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 ten days' treatment with cyclosporin A, 5 mg/kg/day, in 10 adults with atopic dermatitis was investigated using a double-blind, randomized, placebo-controlled, cross-over design. Evaluation was based on itch recording, clinical scoring and immunohistochemical examination of skin biopsy specimens. Cyclosporin A significantly reduced the itch intensity, the eczema score and the consumption of topical hydrocortisone. A significant decrease in serum magnesium and in the total number of blood eosinophils was seen. No other laboratory abnormalities were observed. In lesional skin, Cyclosporin A induced a relative decrease of CD3+ T cells in 5/10 patients, of HLA-DR+ cells in 6/10, and of interleukin-2-receptor positive (CD25+) cells in 4/10. However, these changes in phenotype expression did not seem necessary for itch relief. Relapse of clinical symptoms was seen within 2-30 days of completion of the Cyclosporin A course. The mechanism of the antipruritic effect remains unclear, but the present findings may support the hypothesis that 'pruritogenic cytokines', whose production is inhibited by Cyclosporin A, may be important in the pathogenesis of itch in atopic dermatitis.
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PMID:Antipruritic effect of oral cyclosporin A in atopic dermatitis. 197 58

Atopic dermatitis (AD) is a familial inflammatory skin disorder, which is characterized by extreme pruritus, the typical morphology and distribution, the chronic or chronically relapsing course, and the personal or family case history of atopy (asthma, allergic rhinitis, atopic dermatitis); moreover, we find a variety of additional features, which are either less specific or relatively rare. Although this disease has been well-known since the beginning of the century, we have not clearly understood its pathogenesis so far. This article reviews the reported deviations of the immune system and the alterations of the mediators of inflammation as well as the abnormalities of cyclic nucleotide regulation. These findings are correlated to the clinical symptoms. The following topics have been dealt with in detail: association with HLA-antigens, elevation of serum IgE and generation of IgE immune complexes, numerical and functional deficiencies of T-suppressor cells, involvement of granulocytes, alterations of mediators of inflammation, and particularly, observations on the cAMP-phosphodiesterase. These extremely complex findings, which are based on the interaction between disregulation of the autonomous nervous system and alterations of the immune system, may provide a better understanding of the pathogenesis of atopic dermatitis.
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PMID:[Pathogenesis of atopic dermatitis]. 243 53

A 55-year-old woman with common variable immunodeficiency and mild chronic obstructive lung disease received 3 units of plasma as immunoglobulin replacement therapy. During the administration of the final unit, her temperature rose 1 degree C, with no other observable symptoms. Fifteen minutes later she developed shortness of breath without nausea, vomiting, rash, or pruritus. In 30 min she lost consciousness, was breathless, and cyanotic. Resuscitative efforts failed. Autopsy failed to pinpoint a cause of death. There was no evidence of ABO or Rh incompatibility, bacterial contamination, or hemolysis. There were no neutrophil, platelet or IgA antibodies detectable in the patient or the 3 plasma donors. There were no lymphocytotoxic HLA antibodies in the patient or two of the plasma donors. The third donor had HLA-B35 lymphocytotoxic antibodies that did not agglutinate or aggregate neutrophils. The patient's HLA type was A2, A3; B35, B40. Lymphocytotoxic crossmatches using lymphocytes of the patient were positive with plasma from the third donor but negative with the other two. An eluate prepared from post-mortem lung parenchymal tissue was cytotoxic to 7 of 8 panel lymphocytes positive for the HLA-B35 antigen but not with cells lacking B35. The implicated plasma donor was healthy with a history of 6 pregnancies. This case report illustrates the potential hazard of transfusion of plasma containing HLA antibodies.
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PMID:Fatal pulmonary transfusion reaction to plasma containing donor HLA antibody. 280 Apr 69

In many countries, increasing rates of skin eruptions are attributed to non-steroidal anti-inflammatory drugs (NSAIDs). They are usually mild, and life-threatening reactions such as Stevens-Johnson Syndrome (SJS) or toxic epidermal necrolysis (TEN) are rare. The commonest reactions are pruritus, morbilliform rashes, urticaria and photosensitivity. Urticaria is most frequent in salicylate-sensitive patients, and photosensitivity--a real clinical problem with benoxaprofen--is mainly a phototoxic reaction, predictable from preclinical studies. Other skin reactions are unusual although purpura and cutaneous vasculitis have been attributed to NSAIDs. The main concern is bullous drug reactions--erythema multiforme (EM), SJS and TEN. Whilst EM and SJS have many other causes besides drugs, most cases of TEN are drug-induced. NSAIDs have played an increasing role in the aetiology of TEN and it may be that drugs with a longer serum half-life carry higher risk, especially when administered to patients for infectious complaints who have a predisposing genetic background (HLA-B12). In pre- and post-marketing studies of a new drug, careful attention must be paid to the nature of side-effects, as a high rate of mild reactions belonging to the EM spectrum may be indicative of higher risks of SJS and TEN.
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PMID:Clinical aspects of skin reactions to NSAIDs. 296 Oct 55

Atopic dermatitis (AD) is a familial inflammatory skin disorder which is characterized by extreme pruritus, the typical morphology and distribution, the chronic or chronically relapsing time course and the personal or family history of atopy (asthma, allergic rhinitis, atopic dermatitis). However, there exists a variety of additional features which are either less specific or relatively rare. Although this disease has been well-known since the beginning of the century, the pathogenesis is not clearly understood at present. This review summarizes the reported deviations of the immune system as well as the alterations of the mediators of inflammation and the abnormalities of cyclic nucleotide regulation. These findings will be correlated with clinical symptoms. In particular the following topics were taken into consideration: association with HLA-antigens, elevation of serum IgE and generation of IgE immune complexes, numerical and functional deficiencies of T-suppressor cells, involvement of granulocytes, alterations of mediators of inflammation and especially the observations on the cyclic adenosine monophosphate (cAMP)-phosphodiesterase. These extremely complex findings based on the interaction between disregulation of the autonomous nervous system and alterations of the immune system may provide a better understanding of the pathogenesis of atopic dermatitis.
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PMID:[Pathogenesis of atopic dermatitis]. 299 74

We identified two siblings with exercise-induced anaphylaxis who share the HLA haplotype A3-B8-DR3 with their atopic father. The index case, a 16-year-old female, noted initial episodes at age 13. Intense pruritus, urticaria, facial edema, choking sensation, nausea, hypothermia, and collapse followed vigorous running but not swimming, cycling, racquetball, solar exposure, or cold exposure. Neither antihistamine, antiserotonin, anticholinergic nor epinephrine therapy was entirely effective or protective; only modification of running prevented episodes. Three similar episodes were noted at age 15 years by a brother who, now age 25, relates a 4-year history of seasonal rhinitis and exercise-related urticaria without anaphylactoid reaction. The remainder of the family (father, 47; mother, 46; brother, 22 years) does not have exercise intolerance. The father has allergic rhinitis; his nephew suffers exercise-induced urticaria without collapse. HLA typing revealed the father to be A1-B8-DR3, A3-B8-DR3; the symptomatic daughter to be A3-B8-DR3, A30-B5-DR8; and the symptomatic son to be A3-B8-DR3, A30-B5-DR8. The asymptomatic mother was A30-B5-DR8, A2-B7-DR5 and the asymptomatic son A1-B8-DR3, A30-B5-DR8. We describe exercise-induced anaphylaxis in a unique familial setting, perhaps linked to the HLA haplotype A3-B8-DR3.
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PMID:Familial exercise-induced anaphylaxis. 347 Oct 98

Male HLA-identical twins with numerous congenital abnormalities were discovered to have lichen amyloidosus in similar distribution on their chests and abdomens. Pruritus was absent in both. The finding of identical distribution of nonpruritic lesions was previously reported in familial lichen amyloidosus. This suggests that a subset of these patients have a nevoid condition in which a circumscribed patch of keratinocytes undergoes filamentous degeneration and may appear in identical distribution in family members in the absence of pruritus.
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PMID:Primary cutaneous amyloidosis: identically distributed lesions in identical twins. 372 2

The efficacy of an antigen-free diet on the activity of atopic dermatitis was examined in a double-blind study, comprising 33 adults with severe atopic dermatitis. The antigen-free diet (Vivasorb) was compared to a placebo diet during three weeks of hospitalization. Twenty-five patients were evaluable, two of whom had their diet stopped after a few days due to exacerbation. Nine patients improved, while 16 patients were unchanged. Among those who improved five patients had Vivasorb and four placebo diet. In the remaining group 11 patients had Vivasorb and five had placebo. Four patients reported of less pruritus, sleeplessness and antihistamine consumption (three Vivasorb, one placebo) while 21 did not (13 Vivasorb, eight placebo). Thus, there were no significant differences between the groups. Paraclinical studies of circulating eosinophilocytes, serum IgE, orosomucoid, HLA-antigens, and immunofluorescence of skin biopsies showed no differences between the Vivasorb and the placebo groups. The results from the examination of this relatively small number of patients suggest that elementary intolerance plays little role in the etiology of atopic dermatitis in adults.
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PMID:Antigen-free diet in adult patients with atopic dermatitis. A double-blind controlled study. 608 25

To explore the pruritogenic and inflammatory effects of cytokines, a single dose of 20 micrograms recombinant human interleukin-2 was injected intradermally into eight patients with atopic dermatitis and eight healthy controls. The study was double-blind and randomized with glucose as a negative control. The effects were evaluated by recording local itch and erythema over 72 h and by examining skin biopsies taken at 24 h and 72 h. In patients and controls, interleukin-2 provoked a low-intensity local itch with maximal intensity between 6 h and 48 h and erythema with maximal extension between 12 h and 72 h. In the atopic dermatitis patients, these reactions tended to appear earlier and were less pronounced than in the healthy controls. Interleukin-2 induced dermal mononuclear cell infiltrates consisting mainly of CD3+ cells. A majority of the T cells were CD4+. The number of dermal CD25+, HLA-DR+ and ICAM-1+ cells was also increased at the interleukin-2 induced spongiosis and exocytosis as well as HLA-DR+ and ICAM-1+ keratinocytes. The microscopic findings tended to be more prominent at 72 h than at 24 h in both groups, but with a somewhat slower onset in the atopic dermatitis patients. In conclusion, a single intradermal injection of interleukin-2 induced local itch, erythema, dermal T-cell infiltrates, spongiosis, exocytosis and activation of keratinocytes both in atopic dermatitis patients and in healthy controls.
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PMID:Itch and inflammation induced by intradermally injected interleukin-2 in atopic dermatitis patients and healthy subjects. 748 45

A 63-year-old man was referred to our department on September 14, 1992, because of multiple red papules with severe itching. Pruritic papular eruption (PPE) in a human immunodeficiency virus (HIV)-infected patient was diagnosed based on the histological findings, the reduction in CD4, and positive results for HIV antibody. In September of 1993, papules and erythematous plaques with scales appeared on both the palms and soles. The erythema was pruritic and spread gradually to the extremities and trunk. These plaques with erythema and scales are similar to those of the psoriatic lesions seen in Reiter's syndrome, although the HLA typing was not B27. Immunohistopathological findings of the papules of PPE and plaques of psoriasiform lesions showed that perivascularly infiltrated cells in the dermis were mostly lymphocytes. The lymphocytes in PPE were positive for CD45 and negative for CD3, CD43, and CD45RO, but the lymphocytes in psoriasiform lesions were positive for CD45, CD3, and CD43. Moreover, 20-30% of these lymphocytes were also intensely positive for CD45RO. These observations were similar to those obtained in the lesional skin of HIV-negative psoriasis, suggesting that there were no significant immunohistopathological differences in the abnormality of local cellular immunity related to the formation of psoriasiform lesions in HIV-negative psoriasis and HIV-positive psoriasis.
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PMID:A case of AIDS manifesting pruritic papular eruptions and psoriasiform lesions: an immunohistochemical study of the lesional dermal infiltrates. 765 Feb 42


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