OBJECTIVE: The determinants of serum homocysteine in healthy postmenopausal women remain uncertain. The aim of this study was the assessment of the association of endogenous sex steroids with serum homocysteine levels in healthy postmenopausal women not on hormone therapy. DESIGN: 484 postmenopausal women aged 43-69 years were studied in a cross-sectional design. Parameters assessed were serum FSH, estradiol, total testosterone, SHBG, Free Androgen Index, delta4-Androstendione, Dehydroepiandrosterone sulphate, and homocysteine. RESULTS: Serum FSH correlated positively (r=0.23, p=0.01), while serum estradiol correlated negatively (r=-0.25, p=0.03) with circulating Hcy. This association remained statistically significant after adjustment for age, years since menopause, and BMI. Serum estradiol decreased, while FSH increased linearly with increasing homocysteine quartiles (p=0.04 and p=0.02, respectively). None of the serum androgens assessed correlated with circulating homocysteine. CONCLUSIONS: Endogenous estrogens and not androgens are related to serum homocysteine values in postmenopausal women. Whether this association has clinical implications remains to be clarified.

Background. Lipoprotein(a), Lp(a), has been recognized as an atherogenic and thrombogenic lipoprotein in the general population and in hemodialysis (HD) patients. In addition, fibrinogen and fibronectin may promote atherothrombosis. The aim of this study was to investigate any possible relationship between Lp(a) and thrombogenic coagulation proteins in non-diabetic HD patients. Patients and Methods. Serum Lp(a) and plasma fibrinogen, plasminogen, and fibronectin levels were measured pre-HD in 60 uremic patients (30 male, 30 female) aged 58.6 ± 8.0 years who had been receiving HD treatment for 61.3 ± 50.7 months. The control group comprised 20 age- and sex-matched healthy subjects. All patients were receiving erythropoietin treatment. Results. The mean serum Lp(a) (33.88 ± 34.12 mg/dL) and plasma fibrinogen (329.45 ± 80.62 mg/dL) levels were significantly higher in the HD patients compared with those in the controls (16.70 ± 10.36 and 254.00 ± 43.34 mg/dL, respectively; p < .05 and p < .001, respectively). Plasminogen levels did not differ between the HD patients (11.64 ± 3.22 mg/dL) and the control group (10.67 ± 1.41 mg/dL, p>.05). Fibronectin levels were slightly increased in the HD patients (33.96 ± 5.49 mg/dL) versus in the control group (30.9 ± 5.80 mg/dL, p < .05). There was a significant positive correlation between Lp(a) and fibrinogen levels (r = 0.305, p < .02), as well as between Lp(a) and fibronectin levels (r = 0.360, p < .01). Moreover, there was a significant positive correlation between fibrinogen and fibronectin levels (r = 0.587, p < .0001). Conclusions. According to our results, in non-diabetic HD patients, abnormal serum Lp(a) levels significantly correlated with abnormal levels of fibrinogen and fibronectin. There is a concern that the relationship between these atherogenic and thrombogenic acute-phase proteins may contribute to the increased incidence of atherosclerotic cardiovascular disease in this patient population.

The aim of this study was to assess the association of endogenous sex steroids with bone mineral density (BMD) in healthy postmenopausal women not on hormone therapy. A total of 884 postmenopausal women aged 42-71 years were studied in a cross-sectional design. Parameters assessed were follicle-stimulating hormone, luteinizing hormone, estradiol, total testosterone, sex hormone-binding globulin, free estrogen index (FEI), free androgen index (FAI), Δ4-androstendione (Δ4A), dehydroepiandrosterone sulfate (DHEAS), bone alkaline posphatase, and bone mineral density at the lumbar spine (L-BMD) and femoral neck (N-BMD). Estradiol and FEI associated positively with both L-BMD and N-BMD (r = 0.21-0.47, P < 0.01). These associations remained significant after adjustment for age, years since menopause, and body mass index. FAI correlated positively with both L-BMD and N-BMD (r = 0.18 and 0.33, respectively; P < 0.01). At the multivariate analysis, however, FAI remained the significant determinant only for N-BMD. Δ4A associated positively with N-BMD (r = 0.27, P = 0.001), whereas DHEAS showed no association with BMD at either site. Thus, endogenous steroids are significant determinants of postmenopausal BMD. Endogenous estradiol may be more important for lumbar spine BMD, whereas endogenous androgens are associated mainly with femoral neck BMD. © Springer-Verlag Tokyo 2006.

The EC4 Syllabus for Postgraduate Training is the basis for the European Register of Specialists in Clinical Chemistry and Laboratory Medicine. The syllabus: • Indicates the level of requirements in postgraduate training to harmonise the postgraduate education in the European Union (EU); • Indicates the level of content of national training programmes to obtain adequate knowledge and experience; • Is approved by all EU societies for clinical chemistry and laboratory medicine. The syllabus is not primarily meant to be a training guide, but on the basis of the overview given (common minimal programme), national societies should formulate programmes that indicate where knowledge and experience is needed. The main points of this programme are: • Knowledge in biochemistry, haematology, immunology, etc.; • Pre-analytical conditions; • Evaluation of results; • Interpretations (post-analytical phase); • Laboratory management; and • Quality insurance management. The aim of this version of the syllabus is to be in accordance with the Directive of Professional Qualifications published on 30 September 2005. To prepare the common platforms planned in this directive, the disciplines are divided into four categories: • General chemistry, encompassing biochemistry, endocrinology, chemical (humoral), immunology, toxicology, and therapeutic drug monitoring; • Haematology, covering cells, transfusion serology, coagulation, and cellular immunology; • Microbiology, involving bacteriology, virology, parasitology, and mycology; • Genetics and IVF. © 2006 by Walter de Gruyter.

Background: Intrauterine fetal development is characterized by increased rates of proliferation and apoptosis, while both these processes may be attenuated post-natally. Aim: Tissue polypeptide specific antigen and sFas serum concentrations were determined during pregnancy and post-natally, in order to evaluate their alterations during these crucial periods. Materials and Methods: Forty-seven healthy pregnant women, their full-term newborns and 35 healthy adults (controls) were included in the study. Markers were measured: a) in maternal serum (MS), during the 1st, 2nd, 3rd trimester and at the 1st stage of labor; b) in the umbilical cord (UC), during the 2nd stage of labor; c) in neonatal serum in the 1st (1N) and 5th (5N) day after birth; and d) in controls. Results: The serum TPS concentrations in MS increased significantly with gestational age, being higher in the 3rd trimester and labor, than those in controls (p<0.001). TPS values were significantly lower in the UC, compared to those in MS (p<0.001), while they were markedly elevated in 1N, compared to MS and UC (p<0.001), and subsequently decreased in 5N (p<0.001), remaining higher, than those in the controls (p<0.001). Serum sFas concentrations in the MS depended significantly on gestational age (p<0.001), being significantly lower in the first trimester, than those in the second (p<0.003), the third (p<0.03), in labor and controls (p<0.005). sFas concentrations in the UC were significantly lower than in MS and controls (p<0.001), while they increased significantly in 5 N samples (p<0.01). Conclusion: Our results demonstrate: a) a higher apoptosis rate in the first trimester of pregnancy, possibly affecting maternal immuno-tolerance, followed by a down-regulation during the post-natal period; b) a progressively increased proliferation from the first trimester to parturition, reflecting the fetal and placental growth and development, that seems to be thereafter moderated.

Objective: To assess the association between endogenous sex hormones and risk factors for atherosclerosis in healthy postmenopausal women. Design: Cross-sectional study in a university menopause clinic. Methods: Serum sex hormones and lipid-lipoprotein profile, arterial pressure, homocysteine and insulin resistance, measured by the homeostasis model assessment of insulin resistance (HOMA-111), were assessed in 598 healthy postmenopausal women not on hormone therapy. Results: Compared with women in the lowest testosterone quartile (Q), women in the highest testosterone quartile had higher total cholesterol (Q1: 225.2±41.3 vs Q4: 246.2±38.4 mg/dl, P<0.01), low-density lipoprotein (LDL)-cholesterol (Q1: 146.9±37.2 vs Q4: 171.8±35.3 mg/dl, P<0.001), atherogenic index of plasma (AIP) (Q1: -0.224±0.238 vs Q4:-0.087±0.254, P<0.01), apolipoprotein B (ApoB) (Q1: 100.7±23.1 vs Q4: 113.9±23.8 mg/dl, P<0.001) and higher high-density lipoprotein (HDL)-cholesterol (QI: 60.7±14.5 vs Q4: 52.9±13.0 mg/dl, P<0.01). Accordingly, women in the highest free androgen index (FAI) quartile had higher AIP (Q1: -0.232±0.254 vs Q4: -0.078±0.243, P<0.001) and ApoB (Q1: 102.4±25.5 vs Q4: 114.2±25.8mg /dl, P<0.01) and lower HDL-cholesterol (Q1: 62.0±15.7 vs Q4: 51.9±11.6mg/dl, P<0.001) and apolipoprotein A (Q1: 159.6±25.6 vs Q4: 147.9±24.1 mg/dl, P<0.01) compared with women in the lowest FAI quartile. These differences remained significant after adjustment for age, body mass index (BMI), insulin resistance and social habits. The free estrogen index (FEI) exhibited similar associations to the FAL HOMA-IR showed an independent positive association with total testosterone (Q1: 2.00±1.36 vs Q4: 2.66±1.60, P<0.01), FAI (Q1: 1.70±1.12 vs Q4: 3.04±1.66, P<0.001) and FEI (Q1: 1.70±0.91 vs Q4: 3.08±1.77, P<0.001). Conclusions: Increased androgenicity in healthy postmenopausal women is associated with an unfavorable cardiovascular risk profile. High endogenous estradiol is related to a pro-atherogenic lipid profile, an association which may, in part, be mediated by insulin resistance. © 2006 Society of the European Journal of Endocrinology.