A CASE OF HENOCH-SCHONLEIN PURPURA ASSOCIATED WITH TUBERCULOUS PLEURISY

Abstract

SESSION TITLE: Fellows Chest Infections Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: October 18-21, 2020 INTRODUCTION: Herein we describe a case of Henoch-Schönlein purpura (HSP) associated with tuberculous pleurisy. Complications of these two conditions are extremely rare [1,2]. It has been thought that HSP may be triggered by tuberculosis or by antituberculous treatment. This case highlights the importance of recognizing that HSP can occur during antituberculous treatment. CASE PRESENTATION: An 86-year-old male visited the previous hospital for dyspnea on exertion and fever for 5 days. Chest X-ray revealed left-sided pleural effusion, and he was referred to our department. Chest CT revealed left-sided pleural effusion and calcified nodule in the superior segment of the left lung. Thoracentesis revealed exudative pleural effusion with lymphocyte fraction of 75%. Pleural fluid ADA level was 121.4 IU/L and T-spot TB test was positive. The patient was clinically diagnosed with tuberculous pleurisy because he refused pleural biopsy. Antituberculous treatment with ethambutol /isoniazid/rifampicin was started. 17 days after the initiation of the treatment, systemic eczema and blurred eyes developed, and all drugs were discontinued. These symptoms gradually improved, but palpable purpura appeared in both lower limbs. HSP was suspected and skin and renal biopsy was performed. Pathological examination of the skin revealed leukocytoclastic vasculitis of small vessels without IgA deposition. Pathological examination of the kidney revealed diffuse proliferation of mesangial cells and matrix, endocapillary proliferation, segmental necrotizing lesions, and cellular crescents. Moreover, IgA deposition in mesangium was observed. From these findings, the patient was diagnosed with HSP, and systemic steroid therapy was started. After the steroid treatment, purpura disappeared and urinary protein decreased, so antituberculous drugs were restarted from a small dose. Since then, the dosage of antituberculous drugs has been gradually increased, and treatment can be continued even now. DISCUSSION: HSP is a leukocytoclastic vasculitis that usually affects children. Some precipitating factors have been reported as follows: infections, drugs, malignancy, environmental chemicals, insect bites, trauma, and complement C2 deficiency [1]. HSP is considered as an IgA-mediated immune vasculitis, and palpable purpura is regarded as essential for diagnosis. HSP is rare in adults, but more severe [2]. To the best of our knowledge, there have been 13 cases of HSP associated with tuberculosis [3]. It has been reported that not only tuberculosis but also antituberculosis drugs can cause HSP. In our patient, symptoms of HSP occurred after the initiation of antitubeculous treatment and improved with discontinuation of the drugs and addition of steroids. Therefore, we suspected that HSP was triggered by antituberculous drugs. CONCLUSIONS: This case highlights the importance of recognizing that HSP can occur during antituberculous treatment. Reference #1: 1.Catherine PM, Hayward. Clinical approach to patient with bleeding and bruising. In: Hoffman R, Furie B, McGlave P, Silberstein LE, Shattil SJ, Benz EJ, Heslop H. Hematology basic principles and practice. Philadelphia: Elsevier Saunders publications; 2013. p 1847-56. Reference #2: 2.Laxer RM, Benseler SM. Pediatric Systemic Lupus Erythematosus, Dermatomyositis, Scleroderma, and Vasculitis. In: Firestein GS, Budd RC, Harris ED, McInnes IB, Ruddy S, Sergent JS. Kelley's Textbook of Rheumatology; 9th Ed; vol II. Philadelphia: W.B. Saunders Co, 2000: pp 1171-800. Reference #3: 3.Seth G, Rohatgi A, and Kumar G. Henoch-Schonlein Purpura: An unusual presentation of Disseminated Tuberculosis. Indian Journal of Basic and Applied Medical Research; September 2015: 4; 476-481. DISCLOSURES: No relevant relationships by Yuri Hiramatsu, source=Web Response No relevant relationships by Kazunori Tobino, source=Web Response