Evaluating the association between obesity and development of trigger finger and carpal tunnel syndrome
Jason Sidrak, BS1, Andy Lalka, MPH1, Cailin Delaney, PA-C1, Rajshri Bolson, M.D.2 and Frank A Scott, MD1, (1)University of Colorado, Aurora, CO, (2)Rocky Mountain Regional Veterans Affairs Medical Center, Aurora, CO
Hypothesis: Obesity is known to cause a low-grade inflammatory environment that can influence development of musculoskeletal disorders. The impact of obesity is known in osteoarthritis but there is limited information on obesity-associated upper extremity pathology. We hypothesized that patients with high BMI will develop carpal tunnel syndrome or stenosing tenosynovitis sooner than patients with normal BMI.
Methods: A retrospective chart review was performed for adult patients diagnosed with carpal tunnel syndrome (CTS) or stenosing tenosynovitis (TF) between January 2016 and December 2020 at a large outpatient academic practice. Inclusion criteria were patients over the age of 21, a diagnosis of CTS or TF, and a BMI history of at least 3 years. Exclusion criteria were patients under 21, traumatic etiology of CTS or TF and/or less than 3 years of documented BMI. The primary outcome was age at diagnosis of CTS or TF. A high BMI was considered 30 and above while a normal BMI was 18.5 to 24.9. Summary statistics were produced for covariates of interest then compared between normal and high BMI groups. A stepwise multivariate linear regression model compared the impact of BMI on age of CTS or TF diagnosis after adjusting for co-variates known to accelerate CTS or TF development.
A total of 262 patients met the inclusion criteria. Our univariate analysis showed that patients with high BMI developed CTS or TF an average of 6.4 years (95%CI: 1.9, 10.9, P=0.0053) earlier compared to the normal BMI group, 67.5 and 61.1 years respectively. Our multivariate model found that in the presence of other co-variates, high BMI caused development of CTS or TF 6.2 years sooner than patients with normal BMI (P<0.05). Additionally, current smokers developed CTS or TF 12.5 years sooner than never smokers (P<0.05). Patients with type 1 diabetes developed CTS or TF 18.8 years sooner than non-diabetics (P<0.05). Interestingly, patients with hypertension developed CTS or TF 6.0 years later than those without hypertension (P<0.05).
Patients with high BMI were diagnosed with CTS or TF at a younger age than normal BMI patients after adjusting for other causative co-variates. Smoking and Type 1 diabetes have profound effects of on age of diagnosis of CTS or TF. Obesity is associated with accelerated development of CTS and trigger finer after adjusting for other associated factors. These study results highlight the need for more bench research to investigate underlying inflammatory mechanism of CTS and TF.
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