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  1. ORAM TF
    Med J Malaya, 1954 Jun;8(4):337-42.
    PMID: 13193271
    Matched MeSH terms: Hemochromatosis*
  2. Watanabe M, Roth TL, Bauer SJ, Lane A, Romick-Rosendale LE
    PLoS One, 2016;11(5):e0156318.
    PMID: 27232336 DOI: 10.1371/journal.pone.0156318
    A variety of wildlife species maintained in captivity are susceptible to iron storage disease (ISD), or hemochromatosis, a disease resulting from the deposition of excess iron into insoluble iron clusters in soft tissue. Sumatran rhinoceros (Dicerorhinus sumatrensis) is one of the rhinoceros species that has evolutionarily adapted to a low-iron diet and is susceptible to iron overload. Hemosiderosis is reported at necropsy in many African black and Sumatran rhinoceroses but only a small number of animals reportedly die from hemochromatosis. The underlying cause and reasons for differences in susceptibility to hemochromatosis within the taxon remains unclear. Although serum ferritin concentrations have been useful in monitoring the progression of ISD in many species, there is some question regarding their value in diagnosing hemochromatosis in the Sumatran rhino. To investigate the metabolic changes during the development of hemochromatosis and possibly increase our understanding of its progression and individual susceptibility differences, the serum metabolome from a Sumatran rhinoceros was investigated by nuclear magnetic resonance (NMR)-based metabolomics. The study involved samples from female rhinoceros at the Cincinnati Zoo (n = 3), including two animals that died from liver failure caused by ISD, and the Sungai Dusun Rhinoceros Conservation Centre in Peninsular Malaysia (n = 4). Principal component analysis was performed to visually and statistically compare the metabolic profiles of the healthy animals. The results indicated that significant differences were present between the animals at the zoo and the animals in the conservation center. A comparison of the 43 serum metabolomes of three zoo rhinoceros showed two distinct groupings, healthy (n = 30) and unhealthy (n = 13). A total of eighteen altered metabolites were identified in healthy versus unhealthy samples. Results strongly suggest that NMR-based metabolomics is a valuable tool for animal health monitoring and may provide insight into the progression of this and other insidious diseases.
    Matched MeSH terms: Hemochromatosis/blood; Hemochromatosis/metabolism; Hemochromatosis/veterinary*
  3. Oppenheimer SJ
    Acta Paediatr Scand Suppl, 1989;361:53-62.
    PMID: 2485586
    Iron deficiency is prevalent in childhood in the developed and developing countries. Programs of presumptive therapy, mass supplementation and food fortification have been introduced in many countries. The unresolved debate over the interaction of iron and infection in the clinical setting prompts re-evaluation of these practices. Situations of iron overload are associated with increased susceptibility to certain infections, although the exact mechanisms may vary with the main pathology. Iron treatment has been associated with acute exacerbations of infection, in particular malaria. In most instances parenteral iron was used. In the neonate parenteral iron is associated with serious E. coli sepsis. In one country, with endemic malaria, parenteral iron was associated with increased rates of malaria and increased morbidity due to respiratory disease in infants. In contrast in non-malarious countries studies of oral iron supplementation have if anything shown a reduction in infectious morbidity. Methodological problems in the latter reports indicate the need for further controlled prospective studies with accurate morbidity recording if informed recommendations are to be made.
    Matched MeSH terms: Hemochromatosis/immunology*
  4. Roth TL, Reinhart PR, Kroll JL
    J. Zoo Wildl. Med., 2017 09;48(3):645-658.
    PMID: 28920821 DOI: 10.1638/2017-0010.1
    The aim of this study was to determine if ferritin is a reliable biomarker of iron overload disorder (IOD) progression and hemochromatosis in the Sumatran rhinoceros (Dicerorhinus sumatrensis) by developing a species-specific ferritin assay and testing historically banked samples collected from rhinos that did and did not die of hemochromatosis. Ferritin extracted from Sumatran rhino liver tissue was used to generate antibodies for the Enzyme Immunoassay. Historically banked Sumatran rhino serum samples (n = 298) obtained from six rhinos in US zoos (n = 290); five rhinos at the Sumatran Rhino Conservation Centre in Sungai Dusun, Malaysia (n = 5); and two rhinos in Sabah, Malaysia (n = 3) were analyzed for ferritin concentrations. Across all US zoo samples, serum ferritin concentrations ranged from 348 to 7,071 ng/ml, with individual means ranging from 1,267 (n = 25) to 2,604 ng/ml (n = 36). The ferritin profiles were dynamic, and all rhinos exhibited spikes in ferritin above baseline during the sampling period. The rhino with the highest mean ferritin concentration did not die of hemochromatosis and exhibited only mild hemosiderosis postmortem. A reproductive female exhibited decreases and increases in serum ferritin concurrent with pregnant and nonpregnant states, respectively. Mean (±SD) serum ferritin concentration for Sumatran rhinos in Malaysia was high (4,904 ± 4,828 ng/ml) compared to that for US zoo rhinos (1,835 ± 495 ng/ml). However, those in Sabah had lower ferritin concentrations (1,025 ± 52.7 ng/ml) compared to those in Sungai Dusun (6,456 ± 4,941 ng/ml). In conclusion, Sumatran rhino serum ferritin concentrations are dynamic, and increases often are not associated with illness or hemochromatosis. Neither a specific pattern nor the individual's overall mean ferritin concentration can be used to accurately assess IOD progression or diagnose hemochromatosis in this rhino species.
    Matched MeSH terms: Hemochromatosis/blood; Hemochromatosis/veterinary*
  5. Poddar, Sandeep
    MyJurnal
    Hepatitis C is a liver disease caused by the hepatitis C virus: the virus can cause both acute and chronic hepatitis infection. Patients with chronic hepatitis C virus (HCV) infection appear to have an excellent chance of responding to 6 months of standard therapy with interferon (IFN) and frequently develop systemic iron overload, which exacerbates morbidity. The iron excess in hepatitis C may be due to hereditary hemochromatosis, hematologic diseases, multiple transfusions, porphyria cutanea tarda and chronic alcohol abuse. Different mechanisms proposed to explain the relation between HCV infection and hepatic iron overload. Some revealed that hepatic iron accumulation results from release of iron from damaged liver cells. Consumption of coffee, tea also reduces iron absorption and thereby decrease iron overload in Liver and thereby reduces the oxidative stress of iron overload in liver. The global scenario of this problem has been discussed in the article.
    Matched MeSH terms: Hemochromatosis
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