从“毒热入脉、血脉癥积”理论探讨大动脉炎发病机制

王双瑛; 孟宇航; 孟培培; 杨子婧; 杨卫彬

doi:10.3969/j.issn.1006-2157.2023.06.006

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从“毒热入脉、血脉癥积”理论探讨大动脉炎发病机制

理论研究 | 更新时间：2023-07-05

- 从“毒热入脉、血脉癥积”理论探讨大动脉炎发病机制
- Exploring the pathogenesis of Takayasu arteritis from a theory of "heat-toxin in blood vessels developing into lumps"
- 北京中医药大学学报 2023年46卷第6期页码：770-774
- 作者机构：
  
  1.北京中医药大学研究生院　北京　100029
  2.中国中医科学院西苑医院
  3.解放军总医院京北医疗区
  4.中国中医科学院研究生院
- 作者简介：
  
  王双瑛，女，在读硕士生
  # 杨卫彬，男，博士，主任医师，教授，博士生导师，主要研究方向：中医药防治风湿免疫病与肾脏疾病，E-mail：ywb823@126.com
- 基金信息：
  
  国家自然科学基金面上项目(82074584)
- DOI：10.3969/j.issn.1006-2157.2023.06.006
  中图分类号： R255.6
- 纸质出版日期：2023-06-30，
  
  网络出版日期：2023-04-12，
  
  收稿日期：2022-11-08，
- 稿件说明：
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王双瑛, 孟宇航, 孟培培, 等. 从“毒热入脉、血脉癥积”理论探讨大动脉炎发病机制[J]. 北京中医药大学学报, 2023,46(6):770-774.

WANG Shuangying, MENG Yuhang, MENG Peipei, et al. Exploring the pathogenesis of Takayasu arteritis from a theory of "heat-toxin in blood vessels developing into lumps"[J]. Journal of Beijing University of Traditional Chinese Medicine, 2023,46(6):770-774.
王双瑛, 孟宇航, 孟培培, 等. 从“毒热入脉、血脉癥积”理论探讨大动脉炎发病机制[J]. 北京中医药大学学报, 2023,46(6):770-774. DOI： 10.3969/j.issn.1006-2157.2023.06.006.

WANG Shuangying, MENG Yuhang, MENG Peipei, et al. Exploring the pathogenesis of Takayasu arteritis from a theory of "heat-toxin in blood vessels developing into lumps"[J]. Journal of Beijing University of Traditional Chinese Medicine, 2023,46(6):770-774. DOI： 10.3969/j.issn.1006-2157.2023.06.006.

摘要

大动脉炎是一种慢性肉芽肿性血管炎，其病因不明，大多起病隐匿，为临床难治性疾病，预后欠佳。近年来，毒邪理论在自身免疫病的治疗中受到重视，而毒邪易蕴蓄化热，毒热内伏，诸症渐生。大动脉炎之为病，主因毒邪久郁、化热生火、伤及脉络、血凝不流是其基本病机，病位在血脉，亦与脾、肾关系密切，总属本虚标实之证。脾肾亏虚、精亏血少以致脉道不充、血行滞涩，邪气蕴蓄、化毒生热以致毒热积滞、血脉壅塞，病久邪稽、内舍脏腑以致正气渐亏、诸脏失养。临证以通脉道、行血气为基本治则。活动期重视清解毒热；缓解期重视调脾补肾、滋阴养脉，兼顾解毒通络；瘢痕期则重在通络破积、扶助正气。基于中医学相关理论及西医学病理机制研究，阐述毒热之邪在大动脉炎发病过程中的重要性，提出毒热入脉、血脉癥积是其发病关键，认为可清解毒热以和痹消癥，进而改善患者临床症状，延缓病程进展，为临床治疗该病提供新思路。

Abstract

Takayasu arteritis (TAK) is a chronic granulomatous vasculitis with an unknown etiology that often manifests over time. It has a dismal prognosis and is currently clinically refractory. The theory of poisonous evil has drawn more attention in recent years in the treatment of autoimmune disorders. Poisonous evil tends to accumulate and transform into heat

which causes a variety of symptoms to gradually emerge. Our team believes that the main cause of TAK is the prolonged stagnation of poisonous evil

the transformation of heat into fire

and the damage to the vessels and collaterals. Blood stasis is the basic pathogenesis. This disease is located in the blood vessels

which is also closely related to the spleen and kidney. TAK also belongs to a deficiency in origin and excess in superficislity. Kidney and spleen deficiencies

and a lack of essence and blood

cause only partially filled blood vessels and restricted blood flow. The collection of evil qi and the transformation of heat-toxin culminates in the accumulation of heat-toxin and congestion of blood vessels. The illness persists and the evil qi remains and penetrates the internal organs

causing a lack of vital qi

and the viscera loses its nourishment. Unblocking the blood vessels and boosting blood circulation is the cornerstone of clinical treatment. The focus of treatment is on removing heat-toxin during the active phase

while during the remission phase

the focus is on strengthening the spleen and kidney

nourishing the vessels

taking into consideration detoxification

and dredging collaterals. The goal of the cicatricial period is to dredge collaterals in order to enrich vital qi. Based on relevant theories of traditional Chinese medicine and pathological mechanisms research of western medicine

the significance of heat-toxin in the pathogenesis of TAK is explained. Our team believes that the heat-toxin in blood vessels developing into lumps is the vasculature are the cause of the disease’s morbidity. The heat-toxin can be cleared to remove blood stasis and eliminate lumps

which will improve clinical symptoms

slow the disease’s progression

and provide ideas for clinical treatment.

关键词

毒热血脉癥积大动脉炎发病机制

Keywords

heat-toxinblood vesselslumpsTakayasu arteritispathogenesis

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