Early recognition and combined management with anti-tuberculosis therapy, corticosteroids, and guideline-directed heart failure therapy can lead to complete left ventricular recovery in postpartum immune reconstitution syndrome-mediated fulminant tuberculous myopericarditis.
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Post-caesarean haemodynamic instability warrants TB myopericarditis consideration; leaves open whether MTB antigen triggers fulminant disease.
Background: (MTB) antigen that hypothetically results in acute fulminant tuberculosis myopericarditis. Case summary: A 29-year-old woman develop acute respiratory distress 5 days following caesarean section. On admission vital sign indicating haemodynamic instability. Chest X-ray showed extensive pulmonary consolidation which signified for pulmonary tuberculosis. Echocardiography finding revealed left ventricular (LV) dysfunction with minimal pericardial effusion. Cardiac magnetic resonance imaging showed non-ischaemic late gadolinium enhancement (LGE) distribution. Upon to this finding, acute fulminant tuberculosis myopericarditis diagnosis was established. The patient then stabilized in intensive cardiac care unit with inotropic support, heart failure therapy, steroid, and anti-tuberculosis treatment (ATT). Patient clinical course was favourable and patient discharged at 8th admission day. At 3-month post-discharge visit, the patient showed complete LV recovery and chest X-ray also showed improvement in pulmonary consolidation. Discussion: Important to consider acute fulminant tuberculous myopericarditis that developed immediately in the postpartum period. The IRS-induced acute fulminant tuberculous myopericarditis is reasonable to be considered as an underlying mechanism. Most of the reported cases showed significant improvement after ATT initiation. Clinical vigilance and awareness for early diagnosis and delivering timely management of ATT as effective therapy for tuberculous myopericarditis is of the utmost importance.
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Hendiperdana et al. (2025) studied this question.
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