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[结节性痒疹的发病机制]

[Pathogenesis of prurigo nodularis].

作者信息

Raap U, Günther C

机构信息

Klinik für Dermatologie, Allergologie und Venerologie, Medizinische Hochschule Hannover, Carl-Neuberg-Str. 1, 30625, Hannover, Deutschland,

出版信息

Hautarzt. 2014 Aug;65(8):691-6. doi: 10.1007/s00105-014-2754-y.

Abstract

BACKGROUND

Prurigo nodularis is a chronic reaction pattern associated with severe pruritus that markedly affects the quality of life in patients.

PATHOGENESIS

The pathogenesis of prurigo nodularis is not completely clear. Patients have an increased number of substance P and calcitonin gene-related peptide positive nerves in the dermis. Eosinophils and mast cells are in close vicinity to peripheral nerves and increased in numbers in the inflammatory infiltrate in prurigo nodularis. Nerve growth factor (NGF) is increased in lesional skin of patients and can be released by mast cells and eosinophils. In addition, NGF modulates the functional activity of mast cells and eosinophils. Recently, higher levels of the novel pruritic cytokine IL-31 were found in the skin of patients with prurigo nodularis than other pruritic skin diseases.

CONCLUSION

The pathogenesis of prurigo nodularis seems to be regulated by immunological and neuronal plasticity which will be highlighted in the current article.

摘要

背景

结节性痒疹是一种与严重瘙痒相关的慢性反应模式,显著影响患者的生活质量。

发病机制

结节性痒疹的发病机制尚不完全清楚。患者真皮中P物质和降钙素基因相关肽阳性神经数量增加。嗜酸性粒细胞和肥大细胞靠近外周神经,在结节性痒疹的炎症浸润中数量增加。患者皮损皮肤中神经生长因子(NGF)增加,且可由肥大细胞和嗜酸性粒细胞释放。此外,NGF调节肥大细胞和嗜酸性粒细胞的功能活性。最近,发现结节性痒疹患者皮肤中新型瘙痒细胞因子白细胞介素-31的水平高于其他瘙痒性皮肤病。

结论

结节性痒疹的发病机制似乎受免疫和神经可塑性调节,本文将对此进行重点阐述。

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