Leishmania in SLE mimicking an exacerbation

Systemic lupus erythematosus is a protean disease which may present manifestations that resemble other diseases posing serious problems of differential diagnosis. Visceral leishmaniasis is a parasitic infection, endemic in 88 countries, whose hallmarks may mimic a lupus flare. Fever pancytopenia, splenomegaly, hypergammaglobulinemia, production of autoantibodies and complement consumption are some of the overlapping features between the two diseases. Thus, extra attention must be paid to patients with lupus who present with the mentioned symptoms. Diagnosis of visceral leishmaniasis relies on the detection of leishmania antibodies, on the presence of amastigotes in bone marrow aspirates, biopsies and cultures of the parasite. Treatment is based on the use of i.v. liposomal amphotericin B. The missed recognition of a leishmania infection in a lupus patient may lead to death, since both the omission of a specific anti-parasite treatment and the increase of the immunosuppressive therapy, in the conviction of a lupus flare, accelerate a fatal outcome. In this paper we present a case of visceral leishmaniasis occurring in a lupus patient. The clinical and laboratory features that overlap in the two diseases and the current literature on the topic were discussed

Advances in immunology and rheumatoid arthritis pathogenesis

The pathogenesis of Rheumatoid Arthritis (RA) is still largely unknown. From the seminal experimental studies, suggesting a multifactorial mechanism leaded by an antigen specific activation, the direct role of innate immunity in the disease progression has been recently emphasized. In the natural history of RA, characterized by the three phases of the induction, maintenance and tissue destruction, innate immunity seems to be the central player. On the other hands the recent advances about the molecules involved in the T lymphocyte activation, the T cell role in the mechanism of erosion, and the studies about chemokines in the homing and angiogenesis processes support the theory of an antigen specific activation of the adaptive immune system. Therefore, during RA, the pathogenesis of sinovitis and erosions comes from independent pathways involving either innate and adaptive immunity resulting in the final induction of the articular damage

NK cell count as predictor of clinical response in patients with rheumatoid arthritis treated with rituximab [Corrigendum]

 Lurati A, Bertani L, Marrazza M, Re KA, Bompane D, Scarpellini M. Biologics: Targets and Therapy. 2012;6:83–87.On page 87, the disclosure was listed as ‘The authors report no conflicts of interest in this work.’ in error. The correct disclosure should be ‘An unrestricted publication grant was provided by Roche S.p.A. The authors have no other conflicts of interest to report.’Read the original articl