Investigating the relationship between serum endocan, TNF-α and IL-17A levels with disease severity and metabolic parameters in patients with hidradenitis suppurativa

Hidradenitis suppurativa (HS) is a chronic and inflammatory skin disease that affects the follicular part of the pilosebaceous units, often in the axillary, inguinal, mammary and gluteal regions. Although the etiology of HS is not fully elucidated, it is thought to be a multifactorial disease. Abnormal immune response after hair follicle occlusion is necessary to initiate the development of HS. It is suggested that TNF-α and IL-17A are key cytokines in the pathogenesis of HS. Endocan is a soluble and secretable dermatan sulfate proteoglycan weighing approximately 50 kDa. There are many studies conducted in recent years regarding the role of endocan in the pathogenesis of chronic inflammatory diseases and that its serum levels can be a biomarker. In our study, we aimed to measure the serum levels of endocan, as well as TNF-α and IL-17A, which are thought to have a key role in the pathogenesis of HS, in patient and healthy control groups, due to HS being a chronic inflammatory disease and its close relationship with its comorbidities. Disease severity and its relationship with metabolic parameters were evaluated. 35 HS patients and 35 healthy controls were included in our study. Monocyte, hs-CRP, routine biochemistry and lipid parameters were measured in the patient and control groups. Serum endocan, TNF-α and IL-17A levels were measured by ELISA method. In addition, body mass index (BMI), blood pressure, pulse, waist and hip circumference measurements of all participants were recorded. The data obtained were analyzed with SPSS (Statistical Package for the Social Sciences) v29.0 and Minitab 18 program. In our study, the mean serum endocan level (6108.80 ± 1517.35 pg/ml, 6114.51 ± 1561.89 pg/ml, p=0.906, respectively) and the mean serum IL-17A levels (45,78 ± 24,92 pg/ml, 38,78 ± 12,84 pg/ml, p=0,981, respectively) between the patient and control groups were similar. The mean serum TNF-α level (81.72 ± 51.51 pg/ml, 53.55 ± 32.83 pg/ml, p=0.016, respectively) was found to be significantly higher in the patient group. It was determined that there was no correlation between disease severity serum endocan and IL-17A levels according to the Hurley staging system, but a positive significant correlation with serum TNF-α level. A significant positive correlation was detected between serum endocan and TNF-α levels and monocyte/HDL-C ratio in the patient group. It was thought that our study will illumination on the pathogenesis of HS and endocan, a proteoglycan, may lead to further studies on its relationship with HS. Our results suggest that TNF-α may have a more important role than IL-17A regarding HS pathogenesis. Further studies on large case series at both serum and tissue levels are needed to elucidate the pathogenesis of HS and the role of endocan in HS.