A 29-year-old man presented to the hospital with fever and night sweats for 30 days. The patient recently underwent videolaparoscopic cholecystectomy (hospital stay: September 10-11, 2019). In October 2019, a platelet count of 20,000/microL was the only blood count abnormality. Chest tomography revealed mediastinal adenomegaly, with some lymph nodes forming 2.9 x 2.5 cm clusters in the aorta and alveolar consolidation in the left upper lung lobe (Figure 1). Serology for hepatitis B, hepatitis C, and HIV was negative. 
Bronchoscopy with bronchoalveolar lavage yielded negative results for acid-fast bacilli and fungal and bacterial pathogens. The culture for M. tuberculosis was negative. Rapid molecular detection tests were not conducted. A liquid biopsy of the lavage fluid could not be performed; therefore, an open biopsy was conducted with resection of the para-aortic lymph node and adjacent pulmonary segmentectomy. 
Since platelet count fell further to 4,000/microL and was associated with disseminated ecchymoses and petechiae, intravenous immunoglobulin was initiated at a dose of 0.4 g/kg/day for 5 days, together with 1 mg/kg methylprednisolone. 
The biopsy of the para-aortic lymph node showed foci of caseous necrosis associated with lymphocytic inflammatory infiltrates (Figure 2A). Tests for fungi (periodic acid-Schiff and Grocott methenamine-silver staining) yielded negative results. Neoplasia was not observed. A left upper lobe lung biopsy showed caseous necrosis, adjacent epithelioid histiocytes, organized alveolar pneumonia, alveolar septal or interstitial fibrosis, centriacinar emphysema, and alveolar exudate macrophages (Figure 2B). The specimen was negative for fungi and positive for acid-fast bacilli, and polymerase chain reaction (PCR)-positive for M. tuberculosis. No neoplasia was found. The final histopathological diagnosis was tuberculosis. The clinical and laboratory data suggested a case of ITP triggered by tuberculosis.
Myelography showed hypercellular bone marrow with erythroid and megakaryocytic hyperplasia, preserved cell maturation, and no anomalous cells. Since other causes of thrombocytopenia had been ruled out, and the platelet count response was satisfactory and progressively increased, reaching 120,000/microL in the first 15 days of treatment, ITP was diagnosed.
The patient was discharged in November 2019, and treatment for tuberculosis was initiated with a rifampicin/isoniazid/pyrazinamide/ethambutol (RIPE) regimen. Corticosteroids were simultaneously tapered off, and 50 mg/day of the immunosuppressant azathioprine was introduced because of fluctuations in platelet count while the corticosteroids were being tapered off. During that period, the patient became asymptomatic with no bleeding and platelet count >100,000/mul. In February 2020, three months after discontinuing corticosteroid use, the patient presented with bleeding gums and platelet count of 10,000/mul. The patient was then readmitted to the hospital. Prednisone at 80 mg/day and azathioprine at 100 mg/day were administered. RIPE was maintained, with platelet count >150,000/mul and mucosal and skin bleeding resolving in March.
At the end of March 2020, the patient was discharged for the second time, and weekly tapering of corticosteroids was initiated again. Azathioprine was reduced to 50 mg/day, platelet count was 150,000/microL and there was no bleeding. Outpatient tuberculosis treatment ended in May 2020, with no more reported bleeding and platelet counts being consistently normal in June (218,000/microL) and September 2020 (219,000/microL). By then both corticosteroids and azathioprine had been discontinued (Figure 3).