Abstract
Objectives. We examined the cardiovascular disease risk factor status of men and women with familial hyperlipidaemia (FH) 10-11 years after a clinical trial and asked whether first-degree relatives had undergone lipid testing. Design setting and subjects. Subjects started lipid-lowering drugs in 1987- 88. Of 60 subjects, 12 had died, one emigrated and 35 men and 12 women took part in a follow-up clinical examination in 1998. Results. Total cholesterol level was reduced by 41% and high-density lipoprotein (HDL) cholesterol level increased by 13% compared with baseline (diet alone). Low-density lipoprotein (LDL) cholesterol level was lower at the end of the trial than at follow-up (3.6 ± 1.5 vs. 4.6 ± 2.2 mmol L-1; P = 0.01) and was higher in the group taking a low dose of a statin alone compared with other drug groups. Thus, two-thirds of the subjects required adjustment of lipid-lowering drugs to reach target lipid levels. One-fifth consumed at least two food groups rich in saturated fat regularly. Body mass index (BMI) increased from 25,6 ± 2.9 to 26.8 ± 3.3 kg m-2 (P < 0.001). Five subjects compared with one at baseline had type II diabetes or glucose intolerance; 12 compared with four at baseline had a blood pressure of ≥ 160 mmHg systolic or ≥ 95 mmHg diastolic. Plasma total homocysteine was higher in subjects with coronary artery disease than in subjects without disease (11.7 ± 3.9 vs. 9.0 ± 2.3 μmol L-1: P = 0.01). Barriers to testing for lipids amongst children or siblings included family feuds, fear of increased insurance and psychiatric disease. Conclusion. The majority of subjects were under-treated. Increases in BMI. blood pressure and glucose levels and the diet posed challenges to risk reduction. Plasma homocysteine levels should be considered in this group. Testing of all first-degree relatives may not be achievable because of psychological barriers.
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Tonstad, S., & Hjermann, I. (2000). Cardiovascular risk factors and testing of relatives amongst patients with familial hyperlipidaemia one decade after a clinical trial. Journal of Internal Medicine, 248(2), 111–118. https://doi.org/10.1046/j.1365-2796.2000.00692.x
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