Performance evaluation of the DiaSorin faecal calprotectin assay in monitoring inflammatory bowel disease: a diagnostic accuracy and comparative study

Introduction

Inflammatory bowel disease (IBD) is a chronic, relapsing–remitting inflammatory condition of the gastrointestinal tract. It encompasses two primary subtypes: ulcerative colitis (UC) and Crohn’s disease (CD). UC typically affects the colon in a continuous manner, confined to the mucosal layer, whereas CD presents with transmural inflammation and skip lesions, most commonly involving the ileum but potentially affecting any part of the gastrointestinal tract (1,2). The underlying pathophysiology involves a dysregulated immune response to intestinal microbiota in genetically predisposed individuals (1).

Accurate and timely assessment of disease activity is essential to guide therapeutic decisions, assess treatment response and predict relapse (3,4). This is relevant in the context of tight control strategies shown to improve outcome in CD, such as those demonstrated in the CALM trial (5). While endoscopy remains the gold standard for evaluating intestinal inflammation, it is invasive, costly and unsuitable for frequent monitoring due to associated risks such as bowel perforation, bleeding and patient burden (2,6). Consequently, non-invasive biomarkers are preferred for serial monitoring in clinical practice, particularly in distinguishing between organic and functional gastrointestinal diseases where markers as faecal calprotectin (FC) showed superior diagnostic utility (7).

FC is a 36-kDa calcium- and zinc-binding protein derived predominantly from neutrophils. Its presence in stool is indicative of neutrophil migration to the gastrointestinal mucosa, making it a reliable marker of intestinal inflammation (3,8-10). FC has several advantages as a biomarker: it is resistant to degradation by proteases and bacterial activity both in vitro and in vivo and can be measured reliably in stool samples (9,11).

Robust evidence supports the use of FC for differentiating active from quiescent IBD, with higher diagnostic accuracy than systemic inflammatory markers such as C-reactive protein (CRP) or full blood count (FBC) (10,12,13). Moreover, FC is known to perform well in differentiating IBD from malignancy demonstrating its broad diagnostic utility (14).

It is also useful in predicting relapse in asymptomatic patients, correlating well with endoscopic and histological disease activity (4,15).

The clinical utility of FC is likely to be heavily dependent on the analytical method used (16). Currently, there is no recognised reference method or reference standard for the measurement of calprotectin. Several commercially available assays exist and although they may demonstrate good correlation, they often show poor numerical agreement (11,17-19). Data from external quality assurance (EQA) schemes confirm substantial inter-assay variability in calprotectin measurements. This variability arises from several factors, including faeces heterogeneity (20), different antibody specificity (11,21) and variable extraction recovery (22). For example, the DiaSorin Liaison assay used in this study is a chemiluminescence immunoassay (CLIA) that employs monoclonal antibodies directed against the calprotectin heterocomplex, whereas the BÜHLMANN fCAL^® turbo assay is an uses polyclonal antibodies (2). A head-to-head comparison of extraction devices for the EliA™ Calprotectin assay (Thermo Fisher Scientific) and Smart Prep extraction system (Roche Diagnostics) demonstrated that disagreement between calprotectin assays could arises from the extraction stage and the extraction devices used (22).

In the diagnostic context, applying thresholds validated with one method to results from another could potentially result in misclassification and inappropriate clinical decisions. However, there are relatively few studies that have assessed the impact of different FC methods and cut-off values on monitoring of IBD. A systematic review published in 2017 was unable to provide pooled cut-off values for relapse or mucosal healing because only a limited number of studies were available (15). Even fewer studies have evaluated the DiaSorin assay in the context of monitoring IBD relapse. Notably, a recent meta-analysis [2023] examining the diagnostic accuracy of FC for predicting relapse in patients with IBD included only 24 eligible studies, none of which used the DiaSorin method (23).

Previous research in our region (York Hospital, UK) validated a calprotectin IBD care pathway for monitoring CD patients using FC (24). The pathway is widely used by hospitals in our region, including our hospital (Harrogate), despite the use of different FC methods. The pathway is based on an association between FC level and disease activity and risk of subsequent symptomatic flare (Figure 1) (15,24). The aim of the pathway is neither to miss patients with an active disease nor to over investigate/treat those in clinical remission (24). In clinical practice, this pathway is only applied to patients established on maintenance therapy whether the patient is symptomatic or not. This pathway, however, has been validated using a monoclonal ELISA (EK-CAL calprotectin ELISA, Buhlmann) to determine the FC level in faecal samples and applied a cut-off for FC of ≤100 µg/g to indicate likely quiescent CD and an FC cut-off of >100 µg/g to suggest active disease (2,4,15).

Figure 1 Summary of York IBD care pathway FC cut-offs for monitoring IBD disease (24). FC, faecal calprotectin; IBD, inflammatory bowel disease.

In our laboratory in Harrogate Hospital, FC is currently analysed using the DiaSorin Liaison FC assay. The DiaSorin assay is less widely used for FC measurement and has not been extensively studied as the Buhlmann FC assay. However, it is known that DiaSorin assay produces FC results lower than the Buhlmann FC assay and this is reflected in DiaSorin’s recommended cut-off values (17,19,25). In this study, we aimed to identify the impact of using a different method for FC measurement (DiaSorin) on classification as quiescent or active disease using the cut-off values derived using Buhlmann FC assay to ascertain if this can provide safe and accurate monitoring of IBD patients. We present this article in accordance with the STARD reporting checklist (available at https://jlpm.amegroups.com/article/view/10.21037/jlpm-2025-1-66/rc).

Methods

Sample collection, preparation, and extraction

Samples from adult patients over 18 years old with diagnosed IBD attending IBD monitoring clinics at York Teaching Hospital for monitoring purposes were eligible for inclusion and were recruited as a convenience series over a period of 3 months during 2024. Following routine sampling and calprotectin analysis on the Buhlmann FCAL Turbo method at the biochemistry department at York Teaching Hospitals, samples were anonymised. All anonymised samples were immediately re-sampled using the DiaSorin LIAISON Q.S.E.T. Device plus (REF 319060) used according to the manufacturer’s instruction. The sampling wand of the device is dipped into the stool sample multiple times (3–5 times) and then tightly screwed into the device which contains the extraction buffer. Extracted samples were stored overnight at 4 ℃ before transportation to Harrogate District Hospital laboratory for analysis at 4 ℃ the next day. As per manufacturer instructions, partially extracted samples are stable at room temperature for 8 hours or seven days at 2–8 ℃. Upon receipt in Harrogate laboratory, samples were then homogenised on a multi-tube vortex mixer for 30 min, and then analysed on the DiaSorin LIAISON^® XL analyzer in weekly batches.

This assay comparison was registered as a service evaluation with York Teaching Hospital. Therefore, the local Institutional Review Board deemed the study exempt from review.

FC analysis

FC was measured using the Buhlmann fCAL^® turbo assay (Alpha Laboratories 40 Parham Drive, Eastleigh, Hampshire, SO50 4NU, UK) and the DiaSorin LIAISON^® Calprotectin assay (DiaSorin S.p.A. UK Branch, Central Road, Dartford, Kent, DA1 5LR, United Kingdom). The Buhlmann assay is an immunoturbidimetric method validated against the Buhlmann EK-CAL^® ELISA. Both Buhlmann and DiaSorin platforms were operated according to the manufacturers’ instructions and performed within acceptable internal quality control (IQC) limits during the study. The uncertainty of measurement (UM) for the Buhlmann method at a quality control concentration of 80 µg/g was 13.9%. For the DiaSorin method, UM was 15% at 60 µg/g and 16.6% at 200 µg/g. Calprotectin concentrations were expressed in micrograms per gram of faeces. EQA samples were analysed regularly to ensure accuracy

Clinical validation of DiaSorin FC in IBD patients

Retrospective data from 2020 to 2024 was collected from two UK based neighboring hospitals using DiaSorin FC method, namely; Harrogate District Hospital and Airedale General Hospital. We identified 294 patients records with established diagnoses of IBD based on standard clinical, endoscopic and histological criteria. FC analysed on DiaSorin Liaison was routinely requested in those patients to monitor disease activity or in patients who develop IBD symptoms while on treatment. Patient records were selected for inclusion in the study when there was an FC measurement within one month of an endoscopy. Patients under 18 were excluded from the study. The electronic patient record (EPR) was used to identify and record the type of IBD (UC or CD), clinical symptoms and review colonoscopy reports.

The reference standard was established blindly and independently of the index test as disease activity was defined using the reference standard (endoscopy + histology) prior to evaluation of FC cut-offs. A clinical outcome of either active or quiescent disease was assigned using solely the colonoscopy and histological examination for each patient included in this part of the study. FC results in each patient were converted to categorical data using the cut-off values of ≤100 µg/g to indicate quiescent and >100 µg/g to indicate active disease. The clinical outcome as described above was then used as a gold standard against which the categorical FC results are compared. In addition to evaluating the cut-off value of 100 µg/g, we also evaluated the assay-specific manufacturer-recommended cut-off value of 50 µg/g for the Diasorin FC assay. The ability of DiaSorin FC results to classify patients correctly was assessed by calculation of sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV).

The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was registered as a clinical audit at Harrogate District Hospital and therefore, the local Institutional Review Board deemed the study exempt from review. Individual consent for this retrospective analysis was waived.

Statistical analysis

All statistical analyses and plotting of figures were performed using Analyse-it add-in package (Microsoft Excel 2016, version-3) and Prism (GraphPad, version-10). A mean inter-assay bias of approximately 50%, as reported in UK NEQAS EQA data and published comparisons of FC assays (16,18) was used to simulate the difference in patient classification. Sample size for the analytical comparison was calculated assuming a significance level of 0.05 for detecting a 10% difference in classification between FC assays and a minimum sample size of 45 sample was obtained. Passing-Bablok regression analyses were conducted to show the relationship between Buhlmann and DiaSorin FC results, and a Bland-Altman plot was drawn with bias calculations and 95% confidence intervals (CIs).

Statistically significant differences in analytical results from the two methods were assessed using a Wilcoxon test (paired, non-parametric data). FC results were converted into a patient category/classification (quiescent or active disease) using the cut-off value of 100 µg/g for both FC methods. The proportion of patients falling into each category were then compared for the two calprotectin methods using McNamar’s test of paired proportions.

In the retrospective patient dataset evaluating the performance of the DiaSorin FC assay, patients were sub-classified as having UC or CD. With 144 and 150 patients per CD and UC disease group respectively, the study was designed to evaluate the sensitivity and specificity of the DiaSorin FC assay with a precision of approximately ±8% at a 95% confidence level. Based on expected sensitivity of 80%, this sample size exceeds the minimum required, which was 96 patients with the disease to estimate sensitivity, providing robust reliability for the assay’s diagnostic performance. The classification of disease activity based on laboratory FC results was evaluated against clinical reference standards (colonoscopy plus histology) as the gold standard method. Diagnostic performance was assessed with sensitivity, specificity, PPV, and NPV calculated with 95% CIs. Receiver operating characteristic (ROC) curve analysis was performed to determine optimal DiaSorin cut-offs for maximum clinical validity compared to Buhlmann results.

Results

The impact of different FC assays on patient classification

Fifty-two FC samples were compared using the Buhlmann and DiaSorin methods. FC values ranged from 27 to 1,752 µg/g (Buhlmann) and 5.3 to 674 µg/g (DiaSorin). The mean FC was significantly higher by Buhlmann compared to DiaSorin (mean difference: 361.2 µg/g P<0.001). Graphical comparison (Passing-Bablok) of numerical results from both FC assays revealed a significance negative bias for the DiaSorin assay compared to the Buhlmann assay (y =9.015+0.369 x) (Figure 2A). Altman Bland comparison showed a mean difference of −220.0 µg/g (95% CI: −312.1 to −127.9), indicating that the DiaSorin assay will measure the calprotectin concentration of an identical sample approximately 127.9 µg/g lower than the Buhlmann assay. Ninety-five percent limits of agreement are −799.5 µg/g (95% CI: −958.2 to −139.4) and 359.5 µg/g (95% CI: 200.8–518.2) (Figure 2B).

Figure 2 Graphical comparison of DiaSorin assay versus Buhlmann assay. (A) Shows Passing-Bablock regression. The regression line equation: y =9.015+0.3692 x; 95% CI: for intercept −1.206 to 25.00 and for slope 0.2755 to 0.4458. (B) Shows the Bland-Altman difference plot for the patient samples. The mean difference is −219.995 µg/g (95% CI: −312.1 to −127.9 µg/g). CI, confidence interval; LoA, limits of agreement.

FC results from both FC assays were converted into a patient category/classification (quiescent or active disease) using the cut-off values of 100 µg/g. McNamara’s paired proportions was then used to compare the proportion of patients falling into each category. A significant difference was observed in the classification of patients as having quiescent versus active disease (P<0.05). Using the Buhlmann FC method with a threshold of 100 µg/g, 69% of patients were classified as having active disease whilst 31% were identified as quiescent. In contrast, with the DiaSorin FC method, 50% of patients were classified as active and 50% were classified as quiescent.

Clinical validation of DiaSorin cut-offs

A total of 294 IBD patients were included (144 with CD, 150 with UC); 56% were male and 44% were female (Figure 3). As shown in Table 1, active disease was more common in UC than CD. Although FC levels were slightly higher in UC patients on average, the mean and median values were very similar between disease groups and the difference was not considered clinically or analytically significant.

Figure 3 Selection of the study subjects. CD, Crohn’s disease; IBD, inflammatory bowel disease; UC, ulcerative colitis.

Diagnostic performance of the DiaSorin assay was calculated using both the manufacturer-recommended cut-off value of 50 µg/g faeces and the cut-off of 100 µg/g faeces derived from the Buhlmann FC assay. The values obtained for the different cut-off values for PPV (83.8%, 95% CI: 78.4–88.1 and 88.4%, 95% CI: 83.2–92.0 respectively) and NPV (63.9%, 95% CI: 52.4–74.0 and 65.9%, 95% CI: 55.5–75.0 respectively) were not significantly different as judged by overlap in the CI and P values for PPV is 0.167 and NPV is 0.786 (Table 2). The slight rise in sensitivity at a threshold of 50 µg/g did not translate to an improved NPV because of a high incidence of active disease within our study group, which in turn caused the specificity to decrease. No significant difference in overall diagnostic accuracy was observed between the 100 µg/g cut-off (81.6%) and the 50 µg/g cut-off (78.9%); P=0.25.

Positive and negative likelihood ratios (LRs) were calculated for the overall IBD cohort using the two predefined FC cut-offs to provide prevalence-independent measures of diagnostic performance (Table 3). At the 50 µg/g cut-off, the LR⁺ and LR⁻ values were 2.0 and 0.22 respectively. At the 100 µg/g cut-off, the LR⁺ increased to 2.93, while the LR⁻ was similar at 0.20. These findings indicate that raising the cut-off from 50 µg/g to 100 µg/g enhances rule-in capability (higher LR⁺), while rule-out capability (LR⁻) remains largely unchanged.

ROC curve analysis was used to assess assay performance and determine optimal cut-offs for detecting disease activity status in UC and CD (Table 4). The optimal FC threshold for CD was 272 µg/g [sensitivity 70%, specificity 85%; area under the curve (AUC) =0.78 (95% CI: 0.702–0.860)]. For UC, the optimal threshold was 154 µg/g [sensitivity 83%, specificity 80%; AUC =0.78 (95% CI: 0.658–0.896)]. ROC analysis for the combined IBD cohort (n=294) yielded an AUC of 0.584 (95% CI: 0.502–0.668), with an estimated sensitivity of 88% and specificity of 67% (Figure 4). The ROC-derived optimal cut-off based on the Youden index was approximately 138 µg/g, representing the point that maximised the combined sensitivity and specificity. However, this cut-off value would not offer a clinically meaningful advantage over the predefined cut-offs of 50 µg/g and 100 µg/g.

Figure 4 ROC analysis demonstrating the optimal DiaSorin cut-off for maximum clinical validity for UC and for CD. AUC, area under the curve; CD, Crohn’s disease; CI, confidence interval; ROC, receiver operating characteristic; SE, standard error; UC, ulcerative colitis.

Discussion

FC assays have been widely adopted for non-invasive assessment of intestinal inflammation in patients with IBD. However, considerable inter-assay variability remains a challenge, especially when attempting to apply a standardised clinical protocol across different FC methods (19). UK NEQAS and other research groups consistently reported 50% bias between Buhlmann and DiaSorin platforms, highlighting that large differences in FC results can be seen for different methods as shown in this study (17).

The analytical comparison data in this report showed that applying a uniform cut-off value of 100 µg/g to classify patient results from the two different methods led to inconsistent patient classification, reinforcing the need for assay-specific thresholds to ensure consistency in FC interpretation. In contrast, the retrospective study assessing DiaSorin FC assay performance in a large cohort of individuals with IBD with endoscopy plus histology as a reference standard, was supportive of maintaining a cut-off of 100 µg/g.

Applying a lower, manufacturer-recommended FC cut-off of 50 µg/g resulted in an increase in sensitivity (87.7%), but this improvement was accompanied by a drop in specificity (56.1%) and a corresponding decrease in overall accuracy to 78.9%. Notably, there is no statistically significant difference in diagnostic accuracy parameters between the 100 µg/g and 50 µg/g cut-off (P=0.25). This was further supported by the LR analysis, a prevalence-independent measure, which showed that increasing the cut-off from 50 µg/g to 100 µg/g improved rule-in performance (higher LR⁺), while rule-out performance (LR⁻) remained the same.

At the 100 µg/g cut-off, the DiaSorin assay generated an NPV of 65.9% (95% CI: 55.5–75.0%) in our cohort. This figure is noticeably lower than values reported in earlier studies, many of which found NPVs surpassing 90% when FC was used to rule out active inflammation (10). For example, van Rheenen et al. described an NPV of 93% in symptomatic individuals being evaluated for IBD (26). A recent systematic review reported similarly high NPV, when FC was compared with endoscopic activity (12,27,28). However, it is essential to note that these studies focused on using FC for diagnostic purposes rather than monitoring. Several plausible reasons could explain our lower NPV, including a higher proportion of patients with active disease in our cohort compared to prior publications, which inherently lowers NPV. Although the mean FC concentration measured by the DiaSorin assay was approximately 50% lower than that measured by the Buhlmann assay, this average difference concealed substantial heterogeneity in individual sample results. Such variability likely reflects fundamental differences in assay design, including the recognition of distinct calprotectin epitopes and the recognition of various molecular forms and degradation products (9). It is likely that the two assays are not directly comparable and a result of 100 µg/g on the Buhlmann assay should not be assumed equivalent to 50 µg/g on the DiaSorin platform. This inter-assay variability has been widely recognized, and international consensus recommendations now stress that longitudinal monitoring in individual patients should be performed using the same assay method to avoid misclassification of disease activity (19).

While the DiaSorin assay performed acceptably at both 50 µg/g and 100 µg/g cut-off values, some limitations of the current study must be acknowledged. In this study, only patients who had FC testing within one month of colonoscopy were included and disease activity could have evolved during that interval. Notably, FC levels often normalise more rapidly than mucosal inflammation resolves, potentially leading to false reassurance. This phenomenon has been described in prior studies, including that by Turvill et al. where the mean interval between FC testing and colonoscopy was three weeks—slightly shorter than the one-month window used in our study (24).

As with many retrospective designs, additional constraints include the potential for selection bias, gaps in clinical documentation and reliance on previously recorded endoscopic findings. Nevertheless, the relatively large sample size and the structured use of a clinical pathway enhance the general relevance of our observations and provide data from a “real world” setting.

In our study, the comparison of the cut-offs (50 versus 100 µg/g) yielded comparable but low NPV (63.9% and 65.9% respectively). This suggests that the risk of recurrence/relapse is underestimated using either of the cut-offs. Therefore, we decided to explore the identification of an optimal cut-off value. Using ROC analysis, we identified the optimal cut-offs for UC and CD respectively (154 and 272 µg/g). The increase in the specificity was predictably accompanied with a loss in sensitivity especially for CD patients. Our ROC analysis findings align with a recent meta-analysis that pooled raw data from 24 studies (n=2,260), using various analytical platforms to determine an optimal cut-off for predicting IBD relapse. The analysis identified 152 µg/g as the ideal threshold for patients at high risk of relapse (23). This underscores the need to optimise calprotectin cut-offs for relapse prediction in IBD when using the DiaSorin platform.

It is unlikely that the current study is sufficiently powered to define an optimal cut-off value, therefore, the ROC derived cut-offs in this publication should be considered exploratory and require external validation before implementation in clinical practice. This paper has focused on defining a single optimal cut-off value for dichotomous classification of patient however the previously published York IBD care pathway, utilizes the cut-off value of 100 µg/g as part of a scale includes low, medium and high risk probabilities of relapse and safety netting approach to ensure no patient with active disease is missed. Our results together with the previously published data underscore the need to interpret FC results in the broader context of clinical presentation and, where indicated, direct assessment via endoscopy. Proposing different dichotomous cut-offs for UC and for CD may not be well received in the clinical practice due to concerns regarding practicality and safety netting. Importantly, our findings emphasise the value of evaluating both analytical characteristics and clinical utility when adopting or comparing FC assays in practice. There is a need for a mix of caution and pragmatism when applying cut-offs derived from one FC assay to another FC assay especially in the context of an optimal cut-off for detecting relapse.

Conclusions

FC assays are widely adopted for non-invasive assessment of intestinal inflammation in patients with IBD. Yet, considerable inter-assay variability remains a challenge for the application of unified clinical cut-offs. While the mean FC concentration using the DiaSorin assay is 50% lower than that measured by the Buhlmann assay, applying a cut-off of 100 µg/g established using Buhlmann assay to DiaSorin FC assay results showed no significant differences in classifying patients as having active or quiescent disease. Our findings from ROC analysis, however, underscore the necessity of optimizing diagnostic cut-off values to correctly identify patients with a high relapse probability and improves its rule out capabilities using DiaSorin assays. Future research should focus on prospective, multi-platform comparisons that incorporate clinical outcomes and standardised timing of FC in relation to clinical reference standards.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the STARD reporting checklist. Available at https://jlpm.amegroups.com/article/view/10.21037/jlpm-2025-1-66/rc

Data Sharing Statement: Available at https://jlpm.amegroups.com/article/view/10.21037/jlpm-2025-1-66/dss

Peer Review File: Available at https://jlpm.amegroups.com/article/view/10.21037/jlpm-2025-1-66/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jlpm.amegroups.com/article/view/10.21037/jlpm-2025-1-66/coif). N.J. serves as an unpaid editorial board member of Journal of Laboratory and Precision Medicine from September 2025 to August 2027. M.A., D.T., and N.J. were supported by DiaSorin, which provided reagents and extraction devices to the Harrogate lab—this was specifically for the 52 samples in part 1 of the study. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was registered as a clinical audit at Harrogate District Hospital and therefore, the local Institutional Review Board deemed the study exempt from review. Individual consent for this retrospective analysis was waived.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

1. Abraham C, Cho JH. Inflammatory bowel disease. N Engl J Med 2009;361:2066-78. [Crossref] [PubMed]
2. Reenaers C, Bossuyt P, Hindryckx P, et al. Expert opinion for use of faecal calprotectin in diagnosis and monitoring of inflammatory bowel disease in daily clinical practice. United European Gastroenterol J 2018;6:1117-25. [Crossref] [PubMed]
3. Peyrin-Biroulet L, Sandborn W, Sands BE, et al. Selecting Therapeutic Targets in Inflammatory Bowel Disease (STRIDE): Determining Therapeutic Goals for Treat-to-Target. Am J Gastroenterol 2015;110:1324-38. [Crossref] [PubMed]
4. Wright EK, Kamm MA, De Cruz P, et al. Measurement of fecal calprotectin improves monitoring and detection of recurrence of Crohn's disease after surgery. Gastroenterology 2015;148:938-947.e1. [Crossref] [PubMed]
5. Colombel JF, Panaccione R, Bossuyt P, et al. Effect of tight control management on Crohn's disease (CALM): a multicentre, randomised, controlled phase 3 trial. Lancet 2017;390:2779-89. [Crossref] [PubMed]
6. Sipponen T, Kärkkäinen P, Savilahti E, et al. Correlation of faecal calprotectin and lactoferrin with an endoscopic score for Crohn's disease and histological findings. Aliment Pharmacol Ther 2008;28:1221-9. [Crossref] [PubMed]
7. Tibble JA, Sigthorsson G, Foster R, et al. Use of surrogate markers of inflammation and Rome criteria to distinguish organic from nonorganic intestinal disease. Gastroenterology 2002;123:450-60. [Crossref] [PubMed]
8. Røseth AG, Aadland E, Jahnsen J, et al. Assessment of disease activity in ulcerative colitis by faecal calprotectin, a novel granulocyte marker protein. Digestion 1997;58:176-80. [Crossref] [PubMed]
9. Fagerhol MK. Calprotectin, a faecal marker of organic gastrointestinal abnormality. Lancet 2000;356:1783-4. [Crossref] [PubMed]
10. Lin JF, Chen JM, Zuo JH, et al. Meta-analysis: fecal calprotectin for assessment of inflammatory bowel disease activity. Inflamm Bowel Dis 2014;20:1407-15. [Crossref] [PubMed]
11. Whitehead SJ, French J, Brookes MJ, et al. Between-assay variability of faecal calprotectin enzyme-linked immunosorbent assay kits. Ann Clin Biochem 2013;50:53-61. [Crossref] [PubMed]
12. Mosli MH, Zou G, Garg SK, et al. C-Reactive Protein, Fecal Calprotectin, and Stool Lactoferrin for Detection of Endoscopic Activity in Symptomatic Inflammatory Bowel Disease Patients: A Systematic Review and Meta-Analysis. Am J Gastroenterol 2015;110:802-19; quiz 820. [Crossref] [PubMed]
13. Schoepfer AM, Beglinger C, Straumann A, et al. Fecal calprotectin correlates more closely with the Simple Endoscopic Score for Crohn's disease (SES-CD) than CRP, blood leukocytes, and the CDAI. Am J Gastroenterol 2010;105:162-9. [Crossref] [PubMed]
14. von Roon AC, Karamountzos L, Purkayastha S, et al. Diagnostic precision of fecal calprotectin for inflammatory bowel disease and colorectal malignancy. Am J Gastroenterol 2007;102:803-13. [Crossref] [PubMed]
15. Heida A, Park KT, van Rheenen PF. Clinical Utility of Fecal Calprotectin Monitoring in Asymptomatic Patients with Inflammatory Bowel Disease: A Systematic Review and Practical Guide. Inflamm Bowel Dis 2017;23:894-902. [Crossref] [PubMed]
16. Mirsepasi-Lauridsen HC, Bachmann Holmetoft U, Ingdam Halkjær S, et al. Comparison of three commercial fecal calprotectin ELISA test kits used in patients with Inflammatory Bowel Disease. Scand J Gastroenterol 2016;51:211-7. [Crossref] [PubMed]
17. Labaere D, Smismans A, Van Olmen A, et al. Comparison of six different calprotectin assays for the assessment of inflammatory bowel disease. United European Gastroenterol J 2014;2:30-7. [Crossref] [PubMed]
18. Kittanakom S, Shajib MS, Garvie K, et al. Comparison of Fecal Calprotectin Methods for Predicting Relapse of Pediatric Inflammatory Bowel Disease. Can J Gastroenterol Hepatol 2017;2017:1450970. [Crossref] [PubMed]
19. Oyaert M, Boel A, Jacobs J, et al. Analytical performance and diagnostic accuracy of six different faecal calprotectin assays in inflammatory bowel disease. Clin Chem Lab Med 2017;55:1564-73. [Crossref] [PubMed]
20. Prell C, Nagel D, Freudenberg F, et al. Comparison of three tests for faecal calprotectin in children and young adults: a retrospective monocentric study. BMJ Open 2014;4:e004558. [Crossref] [PubMed]
21. Pathirana WGW, Chubb SP, Gillett MJ, et al. Faecal Calprotectin. Clin Biochem Rev 2018;39:77-90.
22. Oyaert M, Trouvé C, Baert F, et al. Comparison of two immunoassays for measurement of faecal calprotectin in detection of inflammatory bowel disease: (pre)-analytical and diagnostic performance characteristics. Clin Chem Lab Med 2014;52:391-7. [Crossref] [PubMed]
23. Shi JT, Chen N, Xu J, et al. Diagnostic Accuracy of Fecal Calprotectin for Predicting Relapse in Inflammatory Bowel Disease: A Meta-Analysis. J Clin Med 2023;12:1206. [Crossref] [PubMed]
24. Turvill J, Rook L, Rawle M, et al. Validation of a care pathway for the use of faecal calprotectin in monitoring patients with Crohn's disease. Frontline Gastroenterol 2017;8:183-8. [Crossref] [PubMed]
25. De Vos M, Dewit O, D'Haens G, et al. Fast and sharp decrease in calprotectin predicts remission by infliximab in anti-TNF naïve patients with ulcerative colitis. J Crohns Colitis 2012;6:557-62. [Crossref] [PubMed]
26. van Rheenen PF, Van de Vijver E, Fidler V. Faecal calprotectin for screening of patients with suspected inflammatory bowel disease: diagnostic meta-analysis. BMJ 2010;341:c3369. [Crossref] [PubMed]
27. Lasson A, Strid H, Ohman L, et al. Fecal calprotectin one year after ileocaecal resection for Crohn's disease--a comparison with findings at ileocolonoscopy. J Crohns Colitis 2014;8:789-95. [Crossref] [PubMed]
28. Vicente-Steijn R, Jansen JM, Bisheshar R, et al. Analytical and clinical performance of the fully-automated LIAISONXL calprotectin immunoassay from DiaSorin in IBD patients. Pract Lab Med 2020;21:e00175. [Crossref] [PubMed]