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Corpus atrophic gastritis (CAG) is a chronic autoimmune condition characterized by progressive loss of gastric acid secretion and intrinsic factor production, resulting in impaired vitamin B12 absorption and subsequent deficiency.
Long-term intramuscular cyanocobalamin effectively corrects vitamin B12 deficiency in corpus atrophic gastritis, with higher doses needed in patients with advanced gastric damage and macrocytosis.
Corpus atrophic gastritis (CAG) is a chronic autoimmune condition characterized by progressive loss of gastric acid secretion and intrinsic factor production, resulting in impaired vitamin B12 absorption and subsequent deficiency. Persistent vitamin B12 depletion increases the risk of pernicious anemia, neurological dysfunction, and cardiocerebrovascular complications, underscoring the clinical urgency of timely and adequate replacement therapy.
Although intramuscular (IM) cyanocobalamin remains the standard of care, its optimal long-term dosing strategy has not been clearly standardized, particularly in patients with advanced gastric mucosal damage. In this context, the study was designed to assess the long-term effectiveness of two structured IM cyanocobalamin regimens in patients with CAG and vitamin B12 deficiency, while strategically identifying clinical and histological predictors that signal the need for higher annual dosing and a more individualized supplementation approach.
This monocentric, longitudinal real-world cohort study enrolled 213 adult patients with histologically confirmed CAG and documented vitamin B12 deficiency (<220 pg/mL), with a follow-up exceeding 12 months.
All participants initially received an induction regimen of IM cyanocobalamin 5000 µg every 5 days for three doses. Maintenance therapy was then administered according to two schedules:
Serum vitamin B12 normalization served as the primary treatment endpoint. Clinical and biochemical assessments were conducted every 12 ± 6 months. Patients who achieved and maintained vitamin B12 normalization continued TxA, whereas those with persistent deficiency were escalated to TxB. Logistic regression analysis was executed for identifying the predictors of increased cyanocobalamin requisition.
At baseline, 48.3% of patients had anemia and 26.3% presented with macrocytosis without anemia.
The TxA corrected vitamin B12 deficiency in 146 patients (68.5%) and sustained biochemical normalization over a mean follow-up of 42.2 ± 2.6 months. The remaining 67 patients (31.5%) showed persistent deficiency and were escalated to the TxB after a median of 12 months (range 6–36), maintaining correction during a longer follow-up of 50.2 ± 4.1 months. At the longest follow-up, both regimens significantly increased hemoglobin and serum vitamin B12 levels (Table 1).
Multivariate logistic regression identified independent predictors of requiring the higher-dose regimen (Table 2).
In this longitudinal real-world cohort, nearly 70% of patients with CAG achieved sustained vitamin B12 normalization with 20,000 µg/year of IM cyanocobalamin, while about 30% required escalation to 30,000 µg/year. Male sex, advanced gastric mucosal damage, and baseline macrocytosis independently predicted higher dose requirements. These findings underscored the need for individualized dosing and structured long-term monitoring to prevent inadequate replacement and serious hematologic or neurological complications.
Nutrients
Intramuscular Cyanocobalamin Treatment in Patients with Corpus Atrophic Gastritis and Vitamin B12 Deficiency: Efficacy and Predictors of Increased Requirement—A Monocentric Longitudinal Real-Life Cohort Study
Francesco Paolo Schiavone et al.
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