dinoprost and Urticaria

Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) can precipitate adverse reactions in two apparently different clinical conditions: bronchial asthma and chronic idiopathic urticaria (CIU). Recent evidence indicates that the reactions are triggered by the drugs that inhibit cyclooxygenase-1 but not cyclooxygenase-2.. To assess whether patients with CIU and aspirin sensitivity share common eicosanoid alterations with patients who have aspirin-sensitive asthma.. Seventy-four patients with CIU and a history of sensitivity to aspirin and NSAIDs underwent placebo-controlled oral aspirin challenge tests. Concentrations of urinary leukotriene E4 (uLTE4) were measured by ELISA and plasma stable prostaglandin D2 metabolite, 9alpha,11beta prostaglandin F(2) by GC/MS. All measurements were carried out at baseline and after aspirin dosing. Patients were genotyped for the leukotriene C4 synthase (LTC4S) promoter single nucleotide polymorphism.. In 30 of 74 patients, the aspirin challenge was positive, resulting in urticaria/angioedema. In these 30 patients, baseline uLTE4 levels were higher than in nonresponders and the healthy control subjects and increased further (significantly) after the onset of clinical reaction. No such increase occurred in subjects with negative aspirin challenge. Baseline uLTE4 levels correlated with severity of skin reactions. Plasma 9alpha,11beta prostaglandin F(2) levels rose significantly in both aspirin responders and nonresponders, although in the latter group the increase occurred later than in the former. In patients who reacted to aspirin, frequency of (-444)C allele of LTC4S was significantly higher than in patients who did not react.. CIU with aspirin sensitivity is characterized by the eicosanoid alterations, which are similar to those present in aspirin-induced asthma.

Topics: Adult; Alleles; Aspirin; Asthma; Dinoprost; Drug Hypersensitivity; Eicosanoids; Female; Genotype; Glutathione Transferase; Humans; Leukotriene E4; Male; Middle Aged; Polymorphism, Single Nucleotide; Single-Blind Method; Urticaria

Topics: Abdominal Pain; Adult; Anaphylaxis; Angioedema; Anti-Asthmatic Agents; Biomarkers; Cromolyn Sodium; Diarrhea; Dinoprost; Female; Histamine Antagonists; Humans; Leukotriene E4; Male; Mast Cells; Mastocytosis; Middle Aged; Omalizumab; Prostaglandin D2; Treatment Outcome; Tryptases; Urticaria

Little is known about the course of aspirin-induced urticaria. A special regulatory role of cysteinyl leukotrienes and prostaglandin D(2) (PGD(2)) has been postulated.. We performed a long-term observation on clinical course, aspirin sensitivity, and urinary eicosanoids in patients with aspirin-induced urticaria.. For 4 years, we followed up 22 patients with chronic idiopathic urticaria and aspirin hypersensitivity who restrained from the use of aspirin and other COX-1 inhibitors. Aspirin challenges were performed in 2002 (all results were positive) and repeated in 2006. Levels of urinary leukotriene E(4) (LTE(4)) and the main PGD(2) metabolite, 9 alpha 11 beta PGF(2), were measured at the same time points.. During the follow-up period, the severity of urticaria has decreased. In 14 of 22 patients, the results of aspirin challenge remained positive. In 2002, these 14 patients responded to aspirin with a significant increase in urinary LTE(4) and 9 alpha 11 beta PGF(2) levels. When studied 4 years later, they showed a similar response of 9 alpha 11 beta PGF(2) (P = .047) and a tendency toward an increase in LTE(4) level (P = .057). There was a correlation between the urinary LTE(4) concentration after aspirin challenge and the intensity of skin eruptions. The dose of aspirin had no effect on the magnitude of response of both LTE(4) and the PGD(2) metabolite. In the remaining 8 patients, negative aspirin challenge results were not associated with changes in the urinary eicosanoids studied.. Aspirin hypersensitivity manifesting as urticaria/angioedema remains present after 4 years in about two thirds of patients. Aspirin-precipitated skin reactions associate with increased excretion of LTE(4) and PGD(2).

Topics: Adult; Aspirin; Cyclooxygenase Inhibitors; Dinoprost; Drug Eruptions; Female; Follow-Up Studies; Humans; Leukotriene E4; Male; Middle Aged; Urticaria

Eighteen patients with a history of urticaria or asthma, or both, induced by aspirin were studied before and after provocation of symptoms with aspirin. The plasma prostaglandin F2 alpha concentration, which was characteristically raised before challenge, fell significantly at the time of adverse reactions. Repeated administration of aspirin up to a dose of 650 mg daily induced tolerance in most of the patients, and several developed bronchodilator responses to aspirin. Although median total IgE concentrations may be raised in patients with aspirin sensitivity, it appears likely that pharmacological rather than immunological mechanisms are chiefly responsible for the phenomena of aspirin sensitivity and desensitisation.

Topics: Adolescent; Adult; Aspirin; Asthma; Bronchial Provocation Tests; Dinoprost; Dinoprostone; Female; Humans; Immunoglobulin E; Male; Middle Aged; Peak Expiratory Flow Rate; Prostaglandins E; Prostaglandins F; Skin Tests; Time Factors; Urticaria

To study the role played by prostaglandins (PGs) in contact urticaria, concentrations of 13,14-dihydro-15-keto-PGF2 alpha, 6-keto-PGF1 alpha, and thromboxane B2, the stable metabolites of PGF2 alpha, prostacycline and thromboxane A2 were measured by radio-immunoassay of the fluid taken from suction blisters in 11 patients. The blisters were raised on contact urticarial reactions induced by benzoic acid. The effect of peroral indomethacin on contact urticaria from benzoic acid was studied in a further 14 dermatological patients. The levels of these prostanoids in the blister fluid of urticarial skin did not differ from those derived from control blisters raised on apparently normal skin. Premedication with indomethacin, 50 mg t.i.d., completely prevented contact urticarial reactions to benzoic acid in all patients.

Topics: Adolescent; Adult; Benzoates; Benzoic Acid; Dermatitis, Contact; Dinoprost; Epoprostenol; Female; Humans; Indomethacin; Male; Middle Aged; Prostaglandins; Prostaglandins F; Thromboxane A2; Urticaria

Prostaglandins appear to have cytoprotective effects in the upper bowel and are released in increased amounts in patients with abnormal peristalsis and diarrhea. Drugs which interfere with prostaglandin (PG) synthesis often prevent the symptoms of food intolerance and have been reported as improving food-related symptoms in the irritable bowel syndrome.

Topics: Adult; Asthma; Dinoprost; Dinoprostone; Eczema; Female; Food Hypersensitivity; Humans; Intestinal Mucosa; Prostaglandins; Prostaglandins E; Prostaglandins F; Urticaria

Six out of eight patients with a history of aspirin-provoked urticaria/angioedema responded with adverse reactions, including urticaria and bronchospasm, to provoking doses of oral aspirin from 30-515 mg. The other two patients did not react to 1.2 g of aspirin on three occasions. Five of the six patients who had reacted became desensitized after their initial aspirin reaction, tolerating 650 mg on the second day. They then took 650 mg day-1 of aspirin for three weeks, during which time the ingestion of foods which had previously caused a variety of moderate or severe reactions caused no symptoms. The resting plasma PGF2 alpha in ten 'aspirin-sensitive' urticaria patients (24.89 +/- 2.79 pg m-1) was significantly higher than the levels in ten normal subjects (6.75 +/- 1.1 pg ml-1) (P less than 0.01). In the patient group the lowest levels of PGF2 alpha were found in the two patients who subsequently did not experience a positive reaction after aspirin provocation. The PGF2 alpha/PGE2 ratio in 'aspirin-sensitive' urticaria patients (1.83 +/- 0.026) was significantly higher than that in normal subjects (0.63 +/- 0.14) (P less than 0.01).

Topics: Adolescent; Adult; Aspirin; Dinoprost; Dinoprostone; Drug Hypersensitivity; Female; Food Hypersensitivity; Humans; Male; Middle Aged; Prostaglandins E; Prostaglandins F; Urticaria