Adipokines are dysregulated in patients with hidradenitis suppurativa

This is the authors' abstract. We don't add key points for this paper.

Dear Editor, Hidradenitis suppurativa (HS) is characterized by the appearance of painful subcutaneous nodules and dermal abscesses in the axillae, perineum and inframammary folds. The development of HS has been linked to factors such as cigarette smoking and obesity.1 Patients with HS are more likely to have metabolic syndrome than control populations and develop early cardiovascular diseases.2 Adipokines are signalling molecules secreted by adipose tissue and peripheral blood mononuclear cells. The expression of adipokines is dysregulated in obesity and cardiovascular diseases.3,4 We measured the serum levels of adipokines in 30 patients with HS with a mean ± SD body mass index (BMI) of 33·9 ± 11·2 kg m−2. We compared the levels with 20 metabolically healthy lean people with a mean BMI below 25, 32 patients who were nondiabetic obese with a mean BMI of 49 ± 9·2 and 39 patients with psoriasis (BMI 26·1 ± 4·7) with the mean ± SD Psoriasis Area and Severity Index (PASI) of 10·0 ± 3·2 (Table S1; see Supporting Information). The study was approved by the Medical Research Committee of St Vincent's University Hospital. The serum levels of adiponectin, resistin and leptin were measured by enzyme‐linked immunosorbent assays (Quantikine ELISA Kit, R&D Systems Europe, Abingdon, U.K.). Statistical analysis of differences between serum levels of adipokines < 0.001 was performed using GraphPad Prism (GraphPad Software, La Jolla, CA, U.S.A.) and the nonparametric Kruskal–Wallis test and Dunn's multiple comparisons test with significance of P < 0·05. The relationships between levels of adipokines and BMI were analysed by calculating the Spearman's rank correlation coefficient. The mean serum level of adiponectin was decreased significantly in patients with HS (7·8 ± 6·1 μg mL−1) in comparison with healthy lean controls (17·1 ± 7·5 μg mL−1, P < 0·001). Mean serum levels of adiponectin were decreased significantly in the nondiabetic obese group (5·5 ± 3·7 μg mL−1) compared with the psoriasis group (10·6 ± 5·6 μg mL−1, P = 0·002) and healthy lean controls (17·1 ± 7·5 μg mL−1, P < 0·001). There was no significant difference between serum adiponectin levels in patients with HS and psoriasis (P = 0·1201). The levels of resistin and leptin were increased significantly in patients with HS (mean ± SD: resistin, 16·7 ± 7·9 ng mL−1; leptin, 41·1 ± 26·4 ng mL−1) compared with healthy controls (resistin, 10·0 ± 4·8 ng mL−1, P = 0·0237; leptin, 14·3 ± 18·1 ng mL−1, P = 0·003). Resistin and leptin levels in serum were also elevated significantly in the HS group compared with the psoriasis group (resistin, 6·9 ± 1·6 ng mL−1, P < 0·001; leptin, 15·3 ± 16·6 ng mL−1, P < 0.001). The nondiabetic obese group had higher levels of resistin compared with the HS group but this was not statistically significant (resistin, 20·3 ± 10 ng mL−1, P‐value not significant). The nondiabetic obese group had higher levels of resistin compared with the psoriasis group (P < 0·001) and the healthy lean control group (P < 0.001). The nondiabetic obese group had higher levels of leptin in comparison with the HS group (leptin 80 ± 38 ng mL−1, P = 0·02), psoriasis group (P < 0·001) and healthy lean controls (P < 0·001) (Fig. 1a). Patients with hidradenitis suppurativa (HS) have dysregulated levels of adipokines in serum. Serum levels of adiponectin, resistin and leptin were analysed in the HS (n = 30), psoriasis (n = 39), nondiabetic obese [n = 32 for resitin and leptin, n = 27 for adiponectin, body mass index (BMI) > 30] and healthy lean control groups (n = 20, BMI < 25). (a) Dot plots represent individual samples with mean levels of adipokines (red line) in each group. (b) Dot plots represent individual patients with mean BMI (red line) for each group. BMI correlated with levels of adiponectin, resistin and leptin. (c) Graphs present correlations between BMI of all patients in the HS, obese and psoriasis groups and adipokines. r, Spearman's rank correlation coefficient; HC, healthy control; *P < 0·05, **P < 0·01, ***P < 0·001, ****P < 0·0001 by Kruskal–Wallis test and Dunn's multiple comparisons test. There was a strong positive correlation between BMI and serum levels of leptin (r = 0·83, n = 101) and resistin (r = 0·6, n = 101) across all patient groups. This has been described previously. There was a negative correlation between BMI and serum levels of adiponectin (r = −0·4, n = 96) (Fig. 1c). These results demonstrate that serum levels of adipokines are dysregulated in HS and are associated with obesity. Resistin is mainly produced by adipose tissue‐resident macrophages and by circulating monocytes. Leptin stimulates production of interleukin (IL)‐1β, IL‐6, tumour necrosis factor‐α and < 0.001 C‐X‐C motif chemokine ligand 8.5 In contrast, adiponectin attenuates inflammation by induction of IL‐10 and IL‐1RA and its level is decreased in obesity and psoriasis.6 To our knowledge this is the first study to assess the levels of adipokines in patients with HS. Our results indicate that the adipokine balance in HS is shifted towards increased expression of proinflammatory resistin and leptin. The results suggest also that the expression of anti‐inflammatory adiponectin is decreased in patients with HS. Proinflammatory adipokines increased locally in subcutaneous adipose tissue might contribute to the augmentation of inflammatory processes in the skin of patients with HS and in systemic inflammation. These abnormalities in adipokine levels appear to be the result of the increased BMI seen in our HS patients (Fig. 1b, c). It has been speculated that obesity has a pathogenic effect on HS severity as a result of increased low‐grade systemic inflammation and increased skinfold friction. One study has demonstrated that substantial weight loss ameliorated the symptoms of HS and supported the notion that weight control programmes may be beneficial to people with HS.7 The abnormal levels of adipokines found in HS may explain partially the link between obesity, metabolic abnormalities, premature cardiovascular disease and HS.