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Development of Subtle Iron Deficiency During Vitamin E Treatment For Metabolic Dysfunction-Associated Steatotic Liver Disease.

  • 2025-02-17
  • Journal of dietary supplements 22(2)
    • Maren C Podszun
    • Ahmad Samer Alawad
    • Shilpa Lingala
    • Nevitt Morris
    • Wen Chun A Huang
    • Yaron Rotman

Study Design

Type
Clinical Trial
Sample size
n = 20
Population
20 people with MASLD
Methods
Iron status was monitored prospectively; liver histology, hepatic gene expression, hepatic 4-hydroxynonenal, haptoglobin genotype and plasma vitamin E levels were assessed
Blinding
Open-label
Duration
median 11 weeks (range 4-13) of vitamin E treatment; anemia after 23 weeks (16-36)
Funding
Unclear
Vitamin E is an effective treatment for metabolic dysfunction-associated steatohepatitis (MASH) but associated with hemorrhagic complications when used for other indications. We aimed to determine the risk of developing iron deficiency during treatment of metabolic dysfunction-associated steatotic liver disease (MASLD) with vitamin E. Iron status was monitored prospectively in 20 people with MASLD treated with 200 - 800 IU/d vitamin E (https://clinicaltrials.gov/study/NCT01792115). To gain mechanistic insights liver histology, hepatic gene expression, hepatic 4-hydroxynonenal, haptoglobin genotype and plasma vitamin E levels were assessed. We found iron deficiency to occur in 11/20 subjects (55%) after a median 11 weeks (range 4-13) of vitamin E treatment, and anemia to occur in 6 of the 11 (30% of study population) after 23 weeks (16-36). Ferritin (84.5 ± 85.2 to 47.8 ± 54.9μg/L, p < 0.001) and mean corpuscular volume (MCV, 86.2 ± 4.9 to 84.3±4.3fL, p = 0.003) significantly decreased, with a concomitant rise in red-cell distribution width (RDW, 13.4 ± 1.3 to 14.4 ± 1.9%, p = 0.003). A gastrointestinal bleeding source was found in 75% of subjects with complete work-up. Iron deficiency occurred in all diabetics vs. 47% of non-diabetics (p 0.007). Iron deficiency risk was not associated with cirrhosis, platelet count, prothrombin time, haptoglobin genotype, or plasma vitamin E level. Changes in hepatic gene expression and oxidative stress were suggestive of an extrahepatic effect. Iron deficiency resolved with appropriate care even with continued vitamin E treatment. We conclude that occult gastrointestinal bleeding and iron deficiency were frequently observed during vitamin E treatment, possibly reflecting an effect on platelet function. Close monitoring is warranted during the first months of treatment, especially in diabetics and subjects with risk factors for gastrointestinal bleeding.

Research Insights

  • Vitamin E→Developed Anemia

    anemia to occur in 6 of the 11 (30% of study population) after 23 weeks (16-36)

    Effect
    Harmful
    Effect size
    Moderate
    Dose
    200 - 800 IU/d
  • Vitamin E→Improved Iron Levels

    We found iron deficiency to occur in 11/20 subjects (55%) after a median 11 weeks (range 4-13) of vitamin E treatment

    Effect
    Harmful
    Effect size
    Moderate
    Dose
    200 - 800 IU/d
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