Objective Thyroid dysfunction (TD) is a risk factor for coronary heart disease (CHD) events. We study the prevalence and predictors of TD and its impact on characteristics, cardiac function, and ischemic severity of patients with manifest CHD. Patients and methods A total of 200 patients 6–12 months after acute coronary syndrome had at least one vessel − significant stenotic coronary artery lesion. Before elective angiography, patients underwent anthropometric measurement, routine biochemical assay, thyroid hormones, and thyroid peroxidase antibody. Results The prevalence of TD was 17.5%: 12% for hypothyroidism (9.5% subclinical, 2.5% overt) and 5.5% for hyperthyroidism (2.5% subclinical, 3% overt). Compared with the euthyroid group, the hypothyroid group had a significantly higher age, BMI, diastolic blood pressure (BP), atherogic lipid profile, and impaired cardiac functions and higher pulmonary artery systolic pressure (PASP), and the hyperthyroid group had significantly higher systolic BP, ejection fraction (EF), and PASP and significantly lower diastolic BP and lipid profile. Independent predictors for hypothyroidism were age, bradycardia, increased BMI, lower EF, diastolic dysfunction, and atherogenic lipid profile, whereas increased PASP was an independent predictor for hyperthyroidism. Thyroid-stimulating hormone (TSH) was positively correlated and both free triiodothyronine and free thyroxine were negatively correlated to BP, BMI, lipid profile, impaired EF, and coronary atherosclerosis severity. TSH and free thyroxine were positively correlated to PASP, which increased significantly through hypothyroidism to hyperthyroidism. TSH and free triiodothyronine were independent predictors of severity of CHD. Conclusion Age, obesity, impaired cardiac function, and atherogenic lipid profile are predictors of hypothyroidism, and PASP is the predictor of hyperthyroidism among manifest CHD. Thyroid hormones are predictors of severity of coronary atherosclerosis and correlated to cardiac functions and PASP.

Context Android obesity is considered an important predictor of increased mortality and morbidity from diabetes mellitus and cardiovascular disorders. Aim Our research was conducted to assess the level of serum visfatin in android obesity and its relation to anthropometric and biochemical parameters in adults with android obesity. Patients and methods This study was conducted on 136 patients recruited from the outpatient obesity clinic of Specialized Medical Hospital, Mansoura University. The patients were divided into two groups: group I consisted of 65 control nonobese individuals, and group II consisted of 71 obese individuals with android obesity. The obese patients were subdivided into obese diabetic patients (35 patients) and obese nondiabetic patients (36 patients). All participants were subjected to thorough history taking, full clinical examination, and anthropometric measurements to assess body mass index and waist circumference. The changes that appeared in the carbohydrate metabolism were interpreted according to the criteria from the glycometabolic classification of WHO. Plasma glucose levels, lipid profile, and serum visfatin were measured. Results Our study demonstrated a significant elevation of visfatin (P≤0.001) in obese individuals (37.6; 20.7–65.9) compared with that in lean patients (15.3; 7.5–20). Additionally,visfatin levels were higher in the diabetic obese subgroup (45.5; 33.7–65.9) than in the nondiabetic obese subgroup (32; 20.7–46.5). Furthermore, visfatin was positively correlated to blood glucose in the obese group, which suggests a role of visfatin in glycemic control. A significant correlation between visfatin and lipid profile was demonstrated, which may suggest a role for visfatin in lipid homeostasis. Conclusion Serum visfatin was elevated in patients with android obesity, with more significant elevation in patients with android obesity with type 2 diabetes mellitus. It showed potential to be used as a marker of metabolic syndrome as it had a strong relation to android obesity.

Context Diabetic neuropathy is one of the commonest long-term complications of diabetes seen in routine healthcare and considered the most common cause of peripheral neuropathy in developed world. Aim The aim of our work was to measure advanced glycation endproducts (AGEs) and their receptors (RAGEs) in diabetic peripheral neuropathy (DPN), both painful and painless DPN. Patients and methods Our study was conducted on 50 type 2 diabetes mellitus patients with peripheral neuropathy, divided into two subgroups: the first group included 25 patients with painful DPN and the second group included 25 patients with painless DPN. Moreover, a third group included 20 diabetic patients without peripheral neuropathy, and a fourth group that included 20 healthy participants. All groups were subjected to full history taking and clinical examination, anthropometric parameters, the calculation of neuropathy disability score, and nerve conduction studies (peroneal, sural, and tibial nerves). Laboratory investigations included serum AGEs and RAGEs. Results Our study demonstrated that hemoglobin A1c, AGE, and RAGE showed statistically significant difference between the studied groups. Hemoglobin A1c was significantly high in both neuropathic and diabetic groups in comparison with control. Regarding AGE, it was statistically higher in neuropathic group than in control (P<0.011). On the contrary, RAGE was significantly higher in both neuropathic and diabetic groups rather than control (P<0.02). Although the neuropathic group has higher levels of AGE and RAGE than diabetic group, the difference was statistically nonsignificant. Significant difference was found between studied groups regarding nerve conduction studies of sural and tibial nerves. Statistically significant difference was found in the parameters of nerve conduction studies between neuropathic group and both non-neuropathic diabetic and control groups. Conclusion Our study concluded that AGE and RAGE are significantly higher in diabetic patients with neuropathy versus control, with more elevation in neuropathic group than in diabetic without neuropathy.

Introduction Fibroblast growth factor-21 (FGF21) regulates glucose and lipid metabolism and protects against atherosclerosis. Serum FGF21 levels were assessed in newly diagnosed, drug-naive patients with prediabetes (group 1, n=60) and diabetes mellitus type 2 (group 2, n=60), in addition to 40 healthy individuals (group 3, n=40). Results Serum FGF21 levels were significantly increased in groups 1 and 2 compared with group 3 (231.7±59.3 and 260.4±82.5 vs. 22.6±5.31 pg/dl, respectively; P<0.001 for both). Moreover, group 2 had statistically significantly higher FGF21 levels compared with group 1 (P=0.03). Receiver operating characteristic curve analysis identified FGF21 cutoff value of greater than 204 and 30 pg/ml for the diagnosis of diabetes mellitus type 2 and prediabetes, with an area under the curve 0.72 and 1, sensitivity of 82.5 and 100%, and specificity of 60 and 100%, respectively. Using univariate analysis, FGF21 was positively correlated with blood pressure, obesity (BMI and waist–hip ratio), glycemic (glucose and glycosylated hemoglobin) and insulin resistance (fasting insulin and homeostasis model assessment-insulin resistance) parameters, atherogenic lipid profile, liver enzymes, and cardiovascular disease risk score in group 1 and group 2. FGF21 correlated with albumin–creatinine ratio negatively in group 1 and positively in group 2. Independent predictors of FGF21 level were fasting glucose, insulin, and triglyceride in both patient groups. The independent predictors of FGF21 were obesity parameters in group 1 and albumin–creatinine ratio, age, and systolic blood pressure in group 2. Conclusion Among prediabetic patients, FGF21 is an excellent predictor and a novel linkage between metabolic parameters, circulatory system, and nephropathy.

Background Diabetic nephropathy (DN) is the leading cause of renal failure. Diabetic patients with microalbuminuria typically progress to proteinuria and overt DN. Similar to other microvascular complications of diabetes, there are strong associations between glucose control (as measured using HbA1c) and the risk of developing DN. Apelin (APLN), a peptide first isolated from bovine stomach tissue extracts, is the endogenous ligand for the G-protein-coupled APJ receptor that is expressed at the surface of some cell types. APLN and APJ are widely expressed in homogenates from animal organs in a pattern shared with angiotensinogen and the angiotensin receptor. APLN is widely distributed in the central nervous system and periphery, especially in the heart, kidney, lung, and mammary glands. The APLN–APJ system may be involved in the pathogenesis of DN, which may play a renoprotective role partially by antagonizing the angiotensin II–ATIR pathway. Aim The aim of this study was to investigate the relation between serum APLN and different grades of DN in type 2 diabetic patients. Patients and methods This study was conducted on 150 diabetic patients and 20 controls selected from the inpatient department and outpatient clinics of the Internal Medicine Department in Menoufia University Hospital. The selected participants were divided into four groups: group 1 included 20 healthy controls; group 2 included 50 type 2 diabetes mellitus (T2DM) patients with normoalbuminuria; group 3 included 50 T2DM patients with microalbuminuria; and group 4 included 50 T2DM patients with macroalbuminuria. Members of the study groups were subjected to thorough history taking with special emphasis on age, sex, and duration of diabetes mellitus. Investigations included liver profile, complete blood count, fasting and 2 h postprandial plasma glucose, glycosylated hemoglobin (HbA1c), complete urine analysis, kidney function tests (blood urea nitrogen and serum creatinine), urine albumin/creatinine ratio, estimated glomerular filtration rate, and serum APLN. Results Serum APLN was significantly higher in group 4 compared with the other groups, in group 3 compared with groups 1 and 2, and in group 2 compared with group 1. There was a significant positive correlation between serum APLN and serum creatinine, urine albumin/creatinine ratio, and HbA1c. Further, there was a significant negative correlation between serum APLN and estimated glomerular filtration rate in the studied diabetic patients. There was no correlation between serum APLN and BMI in diabetic patients. Conclusion From this study, we can conclude that serum APLN is significantly higher in patients with DN compared with diabetic patients without nephropathy, and there is a positive correlation between serum apelin and the degree of DN. Thus, APLN may play an important role in the development of DN.