Monitoring of iron, lipid and liver profiles in Egyptian hepatitis C virus patients on sofosbuvir therapy.

Hepatitis C virus is a major cause of inflammation of liver tissue. In serious cases the disease can progressed to cirrhosis, fibrosis, hepatocellular carcinoma and end stage liver disease. The research was designed to monitoring the iron, lipid and liver profiles in hepatitis C patients before and during treatment with sofosbuvir antiviral drug. To achieve this aim, the study was conducted on 22 patients with hepatitis C virus infection and 9 control normal volunteers after taking their consent. The monitoring done through biochemical determination of serum iron, ferritin, transferrin as well as total iron binding capacity. Also, serum cholesterol, triglycerides, HDL, LDL, VLDL, AST, ALP, total protein and albumin was determined. The result showed that, the increased serum iron (205.59±8.27 µg/dl), cholesterol (237.96 ± 10.92 mg/dl), triglycerides (246.58 ± 8.23 mg/dl), LDL (172.82 ± 8.47 mg/dl), VLDL (50.91 ± 1.65 mg/dl), AST (164.58 ± 8.45 U/L), ALP (142.61 ± 7.41 U/L) in hepatitis C virus patients was significantly decreased (P < 0.05) upon treatment with sofosbuvir and the decreased serum ferritin (18.55±1.39 ng/dl), transferrin (128.41 ± 6.43 mg/dl), total iron binding capacity (204.41 ± 8.82 mg/dl), total protein (5.81 ± 0.24 g/dl), albumin (2.83 ± 0.09 g/dl) and HDL (14.22 ± 1.17 mg/dl) in hepatitis C virus patients was significantly increased (P < 0.05) upon treatment with sofosbuvir. According to our finding we concluded that, treatment with sofosbuvir 12 week ameliorate disruption of iron, lipid and liver parameters caused by infection with Hepatitis C virus.

Cadmium overload modulates piroxicam-regulated oxidative damage and apoptotic pathways.

Cadmium (Cd) is a common environmental pollutant that threatens humans' and animals' health. Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used drugs due to their wide therapeutic action; however, they have significant side effects. Since, under many circumstances, humans and animals may be co-exposed to Cd and NSAIDs, the current investigation was assigned to explore the intertwining relationship between Cd and NSAIDs. Four groups of male Wister rats were used: control group: rats received saline; Cd group: rats received cadmium (Cd, 2 mg/kg) orally; Px group: rats received a NSAID (piroxicam, Px, 7 mg/kg, i.p.); and Cd+Px group: rats received both Cd+Px. All treatments were given once a day for 28 consecutive days. Then, blood samples, stomach, liver, and kidney tissues were collected. The results indicated that Px provoked gastric ulcer indicated by high ulcer index, while Cd had no effect on the gastric mucosa. In addition, treatment with Cd or Px alone significantly induced liver and kidney injuries indicated by serum elevations of AST, ALT, ALP, ALB, total protein, creatinine, and urea along with histopathological alterations. Significant increases in malondialdehyde and reduction in GSH and CAT contents were reported along with up-regulated expression of Bax and Bcl-2 after Cd or Px exposure. However, when Cd and Px were given in a combination, Cd obviously potentiated the Px-inflicted cellular injury and death in the liver and kidney but not in the stomach when compared to their individual exposure. This study concluded that oxidative stress mechanisms were supposed to be the main modulator in promoting Cd and Px toxicities when given in combination.