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)

Adults with atopic dermatitis (AD), with respiratory atopy only and healthy non-atopic controls were given intradermal injections of substance P (SP), neurokinin A (NKA), neurotensin (NT), vasoactive intestinal polypeptide (VIP), calcitonin gene-related peptide (CGRP) and histamine into the normal-appearing skin on the back. The weal and flare responses were evaluated after 3, 5 and 15 min and the areas calculated using an automatic image analyser. With the three different concentrations used (1, 3 and 30 pmols) a statistically significant (P less than 0.05) reduction in both the weal and flare response to SP, NKA, NT and histamine and a reduced flare to CGRP was observed only in AD patients. Among those with AD there was no uniformity of response to the individual neuropeptide and in general the more severely affected showed a lower reactivity. Dose-response relationships were evaluated for SP and NT (10-320 pmols) in AD and healthy controls. In AD dose-response curves and time-course relationships were similar to controls, but at significantly reduced levels. The itch response to the neuropeptides and histamine was not different in atopics and controls. We suggest that this hyporesponsiveness in AD is the result of natural tachyphylaxis of the target structures (mast cells and blood vessels) and possibly due to a higher availability of neuropeptides in the skin or to a primary abnormal sensitivity of the blood vessels and mast cells to these peptides.
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PMID:Skin reactivity to neuropeptides in atopic dermatitis. 261 Nov 20

Itch sensations and skin reactions induced by histamine iontophoresis at six different current intensities were studied in 27 atopic dermatitis (AD) patients and 20 healthy controls. Subjective itch ratings were assessed on a visual analogue scale (VAS) for 8-min periods after 10-sec histamine application, while changes of skin blood flow were simultaneously measured using two Laser Doppler flowmeters. Ten minutes after each histamine application, the areas of wheal and flare reactions were planimetrically evaluated. When no or weak current was applied, AD patients revealed stronger wheal and flare reactions than controls, possibly due to disturbed skin barrier function. Higher histamine doses, however, produced weaker subjective and vascular reactions in AD patients. In contrast to the controls, AD patients were unable to distinguish between weak and strong histamine stimulation, as shown by their VAS ratings. These results imply that AD patients have an altered histamine response. In particular, their afferent cutaneous nerve fibers show a decreased ability to signal itching to the central nervous system and to release vasoactive neuropeptides upon histamine stimulation.
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PMID:Skin reactions and itch sensation induced by epicutaneous histamine application in atopic dermatitis and controls. 267 98

A controlled trial of 4-weeks oral photochemotherapy (PUVA) on 14 patients with severe symptomatic dermatographism produced a clinically useful reduction in itching in five patients. In four of these patients itching had relapsed to pre-treatment levels within 3 months of finishing the PUVA course. A comparison of the weal and flare responses on exposed and covered (control) skin using a calibrated dermographometer showed no significant change in skin reactivity, even in the patients who experienced symptomatic relief. While PUVA may temporarily reduce itching in some patients with symptomatic dermographism, its use cannot generally be justified for treating this type of physical urticaria.
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PMID:The effect of psoralen photochemotherapy (PUVA) on symptomatic dermographism. 268 Jan 76

We have studied the influence of cold exposure on itch, erythema and wheal, in response to histamine scratch tests, in 14 volunteers. Cooling of the skin to less than 20 degrees C, by application of an ice cube for 30 min on the inside of the forearm, abolished itch and reduced erythema by approximately 50%, whereas the size of the wheal was unaffected by cooling. The observations bear significance for an explanation of the well-known observation that cold relieves itch. A normal itch response seems to require a continuous metabolic process in the skin, which is inhibited at temperatures less than 20 degrees C. The skin symptoms, itching and erythema, among workers in the fish processing industry are mainly localized to the forearms and backs of the hands, but only seldom to the fingers and palms, although they are in direct contact with fish products. Skin temperature measurements have shown that the temperature on the fingers and palms is less than 20 degrees C, while the temperature on the backs of the hands and forearms ranges from 25 to 30 degrees C. We therefore conclude that the skin temperature is an important factor for the location of skin symptoms among workers in the fish processing industry.
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PMID:The relevance of low skin temperature inhibiting histamine-induced itch to the location of contact urticarial symptoms in the fish processing industry. 279 42

The pharmacokinetics and pharmacodynamics of terfenadine were studied in 13 children with allergic rhinitis, mean age 7.45 +/- 0.54 SEM years. Serum concentrations of the active carboxylic acid metabolite of terfenadine (terfenadine metabolite I) were measured before and hourly for 8 hours after administration of a single dose of terfenadine suspension. The mean maximum serum concentration of terfenadine metabolite I, 242 +/- 28 ng/ml, occurred at 2.3 +/- 0.2 hours; the mean serum half-life value was 2.0 +/- 0.1 hours. Wheals and flares after epicutaneous tests with histamine phosphate, 1.0 mg/ml and 0.2 mg/ml, were significantly suppressed from 1 to 8 hours after the terfenadine dose compared to predose values. Maximum wheal suppression occurred at from 3 to 6 hours. Itching was completely suppressed for 8 hours. No serious adverse effects occurred. Terfenadine in children appears to be well absorbed, and its carboxylic acid metabolite has a short serum elimination half-life. The duration of its suppressive effect on the histamine-induced wheal and flare greatly exceeds that expected from consideration of serum terfenadine metabolite I concentrations.
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PMID:The pharmacokinetics and pharmacodynamics of terfenadine in children. 289 38

Antihistamines act by competing with histamine for H1 or H2 histamine receptors on cell membranes. In addition, most of the common antihistamines bind other receptors and thus exert other pharmacologic actions. For all practical purposes, mast cells and basophils are the main physiologic sources of histamine, and the primary usefulness of antihistamines is in diseases characterized by excessive production and release of histamine by these two cell types. Experimental models have proven useful for evaluating antihistamine compounds in humans. In these model systems, a test drug may be employed to block one or more of the known effects of exogenously administered histamine or a histamine agonist. Or the release of endogenous histamine may be brought about in a controlled fashion by agents such as allergens, opiates, or compound 48/80, and the drug's effects on this process may then be measured. In the case of the central nervous system, unfortunately, such models are not available and other means of evaluation must be devised. The dose response and duration of action of orally administered antihistamines can be determined in a simple skin model by their blocking of the wheal and erythema (flare) resulting from an intradermal challenge with histamine, an allergen, or compound 48/80. Antihistamines can also be evaluated in urticaria induced by scratching or cold. Itching that commonly follows injection of histamine or an allergen into the skin is also inhibited by this class of drugs. Most of the commonly used antihistamines are effective in these models, which form the basis for evaluating antihistamines in the treatment of skin diseases. In the nose and conjunctiva, other model strategies are used.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical pharmacodynamics of antihistamines. 289 49

A number of studies of the effects of antihistamines on chronic idiopathic urticaria and itch are reviewed. In chronic idiopathic urticaria, terfenadine has been shown to control the number, size, and duration of skin whealing as well as itch. Likewise, in chronic dermatographic urticaria, the minimal force required to produce whealing is increased, while severity of itch is decreased following treatment with terfenadine. In both conditions, however, wheal formation is not completely inhibited, suggesting the involvement of a mechanism unrelated to histamine. In nonurticarial disease in which histamine is not involved in the pathogenesis, antihistamines appear to work as antipruritics, but by a sedative-related property and not by antagonism of H1-receptors.
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PMID:Antihistamines in the treatment of urticarial disorders. 290 16

A single oral dose of cetirizine, 10 mg, a new H1 antagonist with minimal sedative effects and devoid of anticholinergic activities, was administered to eight healthy subjects. It markedly inhibited the wheal and flare induced 4 hours later by intracutaneously injected histamine and compound 48/80. Dermographism was produced by different pressures (100 to 500 gm/15 mm2) in 10 patients with factitial urticaria. Four hours after 10 mg of cetirizine, the whealing was absent in eight patients and markedly reduced in the other two subjects. In 12 patients with cold urticaria, wheals were induced by 30 seconds to 12 minutes application of an ice cube. Four hours after 10 mg of cetirizine, the urticarial reaction had disappeared in five patients and was decreased in the other patients. No itching was experienced in any of the patients after cetirizine, but the tested areas had an erythema lasting for 20 to 60 minutes.
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PMID:Inhibiting effect of cetirizine on histamine-induced and 48/80-induced wheals and flares, experimental dermographism, and cold-induced urticaria. 295 19

C5a is an 11,000-D fragment of the fifth component of complement (C5) with potent anaphylatoxic and leukocyte chemotactic activities. C5a is believed to play an important role in the pathophysiology of certain skin disorders and systemic diseases with cutaneous manifestations. However, there is very little known about the in vivo reactivity of C5a in man. In this study we examined the effects of intradermal injections of human C5a in 17 normal volunteers. C5a was prepared by interacting highly purified human C5 with zymosan bound alternative pathway C5 convertase under conditions resulting in consumption of approximately 90% of the C5 substrate. C5a produced in this manner was chemotactic for human neutrophils and monocytes (0.5 X 10(-7) to 10(-9) M) and caused neutrophil aggregation and myeloperoxidase release (concentrations greater than or equal to 10(-10) M) in vitro. In vivo, C5a produced immediate wheal and flare reactions in all volunteers, and was active in doses as low as 1 ng (10(-13) mol). Intradermal testing with 20 ng of C5a in eight volunteers produced a maximal mean wheal of 11.75 mm (+/- 0.80 mm SEM) 20 min after anaphylatoxin injection, and a maximal mean erythema of 62.50 mm (+/- 3.27 mm SEM) 10 min after C5a administration. Reactions at C5a test sites were dose-related, associated with marked pruritus in some subjects, resolved without lesion formation, and were not associated with late phase reactions. In vivo testing revealed that human C5a was a more potent mediator of wheal and flare reactions than histamine, 48/80, human C3a, or morphine sulfate. Skin biopsies from eight volunteers 20 min after intradermal injection of 20 ng of C5a revealed a neutrophil-predominant perivascular infiltrate, endothelial cell edema, and sites of leukocytoclasis. Mast cell degranulation was observed on both light and electron microscopy of biopsies from C5a test sites. Although erythema at C5a injection sites was reduced by pretreating volunteers with hydroxyzine, whealing reactions and cellular infiltrates in biopsies were unaffected by this H1-antihistamine. Moderate doses of systemic corticosteroids did not alter clinical or histologic reactions at C5a injection sites in two volunteers. This study, using doses within the potential physiologic range of the anaphylatoxin, provides a comprehensive assessment of the effect of human C5a on normal human skin.
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PMID:Studies of human C5a as a mediator of inflammation in normal human skin. 298 14

Most helminth parasites induce a strong IgE antibody and elevated eosinophil response in their mammalian hosts and a number of in vitro studies have suggested that IgE, possibly in association with eosinophils, may be an essential element of the host protective immunity against helminth infections. To assess the role of IgE in protective immunity, we examined the effect of suppressing the IgE antibody response on rat immunity to Schistosoma mansoni. Suppression was achieved in neonates by injections of rabbit anti-epsilon chain gamma-globulins, control rats received injections of unspecific gamma-globulins. IgE suppression caused a marked reduction of the inflammatory reaction that developed in the skin of immune rats at the site of a cercarial challenge: the early (30 to 60 min) wheal and flare reaction was abolished, and the late cutaneous reaction (6 to 18 h) associated with intense pruritus, edema and local eosinophilia was greatly reduced. This shows that IgE was critical to the recruitment of effector cells and molecules in the skin during the first 24 h following parasite invasion. Worms were recovered 18 to 30 days after a primary infection and 18 days after a challenge infection from IgE-suppressed and control rats. IgE-suppressed rats cured a first infection as rapidly as the control rats; however, they were two to three times less efficient than the controls at eliminating a second or a third challenge. These observations demonstrate that IgE antibodies are essential for the full development of rat acquired protective immunity against Schistosoma mansoni.
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PMID:IgE antibody and resistance to infection. II. Effect of IgE suppression on the early and late skin reaction and resistance of rats to Schistosoma mansoni infection. 308 55


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