Observational studyMusculoskeletal surgery2018
Shoulder adhesive capsulitis and hypercholesterolemia: role of APO A1 lipoprotein polymorphism on etiology and severity.
Observational study in Musculoskeletal surgery, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Suprascapular nerve blocks with 5 mL × 10 mL in the treatment of primary adhesive capsulitis: pilot study of clinical trial.Musculoskeletal surgery · 2025Trial
- Impact of nutritional profile on pain and functionality in patients with frozen shoulder: a cross-sectional observational study.Frontiers in medicine · 2026Article
- The effect of cellular nuclear function alteration on the pathogenesis of shoulder adhesive capsulitis: an immunohistochemical study on lamin A/C expression.Journal of orthopaedics and traumatology : official journal of the Italian Society of Orthopaedics and Traumatology · 2024Article
- The puzzling pathophysiology of frozen shoulders - a scoping review.Journal of experimental orthopaedics · 2020Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeRelationship between shoulder adhesive capsulitis (AC) and hypercholesterolemia is known. The connecting link might be represented by the correlation between HDL and transforming growth factor beta (TGF-β): normally, HDLs stimulate TGF-β expression; the latter is employed in the development of fibrous tissue. We assess whether the presence of the Apo-A1-G75A-polymorphism, which is correlated to an enhanced HDL function, could be a risk factor for the genesis and severity of AC.
methodsPeripheral blood samples of 27 patients [7M; 20F, mean age 54.81 (41-65)] with AC and hypercholesterolemia were submitted to polymerase chain reaction in order to evaluate the Apo-A1-G75A-polymorphism. Genome database was used as control. Two categories were obtained according to AC severity: type I (active forward flexion ≥ 100°) and type II (< 100°). Data were submitted to statistics.
resultsThe prevalence of Apo-A1-G75A-polymorphism in the studied group and in the control group was 22.2% (10AG; 1AA; 16GG) and 19% (OR 1.22, IC 0.59-2.53, p > 0.05), respectively. Patients with type I and II capsulitis were 11 [flexion 148.0° (range 100°-165°)] and 16 [flexion 82.5° (range 50°-95°)], respectively. The prevalence of Apo-A1-G75A in type I was 18.1% (2AG; 9GG) and in type II was 56.3% (8GA; 1AA; 7GG), respectively (RR 1.87, IC 1.005-3.482, p < 0.05).
conclusionsApo-A1-G75A-polymorphism is not necessary for the genesis, but it is a risk factor for severity of AC. LEVEL OF EVIDENCE: III.
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