CASE BASED REVIEW Exacerbation of latent lupus: is the culprit acid-fast bacilli or antitubercular therapy? Harpreet Singh & Sucharita Ray & Maneet Kaur & Vikas Gupta & Harish Kumar & Paulomi Talapatra & Rekha Mathur & Suvrat Arya & Naveen Ghangas Received: 24 January 2013 / Revised: 10 March 2013 / Accepted: 27 March 2013 / Published online: 10 April 2013 # Clinical Rheumatology 2013 Abstract Typical as well as atypical presentations of systemic lupus erythematosus are being increasingly recognized due to improved diagnostic methods. In a tuberculosis-endemic coun- try like India, it was traditionally believed that the occurrence of tuberculosis in lupus was due to the chronic immunosup- pression caused by lupus or because of the use of steroids or isoniazid-induced lupus. Increasingly several patients with no recorded predisposition to lupus with a history of treatment for tuberculosis are coming with evidence of systemic lupus erythematosus rather than a drug-limited story. Whether the development of an autoimmune state is a mere conjecture or the presence of acid-fast bacilli in the body for a prolonged duration causes complex antigenic interactions leading to an antigenic response needs to be looked into. We present a report of three such patients and review the pathogenetic interactions that could possibly explain the role of mycobacterial antigens as a putative antigen in the pathogenesis of lupus. Keywords Epitope spreading . Latent lupus . Lupus . Pathogenesis . Tuberculosis Introduction With increasing population, attendant overcrowded condi- tions, and exposure to newer antigens, pesticides, and diseases, systemic lupus erythematosus, once considered a rare disease, not only is being increasingly diagnosed but is showing several atypical presentations and interactions. Tuberculosis is endem- ic in the country with significant morbidity and mortality rates, and it is not surprising to assume that the two share several complex and hitherto undiscovered interactions, given the propensity for each to lead to a state of profound immunosup- pression in the patient. Several reports of active tuberculosis in SLE and the preponderance of miliary and far-advanced pulmonary tuberculosis as well as a higher incidence of extrapulmonary tuberculosis have been reported in the litera- ture. One of the traits of tuberculosis is to establish a prolonged state of latent disease in an immunocompromised patient like lupus. Several authorities have even suggested that routine isoniazid prophylaxis in patients with SLE with a positive Mantoux reaction, the combined hepatotoxicity of drugs, nonadherence to chemoprophylaxis, propensity for causing lupus flare, and other less validated concerns have prevented routine usage of isoniazid in chemoprophylaxis of lupus [1]. Lupus alone, with the use of cyclophosphamide and corti- costeroids, has been implicated in the immunosuppressed state that acts to establish a latent infection of tuberculosis in the patient [3–5]. However, even without lupus or these agents, tuberculosis exists in a high percentage in normal H. Singh : V. Gupta : R. Mathur : S. Arya : N. Ghangas Department of Medicine, Pt. B. D Sharma PGIMS, Rohtak, Haryana, India e-mail: drhps1@rediffmail.com S. Ray (*) Department of Neurology, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India e-mail: dr.sucharitaray@gmail.com M. Kaur Department of Medicine, Dayanand Medical College & Hospital, Ludhiana, Punjab, India H. Kumar Department of Pulmonary Medicine and Critical Care, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India P. Talapatra Department of Rheumatology, Pt. B. D. Sharma PGIMS, Rohtak, Haryana, India Clin Rheumatol (2013) 32:1233–1236 DOI 10.1007/s10067-013-2250-2