; mild hepatomegaly was found in 16%, splenomegaly in 0.5%. There was no correlation between frequency of symptoms and egg counts. This low morbidity, in spite of intense infections, was confirmed by ultrasound, and may be due to the recent nature of the focus. In the first cohort, 82% of treated subjects still excreted eggs 12 weeks after treatment, though egg counts declined strongly. Antigen detection confirmed these results. Parasitological negativation rates in subsequent cohorts, followed up sooner after treatment, improved but remained remarkably low. The low drug efficacy may be due to very rapid reinfection (though further reinfection after one year was limited), and/or to the lack of immunity in the population. Reduced susceptibility of the local schistosome strain can not be excluded, however. Praziquantel treatment provoked impressive but transient side effects (colics, vomiting, urticaria, oedema), the frequency of which correlated with intensity of infection.
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PMID:Epidemiology, immunology and chemotherapy of Schistosoma mansoni infections in a recently exposed community in Senegal. 782 23

A healthy 3-year-old boy developed acute urticaria five minutes after exposure to tap water in different areas of Jerusalem. Physical examination and baseline laboratory evaluation were within normal limits. The clinical picture and possible mechanisms of aquagenic urticaria are reviewed. This is the youngest patient to be reported.
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PMID:Aquagenic urticaria in a child. 817 Aug 45

Sequential skin testing including immediate patch test (IPT), skin prick test (SPT), and intradermal test (IT) with sodium benzylpenicillin G (Pen G), and SPT with benzylpenicilloyl human serum albumin (BPO-HSA) was done in 58 subjects with a history of probable anaphylactic reaction or shock of unknown cause. Based on positive skin tests, the diagnosis of penicillin anaphylaxis was confirmed in 30 patients. The average age of onset of penicillin allergy was 42 years ranging from 20-70 years. The sex ratio was 2:28 with marked female predominance. Anaphylactic shock, wheezing and urticaria occurred in 21, 20, 19 patients, respectively. Most symptoms were induced by skin tests and inhalation. The results of skin tests in these patients showed that IPT with 500 U/ml of Pen G was not only reliable but also safe. It is suggested that patients suspected of penicillin anaphylaxis should received IPT with 500 U/ml of Pen G as the initial diagnostic step; if a negative reaction occurred, then SPT and IT should be applied with the same concentration of Pen G, until a positive reaction developed or all the skin testing showed negative results. SPT to BPO-HSA was safe, but its positive rate was only 47.8% in our study; it seems to be less important than skin test to Pen G. As a whole, the skin testing procedure we recommend is relatively reliable, safe and practical even in individuals extremely sensitive to penicillin. In addition, once the patient develops a positive IPT, Pen G residue on the testing site should be wiped away rapidly and washed out with cool water thoroughly to disrupt further violent reaction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Skin testing in patients with high risk of anaphylactic reactions to penicillin. 821 54

Since the introduction of sodium metabisulfite as a food preservative, it has been associated with several idiosyncratic reactions (eg, bronchospasm, oculonasal symptoms, and urticaria/angioedema) in sulfite-sensitive individuals. The pathogenic mechanism of these reactions is not yet understood. We report the case of two crewmen on a shrimp trawler who were found dead in the ship's hold. Their deaths had occurred while they were applying dry sodium metabisulfite, referred to as "shrimp dip" in the shrimping industry. Postmortem examinations showed diffuse pulmonary edema consistent with death secondary to asphyxia. Associated findings were visceral congestion. Although it is possible to measure death from sodium metabisulfite with available records, its potential morbidity cannot be estimated. It is known that sodium metabisulfite can react with acids and water, releasing toxic sulfur dioxide (SO2) gas. In addition, SO2 gas reacts with respiratory tissue forming sulfureous acid, and inducing a pulmonary reaction causing hypoxemia. Furthermore, sodium metabisulfite, compared with sodium bisulfite, has a much greater propensity to release SO2 gas. We conclude that there is a need for improved education regarding the potential side effects of sodium metabisulfite, thus eliminating needless occupational morbidity and mortality.
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PMID:Sodium metabisulfite and SO2 release: an under-recognized hazard among shrimp fishermen. 826 51

Six-hundred-and-three people aged 40 or more years, from Maryborough in central Victoria, were enrolled in a randomized longitudinal study, which required daily application of either a SPF 15+, broad-spectrum, water-resistant sunscreen cream or the cream base without the active ingredients. The study duration was 7 months, from September 1991 until April 1992. One-hundred-and-fourteen (18.9%) of these subjects developed an adverse reaction to the cream they were applying. Patch testing, photopatch testing and scratch testing with the ingredients of the creams revealed that only a small proportion (< 10%) of the inflammatory eruptions were allergic in nature. None of the people tested was allergic to the sunscreen active ingredients. History and examination findings, where available, suggested that the majority of adverse responses were consistent with an irritant reaction, both to the sunscreen preparation and the base cream control. A higher than expected proportion of the people who developed an adverse reaction had a personal history consistent with atopy. Other reactions included acneiform eruptions and contact urticaria. A frequency of reactions to sunscreen preparations of over 15% means that further work is necessary to improve both the formulation of such products, and the manner and conditions under which they are used, to ensure satisfactory compliance.
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PMID:The frequency of reactions to sunscreens: results of a longitudinal population-based study on the regular use of sunscreens in Australia. 850 41

Polyfunctional aziridine (PFA) is increasingly used as a water-based cross-linker in 2-component paints, paint primers, lacquers, topcoats and other protective coatings. The cross-linker (PFA hardener) is made by reacting multifunctional acrylic monomer with a highly reactive aziridine compound. During 1992-1993, we came across 2 patients with allergic patch test reactions provoked by PFA hardener. One of the patients was a parquet layer, and the other a printer. Allergic contact dermatitis (ACD) was diagnosed by positive allergic patch test reactions to PFA hardener in a dilution series in pet.:0.3%-1% gave ++ to allergic reactions in both patients, whereas 0.1% gave a weak (+) or questionable reaction (?+), respectively. The methacrylate patch test series was negative in both patients, although gas chromatography/mass spectrometry analysis showed that PFA hardener contained 0.3% of trimethylolpropane triacrylate (TMPTA), a multifunctional acrylic monomer. One of the patients also had symptoms of contact urticaria, and a prick test with PFA hardener (1% aq.) induced a histamine-sized prick test reaction. The positive reactions with the PFA hardener and the negative reactions with the starting chemicals and additives in PFA, namely acrylates, propyleneimine and dimethylethanolamine, indicate that PFA caused ACD. This is in accordance with our previous observations, but differs from the reports of others, whose patients had been sensitized to acrylates present as remnants in the PFA hardener. As test substance, 0.5% PFA hardener in pet. is recommended for patch testing. Testing should be performed in patients with contact dermatitis if exposure to PFA has occurred. Skin prick tests may be of help to detect contact urticaria.
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PMID:Occupational allergic contact dermatitis and contact urticaria caused by polyfunctional aziridine hardener. 856 84

Heat contact urticaria is very rare and it is characterized by the development of wheal limited to the areas of heat contact. We report a case of heat contact urticaria in a 65-year-old women. The wheal was induced by hot bathing, washing in hot water or leaning on hot radiators. Symptoms started within 5 minutes of exposure and lasted 30 to 60 minutes. She had no systemic symptoms. The clinical diagnosis of localized heat urticaria was confirmed by experimental induction of localized wheals. Our investigation showed that the threshold temperature needed for induction of the heat urticaria was 39 degrees C. We tried to investigate the plasma levels of prostaglandin D2 and blood histamine before and after heat challenge. The patient showed marked improvement after a combination treatment of desensitizing by repeated exposure to heat and indomethacine.
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PMID:Heat contact urticaria--a case report. 882 90


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