title: Role of leptin in Legg-Calvé-Perthes disease.
abstract: Obesity is considered a clinical risk sign for Legg-Calvé-Perthes disease (LCPD). Leptin is primarily secreted by adipocytes, and it regulates adipose tissue mass and body weight. Furthermore, obesity is clearly associated with increased leptin levels. We investigated the roles of leptin and the soluble leptin receptor (sOB-R) in LCPD. This matched case-control study included 38 male and 3 female patients with LCPD, and an equal number of age-(range was 4-12) and sex-matched control patients with healthy fractures. Serum leptin and sOB-R levels were quantified with ELISA. The free leptin index (FLI) was defined as the ratio of leptin to sOB-R levels. Serum leptin levels, sOB-R, and FLI were compared between groups. The relationship between leptin, disease severity, and treatment outcomes were analyzed in the LCPD group. There were no significant differences between groups in terms of age, sex, and body mass index (BMI) percentile. Mean leptin levels (p = 0.042), sOB-R levels (p = 0.003), and FLI (p = 0.013) differed significantly between groups. In the LCPD group, the serum leptin levels, sOB-R levels, and FLI differed significantly between the lateral pillar and Stulberg classification groups (p < 0.05). Also, the leptin levels and FLI increased significantly according to the lateral pillar and Stulberg classifications even after adjusting for age and BMI percentile (p < 0.05). Circulating leptin and FLI were significantly higher in the LCPD group. Furthermore, leptin, disease severity, and treatment outcomes were associated. This correlation suggests that leptin might play an important role in LCPD pathogenesis.
authors.affiliation: Department of Preventive Medicine, Chonbuk National University Medical School, 567 Baekje-daero, Deokjin-gu, Jeonju, Jeonbuk, 561-756, Republic of Korea.
authors.forename: Ju-Hyung
authors.initials: JH
authors.lastname: Lee
authors.forename: Lu
authors.initials: L
authors.lastname: Zhou
authors.forename: Keun-Sang
authors.initials: KS
authors.lastname: Kwon
authors.forename: Dongwook
authors.initials: D
authors.lastname: Lee
authors.forename: Byung-Hyun
authors.initials: BH
authors.lastname: Park
authors.forename: Jung Ryul
authors.initials: JR
authors.lastname: Kim
mesh_terms: D015992:Body Mass Index; D016022:Case-Control Studies; D002648:Child; D005260:Female; D005264:Femoral Fractures / Q000000981:diagnostic imaging / Q000453:epidemiology / Q000503:physiopathology*; D005271:Femur Head Necrosis / Q000000981:diagnostic imaging / Q000453:epidemiology / Q000503:physiopathology; D006801:Humans; D007873:Legg-Calve-Perthes Disease / Q000000981:diagnostic imaging / Q000453:epidemiology / Q000503:physiopathology*; D020738:Leptin / Q000097:blood* / Q000502:physiology*; D008297:Male; D009765:Obesity / Q000453:epidemiology / Q000378:metabolism*; D011859:Radiography; D054411:Receptors, Leptin / Q000097:blood / Q000502:physiology; D012307:Risk Factors; D012995:Solubility
chemical_list: D020738:Leptin; D054411:Receptors, Leptin
keywords: Legg-Calvé-Perthes disease; leptin; leptin resistance; pathogenesis; soluble leptin receptor