Session Information
Session Type: ACR Poster Session A
Session Time: 9:00AM-11:00AM
Background/Purpose: To describe the fecal microbiome profile in RA patients and analyze the mechanisms involved in the pathogenesis of RA
Methods:
Design: Controlled, observational, cross-sectional study of established RA cohort.
Patients: Forty consecutive RA patients (ACR/EULAR 2010 criteria) >16 years, selected from a prospective inception cohort (diagnosis of RA between 2007-2011) and 40 sex-age matched healthy controls. Subjects with antibiotics, probiotics, initiation of a new therapy in the previous 3 months or other autoimmune diseases were excluded. Protocol: Cases and controls were evaluated by a rheumatologist. Clinical data of disease activity were collected during the follow-up and analytical values were determined. Fecal samples were frozen within 24 hours of collection. All participants signed informed consent.
Main outcome: Fecal samples exam. Microbial DNA was extracted from fecal samples using QIAamp DNA stool Mini kit. The concentration and quality of DNA was determined by Nanodrop. Secondary outcome: Average DAS28-ESR during the follow-up, HAQ, RF, ACPA and erosive status. Other variables: Demographic, clinical-analytical and therapies (DMARDs).
Statistical analysis: Analysis of microbiota profile: UniFracPCoA (Principal Coordinate Analysis) was performed with the abundance data of operational taxonomic units (OTU) by means of the variance-covariance matrix implemented in Quantitative Insights Into Microbial Ecology(QIIME). The relative abundance of each OTU (taxa) was compared using a Wilcoxon test. The variations of abundance and diversity were compared by statistical analysis of an ANOSIM pathway with PAST and the differences were with P<0.05. The calculation of α and β-diversity was carried out using QIIME.
Results:
Most of subjects were women (75%) with a mean age of 59 years. In RA patients, the average DAS28 was 3.6 (table 1). β-diversity data showed that patients tend to differ from healthy subjects according to their microbiota (p = 0.07). Patients with RA exhibited decreased gut microbiome diversity compared with controls, although was not statistically significant. Regarding in species richness, the analysis suggested an increase of the Collinsella aerofaciens species and enterococcus genera in patients compared with controls. Likewise, an increase of arginine deaminase activity was observed, which belonged, in approximately 90%, to the RA genes of the genus Collinsela. Also, we observed a decrease in other bacterial lineages. On the other hand, RA patients showed an altered metabolic capacity for the transport of zinc and copper in comparison with controls.
Conclusion:
These observations suggest a dysbiosis in RA patients, resulting from the abundance of certain bacterial (i.e Collinsela) and decrease of other bacterial lineages. These alterations could influence in a significant way, by enzymatic or metabolic mechanisms, in the perpetuation of the autoimmunity of the disease.
Table 1.
VARIABLE
|
RA n=40
|
Control n=40
|
P – VALUE
|
Clinical characteristic
|
|
|
|
Age (years), mean (SD)
|
58,5 (9,4) |
58,5 (9,4) |
0,998 |
Sex (female), n (%)
|
30 (75,0) |
30 (75,0) |
1,000 |
Smoke
|
|
|
0,018 |
Non-smoker, n (%)
|
15 (37,5) |
24 (60,0) |
|
Ex-smoker, n (%)
|
16 (40,0) |
5 (12,5) |
|
Smoker, n (%)
|
9 (22,5) |
11 (27,5) |
|
Body mass index, mean (SD)
|
30,3 (5,6) |
28,0 (4,9) |
0,057 |
Obesity, n (%)
|
21 (52,2) |
12 (30,0) |
0,041 |
Laboratory characteristic
|
|
|
|
Rheumatoid factor, n (%)
|
32 (80,0) |
2 (5,0) |
<0,001 |
Anti–cyclic citrullinated peptide, n (%)
|
28 (70,0) |
0 (0,0) |
<0,001 |
CRP, mg/l |
5,02 ± 4,5
|
5,17 ± 7,03
|
0,911 |
ESR mm/h |
17,12 ±11,8
|
12,17 ± 9,4
|
0,041 |
Inflammatory activity
|
|
|
|
Average DAS28 value, mean (SD)
|
3,6 (0,5) |
|
– |
DAS28 at index-date, mean (SD)
|
3,0 (1,1) |
|
– |
Average SDAI value, mean (SD)
|
13,3 (2,8) |
|
– |
SDAI at index-date, mean (SD)
|
9,7 (5,6) |
|
– |
Average CDAI value, mean (SD)
|
12,8 (2,7) |
|
– |
CDAI at index-date, mean (SD)
|
91 (6,1) |
|
– |
Average HAQ value, mean (SD)
|
0,89 (0,6) |
|
– |
HAQ at index-date, mean (SD)
|
1,06 (0,5) |
|
– |
Therapeutic regimen
|
|
|
|
Glucocorticoids (%)
|
7,5 |
– |
|
Sulfasalazine (%) |
15 |
– |
|
Leflunomide (%) |
12,5 |
– |
|
Methotrexate (%) |
72,5 |
– |
|
Hydroxychloroquine (%) |
5 |
– |
|
biologic disease-modifying antirheumatic drugs (%) |
37,5 |
– |
|
To cite this abstract in AMA style:
Mena-Vazquez N, Moreno-Indias I, Ruiz-Limon P, Rojas-Gimenez M, Fuego C, Manrique-Arija S, Ureña-Garnica I, Jimenez-Nuñez FG, Tinahones FJ, Fernandez-Nebro A. Analysis of Intestinal Microbiome Profile of Patients with Established Rheumatoid Arthritis and Healthy Controls [abstract]. Arthritis Rheumatol. 2018; 70 (suppl 9). https://acrabstracts.org/abstract/analysis-of-intestinal-microbiome-profile-of-patients-with-established-rheumatoid-arthritis-and-healthy-controls/. Accessed .« Back to 2018 ACR/ARHP Annual Meeting
ACR Meeting Abstracts - https://acrabstracts.org/abstract/analysis-of-intestinal-microbiome-profile-of-patients-with-established-rheumatoid-arthritis-and-healthy-controls/