Why do patients with atrophic gastritis develop vitamin D deficiency?

Vitamin D Deficiency in Atrophic Gastritis

Patients with atrophic gastritis develop vitamin D deficiency primarily due to reduced gastric acid secretion from parietal cell loss, which impairs the absorption of fat-soluble vitamins including vitamin D, though the exact mechanisms remain incompletely understood and may involve shared autoimmune pathogenic pathways.

Primary Mechanism of Vitamin D Deficiency

The loss of parietal cells in atrophic gastritis—whether from autoimmune destruction in autoimmune gastritis (AIG) or from H. pylori-related damage—leads to hypochlorhydria (reduced gastric acid secretion) 1. This acid deficiency impairs the absorption of multiple micronutrients, including vitamin D 2.

Vitamin D deficiency is the most prevalent nutritional deficiency in patients with chronic atrophic autoimmune gastritis, affecting the majority of patients and often occurring alongside other micronutrient deficiencies 3.

Clinical Evidence and Prevalence

• In one observational study of 122 CAAG patients, 25-OH vitamin D deficiency was present in 76 patients (62%), making it the most common micronutrient deficiency—even more prevalent than vitamin B12 or iron deficiency 3
• Average vitamin D levels in AIG patients were markedly reduced at 9.8 ± 5.6 ng/mL compared to 21.3 ± 12.2 ng/mL in healthy subjects, representing a statistically significant difference 4
• The deficiency appears to correlate with vitamin B12 levels, suggesting potential shared pathogenic mechanisms beyond simple malabsorption 3

Proposed Immunologic Mechanisms

Beyond malabsorption, vitamin D deficiency may have a bidirectional relationship with autoimmune gastritis:

• Vitamin D as a predisposing factor: Hypovitaminosis D may act as a risk factor for developing autoimmune diseases, including AIG, given vitamin D's crucial immunoregulatory and anti-inflammatory properties 4
• The vitamin D receptor is expressed on cells involved in both innate and adaptive immune responses, and these cells can produce and respond to 1,25-dihydroxyvitamin D 4
• Low vitamin D levels may fail to adequately regulate the immune response, potentially allowing or exacerbating the autoimmune attack on gastric parietal cells 5, 4

Correlation with Disease Severity

• Vitamin D levels showed a direct correlation with vitamin B12 levels in CAAG patients 3
• 25-OH vitamin D levels were significantly lower in patients with macronodular ECL cell hyperplasia compared to those with linear or micronodular hyperplasia, suggesting a relationship with disease progression 3
• No significant correlation was found between vitamin D levels and the grading of gastric atrophy itself, BMI, or gastrin levels 3

Clinical Implications for Management

All patients with atrophic gastritis should be screened for vitamin D deficiency alongside iron and vitamin B12 deficiency 6, 7. This is particularly important because:

• Vitamin D is critical for calcium absorption and bone health, and deficiency can lead to bone-related complications in patients already at risk from chronic disease 5
• Adequate vitamin D levels may help regulate immune responses and reduce inflammation in autoimmune conditions 5
• The high prevalence (>60% in some studies) makes screening cost-effective and clinically relevant 3

Important Clinical Pitfall

Unlike vitamin B12 deficiency, which develops slowly due to substantial hepatic stores lasting years, vitamin D deficiency can manifest earlier and may actually precede or contribute to the development of autoimmune gastritis itself 4. Therefore, vitamin D should not be overlooked in favor of only monitoring B12 and iron, despite these being the traditionally emphasized deficiencies in atrophic gastritis 6, 2.