Somayh S. Eissa

Introduction: Obesity is commonly associated with insulin resistance and hyperinsulinemia and is the most important risk factor for type 2 diabetes. Visfatin is an adipokine that exerts insulin-mimetic effects that stimulate muscle and adipocyte glucose transport and inhibit hepatocyte glucose production. Purpose: The aim of this study was to assess levels of visfatin and its relationship to obesity and insulin resistance in type 2 diabetes mellitus. Patients and methods: This study included 40 patients with type 2 diabetes as the patient group: 20 of them were obese (BMI ≥ 30) and 20 were not (BMI < 25). Forty apparently healthy individuals matched for age and sex were included as the control group: 20 of them were obese (BMI ≥ 30) and the other 20 were not (BMI < 25). All patients and controls underwent history taking, physical examination including determination of BMI, and the following laboratory investigations: determination of levels of fasting blood glucose, 2 h postprandial blood glucose, serum cholesterol, triglycerides, fasting insulin, and fasting visfatin; kidney and liver function tests and calculation of homeostasis model of assessment-insulin resistance (HOMA-IR) were also performed. Neither the patients nor controls suffered from any chronic disease other than diabetes. Results: The results of this study revealed a highly significant increase in the fasting serum insulin level, HOMA-IR, and fasting serum visfatin level among diabetic patients (26.10 ± 6.04μIU/ml, 12.18 ± 5.24, 36.70 ± 6.86 ng/ml, respectively) when compared with controls (12.10 ± 3.45μIU/ml, 2.42 ± 0.79, 13.63 ± 3.98 ng/ml, respectively; P < 0.01). Fasting insulin levels, HOMA-IR, and visfatin levels were significantly higher in obese diabetic patients (31.13 ± 4.34μIU/ml, 14.71 ± 6.22, 42.36 ± 4.11 ng/ml, respectively) than in obese controls (14.31±3.11mIU/ml, 2.89±0.77, 16.72 ± 3.16 ng/ml, respectively; P < 0.01). Visfatin levels were higher in nonobese diabetic patients than in nonobese controls. Moreover, visfatin levels were higher in obese diabetic patients (31.04 ± 3.49 ng/ml) than in nonobese diabetic patients (10.54 ± 1.53 ng/ml; P < 0.01). The present study revealed a highly significant positive correlation between levels of visfatin and fasting insulin in both obese and nonobese diabetic patients. Although there was a significant positive correlation between visfatin levels and HOMA-IR, there was no significant correlation between visfatin levels and BMI in obese diabetic patients. Conclusion: Visfatin levels are increased in patients with type 2 diabetes regardless the degree of adiposity.

Premature development of microvascular and macrovascular disease is the most frequent complication of diabetes. It is responsible for diabetic retinopathy, nephropathy, and neuropathy. Moreover, diabetes leads to reduced collateralization in ischemic tissues, which causes a three- to four-fold increase in cardiac mortality in diabetic individuals compared with nondiabetic individuals. The pathophysiological mechanisms responsible for impaired angiogenic activity in diabetes remain unknown. The role of angiogenin in the physiological revascularization process has not been clarified. This work was carried out to determine the serum angiogenin level in type 2 diabetic patients and to determine its correlation with various microangiopathies, cardiovascular complications, and the duration in type 2 diabetic patients. This work was carried out on 88 individuals, 68 type 2 diabetic patients and 20 apparently healthy controls. All individuals were subjected to the following assessments: medical history taking; clinical examination including measurement of BMI; estimation of levels of fasting blood sugar, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, urea, low-density lipoprotein, and creatinine; determination of the albumin/creatinine ratio and complete lipid profile (total cholesterol, triglyceride, high-density lipoproteins); serum angiogenin estimation by enzyme linked immunosorbent assay; fundus examination; ECG and transthoracic echocardiography; and abdominal ultrasonography. Our results indicated a significant decrease in the serum angiogenin level in diabetic patients compared with the control group; an insignificantly low serum angiogenin level in diabetic patients with retinopathy and nephropathy compared with those without retinopathy and nephropathy, respectively; a significant decrease in the serum angiogenin level in patients with coronary artery disease (CAD) compared with diabetic patients without CAD; an insignificant inverse correlation of angiogenin with fasting blood sugar, duration of diabetes mellitus with urea, and creatinine with albumin/creatinine ratio; and an insignificant proportional correlation of angiogenin with ejection fraction in diabetic patients with complications of retinopathy, nephropathy, and CAD in each group separately. This work concluded that the serum angiogenin level is lower in type 2 diabetic patients compared with the control group and it decreases with prolonged duration of diabetes, especially in uncontrolled patients and patients with microangiopathic and cardiovascular complications. As angiogenin is one of most powerful angiogenic factors, we recommend further studies to evaluate the diagnostic, prognostic, and therapeutic value of angiogenin in various microangiopathic and cardiovascular complications of type 2 diabetes.

The platelet count is known to decrease in proportion to the advancement of the stage of liver disease in chronic hepatitis C (CHC) viral infection. The platelet count is currently used as an index for fibrosis staging. The pathophysiology of thrombocytopenia (TCP) in patients with hepatitis C virus (HCV) infection is not completely understood. This work aimed to study the correlations of folic acid (FA), vitamin B₁₂ (Vit B₁₂), homocysteine (Hcy), and thrombopoietin to the platelet count in HCV infection. Sixty-seven patients (51 men and 16 women) with HCV infection were included in this study. All patients were sero-negative for hepatitis B viral markers. In addition, 20 healthy volunteers, matched for sex and age, were included as a control group. All patients and control individuals were subjected to the following: assessment of medical history, thorough clinical examination, and laboratory investigations including the following: complete blood cell counts, viral hepatitis markers, liver and renal function tests, HCV-RNA by quantitative PCR, serum folate, Vit B₁₂, thrombopoietin, and plasma Hcy. Abdominal ultrasonography and ultrasound-guided liver biopsy for histopathologic examinations were carried out for the patients. Patients were divided into two groups of 36 patients with CHC and 31 patients with cirrhosis with HCV liver cirrhosis (LC). The results indicated a significant decrease in the platelet count in CHC and LC patients compared with the healthy control group. There was a highly significant decrease in the FA level in CHC and LC patients compared with the control group; also, a significant decrease in the platelet count was found in LC patients compared with CHC patients. Hcy was significantly increased in CHC and LC patients. There was a nonsignificant decrease in Vit B₁₂ in CHC patients, whereas it was significantly increased in LC patients. There was a nonsignificant decrease in thrombopoietin in CHC patients compared with the control group, whereas in LC patients, there was a highly significant decrease. There was a highly significant positive correlation between the platelet count and FA, but an insignificant correlation between the platelet count and Hcy, Vit B₁₂, thrombopoietin, and viral load. This study concluded that TCP in HCV-related chronic liver diseases is multifactorial and decreased FA is involved in its pathogenesis as an independent risk factor. Increased Hcy may cause TCP through platelet activation and endothelial dysfunction.

Introduction: Hepatitis C virus (HCV) infection and type 2 diabetes are two common disorders with high impact on health worldwide. There is growing evidence to support the concept that HCV is associated with type 2 diabetes. Purpose: This work aimed to study the clinical phenotype of type 2 diabetes in HCV patients. Patients and methods: Our study was conducted upon 100 nonobese, noncirrhotic hepatitis C positive patients who were classified into two groups according to homeostatic model assessment (HOMA) test for insulin resistance (HOMA IR). This study also included 15 nonobese type 2 diabetic patients negative for HCV and hepatitis B virus infection classified as control groups. We excluded alcoholics and drug addicts and patients with conditions that affect blood glucose such as endocrine diseases associated with disordered glucose metabolism and use of drugs. All participants were subjected to full history taking and complete clinical examination including BMI and the following investigations: complete blood count, fasting blood sugar, 2 h postprandial blood sugar, glycosylated hemoglobin, fasting insulin level, cholesterol level, HDL, LDL, triglyceride, serum urea, creatinine, complete urine analysis, liver function tests: total bilirubin, alkaline phosphatase, albumin, prothrombin time, INR, SGOT, SGPT, quantitative PCR for determination of HCV-RNA, surface antigen (HbsAg), abdominal ultrasonography, liver biopsy when needed and possible for HCV patients, and ECG. Results: In this study, we found that the prevalence of type 2 diabetes in group I is 24%. HCV can independently contribute to IR with viral genotypes 1 or 4. We noticed significant positive correlation between fasting insulin and HOMA IR in hepatitis C +ve patients. IR in HCV-infected patients is high irrespective of the degree of liver injury even before a minimal fibrosis is present. Both IR and diabetes can adversely affect the course of chronic hepatitis C, leading to enhanced steatosis and liver fibrosis, and even increase the risk of hepatocellular carcinoma. A significant correlation between HOMA IR and steatosis, a significant positive correlation between fasting insulin and steatosis and a negative correlation between steatosis and BMI in HCV patients was found. No correlation was found between HOMA IR and the viral load (quantitative HCV RNA). Conclusion: We can concluded that diabetic HCV patients had intermediate clinical phenotype lower BMI and LDL than control and development of type 2 diabetes mellitus in HCV patients was significantly higher in nontreated patients than treated patients. Antiviral therapy and clearance of HCV improves IR, β-cell function, the blood glucose abnormalities.

The hepatitis C virus (HCV) is a leading cause of chronic liver disease (CLD), cirrhosis, and hepatocellular carcinoma, as well as the most common indication for liver transplantation in many countries. This work was carried out to study of thrombopoietin (TPO) level in Egyptian patients with chronic hepatitis C and liver cirrhosis with HCV. This work was conducted on 40 patients proved to have chronic liver disease due to chronic HCV infection by positive HCV antibody by enzyme-linked immunosorbent assay, PCR for HCV RNA, abdominal ultrasonography, and histopathological examination. Twenty of these patients had chronic active hepatitis C (CAH) and the other 20 patietns had liver cirrhosis. Fifteen apparently healthy individuals (negative for HCV antibody) were included in a control group. None of the patients had received interferon therapy. Patients with other causes of CLD, chronic renal disease, diabetes, endocrinal hematological, and other debilitating diseases were excluded. All the patients studied were subjected to the following: complete medical history, full clinical examination, laboratory investigations including complete blood picture, liver function tests, fasting blood sugar, 2 h postprandial, HCV antibody and PCR for RNA of HCV; serum TPO level, abdominal ultrasonography, and liver biopsy for histopathological examination. Our results showed a highly significant reduction in the platelet count in patients with CAH (192.55 ± 41.02) and cirrhotic patients (159.800 ± 86.189) in comparison with (322.67 ± 38.12) the control group (P < 0.01). There was nonsignificant increase in TPO in patients with CAH (115.93 ± 71.66) and a significant decrease in TPO in cirrhotic patients (77.504 ± 64.576) in comparison with (107.98 ± 52.53) the control group. In the cirrhotic patients, there was a significant positive correlation between TPO and platelet count, whereas there was no correlation between TPO level and liver enzymes (alanine aminotransferase and aspartate aminotransferase) in all patients. In addition, a significant decrease in TPO was found in cirrhotic patients in comparison with CAH patients. Serum TPO level was elevated in patients with chronic viral C hepatitis as a compensatory response to the reduction of platelet count with still functionally active liver cells, but as the disease progress to cirrhosis which also is associated with thrombocytopenia, TPO production is impaired, with failure to compensate the low platelet count aggravating thrombocytopenia.