Case Presentation: A 26-year-old man from Haiti with no past medical history was hospitalized with a four month history of intermittent fevers, weight loss, and dyspnea. In the ED, he was found to be febrile, tachycardic, and tachypneic with an oxygen saturation of 88% on room air. Physical exam was significant for bilateral rales on auscultation. Labs were significant for leukopenia (3.7 k/µl) and hyponatremia (125 mmol/L). A CT chest revealed diffuse bilateral ground glass opacities with mediastinal and supraclavicular lymphadenopathy. Initial sputum samples were negative for acid-fast bacilli (AFB) and he was HIV negative. He underwent cervical lymph node biopsy, bronchoscopy and bone marrow biopsy, which all showed non-necrotizing granulomatous inflammation. After an extensive unrevealing workup for infection, malignancy, and vasculitis, a diagnosis of sarcoidosis was made. Corticosteroids were initiated with improvement in his pulmonary symptoms, but he continued to spike occasional fevers. After three weeks of incubation, the cervical lymph node specimen stained positive for AFB and TB was confirmed by PCR. Repeat sputum samples were AFB positive. The patient was initiated on therapy with rifampin, isoniazid, pyrazinamide, and ethambutol. Steroids were slowly tapered to 10 mg daily, and patient was discharged with significant clinical improvement.
Discussion: TB and sarcoidosis have long been considered “great imitators” as they present like many other autoimmune disorders, infections and malignancies. Despite presumed exclusion of TB initially, our patient developed active tuberculosis after treatment with high-dose corticosteroids. It is unclear if this was a case of corticosteroid-induced TB reactivation in a patient with sarcoidosis, or if TB was imitating sarcoidosis from initial presentation. In support of the latter, the gold standard for TB diagnosis is an AFB culture, which can take weeks to result. Hospitalists relying on the initial TB sputum smears can make a diagnostic error due to their low sensitivity.
Although the cause of sarcoidosis has not been definitively established, some speculate that a subset of sarcoid is triggered by mycobacterium. Evidence in favor of this theory include the histopathological similarities of their respective granulomas, reports of mycobacterial disease succeeding or antedating sarcoidosis, and findings of mycobacteria in granulomas of sarcoidosis by PCR. Moreover, several studies have shown symptomatic improvement of sarcoid with empiric anti-TB therapy. This case lends support to the theory that mycobacteria may trigger the pathologic changes seen within a subset of sarcoidosis.
Conclusions: Distinguishing between sarcoid and TB (two of the “great imitators”) can be challenging due to similarities in their clinical presentation and diagnostic difficulties. Thus, it is important for hospitalists to keep a low threshold for considering TB when patients being treated for sarcoidosis fail to improve.