Changes in serum levels of calcitonin gene-related peptide, adiponectin, and ghrelin in pregnant women with gestational diabetes mellitus.

AIM: This study was designed to determine serum calcitonin gene-related peptide (CGRP) levels and define whether serum CGRP concentration is associated with adiponectin and ghrelin in pregnant women with gestational diabetes mellitus (GDM). STUDY DESIGN: Thirty-six pregnant women with GDM and 43 normal pregnant women without glucose intolerance were evaluated in this study. The serum concentration of CGRP, adiponectin, and ghrelin were measured in two groups at the last trimester of gestation. MAIN FINDINGS: The serum CGRP level in the GDM group was significantly higher than the control group. Serum levels of adiponectin and ghrelin in the GDM group were significantly lower than in the control group. In pregnant women with GDM, there was a significant negative correlation between serum CGRP level and adiponectin level. However, the correlation between maternal serum CGRP levels and ghrelin levels was not significant. CONCLUSION: Our investigation shows that serum CGRP level was significantly higher in pregnant women with GDM in comparison with the control group. These results suggest that CGRP may play a very important role in GDM pathogenesis.

The strain rate of endometrium measured by real-time sonoelastography as a predictive marker for pregnancy in gonadotropin stimulated intrauterine insemination cycles.

AIM: Sonoelastography is an imaging technique that measures tissue strain quantitatively. This study aims to investigate whether the strain rate of endometrium measured by elastography can predict pregnancy after intrauterine insemination (IUI). METHODS: This study examined 197 gonadotropin-stimulated IUI cycles of 148 women diagnosed with unexplained infertility from February 2019 to November 2020. Endometrial thickness, pattern, and strain rate were measured by transvaginal ultrasonography immediately before the insemination. The endometrium and the parametrial tissue were selected for regions of interest, and the strain rate was calculated. The measurements were analyzed concerning the IUI outcome. RESULTS: Of the 197 IUI cycles, the pregnancy rate was 15.20% (n = 30), and ongoing pregnancy rate was 12.2% (n = 24). The mean strain rates were not different between pregnant and nonpregnant groups (2.68 ± 1.28 vs. 2.81 ± 1.32, p = 0.651). Strain rate was not predictive for pregnancy, shown by receiver operating characteristic curve analysis; the area under the curve was 0.526 (95% CI 0.413-0.639; p = 0.649). Pregnancy rates were significantly affected by the women's age and the inseminated sperm count. In multiple logistic regression analysis, the other parameters, including body mass index, anti-Müllerian hormone, endometrial thickness, endometrial strain rate, and echogenic endometrial pattern, did not significantly change the odds ratio of pregnancy. CONCLUSION: The endometrial strain rate does not significantly affect the pregnancy rates in gonadotropin stimulated IUI cycles. It appears that strain rate does not predict IUI outcome. More research is needed to evaluate the usefulness of sonoelastography in infertility treatments.

Does apical prolapse in addition to early stage anterior prolapse have any effect on lower urinary tract symptoms?

OBJECTIVE: To investigate whether apical prolapse in addition to early-stage anterior prolapse has any effect on lower urinary tract symptoms (LUTS). METHODS: Patients with early-stage pelvic organ prolapse (POP) were retrospectively analyzed at the urogynecology unit of a tertiary referral center. Cases with posterior POP were excluded, and the remaining women were distributed across four main groups: (1) no determinable anterior and/or apical POP (control); (2) isolated anterior POP; (3) anterior + apical POP; and (4) isolated apical POP. Each LUTS symptom in these groups was recorded. Women with isolated anterior POP and women with anterior + apical POP were then compared to define the additional effects of apical prolapse on LUTS. In order to asses; symptoms of urgency, urinary incontinence, stress urinary incontinence, frequency, abnormal emptying, hesitancy, interrupted stream, nocturia, post-micturition dribble, and dysuria were noted and Incontinence Impact Questionnaire (IIQ-7), and domains of Urinary Distress Inventory (UDI-6) were compared between the groups. RESULTS: Of the 225 patients, 66 were excluded from the analysis due to accompanying posterior compartment defect. There was no statistically significant difference for age, systemic disease history, or smoking status between the groups (p > 0.05). However, history of traumatic vaginal delivery was significantly lower in the control group than in the other groups (p = 0.039). The prevalence of hesitancy and interrupted stream were found to be significantly higher in the anterior + apical POP group than in the isolated POP group (p<0.05). Obstructive subscale of the Urinary Distress Inventory was higher both in the isolated anterior POP and anterior + apical POP groups than the control group (p<0.05). CONCLUSION: The current study demonstrates that even minimal loss of apical support accompanying anterior prolapse exacerbates LUTS.

Serum Caspase-1 levels in women with polycystic ovary syndrome.

OBJECTIVE: Caspase-1 is implicated in several important inflammatory diseases and controls adipocyte differentiation and insulin sensitivity. Interleukin-10 (IL-10) is an anti-inflammatory cytokine and plays an important role in chronic inflammatory conditions. This study was planned to determine if there is any relationship between Caspase-1 and IL-10 levels in women with PCOS. MATERIALS AND METHODS: Forty-two women with PCOS and thirty-seven healthy controls were evaluated in this controlled clinical study. Caspase-1 and IL-10 levels, serum lipid sub-fractions, fasting glucose, fasting insulin and other hormones (gonadotropins, androgens), malondialdehyde (MDA) and glutathione (GSH) levels were measured. Homeostasis model assessment (HOMA-IR) was used to estimate insulin resistance. RESULTS: Free androgen index (FAI), HOMA-IR, MDA and Caspase-1 levels were significantly higher in subjects with PCOS. However, the women with PCOS had considerably lower GSH concentration levels than healthy subjects. Serum IL-10 levels were higher in study subjects than in controls, though it was statistically insignificant. Caspase-1 was positively associated with IL-10. CONCLUSION: These outcomes propose that Caspase-1 may have a role in triggering the processes leading to chronic low-grade inflammation in women with PCOS, independent of insulin resistance, androgen excess and oxidative stress. Nevertheless, the precise role of Caspase-1 in the pathogenesis of the disease remains to be elucidated.

Serum HLA-G levels in women with polycystic ovary syndrome.

This study was designed to determine serum human leukocyte antigen-G (HLA-G) levels and establish whether serum HLA-G level is related with insulin resistance, oxidative stress, dyslipidemia and ovarian hyperandrogenism in women with polycystic ovary syndrome (PCOS). Twenty-five patients with PCOS and 23 healthy control women were evaluated in this study. Serum HLA-G, lipid fractions, glucose, insulin, malondialdehyde (MDA), glutathione (GSH), white blood cell (WBC), sex hormone-binding globulin (SHBG) and other hormone (gonadotropins and androgens) levels were measured. The estimate of insulin resistance was calculated by homeostasis model assessment (HOMA-IR). Serum luteinizing hormone (LH), total testosterone, fasting insulin, WBC levels and LH/follicle-stimulating hormone (FSH) ratio, free androgen index (FAI) and HOMA-IR values were significantly higher in patients with PCOS compared with healthy women. However, the women with PCOS had considerably lower serum FSH, SHBG, MDA, GSH and HLA-G levels than healthy subjects. HLA-G was inversely related with HOMA-IR, FAI, LH/FSH ratio and WBC, but positively with high-density lipoprotein cholesterol. Decreased serum HLA-G level may be related with insulin resistance, ovarian hyperandrogenism and oxidative stress in women with PCOS. Nevertheless, the exact role of HLA-G in the pathogenesis of the disease remains to be elucidated.

Serum Fetuin-A levels, insulin resistance and oxidative stress in women with polycystic ovary syndrome.

This study was designed to determine serum Fetuin-A levels and establish whether serum Fetuin-A level is related with insulin resistance, oxidative stress, ovarian hyperandrogenism and dyslipidemia in women with polycystic ovary syndrome (PCOS). Twenty-two patients with PCOS and twenty-one healthy control women were evaluated in this controlled clinical study. Serum Fetuin-A, lipid fractions, glucose, insulin, malondialdehyde (MDA), myeloperoxidase (MPO), glutathione (GSH), superoxide dismutase (SOD) and other hormone (gonadotropins, androgens) levels were measured. The estimate of insulin resistance was calculated by homeostasis model assessment (HOMA-R). The women with PCOS had significantly higher serum fasting glucose, insulin, luteinizing hormone (LH), MDA, Fetuin-A levels, and LH/follicle-stimulating hormone (FSH) ratio, free androgen index (FAI), HOMA-IR than healthy women. However, sex hormone-binding globulin (SHBG) and GSH levels were significantly lower in patients with PCOS compared with controls. Fetuin-A was positively correlated with insulin, HOMA-IR and FAI. Multiple regression analysis revealed that FAI was strong predictor of serum Fetuin-A level. Serum Fetuin-A level was related with insulin resistance and ovarian hyperandrogenism in women with PCOS. These results suggest that Fetuin-A may have a role in triggering the processes leading to insulin resistance and androgen excess in PCOS.

Serum calcitonin gene-related peptide levels in women with polycystic ovary syndrome.

PURPOSE: Calcitonin gene-related peptide (CGRP) is an amino acid neuropeptide with widespread expression. It has potent effects on lipid and energy metabolism. It induces insulin resistance. This study was planned to determine CGRP levels in women with polycystic ovary syndrome (PCOS). METHODS: Forty-seven women with PCOS and 34 healthy controls were evaluated in this controlled clinical study. Serum lipid sub-fractions, postprandial and fasting glucose, insulin and other hormones (gonadotropins, androgens) and CGRP levels were measured. Homeostasis model assessment (HOMA-IR) was used to estimate insulin resistance. RESULTS: Waist measurements, postprandial and fasting glucose and fasting insulin levels and free androgen index and HOMA-IR were significantly higher in subjects with PCOS. However, the women with PCOS had considerably lower high-density lipoprotein cholesterol levels than healthy subjects. Serum CGRP levels were higher in study subjects than in controls, although it was statistically insignificant. CONCLUSIONS: Serum CGRP level was not related with insulin resistance, ovarian hyperandrogenism and dyslipidemia in abdominally obese women with PCOS. These outcomes propose that CGRP may not play a pivotal role in the pathogenesis of PCOS.

Serum total L-carnitine levels in non-obese women with polycystic ovary syndrome.

BACKGROUND: Carnitine plays essential roles in energy production, oxidative stress and glucose metabolism. This study was planned to determine serum total L-carnitine levels in non-obese women with polycystic ovary syndrome (PCOS). METHODS: There were 27 non-obese women with PCOS and 30 healthy, age- and body mass index (BMI) matched controls were evaluated in this controlled clinical study. Serum lipid sub-fractions, fasting glucose, insulin and other hormones (gonadotrophins, androgens) and total L-carnitine levels were measured. Homeostasis model assessment (HOMA-IR) was used to estimate insulin resistance. RESULTS: The women with PCOS had significantly higher serum dehydroepiandrosterone sulfate, total testosterone, free androgen index (FAI), luteinizing hormone (LH), low-density lipoprotein (LDL) cholesterol, non-high density lipoprotein (HDL) cholesterol, fasting insulin levels and HOMA-IR measurement and LH/FSH ratios than healthy women. However, total L-carnitine and sex hormone-binding globulin (SHBG) levels were significantly lower in women with PCOS. L-Carnitine level was negatively correlated with FAI, but positively correlated with SHBG. Multiple regression analysis revealed that SHBG was a strong predictor of serum total L-carnitine level. CONCLUSIONS: Decreased total L-carnitine levels may be associated with hyperandrogenism and/or insulin resistance in non-obese women with PCOS. Long-term studies are needed to evaluate carnitine metabolism in PCOS, especially with regard to the molecular basis.

CCAAT/enhancer binding protein beta regulates aromatase expression via multiple and novel cis-regulatory sequences in uterine leiomyoma.

CONTEXT: Control of aromatase expression in uterine leiomyoma has significant clinical implications because aromatase inhibitors reduce tumor growth and associated irregular uterine bleeding. The mechanisms that regulate aromatase expression in leiomyoma are unknown. OBJECTIVES: We previously demonstrated that the cAMP-responsive proximal promoters I.3 and II regulate aromatase expression in vivo in uterine leiomyoma tissue. Here, we investigated the cellular and molecular mechanisms responsible for promoter I.3/II usage. RESULTS: In smooth muscle cells isolated from leiomyoma (LSMCs), dibutyryl cAMP significantly induced aromatase mRNA and enzyme activity. Reporter constructs of promoter I.3/II deletion and site-directed mutants with selective disruption of cis-regulatory elements in the -517/-16 bp region revealed that five out of seven elements, including three CCAAT/enhancer binding protein (C/EBP) binding sites and two cAMP response elements, were essential for cAMP-induced promoter activity. EMSAs demonstrated that nuclear extracts from LSMCs contain complexes assembled on four of the five cis-elements, with C/EBP binding sites, including a novel -245/-231 bp sequence, clearly associating with C/EBPbeta. Chromatin immunoprecipitation assays revealed that C/EBPbeta binds specifically to the promoter I.3/II region in intact cells. Dibutyryl cAMP significantly induced nuclear C/EBPbeta protein levels in LSMCs in a time-dependent manner. Conversely, knockdown of C/EBPbeta dramatically suppressed cAMP-induced aromatase mRNA and enzyme activity. CONCLUSIONS: C/EBPbeta, which binds to multiple cis-regulatory elements in promoter I.3/II, is a key factor in the transcriptional complex controlling aromatase expression in uterine leiomyoma cells. Definition of this mechanism further may assist in designing inhibitors of aromatase specific for leiomyoma tissue.

Stromal cells of endometriosis fail to produce paracrine factors that induce epithelial 17beta-hydroxysteroid dehydrogenase type 2 gene and its transcriptional regulator Sp1: a mechanism for defective estradiol metabolism.

OBJECTIVE: In endometrium, stromal progesterone receptors mediate production of paracrine factors, which enhance binding of the transcription factor specific protein-1 to the promoter of the gene encoding the 17beta-hydroxysteroid dehydrogenase type 2 enzyme responsible for converting biologically active estradiol to estrone in epithelium. The objective of this study is to define the cellular defect responsible for the disruption of this stromal-epithelial interaction in endometriosis. STUDY DESIGN: We determined the effects of conditioned media generated from primary human eutopic endometrial stromal cells vs endometriotic stromal cells on Ishikawa malignant endometrial epithelial cells. RESULTS: Conditioned media from progestin-pretreated eutopic endometrial stromal cells but not endometriotic stromal cells significantly stimulated specific protein-1 protein levels, 17beta-hydroxysteroid dehydrogenase type 2 messenger RNA levels and promoter activity, and binding activity of specific protein-1 to the 17beta-hydroxysteroid dehydrogenase type 2 promoter region in Ishikawa cells. CONCLUSION: A stromal cell defect in endometriosis blocks formation of progesterone-dependent production of factors leading to 17beta-hydroxysteroid dehydrogenase type 2 deficiency and defective conversion of estradiol to estrone in epithelium.

SP1 and SP3 mediate progesterone-dependent induction of the 17beta hydroxysteroid dehydrogenase type 2 gene in human endometrium.

The opposing actions of estrogen and progesterone during the menstrual cycle regulate the cyclical and predictable endometrial proliferation and differentiation that is required for implantation. Progesterone indirectly stimulates the expression of 17beta hydroxysteroid dehydrogenase type 2 (HSD17B2), which catalyzes the conversion of biologically potent estradiol to weakly estrogenic estrone in the endometrial epithelium. We previously demonstrated upregulation of the HSD17B2 gene in human endometrial epithelial cells by factors secreted from endometrial stromal cells in response to progesterone. We investigated the underlying mechanism by which these stroma-derived, progesterone-induced paracrine factors stimulate HSD17B2 expression. Here, we show that transcription factors SP1 and SP3 interact with specific motifs in HSD17B2 promoter to upregulate enzyme expression in human endometrial epithelial cell lines. Conditioned medium (CM) from progestin-treated stromal cells increased levels of SP1 and SP3 in endometrial epithelial cells and induced HSD17B2 mRNA expression. Mithramycin A, an inhibitor of SP1-DNA interaction, reduced epithelial HSD17B2 promoter activity in a dose-dependent manner. Serial deletion and site-directed mutants of the HSD17B2 promoter demonstrated that two overlapping SP1 motifs (nt -82/-65) are essential for induction of promoter activity by CM or overexpression of SP1/SP3. CM markedly enhanced, whereas anti-SP1/SP3 antibodies inhibited, binding of nuclear proteins to this region of the HSD17B2 promoter. In vivo, we demonstrated a significant spatiotemporal association between epithelial SP1/SP3 and HSD17B2 levels in human endometrial biopsies. Taken together, these data suggest that HSD17B2 expression in endometrial epithelial cells, and, therefore, estrogen inactivation, is regulated by SP1 and SP3, which are downstream targets of progesterone-dependent paracrine signals originating from endometrial stromal cells.

Hormone replacement therapy, C-reactive protein, and fibrinogen in healthy postmenopausal women.

OBJECTIVE: To investigate short-term and long-term effects of combined hormone replacement therapy (HRT) on C-reactive protein (CRP) and fibrinogen plasma concentrations in healthy postmenopausal women. METHODS: In this cross-sectional study 241 healthy postmenopausal women were enrolled. A total of 81 women were receiving the following treatments for 3 months; transdermal 17beta-estradiol (17beta-E2) + medroxyprogesterone acetate (MPA) (n = 21), oral 17beta-E2 + norethisterone acetate (NETA) (n = 27), and conjugated equine estrogens (CEE) + MPA (n = 33). The same combined therapies were implemented in another 58 women for 12 months; transdermal 17beta-E2 + MPA (n = 10), oral 17beta-E2 + NETA (n = 16), and CEE + MPA (n = 32). Control group included 102 healthy postmenopausal women not receiving HRT. The effect of the type and the duration of HRT regimens on plasma levels of CRP, fibrinogen and lipids were investigated. RESULTS: Median CRP concentrations were significantly higher in women receiving oral 17beta-E2 + NETA (P = 0.037) and CEE + MPA (P = 0.0001) for 3 months than in women taking the same types of HRT for 12 months and of those were not on HRT. Median CRP levels were similar in women taking transdermal 17beta-E2 + MPA for 3 and 12 months, compared with controls. Fibrinogen levels were not different between nonusers and any group of HRT users. CONCLUSIONS: These elevated levels of CRP, which appears very recently as a crucial marker for cardiovascular disease, may be responsible for the early increased cardiovascular risk after starting oral combined HRT. But this increased risk in the early period seems to decrease with long-term use. Transdermal 17beta-E2 + MPA had insignificant effect on CRP both in short-term or in long-term use.

Ovarian abscess due to Brucella melitensis.

The case of a 25-y-old woman with brucellar ovarian abscess is reported. Cultures of blood, ascites and a pus specimen yielded Brucella melitensis. The possibility of ovarian abscess being caused by Brucella melitensis should be considered in countries where the infection is endemic.

Decreased total antioxidant status and increased oxidative stress in women with polycystic ovary syndrome may contribute to the risk of cardiovascular disease.

OBJECTIVE: To determine oxidative stress by the level of protein carbonyls and total antioxidant status (TAOS), and whether oxidative stress is associated with increased risk of cardiovascular disease in women with polycystic ovary syndrome (PCOS). DESIGN: Controlled clinical study. SETTING: University hospital. PATIENT(S): Thirty women with PCOS and 31 healthy control women. INTERVENTION(S): Biometric measures and blood samples collection. MAIN OUTCOME MEASURE(S): C-reactive protein (CRP), lipid fractions, glucose, protein carbonyls, insulin, and other hormone (gonadotropins, androgens) levels and TAOS were measured. The estimate of insulin resistance was calculated by homeostasis model assessment (HOMA-R). RESULT(S): The women with PCOS had significantly higher serum fasting insulin, CRP, protein carbonyl levels, HOMA-R, LH levels, and LH/FSH ratios than healthy women. However, TAOS was significantly lower in women with PCOS. TAOS was negatively correlated with fasting insulin, HOMA-R, CRP, and protein carbonyls. Fasting insulin was positively correlated with protein carbonyls. High density lipoprotein (HDL) was inversely associated with fasting insulin, HOMA-R, and protein carbonyls. CONCLUSION(S): Increased oxidative stress and decreased antioxidant capacity may contribute to the increased risk of cardiovascular disease in women with PCOS, in addition to known risk factors such as insulin resistance, hypertension, central obesity, and dyslipidemia.

The short-term effects of different regimens of hormone replacement therapy on left ventricular structure and performance in healthy postmenopausal women. A prospective, controlled echocardiographic study.

OBJECTIVE: To compare the short-term effects of different hormone replacement therapy (HRT) regimens on left ventricular structure and function in healthy postmenopausal women. METHODS: Forty-two apparently healthy postmenopausal women were evaluated prospectively in this controlled study. Subjects were divided into 4 groups. Ten subjects, who did not accept HRT or any other treatments, formed the control group. The remaining subjects were assigned to receive oral estradiol (2 mg/day) + norethisterone acetate (1 mg/day) (n = 11), transdermal estradiol (0.05 mg) + norethisterone acetate (0.25 mg) (n = 11) or tibolone (2.5 mg/day) (n = 10) therapy during 12 weeks. Echocardiography and Doppler techniques were used to assess the cardiac effects of different HRT regimens. RESULTS: After 12 weeks of treatment, there were significant increases in left ventricular ejection fraction (transdermal group: p = 0.008, oral group: p = 0.003, tibolone group: p = 0.005) and cardiac output (transdermal group: p = 0.003, oral group: p = 0.003, tibolone group: p = 0.021) in all treatment groups. In addition, in the transdermal group, a slight increase in left ventricular end-diastolic volume was significant (p = 0.046). CONCLUSION: These data suggest that oral and transdermal HRT regimens and tibolone may contribute to the improvement in left ventricular systolic function without having an effect on left ventricular structure after short-term administration in healthy postmenopausal women.

Association of serum complement (C3, C4) and immunoglobulin (IgG, IgM) levels with hormone replacement therapy in healthy post-menopausal women.

BACKGROUND: Recently published data suggest that hormone replacement therapy (HRT) may increase cardiovascular risk during the early months of therapy. Activation of the immune system is known to be involved in several types of cardiovascular disease. In this cross-sectional study, serum C3, C4, IgG and IgM levels were evaluated in healthy post-menopausal women receiving two different short-term HRT regimens, and in untreated women. METHODS: Serum C3, C4, IgM and IgG levels were assessed in 18 women receiving transdermal 17beta-estradiol (50 micro g/day) + continuous oral medroxyprogesterone acetate (MPA; 2.5 mg/day), in 56 women taking oral conjugated equine estrogen (CEE; 0.625 mg/day) + continuous MPA, and in 80 control women not receiving HRT. RESULTS: The mean serum C3 level was significantly higher in women using oral CEE + MPA than in women receiving transdermal 17beta-estradiol + MPA, and those not on HRT (P = 0.02 and P < 0.001 respectively). Furthermore, women taking oral CEE + MPA had significantly higher mean levels of C4 compared with untreated women (P < 0.01). IgG and IgM levels were similar among women either of the two HRT regimens and between women not on HRT. CONCLUSIONS: Oral HRT may be involved in the development of cardiovascular disease through inflammatory mechanisms, as suggested by increased serum levels of C3 and C4.

Effects of short-time (3 months) tibolone treatment on bone turnover in postmenopausal women.

This study was planned to elucidate the effects of tibolone on bone biochemistry parameters in postmenopausal women at 3 month intervals. There were 56 healthy postmenopausal women enrolled in the study. The women had not received hormone replacement therapy (HRT) previously. Tibolone (2.5 mg/day) was prescribed for 3 months. Serum osteocalcin, calcium, phosphorus, alkaline phosphatase, creatinine and urine calcium, phosphorus creatinine, deoxypyridinoline were measured, and physical examinations were performed at the onset and at the end of the study. The mean serum osteocalcin level and deoxypyridinoline/creatinine (DPD/cr) ratio both decreased significantly (50.3% and 22.9%; P=0.012 and P=0.001, respectively). The slight decreases in serum alkaline phosphatase (4.5%) and urine calcium (13.6%) levels were not statistically significant. There was a positive correlation between DPD/cr and urine calcium ( r=0.66, P=0.001). We conclude that bone formation may be increased early by tibolone after short-term administration.

Effects of short-term transdermal hormone replacement therapy on glycaemic control, lipid metabolism, C-reactive protein and proteinuria in postmenopausal women with type 2 diabetes or hypertension.

BACKGROUND: The study was carried out to evaluate the effects of short-term transdermal hormone replacement therapy (HRT) on glycaemic control, lipid metabolism, C-reactive protein (CRP) and proteinuria in high-risk postmenopausal women. METHODS: A total of 20 well-controlled type 2 diabetic, hypertensive and 21 well-controlled glucose-tolerant, hypertensive postmenopausal women were prospectively enrolled. After 12 weeks of transdermal HRT, the changes in serum lipid sub-fractions, fasting glucose, fructosamine, glycated haemoglobin (HbA(1c)), CRP, creatinine, 24 h urine protein levels, creatinine clearance and blood pressure were evaluated. RESULTS: After 12 weeks of treatment, serum total-cholesterol and low-density cholesterols (LDL-cholesterol) appeared slightly reduced and serum triglyceride slightly elevated, although non-significantly so in both groups. The increase in HDL-cholesterol (P < 0.05) and reduction in very low density (VLDL)-cholesterol (P < 0.05) levels were significant in hypertensive patients. Elevation in the Apolipoprotein A1 (P < 0.05) and reduction in the Apolipoprotein B (P < 0.05) levels were statistically significant in all patients. HRT was associated with significant decreases in serum fasting glucose (P < 0.05) and fructosamine (P < 0.05) levels in diabetic patients. Serum HbA(1c), CRP, creatinine, 24 h urine protein levels, creatinine clearance and systolic and diastolic blood pressure did not change significantly in either group. CONCLUSIONS: There were no detrimental effects of transdermal HRT on lipid profile, glucose metabolism, CRP and urine protein levels in our well-controlled diabetic or hypertensive patients. A decision regarding HRT use should be taken on a case-by-case basis.

QT dispersion in patients with polycystic ovary syndrome.

Cardiac risk factors are observed more frequently in patients with polycystic ovary syndrome (PCOS). On the other hand, increased QT dispersion, which is a risk factor for cardiac arrhythmias and sudden death, has not been investigated in this syndrome. In this study, we evaluated QT dispersion in PCOS patients without overt heart disease. Thirty-six consecutive women with PCOS (mean age 24+/-5 years) and 36 healthy women of similar ages (mean age 24+/-4 years) participated in this study. PCOS was diagnosed if there were polycystic ovaries by ultrasound (enlarged ovaries with > or =8 cysts 2-8 mm in diameter), oligoamenorrhea (intermenstrual interval >35 days), hirsutism (Ferriman-Gallwey score, > or =7) and elevated serum levels of testosterone (> or =2.7 nmol/L). Electrocardiograms were recorded at a paper speed of 50 mm/s. QT intervals were manually measured by a cardiologist. All intervals were corrected for heart rate according to Bazett's formula: QTc interval=QT interval/square root of the RR interval. Mean values of body mass index, heart rate, and blood pressure were not significantly different between the two groups (P>0.05). No significant differences in QT intervals (maximum QT, minimum QT, QT dispersion, minimum corrected QT, maximum corrected QT, and corrected QT dispersion) were observed between the two groups (P>0.05). Our results suggest that the risk of ventricular arrhythmias or sudden cardiac death is not increased in PCOS patients.