Abstract Introduction Reactivation of latent tuberculosis typically occurs as a result of initiation of immunosuppressive medications, HIV infection, malignancy, diabetes, or chronic kidney disease. Less commonly, reactivation TB can occur from severe malnutrition leading to lymphocytopenia and/or pancytopenia. Case Description A man in his late 20’s presented to the emergency department with chief complaint of shortness of breath, productive cough, and weight loss over the last 3 months. He immigrated to Michigan about 12 years ago from Senegal and has since not had any routine medical care. He has not traveled internationally since immigrating and has had no contact with individuals with tuberculosis. Physical exam was notable for tachycardia, hypoxemia, cachexia with BMI of 11, and bilateral lower extremity pitting edema. Computed tomography pulmonary angiography was notable for bilateral acute pulmonary emboli, large cavitary lung lesions and pneumatoceles in bilateral apices and the right middle lobe, and an associated right pneumothorax. Sputum cultures revealed many acid-fast bacilli and PCR was positive for Mycobacterium tuberculosis. Echocardiography demonstrated no evidence of right ventricular dysfunction, however the left ventricular ejection fraction was 20% with global hypokinesis. Further laboratory studies were notable for pancytopenia (with normocytic anemia and lymphopenia including CD4 count 200), hypovolemic hyponatremia, hypoalbuminemia, and mildly elevated transaminases. Fourth generation HIV testing was negative on multiple occasions. Ferritin was reported as 40,000. Soluble IL-2 receptor was markedly elevated. Bone marrow histopathology was non-specific, without evidence of M. tuberculosis or hemophagocytosis. The presumed diagnosis was reactivation of latent tuberculosis due to extreme protein calorie malnutrition and subsequent pancytopenia with lymphocytopenia. Rifampin, isoniazid, pyrazinamide, and ethambutol were started in addition to aggressive nutrition supplements. This resulted in improvement of dyspnea and cough, reduced oxygen requirements, improvement in lymphocytopenia (and CD4 count increased to above 600), and improvement in LVEF to 40% on echocardiography. He was also started on subcutaneous enoxaparin for his pulmonary emboli. Discussion This patient developed extensive cavitary disease and provoked pulmonary emboli as a result of reactivation TB. This case illustrates the possibility of malnutrition and the subsequent relative immunosuppression as an important potential cause of reactivation TB. There were no other apparent triggers of reactivation in this case. Furthermore, left ventricular dysfunction without clinical heart failure developed, likely as a result of malnutrition rather than myocardial involvement of TB. Improvement in clinical status, cell counts, and ejection fraction with nutritional rehabilitation suggest malnutrition is the culprit. This abstract is funded by: None
Connolly et al. (Fri,) studied this question.