Visceral Leishmaniasis or Systemic Lupus Erythematosus Flare?

Systemic lupus erythematosus (SLE) is a multisystem disorder characterised by B-cell hyperactivity with production of multiple autoantibodies. Fever in SLE may be caused by disease exacerbation or by infection. We report a patient of SLE that was later complicated by fever, pancytopenia, and massive splenomegaly. Corticosteroid therapy for SLE might have masked the underlying infection at earlier stage. Despite negative results of rk-39 test and bone marrow biopsy, a very high suspicion for visceral leishmaniasis (VL) led us to go for direct agglutination test (DAT) and polymerase chain reaction (PCR) for leishmanial antigen that revealed positive results. Moreover, significant improvement in clinical and biochemical parameters was noted on starting the patient on antileishmanial therapy. 1. Introduction Systemic lupus erythematosus (SLE) is a chronic autoimmune disease of unknown aetiology, characterised by B cell hyperactivity and production of multiple autoantibodies. Haematological abnormalities of SLE include haemolytic anemia, leucopenia or lymphopenia, and thrombocytopenia, due to the production of autoantibodies [1]. Splenomegaly is not a common sign of SLE, unless there is concurrent infection. On the other hand, visceral leishmaniasis is a chronic parasitic infection caused by Leishmania donovani. There is B cell hyperactivity, resulting in production of autoantibodies such as ANA and others [2]. It is characterised by fever, cytopenias, and splenomegaly. Splenomegaly and hypersplenism are mainly responsible for cytopenias. Immunocompromised patients due to acquired immunodeficiency syndrome, after kidney-transplantation or leukemia are more commonly affected [3]. We report a case of SLE complicated by visceral leishmaniasis, with sharp clinical resemblance to a flare of SLE. A high suspicion for kala azar should always be kept when a patient comes from an endemic area of the disease with fever and splenomegaly, especially when superimposed on a background of an immunocompromised state. 2. Case Report A 30-years-old female presented with complaints of low grade fever, multiple painful small joints with periorbital puffiness and bilateral pedal swelling for one month. She had history of distal phalangeal amputation 1 year back for bilateral upper limb digital infarcts. General examination revealed pallor and bilateral pitting pedal oedema. Palpable spleen 2？cm below subcostal margin was the only significant systemic finding. Haematological investigations revealed haemoglobin 2.56？mmol/L, total leukocyte count 3.4 × 109/L, platelets 59 × 109/L