SAT0474 AUTOIMMUNE MANIFESTATIONS OF VISCERAL LEISHMANIASIS IN CHINESE PATIENTS
Authors: Xixi Chen, Qiao Zhou, Rui Wu, Jia Cheng, Jian Liu, Bin Zhou, LI Long
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Background</h3> Visceral leishmaniasis (VL), caused by the protozoan Leishmania species, is the most severe form of leishmaniasis. The parasite migrates to the internal organs such as the liver, spleen, and bone marrow, and if left untreated, will almost always cause the host to die [1]. Due to polyclonal B cells activation, VL may present signs and symptoms resembling those of rheumatic diseases, especially systemic lupus erythematosus (SLE) [2-4]. This can sometimes lead to mis-diagnosis and treatment of corticosteroids. <h3>Objectives</h3> To analyze 27 Chinese VL patients retrospectively and focused on their autoimmune findings that could help clinicians to differentiate VL from SLE. <h3>Methods</h3> 27 in-hospitalized VL patients in our hospital from 2006 to 2015 were analyzed. VL was diagnosed by the presence of high titers of anti-leishmania antibodies in the blood or by demonstration of intracellular parasites on bone marrow aspiration. All patients were negative for hepatitis B, hepatitis C and human immunodeficiency viruses. Autoimmune antibodies were detected. Levels of serum globulins, complement C3, C4 and RF were evaluated. Coagulation parameters, including prothrombin time (PT) and activated partial thromboplastin time (APTT) were also tested. <h3>Results</h3> The basic characteristics and laboratory findings of the 27 patients were summarized in Table 1. All patients had hepatosplenomegaly. 38.9% had positive ANA, but the titer was no more than 1:320. None of the patients had positive anti-Sm antibody and only 1 had anti-dsDNA antibody. 89.5% had increased IgG level and none had decreased C3 or C4. All patients were cured with sodium stibogluconate, and ANA titers decreased after treatment. <h3>Conclusion</h3> VL may mimic symptoms of SLE due to polyclonal activation of B cells. However, hepatosplenomegaly is a common symptom seen in VL but not so common in SLE. Furthermore, VL patients don't have typical autoantibodies of SLE, their ANA titer are normal to low and they tend to have normal complements, which could help clinicians to differentiate these two diseases. <h3>References</h3> [1] Martins-Melo FR, Lima Mda S, Ramos ANAN Jr., and, et al. Mortality and case fatality due to visceral leishmaniasis in Brazil: a nationwide analysis of epidemiology, trends and s patial patterns. PLoSOne. 2014; 9: e93770. [2] Ozlem Guzel Tunccan, Abdurrahman Tufan, Gülçin Telli, et al. Visceral Leishmaniasis Mimicking Autoimmune Hepatitis, Primary Biliary Cirrhosis, and Systemic Lupus Erythematosus Overlap. Korean J Parasitol. 2012; 50(2): 133–6 [3] Voulgarelis M, Voulgari PV, Serelis J, et al. Visceral leishmaniasis mimicking systemic lupus erythematosus. J Clin Rheumatol. 2010;16(4): 203-4. [4] Drosos AA, Skopouli FN. Visceral leishmaniasis resembling systemic lupus erythematosus. Clin Rheumatol. 2003; 22(6):452-5. <h3>Acknowledgement</h3> Thanks to my colleagues who help me in writing the paper and analyzing all the data. <h3>Disclosure of Interests</h3> None declared