Tuberculous pericarditis is one of the commonest causes of cardiac failure in Transkei and the surrounding regions in southeast Africa. About 20% of patients with clinically diagnosed tuberculous pericardial effusion go on to develop pericardial fibrosis (i.e., construction), a complication which is associated with significant mortality and morbidity. The pathological mechanisms underlying this aberrant inflammatory response are poorly understood, and there is a lack of reliable pointers (clinical or laboratory) in predicting the likelihood of development of constriction. We studied the humoral response to mycobacterial heat shock proteins (65 and 71 kDa) in 25 patients with culture-positive tuberculous pericardial effusion and found a significant correlation between high anti-mycobacterial hsp60 antibody titers (before treatment) and subsequent development of fibrosis (P = 0.035 by logistic regression), which is independent of the effect of the use of prednisolone as adjuvant therapy. Possible mechanisms underlying the pathogenesis of pericardial constriction in tuberculosis are postulated.