The End of the Road for Idiopathic Slipped Capital Femoral Epiphysis?: Commentary on an article by Schuyler J. Halverson, MD, MS, et al.

    loading  Checking for direct PDF access through Ovid

Excerpt

In the article “Leptin Elevation as a Risk Factor for Slipped Capital Femoral Epiphysis Independent of Obesity Status,” Halverson et al. investigate the concept that elevated leptin levels may predispose any child to developing a slipped capital femoral epiphysis (SCFE), regardless of his or her weight (determined by body mass index [BMI]). Despite the well-published association between SCFE and obesity1, this study is based on the observations that there are many more children who are obese than who develop SCFE, most patients who develop SCFE do not have identifiable underlying endocrine or metabolic disease (i.e., the cases are idiopathic)2, hyperleptinemic animal models demonstrate physeal findings similar to those of patients with SCFE, and both patients with SCFE and those with hyperleptinemia have higher rates of obesity and hypertension than control patients. Bringing this concept together through case-controlled comparison, the authors demonstrate that patients who develop SCFE routinely show elevated leptin levels compared with BMI-matched controls no matter the age or BMI status, suggesting a causal relationship between the two.
As a preliminary association in need of further study in a larger context (multicenter reproduction of results), this finding allows the possibility of eliminating the diagnosis of idiopathic SCFE. As is often frustrating in clinical orthopaedic practice, the diagnosis of exclusion represented by an idiopathic condition (in this case, SCFE) frequently leaves the surgeon, patient, and family lacking a satisfactory explanation of the patient’s current situation. By enabling a specific diagnosis to be made (in this case, hyperleptinemia), as the authors mention, a specific cause for the problem is identified and the search for other known medical conditions linked to elevated leptin levels (e.g., cardiovascular, endocrine, pulmonary) may be undertaken with the possibility of proactive treatment and preservation of the patient’s health3.
If further proven to be a causal relationship, associating hyperleptinemia with the diagnosis of SCFE and its readily observable pain and limp, the ramifications of elevated leptin levels are clarified in a much more obvious way than many of the other associated problems, such as hypertension, that may take decades to become manifest in daily life and that may be at a late stage (stroke, heart failure) before detected4. This may lead to additional urgency in the patient and family toward proactive management and avoidance of additional future health issues. It also places the orthopaedic surgeon in the particularly critical position of being able to demonstrate in a concrete and immediate way the possible negative health consequences of hyperleptinemia, allowing other medical providers to move the discussion to other areas with further patient health benefit. As the authors demonstrate in this article with regard to SCFE and hyperleptinemia, combining the findings of clinical and basic-science orthopaedic studies with those of other medical arenas may lead to the elucidation of the true cause of further idiopathic diagnoses such as Blount disease, Legg-Calvé-Perthes disease, and scoliosis, with a possible additional health benefit to our patients beyond their orthopaedic care.

Related Topics

    loading  Loading Related Articles