Leishmaniasis and autoimmune diseases in pediatric age.

Leishmaniasis is a group of diseases caused by the protozoa Leishmania, endemic in the Mediterranean countries. Clinical manifestations can be divided into three different forms: cutaneous leishmaniasis, mucosal leishmaniasis and the visceral leishmaniasis, the most severe form which is potentially lethal if untreated. Immunology and pathogenesis are complex: many different aspects of immune response, resistance and susceptibility to Leishmania have been studied but many others remain to be clarified. The gold standard in diagnosis of visceral Leishmaniasis is the presence of amastigotes in bone marrow or tissue sections. Patients can be initially misdiagnosed as having an autoimmune disease because it may mimic diseases like systemic lupus erythematosus, autoimmune hepatitis, dermatomyositis or others disorders. As in pediatric age the risk of life-threatening complications is very high, leishmaniasis, must be kept in mind to the clinician, in order to avoid wrong diagnosis and an inappropriate immunosuppressive therapy.

Relationship between inflammatory markers, oxidant-antioxidant status and intima-media thickness in prepubertal children with juvenile idiopathic arthritis.

OBJECTIVE: To investigate the presence of possible early atherosclerotic changes in a group of prepubertal children with juvenile idiopathic arthritis (JIA) and to establish the potential beneficial effects of 1-year treatment. MATERIALS AND METHODS: Inflammatory markers (C-reactive protein, erythrocyte sedimentation rate), proinflammatory cytokines (IL-1ß, IL-6, IFN-γ, TNF-α), lipid profile and oxidant-antioxidant status (urinary isoprostanes [PGF-2α]) were assessed in 38 JIA children (12M/26F, mean age 7.05 ± 2.39 years) and compared with 40 controls (18M/22F, mean age 6.34 ± 2.25 years). Carotid intima-media wall thickness (cIMT) was obtained and blood pressure was measured. All parameters were reassessed in JIA children after 1 year of therapy. RESULTS: At baseline JIA children presented compared to controls higher levels of inflammatory markers, proinflammatory cytokines, total cholesterol, LDL cholesterol, and PGF-2α (all p ≤ 0.01). Furthermore, blood pressure and cIMT were significantly increased (both p ≤ 0.01). After a 1-year treatment with non-steroid anti-inflammatory (NSAIDs) and disease-modifying antirheumatic drugs (DMARDs), a significant reduction of all parameters was detected (all p ≤ 0.01). This was associated with a significant reduction in blood pressure and cIMT (both p ≤ 0.01). Within the JIA group, patients requiring etanercept presented worse laboratory values and cIMT measurements at baseline. Nevertheless, the same improvement of all parameters was obtained after a 1-year treatment. In stepwise multiple regression, LDL cholesterol and IL-1ß were mainly related to cIMT. CONCLUSION: Chronic and systemic inflammation seems to lead to early atherosclerotic abnormalities even in pre-pubertal JIA children. Substantial improvement can be obtained with 1-year of appropriate therapy.