Poncet’s disease is a reactive polyarthritis associated with active tuberculosis at another site, without evidence of direct joint invasion by Mycobacterium tuberculosis or another infectious or autoimmune cause. We report the case of a 23-year-old patient with a history of microcephaly, who for six months had joint pain, swelling, and erythema, hand deformities, and weight loss. History-taking was limited by the patient’s baseline condition. There were no reported respiratory or gastrointestinal symptoms, fever, or contact with TB cases. On examination, the patient had low weight (33 kg), clawed fingers, hyperemia, swelling, warmth, and stiffness in metacarpophalangeal and proximal interphalangeal joints. Laboratory data included anemia, negative immunologic markers (rheumatoid factor, anti-CCP, and ANA), and non-reactive rapid tests for HIV, syphilis, and hepatitis. Chest CT showed micronodular opacities and bronchiectasis, while abdominal imaging showed thickening of the cecum and distal ileum wall and enlarged, heterogeneous adjacent lymph nodes. After excluding other etiologies and due to difficulty performing colonoscopy, empirical treatment for intestinal TB was initiated. Progressive clinical improvement followed, including reduced pain and stiffness, regression of inflammatory signs, and weight gain. Follow-up imaging showed resolution of ileocecal changes and supported the diagnosis of Poncet’s disease. This rare, primarily clinical diagnosis is characterized by a symmetric, non-destructive polyarthritis that improves with anti-TB therapy and should be suspected in arthritis cases in endemic regions after ruling out common causes. It most often affects individuals aged 20–40 years, with a female predominance, matching the patient’s profile. Although more commonly associated with pulmonary TB, coexistence with extrapulmonary forms can occur and is even rarer. The likely mechanism involves a systemic immune response with activation of sensitized CD4+ cells and migration of bacterial antigens to the joints. It should be differentiated from tuberculous arthritis, which occurs through hematogenous dissemination of mycobacteria to synovial tissue. Early recognition is essential to avoid therapeutic delay and reduce associated morbidity.
Miranda et al. (Sun,) studied this question.