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PubMed1996

Neurobehavioral dysfunctions associated with dietary iron overload.

Excessive dietary Fe is known to be toxic, but the extent of neurobiological involvement is not clear. In the present study male weanling rats were fed diets containing Fe at 35 (control), 350, 3500, or 20000 ppm for 12 wk. An Fe-deficient group (4 ppm) was included for comparison. Rats were tested for behavioral and body weight changes at various times after initiation of diets, and liver and brain nonheme Fe were measured at term. Excess dietary Fe, primarily at 20000 ppm, significantly decreased activity, habituation, reflex startle, and conditioned avoidance response performance, and enhanced prepulse modulation of startle. Body weights were also markedly decreased. Fe-deficient animals showed similar behavioral effects but more moderate body weight changes. Liver nonheme Fe varied directly with dietary levels. Whole-brain nonheme Fe was significantly reduced in Fe-deficient animals but increased only at the 20000-ppm level. Homeostatic mechanisms appear to regulate whole-brain Fe more effectively under conditions of dietary Fe overload than under conditions of Fe deficiency. The behavioral changes associated with dietary Fe overload may represent secondary consequences of systemic toxicity.

Anemia, Iron-Deficiency↗
PubMed2006

Effective new treatments of iron overload in thalassaemia using the ICOC combination therapy protocol of deferiprone (L1) and deferoxamine and of new chelating drugs.

An expert group of the International Committee on Oral Chelators (ICOC) has recommended a universally effective chelation combination protocol of oral deferiprone (L1) during the day (80-110 mg/kg /day) and subcutaneous deferoxamine (40-60 mg/kg) of a minimum of three nights per week for the rapid, safe and effective depletion of excess body iron in transfused iron loaded patients. Following the clearance of excess cardiac and liver iron load, deferiprone (L1) monotherapy at doses exceeding 80 mg/kg/day has been recommended for preventing the re-accumulation of excess iron in the heart and other organs. New chelators such as deferasirox may also be used in combinations with deferiprone (L1) and deferoxamine, especially in patients not tolerating the deferiprone (L1) / deferoxamine combination.

Deferiprone↗
PubMed1978

On the iron content of human serum ferritin, especially in acute viral hepaptitis and iron overload.

A new method has been developed to measure ferritin iron in human serum. The ferritin is bound to antibodies to ferritin, which are coupled to Sepharose 4-B and separated from the serum by centrifugation. The iron is liberated from the bound ferritin and measured colorimetrically. The detection limit of this method proved to be approx. 15 ng Fe/ml serum. The serum ferritin iron concentration has been compared with the serum ferritin protein concentration. During liver disease with liver cell leakage the mean iron content of serum ferritin proved to be less than the mean iron content in the liver ferritin. The mean iron content in the liver ferritin was 16%, range 7%--32% (n = 8). The mean iron content in serum ferritin from the same patients was 5%, range 0%--14%. Also in two cases of haemosiderosis the serum ferritin iron content was low. It is suggested that ferritin loses part of its iron on passage from the tissue cells to the blood. In some cases of severe liver cell (or other cell) leakage the mean iron content in serum ferritin might be high, because then more or less complete ferritin molecules enter the blood.

Acute Disease↗
PubMed1992

Influence of dietary iron overload on cell proliferation and intestinal tumorigenesis in mice.

Iron-enriched diets caused an increase of tumor rate in two models of dimethylhydrazine(DMH)-induced colon tumorigenesis in mice. The effect was independent of the time the iron-diet was fed, i.e. during DMH-treatment or following the DMH-treatment period. The increase of tumor rate depended on the iron concentration in the diet (0.5-3.5%). The concentration-dependent iron accumulation in the colonic mucosa of mice was paralleled by increments of malonaldehyde contents indicating lipid peroxidation, another factor known to be involved in tumor development. It is suggested that iron exerts cocarcinogenic activity in the DMH-model by stimulating cell proliferation and inducing oxidative stress in the colonic mucosa. This effect of iron is independent of the time of tumor-initiation by DMH, as it is also observed in the period of tumor-promotion/progression after DMH-treatment.

Animals↗
PubMed2003

Comparison between desferrioxamine and combined therapy with desferrioxamine and deferiprone in iron overloaded thalassaemia patients.

Desferrioxamine (DFX) alone (40-50 mg/kg/d s.c. over 8-12 h, five times weekly) was compared with combined DFX twice weekly and deferiprone (75 mg/kg/d) over 12 months in previously poorly chelated thalassaemia patients. Serum ferritin fell from 5506 +/- 635 microg/l (mean +/- SEM) to 3998 +/- 604 microg/l (P < 0.001; n = 14) in the DFX group and from 4153 +/- 517 microg/l to 2805 +/- 327 microg/l in the combined group (P < 0.01; n = 11). Deferiprone plus DFX produced a greater mean urine iron excretion (1.01 mg/kg/24 h) than iron intake from blood transfusion in each patient. Main side-effects were skin reactions (DFX alone), nausea and arthralgia (combined therapy). As chelation therapy, the combined protocol was as effective as DFX five times weekly.

Adolescent↗
PubMed2004

Clinical evaluation of the oral iron chelator deferiprone for the potential treatment of iron overload in bird species.

The clinical use of oral Fe chelators for the treatment of Fe-storage disease in birds requires evaluation. In this study, the efficacy of the Fe chelator deferiprone in reducing hepatic Fe stores, its effects on hematologic, biochemical, and plasma Fe parameters, and its potential toxicity during a 30-day treatment period were investigated in a controlled setting using two model species, the white leghorn chicken (Gallus gallus f. domestica) and the domestic pigeon (Columba livia). A second phase of the study investigated deferiprone-related Fe elimination in the excreta. Deferiprone, administered orally at a dosage of 50 mg/kg twice daily to birds that had been experimentally Fe loaded, significantly reduced hepatic Fe concentrations compared with levels in Fe-loaded and non-Fe-loaded controls. There were no significant alterations in routine clinical hematologic or biochemical parameters, although decreased transferrin saturation was noted in both species. Side effects associated with deferiprone administration were decreased weight gain and significant decreases in plasma Zn concentrations. No mortalities occurred in the pigeons, but there were three deaths in the deferiprone-treated group of Fe-loaded chickens, most likely associated with acute reduction of Fe required for normal enzymatic processes. Histologic changes associated with deferiprone treatment were not noted. Deferiprone caused a dose-dependent increase of Fe in the excreta at oral dosages of 50 and 75 mg/kg once daily in both species. Deferiprone is a promising, orally active Fe chelator for the treatment of Fe overload in birds, although its potential side effects need to be considered.

Administration, Oral↗
PubMed1999

Iron overload in Sub-Saharan Africa: to what extent is it a public health problem?

Excessive deposition of Fe in the organs and tissues of Sub-Saharan Africans was first described in South Africa in 1929. Fe overload, or siderosis, was initially attributed to infections and to metallic poisoning (Cu, Sn, Zn), and then to malnutrition. In 1953 it was hypothesized that it was due primarily to excessive Fe intake derived from foods and drinks prepared in Fe vessels. Recently, in 1992 it was advanced that a gene distinct from any HLA-linked locus may also play a role. As to sequelae, in early research on series of hospital patients, the condition was linked to scurvy, osteoporosis, diabetes, cirrhosis, and latterly, to hepatocellular cancer and tuberculosis. Accordingly, many have concluded that Fe overload is responsible for considerable morbidity and mortality, that adventitious Fe intake should be reduced, and that phlebotomy be recommended for those severely affected. However, there are numerous limitations in the evidence. There are also problems in interpretation, since levels of Fe in the serum are affected additionally by a variety of factors: infection, inflammation, certain cancers and alcohol intake. These considerations complicate attempts to assess to what extent the associations described denote causation, and whether Fe overload has significant ramifications for ill in the general African population. While the adverse sequelae of overload may be less of significance than many believe, the precise pathogenicity of the phenomenon will remain uncertain until further investigations, including prospective studies, are undertaken.

Adult↗