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1 se when she was 18 years old), and secondary haemochromatosis.
2  alloimmune mechanism for recurrent neonatal haemochromatosis.
3 us is a recognized consequence of hereditary haemochromatosis.
4 d symptoms that would suggest a diagnosis of haemochromatosis.
5 ent with clinical observations of hereditary haemochromatosis.
6 han 1% of homozygotes develop frank clinical haemochromatosis.
7 lain how mutations in HFE lead to hereditary haemochromatosis.
8 ated in the iron-overload disease hereditary haemochromatosis.
9 ne of which (Cys282Tyr) is believed to cause haemochromatosis.
10  not all homozygotes present clinically with haemochromatosis.
11  gene is mutated in patients with hereditary haemochromatosis.
12 ric oncology patients suspected of secondary haemochromatosis.
13  evidence of liver involvement with neonatal haemochromatosis: 11 had higher than normal concentratio
14  DBA, multiple blood transfusions, secondary haemochromatosis, advanced liver fibrosis, heart failure
15                                    Secondary haemochromatosis among paediatric oncologic patients is
16     The application of molecular genetics to haemochromatosis and experimental mutagenesis in animals
17  the development of iron overload typical of haemochromatosis and thalassaemia intermedia.
18 atory data and data on signs and symptoms of haemochromatosis as elicited by questionnaire.
19 disorders of systemic iron overload, such as haemochromatosis, brain iron is not increased, which sug
20                                              Haemochromatosis C282Y homozygotes with normal transferr
21 creatitis, pancreatic ductal adenocarcinoma, haemochromatosis, cystic fibrosis, and previous pancreat
22 al ions in humans is a feature of hereditary haemochromatosis, disorders of metal-ion deficiency, and
23                                   Hereditary haemochromatosis due to mutations in the HFE gene leads
24 ingle reaction parameter that mimics a human haemochromatosis gene (HFE) mutation.
25       After identification of the hereditary haemochromatosis gene HFE, and receipt of confirmation t
26                                  The role of haemochromatosis genes in determining susceptibility to
27                   Inheritance of one or more haemochromatosis genes is an important susceptibility fa
28 e normal age distribution of people with the haemochromatosis genotype, and the lack of symptoms in p
29 osatellite alleles that define the ancestral haemochromatosis haplotype had previously been determine
30 h markers of the HLA-A3-containing ancestral haemochromatosis haplotype.
31 identified as highly expressed in hereditary haemochromatosis HCC (HH-HCC) were validated using quant
32 n of HFE, the principal determinant of adult haemochromatosis (HFE1; OMIM 235200) and TfR2, recently
33  the promise of candidate genes for juvenile haemochromatosis (HFE2; OMIM 602390) and neonatal haemoc
34                                              Haemochromatosis (HH) is a clinically and genetically he
35 er and 7 HCC from 3 patients with hereditary haemochromatosis (HH) undergoing surgery.
36                                   Hereditary haemochromatosis (HH), which affects some 1 in 400 and h
37 ations of which are the most common cause of haemochromatosis in the European population.
38                  The most common symptoms of haemochromatosis, including poor general health, diabete
39                                     Neonatal haemochromatosis is a rare disease of gestation that res
40                                   Hereditary haemochromatosis is an iron overloading disorder caused
41 , indicate that the penetrance of hereditary haemochromatosis is much lower than generally thought.
42                       A role of this gene in haemochromatosis is supported by the frequency and natur
43 Overall efficacy of population screening for haemochromatosis is undermined by these observations.
44  recently been reported that causes juvenile haemochromatosis (JH) in the homozygous state.
45 load and deficiency disorders (i.e. anaemia, haemochromatosis, Menkes disease, Wilson's disease), and
46  changing the severity of recurrent neonatal haemochromatosis of administering during pregnancy high-
47 chromatosis (HFE2; OMIM 602390) and neonatal haemochromatosis (OMIM 231100) provide the foundation fo
48 nt haemoglobinopathy, bone marrow pathology, haemochromatosis, or end-stage renal failure requiring d
49 n lead to diseases of iron overload, such as haemochromatosis, or iron limitation anaemias(2).
50              If diagnosed and treated early, haemochromatosis progression can be distinctively altere
51 the human X chromosome, the human hereditary haemochromatosis region, and the BRCA1 pseudogene.
52 e debate on whether population screening for haemochromatosis should be undertaken or whether alterna
53  appears to have modified recurrent neonatal haemochromatosis so that it was not lethal to the fetus
54                     Screening programmes for haemochromatosis that include follow-up identification o
55 arnt from the study of the rare instances of haemochromatosis that involve mutations in newly-identif
56                A disease state simulation of haemochromatosis was created by altering a single reacti
57 ecent pregnancy ended in documented neonatal haemochromatosis were treated with IVIG, 1 g/kg bodyweig