Endocrine Abstracts

During menopause, plasma lipids change in an unfavourable way to a more atherogenic pattern with, increased total and LDL-cholesterol and decreased HDL cholesterol concentrations. Women with POI show increased cardiovascular morbidity and mortality regardless of the cause of the ovarian insufficiency. The treatment of premature ovarian failure in patients presenting extremely low HLD-C is a real challenge.

We present the case of a 29 years old patient who was referred to our clinic for secondary amenorrhoea, headaches and lower limb pain.

Laboratory investigations showed: Thrombocytopenia (80000/100000/ml), FSH=173 mUI/ml, LH=92 mUI/ml, Estradiol<10 pg/ml, normal basal and stimulated cortisol, normal calcium and thyroid function, Cholesterol=74 mg/dL, HDL-col= 3.8/<3 mg/dL, LDL-col=48.6 mg/dL, Triglycerides= 108 mg/dL, Non-HDL=70.2 mg/dl, ApoA1<0.03 g/l (1.08–2.25) very low, ApoB=0.93 g/l (0.6–1.17)- normal. She was started on contraceptive therapy with regular menstrual cycles with no improvement on the lipid panel (HDL-C remained <4 mg/dl). The cardiological and neurological exams didn’t show any signs of premature vascular disease. The haematology exam excluded artifactual or secondary causes of low HDL-C. The thrombocytopenia was defined as essential. Confirming the causes of POI and low HDL-C requires genetic testing which was not performed for financial reasons.

Cardiovascular risk assessment is not well defined in this situations. The association between extremely low HDL-C levels and atherosclerosis still remains unclear in genetic conditions, as well as in the context of POI. HRT would be a better option than monophasic contraceptives. Statin treatment must be individualised. The purpose of the treatment is prolonging the patient’s life and improving the quality of life.

Causes of HDL-C below 20 mg/dl in the absence of severe hypertriglyceridemia are primary monogenic disorders (apolipoprotein A-I mutations, Tangier disease, and lecithin-cholesterol acyltransferase deficiency) or secondary causes (androgen use, malignancy).

Causes of premature ovarian failure are wide ranging: chromosomal and genetic defects (Turner syndrome, fragile-X syndrome, autosomal gene defects), autoimmune disorders, iatrogenic causes, environmental factors.