ライフサイエンスコーパス: hemochromatosis

1 available for the major forms of hereditary hemochromatosis.

2 ad disorders, collectively termed hereditary hemochromatosis.

3 cardiac stress exacerbated by iron overload hemochromatosis.

4 , and review current treatments for neonatal hemochromatosis.

5 myloidosis, cardiac sarcoidosis, and cardiac hemochromatosis.

6 oad, such as the thalassemias and hereditary hemochromatosis.

7 lation is central to the pathogenesis of HFE hemochromatosis.

8 ovel suggestions to improve the treatment of hemochromatosis.

9 rtin, are associated with autosomal dominant hemochromatosis.

10 use of the iron-overload disorder hereditary hemochromatosis.

11 form of the iron overload hereditary disease hemochromatosis.

12 pic expression of Wilson disease and genetic hemochromatosis.

13 inherited disorder of iron metabolism type I hemochromatosis.

14 understanding of Wilson disease and genetic hemochromatosis.

15 rine' focus was elaborated in an overview of hemochromatosis.

16 n-depleted HFE hemochromatosis, and juvenile hemochromatosis.

17 orm of the iron overload disease, hereditary hemochromatosis.

18 e pathogenesis of the iron overload disorder hemochromatosis.

19 d not carry genetic variants associated with hemochromatosis.

20 or cirrhosis, one of the main morbidities of hemochromatosis.

21 and TfR2 cause autosomal-recessive forms of hemochromatosis.

22 TfR2) and HFE are associated with hereditary hemochromatosis.

23 in the HFE gene, responsible for hereditary hemochromatosis.

24 It is defective in hereditary hemochromatosis.

25 ted with the iron overload disorder known as hemochromatosis.

26 ostasis and associated with human hereditary hemochromatosis.

27 r high-risk genetic screening for hereditary hemochromatosis.

28 utweigh the risks and costs of screening for hemochromatosis.

29 (weh(Tp85c-/-)) and in patients with type 4 hemochromatosis.

30 revention of iron accumulation in hereditary hemochromatosis.

31 primary portal for intestinal iron entry in hemochromatosis.

32 ssociated with the iron overloading disorder hemochromatosis.

33 ns reportedly seen in humans with hereditary hemochromatosis.

34 is mutated in the iron-overloading disorder hemochromatosis.

35 lin (HJV) cause severe, early-onset juvenile hemochromatosis.

36 istently identify a link to overt hereditary hemochromatosis.

37 the iron overload phenotype in patients with hemochromatosis.

38 confirm that mutations in HJV cause juvenile hemochromatosis.

39 bling mutations in the TFR2 gene suffer from hemochromatosis.

40 ropoietin, iron deficiency, thalassemia, and hemochromatosis.

41 e liver disease) can cause acquired forms of hemochromatosis.

42 recognized model of the iron-loading disease hemochromatosis.

43 markers in HFE C282Y homozygotes at risk for hemochromatosis.

44 is C, alcoholic liver disease, or hereditary hemochromatosis.

45 es the established treatment for HFE-related hemochromatosis.

46 he first stage of fibrogenesis in hereditary hemochromatosis.

47 f insulin resistance, and iron burden in HFE hemochromatosis.

48 poiesis but is pathologic in thalassemia and hemochromatosis.

49 anemia, sideroblastic anemia, and hereditary hemochromatosis.

50 n accumulation, as observed in patients with hemochromatosis.

51 ngs in advanced iron overload resulting from hemochromatosis.

52 ral history of iron deposition in hereditary hemochromatosis.

53 und to be associated with milder symptoms of hemochromatosis.

54 several organs similar to classic hereditary hemochromatosis.

55 ac diagnoses were familial amyloidosis (11), hemochromatosis (1), restrictive cardiomyopathy and card

56 regulators or the hepcidin gene itself cause hemochromatosis, a common genetic disorder.

57 Type 2 diabetes is a common manifestation of hemochromatosis, a disease of iron overload.

58 Inactivating mutations cause juvenile hemochromatosis, a severe iron overload disorder.

59 se, primary sclerosing cholangitis, neonatal hemochromatosis, acute liver failure (from the Pediatric

60 acute myeloid leukemia, Alzheimer's disease, hemochromatosis, age-related macular degeneration (AMD),

61 Less common causes include hemochromatosis, alpha1-antitrypsin deficiency, autoimmu

62 Patients with C282Y HFE hemochromatosis also have inappropriately low hepcidin l

63 viruses, and oxyradical disorders including hemochromatosis, also generate reactive oxygen/nitrogen

64 uvelin (Hjv)-knockout mice, another model of hemochromatosis, also had increased expression of GLUTs,

65 common HFE mutations resulting in phenotypic hemochromatosis among C282Y heterozygotes have been iden

66 1) What is the risk for developing clinical hemochromatosis among those with a homozygous C282Y geno

67 Hereditary hemochromatosis, an iron overload disease caused by a de

68 Iron overload is the hallmark of hereditary hemochromatosis and a complication of iron-loading anemi

69 e pathophysiology of Wilson disease, genetic hemochromatosis and alpha-1 antitrypsin deficiency as we

70 tion focuses on the disorders Wilson disease hemochromatosis and alpha-one antitrypsin deficiency, an

71 sis and pointing to potential treatments for hemochromatosis and anemia of inflammation (anemia of ch

72 Iron overload in hereditary hemochromatosis and beta-thalassemia intermedia is cause

73 Second, we evaluated mice combining the hemochromatosis and beta-thalassemia phenotypes.

74 nt of clinical conditions such as hereditary hemochromatosis and beta-thalassemia.

75 ned to investigate the presence of the DR in hemochromatosis and describe its associations.

76 myloidosis, cardiac sarcoidosis, and cardiac hemochromatosis and imaging techniques used to facilitat

77 n overload in nearly all forms of hereditary hemochromatosis and in untransfused iron-loading anemias

78 to prevent iron overload in murine models of hemochromatosis and induce iron-restricted erythropoiesi

79 iency results in iron overload in hereditary hemochromatosis and ineffective erythropoiesis.

80 Four selected topics, Wilson disease, hemochromatosis and iron overload disorders, alpha-1 ant

81 data has also advanced our understanding of hemochromatosis and iron overload disorders.

82 The Hemochromatosis and Iron Overload Screening (HEIRS) Stud

83 The Hemochromatosis and Iron Overload Screening (HEIRS) Stud

84 ts and iron dysfunctions, such as hereditary hemochromatosis and iron overload.

85 sm may account for individual variability in hemochromatosis and iron status connected with liver and

86 rders of iron metabolism, such as hereditary hemochromatosis and iron-refractory iron-deficiency anem

87 n is inappropriately decreased in hereditary hemochromatosis and is abnormally increased in the anaem

88 Portal inflammation occurs in hemochromatosis and is independently associated with the

89 ontribute to behavioral symptoms in NBIA and hemochromatosis and is relevant to patients with abnorma

90 own to reduce iron overload in patients with hemochromatosis and may be an option for patients who ca

91 cular insight into immune function in type I hemochromatosis and other disorders of iron homeostasis,

92 e selected disorders-Wilson disease, genetic hemochromatosis and other hereditary iron overload disor

93 ing of the pathophysiology and treatment for hemochromatosis and other iron overload disorders, Wilso

94 ights into the pathophysiology of hereditary hemochromatosis and the anaemia of chronic diseases have

95 on, stimulating the development of the DR in hemochromatosis and this correlates strongly with hepati

96 is commonly found in plasma of patients with hemochromatosis and transfusional iron overload, Zip14-m

97 Advancements in diagnosis of hemochromatosis and Wilson disease may lead to earlier d

98 ons on genetics, diagnosis and management of hemochromatosis and Wilson disease over the past 18 mont

99 s have been made in the genetic diagnosis of hemochromatosis and Wilson disease.

100 For genetic hemochromatosis and Wilson's disease, studies focused on

101 ates for the molecular defect underlying Hfe hemochromatosis, and BMP6-like agonists may have a role

102 y iron deficiency anemia, cancer, hereditary hemochromatosis, and ineffective erythropoiesis, such as

103 mia (ferritin < 10 ng/mL), iron-depleted HFE hemochromatosis, and juvenile hemochromatosis.

104 ver failure, liver transplantation, neonatal hemochromatosis, and the Biliary Atresia Research Consor

105 hepatic and intestinal transport proteins in hemochromatosis, and the histopathologic interpretive ch

106 rs such as the hemophilias, Gaucher disease, hemochromatosis, and the porphyrias.

107 increased in inflammation and suppressed in hemochromatosis, and they may have diagnostic importance

108 included hepatitis B and C virus infections, hemochromatosis, and Wilson's disease.

109 iron homeostasis; all of the known causes of hemochromatosis appear to prevent this system from funct

110 beta-Thalassemia and HFE-related hemochromatosis are 2 of the most frequently inherited d

111 adipocyte ferroportin expression because of hemochromatosis are associated with decreased adipocyte

112 Patients with hemochromatosis are instructed to avoid taking supplemen

113 Patients with hereditary hemochromatosis are known to have an increased risk for

114 e authors draw attention again to hereditary hemochromatosis as a cause of preventable organ dysfunct

115 Hemochromatosis-associated FPN mutations, therefore, eit

116 with up to 10% to 33% eventually developing hemochromatosis-associated morbidity.

117 y BMP6 can be modulated by each of the three hemochromatosis-associated proteins: HJV (hemojuvelin),

118 ced oxidative damage may also play a role in hemochromatosis-associated retinal pathology.

119 definition of the common form of hereditary hemochromatosis became possible, and testing for the com

120 rss6 could be beneficial in individuals with hemochromatosis, beta-thalassemia, and related disorders

121 ermination codon, in a patient with juvenile hemochromatosis but no family history of iron disorders.

122 thought to be ideal venues for diagnosis of hemochromatosis, but diagnosis rates are often low.

123 ty and mortality in patients with hereditary hemochromatosis, but the precise mechanisms leading to d

124 color, Y chromosome R1b haplotypes, and the hemochromatosis C282Y allele; to our knowledge, the firs

125 It is shown that the characteristics of HFE hemochromatosis can be reproduced by increasing the setp

126 oportin disease (FD) is a form of hereditary hemochromatosis caused by mutations in the iron transpor

127 e numerous, but they are only predisposed to hemochromatosis; complete organ disease develops in a mi

128 Hearts from HFE(-/-) mice with hemochromatosis contained slightly more iron overall tha

129 The relationship between the hemochromatosis due to transferrin receptor 2 (TFR2) mut

130 rs to be the ultimate cause of most forms of hemochromatosis, either due to mutations in the hepcidin

131 ans with a form of hereditary iron overload, hemochromatosis, exhibit loss of beta-cell mass.

132 eviously considered screening for hereditary hemochromatosis for a recommendation as a clinical preve

133 odel of hemochromatosis with deletion of the hemochromatosis gene (Hfe(-/-)).

134 Mitochondrial haplogroups and hemochromatosis gene (HFE) polymorphisms have been assoc

135 ity for the C282Y mutation in the hereditary hemochromatosis gene (HFE).

136 wn-regulation of HFE protein [encoded by the hemochromatosis gene (Hfe)] and ferroportin [encoded by

137 allele of Uro-d and two null alleles of the hemochromatosis gene (Uro-d(+/-), Hfe(-/-)) that develop

138 anced greatly with the identification of the hemochromatosis gene and the continued examination of th

139 The C282Y mutation in the HFE hemochromatosis gene occurs more commonly in autoimmune

140 Mice with deficiencies in the hemochromatosis gene product, Hfe, mounted a general inf

141 Mice deficient in the hemochromatosis gene, Hfe, have attenuated inflammatory

142 nificant disease in patients who do not have hemochromatosis genotypes.

143 ample, the role of hepcidin dysregulation in hemochromatosis has been a surprising discovery that pro

144 and that hemojuvelin mutants associated with hemochromatosis have impaired BMP signaling ability.

145 Patients with HJV hemochromatosis have low urinary levels of hepcidin, the

146 er studies have suggested that patients with hemochromatosis have poor post-transplantation survival.

147 st a mechanism by which HFE2 mutations cause hemochromatosis: hemojuvelin dysfunction decreases BMP s

148 Retinal expression of GPR91 was higher in hemochromatosis (Hfe(-/-)) mice than in wild-type (WT) m

149 ASO treatment in mice affected by hemochromatosis (Hfe(-/-)) significantly decreased serum

150 ith disruption of two iron regulatory genes, hemochromatosis (Hfe) and transferrin receptor 2 (Tfr2).

151 lly diverse participants that tested for the hemochromatosis (HFE) C282Y genotype and iron status.We

152 The protein product of the hemochromatosis (HFE) gene modulates uptake of iron and

153 Genotyping for hemochromatosis (HFE) gene status was performed.

154 A specific polymorphism in the hemochromatosis (HFE) gene, H63D, is over-represented in

155 c iron overload: mice with a deletion of the hemochromatosis (Hfe) gene, mice fed a high iron diet, a

156 beta2-M interacts with its receptor, hemochromatosis (HFE) protein, to modulate iron responsi

157 including variants at the transferrin (TF), hemochromatosis (HFE), fatty acid desaturase 2 (FADS2)/m

158 verload was studied in two genetic models of hemochromatosis (HFE-null mouse and HJV-null mouse) and

159 ology of such common disorders as hereditary hemochromatosis (HH) and the anaemia of chronic diseases

160 Mutations in HFE lead to hereditary hemochromatosis (HH) because of inappropriately high iro

161 ansferrin receptor 2 (TFR2) cause hereditary hemochromatosis (HH) by impeding production of the liver

162 HFE-associated hemochromatosis (HH) defined as homozygosity for the C28

163 Mutations in the hereditary hemochromatosis (hh) gene (HFE) explain the siderosis in

164 Hereditary hemochromatosis (HH) is a common autosomal-recessive dis

165 Hereditary hemochromatosis (HH) is a common inherited iron overload

166 Hereditary hemochromatosis (HH) is a highly prevalent genetic disor

167 Hereditary hemochromatosis (HH) is associated with an increased ris

168 Hereditary hemochromatosis (HH) is characterized by increased intes

169 Hereditary hemochromatosis (HH) leads to iron loading because of a

170 ed levels of hepcidin in a murine hereditary hemochromatosis (HH) model increased adipocyte ferroport

171 Type 2 hereditary hemochromatosis (HH) or juvenile hemochromatosis is an e

172 e Hfe and Tfr2 knockout models of hereditary hemochromatosis (HH), signal transduction to hepcidin vi

173 HFE cause the most common form of hereditary hemochromatosis (HH).

174 al complications from HFE-related hereditary hemochromatosis (HH).

175 Here, we provide a comprehensive report of hemochromatosis in a group of patients of Asian origin.

176 By contrast, hemochromatosis in Asia is rare and less well understood

177 genetic screening for HFE-related hereditary hemochromatosis in C282Y homozygotes only.

178 erved in alcoholic liver disease and genetic hemochromatosis in combination with alcohol.

179 P6-SMAD signaling impairment and ameliorates hemochromatosis in Hfe(-/-) mice.

180 h old Hfe-deficient mice, an animal model of hemochromatosis in humans.

181 ns of this gene cause one form of hereditary hemochromatosis in humans.

182 tment on the molecular defect underlying Hfe hemochromatosis in mice.

183 HFE gene testing can be used to diagnose hemochromatosis in symptomatic patients, but analyses of

184 ion in vivo and in vitro in a mouse model of hemochromatosis in which the gene most often mutated in

185 S who was misdiagnosed and treated as having hemochromatosis, in whom a heterozygous c.-160A>G mutati

186 These causes of hereditary hemochromatosis include defects in genes encoding HFE, t

187 y or susceptibility of developing hereditary hemochromatosis, including the relatives of individuals

188 Wilson disease and genetic hemochromatosis involve defects in metal transport with

189 Both Wilson's disease and genetic hemochromatosis involve defects in the transport of heav

190 ll integrity), FOXC2 (vascular development), hemochromatosis (involved in venous ulceration and iron

191 thogenesis of nearly all forms of hereditary hemochromatosis involves inappropriately low expression

192 Hemochromatosis is a disorder of iron overload arising m

193 Hereditary hemochromatosis is a genetic disorder of iron metabolism

194 Hereditary hemochromatosis is a heterogeneous group of genetic diso

195 Juvenile hemochromatosis is a rare autosomal recessive disorder c

196 Hereditary hemochromatosis is an autosomal recessive disorder of ir

197 hereditary hemochromatosis (HH) or juvenile hemochromatosis is an early onset, genetically heterogen

198 Hereditary hemochromatosis is an inherited disorder of increased ir

199 Hereditary hemochromatosis is an iron overload disorder that can le

200 Juvenile hemochromatosis is an iron-overload disorder caused by m

201 Hereditary hemochromatosis is an iron-overload disorder resulting f

202 Hemochromatosis is associated not only with excessive ac

203 Type IV hemochromatosis is associated with dominant mutations in

204 Juvenile hemochromatosis is associated with hepcidin or hemojuvel

205 Excessive iron is also proangiogenic, and hemochromatosis is associated with iron overload.

206 Hereditary hemochromatosis is caused by mutations in the hereditary

207 HFE-associated hemochromatosis is characterized by abnormally high leve

208 Hereditary hemochromatosis is characterized by tissue iron loading

209 Hereditary hemochromatosis is commonly found in populations of Euro

210 Hemochromatosis is considered by many to be an uncommon

211 C282Y substitution diagnostic for hereditary hemochromatosis is developed and evaluated using ferroce

212 anagement of such cofactors in patients with hemochromatosis is important to reduce the risk of liver

213 Because the penetrance of HFE hemochromatosis is low, traditional population screening

214 disease penetrance in HFE-related hereditary hemochromatosis is lower than previously believed, makin

215 Hereditary hemochromatosis is now a complex entity with various cli

216 Therapeutic phlebotomy for hereditary hemochromatosis is relatively safe and presumably effica

217 The most common form of primary hemochromatosis is that caused by C282Y mutation of the

218 Type 1 hemochromatosis is the most common form of the disease a

219 Diagnosis of hereditary hemochromatosis is usually based on a combination of var

220 Juvenile hemochromatosis (JH) is the most severe form, usually ca

221 ng mutations in the RGMc gene cause juvenile hemochromatosis (JH), a rapidly progressing iron storage

222 uidance molecule c (HJV/RGMc) cause juvenile hemochromatosis (JH), a rapidly progressive iron overloa

223 ule C, RgmC) are the major cause of juvenile hemochromatosis (JH).

224 generated Hepc(-/-) mice (a murine model of hemochromatosis) lacking HIF-2 in the intestine and show

225 Despite reports of skin toxicity in hemochromatosis, little is known about iron levels in sk

226 The mainstay of hemochromatosis management is still removal of iron by p

227 factors have been found to cause late-onset hemochromatosis, many patients have unexplained signs of

228 Thus, individuals with hereditary hemochromatosis may be protected with subunit vaccines b

229 FPN-linked hemochromatosis may have a variable pathogenesis dependi

230 Patients with hemochromatosis may have impairment of iron homeostasis

231 sting that hepatic iron levels in hereditary hemochromatosis may not accurately predict the iron cont

232 However, hereditary hemochromatosis may still cause morbidity and mortality

233 Hemochromatosis mice, cytomegalovirus (CMV) infection of

234 cidin, are inappropriately low in hereditary hemochromatosis mouse models and patients with HFE mutat

235 In hereditary hemochromatosis, mutations in HFE lead to iron overload

236 st-transplantation survival of patients with hemochromatosis (n = 177) at 1 year (79.1%), 3 years (71

237 In contrast, during 1997-2006, patients with hemochromatosis (n = 217) had excellent 1-year (86.1%),

238 Evidence suggests that most neonatal hemochromatosis (NH) is the phenotypic expression of ges

239 fection outcomes in patients with hereditary hemochromatosis or thalassemia.

240 man immunodeficiency virus, type 2 diabetes, hemochromatosis, or obesity and thus have implications w

241 in healthy controls, with reduced levels in hemochromatosis (P<0.00006) and elevated levels in infla

242 ries not normally associated with hereditary hemochromatosis (Pakistan, Bangladesh, Sri Lanka, and Th

243 o increase physician awareness of hereditary hemochromatosis, particularly the variable penetrance of

244 ted HIV-1 or when infecting macrophages from hemochromatosis patients expressing mutated HFE.

245 Juvenile hemochromatosis patients have decreased urinary levels o

246 icated in the majority of diagnosed juvenile hemochromatosis patients.

247 Loss of Bmp6 in ECs recapitulated the hemochromatosis phenotype of global Bmp6 knockout mice,

248 a iron levels characteristic of the juvenile hemochromatosis phenotype.

249 Defects in human hemochromatosis protein (HFE) cause iron overload due to

250 Mutations in hemochromatosis protein (HFE) or transferrin receptor 2

251 sis is caused by mutations in the hereditary hemochromatosis protein (HFE), transferrin-receptor 2 (T

252 The hereditary hemochromatosis protein HFE promotes the expression of h

253 stably transfected to express the hereditary hemochromatosis protein HFE these cells have increased f

254 associated proteins: HJV (hemojuvelin), HFE (hemochromatosis protein), and TfR2 (transferrin receptor

255 Lack of functional hereditary hemochromatosis protein, HFE, causes iron overload predo

256 e morphogenetic protein 6 (BMP6), hereditary hemochromatosis protein, transferrin receptor 2, matript

257 Actions of the hereditary hemochromatosis proteins HFE and transferrin receptor 2

258 ical penetrance of HFE-associated hereditary hemochromatosis, raising the possibility that pharmacolo

259 with primary iron overload due to hereditary hemochromatosis reduce morbidity and mortality compared

260 level and, with the assistance of BMP2/4 and hemochromatosis-related proteins hemojuvelin, HFE and tr

261 hepatic fibrosis and cirrhosis in hereditary hemochromatosis relates to the degree of iron loading, b

262 addressing genetic screening for hereditary hemochromatosis remains insufficient to confidently proj

263 The term hemochromatosis represents a group of inherited disorder

264 2 (TfR2) cause a rare form of the hereditary hemochromatosis, resulting in iron overload predominantl

265 We present a case of neonatal hemochromatosis, review genetic and metabolic causes of

266 This paradox could explain the low yields of hemochromatosis screening reported by some liver clinics

267 understanding of the pathogenesis of primary hemochromatosis, secondary iron overload, and anemia of

268 lved as a modulator of the penetrance of HFE hemochromatosis since fat mass is associated with overex

269 subjects participating in the Scripps/Kaiser hemochromatosis study, only 59 had serum ferritin levels

270 at increased risk for developing hereditary hemochromatosis that can be readily identified before ge

271 Today, hereditary hemochromatosis, the paradigmatic iron-loading disorder,

272 Compared with recipients without hemochromatosis, those with hemochromatosis were more li

273 In human hemochromatosis, tissue toxicity is a function of tissue

274 We aimed to compare patients with hemochromatosis to those with other causes of liver dise

275 Mutations in hemochromatosis type 2 (HFE2), which encodes the protein

276 HFE2 (hemochromatosis type 2 gene) is highly expressed in skel

277 theless, TFR2 mutations cause iron overload (hemochromatosis type 3) without overt erythroid abnormal

278 ns in this gene result in a form of juvenile hemochromatosis (type 2A).

279 splant survival of patients with and without hemochromatosis using data provided by the United Networ

280 The prevalence of hereditary hemochromatosis was 1 in 169 patients to 1 in 556 patien

281 of iron overload severity in HFE-associated hemochromatosis, we performed exome sequencing of DNA fr

282 e, but genotypes known to be associated with hemochromatosis were absent.

283 heir regulation in the iron-overload disease hemochromatosis were examined.

284 cipients without hemochromatosis, those with hemochromatosis were more likely to die of cardiovascula

285 hological papers on several forms of non-HFE hemochromatosis were published and Wilson's disease was

286 djustment for gene mutations associated with hemochromatosis, were explored.

287 These disorders include various forms of hemochromatosis, which are characterized by inadequate h

288 Hereditary hemochromatosis, which is characterized by inappropriate

289 patients with the common disease hereditary hemochromatosis, which is often caused by an HFE mutatio

290 esis of this increasingly recognized form of hemochromatosis, which responds poorly to conventional t

291 st-transplantation survival of patients with hemochromatosis, which was previously reported to be poo

292 s isolated from a researcher with hereditary hemochromatosis who died from laboratory-acquired plague

293 as of viral and drug hepatitis, fatty liver, hemochromatosis, Wilson disease, several biliary tract d

294 disease, liver cirrhosis, biliary cirrhosis, hemochromatosis, Wilson's disease) and ICC (biliary cirr

295 nery involved in the pathogenesis of genetic hemochromatosis, Wilson's disease, and alpha1-antitrypsi

296 reased insulin secretion in a mouse model of hemochromatosis with deletion of the hemochromatosis gen

297 mutation in ferroportin 1 produced a form of hemochromatosis with excessive iron in hepatocytes and a

298 in C326 Fpn residue produce a severe form of hemochromatosis with iron overload at an early age.

299 Screening for hemochromatosis with serum ferritin levels will detect t

300 mice have a phenotype resembling hereditary hemochromatosis, with reduced hepcidin expression and ti