Thrombocytopenia in Patients With Chronic Hepatitis C: A Possible Role of HCV on Platelet Progenitor Cell Maturation

A total of 30 patients with chronic hepatitis C (HCV) thrombocytopenia (TP) and 20 healthy controls were studied. Both groups were subjected to complete medical history, clinical examination in addition to assessment of hepatitis markers: level of thrombopoietin (Tpo), Geimsa-stained bone marrow smears, and in vitro short-term megakaryocytic progenitors culture (CFU-MK). Serum Tpo level was significantly elevated in patients with TP HCV. Short-term CFU-MK showed an evident depression in the colony-forming unit-megakaryocyte (CFU-meg). There is a positive correlation between the number of CFU-meg and the platelet count and between serum Tpo level and prothrombin time, transaminase, albumin, and the Child Pugh score of liver disease; a negative correlation between serum Tpo level and the number of CFU-meg and between serum Tpo level and the platelet count. Thus, the level of Tpo could be an indicator of intact functional response of the hepatocytes

Metformin Protects against Diabetic Cardiomyopathy: An Association between Desmin–Sarcomere Injury and the iNOS/mTOR/TIMP-1 Fibrosis Axis

The intermediate filament protein desmin is essential for maintaining the structural integrity of sarcomeres, the fundamental unit of cardiac muscle. Diabetes mellitus (DM) can cause desmin to become dysregulated, following episodes of nitrosative stress, through the activation of the iNOS/mTOR/TIMP-1 pathway, thereby stimulating collagen deposition in the myocardium. In this study, type 2 diabetes mellitus (T2DM) was induced in rats. One group of animals was pre-treated with metformin (200 mg/kg) prior to diabetes induction and subsequently kept on metformin until sacrifice at week 12. Cardiac injuries developed in the diabetic rats as demonstrated by a significant (p p < 0.0001) correlation between desmin tissue levels/sarcomere damage and glycated hemoglobin, heart rate, iNOS, mTOR, and fibrosis was observed. These findings demonstrate an association between damage of the cardiac contractile unit—desmin and sarcomere—and the iNOS/mTOR/TIMP-1/collagen axis of fibrosis in T2DM-induced cardiomyopathy, with metformin exhibiting beneficial cardiovascular pleiotropic effects