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Immunological skin diseases

The present edition of Molecular Immunology on T-Cell Regulation in Allergy, Asthma and Atopic Skin Diseases provides the latest... [Pg.241]

The second part describes the regulation and immunological events in different allergic diseases, such as asthma and atopic skin diseases, in parasite infection and delayed-type hypersensitivity. Special attention is paid to mucosal tolerance, which is important in many respects including... [Pg.241]

Cytotoxic and immunosuppressive drugs, which inhibit the synthesis or action of crucial cellular macromolecules, such as nucleic acids, are used in three broad categories of skin disease hyperproUferative disorders, such as psoriasis immunological disorders, such as autoimmune bullous diseases and skin neoplasms. The pharmacology of these drugs is discussed in Chapter 57. [Pg.493]

Keratinocyte apoptosis has been observed not only during a number of biological processes, such as epidermal differentiation, but also in certain skin diseases in which the epidermis is the target of immunological cytotoxicity [47,48]. [Pg.153]

Immunologic Although chloroquine has been used successfully in the treatment of systemic lupus erythematosus, its exact mechanism of action is not known. Matrix metalloproteinases (MMPs) may play a role in the immune response and tissue damage that occur in autoimmune skin diseases. The effects of chloroquine for 3 months on serum MMP activities and tissue inhibitors of metalloproteinases (TIMPs) have been studied in 25 patients with SLE and in 25 sex- and age-matched controls [4 ]. Before treatment, MMP activities were significantly much higher in the patients with SLE, as were TIMP concentrations. After chloroquine treatment, the MMP activities fell significantly while TIMP concentrations increased... [Pg.441]

Many skin diseases can be induced or worsened by UVR. Among the idiopathic photodermatoses, polymorphic light eruption with delayed reactions to sun exposure (which it is nevertheless correlated to) is the most frequent. Phototoxic or photoallergic dermatitis is more frequent and is due to contact with substances that, by an irritant or immunological mechanism, can... [Pg.363]

Sunderman FW Jr (1989) Chemistry, analysis, and monitoring. In Maibach HI, Menne T (eds) Nickel and the skin immunology and toxicology. CRC Press, Boca Raton, pp 1-8 Tan H-H, Chan MT-L, Goh C-L (1997) Occupational skin disease in workers from the electronics industry in Singapore. Am J Contact Dermatitis 8 210-214... [Pg.533]

Immunologic Skin testing of 26 patients clinically diagnosed with immediate (type I) hypersensitivity to infliximab found seven positives (30%) and six of these had infliximab-reactive serum IgE antibo es. One skin test-positive patient had no detectable IgE antibodies to the mAb [155 ]. After multiple infusions with infliximab, a 61-year-old woman with Crohn s disease experienced an acute anaphylactic reaction immediately after the start of an infusion. Although anti-infliximab IgE antibodies were not detected, the concentration of anti-infliximab IgG was high and this remained the case 1 year after the mAb was discontinued. Substitution of adalimumab for infliximab 1 week after the anaphylactic reaction was tolerated until the 12th day when the patient displayed a delayed, type IV hypersensitivity reaction mediated by IgG antibodies specific for adalimumab [ISb ]. In addition to types I and IV hypersensitivities to infliximab, other immune-mediated reactions representing the other hypersensitivity states also occur to infliximab. This is illustrated by a recent report of a case of a 27-year-old woman of infliximab-induced systemic lupus erythematosus [157 ], an autoimmune connective tissue disease which is both a type II and a type III hypersensitivity response. [Pg.576]

In AD increased S. aureus colonization plays a fundamental role therefore, antistaphylococcal therapy is part of a successful management of the disease. Epidermal lipid deficiencies and barrier dysfunction contribute to enhanced S. aureus attachment to the skin and mediate immunological and inflammatory effects including the release of superantigens, additional exotoxins, and exoenzymes, and perhaps bacterial DNA-triggered mechanisms. Therapeutic possibilities include the use of topical antiseptics in cases of microbial-laden atopic eczema, corticosteroids, and specific antibiotic-antiseptic combinations in cases of localized superinfected atopic eczema and systemic antibiotics in cases of generalized superinfected atopic eczema.48... [Pg.397]

The underlying mechanism of a series of clinical entities associated with beta-lactams, such as maculopapular rash, drug fever, eosinophilia, serum sickness-like disease, vesicular and bullous skin reactions, erythema nodosum, and acute interstitial nephritis, is suspected to be immunological but is still largely unknown. [Pg.486]

Immunological reactions to cromoglicate can involve the pericardium, the lung, the eye, the nasal mucosa, the skin, the joints, and the liver. Rarely, a hypersensitivity reaction can cause fever (4). A survey of the world literature up to 1982 found 13 cases of facial rash, urticaria, and/or generalized dermatitis, and one of nasal congestion. In 19 patients there was bronchospasm and/or pulmonary edema, eventually culminating in shock. Four cases of eosinophilic or granulomatous pulmonary infiltration, one of liver disease and vasculitis, one of pericarditis, and three of polymyositis were reported. [Pg.1018]

The authors suggested that the skin manifestations had been due to graft-versus-host disease triggered by the contrast medium and not a type-IV immunological reaction. Skin biopsy in one of the patients showed typical features of graft-versus-host disease. In addition, the reactions in these patients lasted for longer than one would expect in simple delayed reactions with skin manifestations, which usually resolve within 7-10 days. [Pg.1877]

Skin lesions are the most common industrial exposure symptom. Three distinct skin lesions have been noted following exposure to beryllium dermatitis, ulceration, and granulomas. There appears to be an immunological component to chronic beryllium disease, including the dermal responses. [Pg.266]


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See also in sourсe #XX -- [ Pg.153 ]




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