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Journal articles on the topic 'Haemochromatosis'

Author: Grafiati
Published: 4 June 2021
Last updated: 26 January 2023

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1

Campbell, Rachel. "Haemochromatosis." Nursing Standard 24, no. 22 (February 3, 2010): 59–60. http://dx.doi.org/10.7748/ns.24.22.59.s50.

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2

Fernandes, Tanya. "Haemochromatosis." Nursing Standard 24, no. 3 (September 23, 2009): 58. http://dx.doi.org/10.7748/ns2009.09.24.3.58.c7273.

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3

Campbell, Rachel. "Haemochromatosis." Nursing Standard 24, no. 22 (February 3, 2010): 59. http://dx.doi.org/10.7748/ns2010.02.24.22.59.c7520.

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4

WORWOOD, M. "Haemochromatosis." Clinical & Laboratory Haematology 20, no. 2 (April 1998): 65–75. http://dx.doi.org/10.1046/j.1365-2257.1998.00028.x.

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5

Cayley, William E. "Haemochromatosis." BMJ 336, no. 7642 (February 28, 2008): 506. http://dx.doi.org/10.1136/bmj.39357.698889.94.

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6

Rosenberg, William, and Andrew Davis. "Haemochromatosis." Medicine 30, no. 12 (December 2002): 63–64. http://dx.doi.org/10.1383/medc.30.12.63.28523.

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7

Pietrangelo, A. "Haemochromatosis." Gut 52, no. 90002 (May 1, 2003): 23ii—30. http://dx.doi.org/10.1136/gut.52.suppl_2.ii23.

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8

Adams, Paul C. "Haemochromatosis." European Journal of Gastroenterology & Hepatology 16, no. 9 (September 2004): 857–58. http://dx.doi.org/10.1097/00042737-200409000-00007.

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9

Whittington, C. A., and K. V. Kowdley. "Haemochromatosis." Alimentary Pharmacology & Therapeutics 16, no. 12 (December 2002): 1963–75. http://dx.doi.org/10.1046/j.1365-2036.2002.01371.x.

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10

Adams, Paul C., and James C. Barton. "Haemochromatosis." Lancet 370, no. 9602 (December 2007): 1855–60. http://dx.doi.org/10.1016/s0140-6736(07)61782-6.

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11

Rosenberg, William. "Haemochromatosis." Medicine 35, no. 2 (February 2007): 89–92. http://dx.doi.org/10.1016/j.mpmed.2006.11.014.

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12

Griffiths, W. J. H. "Haemochromatosis." Medicine 39, no. 10 (October 2011): 597–601. http://dx.doi.org/10.1016/j.mpmed.2011.07.004.

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13

Griffiths, William J. H. "Haemochromatosis." Medicine 43, no. 11 (November 2015): 656–60. http://dx.doi.org/10.1016/j.mpmed.2015.08.015.

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14

Griffiths, William J. H. "Haemochromatosis." Medicine 47, no. 12 (December 2019): 808–13. http://dx.doi.org/10.1016/j.mpmed.2019.09.008.

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15

Powell, Lawrie W., Rebecca C. Seckington, and Yves Deugnier. "Haemochromatosis." Lancet 388, no. 10045 (August 2016): 706–16. http://dx.doi.org/10.1016/s0140-6736(15)01315-x.

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16

Crawford, Darrell H. G., and Grant A. Ramm. "Haemochromatosis." Trends in Endocrinology & Metabolism 10, no. 1 (January 1999): 14–17. http://dx.doi.org/10.1016/s1043-2760(98)00103-9.

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17

Cox, T. M. "Haemochromatosis." Blood Reviews 4, no. 2 (June 1990): 75–87. http://dx.doi.org/10.1016/0268-960x(90)90030-v.

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18

Schumacher, H. Ralph. "Haemochromatosis." Best Practice & Research Clinical Rheumatology 14, no. 2 (June 2000): 277–84. http://dx.doi.org/10.1053/berh.2000.0065.

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19

Sheldon, J. H. "Haemochromatosis." Journal of Trace Elements in Experimental Medicine 14, no. 2 (2001): 105–6. http://dx.doi.org/10.1002/jtra.1015.

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20

Wittmann, István, László Wagner, Lajos Markó, Mónika Tamaskó, Boglárka Laczy, Márton Mohás, Judit Cseh, and Béla Melegh. "Importance of hereditary haemochromatosis in the care of diabetes mellitus." Orvosi Hetilap 148, no. 3 (January 1, 2007): 111–15. http://dx.doi.org/10.1556/oh.2007.27901.

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Szerzők a vas- és a szénhidrátanyagcsere kapcsolatait vizsgálták saját és irodalmi eredmények tükrében. Különös hangsúlyt fektettek a szabad gyökös folyamatok ismertetésére, mivel a hereditaer haemochromatosis és a diabetes mellitus is, mint a vas- és a szénhidrátanyagcsere-zavarok leggyakoribbjai oxidatív stressz keltése révén vezetnek szövődményekhez. A nagy vér és szöveti glükózkoncentráció elektronfelesleget eredményez. Ez redukálhatja a redox ciklusban részt vevő, transzport- vagy raktárfehérjéhez nem kötött vasat, és ez vezet az oxidatív stresszhez. A hereditaer haemochromatosis mind a válogatás nélküli, mind pedig a diabeteses populációban a szöveti redox-aktív vas szintjének emelkedését okozhatja. A hereditaer haemochromatosis leggyakoribb mutációit hordozók aránya hazánkban, szelekció nélküli népességben 30,4%-ot és diabetesben 35,8%-ot tesz ki. Az irodalom adatai szerint feltételezhető, hogy már a hereditaer haemochromatosis leggyakoribb mutációi (HFE-C282Y és HFE-H63D) szempontjából heterozigotákban is megemelkedik a szöveti vasszint, bár a fenotípusban a hereditaer haemochromatosis ilyenkor általában nem jelenik meg, mivel penetranciája alacsony. Mégis, ez a megemelkedett vas-ellátottság a már más okból – például diabetes mellitus miatt – károsodott szövetek betegségének progresszóját okozhatja. Másrészt a hereditaer haemochromatosis olyan endothelkárosodáshoz vezethet, ami miatt – a diabetes mellitus manifesztálódását megelőzően – hypertonia alakulhat ki. Feltételezhető, hogy a vérnyomásemelkedés a hereditaer haemochromatosis egyik legkorábbi klinikai jele. Nehezen beállítható hypertonia és szénhidrátanyagcsere-zavar esetén érdemes gondolni a hereditaer haemochromatosis lehetőségére.
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21

Limdi, J. K., and J. R. Crampton. "Hereditary haemochromatosis." QJM 97, no. 6 (May 19, 2004): 315–24. http://dx.doi.org/10.1093/qjmed/hch065.

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22

Hannaway, Liam, and Sophie Wellman. "Genetic haemochromatosis." InnovAiT: Education and inspiration for general practice 13, no. 6 (April 7, 2020): 353–60. http://dx.doi.org/10.1177/1755738020911403.

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Genetic haemochromatosis (GH) is the UK’s most common genetic condition inherited in an autosomal recessive manner. It is an iron overload disorder, in which increased intestinal absorption of iron leads to deposition of iron in organs and tissues, most commonly the liver, heart, pancreas, and joints. GH often presents in an insidious manner, and as a result is significantly underdiagnosed. It is a multi-system disease, in which patient care involves various specialities, including primary care. This article will outline the inheritance, diagnosis, treatment and implications of GH and aims to raise awareness of the condition in general practice.
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23

Cox, Timothy M., and Deirdre K. Lord. "Hereditary haemochromatosis." European Journal of Haematology 42, no. 2 (April 24, 2009): 113–25. http://dx.doi.org/10.1111/j.1600-0609.1989.tb01200.x.

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24

MOERMAN, P., P. PAUWELS, K. VANDENBERGHE, H. DEVLIEGER, J. P. FRYNS, H. VERRESEN, J. JAEKEN, J. LAUWERYNS, and E. EGGERMONT. "Neonatal haemochromatosis." Histopathology 17, no. 4 (October 1990): 345–51. http://dx.doi.org/10.1111/j.1365-2559.1990.tb00739.x.

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25

Tanner, A. R., and Ralph Wright. "HAEMOCHROMATOSIS SCREENING." Lancet 332, no. 8605 (July 1988): 286. http://dx.doi.org/10.1016/s0140-6736(88)92586-x.

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26

Dooley, JS, AP Walker, B. Macfarlane, and M. Worwood. "Genetic haemochromatosis." Lancet 349, no. 9066 (June 1997): 1688–93. http://dx.doi.org/10.1016/s0140-6736(96)09316-6.

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27

Crawford, Darrell H. G., Barbara A. Leggett, and Lawrie W. Powell. "1 Haemochromatosis." Baillière's Clinical Gastroenterology 12, no. 2 (June 1998): 209–25. http://dx.doi.org/10.1016/s0950-3528(98)90131-2.

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28

Bomford, A. B., I. W. Dymock, and E. B. Hamilton. "Genetic haemochromatosis." Gut 32, Suppl (September 1, 1991): S111—S115. http://dx.doi.org/10.1136/gut.32.suppl.s111.

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29

Janssen, M. C. H., and D. W. Swinkels. "Hereditary haemochromatosis." Best Practice & Research Clinical Gastroenterology 23, no. 2 (April 2009): 171–83. http://dx.doi.org/10.1016/j.bpg.2009.02.004.

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30

Alvarenga, Aline Morgan, Pierre Brissot, and Paulo Caleb Junior Lima Santos. "Haemochromatosis revisited." World Journal of Hepatology 14, no. 11 (November 27, 2022): 1931–39. http://dx.doi.org/10.4254/wjh.v14.i11.1931.

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31

George, D. K., G. A. Ramm, L. W. Powell, L. M. Fletcher, N. I. Walker, L. L. Cowley, and D. H. G. Crawford. "Evidence for altered hepatic matrix degradation in genetic haemochromatosis." Gut 42, no. 5 (May 1, 1998): 715–20. http://dx.doi.org/10.1136/gut.42.5.715.

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Background—Altered matrix degradation contributes to fibrosis in some liver diseases but the role of matrix degradation in fibrogenesis associated with genetic haemochromatosis has not previously been addressed.Aims—To measure serum concentrations of tissue inhibitor of metalloproteinase 1 (TIMP-1) and matrix metalloproteinases (MMP), MMP-1, MMP-2, and MMP-3 in patients with haemochromatosis and control subjects.Patients—Forty patients with haemochromatosis and 19 healthy control subjects. Ten of the 40 patients were studied before and after venesection therapy.Methods—Serum levels of TIMP-1, MMP-1, MMP-2, and MMP-3 were measured by enzyme immunoassay and correlated to hepatic iron concentration and degree of histological fibrosis.Results—Serum TIMP-1 was increased in patients with haemochromatosis compared with controls (163 (30) versus 123 (28) ng/ml, p<0.0002). Mean serum TIMP-1 concentration of patients with haemochromatosis without fibrosis was significantly higher than in controls (153 (16) versus 123 (28) ng/ml, p=0.03). Serum TIMP-1 concentration correlated with both hepatic iron concentration and hepatic iron index (r=0.42, p<0.01; r=0.42, p<0.01). Serum MMP-2 concentrations correlated with increasing degree of fibrosis in patients with haemochromatosis (r=0.38, p=0.01). The mean MMP-1:TIMP-1, MMP-2:TIMP-1 and age/sex matched MMP-3:TIMP-1 ratios were significantly lower in patients with haemochromatosis than controls (0.11 (0.06) versus 0.2 (0.14), p=0.02; 3.32 (0.9) versus 3.91 (0.81), p=0.05; and 0.26 (0.12) versus 0.47 (0.27), p=0.007, respectively). Following venesection, MMP-2 and MMP-3 concentrations increased by 11% (p=0.03) and 19% (p=0.03), respectively.Conclusions—This study provides the first evidence of an alteration in matrix degradation in haemochromatosis that may be a contributing factor to hepatic fibrogenesis in this disease.
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32

George, D. K., R. M. Evans, R. W. Crofton, and I. R. Gunn. "Testing for Haemochromatosis in the Diabetic Clinic." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 32, no. 6 (November 1995): 521–26. http://dx.doi.org/10.1177/000456329503200601.

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Random serum transferrin saturation (TS) was measured in 1194 patients attending a diabetic clinic. Twenty-one patients had TS > 55,% and in three of these patients repeat random TS was < 55%. Seventeen patients were recalled for fasting serum TS and ferritin measurement. Ten patients had fasting TS > 55%. The diagnosis of haemochromatosis was confirmed by liver biopsy in a total of six patients, three of whom were previously unsuspected. Haemochromatosis was the possible diagnosis in a further four patients. Family studies using HLA typing confirmed haemochromatosis in four family members, three of whom were asymptomatic. We conclude that measurement of TS is a simple and effective method of finding cases of haemochromatosis in the diabetic clinic.
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33

de Graaff, Barbara, Amanda Neil, Kristy Sanderson, Kwang Chien Yee, and Andrew J. Palmer. "Costs associated with hereditary haemochromatosis in Australia: a cost-of-illness study." Australian Health Review 41, no. 3 (2017): 254. http://dx.doi.org/10.1071/ah15188.

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Objective The aim of the present study was to assess health sector, other sector and time-related (productivity) costs associated with hereditary haemochromatosis from societal, government and patient perspectives for the Australian setting. Methods A national web-based survey of people with haemochromatosis was conducted between November 2013 and February 2015. Participants completed a health survey and resource use diaries. Costs were calculated using a bottom-up approach and calculated in 2015 Australian dollars. Results Cost data were available for 157 participants. From a societal perspective, the estimated annual cost of haemochromatosis was A$274 million. The mean (95% confidence interval) cost for symptomatic patients was almost threefold greater than that of asymptomatic patients (A$10030 (7705–12670) vs A$3701 (2423–5296) respectively). Health sector and productivity-related time loss were the main cost drivers. When extrapolating costs to the Australian population level, asymptomatic haemochromatosis accounted for higher costs than symptomatic haemochromatosis (A$183 million vs A$91 million), reflecting the low clinical penetrance estimate used. Total costs increased when higher clinical penetrance estimates were used. Conclusion The present cost-of-illness study, the first to be published for haemochromatosis, found that although costs were substantial, they could be decreased by reducing clinical penetrance. Development of cost-effective strategies to increase early diagnosis is likely to result in better health outcomes for patients and lower total costs. What is known about the topic? To date, no cost-of-illness study has been conducted for haemochromatosis. Previous economic work in this area has relied on cost estimates based on expert opinion. What does the paper add? This paper provides the first cost estimates for haemochromatosis for the Australian population. These estimates, calculated using a bottom-up approach, were extrapolated to the population level based on the most robust epidemiological estimates available for the Australian population. What are the implications for practitioners? Population screening programs have been widely suggested as an approach to reduce clinical penetrance; however, the lack of high-quality economic analyses has been cited as a barrier to implementation. The present study provides the most robust cost estimates to date, which may be used to populate economic models. In addition, the present study illustrates that reducing clinical penetrance of haemochromatosis is likely to result in substantial reductions in cost.
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34

Haddow, James E., and Thomas B. Ledue. "Preventing Manifestations of Hereditary Haemochromatosis through Population Based Screening." Journal of Medical Screening 1, no. 1 (January 1994): 16–21. http://dx.doi.org/10.1177/096914139400100106.

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To evaluate the efficacy of identifying presymptomatic hereditary haemochromatosis through population based screening. Review the hereditary pattern, prevalence, and clinical manifestations of haemochromatosis. Estimate the detection and false positive rates associated with available screening and diagnostic tests. Develop examples of screening protocols and other components that would be necessary for proper implementation. Identify potential barriers and objections. Hereditary haemochromatosis, an autosomal recessive disorder with a prevalence of three to five per thousand in the general population, is associated with a wide variety of clinical manifestations, usually beginning in mid to late adult years. Identifying and treating this disorder after symptoms appear can arrest its progress but usually cannot reverse existing damage to joints, liver, pancreas, pituitary gland, and other organs. Measuring transferrin saturation in serum is now known to be a reliable screening test for haemochromatosis when applied to a general population of healthy adults, detecting about 80% of cases, with a 0·3% false positive rate. Liver biopsy with iron staining and total iron concentration is the recommended diagnostic test for subjects with positive screening tests. Treatment with phlebotomy can then prevent manifestations. Effective systematic identification and management of presymptomatic haemochromatosis in the general population is best accomplished within the framework of an organised screening programme. Potential barriers include accessibility of young adult populations and attitudes in the health community that severe clinical manifestations are relatively uncommon. It is recommended that pilot programmes be undertaken to determine the feasibility of introducing screening for haemochromatosis as part of routine health care.
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35

Dallos, Tomáš, Enijad Sahinbegovic, Elmar Aigner, Roland Axmann, Maximilian Schöniger-Hekele, Thomas Karonitsch, Tanja Stamm, et al. "Validation of a radiographic scoring system for haemochromatosis arthropathy." Annals of the Rheumatic Diseases 69, no. 12 (August 2, 2010): 2145–51. http://dx.doi.org/10.1136/ard.2009.122119.

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BackgroundArthropathy is one of the earliest and most common manifestations of hereditary haemochromatosis with a significant impact on quality of life. Although its radiographic features are well known, there is no assessment tool for their evaluation.ObjectiveTo develop and validate a novel scoring system for the evaluation of radiographic features of haemochromatosis arthropathy.MethodsA dichotomous scoring system assessing four radiographic features of haemochromatosis arthropathy and a 4-grade scale reflecting severity of radiographic change have been developed. Standard radiographs (hand, wrist, knee and ankle) of 170 subjects (116 male, 54 female) with genetically confirmed haemochromatosis and laboratory signs of iron overload were assessed by three readers and construct validity, feasibility and cross-sectional reliability (intrareader and inter-reader) were assessed.ResultsIntrareader and inter-reader reliability as assessed by percentage pairwise agreement and Cohen's weighed κ were good to excellent for most features and locations evaluated. Radiographic scores correlated well with clinical parameters (bony swollen joint count, hand function and physician's global health assessment; Pearson's correlation, r2=0.18–0.62, p<0.0001). A complete set of radiographs took 3.4±1.2 (mean±SD) min to be assessed. An atlas of characteristic radiographic features was compiled.ConclusionA feasible and reliable radiological assessment tool for the evaluation of haemochromatosis arthropathy has been validated and an atlas of characteristic radiographic features provided.
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36

Bradley, Linda A., James E. Haddow, and Glenn E. Palomaki. "Population Screening for Haemochromatosis: Expectations Based on a Study of Relatives of Symptomatic Probands." Journal of Medical Screening 3, no. 4 (December 1996): 171–77. http://dx.doi.org/10.1177/096914139600300403.

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Objectives— The frequency of symptomatic haemochromatosis in the general population and the potential efficacy of population screening is uncertain. Data from family members of clinically diagnosed index cases were used to estimate the frequency of the haemochromatosis genotype, the proportion of homozygous individuals with clinical manifestations, and the efficacy of transferrin saturation and serum ferritin measurements as screening tests. Setting— English language studies from Europe, North America, and Australia. Methods— Haemochromatosis zygosity was classified only by HLA haplotyping, the most reliable available method. All subsequent analyses were based on family members classified in this way. Results— An estimated 53 individuals per 10 000 are homozygous for haemochromatosis. Overall, 67% of male and 41% of female family members display at least one clinical manifestation; for men, the frequency increases with age. Transferrin saturation levels are 70% or above in an estimated 72% of homozygous men, along with three per 1000 heterozygous or unaffected men. Transferrin saturation levels are 60% or above in an estimated 67% of homozygous women, along with six per 1000 heterozygous or unaffected women. Serum ferritin levels, but not transferrin saturation levels, are associated with clinical manifestations. Conclusions— This information can be used to compare expected versus actual screening performance for intervention trials aimed at detecting haemochromatosis in the general population.
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37

Shubin, Andrew D., Lucia De Gregorio, Christine Hwang, and Malcolm MacConmara. "Combined heart–liver transplantation in a case of haemochromatosis." BMJ Case Reports 14, no. 5 (May 2021): e241508. http://dx.doi.org/10.1136/bcr-2020-241508.

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Hereditary haemochromatosis results in multiorgan dysfunction secondary to iron overload. Haemojuvelin (HJV)-associated haemochromatosis, is a rapidly progressing form of haemochromatosis caused by mutation in the HJV that frequently results in heart and liver failure. Herein, we describe the successful treatment of a 39-year-old woman with decompensated heart failure and liver cirrhosis requiring extracorporeal membrane oxygenation who was successfully treated with combined heart–liver transplantation. Following her life-saving multiorgan transplantation, she was also noted to have rapid correction of her serum ferritin to normal levels. She remains healthy with excellent allograft function and normal iron and ferratin levels 4 years after the procedure. To our knowledge, this case is the first demonstration that combined heart–liver transplantation is a feasible option for patients with heart and liver failure secondary to HJV-associated haemochromatosis and indeed offers a long-standing corrective solution to treat this condition and restore physiologically normal iron metabolism.
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38

Wallace, Daniel F. "Non-HFE haemochromatosis." World Journal of Gastroenterology 13, no. 35 (2007): 4690. http://dx.doi.org/10.3748/wjg.v13.i35.4690.

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39

Hunter, Pam. "Haemochromatosis: a story." Lancet Gastroenterology & Hepatology 7, no. 5 (May 2022): 395. http://dx.doi.org/10.1016/s2468-1253(22)00099-1.

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40

Beutler, E. "Penetrance of haemochromatosis." Gut 52, no. 4 (April 1, 2003): 610—a—611. http://dx.doi.org/10.1136/gut.52.4.610-a.

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41

Edwards, Corwin Q. "Screening for Haemochromatosis." Journal of Medical Screening 3, no. 4 (December 1996): 170. http://dx.doi.org/10.1177/096914139600300402.

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42

Riedel, Hans-Dieter, and Wolfgang Stremmel. "The haemochromatosis gene." Journal of Hepatology 26, no. 4 (April 1997): 941–44. http://dx.doi.org/10.1016/s0168-8278(97)80265-6.

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43

Bomford, Adrian. "Genetics of haemochromatosis." Lancet 360, no. 9346 (November 2002): 1673–81. http://dx.doi.org/10.1016/s0140-6736(02)11607-2.

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44

Camaschella, Clara. "2 Juvenile haemochromatosis." Baillière's Clinical Gastroenterology 12, no. 2 (June 1998): 227–35. http://dx.doi.org/10.1016/s0950-3528(98)90132-4.

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45

Finlayson, N. D. "Hereditary (primary) haemochromatosis." BMJ 301, no. 6748 (August 18, 1990): 350–51. http://dx.doi.org/10.1136/bmj.301.6748.350.

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46

Barton, C. J. "Hereditary (primary) haemochromatosis." BMJ 301, no. 6751 (September 15, 1990): 557. http://dx.doi.org/10.1136/bmj.301.6751.557.

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47

Fellows, I. W. "Hereditary (primary) haemochromatosis." BMJ 301, no. 6752 (September 22, 1990): 609. http://dx.doi.org/10.1136/bmj.301.6752.609-a.

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48

Kelly, I., and R. Dick. "Hereditary (primary) haemochromatosis." BMJ 301, no. 6755 (October 6, 1990): 815. http://dx.doi.org/10.1136/bmj.301.6755.815-a.

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49

Crawford, D. H. G. "The haemochromatosis gene." Australian and New Zealand Journal of Medicine 27, no. 6 (December 1997): 639–41. http://dx.doi.org/10.1111/j.1445-5994.1997.tb00989.x.

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50

Krasin, Elisha, Aviram Gold, Samuel Morgan, and Yaniv Warschawski. "Screening for hereditary haemochromatosis in patients undergoing knee arthroplasty." Bone & Joint Open 2, no. 12 (December 1, 2021): 1062–66. http://dx.doi.org/10.1302/2633-1462.212.bjo-2021-0162.r1.

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Aims Hereditary haemochromatosis is a genetic disorder that is caused by several known mutations in the human homeostatic iron regulator protein ( HFE) gene. Abnormal accumulation of iron causes a joint disease that resembles osteoarthritis (OA), but appears at a relatively younger age and is accompanied by cirrhosis, diabetes, and injury to other organs. Increased serum transferrin saturation and ferritin levels are known markers of haemochromatosis with high positive predictive values. Methods We have retrospectively analyzed the iron studies of a cohort of 2,035 patients undergoing knee joint arthroplasty due to OA. Results No patients had HFE gene C282Y, S65C, or H63D mutations testing. In total, 18 patients (2.96%) of the male cohort and 51 (3.58%) of the female cohort had pathologically increased ferritin levels that may be indicative of haemochromatosis. Seven patients (0.34%) had serum transferrin saturation above 45%. Conclusion The awareness for the diagnosis of this disorder in Orthopaedics is low and needs improvement. Osteoarthritic patients undergoing knee arthroplasty should be routinely screened for haemochromatosis by iron studies and referred to genetic testing when needed. Level of evidence: Level III - Retrospective cohort study. Cite this article: Bone Jt Open 2021;2(12):1062–1066.
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