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 effect of endoscopic thoracic sympathectomy on experimentally histamine-induced itch was studied in seven patients, all of whom were suffering from palmar hyperhidrosis; cutaneous warm, cold, and heat pain perception thresholds were also studied in five of these seven patients. Surgery was effective in abolishing palmar sweating in all patients. No significant differences were seen in itch, flare, wheal, or thermal perception thresholds following sympathectomy as compared to the preoperative period. These findings suggest that the sympathetic system may be of limited importance for somatosensory perception in healthy humans during normal conditions.
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PMID:Sympathectomy does not influence experimental itch and cutaneous temperature perception thresholds. 884 63

There is increasing evidence that neuropeptides may be involved in the pathogenesis of atopic dermatitis (AD). This study examines whether neuropeptide distribution in the skin of patients with AD differs from normal controls. The distribution and density of several neuropeptides were examined in lesional and non-lesional skin of AD patients (n = 5) and in normal controls (n = 4) using indirect immunofluorescence and image analysis. Cholinergic innervation was studied using cholinesterase histochemistry. Staining with the general neuronal marker protein gene product 9 x 5 showed a subepidermal network of nerves with fibres penetrating the epidermis, and nerves around blood vessels, sweat glands and hair follicles. Image analysis of nerves around sweat glands showed a significantly higher nerve density in non-lesional compared with both normal controls and lesional skin (P < 0.05); lesional compared with control skin showed no significant difference. In the epidermis the density of nerves was not significantly greater in non-lesional compared with lesional skin and controls. Calcitonin gene-related peptide immunoreactivity was similar in all subjects except in three of the AD patients, where more nerves appeared to penetrate the epidermis. Substance P immunoreactivity in the papillary dermis was seen in all AD patients but no controls. Vasoactive intestinal polypeptide and neuropeptide Y staining were similar in all groups. Acetylcholinesterase-positive nerves were found around sweat glands in all subjects, the staining being greatest in non-lesional and least in lesional skin. Occasional nerves were seen in the papillary dermis in lesional skin of two out of the four patients. We have demonstrated quantitative differences in nerve growth in clinically normal skin of AD patients, and altered cutaneous neuropeptide expression in these patients which may contribute to the pathogenesis of AD. The cause of atopic dermatitis (AD) has not been fully established but it is believed that there is a complex interaction between genetic susceptibility, precipitating environmental factors and disordered immune responsiveness. There is increasing evidence that neuropeptides may be involved in the pathogenesis of AD. Exacerbations of the disease can be provoked by stress, scratching and sweating which may be the result of neurogenic inflammation. One of the first features of an exacerbation is flushing of the affected skin and pruritus. Several neuropeptides that have been identified in human skin are potent inducers of vasodilation and may induce pruritus. Substance P (SP), calcitonin gene-related peptide (CGRP) and vasoactive intestinal polypeptide (VIP) all cause vasodilation when injected intradermally, and SP and CGRP have been shown to be mediators of the weal and flare reaction. Spantide, a competitive antagonist of SP, has been shown to inhibit immediate and delayed-type hypersensitivity reactions. Part of these responses may be due to release of histamine and indeed elevated concentrations of histamine have been found in vivo in the skin and plasma of patients with AD. In this study the distribution and density of several neuropeptides were examined in lesional and nonlesional skin of AD patients and in normal controls using indirect immunofluorescence and image analysis. Cholinergic innervation was studied using cholinesterase histochemistry. Because many afferent fibres do not express CGRP or SP, the general neuronal marker protein gene product (PGP 9 x 5) was used to assess the overall nerve supply to the skin.
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PMID:Neuropeptides in the skin of patients with atopic dermatitis. 885 37

We assessed the immediate skin reactivity to Dermatophagoides pteronyssinus in children with atopic asthma in order to determine the intensity of the skin reaction, its time course and the end-point allergen concentration. We also examined the correlation between the total and D. pteronyssinus-specific IgE levels and the severity of asthma. Asthmatic children were age- and sex matched to nonatopic children. Significant eosinophilia and elevated serum IgE levels were correlated with the presence of asthma but bore no relation to the severity of the disease. The average end-point allergen concentration was approximately 50 allergy units (AU). The mean wheal diameter ranged from 6.1 mm in mild asthmatics to 7.1 mm in severe cases; this difference, however, was not significant. Most of the patients (85%) reported local pruritus within 120 seconds after allergen injection. The time lag until the start of the reaction and the wheal diameters were correlated with the levels of D. pteronyssinus-specific serum IgE antibodies, and with the end-point allergen concentration. These two variables therefore provide good indicators of the time course and the extent of the skin test reaction in individuals sensitive to the allergen tested.
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PMID:Quantitative skin prick tests and serum IgE antibodies in atopic asthmatics. 909 33

Results of psychophysiological, psychoendocrinological, and psychoneuroimmunological research on the skin in patients with atopic dermatitis were evaluated. 11 investigations were selected and analysed with respect to both design and results. In 6 instances, healthy or ill control groups were included, rarely did the sample size exceed 30. With respect to physiology, blood pressure, heart rate and EDA were most commonly assessed; with respect to immunology, number of leucocytes and differential blood count and with respect to psychology, anxiety, neuroticism and stress perception. The results involving stress induction, itching induction and the relationship of personality and skin parameters were not consistent. The best established relationship is that between skin reactivity (flare, wheal size and pruritus) on the one hand and cognitive appraisal of stress-stimuli and the experimental situation on the other hand. Psychoendocrinological and even more psychoimmunological indicators of the stress of reaction-unlike psychophysiological indicators-were correlated with the skin response. Only half of the studies found an elevated physiological stress reaction in patients with atopic dermatitis.
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PMID:[Psychophysiologic and psychoneuroimmunologic studies in neurodermatitis. Overview and critical evaluation]. 913 89

A 63-year-old insulin-dependent diabetic woman was hospitalized with itchy skin wheals at the injection sites of human insulin. After intradermal skin testing was performed, the erythema and wheal was recorded immediately. The increased titer of human insulin-specific IgE antibody indicated immediate-type allergy against human insulin. Administration of an anti-allergic drug or desensitization for human insulin every 2 hours was not effective. After continuous subcutaneous insulin infusion (CSII) therapy was performed, both the itching and wheal disappeared. The process may be a desensitization through CSII. CSII may be useful in the treatment for human insulin allergy.
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PMID:Immediate-type human insulin allergy successfully treated by continuous subcutaneous insulin infusion. 926 Jul 76

Cytokines have been proposed as histamine-independent itch mediators. To investigate this hypothesis, single doses of interleukin-2 (IL-2, 10 MU/mL) and tumour necrosis factor alpha (TNF-alpha, 10 micrograms/mL) were delivered to the epidermis of 10 healthy volunteers with a controlled skin-prick model; 1% histamine and solvent controls were included in a double-blind, randomized crossover design. Itch ratings (computerized visual analogue scale) were obtained every 20 s for 15 min and cutaneous reactions (weal, flare and temperature) were measured. Reactions were also recorded after 2, 24 and 48 h. The mean itch ratings were: histamine 35.5, IL-2 3.3 (both P < 0.01 compared with control), TNF-alpha 1.6 and solvent control 1.75 (not significant). Weal and flare occurred only with histamine. In two volunteers, an inflammatory papule with transient pruritus developed 12-18 h after applying IL-2. In conclusion, IL-2 showed a rapid, low pruritogenic effect, which may be followed by an inflammatory response. TNF-alpha induced no itching in this setting. Skin-prick testing with appropriate doses of potential pruritogens provides a safe and sensitive model for further chemoreceptor studies.
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PMID:Skin testing of the pruritogenic activity of histamine and cytokines (interleukin-2 and tumour necrosis factor-alpha) at the dermal-epidermal junction. 934 40

As previous experimental studies disproved histamine as the main mediator of eliciting pruritus in atopic eczema (AE), we examined the neurocutaneous sensations in 15 patients with AE and in 15 age- and sex-matched non-atopic controls after i.c. injection of acetylcholine (Ach, 0.5 M, 20 microliters) or buffered saline. The sensory perceptions were rated by the participants of the study with regard to their quality and intensity using a visual analogue scale. Simultaneously, the vascular reactions to Ach were recorded by the examinators via laser Doppler fluxmetry as well as flare and wheal planimetry. In contrast to the approximately equal flare and wheal extensions in either group, the cutaneous sensations differed significantly. The patients complained of 'pure' itching that developed shortly after Ach injection, whereas the control subjects reported only burning pain. Moreover, the patients perceived their sensations significantly earlier and significantly longer than did the controls. The study provides evidence that Ach plays an important role in the pathogeny of pruritus in patients with AE. Further investigations of the neuronal mechanisms involved in this atopy-related effect of Ach have to be performed.
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PMID:Acetylcholine is an inducer of itching in patients with atopic eczema. 937 59

We investigated the antipruritic effect of a 15-min application of dimethindene maleate (Fenistil gel) and other local analgesics (Optiderm, EMLA, Xylocain ointment 5%) on subsequent focal histamine stimulus (20 mC) given by iontophoresis in 12 patients suffering from acute atopic eczema (AE). The results were compared to histamine after pretreatment with the respective placebo and to non-pretreated skin. Wheal and flare areas were planimetrically evaluated. Itch or pain ratings were performed over a 24-min period using a rating scale. The examination also comprised alloknesis, i.e. induction of a perifocal itch sensation by a non-itching mechanical stimulus. None of the antihistaminic and anaesthetic agents reduced the itch intensity significantly. Three of the AE patients had a total lack of alloknesis. We conclude that these substances, when applied for 15 min, are not sufficiently effective in atopic skin suppressing histamine-induced reactions under experimental conditions. The diminished elicitation of alloknesis in these patients may be a result of central nervous system alteration.
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PMID:Experimentally induced pruritus and cutaneous reactions with topical antihistamine and local analgesics in atopic eczema. 941 92

Itching is a well known side-effect of opiate therapy. To gain insight into the possible contribution of opiate receptors to itching we compared the antipruritic effect of naltrexone (Nemexin), an opiate antagonist, to an H1-receptor antagonist and to placebo. In a double blind cross-over study on 15 healthy volunteers, 25 mg naltrexone or placebo was orally given 60 min prior to a histamine stimulus. In a second, otherwise identical experiment, 10 mg cetirizine, an H1 blocker, or placebo was orally given 12 h before the experiment to the same group of volunteers. Histamine was applied iontophoretically to the forearm skin and the following parameters were assessed thereafter: weal and flare size, itch intensity and the extension of the area of alloknesis ('itchy skin') around the application site. Naltrexone had no effect on the vascular histamine reactions 'weal' and 'flare', whereas cetirizine abolished the weal reactions and greatly diminished the flare reactions. Both naltrexone and cetirizine significantly diminished histamine induced itching. In contrast to placebo and cetirizine, naltrexone abolished alloknesis completely in four of 15 volunteers and in the others alloknesis was greatly reduced after naltrexone. Since vascular reactions to histamine are of peripheral origin, whereas alloknesis depends on central nervous mechanisms, our findings suggest a pronounced centrally mediated action of naltrexone on histamine induced pruritus.
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PMID:Opiate and H1 antagonist effects on histamine induced pruritus and alloknesis. 941 11

Histamine releasing autoantibodies play a central role in the pathogenesis of chronic urticaria (CU) in approximately 30% of affected patients. We investigated the therapeutic effect of high-dose intravenous immunoglobulin (IVIG) on disease activity in patients with severe CU of autoimmune aetiology. Autoimmune urticaria was diagnosed by the development of a weal-and-flare reaction to the intradermal injection of autologous serum and by serum-induced histamine release from the basophil leucocytes of healthy donors in vitro. Ten patients with severe, autoimmune CU, poorly responsive to conventional treatment, were treated with IVIG 0.4 g/kg per day for 5 days. The outcome on cutaneous wealing and itch was monitored using urticaria activity scores, visual analogue scales and autologous intradermal serum tests. Clinical benefit was noted in nine of 10 patients: three patients continue in prolonged complete remissions (3 years follow-up), two had temporary complete remissions, and symptoms in four patients improved subsequent to treatment. There was significant improvement in the urticaria activity scores and visual analogue scores at 2 (P < 0.01) and 6 weeks (P < 0.01) post-IVIG compared with the baseline values (Wilcoxon matched pairs). The diminution in urticarial activity in the majority of patients corresponded with a reduced weal-and-flare response to the intradermal injection of autologous post-treatment serum compared with the pretreatment serum. Minor side-effects were common, but there were no serious or long-term adverse effects. IVIG represents a novel therapeutic option in selected patients with recalcitrant CU associated with histamine releasing autoantibodies.
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PMID:Intravenous immunoglobulin in autoimmune chronic urticaria. 953 30


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