BACKGROUND: Slipped capital femoral epiphysis (SCFE) is strongly associated with childhood obesity, yet the prevalence of obesity is orders of magnitude greater than the prevalence of SCFE. Therefore, it is hypothesized that obesity is not, by itself, a sufficient condition for SCFE, but rather one component of a multifactorial process requiring preexisting physeal pathology. Leptin elevation is seen to varying degrees in patients with obesity, and as leptin has been shown to cause physeal pathology similar to the changes seen in SCFE, we propose that leptin may be a factor distinguishing between patients with SCFE and equally obese children without hip abnormalities. METHODS: Serum leptin levels were obtained from 40 patients with SCFE and 30 control patients with approximate body mass index (BMI) matching. BMI percentiles were calculated according to Centers for Disease Control and Prevention population data by patient age and sex. Patients were compared by demographic characteristics, leptin levels, odds of leptin elevation, and odds of SCFE. RESULTS: The odds of developing SCFE was increased by an odds ratio of 4.9 (95% confidence interval [CI], 1.31 to 18.48; p < 0.02) in patients with elevated leptin levels, regardless of obesity status, sex, and race. When grouping patients by their obesity status, non-obese patients with SCFE showed elevated median leptin levels at 5.8 ng/mL compared with non-obese controls at 1.7 ng/mL (p = 0.006). Similarly, obese patients with SCFE showed elevated median leptin levels at 17.9 ng/mL compared with equally obese controls at 10.5 ng/mL (p = 0.039). Serum leptin levels increased in association with obesity (p < 0.001), with an increase in leptin of 0.17 ng/mL (95% CI, 0.07 to 0.27 ng/mL) per BMI percentile point. CONCLUSIONS: To our knowledge, this study is the first to clinically demonstrate an association between elevated serum leptin levels and SCFE, regardless of BMI. This adds to existing literature suggesting that SCFE is a multifactorial process and that leptin levels may have profound physiological effects on the development of various disease states. Despite a strong association with adiposity, leptin levels vary between patients of equal BMI and may be a vital resource in prognostication of future obesity-related comorbidities. LEVEL OF EVIDENCE: Prognostic Level III. See Instructions for Authors for a complete description of levels of evidence.
BACKGROUND:Slipped capital femoral epiphysis (SCFE) is strongly associated with childhood obesity, yet the prevalence of obesity is orders of magnitude greater than the prevalence of SCFE. Therefore, it is hypothesized that obesity is not, by itself, a sufficient condition for SCFE, but rather one component of a multifactorial process requiring preexisting physeal pathology. Leptin elevation is seen to varying degrees in patients with obesity, and as leptin has been shown to cause physeal pathology similar to the changes seen in SCFE, we propose that leptin may be a factor distinguishing between patients with SCFE and equally obesechildren without hip abnormalities. METHODS: Serum leptin levels were obtained from 40 patients with SCFE and 30 control patients with approximate body mass index (BMI) matching. BMI percentiles were calculated according to Centers for Disease Control and Prevention population data by patient age and sex. Patients were compared by demographic characteristics, leptin levels, odds of leptin elevation, and odds of SCFE. RESULTS: The odds of developing SCFE was increased by an odds ratio of 4.9 (95% confidence interval [CI], 1.31 to 18.48; p < 0.02) in patients with elevated leptin levels, regardless of obesity status, sex, and race. When grouping patients by their obesity status, non-obesepatients with SCFE showed elevated median leptin levels at 5.8 ng/mL compared with non-obese controls at 1.7 ng/mL (p = 0.006). Similarly, obesepatients with SCFE showed elevated median leptin levels at 17.9 ng/mL compared with equally obese controls at 10.5 ng/mL (p = 0.039). Serum leptin levels increased in association with obesity (p < 0.001), with an increase in leptin of 0.17 ng/mL (95% CI, 0.07 to 0.27 ng/mL) per BMI percentile point. CONCLUSIONS: To our knowledge, this study is the first to clinically demonstrate an association between elevated serum leptin levels and SCFE, regardless of BMI. This adds to existing literature suggesting that SCFE is a multifactorial process and that leptin levels may have profound physiological effects on the development of various disease states. Despite a strong association with adiposity, leptin levels vary between patients of equal BMI and may be a vital resource in prognostication of future obesity-related comorbidities. LEVEL OF EVIDENCE: Prognostic Level III. See Instructions for Authors for a complete description of levels of evidence.
Authors: Evangelia Charmandari; Martina Weise; Stefan R Bornstein; Graeme Eisenhofer; Margaret F Keil; George P Chrousos; Deborah P Merke Journal: J Clin Endocrinol Metab Date: 2002-05 Impact factor: 5.958
Authors: W F Blum; P Englaro; S Hanitsch; A Juul; N T Hertel; J Müller; N E Skakkebaek; M L Heiman; M Birkett; A M Attanasio; W Kiess; W Rascher Journal: J Clin Endocrinol Metab Date: 1997-09 Impact factor: 5.958
Authors: Y Lampl; Y Eshel; A Kessler; A Fux; R Gilad; M Boaz; Z Matas; M Sadeh Journal: J Neurol Neurosurg Psychiatry Date: 2002-05 Impact factor: 10.154
Authors: M Witbreuk; F J van Kemenade; J A van der Sluijs; E P Jansma; J Rotteveel; B J van Royen Journal: J Child Orthop Date: 2013-03-30 Impact factor: 1.548
Authors: Daniel C Perry; Barbara Arch; Duncan Appelbe; Priya Francis; Joanna Craven; Fergal P Monsell; Paula Williamson; Marian Knight Journal: Bone Joint J Date: 2022-04 Impact factor: 5.385