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

Background and Objectives: Corpus atrophic gastritis (CAG) is associated with vitamin B₁₂ deficiency due to impaired gastric acid and intrinsic factor secretion. Untreated vitamin B₁₂ deficiency can lead to pernicious anemia, severe neurological consequences, and acute cardiocerebral-vascular events. Timely vitamin B₁₂ supplementation is relevant; however, the dosage of intramuscular (IM) vitamin B₁₂ supplementation has not been standardized to date. The objective was to assess the efficacy of a 1st and 2nd treatment schedule of IM-cyanocobalamin treatment in CAG patients with vitamin B₁₂ deficiency at long-term follow-up and to identify the predictors of increased cyanocobalamin requirement. Methods: This monocentric real-life cohort study included 213 CAG patients with vitamin B₁₂ deficiency. Inclusion criteria were adult age, histological diagnosis of CAG with vitamin B₁₂ deficiency (<220 pg/mL), and follow-up of more than 12 months. The 1st-treatment-schedule (TxA) was 5000 µg IM cyanocobalamin every 5 days for 3 times, followed by 5000 µg IM cyanocobalamin every 3 mos (20,000 µg/yr); the 2nd-treatment-schedule (TxB) was 5000 µg IM cyanocobalamin every 5 days for 3 times, followed by 5000 µg IM cyanocobalamin every 2 mos (30,000 µg/yr). The treatment endpoint was serum vitamin B₁₂ normalization. Clinical-biochemical follow-up was scheduled every 12 ± 6 mos: patients who satisfied the endpoint maintained the TxA, otherwise, TxB was prescribed. Results: Of the 213 CAG patients with vitamin B₁₂ deficiency, 48.3% had anemia, and 26.3% macrocytosis without anemia. TxA efficaciously corrected vitamin B₁₂ deficiency in 146 (68.5%) patients, maintaining efficacy until the longest available follow-up (42.2 ± 2.6 months). The remaining 67 patients (31.5%) were switched to TxB due to persistent vitamin B₁₂ deficiency observed at 12 (6–36) months and were maintained until the longest available follow-up (50.2 ± 4.1 months). At the longest available follow-up, a significant increase in Hb (TxA: 11.9 ± 0.2 to 13.1 ± 0.1 g/dL, p < 0.001; TxB: 12.2 ± 0.3 to 13.6 ± 0.2 g/dL, p = 0.003) and serum vitamin B₁₂ (TxA: 168 ± 7 to 402 ± 19 pg/mL, p < 0.0001; TxB: 157 ± 12 to 340 ± 24 pg/mL, p < 0.0001) was shown in both schedules. A significant decrease in MCV was shown in TxB only (p = 0.0003). In logistic regression, switching to TxB was significantly associated with severe corpus intestinal metaplasia (OR 11.0, 95% CI 2.8–43.7), macrocytosis at CAG diagnosis (OR 2.7, 95% CI 1.2–6.3), and male sex (OR 2.4, 95% CI 1.1–5.2). Conclusions: In this real-world setting, at long-term follow-up, nearly 70% of CAG patients with vitamin B₁₂ deficiency restored their vitamin B₁₂ levels with 20,000 µg/yr of cyanocobalamin, while the remaining 30% required 30,000 µg/yr. Male vitamin B₁₂-deficient CAG patients with advanced gastric damage and severe macrocytosis required higher dosages of cyanocobalamin. They should be carefully monitored to avoid suboptimal supplementation and potentially dangerous consequences of vitamin B₁₂ deficiency.