Visceral leishmaniasis mimicking systemic lupus erythematosus: Case series and a systematic literature review.

OBJECTIVE: Systemic lupus erythematosus (SLE) is an autoimmune disease that may present manifestations that resemble other diseases. Visceral leishmaniasis (VL) is a parasitic infection whose hallmarks may mimic SLE symptoms. Here, we report a case series and evaluate the published, scientific evidence of the relationship between SLE and VL infection. METHODS: To assess original studies reporting cases of VL-infected patients presenting manifestations that are capable of leading to inappropriate suspicions of SLE or mimicking an SLE flare, we performed an extensive search in several scientific databases (MEDLINE, LILACS, SciELO, and Scopus). Two authors independently screened all citations and abstracts identified by the search strategy to identify eligible studies. Secondary references were additionally obtained from the selected articles. RESULTS: The literature search identified 53 eligible studies, but only 17 articles met our criteria. Among these, 10 lupus patients with VL mimicking an SLE flare and 18 cases of VL leading to unappropriated suspicions of SLE were described. The most common manifestations in patients infected with VL were intermittent fever, pancytopenia, visceromegaly, and increased serum level of acute phase reactants. The most frequent autoantibodies were antinuclear antibodies, rheumatoid factor, and direct Coombs' test. CONCLUSION: In endemic areas for VL, the diagnosis of SLE or its exacerbation may be a clinical dilemma. Hepatosplenomegaly or isolated splenomegaly was identified in the majority of the reported cases where VL occurred, leading to unappropriated suspicions of SLE or mimicking an SLE flare. Furthermore, the lack of response to steroids, the normal levels of complement proteins C3 and C4, and the increased level of transaminases suggest a possible infectious origin.

A longterm prospective real-life experience with leflunomide in juvenile idiopathic arthritis.

OBJECTIVE: To describe a clinical practice with leflunomide (LEF) in juvenile idiopathic arthritis (JIA). METHODS: Patients with JIA seen between May 2008 and May 2012 and considered nonresponsive to methotrexate (MTX) were given LEF and prospectively followed. Primary outcome was a 28-joint Disease Activity Score (DAS28) of low disease activity (< 3.2) in less than 6 months. Childhood Health Assessment Questionnaire (CHAQ) scores and safety data were recorded. RESULTS: Forty-three patients (33 female) were included with 25 (58.1%) polyarticular, 10 oligoarticular (7 extended; 3 persistent), 6 systemic, and 2 enthesitis-related. Ten (23.2%) were rheumatoid factor-positive and 7 (16.3%) had antinuclear antibodies. Prior drugs other than MTX: 11 (25.5%) chloroquine diphosphate + MTX and 2 (4.6%) sulfasalazine + MTX; mean prednisone dose was 6.4 ± 9.3 mg. The MTX dose prior to LEF was 14.5 ± 4.5 mg/m(2)/week. LEF dose and duration of therapy were 16.6 ± 5.2 mg/d and 3.6 ± 2.2 years, respectively. Nineteen patients (44.2%) interrupted LEF: 1 entered remission, 11 were nonresponsive, and 7 were intolerant (16.2%). Baseline DAS28 (5.57 ± 0.7) dropped to 3.7 ± 1.2 at final analysis (p < 0.001) and 16 patients (37.2%) had a low DAS28 [< 3.2; 12 (27.9%) while taking LEF + MTX and 4 (9.3%) while taking monotherapy]. At last followup, the number of patients with DAS28 > 5.1 dropped from 34 (79%) to 9 (20.9%) and CHAQ scores from 0.86 ± 0.7 to 0.44 ± 0.5 (p < 0.001). CONCLUSION: LEF isolated or combined with MTX is effective and safe to treat JIA in patients refractory to MTX.

Reversible heart failure in a patient receiving etanercept for ankylosing spondylitis.

A 42-year-old man with ankylosing spondylitis that was refractory to nonsteroidal anti-inflammatory drugs as well as various disease-modifying antirheumatic drugs was subjected to anti-TNF compounds. Administration of infliximab and adalimumab gave excellent clinical response but was discontinued due to adverse events. Introduction of etanercept was also clinically effective but followed by development of severe heart failure. Discontinuation of etanercept led to control of heart function. The unusually though potentially life-threatening possibility of heart failure secondary to anti-TNF use in ankylosing spondylitis merits attention.

Combined glucosamine and chondroitin sulfate provides functional and structural benefit in the anterior cruciate ligament transection model.

Evidence that combined glucosamine sulfate and chondroitin sulfate (Gluchon) or isolated glucosamine (Glu) modifies joint damage in osteoarthritis (OA) is still lacking. We studied joint pain and cartilage damage using the anterior cruciate ligament transection (ACLT) model. Wistar rats were subjected to ACLT of the right knee (OA) or sham operation. Groups received either Glu (500 mg/kg), Gluchon (500 mg/kg glucosamine +400 mg/kg chondroitin) or vehicle (non-treated--NT) per os starting 7 days prior to ACLT until sacrifice at 70 days. Joint pain was evaluated daily using the rat-knee joint articular incapacitation test. Structural joint damage was assessed using histology and biochemistry as the chondroitin sulfate (CS) content of cartilage by densitometry (microgram per milligram dried cartilage), comparing to standard CS. The molar weight (Mw) of the CS samples, used as a qualitative biochemical parameter, was obtained by comparing their relative mobility on a polyacrylamide gel electrophoresis to standard CS. Gluchon, but not Glu, significantly reduced joint pain (P < 0.05) compared to NT. There was an increase in CS content in the OA group (77.7 +/- 8.3 microg/mg) compared to sham (53.5 +/- 11.2 microg/mg) (P < 0.05). The CS from OA samples had higher Mw (4:62 +/- 10(4) g/mol) compared to sham (4:18 +/- 0.19 x 10(4) g/mol) (P < 0.05). Gluchon administration significantly reversed both the increases in CS content (54.4 +/- 12.1 microg/mg) and Mw (4:18 +/- 0.2 x 10(4) g/mol) as compared to NT. Isolated Glu decreased CS content though not reaching statistical significance. Cartilage histology alterations were also significantly prevented by Gluchon administration. Gluchon provides clinical (analgesia) and structural benefits in the ACLT model. This is the first demonstration that biochemical alterations occurring in parallel to histological damage in OA are prevented by Gluchon administration.

[Zymosan induced arthritis in rats--mechanisms involved in hypernociception and cartilage lyses]. / Artrite induzida por zymosan em ratos--mecanismos envolvidos na hipernocicepçao e na lise da cartilagem articular.

The authors present the experience of the group in the study of the mechanisms of hypernociception (pain) and articular cartilage lesion in the zymosan-induced arthritis model in rats.