What is the relationship between Alcohol Use Disorder (AUD) and iron metabolism?

From the Guidelines

Alcohol Use Disorder (AUD) is associated with iron metabolism alterations, leading to both iron overload and deficiency states, and management should prioritize addressing the underlying alcohol use and monitoring iron indices. The relationship between AUD and iron metabolism is complex, with chronic excessive alcohol consumption contributing to oxidative stress and activating fibrogenesis, which can lead to iron overload in the liver 1. Patients with hereditary haemochromatosis who consume more than 60 g of alcohol per day have an increased risk of developing advanced ALD 1. However, heterozygosity for HFE mutations is reported higher in patients with AUD and associated with mild iron overload, but it has no major influence on the progression of ALD 1.

Key points to consider in the management of AUD and iron metabolism include:

• Iron metabolism markers, such as ferritin and transferrin saturation, are frequently elevated in patients with ALD, although to a lesser extent than in patients with homozygous haemochromatosis 1
• AUD can also cause iron deficiency anemia through poor nutrition, gastrointestinal bleeding from alcohol-related gastritis, and impaired bone marrow function
• For patients with AUD and elevated iron levels, phlebotomy and alcohol cessation are recommended
• For those with iron deficiency, oral iron supplementation is advised, taken with vitamin C to enhance absorption and between meals to avoid interference from food
• All AUD patients should receive thiamine, folate, and a multivitamin to prevent nutritional complications

Regular monitoring of iron indices and addressing the underlying alcohol use through counseling, support groups, and medications like naltrexone or acamprosate when appropriate is essential for proper management of AUD and iron metabolism alterations 1.

From the Research

Relationship Between Alcohol Use Disorder (AUD) and Iron Metabolism

• The relationship between AUD and iron metabolism is complex, with studies suggesting that patients with AUD frequently suffer from malnutrition, which may result in insufficient iron distribution and iron overload or deficiency 2.
• Iron metabolism in patients with AUD can be described by a combination of biochemical and hematological parameters, including soluble transferrin receptor, ferritin, C-reactive protein (CRP), and hemoglobin concentrations 2.
• Studies have shown that patients with AUD have increased levels of ferritin and soluble transferrin receptor compared to social drinkers, indicating potential iron overload 2, 3.
• Additionally, AUD patients have been found to have higher serum transferrin saturation, which can predict withdrawal symptoms and cumulative dose of benzodiazepine treatment during detoxification 3.
• The HFE rs1799945 polymorphism has been associated with elevated peripheral iron and can serve as a predictor of withdrawal severity in AUD patients 3.
• Thiamine deficiency, which is common in AUD, may also contribute to brain iron overload and alcohol-related dementia by impairing the integrity of the blood-brain barrier 4.

Iron Overload and Deficiency in AUD

• Iron overload is relatively frequent in AUD patients, with one study finding that 9% of patients had iron overload 2.
• Functional iron deficiency and reduced iron supply have also been observed in AUD patients, although to a lesser extent than iron overload 2.
• The mechanisms underlying iron overload and deficiency in AUD are not fully understood, but may involve malnutrition, inflammation, and genetic factors 2, 3.

Clinical Implications

• The relationship between AUD and iron metabolism has important clinical implications, particularly in the management of withdrawal symptoms and prevention of alcohol-related dementia 3, 4.
• Further research is needed to fully understand the mechanisms underlying iron metabolism in AUD and to develop effective therapeutic interventions 2, 3, 4.