scholarly journals Association of ankylosing spondylitis activity indicators in a Russian population of patients with STAT4 rs7574865 gene polymorphism

2019 ◽  
Vol 13 (2) ◽  
pp. 55-60
Author(s):  
M. Yu. Krylov ◽  
A. S. Starkova ◽  
E. Yu. Samarkina ◽  
T. V. Dubinina ◽  
Sh. F. Erdes
Keyword(s):  
Ankylosing Spondylitis ◽  
Gene Polymorphism ◽  
Autoimmune Diseases ◽  
Disease Activity ◽  
Topoisomerase I ◽  
Association Studies ◽  
Russian Population ◽  
Control Group ◽  
Genome Wide Association Studies ◽  
Hla B27

Family and twin studies have shown that ankylosing spondylitis (AS) has a hereditary nature that is based on a strong association with the leukocyte antigen HLA-B27. However, only 1–5% of HLA-B27 carriers develop AS, which indicates that there are other genetic markers involved in the formation of a predisposition to this disease. A number of genome-wide association studies have convincingly confirmed the role of the STAT4 gene. This gene encodes the protein – the signal transducer and activator of transcription (STAT) protein, which is a predisposing factor for the development of many autoimmune diseases. There are not so many studies of the relationship of STAT4 polymorphisms to the predisposition to AS, and there are no these studies regarding the Russian population.Objective: to study whether there is a possible association of STAT4 rs7574865 gene polymorphism with the predisposition to AS and to assess the activity of this disease using BASDAI and ASDAS scores in the Russian patient population.Patients and methods. A cohort of 203 individuals, including 100 patients (79 men and 21 women) with AS, and 103 healthy volunteers (a control group) was surveyed. Age, gender, duration, and specific features of AS onset, ESR, and CRP levels were assessed. BASDAI and ASDAS scores were calculated to evaluate disease activity.Results and discussion. There was a significant relationship between STAT4 polymorphism and C-reactive protein (CRP) levels and BASDAI and ASDAS-CRP scores. The TT genotype carriers had significantly higher mean activity indices compared to the GG (p=0.001) and GT (p=0.005) genotype carriers for CRP, BASDAI (p=0.0001 and p=0.009, respectively) and ASDAS-CRP (p=0.009 and p=0.001, respectively). High disease activity (BASDAI >4 and ASDAS-CRP >3.5) was also associated with the high frequency of the T allele (p=0.046 and p=0.004, respectively). The value of STAT4 rs7574865 gene polymorphism in the pathogenesis of autoimmune diseases is confirmed by a study in which the T allele in STAT4 rs7574865 enhances mRNA transcription and protein expression. Italian authors have shown that there is a relationship between the minor T allele of rs7574865 and the high risk of arthritis. We have previously established a relationship between the T allele and the predisposition to diffuse systemic scleroderma, interstitial lung damage, and elevated anti-topoisomerase I antibody levels.Conclusion. The present study has shown for the first time a significant association of STAT4 rs7574865 polymorphism with the main AS activity indicators: CRP levels, BASDAI and ASDAS-CRP scores. The studied polymorphism may be a new genetic marker for predicting the severity of AS. 

scholarly journals Arthritis Associated with Crohn's Disease

1990 ◽  
Vol 4 (8) ◽  
pp. 497-502 ◽  
Author(s):  
JM Gilvarry ◽  
F Keeling ◽  
O Fitzgerald ◽  
JF Fielding
Keyword(s):  
Crohn’S Disease ◽  
Ankylosing Spondylitis ◽  
Crohn's Disease ◽  
Disease Activity ◽  
Disease Onset ◽  
Close Correlation ◽  
Control Group ◽  
Hypertrophic Osteoarthropathy ◽  
Hla B27 ◽  
Peripheral Arthritis

A controlled prospective study was undertaken to determine the incidence and characteristic features of peripheral arthritis, sacroiliitis, ankylosing spondylitis and hypertrophic osteoarthropathy in a group of patients with Crohn's disease, and to define the relationship of such arthritides with disease site, duration and activity. Peripheral arthritis occurred in 14.5% of the patients; it was not seen in the control group. This arthritis, which tended to be pauciarticular, was more common in females with large bowel disease and post dated the bowel symptoms in all but one patient. There was close correlation with disease activity. Radiographic sacroiliitis occurred in 12.7% of the patients and ankylosing spondylitis in 7.3%; neither of these were seen in the control group. Sacroiliitis was more common in females and showed no correlation with either disease activity or human lymphocyte antigen (HLA) B27. Ankylosing spondylitis was seen equally in males and females and showed close correlation with both disease activity and HLA B27. Hypertrophic osteoarthropathy occurred in 9.1% of patients. It was not seen in the control group. All patients were asymptomatic. It showed no correlation with disease activity, finger clubbing, age of disease onset, or HLA B27.

scholarly journals Perspectives on the Genetic Associations of Ankylosing Spondylitis

2021 ◽  
Vol 12 ◽  
Author(s):  
B. Paul Wordsworth ◽  
Carla J. Cohen ◽  
Connor Davidson ◽  
Matteo Vecellio
Keyword(s):  
Ankylosing Spondylitis ◽  
Association Studies ◽  
Regulation Of Gene Expression ◽  
Risk Scores ◽  
Genome Wide Association Studies ◽  
Hla B27 ◽  
Genetic Associations ◽  
Functional Polymorphisms ◽  
Intergenic Regions ◽  
Specific Regulation

Ankylosing spondylitis (AS) is a common form of inflammatory spinal arthritis with a complex polygenic aetiology. Genome-wide association studies have identified more than 100 loci, including some involved in antigen presentation (HLA-B27, ERAP1, and ERAP2), some in Th17 responses (IL6R, IL23R, TYK2, and STAT3), and others in macrophages and T-cells (IL7R, CSF2, RUNX3, and GPR65). Such observations have already helped identify potential new therapies targeting IL-17 and GM-CSF. Most AS genetic associations are not in protein-coding sequences but lie in intergenic regions where their direct relationship to particular genes is difficult to assess. They most likely reflect functional polymorphisms concerned with cell type-specific regulation of gene expression. Clarifying the nature of these associations should help to understand the pathogenic pathways involved in AS better and suggest potential cellular and molecular targets for drug therapy. However, even identifying the precise mechanisms behind the extremely strong HLA-B27 association with AS has so far proved elusive. Polygenic risk scores (using all the known genetic associations with AS) can be effective for the diagnosis of AS, particularly where there is a relatively high pre-test probability of AS. Genetic prediction of disease outcomes and response to biologics is not currently practicable.

A brief history of ankylosing spondylitis

2016 ◽  
Author(s):  
Stefan Siebert ◽  
Sengupta Raj ◽  
Alexander Tsoukas
Keyword(s):  
Ankylosing Spondylitis ◽  
Clinical Features ◽  
Association Studies ◽  
Genome Wide Association ◽  
Genome Wide Association Studies ◽  
Hla B27 ◽  
The Past ◽  
Genome Wide ◽  
Clinical Radiology ◽  
History Of

The history of ankylosing spondylitis (AS) dates back to the discovery of skeletons with characteristic spinal changes. The disease was further defined by correlating pathological and clinical features, and the development of clinical radiology. Subsequent epidemiology and familial studies highlighted the association with other related conditions as part of the spondyloarthritides. The discovery of HLA-B27 confirmed this association. Over the past two decades, genome-wide association studies, and advances in imaging and immunology have yielded dramatic insights into the disease and the development of highly effective therapies.

scholarly journals Analysis of 47 Non-MHC Ankylosing Spondylitis Susceptibility Loci Regarding Associated Variants across Whites and Han Chinese

2019 ◽  
Vol 47 (5) ◽  
pp. 674-681
Author(s):  
Xuqi Zheng ◽  
Qiuxia Li ◽  
Xiaomin Li ◽  
Yanli Zhang ◽  
Xinyu Wu ◽  
...  
Keyword(s):  
Ankylosing Spondylitis ◽  
Interaction Analysis ◽  
Association Studies ◽  
Critical Role ◽  
Population Attributable Risk ◽  
Han Chinese ◽  
Systematic Evaluation ◽  
Genome Wide Association Studies ◽  
Hla B27 ◽  
Susceptibility Loci

Objective.To present a systematic evaluation of 47 non-MHC ankylosing spondylitis (AS) susceptibility loci that have been initially discovered through white genome-wide association studies in Han Chinese.Methods.Originally, 10,743 samples representing north and south Chinese in 4 datasets were obtained. After data quality control and imputation, metaanalysis results of 94,621 variants within 47 loci were extracted. Four ERAP1 single-nucleotide polymorphisms (SNP) and HLA-B27 tag SNP rs13202464 were used for interaction analysis. Population-attributable risk percentages of AS-associated variants were compared. Functional annotations of AS-associated variants were conducted using HaploReg, RegulomeDB, and rVarBase databases.Results.We revealed 16 AS-associated variants with nominal evidence in Han Chinese, including rs10865331 (p = 6.30 × 10−10), rs10050860 (p = 4.09 × 10−5) and rs8070463 (p = 1.03 × 10−4). Potential susceptible SNP within these 47 loci were also identified, such as rs13024541 (2p15), rs17401719 (5q15), and rs62074054 (17q21). Epistatic interactions between 3 ERAP1 SNP (rs17401719, rs30187, and rs10050860) and HLA-B27 were confirmed. Among the 16 AS-associated variants, rs30187 showed weaker risk effect, while rs10050860 and rs12504282 seemed to attribute more risk in Han Chinese than in whites. Further genomic annotation pinpointed 35 candidate functional SNP, especially in the 2p15, ERAP1, and NPEPPS-TBKBP1 regions.Conclusion.Our results provided a detailed spectrum of all the reported non-MHC AS susceptibility loci in Han Chinese, which comprehensively exhibited the ethnic heterogeneity of AS susceptibility and highlighted that 2p15, ERAP1, and NPEPPS-TBKBP1 regions may play a critical role in AS pathogenesis across diverse populations.

TLR1 and PRKAA1 Gene Polymorphisms in the Development of Atrophic Gastritis and Gastric Cancer

2018 ◽  
Vol 27 (4) ◽  
pp. 363-369 ◽  
Author(s):  
Gintare Dargiene ◽  
Greta Streleckiene ◽  
Jurgita Skieceviciene ◽  
Marcis Leja ◽  
Alexander Link ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Atrophic Gastritis ◽  
Genetic Polymorphisms ◽  
Association Studies ◽  
Control Group ◽  
Similar Distribution ◽  
Genome Wide Association Studies ◽  
Increased Risk ◽  
Infection Susceptibility ◽  
H Pylori

Background & Aims: Previous genome-wide association studies showed that genetic polymorphisms in toll-like receptor 1 (TLR1) and protein kinase AMP-activated alpha 1 catalytic subunit (PRKAA1) genes were associated with gastric cancer (GC) or increased Helicobacter pylori (H. pylori) infection susceptibility. The aim of this study was to evaluate the association between TLR1 and PRKAA1 genes polymorphisms and H.pylori infection, atrophic gastritis (AG) or GC in the European population.Methods: Single-nucleotide polymorphisms (SNPs) were analysed in 511 controls, 340 AG patients and 327 GC patients. TLR1 C>T (rs4833095) and PRKAA1 C>T (rs13361707) were genotyped by the real-time polymerase chain reaction. H. pylori status was determined by testing for anti-H. pylori IgG antibodies in the serum.Results: The study included 697 (59.2%) H. pylori positive and 481 (40.8%) H. pylori negative cases. We observed similar distribution of TLR1 and PRKAA1 alleles and genotypes in H. pylori positive and negative cases. TLR1 and PRKAA1 SNPs were not linked with the risk of AG. TC genotype of TLR1 gene was more prevalent in GC patients compared to the control group (29.7% and 22.3% respectively, p=0.002). Carriers of TC genotype had a higher risk of GC (aOR=1.89, 95% CI: 1.26–2.83, p=0.002). A similar association was observed in a dominant inheritance model for TLR1 gene SNP, where comparison of CC+TC vs. TT genotypes showed an increased risk of GC (aOR=1.86, 95% CI: 1.26–2.75, p=0.002). No association between genetic polymorphism in PRKAA1 gene and GC was observed.Conclusions: TLR1 rs4833095 SNP was associated with an increased risk of GC in a European population, while PRKAA1 rs13361707 genetic variant was not linked with GC. Both genetic polymorphisms were not associated with H. pylori infection susceptibility or the risk of AG.

scholarly journals Association analysis of juvenile idiopathic arthritis genetic susceptibility factors in Estonian patients

2021 ◽  
Author(s):  
Tiit Nikopensius ◽  
Priit Niibo ◽  
Toomas Haller ◽  
Triin Jagomägi ◽  
Ülle Voog-Oras ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Juvenile Idiopathic Arthritis ◽  
Autoimmune Diseases ◽  
Genetic Risk ◽  
Association Studies ◽  
Control Sample ◽  
Case Control ◽  
Genome Wide Association ◽  
Genome Wide Association Studies ◽  
Genome Wide

Abstract Background Juvenile idiopathic arthritis (JIA) is the most common chronic rheumatic condition of childhood. Genetic association studies have revealed several JIA susceptibility loci with the strongest effect size observed in the human leukocyte antigen (HLA) region. Genome-wide association studies have augmented the number of JIA-associated loci, particularly for non-HLA genes. The aim of this study was to identify new associations at non-HLA loci predisposing to the risk of JIA development in Estonian patients. Methods We performed genome-wide association analyses in an entire JIA case–control sample (All-JIA) and in a case–control sample for oligoarticular JIA, the most prevalent JIA subtype. The entire cohort was genotyped using the Illumina HumanOmniExpress BeadChip arrays. After imputation, 16,583,468 variants were analyzed in 263 cases and 6956 controls. Results We demonstrated nominal evidence of association for 12 novel non-HLA loci not previously implicated in JIA predisposition. We replicated known JIA associations in CLEC16A and VCTN1 regions in the oligoarticular JIA sample. The strongest associations in the All-JIA analysis were identified at PRKG1 (P = 2,54 × 10−6), LTBP1 (P = 9,45 × 10−6), and ELMO1 (P = 1,05 × 10−5). In the oligoarticular JIA analysis, the strongest associations were identified at NFIA (P = 5,05 × 10−6), LTBP1 (P = 9,95 × 10−6), MX1 (P = 1,65 × 10−5), and CD200R1 (P = 2,59 × 10−5). Conclusion This study increases the number of known JIA risk loci and provides additional evidence for the existence of overlapping genetic risk loci between JIA and other autoimmune diseases, particularly rheumatoid arthritis. The reported loci are involved in molecular pathways of immunological relevance and likely represent genomic regions that confer susceptibility to JIA in Estonian patients. Key Points• Juvenile idiopathic arthritis (JIA) is the most common childhood rheumatic disease with heterogeneous presentation and genetic predisposition.• Present genome-wide association study for Estonian JIA patients is first of its kind in Northern and Northeastern Europe.• The results of the present study increase the knowledge about JIA risk loci replicating some previously described associations, so adding weight to their relevance and describing novel loci.• The study provides additional evidence for the existence of overlapping genetic risk loci between JIA and other autoimmune diseases, particularly rheumatoid arthritis.

scholarly journals Functional genomics of autoimmune diseases

2021 ◽  
pp. annrheumdis-2019-216794
Author(s):  
Akari Suzuki ◽  
Matteo Maurizio Guerrini ◽  
Kazuhiko Yamamoto
Keyword(s):  
Autoimmune Diseases ◽  
Association Studies ◽  
Linkage Disequilibrium Block ◽  
Causal Variant ◽  
Genome Wide Association Studies ◽  
Coding Region ◽  
Risk Variants ◽  
Non Coding Rna ◽  
Genome Wide ◽  
Long Non Coding Rna

For more than a decade, genome-wide association studies have been applied to autoimmune diseases and have expanded our understanding on the pathogeneses. Genetic risk factors associated with diseases and traits are essentially causative. However, elucidation of the biological mechanism of disease from genetic factors is challenging. In fact, it is difficult to identify the causal variant among multiple variants located on the same haplotype or linkage disequilibrium block and thus the responsible biological genes remain elusive. Recently, multiple studies have revealed that the majority of risk variants locate in the non-coding region of the genome and they are the most likely to regulate gene expression such as quantitative trait loci. Enhancer, promoter and long non-coding RNA appear to be the main target mechanisms of the risk variants. In this review, we discuss functional genetics to challenge these puzzles.

scholarly journals THU0389 OBESITY IS A STRONG PREDICTOR OF WORSE CLINICAL OUTCOMES AND TREATMENT RESPONSES TO BIOLOGICS IN PATIENTS WITH ANKYLOSING SPONDYLITIS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 429.2-429
Author(s):  
L. Hu ◽  
X. Ji ◽  
F. Huang
Keyword(s):  
Ankylosing Spondylitis ◽  
Disease Activity ◽  
Clinical Outcomes ◽  
Normal Weight ◽  
Low Grade ◽  
Hla B27 ◽  
Treatment Responses ◽  
The Impact ◽  
Overweight Or Obesity

Background:Obesity population are rising rapidly and have become a major health issue. Studies have shown that obesity is a low-grade inflammatory status characterized by increase in proinflammatory cytokines.Objectives:To examine the impact of overweight or obesity on disease activity and treatment responses to biologics in patients with ankylosing spondylitis (AS) in a real-world setting.Methods:Body mass index (BMI) is available in 1013 patients from the Chinese Ankylosing Spondylitis Imaging Cohort (CASPIC). Differences in clinical outcomes (such as BASDAI, ASDAS, BASFI, and ASAS HI) and treatment responses to biologics (ΔBASDAI and ΔASDAS) over 3, 6, 9, and 12 months are assessed between BMI categories (normal weight BMI <24 kg/m2; overweight BMI=24-28 kg/m2; obesity BMI ≥28 kg/m2) using Kruskal-Wallis test. The association between BMI and clinical characteristics and treatment responses to biologics was determined, and multivariate median regression analyses were conducted to adjust for confounders (such as age, gender, smoke, and HLA-B27).Results:Among 1013 patients with AS, overweight accounts for 33%, while obesity for 12.4%. There were significant differences between patients who were obese or overweight and those with a normal weight regarding clinical outcomes (BASDAI: 2.90/2.56 vs 2.21; ASDAS-CRP: 2.20/1.99 vs 1.81; BASFI: 2.13/1.69 vs 1.38; ASAS HI: 6.87/5.29 vs 5.12 and BASMI: 2.35/1.76 vs 1.62; all P<0.05). After adjusting for age, gender, smoke, and HLA-B27, obesity remained associated with higher disease activity (BASDAI: β=0.55, P=0.005; ASDAS-CRP: β=0.40, P<0.001), poorer functional capacity (BASFI: β=0.58, P=0.001), worse health index (ASAS HI: β=1.92, P<0.001) and metrology index (BASMI: β=0.71, P=0.013). For TNFi users, BMI was found to be negatively correlated with changes in disease activity (ΔBASDAI and ΔASDAS) in the multivariate regression model (all P<0.05), and overweight and obese patients showed an unsatisfactory reduction in disease activity during 3-month, 6-month, 9-month, and 12-month follow-up period, compared to normal weight patients (all P<0.05).Conclusion:Overweight or obesity impacts greatly on clinical outcomes and treatment responses to biologics in patients with ankylosing spondylitis, which argues strongly for obesity management to become central to prevention and treatment strategies in patients with AS.References:[1]Maachi M, Pieroni L, Bruckert E, et al. Systemic low-grade inflammation is related to both circulating and adipose tissue TNFalpha, leptin and IL-6 levels in obese women. Int J Obes Relat Metab Disord 2004;28:993–7.Figure 1.Changes of disease activity for TNFi users during 3-, 6-, 9- and 12-month follow-up according to BMI categories. a: vs. normal weight, P<0.05 in 3 months; b: vs. normal weight, P<0.05 in 6 months; c: vs. normal weight, P<0.05 in 9 months; d: vs. normal weight, P<0.05 in 12 months.Acknowledgments:We appreciate the contribution of the present or former members of the CASPIC study group.Disclosure of Interests:None declared

scholarly journals Application of Genetic Studies to Flow Cytometry Data and Its Impact on Therapeutic Intervention for Autoimmune Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Valeria Orrù ◽  
Maristella Steri ◽  
Francesco Cucca ◽  
Edoardo Fiorillo
Keyword(s):  
Flow Cytometry ◽  
Autoimmune Disease ◽  
Autoimmune Diseases ◽  
Immune Cell ◽  
Disease Risk ◽  
Association Studies ◽  
Large Fraction ◽  
Surface Protein ◽  
Genome Wide Association Studies ◽  
Human Immune System

In recent years, systematic genome-wide association studies of quantitative immune cell traits, represented by circulating levels of cell subtypes established by flow cytometry, have revealed numerous association signals, a large fraction of which overlap perfectly with genetic signals associated with autoimmune diseases. By identifying further overlaps with association signals influencing gene expression and cell surface protein levels, it has also been possible, in several cases, to identify causal genes and infer candidate proteins affecting immune cell traits linked to autoimmune disease risk. Overall, these results provide a more detailed picture of how genetic variation affects the human immune system and autoimmune disease risk. They also highlight druggable proteins in the pathogenesis of autoimmune diseases; predict the efficacy and side effects of existing therapies; provide new indications for use for some of them; and optimize the research and development of new, more effective and safer treatments for autoimmune diseases. Here we review the genetic-driven approach that couples systematic multi-parametric flow cytometry with high-resolution genetics and transcriptomics to identify endophenotypes of autoimmune diseases for the development of new therapies.

scholarly journals Assessment of Ankylosing Spondylitis Activity During Pregnancy Using Different Disease Activity Indices

2020 ◽  
Vol 58 (5) ◽  
pp. 503-511
Author(s):  
O. A. Krichevskaya ◽  
Z. M. Gandaloeva ◽  
S. I. Glukhova ◽  
I. Yu. Skripkina ◽  
A. B. Demina ◽  
...  
Keyword(s):  
Back Pain ◽  
Ankylosing Spondylitis ◽  
Disease Activity ◽  
Pregnant Women ◽  
Activity Index ◽  
Disease Activity Index ◽  
Control Group ◽  
Mean Values ◽  
In Pregnancy ◽  
Activity Indices

Objective: Assessment of ankylosing spondylitis activity patterns during pregnancy using BASDAI (Bath Ankylosing Spondylitis Disease Activity Index) and ASDAS-CRP (Ankylosing Spondylitis Disease Activity Score — C-Reactive Protein) disease activity indices.Materials and methods. The prospective study included 36 pregnant women with AS (modified New York AS criteria, 1984). Patients’ mean age was 31.6±4.8 years, mean age at AS onset was 21.8±10.9, and disease duration 134.9±89.3 months. The control group included 30 healthy pregnant women with no history of back pain and arthritis, their mean age was 28.2±4.5 years. In the I trimester of pregnancy 10 (33.3%) As patients experienced back pain, while in the III trimester already 15 (50%) had back pain. Throughout pregnancy, the intensity of back pain in the I, II и III trimesters based on numeric scale was on average 1.9±0.9; 2.1±1.1 and 2.1±0.8. BASDAI and ASDAS-CRP were used to measure disease activity on gestational Weeks 10–11, 20–21 and 31–32. The time of conception BASDAI score was assessed retrospectively at the 1st visit.Results and discussion. BASDAI mean values at the time of conception and I, II и III trimesters of pregnancy were: 2.3±1.9; 2.8±1.72 (p<0,05 vs month of conception); 3.2±1.9 and 3.3±2.1 respectively. Mean ASDAS-CRP in the I, II и III trimesters were 1.9±0.7; 2.3±0.9 and 2.2±0,8 respectively. There was a trend to CRP increase in the II and III trimesters vs the I: median CRP values in the I, II and III trimesters were 5.7 [1.6; 6.2], 8.0 [2.1; 9.6] and 7.9 [2.0; 9.2] mg/L, respectively. Percentages of patients with high disease activity based on BASDAI scores in the I, II and III trimesters were 30.6; 34.3 and 34.3%; based on ASDAS-CRP — 36.1; 57.5 and 53%, respectively. Throughout pregnancy, BASDAI scores were lower in the control group than in AS patients (p<0.01). However, no differences were found when comparing BASDAI values of AS patients and healthy women with back pain during pregnancy. The level of fatigue did not differ between pregnant women with AS (median 5[3; 7] and 5[3; 6]) and healthy controls (5[3; 8] and 5[4; 6]) in the I and II trimesters, while in the III trimester, fatigue in healthy pregnant women (6[4; 8]) was more pronounced than in AS patients (5[3; 6], p=0.01). Throughout pregnancy, the intensity of back pain in AS patients and healthy pregnant women with back pain did not differ (p<0.05). Median pain intensity in the I, II and III trimesters was 3[2; 4]; 4[3; 5]; 3[2; 6] and 2,5[1; 4]; 3[2; 7]; 4[2; 6], respectively. A high (rs ≥0,7) correlation of all BASDAI components with the index itself in each trimester of pregnancy, except for joint pain in the month of conception, and in the I and III trimesters was established in the group of pregnant women with AS. The control group had quite high correlation (rs >0.7) of fatigue severity with the BASDAI index in the I and II trimesters of pregnancy and moderate correlation (rs >0.53) in the III trimester; as wells as moderate (rs >0.5-0.69) correlation between back pain and BASDAIConclusion. A trend towards increasing AS activity based on BASDAI and ASDAS-CRP scores and CRP levels was established for the first half of pregnancy. Later in pregnancy these increased values failed to return to normal until the end of gestation. The percentage of AS patients with highto-moderate disease activity throughout pregnancy was lower based on BASDAI score vs based on ASDAS-CRP. Some BASDAI components (fatigue and back pain) reflect not only the activity of AS, but also changes associated with physiological pregnancy. The BASDAI index requires adaptation for use in pregnancy

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