ReviewMedicine2026
Coexistence of papulonecrotic tuberculid and Poncet's disease: A case report of dual tuberculin hypersensitivity reactions and literature review.
Review in Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
rationalePapulonecrotic tuberculid (PNT) and Poncet's disease (PD) are rare, immune-mediated reactions to Mycobacterium tuberculosis (MTB) that occur without direct bacterial isolation. The concurrent manifestation of both conditions in a single individual is exceptionally rare, with only limited cases documented in the literature. This report documents a singular case of concurrent PNT and PD, illustrating multisystem delayed-type hypersensitivity as an exceptional manifestation of MTB. PATIENT CONCERNS: A 30-year-old male presented with a 3-year history of recurrent, symmetrical necrotic papules on the extremities and trunk, evolving through sequential stages from papule to central necrosis, crusting, and varioliform scarring. He also reported episodes of inflammatory polyarthritis involving the knees, elbows, wrists, and metacarpophalangeal joints. He had sustained household contact with a grandmother diagnosed with pulmonary tuberculosis. DIAGNOSES: Laboratory testing revealed elevated total immunoglobulin E (>2000 IU/mL), an increased erythrocyte sedimentation rate (ESR = 31 mm/h), and elevated C-reactive protein (CRP = 29 mg/L). Tuberculin skin testing was positive (13 mm × 13 mm), and interferon-gamma release assay was positive. Skin biopsy revealed leukocytoclastic vasculitis, epithelioid necrotizing granulomas, and multinucleated giant cells. He was diagnosed with PNT and PD as hypersensitivity reactions to latent MTB infection.
interventionsStandard antitubercular therapy (isoniazid, rifampicin, and ethambutol) was administered. OUTCOMES: Complete resolution of cutaneous and articular symptoms was achieved within the 6-month follow-up period. LESSONS: Concurrent PNT and PD underscore the potential of MTB to trigger synchronous multisystem immune reactions. The observed elevated immunoglobulin E levels suggest a possible T helper 2-skewed immunologic background, broadening the understanding of tuberculous hypersensitivity syndromes. In tuberculosis-endemic areas, clinicians should maintain a high index of suspicion for such atypical presentations to avoid diagnostic delays and prevent chronicity. Anti-MTB therapy remains the definitive and effective treatment for these immune-mediated phenotypes.
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