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Biomedical subjects

Sophia N Kalantaridou

Publications and source records attributed to Sophia N Kalantaridou.

13 recordsLinked to original sources
PubMed2007

Combined thrombophilic mutations in women with unexplained recurrent miscarriage.

PROBLEM: To compare the prevalence of five common thrombophilic polymorphisms and their combination in women with recurrent miscarriage and a control group. METHOD OF STUDY: Genomic analysis using polymerase chain reaction (PCR) was carried out in patients with two or more miscarriages and controls for Factor V Leiden, Factor V A1299H (HR2), Factor II G20210A, MTHFR C677T and MTHFR A1298C. Secondary analyses were made for number of miscarriages and gestational age at miscarriage. RESULTS: None the mutations was associated with significantly increased risk for recurrent miscarriage. The prevalence of combined thrombophilias (4/88 versus 2/88) did not increase the risk for miscarriage (OR 2.04, 95% CI 0.36-11.47). Although virtually all patients with thrombophilia had miscarriages 10 weeks' subgroup. There was no difference in the distribution of Factor V Leiden (P=1.000), FII G20210A (P=0.652), and MTHFR C677T (P=0.869) between patients with two and three or more miscarriages, whereas MTHFR A1298C was more common among patients with two miscarriages (P=0.017). CONCLUSIONS: Combinations of the five thrombophilic mutations studied are an uncommon event with heterogeneous pattern and they do not significantly increase the risk for miscarriage.

Abortion, Habitual↗
PubMed2006

Hormonal and cytokine regulation of early implantation.

Implantation of the blastocyst into the endometrium is a delicately controlled process and a prerequisite for the furtherance of the mammalian species. A complex network of molecules is involved in preparing both the endometrium and blastocyst for a successful interaction. However, the exact molecular steps are poorly understood. Studies so far have shown that disruption of certain pathways results in fertility defects. Impaired implantation is currently considered to be the most important limiting factor for the establishment of viable pregnancies in assisted reproduction. It is expected that elucidating the molecular background of the process will enable accurate diagnosis and effective treatment of infertility.

Animals↗
PubMed2006

Premature ovarian failure, endothelial dysfunction and estrogen-progestogen replacement.

Cardiovascular disease, including coronary artery disease, stroke and peripheral vascular disease, is the leading cause of death among women. Vascular endothelial dysfunction is an early marker of atherosclerosis. Women with premature ovarian failure (or premature menopause) present an increased risk for cardiovascular disease, which might be attributed to the early onset of vascular endothelial dysfunction, associated with sex steroid deficiency. Cyclical estrogen and progestogen therapy has been shown to restore endothelial function in these young women. Further research is required to assess primarily the long-term effects of hormone replacement therapy on cardiovascular and overall prognosis in young women with premature ovarian failure, as well as the effects of different doses, duration and routes of hormone administration in these women.

Adult↗
PubMed2006

Testosterone deficiency in young women with 46,XX spontaneous premature ovarian failure.

OBJECTIVE: To determine whether women with 46,XX spontaneous premature ovarian failure have lower serum free-T levels than do control women. DESIGN: Cross-sectional. SETTING: National Institutes of Health Clinical Research Center. PATIENT(S): Women with 46,XX spontaneous premature ovarian failure (n = 130). INTERVENTION(S): Evaluation while off any estrogen therapy and then again after receiving a standardized hormone regimen. Regularly menstruating control women (n = 65) were sampled during the midfollicular phase. MAIN OUTCOME MEASURE(S): Serum total T by RIA after extraction and column chromatography, free T by equilibrium dialysis, and sex hormone-binding globulin by immunoradiometric assay. RESULT(S): While off estrogen therapy patients had a median serum free-T concentration that was statistically significantly lower than controls (2.2 vs. 3.3 pg/mL). This dropped significantly lower to 1.9 pg/mL while the patients were on physiologic transdermal E(2) therapy. This is despite the fact that sex hormone-binding globulin levels did not change. While on E(2) therapy, 13% of women (95% confidence interval, 7.9%-20.3%) had serum free-T levels below the lower limit of normal (<1.1 pg/mL). CONCLUSION(S): As a group, young women with 46,XX spontaneous premature ovarian failure have reduced circulating free-T levels, both during an interval off of estrogen therapy and while on physiologic transdermal E(2) therapy.

Chromosomes, Human, X↗
PubMed2006

Testosterone therapy in premenopausal women.

Testosterone therapy for postmenopausal women and women with surgical menopause, albeit controversial, is becoming more widespread. However, only limited data are available to support its use in premenopausal women. Androgens have important biological roles in young women, influencing bone and muscle mass, mood and well-being, and libido. Pathophysiological states affecting ovarian and adrenal function or both may result in androgen deficiency in premenopausal women. Young women with hypothalamic amenorrhea, premature ovarian failure, oophorectomy, premenstrual syndrome, acquired immunodeficiency wasting syndrome, adrenal insufficiency, and hypopituitarism may have testosterone deficiency. Young women with loss of libido may also have testosterone deficiency. Medications that may lead to testosterone insufficiency include oral estrogen, oral contraceptives, and corticosteroids. Testosterone deficiency in young women may be underdiagnosed because the symptoms generally are nonspecific and the measurement of total and free testosterone is inaccurate with commonly used techniques. Only a few studies investigating the effects of testosterone therapy have been performed thus far in premenopausal women. Long-term trials evaluating safety and effectiveness of testosterone therapy in premenopausal women are lacking. Common adverse effects include hirsutism and acne, which reverse with discontinuation of treatment. The availability of testosterone regimens specifically designed for women is expected to help maintain testosterone levels within the normal range and clarify whether the apparent beneficial effects of testosterone therapy are physiological or pharmacological.

Adult↗
PubMed2006

Corticotropin-releasing hormone modulates human trophoblast invasion through carcinoembryonic antigen-related cell adhesion molecule-1 regulation.

Abnormalities in the process of trophoblast invasion may result in abnormal placentation. Both the embryonic trophoblast and maternal decidua produce corticotropin-releasing hormone (CRH), which promotes implantation. Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1), which is expressed in extravillous trophoblasts (EVTs) of normal human placenta, may also function in tro-phoblast/endometrial interactions. We investigated whether locally produced CRH plays a role in trophoblast invasion, primarily by regulating CEACAM1 expression. We examined cultures of freshly isolated human EVTs, which express CEACAM1, and an EVT-based hybridoma cell line, which is devoid of endogenous CEACAM1. CRH inhibited EVT invasion in Matrigel invasion assays, and this effect was blocked by the CRH receptor type 1 (CRHR1)-specific antagonist antalarmin. Additionally, CRH decreased CEACAM1 expression in EVTs in a dose-dependent manner. After transfection of the hybridoma cell line with a CEACAM1 expression vector, the invasiveness of these cells was strongly enhanced. This effect was inhibited by addition of blocking monoclonal antibody against CEACAM1. Furthermore, blocking of endogenous CEACAM1 in EVTs inhibited the invasive potential of these cells. Taken together these findings suggest that CRH inhibits trophoblast invasion by decreasing the expression of CEACAM1 through CRHR1, an effect that might be involved in the pathophysiology of clinical conditions, such as preeclampsia and placenta accreta.

Antigens, CD↗
PubMed2005

A pilot study of an investigational testosterone transdermal patch system in young women with spontaneous premature ovarian failure.

CONTEXT: Evidence suggests that young women with spontaneous premature ovarian failure (sPOF) have significantly lower androgen levels than age-matched regularly menstruating women. OBJECTIVE: The objective of the study was to evaluate an investigational testosterone transdermal patch (TTP) designed to deliver the normal ovarian production rate of testosterone. DESIGN: This was an open-label study (2-month baseline period followed by 2-month treatment period). PATIENTS: Nine women with sPOF and a history of regular bleeding patterns on standard estrogen/progestogen cyclic treatment participated in the study. One subject with abnormal baseline levels was excluded. INTERVENTION: Four consecutive 28-d cycles of transdermal estradiol (E2; 0.1 mg/d) and sequential oral medroxyprogesterone acetate (MPA; 10 mg/d for the last 12 d of each cycle). During cycles 3 and 4, an investigational TTP (nominal delivery 150 microg/d) was applied twice weekly to the abdomen. MAIN OUTCOME MEASURES: Steady-state pharmacokinetic profiles of free and total testosterone and scheduled vaginal bleeding patterns were studied. RESULTS: The mean (95% confidence interval) of the time-average free testosterone levels during TTP treatment was 7.5 (4.9-9.9) pg/ml; 26.0 (17.2-34.6) pmol/liter (with E2), and 6.9 (4.9-8.8) pg/ml; 23.9 (17.2-30.5) pmol/liter (with E2 and MPA). The confidence intervals of the means include the upper limit of normal for premenopausal women, i.e. 6.8 pg/ml (23.5 pmol/liter), although the mean values are slightly above this. CONCLUSIONS: The addition of TTP to cyclic E2/MPA therapy in women with sPOF produced mean free testosterone levels that approximate the upper limit of normal. A 3-yr study to assess safety and effectiveness in this population is in progress.

Administration, Cutaneous↗
PubMed2005

Predictors of endothelial dysfunction in young women with polycystic ovary syndrome.

CONTEXT: Women with polycystic ovary syndrome (PCOS) may be at increased risk for cardiovascular disease. Endothelial dysfunction is an early marker of atherosclerosis. OBJECTIVES: The objectives of this study were to 1) compare endothelial function in young women with PCOS and regularly menstruating control women, and 2) to identify the determinants of endothelial function and investigate its relationship with body mass index in women with PCOS. DESIGN: This was a cross-sectional study. SETTING: This study was conducted at a tertiary cardiovascular research center. PATIENTS: Sixty-two young women with PCOS (mean age, 22.7 yr) and 17 control women, matched as a group for age and body mass index, were studied. Twenty-three women with PCOS were lean, 21 were overweight, and 18 were obese. MAIN OUTCOME MEASURES: Endothelium-dependent and -independent vascular function was assessed by measuring flow-mediated dilation (FMD) and nitrate-mediated dilation in the brachial artery (diameter change during hand hyperemia and after sublingual glyceryl trinitrate administration, respectively). RESULTS: FMD and nitrate-mediated dilation were significantly lower in PCOS than in control women (reduced by approximately 50 and 25%, respectively; both P < 0.0005). Insulin resistance, total testosterone, and total cholesterol were independent predictors of FMD, accounting for 21, 10, and 9% of the variance, respectively (P < 0.005 for all). A trend of deterioration in FMD from lean to overweight and obese PCOS women was observed, but differences among groups were not statistically significant. CONCLUSIONS: Women with PCOS have significant endothelial dysfunction at an early age (i.e. early 20s), and largely independent of obesity. This suggests that women with PCOS are at increased risk for early onset cardiovascular disease and may gain particular benefit from measures to improve endothelial function.

Adult↗
PubMed2004

Reproductive functions of corticotropin-releasing hormone. Research and potential clinical utility of antalarmins (CRH receptor type 1 antagonists).

BACKGROUND: The hypothalamic-pituitary-adrenal (HPA) axis exerts a complex, mostly inhibitory, effect on the female reproductive system. In addition, the principal regulator of this axis, the hypothalamic neuropeptide corticotropin-releasing hormone (CRH) and its receptors have been identified in most female reproductive tissues, including the ovary, uterus, and placenta. Furthermore, CRH is secreted in peripheral inflammatory sites where it exerts strong inflammatory actions. Antalarmins (CRH receptor type 1 antagonists) have been used to elucidate the roles of CRH in stress, inflammation and reproduction. METHOD OF STUDY: We review existing data on the effects of CRH in the female reproductive system. RESULTS: Ovarian CRH participates in female sex steroid production, follicular maturation, ovulation and luteolysis. Uterine CRH participates in decidualization, implantation, and early maternal tolerance. Placental CRH participates in the physiology of pregnancy and the onset of parturition. Circulating placental CRH is secreted mostly during the latter half of pregnancy and is responsible for the concurrently increasing physiologic hypercortisolism of this period. After labor and delivery, this hypercortisolism is ensued by a transient suppression of hypothalamic CRH secretion, which may explain the postpartum blues and depression and the increased autoimmune manifestations depression of period, the postpartum period. CONCLUSIONS: These data show that CRH is present in female reproductive tissues, and is regulating key reproductive functions with an inflammatory component, such as ovulation, luteolysis, implantation, and parturition.

Animals↗
PubMed2004

Impaired endothelial function in young women with premature ovarian failure: normalization with hormone therapy.

Normal menopause is associated with vascular endothelial dysfunction, an early stage of atherosclerosis. The effect of premature ovarian failure (or premature menopause) on endothelial function in young women is unknown. Endothelial function was assessed in 18 women with premature ovarian failure before and after 6 months of hormone therapy and was compared with the endothelial function of 20 age- and body mass index-matched premenopausal women. Brachial artery diameter was measured both during hyperemia (an index of endothelium-dependent vasodilation) and in response to glyceryl trinitrate (an index of endothelium-independent vaso-dilation). Flow-mediated dilation was significantly lower in women with premature ovarian failure at baseline (increase in brachial artery diameter during hyperemia by 3.06 +/- 4.33%) than in control women (increase by 8.84 +/- 2.15%; P < 0.0005). Glyceryl trinitrate-induced vasodilation did not differ between the groups. After hormone therapy for 6 months, flow-mediated dilation was improved in women with premature ovarian failure, increasing by more than 2-fold (7.41 +/- 3.86%; P < 0.005 compared with pretreatment) and reaching normal values (P not significant compared with control women). Glyceryl trinitrate-induced vasodilation did not change after treatment in women with premature ovarian failure. Young women with premature ovarian failure have significant vascular endothelial dysfunction. Early onset of endothelial dysfunction associated with sex steroid deficiency may contribute to the increased risk of cardiovascular disease and mortality in young women with premature ovarian failure. Hormone therapy restores endothelial function within 6 months of treatment.

Adult↗
PubMed2003

Ovarian antibodies as detected by indirect immunofluorescence are unreliable in the diagnosis of autoimmune premature ovarian failure: a controlled evaluation.

BACKGROUND: Ovarian antibodies as detected by indirect immunofluorescence have been used to detect ovarian autoimmunity, but to our knowledge the rate of false positive findings using this method has never been reported. METHODS: Here we examine whether a commercially available ovarian antibody test system, using cynomologous monkey ovary, might be useful in the diagnosis of autoimmune premature ovarian failure. The test was performed in a blinded manner in 26 young women with 46,XX spontaneous premature ovarian failure, in 26 control women with regular menstrual cycles (matched for age, race, and parity) and 26 control men (matched for age and race). We also compared the frequency of other autoantibodies associated with ovarian autoimmunity. RESULTS: As a group young women with premature ovarian failure had an increased incidence of thyroid and gastric parietal cell autoimmunity (p < 0.05). Unexpectedly, however, nearly one third (31%) of normal control women had ovarian antibodies using the commercially available test. One half of young women with premature ovarian failure were found to have ovarian antibodies (P = 0.26). In our own laboratory we found similar results and we were unable to improve the specificity of the test. None of 26 men were found to have ovarian antibodies (P < 0.001). CONCLUSION: Since approximately one third of normal women were found to have ovarian antibodies using the system under study, we conclude that ovarian antibodies as detected by this indirect immunofluorescence method have poor specificity. The specificity of any ovarian antibody test should be established before it is used clinically.

Journal Article↗
PubMed2003

Roles of reproductive corticotropin-releasing hormone.

Corticotropin-releasing hormone (CRH), the principal regulator of the hypothalamic-pituitary-adrenal axis, as well as its receptors, have been identified in most female reproductive tissues, including the uterus, placenta, and ovary. Endometrial CRH may participate in decidualization, implantation, and early maternal tolerance; placental CRH may participate in the physiology of pregnancy and the onset of parturition, and ovarian CRH may participate in follicular maturation, ovulation, and luteolysis. The hypercortisolism of the latter half of pregnancy can be explained by increased levels of placental CRH in plasma. This hypercortisolism is followed by a transient suppression of hypothalamic CRH secretion in the postpartum period, which may explain the blues or depression and autoimmune phenomena frequently observed during this period.

Animals↗