1993 年 21 巻 8 号 p. 573-577
Hypothyroidism (Hypo) has been clinically associated with accelerated and premature coronary atherosclerosis. At the same time, lipoprotein (a) [Lp (a)] is known to provoke atherosclerosis and has been confirmed as a major independent risk factor for cardiovascular and cerebrovascular diseases. In this study we examined the role of plasma Lp (a) levels in patients with Hypo.
Plasma Lp (a) levels in 2 men and 21 women aged 25 to 67 (mean 49) years with untreated Hypo ranged from 2.0 to 58.4 (group A: mean±SE; 19.2±3.0) mg/dl. Levels in 34 healthy men and 72 healthy women aged 30 to 75 (mean 50) years ranged from 0.2 to 46.1 (group B: 11.8±0.8) mg/dl, and those of 2 men and 15 women aged 21 to 77 (mean 58) years with Hypo undergoing treatment for at least 1 year ranged from 1.6 to 47.1 (group C: 13.9±3.2) mg/dl. The mean value for Lp(a) in group A was significantly higher than that of group B (p<0.05), while the value in group C tended to be lower. Following levothyroxine administration to the 17 patients in group A, Lp (a) value for the group declined to 11.9±2.4 (range from 1.5 to 34.6) mg/dl, which followed a similar pattern in group C. In addition, the incidence of Lp (a) levels above 25mg/dl, which is considered highly atherogenic, was higher in group A than in group B (30.4 vs 6.6%, respectively, p<0.001). While 11.8% of group C and 17.6% of group A during treatment had high Lp (a) levels, both tended to be lower than that of group A. A significant correlation was noted between changes of plasma Lp (a) and those of TSH in group A before and during treatment (p<0.05).
In conclusion, plasma Lp (a) was increased in patients with Hypo, and tended to be lower during treatment. These increased plasma Lp (a) levels may contribute to the increased risk of premature atherosclerosis in the Hypo state.