Antimalarials are widely used for the treatment of systemic lupus erythematosus. However, their mechanisms of action have not been fully elucidated. Literature data indicate that matrix metalloproteinases may play a role in the immune response and tissue damage that occur in autoimmune skin diseases. The aim of this study was to determine the effect of 3 months of chloroquine treatment on serum levels of MMP-9 and TIMP-1 in patients with systemic lupus erythematosus. The study group consisted of 25 patients with systemic lupus erythematosus and 25 sex- and age-matched healthy volunteers. Before drug administration, serum levels of MMP-9 and TIMP-1 were determined by enzyme-linked immunosorbent assay. The same procedure was performed after chloroquine treatment. We found significantly higher median serum levels of MMP-9 in patients with systemic lupus erythematosus before therapy (57.20 ng/ml) when compared with controls (44.50 ng/ml) (p < 0.001). After chloroquine therapy the median MMP-9 serum level of systemic lupus erythematosus patients decreased significantly (43 ng/ml; p < 0.001). Before treatment the median TIMP-1 serum level in the patients with systemic lupus erythematosus was significantly higher than in the control group (500 vs. 200 ng/ml; p < 0.001), and after therapy it increased significantly (750 ng/ml TIMP-1; p < 0.001). The results suggest that chloroquine treatment may affect the matrix metalloproteinase network, and this effect may contribute to the immunoregulatory and anti-inflammatory properties of antimalarials.

Endothelial function impairment may constitute a link between nephrotic syndrome and atherosclerosis. We assessed changes in plasma thrombomodulin, von Willebrand factor and plasminogen activator inhibitor-1 at different stages of idiopathic nephrotic syndrome in children and correlated them with clinical and biochemical parameters. The study group included 132 nephrotic children (aged 2–18 years) divided into four groups, i.e. in acute phase of the disease with proteinuria, during steroid-induced remission, steroid-free remission, and in long-term, steroid-free remission. Forty-one healthy children served as controls. Plasma thrombomodulin, plasminogen activator inhibitor-1 and von Willebrand factor activity were increased in children with early nephrotic relapse. They systematically decreased in later stages of the disease but the increase in von Willebrand factor persisted in drug-free remission. These disturbances were dependent on the degree of proteinuria and serum albumin concentration. The study revealed that nephrotic children show markers of endothelial dysfunction that are dependent on the disease activity. This leads to the hypothesis that children with severe clinical course of nephrotic syndrome may be at high risk of accelerated atherogenesis.

As most studies on pemphigus vulgaris (PV) pathogenesis concern its active stage, we aimed to evaluate the serum concentration of TNF-α, IL-1, and IL-6 in PV patients in clinical remission. The study group consisted of sera from 19 PV patients in active stage and from 24 patients in clinical remission. 19 sera taken from healthy subjects served as the controls. Serum IL-6 concentrations in PV active and PV remission group were significantly higher when compared to the controls (P < .05). In patients in active stage of PV, a significant correlation between serum IL-1 and IL-6 concentrations was found (r P = 0.46; P < .05). We also found a negative correlation between TNF-α level and pemphigus antibodies titer in the patients from the remission group (r S = −0.47303; P < .02). Our data suggest that IL-6 and TNF-α may be involved in maintaining immunological disturbances in remission stage of PV.

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The aim of this study was to evaluate changes in urine and plasma concentrations of cystatin C in children with a relapse of the idiopathic nephrotic syndrome(INS). The study group comprised 12 children with INS with proteinuria and 12 children in an 8-week remission,both treated with steroids. Twelve healthy children served as controls. Cystatin C was detectable in the urine of children with proteinuria. The study suggests that massive proteinuria may influence renal cystatin C handling.