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)

Research on itch has been hampered by difficulties in measuring the itch sensation. A microcomputer-based system, where the patients themselves record their symptoms on portable data loggers can be used for quantitative measurements of clinical itch and for the detection of antipruritic effects of drugs. By using this system we have found that itch in atopic dermatitis is not inhibited by antihistamines but by cyclosporin A, a drug inhibiting cytokine production. Thus histamine is not a major pruritogen in atopic dermatitis. A hypothesis is proposed that cytokines are involved in itch in atopic dermatitis.
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PMID:Some methods for evaluating clinical itch and their application for studying pathophysiological mechanisms. 141 79

Atopic dermatitis is a genetically determined inflammatory condition in which the primary defect is expressed in one or more hematopoietic cells that infiltrate the skin. It is a multifactorial disease with inflammation triggered by a variety of factors. Among these, atopic dermatitis has been experimentally induced and reproduced by emotional-stress interviews and food challenges only. The inflammatory events of atopic dermatitis appear to initiated by mast cells, but eosinophils, monocytes, and T lymphocytes (predominantly CD4) also are present in lesions. The secondary effects of inflammation are a dry, brittle stratum corneum and pruritus, causing excoriation and a lichenified epidermal layer resulting from chronic rubbing. Therapeutic approaches to atopic dermatitis may be directed at several points in the evolution of the disease. Agents including emollients are needed to preserve and restore the stratum corneum barrier, and effective antipruritics are required to reduce the self-inflicted damage to the involved skin. Various other agents may be needed to antagonize mediators or cytokines and to inhibit cytokine expression and release from lesional, immune-effector cells. Likewise, new phosphodiesterase inhibitors, calcium-active agents, and antiallergic drugs may be used to reduce the quantity and pathologic functioning of inflammatory infiltrating cells in the skin.
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PMID:Atopic dermatitis: new therapeutic considerations. 167 14

The clinical and immune modulatory effects of interleukin-2 (IL-2) and interferon (INF) alfa-2a were examined in a phase II study in patients with metastatic renal cell carcinoma (six patients) and melanoma (eight patients). Treatment consisted in IL-2 3 MU/m2 continuous infusion days 1-4 and INF alfa-2a 6 MU/m2 subcutaneously day 1 and 4, both given on alternate weeks. Tumour response was assessed after four cycles of treatment or earlier, if necessary. Patients with stable disease or response were to be continued for another nine cycles or up to disease progression. The 14 patients received a total of 60 cycles of treatment. Major toxicities (WHO Grade III/IV) were fever, capillary leak syndrome with hypotension, nausea and vomiting, erythema with pruritus, leuco- and thrombopenia and sepsis with staphylococcus aureus. Five of 14 patients (36%) developed a self limiting autoimmune thyroiditis with HLA-DR expression on thyrocytes. Long term treatment toxicity was moderate with an average weight loss of 5% and an average fall in Karnofsky index of 10% compared to baseline. No responses were seen in renal cell carcinoma, two patients with melanoma had a partial and two a minor response with a duration of 1-7 months. Serial measurements of immune modulatory parameters showed a functional response to treatment with an increase of NK- and LAK-activity during the first two cycles, followed by a plateau and decrease during the third and fourth cycles. These findings were paralleled by a successive decline in treatment induced INF gamma response. These findings suggest, that alternative weekly treatment with IL-2 and INF alfa-2a results in an exhaustion of lytic capacity of NK- and LAK-cells and an attenuation of secondary cytokine release.
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PMID:Clinical and immune modulatory effects of alternative weekly interleukin-2 and interferon alfa-2a in patients with advanced renal cell carcinoma and melanoma. 199 8

Neutrophil attractant/activation protein-1 (NAP-1) is a recently described cytokine that attracts neutrophils, but not monocytes or eosinophils. This leukocyte specificity is not absolute, in that NAP-1 attracts basophils and small numbers of lymphocytes. Our purpose was to determine in vivo effects of NAP-1, and to compare them to the reported action of the complement attractant, C5a. Intradermal injection into normal human subjects of 40 microliters of NAP-1, over a concentration range of 4 x 10(-8) M to 10(-6) M, caused no symptoms or signs such as wheal-and-flare, itching, induration, or tenderness. However, biopsies of injection sites showed perivascular neutrophil infiltration as early as 30 min, which increased at 1 and 3 h. The mean number of neutrophils per mm2 of dermis for 15 biopsies taken 3 h after intradermal injection of 2 x 10(-7) M or 10(-6) M NAP-1 was 164 +/- 41; the response to saline or a NAP-1 inactive fragment was 5 or less. Intradermal NAP-1 did not cause basophil or lymphocyte infiltration. Consistent with the absence of a wheal-and-flare, acid toluidine blue-stained sections showed no evidence of mast cell degranulation, in contrast to previously reported results with C5a. Thus, the predominant response by human subjects to intradermal NAP-1 was neutrophil accumulation in proximity to dermal blood vessels.
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PMID:Neutrophil recruitment by intradermally injected neutrophil attractant/activation protein-1. 202 77

Atopic dermatitis shows a familial disposition and is characterised clinically by extreme pruritus, typical eczematoid pathology and distribution on the integument, a chronic relapsing course, and a personal or familial history of atopic diseases (allergic bronchial asthma, rhinitis and allergic conjunctivitis, atopic dermatitis), as well as numerous other stigmata and microsymptoms. Although numerous exogenous factors help trigger the disease, more recent findings point to an immunological basis. In recent years, numerous cellular malfunctions of immune cells have been reported, with disturbances in T-lymphocyte predominating. The latest investigations now suggest that the reported changes in the immune response are due to an imbalance in the cytokine network. Thus, it has been observed that disturbances of cytokine production depend upon the severity of the disease, and show an AD-characteristic pattern. The pathogenesis of atopic dermatitis however, is not yet fully understood.
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PMID:[Pathogenesis of atopic dermatitis]. 204 39

Acquired immunodeficiency syndrome was first recognized as a new disease in 1981 because of the unusual association of Kaposi's sarcoma and Pneumocystis carinii pneumonia in young men. The skin remains one of the most important clinical markers for acquired immunodeficiency syndrome, now recognized as the end stage of infection with the human immunodeficiency virus (HIV). Indeed, an urticarial viral exanthem appearing during seroconversion may allow early identification of newly infected individuals who might benefit from administration of antiviral therapy during plasma viremia. The "asymptomatic HIV infection" is often accompanied by multiple skin complaints, which commonly include xerosis, pruritus, psoriasis/seborrheic dermatitis, and pruritic papular eruptions, the cause of which remains controversial. Psoriasis and Kaposi's sarcoma lesions share features including angiogenesis, dermal dendrocytes infected with HIV, and epidermal hyperproliferation, and are manifested by mice transgenic for HIV provirus or Tat-ltr. Changes in the immune system including T-cell function, antigen response, and shifting cytokine expression as well as a propensity for autoimmune reactions must underlie the skin immunodysfunction occurring in the setting of HIV infection. One of the most unsettling controversies suggested by in vitro data is that ultraviolet light, an effective therapy for HIV-related skin disorders, may actually activate the virus.
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PMID:Human immunodeficiency virus and the skin: selected controversies. 761 89

Long-term treatment with interferon alpha (IFN-alpha) has recently been shown to reduce the bone marrow infiltrate and cutaneous lesions in systemic mast cell disease. We therefore administered this cytokine to six patients with urticaria pigmentosa for up to 12 months, using subcutaneous injections of 5 x 10(6) U, initially five times, and subsequently three times a week. The generally well-tolerated therapy resulted in marked improvement of the cutaneous symptoms, especially in three of the patients who suffered from very severe pruritus. Two of the patients with bone marrow infiltration showed normal findings after treatment. However, in none of the patients was there any change in the skin lesions, or decrease in the degree of cutaneous mast cell infiltration, as evidenced by light and electron microscopic examination. These findings indicate that IFN-alpha is highly effective in the control of symptoms, but otherwise does not influence the cutaneous lesions of urticaria pigmentosa.
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PMID:Treatment of urticaria pigmentosa using interferon alpha. 876 58

Recombinant gamma interferon (IFN-gamma) was employed to treat adult-type atopic dermatitis. Eight cases received subcutaneous injections of 500,000 JRU of IFN-gamma for 8 weeks. They responded relatively well to this treatment; however, the overall response to the treatment was not significantly better than that to conventional therapy in the control group. There was no significant suppression of itch or erythema. Swelling was reduced at the 8th week in the treatment group. Frequency of flushing attacks on the face was reduced and disappeared within four weeks in 6 of these patients; however, a similar reduction of frequency was observed in the control group. Papular and lichenified lesions on the trunk and extremities responded significantly to the treatment later than 5 weeks after its initiation. Serum IgE level was not affected by the treatment. Seven had the same level of serum IgE before and after the treatment. The serum cytokine level in the treated patients was also unaltered. Therefore, although IFN-gamma treatment has some benefit in the treatment of severe cases of atopic dermatitis, it should be applied to limited cases because of its high cost.
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PMID:Gamma-interferon therapy for severe cases of atopic dermatitis of the adult type. 773 73

We have described a patient with hyperprolactinemic galactorrhea associated with Hodgkin's disease and severe pruritus. Prolactin levels increased in parallel with the development of constitutional symptoms and returned to normal during successful treatment with chemotherapy. Explanations for the development of galactorrhea include chronic chest wall excoriation due to severe pruritus and cytokine-mediated pituitary prolactin release.
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PMID:Hyperprolactinemic galactorrhea in a patient with Hodgkin's disease and intense pruritus. 832 94

Knowledge of biochemical and molecular events during burn wound healing may optimize treatment of patients with thermal injuries. Substance P (SP), a neuropeptide present in C fibers of the skin, has been implicated as a mediator of inflammation and wound healing. This neuropeptide induces vasodilitation and vascular permeability by stimulating endothelial cells to round up, vascular smooth cells to relax, and mast cells to release histamine. SP also induces cytokine release by macrophages and neutrophils. Because many of the functions of SP seemed relevant to wound repair in burns, we used immunocytochemistry to characterize SP+ nerve fibers in healing human burn wounds. Deep partial-thickness burns collected from 20 patients at the time of excision and grafting were formalin fixed, paraffin-embedded, sectioned, and labeled with a monoclonal antibody to SP with use of an immunoperoxidase technique. Our tissue samples included normal skin and 20 specimens from postburn days 2 through 49. In normal adult skin, SP+ nerve fibers surrounded vessels throughout the skin and extended from the papillary dermis into the epidermis. SP+ fibers were absent in early wound beds. SP immunostaining did occur in the advancing epidermis, endothelial cells, and mast cells. SP+ fibers could be identified in the deep dermis and subjacent to the advancing epithelium before the wound beds. Maximum numbers of SP+ fibers were present subjacent to the advancing epithelium at 2 weeks after burn injury. After 4 weeks, the distribution of SP+ fibers in reepithelialized areas was similar to that of normal skin. Our data corroborate published reports of SP+ fiber regeneration in guinea pig burns and correlates with clinical observations of pain and pruritus in patients with thermal injuries. The absence of SP+ fibers in the early wounds with SP immunostaining in the epidermis and extracellular matrix suggests that SP may be released from injured nerves and supports neurogenic mediation of inflammation and vasodilitation in early wound repair. Repopulation of the wound beds with SP+ fibers appeared to follow neovascularization originating in the deep reticular dermis and wound edge.
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PMID:Substance P has a role in neurogenic mediation of human burn wound healing. 888 61


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