role of serum adiponectin levels in women with polycystic ovarian syndrome

Background: adiponectin is a recently identified adipocyte-derived collagen-like protein. In humans, adiponectin levels were found to be decreased in obese, compared to normal individuals, whereas high adiponectin levels are independently associated with increased insulin sensitivity. The specific role of adiponectin in these metabolic conditions is not clear: it may have a causative role, or it could be regulated by insulin and serve as a marker for insulin resistance. Adiponectin levels hold great promise for use in clinical applications as a potent indicator of underlying metabolic complications

Aim of the work: the present study was aimed to evaluate the link between adiponectin and polycystic ovarian syndrome [PCOS] and the potential use of adiponectin as a biomarker for PCOS

Patients and methods: the study included 84 female patients presenting to the Reproductive and Infertility Clinics at Ain Shams University Maternity Hospital, starting from June 2016 till January 2017. They were divided into four groups based on the diagnosis of polycystic ovarian syndrome [PCOS]; Cases were selected as: Group I non-obese PCOS group [n = 21], Group II obese PCOS group [n = 21]. Controls were selected as: Group III non-obese control group [n = 21] and Group IV obese control group [n = 21]. All the Control subjects had normal, regular menstruation, normal ovarian findings on ultrasound, and normal luteinizing hormone [LH] and follicle-stimulating hormone [FSH] levels. None displayed hirsutism. PCOS subjects were enrolled when they had satisfied two of the three following inclusion criteria: 1. Oligomenorrhea or amenorrhea. 2. Clinical or biochemical hyperandrogenism. 3. Ultrasonographic polycystic ovarian morphology. Serum adiponectin, metabolic and hormonal parameters were compared in PCOS patients with BMI matched controls. Measurement of plasma adiponectin levels done by Enzyme Immunoassay kit in Ain Shams University Maternity Hospital lab

Results: serum adiponectin level was significantly lower among cases than controls [p value < 0.001]. No significant difference was found between cases and controls regarding their hormonal profile except for testosterone and insulin levels which were significantly higher among cases [p value <0.001]. As regard insulin resistance, there was a significant difference where cases were higher than control [p value <0.001]

Conclusion: it could be concluded that PCOS was found to correlate with low adiponectin levels, independently of BMI. The relationships between adiponectin and insulin resistance and sensitivity, metabolic syndrome, and BMI in women with PCOS suggest that adiponectin potentially could serve as a marker for disease risk and provide opportunity for earlier intervention if knowledge is successfully translated from laboratory to clinical practice

association of angiotensin-1 converting enzyme [ACE] serum level and [I/D] polymorphism in Egyptian preeclamptic women

Preeclampsia [PE] a major cause of maternal and neonatal mortality and morbidity worldwide in which hypertensive disorders during pregnancy account for 25.7% of maternal deaths. Both maternal and fetal genetic factors may predispose towards pre-eclamptic pregnancy, especially severe forms. However, preeclampsia is thought to be the result of the interplay between important genetic components and environmental influences; still, factors and mechanisms that lead to preeclampsia remain mysterious. Insertion/deletion [I/D] polymorphism of ACE gene has attracted significant attention and has been extensively investigated with its serum activity in a spectrum of cardiovascular phenotypes

Aim to study the potential association of I/D polymorphism of ACE gene in PE Egyptian women that gets us closer to understanding the disease

Patients and Methods: one hundred hypertensive and age-matched normotensive primigravida were recruited from Minufiya university Hospital. Routine investigations were done for PE diagnosis. DNA was extracted from whole blood of patients and healthy controls. All samples were genotyped for ACE I/D polymorphism according to Rigat et al. using amplification and PCR of known allelic variants. ACE genotype was identified and followed by serum concentration of ACE activity for both groups

Results: ACE DD genotype was found in 60% of PE patients while 34% of normotensive subjects [P 0.05], although D allele was higher among cases than controls, but it did not show significance [P > 0.05]. High significance was revealed when comparing the mean total ACE activity in the hypertensive patients [32.74 IU/l] and normotensive subjects [28.06 IU/l] [P <0.001]. The ACE activity in cases and controls carrying DD allele differed significantly [P<0.001]. In contrast the other ACE genotype ID and II did not show significance between cases and controls

Conclusion: these findings might bear implications for precise management of pregnancy in high-risk DD genotype women. Further large scale evaluation was required to provide added marker for risk assessment for PE patients

Serum and ascitic fluid leptin levels in cirrhotic patients: relation to other clinicopathologic parameters

Leptin is an adipocytokine peptide involved in the homeostasis of body composition. Alterations in leptin regulation have been observed in liver cirrhosis. We aimed to assess serum and ascitic fluid leptin levels in a group of patients with decompensated liver cirrhosis and to evaluate these levels in relation to tumor necrosis factor-alpha levels. We assessed both serum and ascitic fluid leptin levels by a radioimmunoassay method, in 40 patients with posthepatic cirrhosis. We calculated body mass index [BMI] as Kg/m2 in all patients and assessed other laboratory biochemical parameters of liver functions. We excluded patients with Spontaneous bacterial peritonitis and all forms of non cirrhotic ascites. Both serum and ascitic leptin levels were correlated with BMI. Ascitic fluid leptin levels [13.1 +/- 10.9 ng/ml] were twice as high as serum levels [7.0 +/- 6.4 ng/ml] and the ascitic fluid/serum ratio of leptin was >1 in all patients. We suggested that this parameter can be used as one of the characteristics of cirrhotic ascites. Serum and ascitic fluid leptin levels were positively highly correlated [r = 0.76 p<0.001] while no correlation was found between TNF-alpha levels in serum and ascites [r=0.29 p>0.05]. We concluded from this study that ascitic fluid leptin levels of cirrhotic patients with sterile ascites are on average two times higher than circulating levels of this hormone, a useful marker of characterizing cirrhotic ascites. These findings suggest that intra-abdominal production of leptin in cirrhotic ascites by peritoneal adipocytes may explain this local rise of leptin levels and this is largely regulated and interrelated to TNF-alpha. Both proinflammatory adipocytokines are related to the metabolic picture in cirrhotic patients particularly anorexia, cachexia and increased energy expenditure. This may represent a therapeutic target in the future by means of introducing anticytokine therapy or chemoprophylactic measures that may ameliorate the release of these cytokines from stimulated monocytes, T-cells or from adipocytes

Evaluation of the pathological role of lymphocyte apoptosis in juvenile autoimmune diseases

To elucidate the involvement of APO-1 antigen in human autoimmune diseases, APO-1 antigen expression, on peripheral lymphocytes from children with systemic lupus erythematosus [SLE], juvenile rheumatoid arthritis [JRA] and normal controls, was analyzed. Significantly higher levels of APO-1 were detected on freshly isolated lymphocytes in both diseases. However, there was a significant increase in APO-1 in active SLE than in control, while there was no significant difference in APO-1 expression between active JRA and control. There was a positive significant correlation between APO-1 expression and in vitro apoptosis of lymphocytes and an inverse relationship although insignificant between APO-1 expression and total lymphocyte count in SLE. To address the question of whether altered apoptosis might provide a source of extracellular nuclear Ags in SLE, in vitro apoptosis of lymphocytes isolated from children with SLE, JRA and normal controls was examined. After culture for 48 hours, there was a significant increase of in vitro apoptosis of lymphocytes in active SLE compared with the control group, while there was no significant difference in in-vitro apoptosis in active JRA compared with the control group. The increase of APO-1 expression and in vitro apoptosis of lymphocytes could not be accounted for by corticosteroid or cytotoxic medication