Autoantibodies to Gastric Parietal Cells in Rheumatoid Arthritis Patients
Status: | Completed |
---|---|
Conditions: | Arthritis |
Therapuetic Areas: | Rheumatology |
Healthy: | No |
Age Range: | 18 - Any |
Updated: | 7/11/2015 |
Start Date: | June 2013 |
End Date: | January 2015 |
Contact: | Matthew B Carroll, MD |
Email: | matthew.carroll.1@us.af.mil |
Phone: | 228-376-3629 |
Presence of Autoantibodies to Gastric Parietal Cells and Subsequent Vitamin B12 Deficiency in Rheumatoid Arthritis Patients
A review of the literature reveals that very few studies have assessed the potential
co-existence of vitamin B12 deficiency due to gastric parietal cell autoantibodies. While
Segal et al. in 2004 published a study which found that 49% of patients with RA had vitamin
B12 deficiency, no assessment of the etiology or the presence of autoantibodies was made.
While Goeldner et al. in 2011 and Datta et al. in 1990 demonstrated that anti-gastric
parietal cell antibodies (anti-GPC Ab) were found in <5% to 28% of RA patients respectively,
no additional testing was implemented to determine the significance, specifically whether or
not the presence of anti-GPC Ab related to vitamin B12 deficiency.
The purpose of this study is to determine the prevalence and metabolic significance of
anti-GPC Ab in three cohorts: (1) a group of patients with Rheumatoid Arthritis, (2) a
group of patients with autoimmune thyroid disease (AITD), and (3) a group of patients with
neither RA or AITD. To determine the significance of the presence of anti-GPC Ab, testing
of the current serum B12 level along with a metabolite dependent on adequate vitamin B12
levels (Methylmalonic acid) will be tested.
co-existence of vitamin B12 deficiency due to gastric parietal cell autoantibodies. While
Segal et al. in 2004 published a study which found that 49% of patients with RA had vitamin
B12 deficiency, no assessment of the etiology or the presence of autoantibodies was made.
While Goeldner et al. in 2011 and Datta et al. in 1990 demonstrated that anti-gastric
parietal cell antibodies (anti-GPC Ab) were found in <5% to 28% of RA patients respectively,
no additional testing was implemented to determine the significance, specifically whether or
not the presence of anti-GPC Ab related to vitamin B12 deficiency.
The purpose of this study is to determine the prevalence and metabolic significance of
anti-GPC Ab in three cohorts: (1) a group of patients with Rheumatoid Arthritis, (2) a
group of patients with autoimmune thyroid disease (AITD), and (3) a group of patients with
neither RA or AITD. To determine the significance of the presence of anti-GPC Ab, testing
of the current serum B12 level along with a metabolite dependent on adequate vitamin B12
levels (Methylmalonic acid) will be tested.
Background: Organ specific antibodies such as anti-gastric parietal cell antibodies
(anti-GPC Ab) have been found in a variable number of patients with RA, but it is unclear
what significance these antibodies have on actual vitamin B12 levels. Patients with RA have
been found to have vitamin B12 deficiency up to near 50% but it is unclear if this
deficiency is due to anti-GPC Ab.
Hypothesis: By virtue of the aberrant autoimmune process that occurs in RA, patients with
RA are more likely to have anti-GPC Ab and more likely than a control arm or participants
with autoimmune thyroid disease (AITD) to have vitamin B12 deficiency.
Method: 135 patients will be consented; 45 to the RA arm, 45 to an AITD arm, and 45 to a
control arm. Exclusion criteria will filter patients who would have other reasons for
altered vitamin B12 absorption, such as inflammatory bowel disease, surgery, or medication
use. After obtaining consent subjects will be sent to lab a serum anti-GPC Ab test
(obtainable in an SLE panel), RF, B12/folate (as available for ordering in CHCS), methyl
malonic acid, and (for the control arm subjects and AITD subjects) an anti-CCP IgG.
Patients will also complete a one-sided, one page questionnaire asking them about dietary
and medication exposures.
Outcomes: (1) Determine whether evidence of serum vitamin B12 deficiency, as measure by
either a low vitamin B12 level or elevated methylmalonic acid, will be more common in RA
patients with anti-GPC Ab. (2) Determine the prevalence of anti-GPC Ab in a group of
patients with RA as compared to a group of patients with AITD and with no known systemic or
organ specific autoimmune condition.
(anti-GPC Ab) have been found in a variable number of patients with RA, but it is unclear
what significance these antibodies have on actual vitamin B12 levels. Patients with RA have
been found to have vitamin B12 deficiency up to near 50% but it is unclear if this
deficiency is due to anti-GPC Ab.
Hypothesis: By virtue of the aberrant autoimmune process that occurs in RA, patients with
RA are more likely to have anti-GPC Ab and more likely than a control arm or participants
with autoimmune thyroid disease (AITD) to have vitamin B12 deficiency.
Method: 135 patients will be consented; 45 to the RA arm, 45 to an AITD arm, and 45 to a
control arm. Exclusion criteria will filter patients who would have other reasons for
altered vitamin B12 absorption, such as inflammatory bowel disease, surgery, or medication
use. After obtaining consent subjects will be sent to lab a serum anti-GPC Ab test
(obtainable in an SLE panel), RF, B12/folate (as available for ordering in CHCS), methyl
malonic acid, and (for the control arm subjects and AITD subjects) an anti-CCP IgG.
Patients will also complete a one-sided, one page questionnaire asking them about dietary
and medication exposures.
Outcomes: (1) Determine whether evidence of serum vitamin B12 deficiency, as measure by
either a low vitamin B12 level or elevated methylmalonic acid, will be more common in RA
patients with anti-GPC Ab. (2) Determine the prevalence of anti-GPC Ab in a group of
patients with RA as compared to a group of patients with AITD and with no known systemic or
organ specific autoimmune condition.
Inclusion Criteria:
- Adult, age 18 and older
- RA arm: History of Rheumatoid Arthritis
- AITD arm: History of an autoimmune thyroid disease without a history or clinically
obvious manifestation of an organ specific or systemic autoimmune process.
- Control arm: No history of RA and no history or clinically obvious manifestation of
an organ specific or systemic autoimmune process.
Exclusion Criteria:
- Known vitamin B12 deficiency for which the participant was formerly treated or
continues to receive therapy.
- Active malabsorptive state to include but not limited to celiac disease, inflammatory
bowel disease, etc.
- Surgically induced malabsorptive state to include but not limited to Roux-en-Y
Gastric bypass
- Use of medications that may interfere with vitamin B12 absorption
- Patients with a thyroid condition not consistent with an autoantibody process (i.e.
congenital absence of the thyroid, infectious thyroiditis, thyroidectomy for
non-autoimmune process, toxic multinodular goiter) will be excluded from the
autoimmune thyroid arm.
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