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Background: Type 2 diabetes is a part of metabolic syndrome associated with a higher risk of vascular complications. Diabetes is characterized by changes in platelet morphology, function, and platelet hyperactivity so, it's considered a prothrombotic condition. Morbidity and mortality in people with type 2 diabetes-related to micro and macrovascular complications. Novel biomarkers are needed to identify and treat people at higher risk. Objective: The main objective of this controlled cross-sectional study was to evaluate Platelet volume indices (PVI) in subjects with type 2 diabetes with and without complications in comparison to subjects without diabetes. Methods: Hundred and thirty-five subjects aged from 35 to 60 years were subdivided into 3 groups. Group A includes 55 subjects with type 2 diabetes with complications. Group B includes 45 subjects with type 2 diabetes without complications. Group C includes 35 normal healthy subjects. Detailed clinical history was taken. Also, PVI, fasting blood glucose (FBG), hemoglobin A1c, and creatinine were obtained. Results: Mean Platelet Volume (MPV), Platelet Distribution Width (PDW), Plateletcrit (PCT), and Platelet large cell ratio (P-LCR) were significantly higher among subjects with retinopathy, nephropathy, and neuropathy than other subjects with diabetes who didn't develop complications (P<0.001). At cutoff value > 11.9 fL, MPV have diagnostic sensitivity 80% and specificity 97.8%. Whereas PDW >16.9fL has a sensitivity of 74.5% and specificity of 100% for diabetic microvascular complications (retinopathy, nephropathy, and neuropathy). Conclusion: MPV and PDW may be considered as possible biomarkers for the early detection of diabetic microvascular complications.

Abstract:The most reliable determination of severity and prognosis in chronic viral hepatitis is the histological staging of the disease, which comprises an invasive procedure and is often not well accepted by patients. The search for alternative non-invasive methods is mandatory especially in follow-ups after initial assessment by biopsy. The aim of this study was to evaluate the role of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) in patients under interferon alpha therapy whether responsive or non-responsive to therapy. Thirty chronic hepatitis C patients (CHC) under combined therapy of interferon-α with ribavirin, whether responsive or non-responsive, were included in the study as well as ten healthy controls. Serum VCAM-1 and ICAM-1 levels were calculated using commercial enzyme linked immunosorbent assay (ELISA) kits. Before the therapy, sICAM-1 and sVCAM-1 levels were significantly higher among CHC patients (96.9 ± 39.74 and 679.4 ± 218.98 ng/mL, respectively) than in the control group (14.3 ± 4.32 and 108.9 ± 49.21 ng/mL, respectively), (p < 0.05 for both). They were higher among non-responsive than in responsive patients. Comparisons in soluble ICAM-1 (sICAM-1) levels of responsive persons during treatment revealed a statistically significant increase at baseline (81.27 ± 25.797) versus its value after one month (52.33 ± 12.76), p < 0.05 and after three months (49.67 ± 14.42), p < 0.05. However, no statistically significant difference was detected between one and three-month sICAM-1 levels post-therapy commencement (p = 0.055). Also, no statistically significant difference was detected between sVCAM-1 levels at baseline (521.47 ± 137.29) versus three months after therapy initiation (517.53 ± 130.6), p = 0.854. The occurrence of a significant decrease in sICAM-1 level as early as one month after therapy in responsive patients only allows us to conclude that sICAM-1 could be used as an early marker in CHC patients under interferon therapy to predict prognosis and guide the treatment, whereas sVCAM-1 does not present any difference between the studied groups.

Background The stage of liver fibrosis is the most important predictive factor for initiation and duration of antiviral treatment, where patients with early fibrosis stages respond to treatment better with a higher sustained virologic response rate. Several noninvasive tests to stage the degree of fibrosis in patients with chronic hepatitis C virus (HCV) infection have been used. No single test is known to have high accuracy and the results of each test must be carefully interpreted. The objective of the study is to evaluate the value of serum fibronectin (FN) as a noninvasive predictor for the assessment of HCV-induced liver fibrosis. Patients and methods A total of 100 patients with chronic HCV infection proved by HCV antibodies and HCV RNA preparing for antiviral treatment were exposed to full history, physical examination, and laboratory assessment. Serum FN level and fibroscan were done for all patients. According to the results of fibroscan, the patients were divided into four groups of liver fibrosis and compared. Results All patients were proved to have HCV viremia with average PCR of 1990.52 ±3144.29 copies/ml. A statistically significant difference was found as regards FN, fibroscan, and APRI score between patients with fibrosis in comparison to patients without fibrosis. According to fibroscan results, 20 patients were found with fibrosis stage 0, 24 patients with stage 1, 24 patients with stage 2, eight patients with stage 3, and 24 patients with stage 4 (cirrhosis). On comparison of different stages of fibrosis as regards FN level, we found no statistically significant difference between stages. FN have a sensitivity of 67.5% and a specificity of 47.4% with 84.4% positive predictive value. Conclusion FN is a good noninvasive marker for the assessment of liver fibrosis in patients with chronic HCV. Larger scale multicenter studies are needed to assess its validity in the detection of fibrosis caused by causes other than HCV.

Several antibodies, including anticardiolipin antibodies (ACA), have been detected among chronically infected hepatitis C virus (HCV) patients. The present work aimed at ascertaining the clinical significance of ACA levels among HCV infection associated with two commonly encountered diseases, thrombocytopenia and arteriovenous-shunt malfunction. Six groups were studied, 11 HCV-positive thrombocytopenic patients (group I), 14 HCV-positive non-thrombocytopenic patients (group II) and 15 healthy controls (group III), 11 anti-HCV-positive hemodialysis patients with non-functioning shunt (group IV), 14 anti-HCV-positive hemodialysis patients with patent shunt (group V) (Bain Medical Equipment Co., China) and 15 healthy controls (group VI). Anticardiolipin antibody (ACA) assay was performed on all patients and controls whereas tumor necrosis factor α (TNF-α) assay was carried out on thrombocytopenic patients and controls. Thrombocytopenic groups presented an inverse correlation between IgG ACA levels and both thrombocytopenia and TNF-α levels. During the follow-up period, no other clinical manifestations related to ACA were developed. Hemodialysis groups showed a significant elevation in IgG ACA levels in groups IV and V compared to the controls, with statistically higher levels in group IV than group V. Three group IV patients were hypercholesterolemic. We can conclude that induction of proinflammatory cytokines such as TNF-α by persistent HCV infection may promote the generation of ACA. Complications of HCV, including thrombocytopenia and thrombosis in arteriovenous shunt, are more strongly correlated with IgG ACA than with IgM ACA.

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