Gynecologic problems among elderly women in comparison with women aged between 45-64 years.

BACKGROUND: As women age, they face a variety of co-morbid medical problems as well as gynecologic problems that may differ from those of younger women. Clinicians should know how to screen and manage those problems among elderly women. OBJECTIVE: With this background, the study was designed to assess the gynecologic problems on admission among elderly women and women aged between 45-64 years. METHODS: A retrospective analysis of symptom distribution of 200 women aged over 65 years and 200 women aged between 45-64 years from January 1999 to December 2003 was performed in an university clinic. PARTICIPANTS: Geriatric women and women aged between 45-64 years with gynecologic complaints on admission to outpatient clinics between January 1999 and December 2003. Analyses of demographic data and data related to symptom distribution, using appropriate parametric and non-paramertic statistical tests, were performed. RESULTS: Geriatric women had a higher number of pregnancies (p < 0.01) but lower percentage of hormone replacement therapy use (p < 0.1) compared to women aged 45-64 years. No significant difference was observed in terms of the age at menopause. Vaginal fullness was felt most commonly by elderly women (p < 0.01) in contrast to menopausal vasomotor symptoms which were relevant in the younger age group (p < 0.01). As a clinical diagnosis, pelvic relaxation with uterine prolapse and genital malignancies were the common two diagnoses among geriatric women (p < 0.05). Postmenopausal vaginal bleeeding was observed more often among geriatric women compared to women aged 45-64 years (19.5% vs 12%, p = 0.03). Endometrial and ovarian cancer distribution did not differ among the two groups when the initial complaint was postmenopausal bleeding. CONCLUSION: Type and management of gynecologic problems in women aged over 65 can be challenging and differ from those for younger women. Thus, caring for these women in their reproductive years as well as in later life should be an aim for all obstetrician-gynecologists.

A ten-year gestational diabetes mellitus cohort at a university clinic of the mid-Anatolian region of Turkey.

OBJECTIVE: The study attempts to analyze a 10-year retrospective cohort of gestational diabetes mellitus (GDM) cases, elucidating the maternal complications and perinatal morbidity and mortality. STUDY DESIGN: The study participants were 110 diabetic singleton pregnancies receiving obstetric care at the Department of Obstetrics and Gynecology, Osmangazi University School of Medicine in Eskisehir, Turkey from January 1995 to December 2004. In 70 of the GDM cases, mean age, diagnostic criteria used to define GDM, gestational age at delivery, presence of additional risk factors, method of clinical management, mode of delivery, fetal birthweights and newborn characteristics were assessed. RESULTS: The prevalence of GDM in the past ten-year period was 3.1% (110/3548). Mean age of enrolled GDM cases was 32.6 +/- 5.3 years. With regard to diagnostic criteria of GDM, 24 (37.1%) cases were diagnosed based on a 100 g, three-hour oral glucose tolerance test (OGTT), while 18 (25.7%) cases were referred to our unit without any information on the specific criteria of GDM diagnoses. In less than a third of the cases (25.7%), a one-hour 50 g glucose challenge test (GCT) resulted > or =185 mg/dl completing the diagnoses. More than half of the cases (57.1%) revealed controlled glucose homeostasis on diet, while 30 (42.9%) pregnant women needed insulin therapy to control blood glucose levels to within normal physiologic limits. Fetal macrosomia was present in 18 (25.7%) pregnancies. Meanwhile, most of the fetuses (62.9%) were within the normal growth percentiles throughout the pregnancy. There was no difference detected in body mass index (BMI) of women undergoing cesarean section and spontaneous vaginal births (25.1 +/- 1.2 vs 26.2 +/- 2.3 kg/m2, respectively, p = 0.45). Vacuum extraction and forceps applications were indicated in 10% of all GDM groups. Fetuses born to women having cesarean section were heavier at birth compared to those of women having vaginal births (3940 +/- 320 g vs 430 +/- 117 g, p = 0.08) Most frequent neonatal morbidity was hyperbilirubinemia in 25 (35.7%) newborns. Interestingly, of those women with GDM, only ten (14.3%) cases consented to follow-up evaluation of glucose intolerance between six and eight weeks postpartum. CONCLUSIONS: Proposed risks from abnormal glucose intolerance in pregnancy are multiple. Early diagnosis, patient education, proper follow-up and postpartum testing in women with GDM will certainly decrease poor perinatal outcomes, enabling also a secondary prevention of type 2 diabetes in the long term.

Antioxidant effect of taurine against lead-induced oxidative stress.

Oxidative stress is proposed as a molecular mechanism in lead toxicity, which suggests that antioxidants might play a role in the treatment of lead poisoning. The present study was designed to investigate whether taurine has a beneficial effect both on Chinese hamster ovary (CHO) cells and on Fisher 344 (F344) rats following lead exposure. Therefore, oxidative stress parameters (glutathione, malondialdehyde levels, catalase, and glucose-6-phosphate dehydrogenase [G6PD] activities) of lead-exposed CHO cells and F344 rats were determined following taurine treatment. Taurine was found to be effective in (1) increasing glutathione levels that had been diminished by lead; (2) reducing malondialdehyde levels, an end-product of lipid peroxidation; (3) decreasing catalase and erythrocyte G6PD activity, which had been increased by lead exposure; and (4) improving cell survival of CHO cells. However, taurine had no effect on blood and tissue lead levels when 1.1 g/kg/day taurine was administered to F344 rats for 7 days, following 5 weeks of lead exposure (2,000 ppm lead acetate). As a result, taurine seems to be capable of fortifying cells against lead-induced oxidative attack without decreasing lead levels. Therefore, administration of taurine, accompanied by a chelating agent, might increase its effectiveness in the treatment of lead poisoning.

Can antioxidants be beneficial in the treatment of lead poisoning?

Recent studies have shown that lead causes oxidative stress by inducing the generation of reactive oxygen species, reducing the antioxidant defense system of cells via depleting glutathione, inhibiting sulfhydryl-dependent enzymes, interfering with some essential metals needed for antioxidant enzyme activities, and/or increasing susceptibility of cells to oxidative attack by altering the membrane integrity and fatty acid composition. Consequently, it is plausible that impaired oxidant/antioxidant balance can be partially responsible for the toxic effects of lead. Where enhanced oxidative stress contributes to lead-induced toxicity, restoration of a cell's antioxidant capacity appears to provide a partial remedy. Several studies are underway to determine the effect of antioxidant supplementation following lead exposure. Data suggest that antioxidants may play an important role in abating some hazards of lead. To explain the importance of using antioxidants in treating lead poisoning the following topics are addressed: (i) Oxidative damage caused by lead poisoning; (ii) conventional treatment of lead poisoning and its side effects; and (iii) possible protective effects of antioxidants in lead toxicity.

Antioxidant role of alpha-lipoic acid in lead toxicity.

The assumption of oxidative stress as a mechanism in lead toxicity suggests that antioxidants might play a role in the treatment of lead poisoning. The present study was designed to investigate the efficacy of lipoic acid (LA) in rebalancing the increased prooxidant/antioxidant ratio in lead-exposed Chinese hamster ovary (CHO) cells and Fischer 344 rats. Furthermore, LA's ability to decrease lead levels in the blood and tissues of lead-treated rats was examined. LA administration resulted in a significant improvement in the thiol capacity of cells via increasing glutathione levels and reducing malondialdehyde levels in the lead-exposed cells and animals, indicating a strong antioxidant shift on lead-induced oxidative stress. Furthermore, administration of LA after lead treatment significantly decreased catalase and red blood cell glucose-6-phosphate dehydrogenase activity. In vitro administration of LA to cultures of CHO cells significantly increased cell survival, that was inhibited by lead treatment in a concentration-dependent manner. Administration of LA was not effective in decreasing blood or tissue lead levels compared to a well-known chelator, succimer, that was able to reduce them to control levels. Hence, LA seems to be a good candidate for therapeutic intervention of lead poisoning, in combination with a chelator, rather than as a sole agent.

Captopril as an antioxidant in lead-exposed Fischer 344 rats.

Recent studies suggest that lead induces oxidative stress in various tissues. Captopril ([2S]-1-[3-mercapto-2-methylpropionyl]-L-proline), an angiotensin-converting enzyme inhibitor, is a well-known antihypertensive agent and is also believed to function as an antioxidant. In the present study the antioxidant effect of captopril on lead-induced oxidative stress was studied in Fischer 344 rats. Their liver, brain and kidneys were assayed for glutathione (GSH), glutathione disulfide (GSSG), malondialdehyde concentrations, and catalase activities. The results from animals treated with captopril were compared to results of control and lead-exposed non-treated groups. The captopril-treated samples showed higher GSH:GSSG ratios in the liver, brain and kidneys, as well as slightly decreased malondialdehyde concentrations. The catalase activity was not significantly affected.

Effects of some sulfur-containing antioxidants on lead-exposed lenses.

Lead (Pb) is known to negatively affect glutathione (GSH) metabolism in the lens. The present study examined the effects of Captopril, Taurine, and alpha-Lipoic acid on the Pb-induced GSH depletion and lipid peroxide increase in the lenticular system. Captopril administration returned the GSH, cysteine (CYS), and malondialdehyde (MDA) levels to near normal. Following Taurine administration the GSH, CYS and MDA levels were intermediate between the control group and the Pb group levels. Alpha-Lipoic acid administration, however, only increased the CYS levels. No significant changes in oxidized glutathione (GSSG) levels were observed in any treatment group.

Effects of N-acetylcysteine and 2,3-dimercaptosuccinic acid on lead induced oxidative stress in rat lenses.

Lead (Pb) is known to disrupt the pro-oxidant/anti-oxidant balance of tissues which leads to biochemical and physiological dysfunction. The present study investigated the effects of exposure on the redox status of the lenses of Fisher 344 rats and examined whether antioxidant or chelator administration reversed these changes. Animals were given 5 weeks of 2000 ppm Pb exposure followed by 1 week of either antioxidant, chelator or distilled water administration. Glutathione (GSH) and cysteine (CYS) levels decreased in the Pb-exposed group. N-acetylcysteine or 2,3-dimercaptopsuccinic acid (Succimer) supplementation following Pb intoxication resulted in increases in the GSH and CYS levels. Protein bound glutathione (PSSG) and cysteine (PSSC) increased following Pb exposure. In the Succimer-treated animals, the PSSG decreased significantly. The glutathione disulfide (GSSG) levels remained unchanged. Malondialdehyde (MDA) levels, a major lipid peroxidation byproduct, increased following Pb exposure and decreased following Succimer treatment. Our results suggest that antioxidant supplementation, as well as chelation, following Pb exposure may enhance the reductive status of lenses.

Antioxidant effects of N-acetylcysteine and succimer in red blood cells from lead-exposed rats.

This study examined whether lead-induced alterations in selected parameters that are indicative of oxidative stress accompany the toxic effects of lead in red blood cells (RBCs) in vivo. It also explored the possibility that treatment with N-acetylcysteine (NAC) or succimer (meso-2,3-dimercaptosuccinic acid) was capable of reversing parameters indicative of lead-induced oxidative stress. Fisher 344 rats were given 2000 ppm lead acetate in their drinking water for 5 weeks. The lead was then removed and the animals were given NAC (800 mg/kg/day) or succimer (90 mg/kg/day) in their drinking water for 1 week, after which the RBCs were harvested. Animals not given lead and those given lead, but not NAC or succimer, served as negative and positive controls, respectively. At the end of the experiment, blood-lead levels were 35 +/- 4 microg/dl in lead-treated animals, which were reduced to 2.5 +/- 1 microg/dl by treatment with succimer and to 25 +/- 3 microg/dl by treatment with NAC. Lead-exposed animals demonstrated signs of anemia as evidenced by anisocytosis, poikilocytosis, and alterations in hemoglobin, hematocrit, and mean corpuscular volume. Lipid peroxidation, as evidenced by increased malondialdehyde (MDA) content, as well as decreases in reduced glutathione (GSH) and increases in catalase and glucose 6-phosphate dehydrogenase (G6PD) activity were noted in RBCs from lead-treated rats, suggesting that the lead induced oxidative stress. In addition, a significant reduction in blood delta-aminolevulinic acid dehydratase (ALAD) activity suggested that accumulation and autooxidation of delta-aminolevulinic acid might contribute to lead-induced oxidative stress. Treatment with either NAC or succimer reversed lead-induced alterations in MDA and GSH content, but only succimer appeared to partially restore ALAD activity. These results provide in vivo evidence supporting the hypothesis that lead induces oxidative stress in RBCs, which is reversible by treatment with a thiol antioxidant (NAC), as well as a chelating agent (succimer).

Pro-oxidant effects of delta-aminolevulinic acid (delta-ALA) on Chinese hamster ovary (CHO) cells.

delta-Aminolevulinic Acid (delta-ALA) is a heme precursor accumulated in lead poisoning and acute intermittent porphyria. Although no single mechanism for lead toxicity has yet been defined, recent studies suggest at least some of the lead-induced damage may originate from delta-ALA-induced oxidative stress. The present study was designed to test the hypothesis that delta-ALA accumulation in Chinese hamster ovary (CHO) cells contributes to the cumulative oxidative challenge of lead poisoning as indicated by the oxidative stress parameters glutathione (GSH), glutathione disulfide (GSSG), malondialdehyde equivalents (MDA), and catalase (CAT). It will also examine the possibility that this oxidative challenge can be reversed by treatment with an antioxidant such as N-acetylcysteine (NAC). First in vitro administration of delta-ALA to CHO cells was found to have a concentration-dependent inhibitory effect on colony formation and cell survival. NAC administration was shown to alleviate this inhibition in CHO survival. The oxidative status of CHO cell cultures exposed to increasing concentrations of delta-ALA was then examined. Decreases in GSH levels (P < 0.05) were observed in the delta-ALA-treated cultures as compared to the controls, while GSSG and MDA levels were significantly increased in delta-ALA-treated cells (P < 0.05). CAT activity was not significantly affected. NAC administration concurrent with delta-ALA exposure resulted in GSH and GSSG levels similar to the control levels, while no significant improvement in MDA was observed. These results indicate a state of oxidative stress and suggest that the delta-ALA- induced inhibitory effect on CHO colony formation may be due to its pro-oxidant effect. To assess whether this oxidative challenge would induce antioxidant increases during extended exposure to delta-ALA, CHO cells were exposed to 5 mM delta-ALA for increasing time periods. The GSH and GSSG levels were measured and a rebound effect was observed after 12 h of delta-ALA exposure.