Abstract
Mycobacterium tuberculosis (Mtb) has been implicated in the pathogenesis of Takayasu’s arteritis (TA), but there is no direct evidence substantiating the association. Several cases series and laboratory studies provide indirect evidence on the role of Mtb and other related species in the immunopathogenesis of TA. This association could be explained by the molecular mimicry between mycobacterium heat shock protein (mHSP 65) and the human homologue (hHSP60) driving immune response in TA. Two different histopathological studies that have evaluated the presence of mycobacteria in aortic tissue have reported contradictory results. This may be due to regional differences in the prevalence of Mtb, ethnicity, and study methodology. Recent progress in identifying susceptibility genes and study of TNFα-308 gene polymorphism has opened up new avenues for research on mycobacterium theory. Based on the currently available data, three different models have been proposed. Among these, two models favor the mycobacterium theory, while one does not. Transcriptomic and proteomic studies of mycobacteria could help in identifying specific or common traits of mycobacteria that are relevant to the development and reactivation of TA.
Highlights
Takayasu’s arteritis (TA) is a rare chronic pan arteritis of aorta and its major branches
Genetic background has been implicated in the predisposition to TA and exogenous factors, Mycobacterium tuberculosis (MTb) as possible etiological agents, there is no convincing data to substantiate the findings
This review evaluates the available literature evidence linking mycobacteria infections with the etiopathogenesis of TA
Summary
Takayasu’s arteritis (TA) is a rare chronic pan arteritis of aorta and its major branches. Studies done during the last fifty years in Japan, Korea, India, and South Africa have reported either tubercular hypersensitivity or evidence of active TB in patients with TA series (Table 1).[4]. Case studies suggesting an association between TA and tuberculosis Possible relationship between TA and latent and active tuberculosis (TB) was first suggested by Shimizu and Sano in 1948.1 This hypothesis was based on the detection of Langhans giant cells granulomas in the arterial specimens of patients with TA. These granulomas morphologically resembled to those found in the tuberculous lesions. A case series of twenty TA patients from India has found that the chances of having TA in active TB patients were 44.8 times more when compared to general population, in whom the prevalence rate of TB was 1.5 times in the year 1970.5 A systematic search of the Medline database has identified 9 cases of TA with active TB, mainly in the lymph nodes and lungs and occasionally in the internal organs such as kidneys.[6, 7] One case had a rare form of skin TB (papulonecrotic tuberculide), while another subjects had cold agglutins and cryoglobulins, which disappeared
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