Introduction
Corpus atrophic gastritis (CAG) is associated with vitamin B12 deficiency. Untreated vitamin B12 deficiency can lead to megaloblastic anaemia (also known as Pernicious Anaemia) and other potential serious clinical manifestations such as acute cardiocerebral events and severe neurological consequences, thus timely B12 supplementation is relevant. To date, the dosage of intramuscular B12 supplementation in CAG patients with vitamin B12 deficiency is not standardized.
Aims & Methods
The aim was to assess the efficacy of cyanocobalamin treatment (Tx) at long term follow-up and predictors of increased cyanocobalamin requirement.
A monocentric retrospective longitudinal cohort study was conducted on 190 pts (62.1% F, age 63±1 yrs) consecutively diagnosed (2007-2021) with CAG and vitamin B12 deficiency. Inclusion criteria were age >18 years, histological diagnosis of CAG (updated Sydney System), serum B12 <250 pg/ml, intramuscular cyanocobalamin supplementation, and follow-up of at least 12 mos. Demographic, clinical, biochemical, and histological data were retrospectively collected. After the diagnosis of vitamin B12 deficiency pts were first treated with TxA schedule (5000μg intramuscular cyanocobalamin every 5 days for 3 times, followed by 5000μg intramuscular every 3 mos (20000μg/yr)), and revaluated at follow up. If TxA was not sufficient to restore B12 levels, TxB was prescribed (5000μg intramuscular cyanocobalamin every 5 days for 3 times, followed by 5000μg intramuscular cyanocobalamin every 2 mos (30000μg/yr)). Primary Tx endpoint was B12 normalization. Baseline and follow-up data of pts on TxA and TxB were compared by Student's t-test. Logistic regression was performed to find out predictors of increased B12 need.
Results
Macrocytic anaemia was mild, moderate and severe in 60, 17, 14 out of 190 pts, while 94 pts had vitamin B12 deficiency without anaemia. TxA efficaciously corrected vitamin B12 deficiency in 130 (68.4%) pts and was maintained until longest available follow-up (41±2.4 mos). The remaining 60 (31.6%) pts, due to persistent vitamin B12 deficiency observed at 12 (6-48) mos, were switched to TxB which was then maintained until longest available follow-up (49.9±4.1 mos). At longest available follow-up, a significant increase of Hb (TxA: 12±0.2 vs 13.1±0,2; TxB: 12.1±0.4 vs 13.8±0.2, p<0,0001) and B12 (TxA: 162.9±8.6 vs 400±22.2; TxB: 142.3±11.2 vs 323.4±22.3, p<0.001) was shown in both schedules. A significant decrease of MCV was shown in TxB only (96.4± 2.1 vs 88.1±0.9,p=<0.0001). At logistic regression, switch to TxB was associated with severe intestinal metaplasia (OR10.6, IC 95% 2.6-43.0, p=0.0009) and macrocytosis at diagnosis (OR2.8, IC95% 1.1-6.9, p=0.0231), and male gender (OR 2.5, IC95% 1.1-5.7, p=0,0213), while other features such as age, severity of vitamin B12 deficiency, previous vitamin B12 therapy, concomitant iron deficiency were not significantly associated with increased need of intramuscular cyanocobalamin.
Conclusion
At long term follow-up, about 70% of pts restore vitamin B12 deficiency with 5000μg intramuscular cyanocobalamin every 3 mos, while only 30% require an increased dosage of 5000μg intramuscular cyanocobalamin every 2 mos. In particular, male pts with severe intestinal metaplasia and macrocytosis at diagnosis require a higher dosage of cyanocobalamin to obtain B12 normalization. In CAG pts with vitamin B12 deficiency regular clinical-biochemical follow-up is important to monitor efficacy of B12 treatment to restore B12 levels and to treat and prevent clinical manifestations of vitamin B12 deficiency.
References
Lenti MV, Rugge M, Lahner E, Miceli E, Toh B-H, Genta RM, et al. Autoimmune gastritis. Nat Rev Dis Primers. (2020);
Green R, Allen L, Bjørke-Monsen A et al. Vitamin B 12 deficiency. Nature reviews | Disease primers (2017);
Devalia V, Hamilton MS et al. Guidelines for the diagnosis and treatment of cobalamin and folate disorders. British Journal of Haematology (2014);
