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EN
With the increasing importance of early type 2 diabetes (DM2) and obesity detection, it is useful to reevaluate leptin role in these conditions. Our study aimed at investigating circulating leptin concentrations in a group of patients with DM2, and at assessing in detail whether leptin concentrations correlate with selected biochemical, clinical parameters and markers of systemic inflammation in patients with DM2 and in healthy volunteers. In our work, we analysed samples and data drawn from 71 patients aged 61.4 ± 11.7 years, who have been diagnosed with type 2 diabetes, as well as from a healthy control group (HC) consisting of 51 healthy subjects with a mean age of 57.8 ± 13.7 years. Therein, the concentration of leptin in the DM2 patients was significantly higher than in the HC (p < 0.01), with median value of 16.59 (IQR 8.58-33.39) ng/ml in the DM2, vs median value of 6.66 (IQR 4.52-21.40) ng/ml in the HC. In the analysis of variance, higher leptin concentrations were revealed in the DM2 group as compared to the HC, and this figure remained significant after adjusting for gender and age (p < 0.001). Moreover, it was independent of HOMA-IR (p = 0.003). However, the differences in leptin levels between the groups disappeared when additional adjustments for anthropometric parameters (BMI, waist circumference) were applied (p = 0.088). Beyond the aforementioned, significant positive correlations were found in the DM 2 group between leptin level and CRP (r=0.256; p < 0.05) and IL-6 (r = 0.345; p < 0.01). Among the selected variables, only gender and BMI were included in the predictive model explaining the variability of leptin, and, in total, were responsible for 72.6% of the original variation of the studied adipocytokine. The results of this study have led to conclusion that leptin may participate in the complex pathogenesis of DM2 and be a predictor of the development of this disease. As higher concentrations of leptin coexist with obesity, and this situation correlates positively with markers of inflammation (CRP, IL-6), leptin level, hence, should be considered in the pathogenesis of DM2.
EN
Osteoarthritis is the most common rheumatoid disease. It may develop as a primary disease of the motor organ or as a secondary one in the course of other inflammatory joint diseases. Similarly to the majority of rheumatoid conditions, the pathogenesis of osteoarthritis has not been fully explained. The fact that its development is determined by adipocytokines, which are inflammatory mediators produced in the adipose tissue, has been known for several years. Additionally, inflammatory processes taking place in the adipose tissue that lead to degenerative changes are the main subject of studies conducted by various immunological laboratories. Degenerative changes in patients with osteoarthritis are frequently accompanied by secondary inflammation with cellular infiltrations in the synovial membrane. In numerous cases, the intensification of inflammatory lesions resembles changes seen in arthritis, particularly in rheumatoid arthritis, which inhibits the differential diagnosis by means of imaging examinations. This may have significant clinical implications, e.g. with respect to sonography, which is the basic imaging examination in diagnosing rheumatoid arthritis, monitoring the efficacy of implemented treatment or confirming remission. This article discusses the pathogenesis of three elements of osteoarthritis, i.e. synovitis (due to the difficulties in differentiation of synovitis in the course of osteoarthritis and in rheumatoid arthritis) as well as osteophytes and subchondral sclerosis (due to the significance of the inflammatory factor in their development).
PL
Choroba zwyrodnieniowa stawów jest najczęstszą chorobą reumatyczną. Może się rozwijać jako pierwotne schorzenie narządu ruchu lub wtórnie w przebiegu innych zapalnych chorób stawów. Podobnie jak w przypadku większości chorób reumatycznych patogeneza choroby zwyrodnieniowej stawów nie została w pełni wyjaśniona. O tym, że istotną rolę w jej rozwoju odgrywają adipocytokiny, czyli mediatory zapalne produkowane w tkance tłuszczowej, wiadomo od kilku lat, a procesy zapalne zachodzące w tkance tłuszczowej, prowadzące do rozwoju zmian zwyrodnieniowych, są wiodącym tematem badań wielu laboratoriów immunologicznych. Zmianom degeneracyjnym u chorych na chorobę zwyrodnieniową często towarzyszy wtórny proces zapalny z obecnością nacieków komórkowych w błonie maziowej. W wielu przypadkach duże nasilenie zmian zapalnych jest podobne jak w innych jednostkach chorobowych, zwłaszcza w reumatoidalnym zapaleniu stawów, co utrudnia różnicowanie przy użyciu badań obrazowych. Może to mieć znaczące implikacje kliniczne, np. w odniesieniu do ultrasonografii, która jest podstawowym badaniem obrazowym w diagnostyce, monitorowaniu skuteczności leczenia czy w potwierdzaniu remisji u chorych na reumatoidalne zapalenie stawów. W niniejszym artykule omówiono patogenezę trzech elementów obrazu chorobowego choroby zwyrodnieniowej stawów, tj. zapalenia błony maziowej, z uwagi na trudności różnicowania synovitis w przebiegu tej choroby i reumatoidalnego zapalenia stawów, oraz osteofitów i podchrzęstnej sklerotyzacji, ze względu na istotne znaczenie czynnika zapalnego w ich powstawaniu.
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