Shoulder adhesive capsulitis and hypercholesterolemia: role of APO A1 lipoprotein polymorphism on etiology and severity

Abstract

Purpose: Relationship 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.

Methods: Peripheral 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.

Results: The 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).

Conclusions: Apo-A1-G75A-polymorphism is not necessary for the genesis, but it is a risk factor for severity of AC.

Level of evidence: III.

Keywords: Adhesive capsulitis; Adhesive capsulitis severity; Frozen shoulder; Frozen shoulder etiology; Hypercholesterolemia; Lipoproteins.