Gamze Serarslan1, Oğuzhan Özcan2, Ebru Okyay3, Bahar Ünlü2, Mehmet Karadağ4. 1. Tayfur Ata Sökmen Medical Faculty, Department of Dermatology, Hatay Mustafa Kemal University, Antakya, Hatay, Turkey. gserarslan@hotmail.com. 2. Tayfur Ata Sökmen Medical Faculty, Department of Biochemistry, Hatay Mustafa Kemal University, Antakya, Hatay, Turkey. 3. Tayfur Ata Sökmen Medical Faculty, Department of Dermatology, Hatay Mustafa Kemal University, Antakya, Hatay, Turkey. 4. Tayfur Ata Sökmen Medical Faculty, Department of Biostatistics, Hatay Mustafa Kemal University, Antakya, Hatay, Turkey.
Abstract
BACKGROUND/AIMS: Alopecia areata (AA) is considered an organ-specific autoimmune disease of hair follicles. Adipose tissue plays a role in lipid metabolism and glucose metabolism and secretes adipokines such as leptin and adiponectin. Dysregulation in the adipokine balance may be associated with metabolic syndrome. We aimed to determine serum adipokine levels in AA patients and compare them with healthy controls, and to determine whether there was metabolic syndrome and insulin resistance in the AA patients. METHODS: A total of 70 participants were included in the study. Patients were divided into two subgroups: patients with scalp hair loss were in subgroup 1 (AA1). Patients with beard and eyebrow hair loss were in subgroup 2 (AA2). Serum adiponectin, leptin, TNF-α, insulin, fasting glucose, TG, and HDL were analyzed. RESULTS: Thirty-six (25 male, 11 female) patients with AA and 34 (18 male, 16 female) healthy subjects were included in the study. Metabolic syndrome was detected in three of the AA patients and in two of the healthy subjects. Serum leptin, adiponectin, TNF-α, TG, HDL, and insulin levels and HOMA-IR scores were not statistically significant in patients compared with control subjects, except fasting glucose levels (p = 0.035). However, serum leptin and adiponectin levels were significantly higher in AA1 (n = 25) subgroup compared with the control group (p = 0.029, p = 0.026 respectively). There was a statistically significant increase in the fasting glucose level, while there were no differences in other parameters between the AA2 (n = 11) subgroup and the control group. CONCLUSIONS: To our knowledge, this is the first report indicating that adiponectin and leptin probably has a role in the pathogenesis of AA with scalp hair involvement.
BACKGROUND/AIMS: Alopecia areata (AA) is considered an organ-specific autoimmune disease of hair follicles. Adipose tissue plays a role in lipid metabolism and glucose metabolism and secretes adipokines such as leptin and adiponectin. Dysregulation in the adipokine balance may be associated with metabolic syndrome. We aimed to determine serum adipokine levels in AA patients and compare them with healthy controls, and to determine whether there was metabolic syndrome and insulin resistance in the AA patients. METHODS: A total of 70 participants were included in the study. Patients were divided into two subgroups: patients with scalp hair loss were in subgroup 1 (AA1). Patients with beard and eyebrow hair loss were in subgroup 2 (AA2). Serum adiponectin, leptin, TNF-α, insulin, fasting glucose, TG, and HDL were analyzed. RESULTS: Thirty-six (25 male, 11 female) patients with AA and 34 (18 male, 16 female) healthy subjects were included in the study. Metabolic syndrome was detected in three of the AA patients and in two of the healthy subjects. Serum leptin, adiponectin, TNF-α, TG, HDL, and insulin levels and HOMA-IR scores were not statistically significant in patients compared with control subjects, except fasting glucose levels (p = 0.035). However, serum leptin and adiponectin levels were significantly higher in AA1 (n = 25) subgroup compared with the control group (p = 0.029, p = 0.026 respectively). There was a statistically significant increase in the fasting glucose level, while there were no differences in other parameters between the AA2 (n = 11) subgroup and the control group. CONCLUSIONS: To our knowledge, this is the first report indicating that adiponectin and leptin probably has a role in the pathogenesis of AA with scalp hair involvement.
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