Severe Thrombocytosis in a Patient with Pulmonary Tuberculosis: A Case Report
Keywords:
Thrombocytosis, Tuberculosis, Pulmonary, Platelet, ImmunologyAbstract
Platelets are key players in the immunopathology of pulmonary tuberculosis (TB), and thrombocytosis is a rare complication of the disease. Thrombocytosis is defined as platelet counts exceeding 450 x 109/L. In TB, thrombocytosis is associated with other hematological changes and an increased risk of venous thromboembolism (VTE). An 80-year-old Chinese gentleman presented with a chronic cough for 2 weeks, without fever, weight loss, night sweats, family history of blood dyscrasia, or prior thrombotic events. Full blood count (FBC) showed leukocytosis with high white blood cells (WBC) (22.63 x 103/uL), neutrophils (19.49 x 103/uL), and platelets (1808 x 109/L). Peripheral blood film (PBF) showed leukocytosis with neutrophilia, monocytosis, and basophilia. Red blood cells (RBC) showed microcytic hypochromic anemia, and platelets were grossly increased with circulating megakaryocyte fragments. Essential thrombocytosis was suspected based on persistent thrombocytosis (normal range 150–450 x 109/L) for 1 week during admission; however, JAK2 mutation analysis was negative. Suspicion of pulmonary TB due to cough was confirmed via Gene-Xpert MTB/RIF sputum test (PCR). Subsequently, anti-tuberculosis therapy was initiated, and the patient responded well. The patient’s platelet count was monitored, but the patient was not on any VTE prophylaxis. Platelets may directly sense Mycobacterium tuberculosis (M. tuberculosis). As a rapid innate immune response, platelets become activated and granulated, releasing pro-inflammatory cytokines. Platelets then undergo structural changes and upregulate platelet-activated gene transcripts. Tissue damage in TB results from platelet interactions with other leukocytes, which produce matrix metalloproteinases (MMPs) and cytokines such as Interleukin-10 (IL-10) that inhibit the host immune response. Conclusion: There should be a high index of suspicion for TB infection in patients presenting with respiratory symptoms and severe thrombocytosis, especially in older patients. Antiplatelet therapy may be considered alongside the standard antitubercular drug regimen as a potential host-directed therapy to improve outcomes and prevent VTE complications in patients with pulmonary TB and severe thrombocytosis.
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