Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085593 (chills)
 4,268 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Generalized pustular psoriasis is one of life-threatening skin diseases which represents sudden onset of severe systemic symptoms such as high fever and chill as well as burning erythema and aseptic pustules over the entire skin. Although the precise mechanism of this rare disease is unknown, several lines of clinical and experimental observations have suggested that certain immunological mechanisms play important roles in the pathogenesis of this disease. In this study, in order to attain better understanding of the immunological events involved in generalized pustular psoriasis, several in vivo and in vitro immunological experiments have been performed. The results obtained are as follows: 1) sera from patients contained high amount of inflammatory cytokines, 2) peripheral blood mononuclear cells(PBMC) showed high proliferative responses to bacteria-derived super antigens, 3) PBMC from patients produced a large amount of cytokines when stimulated by mitogens in vitro, 4) endothelial cells in the lesional skins of patients exhibited enhanced expression of adhesion molecules, and 5) the expressions of these adhesion molecules on human endothelial cells were differently regulated by several cytokines. These results suggest that the activation of peripheral blood mononuclear cells by bacteria-derived super antigens followed by cytokine production, and the induction of the adhesion molecules expressions on the endothelial cells are important immunological events in the forming the characteristic clinical symptoms of generalized pustular psoriasis.
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PMID:[Analysis of immunological mechanisms in the pathogenesis of generalized pustular psoriasis]. 1033 Oct 61

Generalized pustular psoriasis (GPP) is a serious dermatological disease characterized by fever, chills, rigors, and generalized pustule formation on the skin. Previous analyses in Japan have led to the proposal to divide GPP into two groups, one with a history of ordinary psoriasis (pso(+) GPP) and the other without a history of psoriasis (pso(-) GPP). Clinically the onset of the pustular outbreak is earlier in pso(-) GPP, which occurs more frequently after infections, whereas pso(+) GPP occurs more frequently following corticosteroid therapy. Substantial differences are also noted in HLA analyses. Activation of neutrophils is a basic mechanism in both types of GPP. Although the epidermal structural changes in GPP are usually not so prominent as those in psoriasis vulgaris, pso(+) GPP shows a more psoriasiform architecture than pso(-) GPP. Analysis of epidermal cell proliferation in GPP indicates that it is not less than that seen in psoriasis vulgaris. The occasional psoriasiform epidermal architecture especially seen in pso(+) GPP may be considered to be a steady-state condition achieved after epidermal cell proliferation has continued for a sustained period. Various inflammatory cytokines appear to be involved in the neutrophilic infiltrate seen in GPP.
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PMID:Pathophysiology of generalized pustular psoriasis. 1267 33