Non-alcoholic steatohepatitis (NASH) and hereditary hemochromatosis (HHC)

Jawaid, Qaiser; LeClair, Paula; Tortorelli, Kristina; Cobb, Joseph; Lambrecht, Richard W.; Bonkovsky, Herbert L.

doi:10.1016/s0016-5085(98)85132-9

Cited by 5 publications

(4 citation statements)

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“…One possible explanation for this discrepancy is ''referral bias'' or ''ascertainment bias.'' Unlike the patients reported in previous studies, 6,[15][16] our patients were seen at a referral center without a special interest in disorders of iron storage. Given the relatively high prevalence of NAFL (3% and 20% in lean and obese individuals, respectively) 4,8 and C282Y mutation (6.7%) in the general population, 16,19 the co-occurrence of these 2 conditions is possible.…”

Section: Discussionmentioning

confidence: 94%

“…Given the relatively high prevalence of NAFL (3% and 20% in lean and obese individuals, respectively) 4,8 and C282Y mutation (6.7%) in the general population, 16,19 the co-occurrence of these 2 conditions is possible. However, the 3-to 5-fold higher prevalence of the HFE mutation seen in these previous studies in NAFL patients (21%-31%) 15,16 is most likely the reflection of this referral or ascertainment bias.…”

Section: Discussionmentioning

confidence: 99%

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Hepatic iron and nonalcoholic fatty liver disease

et al. 1999

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Increased iron is suspected to enhance hepatic injury associated with nonalcoholic fatty liver disease (NAFL).Nonalcoholic steatohepatitis (NASH) is a form of nonalcoholic fatty liver (NAFL) with the potential for progression into cirrhosis. 1-7 Risk factors associated with NASH include obesity, type II diabetes, and hyperlipidemia. [8][9] In a more recent study, NASH was described in patients who lacked these risk factors. 6 Although fatty liver alone seems to be benign, NASH can have a progressive course.

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Hepatic iron and nonalcoholic fatty liver disease

et al. 1999

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“…There was an association between the presence of the C282Y mutation and iron overload, as manifested by the hepatic iron concentration (P<0.005), hepatic iron index P<0.005), and stainable iron (P<0.005), as well as with the degree of fibrosis. We reported recently [37] that patients with NASH have an increased prevalence of heterozygosity (61%, P = 0.02), and of homozygosity (8.3%, P=0.0001) for either or both of the mutations compared wit controls. The presence of the C282Y mutation alone (2.7%, P=0.047 for homozygosity) and of the H63D mutation (5.6% homozygous and 44.4% heterozygous) were statisti cally increased when compared with controls.…”

Section: Table 1 Nonhemochromatotic Disorders Of the Liver In Which Imentioning

confidence: 91%

Role of HFE gene mutations in liver diseases other than hereditary hemochromatosis

Bonkovsky

Obando

1999

Curr Gastroenterol Rep

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Heavy iron overload, as occurs in primary and secondary hemochromatosis, may cause fibrosis of parenchymal organs, including the heart, liver, and pancreas, and it is a risk factor for the development of hepatocellular carcinoma. Recent evidence indicates that lesser degrees of hepatic iron deposition are also risk factors for nonhemochromatotic liver disease. For example, several recent studies showed extraordinarily high prevalences (about 60% to 75%) of HFE mutations in patients with porphyria cutanea tarda and significantly increased prevalences of these mutations in patients with nonalcoholic steatohepatitis from Australia and the United States. It is less well established that the prevalence of the HFE mutations is increased in alcoholic liver disease and in chronic viral hepatitis, but in both conditions, patients harboring one of these mutations, especially C282Y, are more likely to have advanced hepatic fibrosis or cirrhosis. Thus, these mutations both incite and exacerbate nonhemochromatotic liver disease. In this review, we summarize current knowledge of these associations and emphasize important unresolved questions that require further study.

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“…80 Patients frequently have obesity, hyperlipidemia, or diabetes, but some patients have no obvious etiologic factors. Several studies have now documented abnormal iron levels in serum and liver in up to 50% of patients with NASH [80][81][82] and a higher than expected frequency of the C282Y mutation (homozygosity in 3%-8% and heterozygosity in 14%-21%). Thus, iron may act as a cofactor in causing liver disease in this syndrome.…”

Section: Genotype and Phenotype In Hemochromatosismentioning

confidence: 97%