ascorbic-acid and Liver-Failure

Topics: Antioxidants; Ascorbic Acid; Ascorbic Acid Deficiency; Child; Female; Humans; Kidney Transplantation; Liver Failure; Liver Transplantation; Membrane Lipids; Oxidative Stress; Renal Insufficiency; Scurvy; Tissue and Organ Procurement; Tocopherols

First described in the 1500 s, scurvy is infrequently seen in industrialized countries today, although vulnerable patient groups remain. A 15-yr-old girl underwent liver transplantation at age 26 months for a primary diagnosis of biliary hypoplasia, and subsequently developed late allograft failure and progressive renal insufficiency culminating in listing for combined liver retransplantation and kidney transplantation at age 13 yr. She required regular hemodialysis treatment for 12 months prior to deceased donor organ availability, with a complicated clinical course including recurrent septic episodes and severe cachexia. Ten months after initiation of hemodialysis, she presented with severe bone pain, purpura, ecchymoses, gingival hyperplasia, mucosal bleeding, and subconjunctival hemorrhages. Serial serum ascorbic acid levels were found to be extremely low (<10 micromol/L) despite routine supplementation both in her dialysate and via regular oral supplementation. Histopathology from skin biopsy revealed purpura, hyper- and parakeratosis, and follicular plugging. She had ECG and 2D echocardiogram disturbances, as well as osteopenia and sclerosis of the extremities on radiological evaluations. Therapy with high-dose ascorbic acid (1 g/day orally) led to complete resolution of skin lesions. This case highlights the importance of awareness and recognition of this historic diagnosis, and particularly in children with end-stage organ disease with severely compromised nutrition.

Topics: Adolescent; Antioxidants; Ascorbic Acid; Ascorbic Acid Deficiency; Biopsy; Female; Humans; Kidney Transplantation; Liver Failure; Liver Transplantation; Renal Dialysis; Renal Insufficiency; Reoperation; Scurvy; Tissue and Organ Procurement

Increasing evidence has shown that reactive oxygen species (ROS) are important mediators in liver ischemia/reperfusion injury(IRI). ROS include hydrogen peroxide (H(2)O(2)), superoxide anion (O(-2)), and hydroxyl radical (HO(-)), which may be generated by activated Kupffer cells in the liver, contributing to reperfusion injury. Hepatic IRI is a multistep process that damages liver graft function. To establish a series of therapeutic strategies to improve the outcome of liver transplantation, a good understanding of the mechanisms of IRI is essential. However, the detail mechanisms of how ROS lead to hepatocyte damage in IRI remains unclear. The aim of this review was to describe recent developments in the field of oxidative stress research. The first part of this review focused on the key roles and possible mechanisms of ROS in hepatic IRI. The second part of this review summarizes some findings including novel and classic antioxidant methods to ameliorate the hepatocyte damage during IRI.

Topics: Antioxidants; Ascorbic Acid; Free Radical Scavengers; Glutathione Peroxidase; Humans; Ischemic Preconditioning; Liver Circulation; Liver Failure; Liver Transplantation; Peroxidases; Peroxiredoxins; Reactive Oxygen Species; Reperfusion Injury; Thioredoxins