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)

The second-generation H1-receptor antagonists do not penetrate into the central nervous system as readily as the first-generation H1-receptor antagonists do. They bind preferentially to peripheral rather than central H1-receptors. They cause no more sedation than placebo does. These medications differ considerably from one another in some aspects of basic pharmacology and in pharmacokinetics and pharmacodynamics. An understanding of these differences will facilitate their optimal clinical usage. The second-generation H1-receptor antagonists are replacing the first generation H1-receptor antagonists in the symptomatic treatment of allergic rhinoconjunctivitis, and in relieving pruritus in patients with urticaria. They have a mild beneficial effect in patients with chronic asthma. They have not supplanted the first generation H1-receptor antagonists in atopic dermatitis treatment or as adjunctive treatment of pruritus and other symptoms in patients with anaphylaxis.
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PMID:Second-generation H1-receptor antagonists. 167 Sep 85

Six of nine adults who developed Red Sea coral contact dermatitis had seafood allergies. Contact with the "fire" coral was followed by a series of skin eruptions starting with an immediate pruritic urticaria-like lesion which forced the victims out of the water. Within minutes the affected area became erythematous and edematous with eventual blister formation approximately 6 hours after the initial contact. The blisters resolved, leaving violaceous papules and plaques in a streaky fashion corresponding to where the coral brushed the skin. The lesions became shiny and lichenoid in 3 weeks while pruritus persisted. Treatment with topical corticosteroids and oral antihistamines reduced the severity of the disease but did not stop its evolution to the lichenoid stage. Complete resolution usually occurred after 15 weeks, leaving residual hyperpigmented macules.
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PMID:Red sea coral contact dermatitis. 167 31

The efficacy of cetirizine dihydrochloride, a new H1-antagonist claimed to have minimal sedative property was evaluated in 28 patients with chronic idiopathic urticaria. Cetirizine 10 mg and placebo were compared in a double-blind cross-over trial. Response was measured by patients with daily charts on itch and wheals. Response was also assessed by patients and investigators while on cetirizine and placebo on an analogue scale. The mean analogue score by the investigator while on cetirizine (64.6 mm) was better than while on placebo (47.0 mm) (p = 0.008). Reduction of itch with cetirizine was significantly greater than with placebo. The mean itch scores for placebo and cetirizine were 21.2 and 14.5 respectively (p = 0.01) showing a significant improvement of itch by cetirizine. The mean score for wheal response for placebo and cetirizine were 21.0 and 16.16 respectively (p = 0.07 NS) showing a reduction of wheal from cetirizine was greater than placebo but the difference was not statistically significant. The patients' mean visual analogue score for placebo was 38.4 and for cetirizine was 57.5 (p = 0.006). Cetirizine was significantly better in controlling symptoms of chronic urticaria than placebo. Five of the 28 (17.9%) patients reported mild drowsiness while taking cetirizine. Two patients reported drowsiness while on placebo. Tolerance was reported as good in 85%, moderate in 10% and bad in 5% according to patients' assessment, while tolerance was excellent and good in 80%, moderate in 15% of patients according to investigator's assessment.
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PMID:Cetirizine vs placebo in chronic idiopathic urticaria--a double blind randomised cross-over study. 168 78

The focus of this study on coital allergy is on discussing the basis for and clinical implications of the immunological reactions that mediate allergic reactions to semen. Allergic reactions to antigens in seminal plasma occur in the case of acute systemic hypersensitivity (ACH), localized postcoital allergic seminal vulvovaginitis, and/or hypersensitivity to exogenous allergens in semen. In the few cases (30 cases at present), ACH may manifest itself in generalized urticaria, orbital and vulval edema, vulval and generalized pruritus, bronchospasm, lower abdominal pain, hypotension, and loss of consciousness. There may be a family history of atopy. Symptoms may appear over months or years before reaching a severe level. The usual case is the appearance after the 1st coital act or after a change in coital, genital, or reproductive occasions. It is not specific to a particular male partner. It may be self-limiting. Condom usage or abstinence may lead to abatement. Localized vulvovaginitis may occur simultaneously with ACH or exist alone. The symptoms are local pruritus, burning, swelling, erythema, and urticaria in varying degrees for up to a week and occur during or after coitus. Douching or vulval irrigations may ameliorate symptoms. Misdiagnosis as genital herpes or infective vulvovaginitis may occur in mild cases. Exogenous allergens derived from drugs, food, and other sources presenting in the semen may contribute to hypersensitivity. This is different from reactions to intrinsic components of seminal plasma. Vaginal exposure to chemical products such as soaps or to airborne particles such as pollen may produce allergic responses. Another possibility is that genital candidiasis may produce local Ige antibodies, and PGE2 induced suppression of cell-mediated immunity. The immunological mechanisms are described as type I hypersensitivity reactions with the antigen reacting with reaginic antibodies of the Ige class which are bound to mast cell or circulating basophils. The antigens and the immune reactions are specified. In the clinical diagnosis, the rare acute systemic form is obvious, but the atypical, recurrent, and intractable forms of vulvovaginitis require investigation with skin tests. Treatment may involve artificial insemination for those seeking pregnancy, immunotherapy, or antihistamines, rather than use of a condom or abstinence.
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PMID:Allergy to coitus. 168

A controlled and completely randomized study was carried out with the aim of assessing the efficacy and safety of oxatomide gel in comparison with another preparation for topical use, dechlorpheniramine. Twenty-seven patients (sixteen F, eleven M) aged between 21 and 72 years (mean age 39) suffering from chronic idiopathic urticaria were treated for 15 days with oxatomide gel at 5% or dechlorpheniramine cream at 1%; 15 days of follow-up without therapy were then observed. Both the treatments allowed significant control of cutaneous symptoms. In particular, in the group treated with oxatomide there was a more marked reduction in itching and in the number of weals (p less than 0.01 between times), and in the dechlorpheniramine group in the severity of erythema (p less than 0.01 between times). During the follow-up period, a distinct flare-up of symptoms was observed only in the dechlorpheniramine group. Acceptability and safety, both clinical and biological, were good for both products.
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PMID:Treatment of chronic idiopathic urticaria with topical preparations: controlled study of oxatomide gel versus dechlorpheniramine cream. 168 44

Histamine, which is stored mainly in mast cells and basophils, is a prominent contributor to allergic disease. Elevations in plasma or tissue histamine levels have been noted during anaphylaxis and experimental allergic responses of the skin, nose, and airways. Of the four cardinal signs of asthma (bronchospasm, edema, inflammation, and mucus secretion), histamine is capable of mediating the first two through its H1 receptor and mucus secretion through its H2 receptor. Of the five cardinal signs of allergic rhinitis (pruritus, mucosal edema, sneezing, mucus secretion, and late-phase inflammatory reactions), histamine is capable of mediating the first three through its H1 receptor. In the nose, mucus secretion can be reflexively mediated by H1 and possibly also by H2 receptors. In the skin the cardinal features of urticaria (vasodilation, vascular permeability, and pruritus) can be mediated by stimulation of the H1 receptor. In anaphylaxis histamine H1-receptor stimulation can mediate vascular permeability, smooth muscle contraction, and tachycardia, whereas H2-receptor stimulation can mediate mucus secretion. Stimulation of both receptors can mediate vasodilation and reduce peripheral vascular resistance. Thus although histamine is only one of many mediators of allergic disease, it plays a primary role in allergic rhinitis, urticaria, anaphylaxis, and to a lesser degree, asthma.
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PMID:The role of histamine in allergic diseases. 169 87

Histamine, the main amine released during allergic reactions, can provoke coronary arterial spasm manifested as angina pectoris. This has been shown during clinical and laboratory studies. The effects of histamine on cardiac function are mediated via H1- and H2- receptors situated on the four cardiac chambers and coronary arteries. Coronary arteries of cardiac patients are hyperactive and contain stores of histamine which can initiate coronary artery spasm. Clinical observations indicate that angina pectoris or acute myocardial infarction can be provoked by acute allergic reaction. The coincidental occurrence of chest pain and allergic reaction accompanied by clinical and laboratory findings of classical angina pectoris seems to constitute the syndrome of allergic angina. The clinical symptoms of allergic angina include chest discomfort, dyspnoea, faintness, nausea, pruritus and urticaria. They are accompanied by signs such as hypotension, diaphoresis, pallor and bradycardia. There are also electrocardiographic findings indicating myocardial ischaemia, arrhythmias and conduction defects. Thus, in patients undergoing acute allergic reaction, the development of chest pain could be explained by the mechanism of coronary arterial spasm provoked by the release of histamine, which constitutes the syndrome of allergic angina.
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PMID:Histamine-induced coronary artery spasm: the concept of allergic angina. 179 97

A case of a ten year old adopted girl is presented, who had gastrointestinal disturbances, anal pruritus and relapses of urticaria from her fourth year of age. By means of radiological and endoscopis analysis, multiple gastrointestinal polyposis was established. Pathohistological examination of the polyp indicated that tubular adenomas were in question, therefore in the case of this girl it can be stated that she has diffuse tubular gastrointestinal adenomatous polyposis, which is a characteristic of Gardner's syndrome. At the moment of the setting of the diagnosis, the girl had no skin changes nor did she have any radiological changes on the bones of her skull. The first skin changes appeared one year after the diagnosis was set, and they were in the form of maculopapular nodules, comedos of the closed and open type on the forehead and chin.
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PMID:[Multiple gastrointestinal polyps]. 180 74

Seventy-one male employees whose working environment was a temperature and dust controlled low-humidity 'Clean Room' and 144 male employees working in a natural factory environment were compared by means of period percentage prevalences of occurrence, severity and frequency of subjective symptoms of facial dermatitis. Using a cross-sectional interviewer-administered questionnaire it was possible to assess the percentage prevalence of each of 3 facial dermatitis symptoms among both low humidity exposed and non-exposed workers. The two prevalences were compared by calculating a ratio (the percentage prevalence ratio or PPR) of the prevalence of symptoms in the exposed, to that in the non-exposed workforce. A confidence interval (CI) for the PPR was also calculated. For the symptom of itching, the PPR was 1.65 (CI 1.32-2.07) in favour of the study group, whilst for the symptoms of redness and urticaria the PPRs were 1.96 (CI 1.54-2.48) and 2.53 (CI 1.40-4.59) respectively. The occurrence of a greater prevalence of all symptoms in the low-humidity exposed workforce confirms the clinical and laboratory reports of previous workers. A comparison was also made between the two groups of workers of both the severity, and the frequency of occurrence of symptoms. Whilst there was no statistically significant difference between the exposed and non-exposed groups for prevalence of one symptom, among those who had experienced two symptoms there was a PPR of 2.43 (CI 1.37-4.30) between the two groups. Furthermore, among those workers who had experienced all 3 symptoms of facial dermatitis there was a PPR of 3.38 (CI 1.18-8.93) in favour of the low-humidity exposed workforce.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clean rooms and itchy faces. 182 37

The effects of oral cetirizine on spontaneous and provoked urticaria were evaluated in two studies. In a double-blind crossover trial, 30 patients with idiopathic urticaria received 10 or 20 mg of cetirizine or placebo. Cetirizine was significantly more effective than placebo in reducing the incidence of erythema, wheals, and pruritus. No serious side effects were reported. In the second study of ten patients with chronic urticaria, immediate and delayed reactions to injected autologous serum, histamine, kallikrein, and synthetic platelet-activating factor (PAF)-acether were inhibited by 10 mg of cetirizine. These results suggest that the mechanism of action of cetirizine may involve inhibition of PAF-induced influx of eosinophils.
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PMID:Cetirizine in the treatment of chronic urticaria. 182 14


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