Serum ferritin levels predict histological severity in patients with nonalcoholic fatty liver disease in India

Parikh, Pathik; Patel, Jatin; Ingle, Meghraj; Sawant, Prabha

doi:10.1007/s12664-015-0572-5

Cited by 12 publications

(15 citation statements)

References 29 publications

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Section: Discussionmentioning

confidence: 89%

“…The best cutoff value of serum ferritin was found to be 51.95 ng/mL, for predicting the occurrence of fibrosis on top of NAFLD in the current study, with a 65% sensitivity and a 60% specificity with AUC 0.658. Similarly, Parikh et al 35 found that the cutoff value of 48 ng/mL was the best to predict fibrosis in NAFLD with AUC 0.779. On the other hand, Manousou et al 8 found that the cutoff value of serum ferritin 240 ng/mL or more combined with BMI >28.2 identified patients at risk of developing fibrosis with an 82% sensitivity and a 79% specificity.…”

Section: Discussionmentioning

confidence: 89%

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Serum ferritin as a non‐invasive marker in the prediction of hepatic fibrosis among Egyptian patients with non‐alcoholic fatty liver disease

et al. 2017

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Background and AimMany studies have found a relationship between hepatic iron, serum ferritin, and non‐alcoholic fatty liver disease (NAFLD) or its progress. The aim of this study is to assess the value of serum ferritin as a non‐invasive marker in the prediction of hepatic fibrosis in NAFLD.MethodsThis study included 113 subjects who were classified into three groups. Group I included 30 healthy subjects as control with no clinical, radiological, and histological features of NAFLD. Group II included 31 NAFLD patients without hepatic fibrosis. Group III included 52 patients with hepatic fibrosis on top of NAFLD.ResultsSerum ferritin was determined using ferritin ELISA kit. Fibrosis 4 score was calculated. Liver biopsy was conducted for included patients. Significantly higher levels of serum ferritin were found in patients with hepatic fibrosis on top of NAFLD than controls. Receiver operating characteristic curve analysis revealed that an optimum cutoff level of 51.95 ng/mL was the best to predict fibrosis on top of NAFLD with diagnostic sensitivity and specificity of 65% and 60%, respectively, and area under the curve = 0.658.ConclusionHigher serum ferritin was found in patients with hepatic fibrosis on top of NAFLD. Serum ferritin was found to be a predictor of fibrosis on top of NAFLD with moderate sensitivity and specificity.

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Section: Discussionmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 89%

Serum ferritin as a non‐invasive marker in the prediction of hepatic fibrosis among Egyptian patients with non‐alcoholic fatty liver disease

et al. 2017

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“…A wide range of indirect and direct inflammatory parameters were found to be significantly higher in NAFLD or NASH patients when compared with control subjects (e.g., aspartate aminotransferase, thioredoxin, C-reactive protein, α-2-macroglobulin, ceruloplasmin, malondialdehyde, hepatic 8-oxodG, nitric oxide, interleukin-6, interleukin-8, and tumor necrosis factor-α). Most studies also found ferritin levels to be significantly higher in NASH patients compared with control subjects and/or patients with HS and NAFLD patients compared with control subjects 27,36,37,42,[45][46][47][48][49] (►Supplementary Table S2 [online only]). Most of the studies showed no signs of biochemical or histological iron overload to explain the higher ferritin levels.…”

Section: Hyperferritinemia Related To Inflammationmentioning

confidence: 99%

Hyperferritinemia in Nonalcoholic Fatty Liver Disease: Iron Accumulation or Inflammation?

et al. 2019

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Hyperferritinemia, observed in inflammation, iron overload as well as in combination of both, is found in ∼30% of nonalcoholic fatty liver disease (NAFLD) patients. The authors summarized the evidence regarding the potential cause of hyperferritinemia in NAFLD, as this may affect the indicated therapy. A systematic literature search was conducted in EMBASE, PubMed, MEDLINE, and the Cochrane library. In the majority of NAFLD patients, hyperferritinemia is due to inflammation without hepatic iron overload. In a smaller group, a dysmetabolic iron overload syndrome (DIOS) is found, showing hyperferritinemia in combination with mild iron accumulation in the reticuloendothelial cells. The smallest group consists of NAFLD patients with hemochromatosis. Phlebotomy is only effective with hepatocellular iron overload and should not be the treatment when hyperferritinemia is related to inflammation, whether or not combined with DIOS. Treatment with lifestyle changes is to date probably the more effective way until new medication is becoming available.

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“…4 b). In such patients, hyperferritinemia is an indicator of more advanced fibrosis or accelerated disease progression [46] . However, studies on the effects of phlebotomy have revealed conflicting results, where initial findings that therapeutic venesection improves insulin sensitivity have not been reproduced more recently [47] .…”

Section: Evaluation Of Patients With Suspected Iron Overload Hyperfermentioning

confidence: 99%

Pathogenesis, Diagnosis and Treatment of Hemochromatosis

Zoller¹,

Henninger

2016

Dig Dis

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Hemochromatosis is a common cause of chronic liver disease and HFE genotyping allows decisive and non-invasive diagnosis. Molecular and clinical genetic studies have led to the identification of genes other than HFE in patients with inherited diseases associated with increased hepatic iron storage that can cause hemochromatosis, which adds complexity to a diagnostic approach to patients with suspected hemochromatosis. Despite major advances in genetics, hepatic iron quantification by non-invasive methods therefore remains the key to the diagnosis of hemochromatosis. Although associated with homozygosity for the C282Y polymorphism in the HFE gene in >80% of patients, hemochromatosis is a complex genetic disease with strong environmental disease modifiers. Testing for mutations in the non-HFE hemochromatosis genes transferrin receptor 2, hemojuvelin, HAMP and SLC40A1 is complex, costly and time-consuming. Demonstration of hepatic iron overload by liver biopsy or MRI is therefore required before such complex tests are carried out. The pathogenesis of chronic liver disease in hemochromatosis is mainly attributed to the redox potential of tissue iron, and only the more recent studies have focused on the toxic properties of circulating iron. Considering the fact that an increased saturation of transferrin and high iron in plasma are the hallmark of all hemochromatosis forms, an alternative view would be that toxic iron in the circulation is involved in the pathogenesis of hemochromatosis. Recent studies have shown an increased concentration of redox-active iron in plasma in patients with increased transferrin saturation. This finding supports the hypothesis that tissue iron may be the ‘smoking gun' of iron-induced organ damage. Taken together, caring for patients with suspected or established hemochromatosis still remains a challenge, where understanding the genetics, biochemistry and cell biology of hemochromatosis will aid better diagnosis and treatment of affected individuals.

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Serum ferritin levels predict histological severity in patients with nonalcoholic fatty liver disease in India

Abstract: Serum ferritin was low in Indian individuals, and levels even within apparently normal range indicated fibrosis and cirrhosis. A cutoff level of 48.0 IU/mL distinguished fibrosis in NAFLD. Fibroscan correlated well with serum ferritin levels.

Cited by 12 publications

References 29 publications

Serum ferritin as a non‐invasive marker in the prediction of hepatic fibrosis among Egyptian patients with non‐alcoholic fatty liver disease

Serum ferritin as a non‐invasive marker in the prediction of hepatic fibrosis among Egyptian patients with non‐alcoholic fatty liver disease

Hyperferritinemia in Nonalcoholic Fatty Liver Disease: Iron Accumulation or Inflammation?

Pathogenesis, Diagnosis and Treatment of Hemochromatosis

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