Effective vitamin B12 treatment can reduce serum antigastric parietal cell antibody titer in patients with oral mucosal disease.

BACKGROUND/PURPOSE: Patients with serum antigastric parietal cell antibody (GPCA) positivity may have vitamin B12 deficiency and some oral symptoms. This study assessed the changes of serum GPCA titer in GPCA-positive patients after effective vitamin B12 treatment. METHODS: Two hundred and ten GPCA-positive oral mucosal disease patients became oral symptom free (complete response) after 1.0-67.1 months of treatment with regular and continuous intramuscular injection of vitamin B12 once per week. The changes of serum GPCA titers after treatment were evaluated in these 210 patients. RESULTS: We found a significant drop of the GPCA positive rate from 100% to 42.9% in our 210 complete response patients after effective vitamin B12 treatment (p < 0.001). When 210 patients were further divided into seven subgroups according to the low to high serum GPCA titers, we noted that the higher serum GPCA titers decreased to significantly lower levels after treatment in all seven subgroups (all p < 0.001). However, serum GPCA titers increased to significantly higher levels in 46 GPCA-positive control patients receiving only oral administration of two vitamin BC capsules (containing 10 µg of vitamin B12) plus deficient hematinic supplements per day after a follow-up period of 2.7-27 months. A maintenance vitamin B12 treatment once a month could retain the GPCA-negative status in 87% of treated-to GPCA-negative patients compared with those (10%) without further maintenance vitamin B12 treatment. CONCLUSION: Regular and continuous effective vitamin B12 treatment can reduce the relatively higher serum GPCA titers to significantly lower or undetectable levels in GPCA-positive patients.

Significant reduction of serum homocysteine level and oral symptoms after different vitamin-supplement treatments in patients with burning mouth syndrome.

BACKGROUND: Serum homocysteine level is a biomarker of cardiovascular disease. METHODS: In this study, 399 primary and secondary burning mouth syndrome (BMS) patients without or with hematinic deficiencies were treated with vitamin BC capsules plus none, one, or two deficient hematinics depending on the corresponding deficiency statuses of the patients. One hundred and seventy-seven patients showed complete remission of all oral symptoms after treatment. The blood homocysteine, vitamin B12, folic acid, iron, and hemoglobin concentrations at baseline and after treatment till all oral symptoms had disappeared in these 177 complete-response BMS patients were measured and compared by paired t-test. RESULTS: For BMS patients with concomitant deficiencies of vitamin B12 only (n = 48), folic acid only (n = 12), vitamin B12 plus folic acid (n = 9), or vitamin B12 plus iron (n = 15), supplementations with vitamin BC capsules plus corresponding deficient hematinics could significantly reduce the abnormally high serum homocysteine levels to normal levels after a mean treatment period of 5.4-8.2 months (all P-values < 0.01). For BMS patients without definite hematinic deficiencies (n = 62), supplementation with vitamin BC capsules only could also significantly decrease the relatively higher homocysteine levels to significantly lower levels after a mean treatment period of 10.2 months (P < 0.001). CONCLUSION: Specific supplementations with vitamin BC capsules plus none or corresponding deficient vitamin B12 and/or folic acid can reduce the abnormally high serum homocysteine levels to normal levels in BMS patients without or with deficiencies of corresponding hematinics.

Zinc deficiency may be a cause of burning mouth syndrome as zinc replacement therapy has therapeutic effects.

BACKGROUND: Zinc is known to play an important role for growth and development, the immune response, neurological function, and reproduction. Although the etiology of burning mouth syndrome (BMS) is unknown, zinc deficiency may be implicated in the pathogenesis of BMS. The aim of this study was to demonstrate a causal relationship between zinc deficiency and BMS and to assess whether zinc replacement is an effective therapy for BMS. METHODS: Serum zinc level was evaluated in 276 patients with BMS. To assess the therapeutic effect of zinc replacement, patients with zinc deficiency were administered a zinc supplement (14.1 mg/day). Pain intensity 6 months after zinc replacement was evaluated using an 11-point numerical scale. We also developed an animal model of zinc deficiency to assess the effects of zinc deficiency on the oral mucosa. RESULTS: Of the 276 patients with BMS, 74 (26.8%) had low serum zinc levels. Zinc replacement therapy lowered the mean numerical pain scale in these patients from 8.1 to 4.1, compared with a mean decrease from 7.7 to 6.7 in a control group (P = 0.004). In our animal model of zinc deficiency, the main pathologic findings were hyperkeratinization and increased mitosis on the dorsum of the tongue, although there were no gross oral mucosal lesions. CONCLUSIONS: Zinc deficiency might play a role in some patients with BMS. In such patients, appropriate zinc replacement therapy is effective in relieving symptoms.