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A longitudinal study of fecal calprotectin and the evolution of inflammatory bowel disease in ankylosing spondylitis

  • Hans Strid2,iii,
  • Arne Ståhl4,
  • Anna Demingerane,
  • Hans Carlstenane,
  • Lena Öhmanfour,five &
  • Helena Forsblad-d'Elia1,6

Arthritis Research & Therapy book 19, Article number:21 (2017) Cite this article

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Abstruse

Background

Patients with ankylosing spondylitis (As) are at increased chance of developing inflammatory bowel disease (IBD). Nosotros aimed to determine the variation in fecal calprotectin in Every bit over 5 years in relation to affliction activity and medication and also to study the incidence of and predictors for development of IBD.

Methods

Fecal calprotectin was assessed at baseline (n = 204) and at five-year follow-up (n = 164). The patients answered questionnaires and underwent clinical evaluations. At baseline and at 5-year follow-upward, ileocolonoscopy was performed in patients with fecal calprotectin ≥500 mg/kg and ≥200 mg/kg, respectively. The medical records were checked for diagnoses of IBD during the follow-up period.

Results

Fecal calprotectin >50 mg/kg was institute in ii-thirds of the patients at both report visits. In 80% of the patients, fecal calprotectin changed past <200 mg/kg betwixt the ii measuring points. Baseline fecal calprotectin was positively correlated with Ankylosing Spondylitis Disease Activity Score based on C-reactive protein, Bathroom Ankylosing Spondylitis Disease Activity Index, Bathroom Ankylosing Spondylitis Functional Index, C-reactive protein, erythrocyte sedimentation rate, and fecal calprotectin at 5-year follow-up. The utilise of nonsteroidal anti-inflammatory drugs (NSAIDs) was associated with higher fecal calprotectin, and three-calendar week abeyance of NSAIDs resulted in a drop of a median 116 mg/kg in fecal calprotectin. The use of tumor necrosis factor (TNF) blockers was associated with lower fecal calprotectin at both visits, but the users of TNF receptor fusion proteins had significantly higher fecal calprotectin than users of anti-TNF antibodies at 5-year follow-upwardly. The v-year incidence of Crohn's illness (CD) was 1.5% and was predicted by loftier fecal calprotectin.

Conclusions

Fecal calprotectin was elevated in a majority of the patients and was associated with disease action and medication at both visits. CD developed in ane.v% of the patients with Equally, and a loftier fecal calprotectin was the main predictor thereof. The results back up a link between inflammation in the gut and the musculoskeletal organization in Every bit. We propose that fecal calprotectin may be a potential biomarker to identify patients with As at risk of developing IBD.

Trial registration

ClinicalTrials.gov identifier: NCT00858819. Registered 9 March 2009. Last updated 28 May 2015.

Background

Ankylosing spondylitis (Every bit), Crohn's disease (CD), and ulcerative colitis (UC) are inflammatory diseases that have many common features. Several adventure genes are shared between the spondylarthritides and inflammatory bowel disease (IBD), and the diseases tin show coinheritance [1–four]. Patients with IBD can develop peripheral arthritis (10–20%), sacroiliitis (10–20%), and inductive uveitis (0.5–3%) [five–nine]. Studies have revealed the presence of endoscopic and histologic gut inflammation in forty–60% of patients with Equally and in 46% of patients with early spondylarthritis (SpA) [ten–13]. The subclinical gut inflammation in AS is often localized to the colon or the distal ileum. Histologically, the inflammation has been divided into an astute class and a chronic form, the latter resembling CD and conferring an increased risk for subsequent development of IBD [fourteen–sixteen]. Approximately 5–10% of patients with SpA eventually develop IBD, with CD existence more than common than UC [17, 18]. There is a lack of knowledge near what predicts the evolution of IBD in Every bit, even so, and clinical studies on the subject are rare [19].

Fecal calprotectin is an unspecific marker for gut inflammation. Calprotectin belongs to the family of calcium-binding calgranulins (or S100 proteins) and consists of heterodimers of the two proteins S100A8 and S100A9. Calprotectin is an abundant protein in the neutrophils, constituting up to 40–threescore% of the cytosolic poly peptide content, and it is also found in gut epithelial cells, monocytes, and macrophages. The level of calprotectin in feces is proportional to the level of neutrophil inflammation in the gut [20]. Fecal calprotectin is clinically used to discriminate IBD from irritable bowel syndrome and correlates well with clinical, endoscopic, and histologic measures of disease activeness in IBD [21, 22]. Fecal calprotectin is also increased in enteropathy caused past nonsteroidal anti-inflammatory drugs (NSAIDs) [23].

We accept previously investigated the levels of fecal calprotectin in a cohort of 204 patients with AS. We constitute that 68% of the patients had elevated levels (>50 mg/kg) and that fecal calprotectin was associated with higher disease activity but not with gastrointestinal symptoms [24]. The same patients were then invited to exist reexamined at a five-twelvemonth follow-upwards test.

The aims of this v-year prospective study on Every bit were (1) to investigate the intraindividual variations in fecal calprotectin over time in relation to affliction activity, illness manifestations, and medication; (2) to study the five-year incidence of IBD; and (iii) to identify predictors for the development of IBD.

Methods

Patients

All patients fulfilling the modified New York criteria for AS who were registered at the rheumatology clinics at Sahlgrenska University Hospital and the hospitals of Borås and Alingsås were invited to participate in the study in 2009, hereafter called baseline [24, 25]. Exclusion criteria were diagnosed IBD, psoriasis, dementia, pregnancy, and difficulties in understanding the Swedish language. Altogether, 204 patients were included at baseline and 164 (eighty%) patients were reexamined at the 5-year follow-up in 2014. All patients gave their written informed consent. The study was approved past the regional ethics committee in Gothenburg and was carried out in accordance with the Helsinki declaration. A flowchart of the enrollment of the patients and the study procedures is shown in Fig. 1. The patients underwent the same assessments at both visits, including concrete examinations and responding to questionnaires. Blood and stool samples were nerveless. The medical records of all the included patients at baseline were checked for ileocolonoscopies, episodes of gut inflammation, or diagnoses of IBD.

Fig. 1
figure 1

Flowchart of the written report procedures. Ileocolonoscopies were performed at different thresholds of fecal calprotectin at baseline and 5-year follow-upward. F-cal Fecal calprotectin, NSAID Nonsteroidal anti-inflammatory drug

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Questionnaires

The Ankylosing Spondylitis Illness Action Score based on C-reactive protein (ASDASCRP), Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), Bathroom Ankylosing Spondylitis Patient Global Score, and Bath Ankylosing Spondylitis Functional Index (BASFI) were used to assess disease activity and physical function. Back mobility was measured for the calculation of Bath Ankylosing Spondylitis Metrology Index (BASMI) [26].

Stool samples

Stool samples were nerveless past the patients and sent to the laboratory, where the samples were immediately frozen. After thawing of the samples, fecal calprotectin was analyzed using an enzyme-linked immunosorbent assay (ELISA) kit (Bühlmann Laboratories AG, Schönenbuch, Switzerland). The same ELISA kit and procedures were used at baseline and at five-yr follow-up. In the general population, fecal calprotectin is <50 mg/kg, according to the manufacturer of the kit.

Claret samples

Claret samples were analyzed for hemoglobin, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) using standard laboratory technique. Serum calprotectin was analyzed at baseline by ELISA (PhiCal; Immundiagnostik AG, Bensheim, Federal republic of germany) following the manufacturer's instructions. According to the manufacturer, the normal range for serum calprotectin is 500–3000 ng/ml.

Ileocolonoscopy

At baseline, all patients with fecal calprotectin ≥500 mg/kg were asked to ship in a new stool sample. NSAID use was not stopped. If their fecal calprotectin remained ≥500 mg/kg, the patients were advised to undergo a clinical routine ileocolonoscopy (Fig. 1). At five-yr follow-upward, all patients with fecal calprotectin ≥200 mg/kg were asked to send in another stool sample later on pausing NSAID medication for 3 weeks. If their fecal calprotectin remained >200 mg/kg when retested, the patients were referred for ileocolonoscopy. Before the ileocolonoscopy, NSAIDs were again paused for 3 weeks. At 5-year follow-upward, all ileocolonoscopies were performed past one endoscopist (HS) and followed the same procedure.

Data analyses

Data from all patients who participated at baseline (north = 204) were analyzed with the aim of determining the five-yr incidence of IBD and the predictors thereof. For all other data analyses, simply the patients who participated both at baseline and at v-year follow-up (n = 164) were included.

Statistical analyses

Statistical analyses were performed using IBM SPSS Statistics 23 software (IBM, Armonk, NY, USA). Descriptive statistics are presented as median and IQR. In comparisons between groups, the Isle of man-Whitney U test was used for continuous variables, and the chi-square test or Fisher's exact exam was used for categorical variables. The Wilcoxon signed-rank exam was used for repeated measurements. Correlations were calculated using Spearman'due south correlation (r south). Owing to its skewed distribution, fecal calprotectin was log-transformed and used every bit an outcome in linear regression with a stepwise model. All tests were two-tailed, and p ≤ 0.05 was considered statistically significant.

Results

Characteristics of the study population

In full, 164 patients, comprising 45% women and 55% men, completed the report and were examined at the 2 report visits (baseline and 5-yr follow-upwards). The characteristics of the report population are provided in Table i.

Table 1 Characteristics of the 164 patients with ankylosing spondylitis at baseline and 5-year follow-up

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Intraindividual variation in fecal calprotectin betwixt baseline and 5-twelvemonth follow-up

Fecal calprotectin was elevated (>50 mg/kg) in 70.7% (116 of 164) of the patients at baseline and in 63.4% (104 of 164) of the patients at 5-year follow-upwards. The levels of fecal calprotectin did non differ betwixt baseline and follow-up (p = 0.660) (Table 1).

The alter in fecal calprotectin between baseline and the 5-twelvemonth follow-upwards was ≤l mg/ml in 48% of the patients, 51–100 mg/kg in 16%, and 101–200 mg/kg in 16%. The median change between baseline and five-yr follow-up for calprotectin was one.5 (IQR −52.7 to 52.7) mg/kg. The intraindividual correlation coefficient for fecal calprotectin at baseline and follow-up was r South = 0.512 (p < 0.001) (Fig. 2a).

Fig. 2
figure 2

a Scatterplot of fecal calprotectin at baseline and 5-year follow-up in 164 patients with ankylosing spondylitis (AS). b Fecal calprotectin earlier and after a 3-week suspension of nonsteroidal anti-inflammatory drug (NSAID) use at 5-yr follow-up in 33 patients with AS

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Fecal calprotectin correlates with disease action and physical function

At both visits, fecal calprotectin was positively and significantly correlated with parameters reflecting college disease activity and poorer function at the aforementioned visit, such as CRP, ESR, ASDASCRP, BASDAI, BASFI, and BASMI. In addition, fecal calprotectin at baseline was positively associated with higher levels of CRP, ESR, ASDASCRP, and BASFI at 5-year follow-upward (Tabular array two).

Tabular array 2 Spearman'south correlations betwixt fecal calprotectin and parameters reflecting disease activity and physical part at baseline and 5-year follow-up

Full size tabular array

The patients who were smoking at baseline (nine%) had, in comparison with nonsmokers, significantly higher fecal calprotectin at 5-yr follow-upwardly (median [IQR] 107 [43–402] vs. 85 [45–221] mg/kg, p = 0.026). Baseline serum calprotectin was also positively correlated with fecal calprotectin, both at baseline (rS = 0.252, p = 0.001) and at v-year follow-upwardly (r S = 0.170, p = 0.030).

Fecal calprotectin and medication

The medications used at baseline and 5-yr follow-up are listed in Table 1. Fecal calprotectin was significantly higher in NSAID users than in nonusers at both study visits (baseline median [IQR] 105 [45–262] vs. 68 [44–93] mg/kg, p = 0.032; 5-yr follow-upwards 93 [44–215] vs. 40 [23–120] mg/kg, p = 0.011) (Fig. 3a). The users of anti-tumor necrosis cistron (anti-TNF) antibodies (infliximab, adalimumab, golimumab) had significantly lower fecal calprotectin than patients without TNF blocker therapy at both visits (baseline 43 [17–84] vs. 99 [54–256] mg/kg, p = 0.004; v-year follow-up 48 [26–135] vs. 89 [40–210] mg/kg, p = 0.022), whereas no such difference was found between users of TNF receptor fusion proteins (etanercept) and nonusers of TNF blockers. At 5-yr follow-up, the patients treated with TNF receptor fusion proteins had significantly college fecal calprotectin than the patients treated with anti-TNF antibodies (200 [93–555] vs. 48 [26–135] mg/kg; p = 0.016) (Fig. 3b). Comedication with methotrexate and a TNF blocker was mutual. Methotrexate was mostly taken in low doses (5–fifteen mg weekly). At 5-year follow-up, the utilise of methotrexate among patients on anti-TNF antibodies was not significantly dissimilar from the use in patients taking etanercept (xviii of 33 [54.5%] vs. 2 of 6 [33%]; p = 0.407 by Fisher'southward exact test).

Fig. three
figure 3

a Box plot showing the association between fecal calprotectin and frequency of NSAID intake at 5-year follow-up. b Box plot showing the distribution of fecal calprotectin among patients on anti-TNF antibodies (infliximab, adalimumab, golimumab) vs. no TNF blocker therapy vs. TNF receptor fusion proteins (etanercept) at 5-twelvemonth follow-up. Values are median (horizontal lines), IQR (boxes), and total range (whiskers). NSAID Nonsteroidal anti-inflammatory drug, TNF Tumor necrosis factor

Total size image

Although the patients treated with TNF blockers had a significantly lower frequency of NSAID intake than the patients without TNF blockers, the meaning differences in fecal calprotectin between users and nonusers of disease-modifying antirheumatic drugs and/or TNF blockers remained afterwards adjustment for NSAID use. Linear regression analysis was performed with log-transformed fecal calprotectin at five-year follow-up as an outcome measure out, and the following baseline values were used as covariates: sexual activity, historic period, serum calprotectin, fecal calprotectin, CRP, ASDASCRP, BASFI, smoking, and use of NSAIDs and anti-TNF antibodies/TNF receptor fusion proteins. Only fecal calprotectin at baseline (β = 0.001, SE = 0.000, 95% CI 0.0008–0.0015, p < 0.001) and smoking at baseline (B = 0.241, SE = 0.121, 95% CI 0.002–0.479, p = 0.048) remained independently associated with higher fecal calprotectin at v-year follow-up (R 2 = 0.247).

Gastrointestinal symptoms

A loftier frequency of gastrointestinal symptoms (diarrhea, presence of blood or mucus in stools, obstipation, intestinal pain, tenesmus, reflux symptoms, and epigastric pain) was reported by the participants both at baseline and at 5-year follow-upwardly (Tabular array 1). There were no significant associations between the levels of fecal calprotectin and gastrointestinal symptoms at any of the time points, notwithstanding.

Fecal calprotectin before and subsequently of iii-week NSAID pause

At 5-year follow-up, the patients who had fecal calprotectin ≥200 mg/kg (n = 40 [24%]) were asked to ship in a new stool sample after pausing NSAID employ for 3 weeks, which a total of 33 patients did. After the 3-week NSAID pause, fecal calprotectin dropped past 116 (−twenty to 289) mg/kg from a range of 410 (295–510) mg/kg to 290 (120–480) mg/kg (p = 0.005) (Fig. 2b).

Evolution of gut inflammation during 5 years of follow-upwardly

Ileocolonoscopies were performed in 8 patients at baseline and in 16 patients at five-yr follow-upwardly (Fig. 1). The findings from the ileocolonoscopies are summarized in Table 3. Altogether, 10 (41.7%) of the 24 patients who underwent ileocolonoscopy had inflammatory changes in the gut biopsies. In addition, v patients (20.8%) had only macroscopic changes.

Table 3 Development of gut inflammation in 204 patients with ankylosing spondylitis betwixt baseline and 5-year follow-upwardly

Full size table

At 5-twelvemonth follow-upwardly, 3 patients (1.five%) were diagnosed with CD (corresponding to an annual incidence of 294 new cases per 100,000 person-years), and i patient (0.5%) was diagnosed with lymphocytic colitis. No cases of UC were plant. Additionally, v patients (2.5%) demonstrated characteristics of subclinical CD with aphthous ulcerations and/or chronic inflammation in the distal ileum, and another six patients (ii.9%) had ulcerations and/or chronic inflammation in the colon. In total, 15 patients (7.4%) demonstrated characteristics of inflammation in the big or small intestine during the v-year follow-up period.

Predictors for development of CD

At baseline, the patients who adult CD had, in comparison with the other patients, college fecal calprotectin (570 [271–570] mg/kg vs. 85 [43–230]; p = 0.014) and more often reported having diarrhea containing mucus (iii of 3 vs. xxx of 201; p = 0.004). No pregnant associations were found between the evolution of CD and the other baseline parameters. A receiver operating characteristic (ROC) curve was created with baseline fecal calprotectin every bit the test variable and development of CD as the chiselled state variable. The surface area nether the curve was 0.913 (95% CI 0.805–1.000; p = 0.014). Using a threshold for baseline fecal calprotectin of 266 mg/kg, based on this ROC curve, the sensitivity for development of CD was 100% and the specificity was 78.vii%.

Discussion

In this longitudinal 5-twelvemonth study of a well-characterized accomplice of patients with Every bit, we followed the intraindividual variation in fecal calprotectin in relation to disease activity and medication, and we determined the incidence and predictors for IBD. Fecal calprotectin was elevated (>l mg/kg) in approximately 2-thirds of the patients at both the baseline and v-year follow-up visits. The intraindividual variation was moderate; in eighty% of the patients, fecal calprotectin changed <200 mg/kg between the two measurement time points. Smoking and elevated fecal calprotectin at baseline were the strongest predictors for high fecal calprotectin at v-yr follow-upwards. Of the 204 patients included at baseline, 1.5% were diagnosed with CD and 0.5% with lymphocytic colitis at 5-yr follow-upwardly. High fecal calprotectin and presence of fungus in diarrhea at baseline were the main predictors of evolution of CD in this cohort.

Our results bespeak that gut inflammation in AS is associated with higher disease activity in rheumatic illness. Increased fecal calprotectin at baseline was associated with higher ASDASCRP, BASDAI, BASFI, CRP, and ESR at five-year follow-up. Early prospective studies showed a link between active gut inflammation and persistence of joint and spine inflammation every bit well as more than chronic radiographic changes in the sacroiliac joint and spine [xviii, 27]. Researchers in two cantankerous-sectional studies reported higher fecal calprotectin in AS than in healthy control subjects [28, 29]. One of the studies showed a positive correlation betwixt fecal calprotectin and BASDAI, BASFI, ESR, and CRP [29]. In studies with the Belgian Inflammatory Arthritis and spoNdylitis cohorT (GIANT) of early on SpA, the presence of histological gut inflammation was associated with higher BASDAI and college BASMI and was also linked to a greater caste of bone marrow edema in the sacroiliac joints visualized by magnetic resonance imaging [13, thirty]. The longitudinal results of our study support they hypothesis that inflammation in the gut and the musculoskeletal system may be linked. If gut inflammation is the cause or the upshot of locomotor disease is unknown, however, and fecal calprotectin is simply a surrogate measure for gut inflammation.

In a recent report based on the GIANT accomplice, fecal calprotectin, serum calprotectin, and CRP were also significantly higher in patients with microscopic gut inflammation [31]. We found that serum calprotectin at baseline was positively correlated with fecal calprotectin, both at baseline and at v-year follow-up, only serum calprotectin was not a pregnant predictor for the evolution of CD.

In the present study, the employ of anti-TNF antibodies was associated with lower fecal calprotectin, whereas use of TNF receptor fusion proteins was associated with college levels of fecal calprotectin, at 5-year follow-upwards. Infliximab and adalimumab, but not etanercept, are efficacious in the treatment of CD and UC [32]. Similarly, in earlier studies, more flares and onset of IBD were observed in patients with AS treated with etanercept than in patients treated with infliximab [33, 34].

The 5-year incidence of CD in the nowadays report was 1.5%, which corresponds to an annual incidence of 294 new cases per 100,000 person-years. This can be compared with the highest reported almanac incidence of CD in the general population of 12.7 per 100,000 person years in Europe and 20.2 per 100,000 person-years in North America [35]. Mielants et al. reported an incidence of IBD of v% in a cohort of 217 patients with SpA or Equally during a median follow-up of 5.5 years [19]. Similarly to our study, CD was more than common than UC in their report. In dissimilarity to our study, ileocolonoscopy was performed on all patients at inclusion, and 49 patients underwent a second endoscopy. Because patients with fecal calprotectin <200 mg/kg were not examined with endoscopy in our study, cases with IBD despite lower fecal calprotectin may have been missed. Moreover, the before studies were performed in the "prebiologic era," which may take affected the results. Furthermore, a few patients with persistently elevated fecal calprotectin declined ileocolonoscopy.

In our study, elevated fecal calprotectin and presence of fungus in diarrhea at baseline were the simply significant predictors of the evolution of CD. The low number of new cases of CD (n = 3) may have affected the robustness of the results and the possibility of finding other significant predictors.

The high use of NSAIDs amongst patients with AS is a problem when studying gut inflammation. NSAID-induced enteropathy is difficult to distinguish from AS-associated gut inflammation and is associated with increased fecal calprotectin [23]. In the present study, NSAID employ was stopped for 3 weeks before retesting fecal calprotectin and before ileocolonoscopies, which resulted in a drop of a median of 116 mg/kg in fecal calprotectin. We constitute that 3-week abeyance of NSAID use before testing fecal calprotectin was a reasonable class of action and acceptable for most patients.

The strengths of the present study are its prospective blueprint with two measurement time points, the relatively large and well-characterized cohort, and cessation of NSAIDs before ileocolonoscopy at follow-up. The written report's weaknesses are that ileocolonoscopy was not performed in all patients, which may have resulted in a lower incidence of IBD. The ileocolonoscopies were likewise performed at different thresholds of fecal calprotectin at baseline and 5-yr follow-upwards (Fig. one).

Conclusions

Fecal calprotectin was elevated in 2-thirds of the patients with Every bit and was positively associated with parameters reflecting higher disease activity and poorer concrete office at both report visits. Use of NSAIDs and TNF receptor fusions proteins was associated with higher levels of fecal calprotectin, whereas employ of anti-TNF antibodies was associated with lower levels of fecal calprotectin. Further studies are needed to show whether anti-TNF treatment has an outcome on subclinical gut inflammation in AS and whether it tin can prevent the development of IBD. The v-twelvemonth incidence of CD was 1.5%, and elevated fecal calprotectin at baseline was the strongest predictor of the evolution of IBD. On the basis of these results, we propose that fecal calprotectin may be a potential biomarker to identify patients with AS at take a chance of developing IBD. Thus, fecal calprotectin quantification should be considered, especially in patients with loftier disease activeness and gastrointestinal symptoms. If possible, NSAIDs should be stopped temporarily before measuring fecal calprotectin to reduce the confounding effect of NSAID enteropathy on the measurement.

Abbreviations

As:

Ankylosing spondylitis

ASDAS:

Ankylosing Spondylitis Affliction Activity Score

ASDASCRP :

Ankylosing Spondylitis Illness Activity Score based on C-reactive protein

BASDAI:

Bath Ankylosing Spondylitis Disease Activeness Index

BASFI:

Bathroom Ankylosing Spondylitis Functional Index

BAS-G:

Bath Ankylosing Spondylitis Patient Global Score

BASMI:

Bath Ankylosing Spondylitis Metrology Alphabetize

CD:

Crohn's illness

CRP:

C-reactive poly peptide

DMARD:

Disease-modifying antirheumatic drug

ELISA:

Enzyme-linked immunosorbent assay

ESR:

Erythrocyte sedimentation rate

Giant:

Belgian Inflammatory Arthritis and spoNdylitis cohorT

IBD:

Inflammatory bowel affliction

NSAID:

Nonsteroidal anti-inflammatory drug

ROC:

Receiver operator characteristic

SpA:

Spondylarthritis

TNF:

Tumor necrosis factor

UC:

Ulcerative colitis

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Acknowledgements

We give thanks all the patients who participated in the written report.

Funding

This work was supported by grants from the Health and Medical Intendance Executive Board of the Västra Götaland, Rune and Ulla Amlövs Foundation for Rheumatology Research, Göteborg Clan against Rheumatism, the Swedish Clan Confronting Rheumatism, the Medical Society of Göteborg, and the Region Västra Götaland (agreement concerning research and education of doctors), Decision-making Chronic Inflammatory Diseases with Combined Efforts (COMBINE), the Margareta Rheuma Research Foundation, and the Swedish Lodge of Medicine.

Availability of information and materials

The datasets analyzed during the present written report are available from the corresponding author on reasonable request.

Authors' contributions

EK participated in the blueprint of the study, examined the patients, collected information, performed statistical analyses, and drafted the manuscript. HS participated in the design of the study, performed the ileocolonoscopies, and participated in the drove and estimation of data. AS was responsible for the fecal analyses and interpretation of data. Ad participated in the design of the study, examined the patients, and nerveless information. HC participated in the design of the study and the interpretation of data. LÖ participated in the pattern of the study and the collection and interpretation of data. HFd'E supervised the study and was responsible for written report design and interpretation of data. All authors critically reviewed the manuscript, approved the final version to be published, and agreed to be accountable for all aspects of the work.

Competing interests

The authors declare that they accept no financial or nonfinancial competing interests.

Consent for publication

Not applicable.

Ethics approval and consent to participate

The written report was canonical by the regional ideals committee in Gothenburg and was carried out in accordance with the Helsinki announcement. All participants gave their written informed consent.

Author information

Affiliations

  1. Department of Rheumatology and Inflammation Research, Sahlgrenska Academy at the Academy of Gothenburg, Guldhedsgatan 10A, S-413 46, Gothenburg, Sweden

    Eva Klingberg, Anna Deminger, Hans Carlsten & Helena Forsblad-d'Elia

  2. Department of Internal Medicine, Södra Älvsborgs Sjukhus, Borås, Sweden

    Hans Strid

  3. Department of Internal Medicine and Clinical Nutrition, Sahlgrenska Academy at the Academy of Gothenburg, Gothenburg, Sweden

    Hans Strid

  4. Department of Microbiology and Immunology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden

    Arne Ståhl & Lena Öhman

  5. Sweden Schoolhouse of Health and Education, University of Skövde, Skövde, Sweden

    Lena Öhman

  6. Rheumatology Unit, Section of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden

    Helena Forsblad-d'Elia

Corresponding author

Correspondence to Eva Klingberg.

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Klingberg, E., Strid, H., Ståhl, A. et al. A longitudinal report of fecal calprotectin and the evolution of inflammatory bowel affliction in ankylosing spondylitis. Arthritis Res Ther nineteen, 21 (2017). https://doi.org/10.1186/s13075-017-1223-2

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  • DOI : https://doi.org/10.1186/s13075-017-1223-2

Keywords

  • Ankylosing spondylitis
  • Spondylarthritis
  • Inflammatory bowel disease
  • Fecal calprotectin
  • Crohn's disease
  • Ulcerative colitis
  • Intestinal inflammation

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