Hepatic iron in dialysed patients given intravenous iron dextran

Article Abstract:

Anemia is considered to be a condition in which there is an inadequate number of red blood cells. Common causes include blood loss, impaired blood cell production, poor nutrition and chronic illness. Patients with kidney disease who receive hemodialysis (blood filtration) lose blood in the dialysers, the gastrointestinal tract, and repeated laboratory testing. Unless iron supplementation is given, this blood loss leads to iron deficiency anemia, which increases the patient's burden of disease. Iron supplementation can be administered orally or intravenously. Erythropoietin, a hormone that stimulates the production of red blood cells, can now be administered to dialysis patients to prevent or treat anemia. New erythropoietin treatment protocols require that the patient have an adequate level of available iron. Previous studies have not determined whether orally or intravenously administered iron is more likely to cause toxic effects on the liver (where iron is stored), and whether some degree of liver toxicity is acceptable when treating anemia in this patient population. To explore the relation between iron storage and liver damage, 22 dialysis patients, 13 of whom received intravenous iron-dextran, were assessed. Measurements of liver iron content, plasma iron, transferrin (transported form), and ferritin (stored form) were compared with liver tissue specimens. Five liver biopsies were obtained from living patients, and 15 from necropsy examinations. Iron concentrations, measured chemically and histologically (in tissue), correlated closely. Liver fibrosis was nonspecific and minimal. While there was a risk of liver damage in the patients who received iron-dextran, the potential risk was outweighed by the benefits derived from increased levels of hemoglobin (the oxygen-carrying pigment of red blood cells that contains iron). The use of intravenous iron-dextran in dialysis patients requires further evaluation, since treatment with erythropoietin is likely to increase and it requires a constantly available iron supply. (Consumer Summary produced by Reliance Medical Information, Inc.)

Causes of, Drug therapy, Dialysis, Dialysis (Chemical process), Chronic kidney failure, Iron deficiency anemia, Iron-dextran complex

---

Dietary calcium and iron: effects on blood pressure and hematocrit in young spontaneously hypertensive rats

Article Abstract:

In the strain of rats which have been bred to be spontaneously hypertensive (SHRs), young weaned rats develop increased blood pressure within four days of restriction of dietary calcium, while the opposite effect occurs when the rats are given supplemental calcium. Similar effects occur in older animals but take several weeks to occur. The pressure changes may possibly be caused by changes in hematocrit, an index of the number of red blood cells in a volume of blood. Increased dietary calcium causes a decrease in hematocrit, which in turn lowers blood viscosity and reduces peripheral resistance. In adult SHRs but not a related strain of rats, lowering the hematocrit by varying techniques leads to reduced blood pressure. To determine whether dietary calcium affects blood pressure in SHRs through effects on hematocrit, young male SHRs were treated with one of four diets with varied iron content (essential for red blood cell synthesis), and the effects of varying dietary ratios of calcium to iron on blood pressure were evaluated. As expected, hematocrit decreased as dietary iron decreased. However, blood pressure did not vary with hematocrit. Red blood cell number, size, hemoglobin (oxygen-carrying protein in the blood for which iron is essential) content, and iron levels all decreased with decreases in dietary iron. In another group of SHRs, levels of both dietary iron and calcium were varied, with two groups having similar ratios of iron to calcium. In these rats, the dietary manipulations did not produce consistent and similar changes in both hematocrit and blood pressure. The results suggest that dietary calcium exerts effects on blood pressure relatively independently of changes in hematocrit. Further study of this phenomenon is needed. (Consumer Summary produced by Reliance Medical Information, Inc.)

Blood pressure, Calcium in the body, Calcium (Nutrient), Hematocrit

---

Prevention of postischaemic lipid peroxidation and liver cell injury by iron chelation

Article Abstract:

In an experiment with rats, blood flow into the liver was intentionally stopped by clamping the spot where vessels and ducts enter the organ (hilar pedicle) for 30 minutes while several experiments were done. Decreased blood flow to the liver (ischemia) causes liver cell damage and causes iron to be released which, in turn, causes lipid peroxidation, an enzymatic activity indicating liver damage. The rats were then treated with nothing or with various doses of the iron chelating agent desferrioxamine (deferoxamine, DFR), which binds the iron together and isolates it. The effects of resuming blood flow (reperfusion) was also studied on both groups of rats. The drug was administered intravenously five minutes before either ischemia or reperfusion. The drug DFR reduced the amount of malondialdehyde (MDA), a product of lipid peroxidation, indicating a decrease in liver cell damage. Iron chelation significantly decreases lipid peroxidation, and therefore reduces damage to liver cells during liver ischemia.

Evaluation, Ischemia, Chelation therapy

Similar abstracts:

• Abstracts: Obstetric complications in a patient with Bernard-Soulier syndrome. Obstetric and perinatal outcomes from the Australian and New Zealand Twin-Twin Transfusion Syndrome Registry
• Abstracts: Penicillin-resistant pneumococci from pediatric patients in the Washington, DC, area. Pediatric Resident and Faculty Knowledge of the Denver II
• Abstracts: Cancer risk in relatives of patients with common colorectal cancer. Zinc acetate lozenges to treat the common cold
• Abstracts: Quality indicators for patient information in short-stay units
• Abstracts: Switching from insulin to oral sulfonylureas in patients with diabetes due to Kir6.2 mutations

This website is not affiliated with document authors or copyright owners. This page is provided for informational purposes only. Unintentional errors are possible.