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

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. LevelofEvidence III.