Birthweight of Full-Term Twin Infants in Relation to Sex-Pair

ABSTRACT

BACKGROUND

Nigeria has one of the highest twining rates in the world. Twin gestation is known to have a negative influence on birthweight but the effect of sex-pair is not well established.

OBJECTIVE

To determine the effect of sex-pair on birthweight of twins.

METHODS

The birthweights and sex-pairs of 104 live-born full-term twin pairs were recorded and analyzed. The mean birthweight of different-sex twin pair was compared with that of same-sex twin pair. Also the mean birthweight sum of different-sex twin pair was compared with that of same-sex twin pair. The relative incidence of low birthweight (LBW) and birthweight discordance in different-sex twin pair and same-sex twin pair were examined.

RESULTS

Comparing the mean birthweight of different-sex twin pair with that of same-sex twin pair, it was 2503±428g (95% confidence interval, CI: 2369–2637) versus 2398±442g (95% CI: 2291–2505), t=0.851, P>.05. The overall mean birthweight sum of different-sex twin pair was 3889±492g (95% CI: 3679–4099) while for same-sex twin pair it was 3665±512g (CI: 3493–3837), P>0.05. The mean birthweight sum for male-male twin pair was 3903±536g (95% CI: 3648–4158), while that of female-female twin pair was 3426±560g (95% CI: 3160–3192), P<0.05. The mean birthweight of female infants in male-female twin pair was 2081±492g (95% CI: 1703–2459) compared to 1795±502g (95% CI: 1635–1955) for female infants in female-female twin pair, P>0.05. The figures for the male infants in male-female pair and male-male twin pair were 2136±468g (95% CI: 1945–2327) and 1976±519g (95% CI: 1804–2148), respectively, P>0.05. Frequency of delivery of LBW twin pairs were: (1) different-sex 51.3%, (2) male same-sex 43.8%, and (3) female same-sex 75.8%. Out of 59 LBW twin pairs, 20 (33.9%) were different-sex twins pair while the remaining 39 (66.1%) were same-sex twin pairs. Of 30 birthweight discordant pairs, 12 (40.0%) were different-sex twin pair while 18 (60.0%) were same-sex twin pair, corresponding to a ratio of 1:1.5.

CONCLUSION

In twin gestations, cohabitation in utero of fetuses of different gender influenced their intrauterine growth.

Incretin-based Therapies: A Focus on Alpha Cells and Glucagon Secretion

ABSTRACT

Conventional therapies for type 2 diabetes mellitus effectively reduce hyperglycemia. However, they are often associated with hypoglycemia and other adverse side effects. In patients with diabetes, the secretion of glucagon is often not inhibited in the presence of elevated blood glucose, thus exacerbating hyperglycemia. Alpha-cell dysfunction is also a characteristic of type 2 diabetes. However, based solely on their mechanism of action, none of the conventional therapies represents a tool for modulating glucagon secretion. Incretin-based therapies lower glucose using novel mechanisms based on the action of the gut hormones GLP-1 and GIP. The physiological mechanism of incretin's action suggests different areas in which incretin therapies may be more advantageous compared to other medications. In particular, GLP-1 has been shown to inhibit glucagon release after meal ingestion with a decreased risk of hypoglycemic episodes compared to other therapies. Improvement in alpha-cell function via incretin-based therapies results in better postprandial and fasting glycemic profiles. Moreover, due to the wide distribution of GLP-1 receptors in human tissues, incretin-based therapies may have other beneficial effects on beta-cells, body weight, lipid profile, cardiovascular risk, and other extra-pancreatic properties.

A Review of Diabetes Treatments and Their Effects on Glycemic Control and Complications of Diabetes

ABSTRACT

INTRODUCTION

The incidence and prevalence of diabetes continues to rise across the world, therefore effective management of this disease is required to reduce the morbidity and mortality associated with this condition via the reduction of hyperglycemia and the macrovascular and microvascular complications of diabetes.

OBJECTIVES

To review the literature and provide an overview of the available treatments for diabetes and their effects on hyperglycemia, glycemic control (measured using glycated hemoglobin [HbA1c]), and diabetes complications.

METHODS

English language articles (including randomized controlled trials, systematic reviews, and meta-analyses) dealing with the relevant subject matter were obtained by searching PubMed.

RESULTS

When used as monotherapy, oral and noninsulin injectable diabetes treatments appear to reduce HbA1c by about 1%, insulin reduces HbA1c by >1%, orlistat reduces HbA1c by about 0.6%, and bariatric surgery reduces HbA1c by >2%. Different treatments have variable effects on pre- and postprandial hyperglycemia. Combinations of treatments produce further HbA1c reductions. Each treatment has its own side effect profile and some have been demonstrated to reduce diabetes complications, as well as reduce the progression from prediabetic states to type 2 diabetes.

CONCLUSION

A variety of options exist for the treatment of diabetes, and the benefits and side effects of each treatment need to be weighed carefully to guide the choice and combination of treatments offered to patients.

Clinical Implications of Visfatin/PBEF/Nampt for Development of Vascular Inflammation and Atherosclerosis

ABSTRACT

In the last years, the adipose tissue has been acknowledged as an endocrine organ that releases a heterogeneous series of compounds, the so-called adipokines. In 2005, visfatin was first identified as a new adipokine with insulin-mimetic properties, identical to the pre-B cell colony-enhancing factor (PBEF) and exhibiting intrinsic nicotinamide phosphoribosyltransferase (Nampt) enzymatic activity. For this reason, this adipocytokine is currently termed visfatin/PBEF/Nampt. The circulating levels of visfatin/PBEF/Nampt are elevated in metabolic conditions, such as obesity and type 2 diabetes, and although this observation is subject to controversy, they positively correlate with markers of systemic inflammation. In the context of cardiovascular diseases, visfatin/PBEF/Nampt is emerging as a new clinical marker of atherosclerosis, endothelial dysfunction, and vascular damage with a potential prognostic value. A growing bulk of evidence further unveils that visfatin/PBEF/Nampt can not only be a clinical marker, but also an active player in promoting vascular inflammation and atherosclerosis. Hence, through its actions on cytokine and chemokine secretion, macrophage survival, leukocyte recruitment by endothelial cells, vascular smooth muscle inflammation, and plaque destabilization, visfatin/PBEF/Nampt arises as an active player in plaque development and progression. Further in depth research is required to understand the mechanisms mediating the cellular actions of this adipocytokine and to identify the factors that regulate its cellular synthesis and release in different clinical situations. Such knowledge will help determine whether visfatin/PBEF/Nampt can represent a valuable therapeutical target in the context of cardio-metabolic diseases.

Podocyte Biomarkers in Urine: Relevance and Potential

ABSTRACT

Proteinuria and/or albuminuria are widely used for noninvasive assessment of kidney diseases. However, proteinuria is a nonspecific indicator of many forms of kidney injury, systemic disease, and physiologic alteration in glomerular filtration of proteins. This includes diabetic nephropathy and causes of proteinuria that progress to end-stage kidney disease (ESKD) and those that do not. Therefore proteinuria per se is not considered to be sufficiently precise an endpoint to serve either as a diagnostic tool for specific diseases of the kidney or as a surrogate for ESKD in clinical trials, although within a defined disease setting proteinuria is a powerful monitoring tool. Progression of glomerular diseases is the mechanism by which cumulative glomerular injury results in progressive loss of kidney structure and function eventually causing ESKD. Several lines of evidence strongly suggest that a major cause of glomerulosclerosis is podocyte depletion from glomeruli. Since podocytes are resident on the outer surface of the glomerular basement membrane, when they or their products detach they can be detected in urine. This potentially provides a noninvasive mechanism for monitoring podocyte well-being and raises the possibility that biomarkers of podocyte injury, stress, or loss could be used in combination with proteinuria to more reliably detect and monitor progression and response to treatment. Several potential urine podocyte biomarkers have been described including podocytes themselves and fragments of podocytes, podocyte proteins and mRNAs, and exosomes. Here we review recent urine podocyte biomarkers that could potentially complement proteinuria for monitoring the progression process in the clinic.

Cardio-Metabolic Syndrome: Definition, Management, and Prognosis

ABSTRACT

The metabolic syndrome, a constellation of clinical signs including obesity, insulin resistance, dyslipidemia, and hypertension, is of growing prevalence in the world. Concerns include the multitude of risk factors associated with having this syndrome. Mortality is increased along with the increased susceptibility of a cardiovascular event such as myocardial infarction, stroke, or some form of athrogenic disease. Throughout the world there is a positive correlation seen between age and prevalence of the metabolic syndrome. Older individuals (> 70 years of age) are the highest group with this syndrome. Women also seem to be more at risk than men. There are currently three widely used definitions for the metabolic syndrome. Accordingly, identifying patients depend on which definition is used and discrepancies can occur between studies. Although there are many contributors to the pathophysiology of the metabolic syndrome, a recurrent theme is abdominal obesity and insulin resistance. Both these entities can explain the clinical criteria seen when identifying patients with this syndrome. Current therapies include weight reduction through dieting, lifestyle modifications, and perhaps pharmacological treatments. As the metabolic syndrome is gaining more recognition, emerging therapies are targeting the molecular biology behind this syndrome.

Cardiorenal Syndrome Type-5: The Case of Diabetes Mellitus and the Effect of Nephropathy on the Cardiovascular Outcome

ABSTRACT

Cardiorenal syndrome is defined as a pathophysiological disorder of the heart and kidneys in which acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. This syndrome is classified into 5 types. Secondary (type 5) cardiorenal syndrome is characterized by the presence of combined cardiac and renal dysfunction due to acute or chronic systemic disorders. In the chronic setting, diabetes mellitus represents such a systemic condition that affects both the cardiac and renal system. Diabetes is a known risk factor for cardiovascular disease (CVD). Also, some diabetic patients develop nephropathy. The fibrogenic cytokine transforming growth factor-beta and the vascular endothelial growth factor are implicated in the development of the cardinal features of diabetic nephropathy. It is suggested that endothelial dysfunction may lead to simultaneous development and progression of renal and cardiac pathology in diabetes. While the risk of microvascular complications can be reduced by intensive glycemic control in patients with type 1 and type 2 diabetes mellitus, intensified intervention involving other vascular risk factors like hypertension and dyslipidemia demonstrated benefits in terms of both macrovascular and microvascular complications. In addition, treatments with angiotensin-converting enzyme inhibitors or angiotensin II receptor antagonists were shown to be associated with a significant reduction in the risk for renal disease progression that was paralleled by a reduction of the cardiovascular risk.

The Effect of Hypogonadism and Testosterone Replacement Therapy on Components of the Cardio-Metabolic Syndrome and Diabetes Mellitus

ABSTRACT

There is increased awareness of the association between hypogonadotropic hypogonadism (HH) and the components of the cardiac metabolic syndrome (CMS) and type 2 diabetes mellitus (T2DM). The indications for treatment, as established by the Endocrine Society, focus on addressing the decreased sexual function, bone mineral density, and on improving the sense of well-being of those patients with biochemical evidence of HH. Recent studies, however, suggest that treating HH also improves insulin resistance in T2DM and each of the components of the CMS. Larger studies of testosterone administration need to be conducted to more clearly outline benefits and balance them against the risks of prostatic and cardiovascular disease (CV) as well as other adverse outcomes. The present article explains the pathophysiology of HH, reviews the articles highlighting this association, and discusses the clinical evidence supporting the effects of testosterone replacement therapy and its potential adverse effects in patients with T2DM and CMS.

Antidiabetic Potential of Commonly Consumed Cereals—A Review

ABSTRACT

Diabetes mellitus (DM) is a common disease affecting several million individuals worldwide. Over the last century, changes in human behavior and lifestyle have resulted in a dramatic increase in the incidence of diabetes world over. Though oral hypoglycemic agents and insulin are the mainstay of treatment of diabetes, they have prominent side effects and fail to significantly alter the course of diabetic complications. Lifestyle modifications including appropriate diet and exercise programs have been found to be greatly effective in the management of the disease. Diet therapy, especially, is showing a bright future in the therapy of DM. In particular, the commonly consumed cereal grains have been reported to possess antidiabetic properties.

There are a variety of grains and grain products which can be beneficial in lowering glucose and insulin responses. The synergistic effect of several whole-grain components such as dietary fiber, phytochemicals, vitamin E, Mg, or others may be involved in the reduction of the risk for type 2 diabetes mellitus (T2DM). Hence, replacing low fiber grain foods such as white bread with whole grain higher fiber or higher amylose content products will reduce risk of developing insulin resistance and obesity and improve the health of the population.

Incidence and Risk Factors of Severe Obstetric Hemorrhage

ABSTRACT

Severe obstetric hemorrhage is the main cause of severe maternal morbidity and mortality worldwide. The incidence of severe hemorrhage varies considerably, even among countries with high resource settings. Uterine atony is the main cause of severe obstetric hemorrhage, followed by retained placental tissues and trauma of the genital tract. Preexisting or acquired coagulopathy accounted for almost 1% of severe obstetric hemorrhage. The mode of delivery is the most important risk factor for severe obstetric hemorrhage, especially an emergency cesarean section (CS), followed by elective CS. Other important risk factors included multiple pregnancy, von Willebrand's disease, HELLP syndrome, anemia, macrosomia, cardiac disease, chorioamnionitis, induction, prolonged labor, and older age. Mothers with a history of unexplained severe obstetric hemorrhage should be investigated for preexisting or acquired bleeding disorders, and should receive conjoined care by a hematologist, obstetrician, and anesthesiologist during pregnancy and labor as well as in the postpartum period.

Severe obstetric hemorrhage is a relatively frequent complication. Increasing knowledge of risk factors may contribute to reducing its incidence and impact. The findings call for reviewing labor management, as well as screening for different bleeding disorders.

Endothelial Dysfunction in Young People With Diabetes Mellitus in the Absence of Clinical Vascular Disease: A Review

ABSTRACT

Endothelial dysfunction is an early surrogate of future vasculopathy. Children and adolescents with diabetes have a high future risk of clinical vascular disease and we and others have demonstrated that biophysical abnormalities of endothelial dysfunction and the markers of endothelial cell activation tend to be perturbed early in this group of patients. The endothelial dysfunction is manifest well in advance of clinical vascular disease. The mechanisms of early endothelial dysfunction are complex and many underlying factors act in concert to initiate such dysfunction: with the sustained hyperglycemia acting as a prime mover; the subsequent metabolic derangements as perpetuators; and along with obesity, smoking, and lack of physical exercise, all contribute to a progression of this dysfunction into full angiopathy. Strategies to ameliorate such dysfunction have been explored. This review aims at shedding light on this area that has received much attention in the last two decades.