RESUMEN
Fractional laser therapy improves skin texture, range of motion, and quality of life for patients with traumatic scars. Nevertheless, anecdotal evidence suggests declining insurance coverage for laser therapy. We aimed to characterize the landscape of insurance coverage for fractional laser therapy present our six-year reimbursement trends. We cross-sectionally analyzed the 60 largest American health insurers by enrollee size and market share. For each, we identified their laser therapy policy for scar revision and extracted their documentation, prior, and continuing authorization requirements and treatment guidelines. We also collected retrospective institutional claims data from 2017 to 2022 to investigate trends in reimbursement. Of the 60 largest health insurers, we identified 11 (18.3%) policies on scar revision and 40 policies (66.7%) on reconstructive surgery, including scar revision. Nineteen policies considered laser therapy medically necessary with evidence of functional impairment refractory to prior treatment. Three insurers denied laser coverage under any circumstance. Of the 1,531 claims submitted by our institution for burn scar laser therapy, 13.8% were denied. Patients with Medicare (ORadj, 3.78) or Medicaid (ORadj, 2.80) had significantly greater odds of coverage than privately insured patients (p<0.01). There was a 14.5% annual reduction in the odds of reimbursement during the study period (ORadj, 0.86, p < 0.01). Laser therapy is a powerful treatment that is not widely available to patients with traumatic scars. Our institutional data suggest this access may be further eclipsed by decreasing trends in coverage since 2017. Strategies are needed to protect patient access to this life-changing treatment.
RESUMEN
Familial cardiomyopathy is an inherited disease that affects the structure and function of heart muscle and has an extreme range of phenotypes. Among the millions of affected individuals, patients with hypertrophic (HCM), dilated (DCM), or left ventricular non-compaction (LVNC) cardiomyopathy can experience morphologic changes of the heart which lead to sudden death in the most detrimental cases. TNNC1, the gene that codes for cardiac troponin C (cTnC), is a sarcomere gene associated with cardiomyopathies in which probands exhibit young age of presentation and high death, transplant or ventricular fibrillation events relative to TNNT2 and TNNI3 probands. Using GnomAD, ClinVar, UniProt and PhosphoSitePlus databases and published literature, an extensive list to date of identified genetic variants in TNNC1 and post-translational modifications (PTMs) in cTnC was compiled. Additionally, a recent cryo-EM structure of the cardiac thin filament regulatory unit was used to localize each functionally studied amino acid variant and each PTM (acetylation, glycation, s-nitrosylation, phosphorylation) in the structure of cTnC. TNNC1 has a large number of variants (> 100) relative to other genes of the same transcript size. Surprisingly, the mapped variant amino acids and PTMs are distributed throughout the cTnC structure. While many cardiomyopathy-associated variants are localized in α-helical regions of cTnC, this was not statistically significant χ2 (p = 0.72). Exploring the variants in TNNC1 and PTMs of cTnC in the contexts of cardiomyopathy association, physiological modulation and potential non-canonical roles provides insights into the normal function of cTnC along with the many facets of TNNC1 as a cardiomyopathic gene.
