Haemochromatosis
Haemochromatosis is now known to be an iron-storage disease with genetic heterogeneity but with a final common metabolic pathway resulting in inappropriately low production of the hormone hepcidin. This leads to increase in intestinal absorption and deposition of excessive amounts of iron in parench...
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| Published in | The Lancet (British edition) Vol. 388; no. 10045; pp. 706 - 716 |
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| Main Authors | , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Elsevier Ltd
13.08.2016
Elsevier Limited Elsevier |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0140-6736 1474-547X 1474-547X |
| DOI | 10.1016/S0140-6736(15)01315-X |
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| Abstract | Haemochromatosis is now known to be an iron-storage disease with genetic heterogeneity but with a final common metabolic pathway resulting in inappropriately low production of the hormone hepcidin. This leads to increase in intestinal absorption and deposition of excessive amounts of iron in parenchymal cells which in turn results in eventual tissue damage and organ failure. A clinical enigma has been the variable clinical expression with some patients presenting with hepatic cirrhosis at a young age and others almost asymptomatic for life. Research is unravelling this puzzle by identifying environmental factors—especially alcohol consumption—and associated modifying genes that modulate phenotypic expression. A high index of suspicion is required for early diagnosis but this can lead to presymptomatic therapy and a normal life expectancy. Venesection (phlebotomy) therapy remains the mainstay of therapy, but alternative therapies are the subject of current research. |
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| AbstractList | Haemochromatosis is now known to be an iron-storage disease with genetic heterogeneity but with a final common metabolic pathway resulting in inappropriately low production of the hormone hepcidin. This leads to increase in intestinal absorption and deposition of excessive amounts of iron in parenchymal cells which in turn results in eventual tissue damage and organ failure. A clinical enigma has been the variable clinical expression with some patients presenting with hepatic cirrhosis at a young age and others almost asymptomatic for life. Research is unravelling this puzzle by identifying environmental factors—especially alcohol consumption—and associated modifying genes that modulate phenotypic expression. A high index of suspicion is required for early diagnosis but this can lead to presymptomatic therapy and a normal life expectancy. Venesection (phlebotomy) therapy remains the mainstay of therapy, but alternative therapies are the subject of current research. Haemochromatosis is now known to be an iron-storage disease with genetic heterogeneity but with a final common metabolic pathway resulting in inappropriately low production of the hormone hepcidin. This leads to increase in intestinal absorption and deposition of excessive amounts of iron in parenchymal cells which in turn results in eventual tissue damage and organ failure. A clinical enigma has been the variable clinical expression with some patients presenting with hepatic cirrhosis at a young age and others almost asymptomatic for life. Research is unravelling this puzzle by identifying environmental factors-especially alcohol consumption-and associated modifying genes that modulate phenotypic expression. A high index of suspicion is required for early diagnosis but this can lead to presymptomatic therapy and a normal life expectancy. Venesection (phlebotomy) therapy remains the mainstay of therapy, but alternative therapies are the subject of current research.Haemochromatosis is now known to be an iron-storage disease with genetic heterogeneity but with a final common metabolic pathway resulting in inappropriately low production of the hormone hepcidin. This leads to increase in intestinal absorption and deposition of excessive amounts of iron in parenchymal cells which in turn results in eventual tissue damage and organ failure. A clinical enigma has been the variable clinical expression with some patients presenting with hepatic cirrhosis at a young age and others almost asymptomatic for life. Research is unravelling this puzzle by identifying environmental factors-especially alcohol consumption-and associated modifying genes that modulate phenotypic expression. A high index of suspicion is required for early diagnosis but this can lead to presymptomatic therapy and a normal life expectancy. Venesection (phlebotomy) therapy remains the mainstay of therapy, but alternative therapies are the subject of current research. Summary Haemochromatosis is now known to be an iron-storage disease with genetic heterogeneity but with a final common metabolic pathway resulting in inappropriately low production of the hormone hepcidin. This leads to increase in intestinal absorption and deposition of excessive amounts of iron in parenchymal cells which in turn results in eventual tissue damage and organ failure. A clinical enigma has been the variable clinical expression with some patients presenting with hepatic cirrhosis at a young age and others almost asymptomatic for life. Research is unravelling this puzzle by identifying environmental factors—especially alcohol consumption—and associated modifying genes that modulate phenotypic expression. A high index of suspicion is required for early diagnosis but this can lead to presymptomatic therapy and a normal life expectancy. Venesection (phlebotomy) therapy remains the mainstay of therapy, but alternative therapies are the subject of current research Summary Haemochromatosis is now known to be an iron-storage disease with genetic heterogeneity but with a final common metabolic pathway resulting in inappropriately low production of the hormone hepcidin. This leads to increase in intestinal absorption and deposition of excessive amounts of iron in parenchymal cells which in turn results in eventual tissue damage and organ failure. A clinical enigma has been the variable clinical expression with some patients presenting with hepatic cirrhosis at a young age and others almost asymptomatic for life. Research is unravelling this puzzle by identifying environmental factors—especially alcohol consumption—and associated modifying genes that modulate phenotypic expression. A high index of suspicion is required for early diagnosis but this can lead to presymptomatic therapy and a normal life expectancy. Venesection (phlebotomy) therapy remains the mainstay of therapy, but alternative therapies are the subject of current research. |
| Author | Deugnier, Yves Powell, Lawrie W Seckington, Rebecca C |
| Author_xml | – sequence: 1 givenname: Lawrie W surname: Powell fullname: Powell, Lawrie W email: lawrie.powell@qimrberghofer.edu.au organization: Centre for the Advancement of Clinical Research, Royal Brisbane and Women's Hospital, Brisbane, The University of Queensland, Brisbane, Australia – sequence: 2 givenname: Rebecca C surname: Seckington fullname: Seckington, Rebecca C organization: Faculty of Medicine and Biomedical Sciences, The University of Queensland, Brisbane, Australia – sequence: 3 givenname: Yves surname: Deugnier fullname: Deugnier, Yves organization: University Hospital and University of Rennes 1, Rennes, France |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26975792$$D View this record in MEDLINE/PubMed https://univ-rennes.hal.science/hal-01295665$$DView record in HAL |
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| Snippet | Haemochromatosis is now known to be an iron-storage disease with genetic heterogeneity but with a final common metabolic pathway resulting in inappropriately... Summary Haemochromatosis is now known to be an iron-storage disease with genetic heterogeneity but with a final common metabolic pathway resulting in... |
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| SubjectTerms | Alcohol Alcohol Drinking - adverse effects Cation Transport Proteins - genetics Disease Management Environmental Exposure Environmental factors Europe - epidemiology European Continental Ancestry Group - genetics Ferritins - blood Genetic disorders Genetic Testing Genotype Genotype & phenotype Hemochromatosis - diagnosis Hemochromatosis - genetics Hemochromatosis - physiopathology Hemochromatosis - therapy Hemochromatosis Protein Hepcidins - deficiency Heterogeneity Histocompatibility Antigens Class I - genetics Humans Internal Medicine Iron Iron - metabolism Life expectancy Life Sciences Liver Liver - drug effects Liver - metabolism Liver diseases Liver Diseases - etiology Liver Diseases - physiopathology Liver Diseases - therapy Mass Screening - methods Mass Screening - standards Membrane Proteins - genetics Mutation Pathology Phenotype Phlebotomy Polymorphism, Single Nucleotide Receptors, Transferrin - genetics Risk Factors Sex Factors Studies Uncertainty |
| Title | Haemochromatosis |
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