Dysmetabolic Iron Overload Syndrome: Raised Ferritin With Metabolic Syndrome

Table of Contents

1. What the Name Describes
2. How Common It Is
3. How It Differs From HFE Hemochromatosis
4. What a High Ferritin Does and Does Not Mean
5. Proposed Mechanisms, Sorted by Type of Evidence
6. Findings Reported Alongside It
7. Bloodletting Trials: Results in Both Directions
8. What Happens After Iron Is Removed
9. Diet, Weight and Lifestyle Findings
10. What Is Not Known
11. Key Research Papers
12. Connections
13. Featured Videos

What the Name Describes

The syndrome was first described in The Lancet in 1997. Moirand and colleagues in Rennes, France, studied 65 people who had unexplained iron in the liver and a normal transferrin saturation (the share of the blood's iron-carrying protein that is loaded with iron). Their median liver iron concentration was 65 µmol/g of dry liver, against a normal value below 36 µmol/g; their median ferritin was 566 µg/L; and their median transferrin saturation was 32%. Ninety-five per cent had one or more of obesity, raised blood fats, abnormal glucose handling or high blood pressure. The authors called it "a new non-HLA-linked iron-overload syndrome" and wrote that it "suggests a link between iron excess and metabolic disorders".

Two years later the same group described 161 people with unexplained liver iron who did not carry two copies of the C282Y variant of the HFE gene. Most (94%) had features of the insulin-resistance syndrome, defined in that study as a body mass index above 25, diabetes or raised blood fats. Liver iron ranged from 38 to 332 µmol/g (median 90). Transferrin saturation was raised in 35% of them, with a median of 42%. The authors called the pattern insulin resistance-associated hepatic iron overload.

A 2017 review by three of the Rennes researchers gives the definition most later papers repeat. Dysmetabolic iron overload syndrome is:

• a raised ferritin (hyperferritinemia) with a normal or moderately raised transferrin saturation;
• one or more metabolic abnormalities: a raised body mass index with fat carried around the abdomen, raised blood pressure, abnormal blood fats, abnormal blood sugar, or fatty inflammation of the liver (steatohepatitis);
• mild excess iron in the liver on magnetic resonance imaging (MRI) or liver biopsy;
• no other identifiable cause of iron excess.

A related label, dysmetabolic hyperferritinemia, describes the raised ferritin and the metabolic features without proof of extra iron in the liver. A 2020 review asked whether the two are "two related conditions or different entities" and noted that their clinical presentation "overlaps almost completely". In 2023 a multidisciplinary global panel of researchers published a consensus statement proposing an updated definition and a provisional staging system for metabolic hyperferritinemia (a raised ferritin with metabolic dysfunction). A 2024 validation study applied it using three ferritin grades: grade 1 from 200 µg/L in women or 300 µg/L in men up to 550 µg/L; grade 2 from 550 to 1,000 µg/L; and grade 3 above 1,000 µg/L. The panel wrote that "validated criteria for the non-invasive diagnosis of metabolic hyperferritinaemia and the staging of iron overload are still lacking".

An Italian biopsy study of 81 people with unexplained liver iron, published in 2008, found that two or more features of metabolic syndrome together with a fatty liver marked out a group with moderate iron overload, iron sitting mainly in the liver's lining (sinusoidal) cells, and a normal transferrin saturation. People with a transferrin saturation of 60% or more had heavier iron loading, few or no metabolic abnormalities and a pattern that resembled hemochromatosis.

How Common It Is

Counts vary widely, mainly because studies define the condition differently and few measure liver iron directly.

• In the general middle-aged population. In the Paracelsus 10,000 cohort from Salzburg, Austria, 1,111 of 8,408 people aged 40 to 77 (13%) had a raised ferritin, and 69% of them were men. Applying the 2023 consensus criteria, 81% of those with a raised ferritin met the metabolic criteria for metabolic hyperferritinemia. This counts raised ferritin with metabolic features; it does not show how many had extra iron in the liver.
• Among people referred for a high ferritin. In 132 consecutive referrals to a hospital in the Basque Country, Spain, metabolic syndrome was found in 55% of the men and 59% of the women assessed for it. In a larger Basque cohort of 276 referrals, 49% had metabolic syndrome.
• Among people with metabolic syndrome. In an Egyptian study, 64 of 101 people with high blood pressure had metabolic syndrome, and 6 of those 64 (9.3%) met the criteria for dysmetabolic iron overload syndrome. A 2020 review states that the syndrome is seen in 15% of people with metabolic syndrome.
• Among people with fatty liver. A 2026 meta-analysis of 16 studies with 49,754 patients found a raised ferritin in 26.4% of people with metabolic dysfunction-associated steatotic liver disease (MASLD, the newer name for non-alcoholic fatty liver disease), higher in Asia (30.9%) than in North America (20.2%). A 2019 systematic review put the figure at about 30%.

The 2020 review calls dysmetabolic iron overload syndrome "the most frequent iron overload condition". The Basque studies, described further down, found that many people with a high ferritin and metabolic syndrome had little or no measurable extra liver iron, which is why the raised-ferritin counts above are larger than the number with true iron overload.

How It Differs From HFE Hemochromatosis

Hereditary hemochromatosis, mostly caused by two copies of the C282Y variant of the HFE gene, is described on the Hemochromatosis page. The studies on this page compare the two conditions in four ways.

• Genetics. By definition, people with dysmetabolic iron overload syndrome do not carry two copies of C282Y. HFE variants are not absent, though. In Mendler's 161 patients the C282Y variant appeared on 20% of chromosomes against 9% in controls, and H63D on 30% against 17%. The excess came from a higher share of compound heterozygotes (one C282Y and one H63D), who carried slightly more iron. Patients with no HFE variant had similar iron levels to most other genotypes. In the 132 Basque referrals, two copies of H63D were found in 17.5% against 7.76% of controls. The 2023 consensus statement says genetic variants that affect iron handling are "the main determinants" of ferritin in people with metabolic dysfunction.
• Transferrin saturation. In hemochromatosis it is typically high. In the original 1997 series it was normal (median 32%). In the 2008 Italian biopsy study, a transferrin saturation of 60% or more went with the hemochromatosis-like pattern, while a normal saturation went with the metabolic pattern. Not every patient fits neatly: 35% of Mendler's patients had a raised saturation.
• How much iron the gut absorbs. In hemochromatosis the gut absorbs too much iron. In a French study using a labelled form of iron, men with dysmetabolic iron overload syndrome absorbed less iron than overweight controls with normal iron stores, and much less than lean controls. In a 2020 trial using a standard iron-rich meal containing 43 mg of iron, iron absorption was 3.5 times higher in people with hemochromatosis than in people with the metabolic syndrome.
• How much liver iron. The 1997 patients had significantly less liver iron than people with genetic hemochromatosis and were older. Typical liver iron values in the metabolic syndrome studies sit in the mild range: median 65 µmol/g (1997), median 90 (1999), a mean of 78 in 16 men (2009) and a mean of 80 in 58 patients (2014). A 2026 Italian study of 570 people with a raised ferritin found that a transferrin saturation of 60% or more, or a saturation below 60% with a ferritin of 963 µg/L or more, identified over 95% of those with the highest liver iron grade (above 7 mg/g).

One finding cuts the other way. A 2001 study of 56 phlebotomised patients with insulin resistance-associated iron overload reported that they gave up a similar total amount of iron as C282Y homozygotes, while their ferritin was three times higher. The authors concluded that ferritin overestimated their iron stores. A 2015 case-control study measured the iron removed by bloodletting: 2.5 g in 12 people with dysmetabolic iron overload syndrome against 0.8 g in 12 overweight people with normal ferritin.

The two conditions also look alike in some respects. In a 2024 study of 20 people with each condition, the pattern of oxidised fat molecules in the blood (oxylipins) did not separate the two groups, apart from one molecule, 20-hydroxyeicosatetraenoic acid, which was higher in the metabolic group and tracked with high blood pressure.

What a High Ferritin Does and Does Not Mean

Ferritin is the protein that stores iron inside cells, and a small amount of it circulates in the blood. Its level tracks iron stores, but it also rises for reasons that have nothing to do with extra iron. The studies found that a high ferritin in someone with metabolic features is often not a sign of iron overload.

• Inflammation. A 2019 systematic review of hyperferritinemia in fatty liver concluded that in most people with fatty liver disease, a raised ferritin is due to inflammation without iron overload in the liver. A smaller group had dysmetabolic iron overload syndrome with mild iron in the liver's scavenger cells, and the smallest group had hemochromatosis.
• Liver disease itself. In 628 adults with biopsy-proven fatty liver disease in the United States NASH Clinical Research Network, a ferritin above 1.5 times the upper limit of normal (above 300 ng/mL in women and 450 ng/mL in men) went with more liver iron and more severe liver disease. It was independently associated with advanced fibrosis (odds ratio 1.66) and with a higher disease activity score. The higher activity score held even in patients with no iron in the liver.
• Alcohol. In 3,375 Australian adult twins, serum iron and ferritin rose step by step across classes of alcohol intake, and beer had a larger effect than wine or spirits. The authors concluded that "alcohol intake at low level increases ferritin". Alcohol was common in the referral studies: 18.1% of the 132 Basque referrals drank 60 g or more a day, and a significant alcohol intake was recorded in 38.2% of the 179 people in a 2026 Spanish bloodletting programme.
• Little or no extra liver iron. In the 2016 Basque study, people with a high ferritin and metabolic syndrome had a mean liver iron of 27.8 µmol/g on magnetic resonance imaging, within the normal range, and not different from people with a high ferritin without metabolic syndrome. In the larger 276-person Basque cohort, mean liver iron was 37.7 µmol/g with metabolic syndrome and 43.4 µmol/g without it, again not significantly different. In the 132 Basque referrals overall, magnetic resonance imaging found iron overload in 33%. In the 570-person Italian study, 66.1% had a liver iron of 3 mg/g or less, the lowest grade.

For this reason the Liver Problems page describes transferrin saturation as the more specific test, and the studies above confirmed extra liver iron with magnetic resonance imaging or biopsy. The Ferritin Test and Iron Panel pages explain the blood tests themselves.

Proposed Mechanisms, Sorted by Type of Evidence

Why iron would build up in people with insulin resistance is still debated. The 2017 Rennes review calls it "a multifactorial and dynamic process triggered by an excessively rich diet, facilitated by environmental and genetic cofactors and implying a cross-talk between the liver and visceral adipose tissue". That is the authors' interpretation, not a tested finding. The pieces below are grouped by the kind of evidence behind them.

Hepcidin is raised, not lowered (measured in people)

Hepcidin is the liver hormone that limits how much iron the gut absorbs and how much iron storage cells release; the Iron Absorption and the Hepcidin Gate animation shows how it works. In hemochromatosis hepcidin is too low. In the metabolic syndrome the human measurements point the other way:

• In 10 people with dysmetabolic hyperferritinemia in Vancouver, urinary hepcidin was about twice that of healthy controls (median 1,584 against 799 ng/mg of creatinine, p = 0.05), while transferrin saturation did not differ (38% against 36%). Seven of the ten had mild liver iron on magnetic resonance imaging.
• In the French iron-absorption study, absorption fell as plasma hepcidin rose (r = −0.61), and also fell with the insulin-resistance score and with C-reactive protein, a marker of inflammation.
• In 1,391 people from the Val Borbera population in Italy, serum hepcidin rose steadily with each additional feature of metabolic syndrome, in step with ferritin. In men, ferritin was the only independent predictor of hepcidin. The authors read this as the normal feedback loop still working: hepcidin rises as iron stores rise.

Hepcidin resistance (a small challenge study in people)

A 2016 Milan study gave an oral iron dose to 18 people with dysmetabolic iron overload syndrome, 18 with fatty liver, 23 healthy people and 10 with hemochromatosis. The metabolic group made more hepcidin than any other group, but that hepcidin spike was less able to hold down the rise in transferrin saturation early in the test. The authors proposed "a hepcidin resistance state" and wrote that "further studies are required" to find the molecular cause.

Inflammation and fat tissue (human tissue and laboratory work)

In liver and fat tissue from severely obese patients, hepcidin was made in fat tissue as well as in the liver, and more of it was made in the fat of obese patients. Fat-tissue hepcidin tracked with interleukin-6 and C-reactive protein, two markers of inflammation, and interleukin-6 raised hepcidin in fat tissue in the laboratory. Sixty-eight per cent of these patients had a low transferrin saturation. The authors called hepcidin "a proinflammatory adipokine" and linked it to the low blood iron of inflammation in obesity, not to iron build-up.

Insulin resistance (association in people)

The tie to insulin resistance comes mainly from how often the two occur together: 94% of Mendler's patients and 95% of Moirand's had metabolic features. In the absorption study, iron absorption fell as insulin resistance rose. These are associations. Whether insulin resistance causes the iron build-up, the iron worsens insulin resistance, or both come from a shared cause is not settled. The bloodletting trials below were partly a test of the second idea.

Diet (animal work and review opinion)

The "excessively rich diet" trigger in the Rennes review is an interpretation. No human study read for this page tested it.

Findings Reported Alongside It

• Liver scarring. In the 1999 French series, portal fibrosis was present in 62% of patients (grade 2 or 3 in 12%), and it went with fatty liver, inflammation and older age, not with the amount of liver iron. Fatty liver was present in 25% and steatohepatitis in 27%. In the 2026 meta-analysis, a raised ferritin in fatty liver disease was associated with a higher rate of liver-related events (hazard ratio 2.02).
• Mortality. In United States National Health and Nutrition Examination Survey data analysed in 2024, metabolic hyperferritinemia as a whole was not significantly linked to death from any cause, but grades 2 and 3 (ferritin above 550 µg/L) were.
• Male hormones. In 50 men with moderate dysmetabolic iron excess, 8% had a low total testosterone and 26% a low bioavailable testosterone. Higher liver iron went with higher sex hormone-binding globulin and lower luteinizing hormone.
• Stress hormones. In the Egyptian study, adrenaline, noradrenaline and dopamine levels did not differ between people with and without the syndrome. The people with the syndrome were older and had a lower body mass index than the other patients with high blood pressure.

These are associations from observational studies and do not show that the iron caused the finding.

Bloodletting Trials: Results in Both Directions

Removing blood (phlebotomy or venesection) is the standard treatment for hemochromatosis. Whether it helps people with metabolic iron excess has been tested many times. The results split by study design: uncontrolled and matched studies were mostly positive, while the two largest randomized trials were null.

Studies that reported a benefit

• 2001, Rennes (uncontrolled). Fifty-six patients were bled weekly or every two weeks. Women gave up a median 0.6 g of iron in 2.8 months and men 1.8 g in 5 months. Fatigue and/or joint pain improved in 6 of 7 patients who had them, and the bloodletting was well tolerated. The authors recommended venesection.
• 2007, Italy (case-control, fatty liver with high ferritin). Sixty-four bled patients were matched with 64 who received diet and lifestyle advice only. After 8 months, insulin and an insulin-resistance score fell more with iron depletion (p = 0.0016 and p = 0.0042), with larger effects in people with higher ferritin and in carriers of HFE variants.
• 2011, Italy (observational, propensity-adjusted). In 198 people with fatty liver at three centres (79 bled, 119 advice only), venesection was linked to a normal insulin-resistance score (odds ratio 3.00) and a normal level of alanine aminotransferase (ALT), a liver enzyme (odds ratio 2.56).
• 2014, Milan (randomized, 38 patients). People with fatty liver and ferritin of 250 ng/mL or more were assigned to bloodletting or lifestyle change alone. Among the 21 who followed the protocol, liver biopsy improved in 8 of 12 bled patients (67%) against 2 of 9 controls (22%), p = 0.039. Liver enzymes were lower at two years in the bled group.
• 2016 meta-analysis. Four studies with 438 participants found a lower insulin-resistance score after bloodletting (mean difference 0.84, 95% confidence interval 0.01 to 1.67, with high variation between studies), lower alanine aminotransferase and triglycerides and higher high-density lipoprotein cholesterol.

Studies that found no benefit

• 2006, Rennes (randomized, 48 patients). Bloodletting every 14 days took ferritin from 715 to 74 µg/L. Activity of the liver enzyme cytochrome P450 2E1, the trial's main measure, did not change differently between groups. Low-density lipoprotein cholesterol fell more in the bled group.
• 2011, Rennes (randomized, 50 men). Iron depletion did not significantly improve any hormone level.
• 2015, Western Australia (randomized, 74 patients with fatty liver). Over 6 months the bled group had a median of 7 sessions and a larger fall in ferritin (−148 against −38 ng/mL). There was no difference in liver fat on magnetic resonance imaging (17.7% against 15.5%), alanine aminotransferase, a liver-cell injury marker, insulin resistance or a lipid-peroxidation marker. Patients who started with a high ferritin did no better.
• 2017, eight French centres (randomized, 274 patients). This is the largest trial. All participants had dysmetabolic iron overload syndrome without diabetes and liver iron above 50 µmol/g on magnetic resonance imaging. For one year, 146 were bled to keep ferritin below 50 µg/L and 128 received lifestyle and diet advice alone. Ferritin ended at 71 against 733 µg/L after removal of 4.9 L of blood. Fasting blood sugar did not differ (5.44 against 5.49 mmol/L, p = 0.57). The insulin-resistance score was worse in the bled group (3.39 against 2.40, p = 0.002). Weight changed by +0.5% against −0.6%, and liver enzymes, a fatty-liver index and a fibrosis score did not differ. Fatigue was reported by 25.3% of bled patients against 2.3% of controls. The authors concluded that iron depletion "does not improve metabolic and hepatic features, is associated with weight gain, and is not as well tolerated as expected".
• 2018 meta-analysis. Nine studies with 820 patients (427 bled, 393 lifestyle alone) found no improvement in the insulin-resistance score, insulin or aspartate aminotransferase. Alanine aminotransferase fell by 6.6 IU/L, an effect the authors called very small. No study showed improvement in liver inflammation or fibrosis. They concluded that current evidence does not support phlebotomy in this syndrome or in fatty liver disease.

The 2018 analysis is the larger of the two meta-analyses (nine studies and 820 patients, against four studies and 438). The 2017 Rennes review states that phlebotomy "cannot be currently considered as a valuable option" in this syndrome, and the 2023 consensus panel found "no clear evidence of a benefit for iron depletion therapy". By contrast, the 2001 Rennes paper and the 2020 Milan review regard bloodletting with diet and lifestyle change as a treatment approach. A 2019 systematic review stated that phlebotomy works only where iron sits in the liver cells themselves, not where a high ferritin reflects inflammation. In the 2026 Spanish review of 179 people in a bloodletting programme, metabolic syndrome with a high ferritin accounted for 33% of them. Only 48% fitted the authors' standard of hemochromatosis with significant liver iron, and the authors wrote that "a high percentage do not benefit from it".

Bloodletting has measured downsides in these trials: fatigue in a quarter of bled patients in the largest trial, and a small weight gain. The Berberine and Iron Overload page also reports the 274-person trial.

What Happens After Iron Is Removed

A Rennes follow-up study traced 58 patients who had finished bloodletting between 1998 and 2003 and had no treatment afterwards. They had started with a mean liver iron of 80 µmol/g and had 2.2 g of iron removed. After a mean of 71 months, 64% had iron overload again. The ferritin level at diagnosis was the only factor linked to recurrence. The authors suggested periodic follow-up to find those who might need maintenance treatment.

Diet, Weight and Lifestyle Findings

• Weight loss. In the 274-person trial, the patients who lost weight saw improvements in blood sugar, the insulin-resistance score, ferritin, blood fats and liver tests, whether or not they had been bled. The trial authors concluded that "sustained modification of diet and lifestyle habits remains the first therapeutic intervention".
• A low-calorie diet alone. In the 2001 Rennes study, ten patients treated with a low-calorie diet alone kept a stable ferritin. The authors concluded that body iron was "not modified by a low calorie diet".
• Weight-loss surgery. In a Brazilian study of 42 people (92.9% women) who had gastric bypass surgery and later a second operation with a repeat liver biopsy, the share with liver iron overload fell from 16.7% to 2.4% over a mean 20.6 months, with a 26.7% loss of body weight. Ferritin fell from 220.8 to 101.6 ng/mL, but hemoglobin also fell, from 13.7 to 12.1 g/dL. This was an exploratory study without a comparison group.
• A plant polyphenol with meals. In a double-blind crossover trial, 100 mg of procyanidins (a group of plant polyphenols) taken with an iron-rich test meal did not reduce iron absorption in people with the metabolic syndrome or in people with hemochromatosis. The meal itself raised serum iron only modestly in the metabolic group (8% to 9.1%).

In the absorption studies, people with the syndrome absorbed less iron than controls and far less than people with hemochromatosis. No study read for this page tested a diet aimed at cutting iron absorption in them apart from the procyanidin meal; the diet and lifestyle findings concern weight and metabolic health. The Metabolic Syndrome, Insulin Resistance and Fatty Liver Disease pages cover that research.

What Is Not Known

• A shared definition. Studies use different ferritin cut-offs, different definitions of metabolic syndrome, and sometimes no liver iron measurement. The 2023 consensus states that validated non-invasive criteria and staging are still lacking.
• Whether the iron matters. The consensus calls a causal role for iron in insulin resistance and organ damage a hypothesis. The large randomized trials did not find that removing iron improved blood sugar, insulin resistance or liver tests.
• The mechanism. Hepcidin is raised, yet iron builds up. Whether "hepcidin resistance", inflammation, fat-tissue signalling or genetic variants explain this has not been settled.
• Long-term outcomes. No trial found for this page has followed bled and unbled patients long enough to compare liver cancer, heart disease or death.
• Who might benefit from iron removal. Some studies suggest larger effects in people with HFE variants or higher ferritin, and the 2019 review limits possible benefit to iron inside liver cells. None of these subgroups has been tested in a dedicated trial.
• Diet. No dietary trial measuring liver iron in this syndrome was found, apart from the single-meal procyanidin study.

Key Research Papers

1. Moirand R, Mortaji AM, Loréal O, Paillard F, Brissot P, Deugnier Y. A new syndrome of liver iron overload with normal transferrin saturation. Lancet. 1997;349(9045):95-7. PubMed PMID: 8996422
2. Mendler MH, Turlin B, Moirand R, Jouanolle AM, Sapey T, Guyader D, et al. Insulin resistance-associated hepatic iron overload. Gastroenterology. 1999;117(5):1155-63. PubMed PMID: 10535879
3. Riva A, Trombini P, Mariani R, Salvioni A, Coletti S, Bonfadini S, et al. Revaluation of clinical and histological criteria for diagnosis of dysmetabolic iron overload syndrome. World J Gastroenterol. 2008;14(30):4745-52. PubMed PMID: 18720534
4. Deugnier Y, Bardou-Jacquet É, Lainé F. Dysmetabolic iron overload syndrome (DIOS). Presse Med. 2017;46(12 Pt 2):e306-e311. PubMed PMID: 29169710
5. Valenti L, Corradini E, Adams LA, Aigner E, Alqahtani S, Arrese M, et al. Consensus Statement on the definition and classification of metabolic hyperferritinaemia. Nat Rev Endocrinol. 2023;19(5):299-310. PubMed PMID: 36805052
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7. Ruivard M, Lainé F, Ganz T, Olbina G, Westerman M, Nemeth E, et al. Iron absorption in dysmetabolic iron overload syndrome is decreased and correlates with increased plasma hepcidin. J Hepatol. 2009;50(6):1219-25. PubMed PMID: 19398238
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11. Jézéquel C, Lainé F, Laviolle B, Kiani A, Bardou-Jacquet E, Deugnier Y. Both hepatic and body iron stores are increased in dysmetabolic iron overload syndrome. A case-control study. PLoS One. 2015;10(6):e0128530. PubMed PMID: 26030828
12. Castiella A, Urreta I, Zapata E, Zubiaurre L, Alústiza JM, Otazua P, et al. Liver iron concentration in dysmetabolic hyperferritinemia: Results from a prospective cohort of 276 patients. Ann Hepatol. 2020;19(1):31-35. PubMed PMID: 31587985
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14. Castiella A, Zapata E, Zubiaurre L, Ma Alustiza J, De Juan MD, Iribarren A, et al. Impact of H63D mutations, magnetic resonance and metabolic syndrome among outpatient referrals for elevated serum ferritin in the Basque Country. Ann Hepatol. 2015;14(3):333-9. PubMed PMID: 25864213
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16. Souza M, Lima LCV, Villela-Nogueira CA. Prevalence and Characteristics of Hyperferritinemia in Metabolic Dysfunction-Associated Steatotic Liver Disease: A Meta-Analysis. Liver Int. 2026;46(4):e70569. PubMed PMID: 41873565
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21. Lainé F, Ruivard M, Loustaud-Ratti V, Bonnet F, Calès P, Bardou-Jacquet E, et al. Metabolic and hepatic effects of bloodletting in dysmetabolic iron overload syndrome: A randomized controlled study in 274 patients. Hepatology. 2017;65(2):465-474. PubMed PMID: 27685251
22. Adams LA, Crawford DH, Stuart K, House MJ, St Pierre TG, Webb M, et al. The impact of phlebotomy in nonalcoholic fatty liver disease: A prospective, randomized, controlled trial. Hepatology. 2015;61(5):1555-64. PubMed PMID: 25524401
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25. Valenti L, Moscatiello S, Vanni E, Fracanzani AL, Bugianesi E, Fargion S, et al. Venesection for non-alcoholic fatty liver disease unresponsive to lifestyle counselling--a propensity score-adjusted observational study. QJM. 2011;104(2):141-9. PubMed PMID: 20851820
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PubMed Topic Searches

1. PubMed: dysmetabolic iron overload syndrome
2. PubMed: metabolic hyperferritinemia
3. PubMed: phlebotomy in fatty liver disease, randomized trials
4. PubMed: hepcidin and the metabolic syndrome
5. PubMed: hyperferritinemia and liver iron on magnetic resonance imaging
6. PubMed: serum ferritin and alcohol intake

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Connections

• Hematology — the blood-disorders section this page belongs to
• Hemochromatosis — the inherited iron-loading disease compared on this page
• Iron Overload: Liver Problems — how excess iron injures the liver
• Berberine and Iron Overload — what has and has not been measured
• Iron Overload and Iron Toxicity — the wider iron-overload overview
• Fatty Liver Disease (MASLD) — the liver condition most often found with a high ferritin
• Metabolic Syndrome — the cluster of features that defines this syndrome
• Insulin Resistance — the metabolic state most of these patients share
• Ferritin Test — the blood test that usually starts the question
• Iron Panel — ferritin, iron and transferrin saturation together
• Iron Absorption and the Hepcidin Gate — an animation of how hepcidin controls iron

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