Hematinic deficiencies and hyperhomocysteinemia in gastric parietal cell antibody-positive or gastric and thyroid autoantibodies-negative atrophic glossitis patients.

Background/purpose: Our previous study found that 177 of 1064 atrophic glossitis (AG) patients have serum gastric parietal cell antibody (GPCA) positivity only (so-called GPCA ⁺ AG patients). This study assessed whether serum GPCA positivity or AG itself was a significant factor causing hematinic deficiencies and hyperhomocysteinemia in GPCA ⁺ AG or GPCA-negative, thyroglobulin antibody (TGA)-negative, and thyroid microsomal antibody (TMA)-negative AG (GPCA־TGA־TMA־AG) patients.
Methods: The mean blood hemoglobin (Hb), iron, vitamin B12, folic acid, and homocysteine levels were measured and compared between any two of three groups of 177 GPCA ⁺ AG patients, 476 GPCA־TGA־TMA־AG patients, and 532 healthy control subjects.
Results: GPCA ⁺ AG patients had significantly lower mean blood Hb and iron (for women only) levels and a significantly higher mean serum homocysteine level than healthy control subjects. Moreover, GPCA ⁺ AG patients had significantly greater frequencies of blood Hb, iron, and vitamin B12 deficiencies and hyperhomocysteinemia than healthy control subjects. GPCA ⁺ AG patients have a lower mean serum vitamin B12 level and a significantly higher mean serum homocysteine level as well as significantly greater frequencies of vitamin B12 deficiency and hyperhomocysteinemia than GPCA־TGA־TMA־AG patients. Moreover, GPCA־TGA־TMA־AG patients did have significantly lower mean blood Hb and iron levels and significantly greater frequencies of blood Hb, iron, vitamin B12, and folic acid deficiencies and hyperhomocysteinemia than healthy control subjects.
Conclusion: The GPCA is a major factor causing vitamin B12 deficiency and hyperhomocyteinemia in GPCA ⁺ AG patients. AG itself does play a significant role in causing anemia, hematinic deficiencies, and hyperhomocysteinemia in both GPCA ⁺ AG and GPCA־TGA־TMA־AG patients.
(Copyright © 2019. Published by Elsevier B.V.)