Takayasu’s Arteritis and Its Potential Pathogenic Association with Mycobacterium tuberculosis

Takayasu’s arteritis is an idiopathic, inflammatory disease which involves largeand medium-sized arteries, specially the aorta, its major branches and the pulmonary arteries. In contrast to other vasculitides, Takayasu’s arteritis is restricted to certain geographical areas. Initially thought to be confined to Japan and Korea, it has now been reported with increased frequency in Mexico, India, China, South America, South Africa, and the Mediterranean basin; while, the disease continues to be exceptionally described in individuals from the United States, North and Central Europe and other high-income regions. The etiology of Takayasu’s arteritis is unclear and attempts to clarify it are still limited. There are clinical and laboratory features suggesting an autoimmune basis, while others raise a question that aortitis may be the expression of delayed-type hypersensitivity reaction to tuberculin or other sensitizers. Finally, the occurrence of Takayasu’s arteritis in homozygotic twins suggests a genetic background for predisposition. A possible relationship between Takayasu’s arteritis with both latent and active tuberculosis was suggested long time ago. Both diseases show similar chronic inflammatory lesions on histology, with occasional granuloma formation into the arterial walls. Delayed hypersensitivity to tuberculin is frequently found to be increased in patients with Takayasu’s arteritis from almost all ethnicities. Isolated cases of Takayasu’s arteritis coexisting with both latent and active tuberculosis, and improvement of arteritis after antituberculous treatment have been occasionally described. Finally, there are studies showing increased humoral and cellular immune responses directed toward mycobacterial 65 kDa heat shock protein (HSP) and its human homolog 60 kDa HSP. All these indirect evidences support that Mycobacterium tuberculosis and probably other mycobacteria may play a role in the immunopathogenesis of Takayasu’s arteritis, possibly through molecular mimicry mechanisms; however, results of several recent studies are challenging this old but still valid etiopathogenic hypothesis of association. Analyzing this possible link is not futile because the potential risk of using anti-tumour necrosis factor (TNF) therapies in the treatment of patients with Takayasu’s arteritis and the increasing use of Bacille CalmetteGuérin (BCG) for vaccination purposes around the world.