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肿瘤坏死因子:麻风病治疗前后反应中的状况

Tumor necrosis factor: status in reactions in leprosy before and after treatment.

作者信息

Bhattacharya S N, Chattopadhaya D, Saha K

机构信息

Department of Dermatology and Venereology, Lady Hardinge Medical College, New Delhi, India.

出版信息

Int J Dermatol. 1993 Jun;32(6):436-9. doi: 10.1111/j.1365-4362.1993.tb02816.x.

Abstract

BACKGROUND

Tumor necrosis factor-alpha (TNF) is an important mediator of immunologic responses to chronic infections.

METHOD

Sera from 25 patients with acute reactions (6 with type 1 upgrading, 8 with type 1 downgrading, and 11 with type 2 reaction) were assayed for TNF before treatment and after clinical remission of the acute episode. The results were compared with serum TNF levels in healthy controls and fresh pauci- and multibacillary leprosy patients.

RESULTS

TNF levels in acute reactions were higher than in the control groups (significant only in upgrading reaction). In type 1 reaction, serum TNF concentrations fell to approximately the levels of the control patients following treatment and clinical remission. In type 2 reaction, however, levels of TNF were seen to rise further (became statistically significant) as a result of therapy induced clinical remission.

CONCLUSIONS

The rise in TNF-alpha level in reactions in leprosy is significant and indicates its active role in immunopathogenesis. The corresponding decline in TNF-alpha levels seen following regression of type 1 (lepra) reactions was not observed in the case of type 2 (ENL) reaction. This probably reflects the enhancement of cellular immunity in such cases and/or an attempt by the immunologic process to overcome specific inhibitors.

摘要

背景

肿瘤坏死因子-α(TNF)是对慢性感染免疫反应的重要介质。

方法

检测25例急性反应患者(6例1型升级反应、8例1型降级反应和11例2型反应)在治疗前及急性发作临床缓解后的血清TNF水平。将结果与健康对照以及新发少菌型和多菌型麻风患者的血清TNF水平进行比较。

结果

急性反应患者的TNF水平高于对照组(仅在升级反应中有显著性差异)。在1型反应中,治疗及临床缓解后血清TNF浓度降至大致与对照患者相同的水平。然而,在2型反应中,由于治疗诱导的临床缓解,TNF水平进一步升高(具有统计学显著性)。

结论

麻风反应中TNF-α水平升高具有显著性,表明其在免疫发病机制中起积极作用。1型(麻风)反应消退后TNF-α水平相应下降的情况在2型(结节性红斑型麻风反应)反应中未观察到。这可能反映了此类病例中细胞免疫的增强和/或免疫过程克服特异性抑制剂的尝试。

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