OBJECTIVE: Previous studies have suggested that Mycobacterium tuberculosis (MT) could be involved in the pathogenesis of Takayasu's arteritis (TA). The search for MT in arterial lesions of TA has never been assessed directly by sensitive methods. Our aim was to assess the presence of MT in arterial samples obtained in patients with TA. METHODS: Fresh arterial samples were collected from 10 consecutive patients (9 women and 1 man, median age 42 yrs, range 19-67 yrs) with a diagnosis of TA according to the American College of Rheumatology criteria who underwent vascular surgical procedures for their disease. Three patients had recent onset of TA and 7 had longstanding disease. No patient had evidence of active tuberculosis. Arterial biopsies were collected during vascular surgical procedures, and were systematically studied by a pathologist specializing in vascular diseases. Presence of MT was assessed in the biopsies by acid-fast and auramine-fluorochrome stainings, mycobacterial cultures, and direct amplification test (DAT) for MT. RESULTS: Histological examination showed active (n = 5) and inactive (n = 5) arterial lesions. MT was not detected in arterial lesions of either active or inactive TA, by acid-fast and auramine-fluorochrome staining, mycobacterial cultures, or DAT. No DAT inhibitors were found. CONCLUSION: Our study does not support a direct role of MT in the pathogenesis of arterial lesions in either recent or longstanding TA, but does not exclude the possibility of a cross-reaction between mycobacterial and arterial antigens.
OBJECTIVE: Previous studies have suggested that Mycobacterium tuberculosis (MT) could be involved in the pathogenesis of Takayasu's arteritis (TA). The search for MT in arterial lesions of TA has never been assessed directly by sensitive methods. Our aim was to assess the presence of MT in arterial samples obtained in patients with TA. METHODS: Fresh arterial samples were collected from 10 consecutive patients (9 women and 1 man, median age 42 yrs, range 19-67 yrs) with a diagnosis of TA according to the American College of Rheumatology criteria who underwent vascular surgical procedures for their disease. Three patients had recent onset of TA and 7 had longstanding disease. No patient had evidence of active tuberculosis. Arterial biopsies were collected during vascular surgical procedures, and were systematically studied by a pathologist specializing in vascular diseases. Presence of MT was assessed in the biopsies by acid-fast and auramine-fluorochrome stainings, mycobacterial cultures, and direct amplification test (DAT) for MT. RESULTS: Histological examination showed active (n = 5) and inactive (n = 5) arterial lesions. MT was not detected in arterial lesions of either active or inactive TA, by acid-fast and auramine-fluorochrome staining, mycobacterial cultures, or DAT. No DAT inhibitors were found. CONCLUSION: Our study does not support a direct role of MT in the pathogenesis of arterial lesions in either recent or longstanding TA, but does not exclude the possibility of a cross-reaction between mycobacterial and arterial antigens.
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