A 66‐year‐old woman presented with vomiting, bilateral leg pain, and a fall. Over the past 6 months, the patient had complained of an unsteady gait, intermittent shooting pains from the knees to the thighs, polyuria, and generalized fatigue. Eighteen months prior, a bone marrow biopsy (BMBx) performed because of thrombocytopenia revealed caseating and noncaseating granulomas with rare acid‐fast bacilli (AFB). Pulmonary evaluation was negative, and the patient was treated over 6 months with rifampin, isoniazid, pyrazinamide, and ethambutol for extrapulmonary tuberculosis. Thereafter, she presented twice with hypercalcemia (as high as 13.3) and renal failure. A workup including ACE level, PTH, PTHrP, serum protein electrophoresis, and vitamin D levels was unrevealing. A repeat BMBx revealed noncaseating granulomas without AFB. She was treated with a brief course of steroids, complicated by hyperglycemia. On admission, the patient was ill‐appearing, but vital signs were normal. She had icteric sclera, and neck exam revealed no lymphadenopathy (LAN). Lungs were clear, and cardiac exam revealed a 3/ 6 aortic systolic murmur. She had splenomegaly. Neurologic exam revealed ataxic gait, and the patient was unable to arise from a sitting position. Laboratory data revealed hypercalcemia of 12.1 mg/dL and an elevated Cr of 1.8 mg/dL. An ACE level was elevated, at 206 U/L. Hematologic profile revealed anemia (hemoglobin 8.5 g/dL) and thrombocytopenia as low as 52,000 along with a low fibri‐nogen and elevated D‐dimer, suggesting disseminated intra‐vascular coagulation. A mediastinal lymph node biopsy revealed noncaseating granulomas, and repeat BMBx confirmed the absence of AFB. A QuantiFERON assay was negative, and the patient was noted to be anergic. High‐dose steroids were initiated with improvement in hypercalcemia and constitutional symptoms.
An association between mycobacterial infection and sarcoidosis has long been implicated because of overlapping pathologic manifestations. With the advent of molecular techniques, mycobacterial DNA have been detected by polymerase chain reaction in granulomatous tissues, but the organisms have never been seen or cultured. In this patient, we report the identification of AFB in the BM; however, mycobacteria could not be cultured. Empiric therapy for tuberculosis was initiated but did not lead to a resolution of symptoms; instead, it delayed the diagnosis and treatment of sarcoidosis. In addition, concerns over possible reactivation of mycobacterial infection necessitated additional testing before steroid therapy could be started. Indeed, identification of AFB created a therapeutic dilemma, but this case illustrates that antituberculous therapy has a limited role in the management of patients with sarcoidosis.
A causal link between mycobacterial infection and sarcoidosis has been implicated in the literature, but our experience suggests that treatment with antituberculous therapy does not alter the natural history of sarcoidosis, but delays the diagnosis and treatment.
J. Powell ‐ none; E. Esquivel ‐ none
To cite this abstract:Powell J, Esquivel E. In a Case of Sarcoidosis: Are Mycobacteria Innocent or Guilty As Charged?. Abstract published at Hospital Medicine 2011, May 10-13, Dallas, Texas. Abstract 373. Journal of Hospital Medicine. 2011; 6 (suppl 2). https://www.shmabstracts.com/abstract/in-a-case-of-sarcoidosis-are-mycobacteria-innocent-or-guilty-as-charged/. Accessed September 20, 2019.