# Faecal calprotectin: Marker of intestinal inflammatory process in anorexia nervosa? A preliminary study

Dina Moubayed, Pierre Philippe Piché-Renaud, Camille Provost, Christophe Faure, Danielle Taddeo, Olivier Jamoulle, Jean Yves Frappier, Chantal Stheneur

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Dina Moubayed, Pierre Philippe Piché-Renaud, Camille Provost, Christophe Faure, Danielle Taddeo, et al.. Faecal calprotectin: Marker of intestinal inflammatory process in anorexia nervosa? A pre-liminary study. European Eating Disorders Review, 2023, 31 (5), pp.709-716. 10.1002/erv.2983 . hal-04190796

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BRIEF REPORT

WILEY

# Faecal calprotectin: Marker of intestinal inflammatory process in anorexia nervosa? A preliminary study

Dina Moubayed<fnref n="1" />,<fnref n="2" /> ID

Pierre-Philippe Piché-Renaud<fnref n="3" />

Camille Provost<fnref n="2" />

Christophe Faure<fnref n="1" />,<fnref n="2" />

Danielle Taddeo<fnref n="1" />,<fnref n="2" />

Olivier Jamoulle<fnref n="1" />,<fnref n="2" />

Jean-Yves Frappier<fnref n="1" />,<fnref n="2" />

Chantal Stheneur<fnref n="4" />,<fnref n="5" /> ID

**Correspondence**

Dina Moubayed, CHU Sainte-Justine, 3175 Chemin de la Côte-Sainte-Catherine, Montréal, QC H3T 1C5, Canada.

Email: moubayeddina@gmail.com

**Handling Editor:** Beate Herpertz-Dahlmann

**Funding information**

CHU Sainte-Justine

**Abstract**

**Purpose:** Anorexia Nervosa (AN) is a serious and potentially lethal mental disorder characterised by a deliberate quest to reduce one's weight. It can have multiple physical and psychological consequences. The clinical presentation of AN can include gastrointestinal symptoms, however, the pathophysiology of these symptoms in the context of AN remains uncertain. It is hypothesised that patients with AN may have an increase in intestinal permeability, which could lead to an increase in faecal calprotectin (fCP), a marker of intestinal inflammation. No relation between AN and elevation of fCP has been previously described in literature.

**Methods:** Eight patients hospitalised for AN have a dosage of fCP.

**Results:** Calprotectine was found to be elevated in 50% of cases, with or without any underlying comorbid gastrointestinal disease. Only the duration of illness tended to be associated with the increase in fCP suggesting a greater alteration as a function related to the time of denutrition.

**Conclusion:** Although these findings provide insights in the potential pathophysiology of gastrointestinal symptoms in AN, further studies that evaluate the factors associated with elevated fCP in patients with AN are needed.

**KEYWORDS**

anorexia nervosa, faecal calprotectin, gastrointestinal, inflammation, inflammatory bowel disease, intestinal permeability

**Key points**

**What is already known on this subject?**

* To our knowledge, our study is the first to describe faecal calprotectin (fCP) levels in patients who are malnourished due to anorexia nervosa (AN) and describe the patients' clinical characteristics in order to better explain the gastrointestinal tract implication in AN symptoms.

<footnote n="1">¹Centre Hospitalier Universitaire Sainte-Justine, Montréal, Quebec, Canada</footnote>

<footnote n="2">²Université de Montréal, Montréal, Quebec, Canada</footnote>

<footnote n="3">³Division of Infectious Diseases, The Hospital for Sick Children, Toronto, Ontario, Canada</footnote>

<footnote n="4">⁴Paris Saclay University, UVSQ, INSERM, CESP, Villejuif, France</footnote>

<footnote n="5">⁵Clinique FSEF Varennes Jarcy, Varennes Jarcy, France</footnote>
**What this study adds?**

* This study's finding of a possible elevation of fCP in patients with AN raises interesting questions on the pathophysiology of AN, and the possibility of an underlying inflammatory process in these patients. Although this is a preliminary study, as the sample size is small, it is therefore important for clinicians to acknowledge that fCP can be elevated in patients with AN without any other disease. The literature remains scarce regarding the relationship between the gastrointestinal tract and AN, although it is a predominant aspect of the symptomatology of the disease. This offers opportunities and strengthen the need for further research on the effects of restriction, renutrition and weight gain on the gastrointestinal tract in patients with AN, and the possible role and use of fCP in this disease.

# 1 | INTRODUCTION

Anorexia Nervosa (AN) is a severe pathology in both the short and the long term, with high morbidity and mortality rates. The DSM-5 defines AN as a restriction of energy intake, leading to a significantly lower than expected body weight. This is accompanied by an intense fear of gaining weight or persistent behaviour that interferes with weight gain, even when the individual is already underweight. At the beginning, patients usually have a misperception of their body weight and fail to recognise the seriousness of their low body weight.

There is a strong connection between AN and gastrointestinal symptoms. Abdominal symptoms are present throughout the restriction period as well as during the renutrition period (Mascolo et al., 2017). Studies suggest a prevalence of functional gastrointestinal disorders, prior to eating disorder (ED) treatment, ranging from 56% to 97%, depending on the population examined (Boyd et al., 2005; Perez et al., 2013). Patients usually complain of postprandial fullness, epigastric pain, nausea, dysphagia, bloating and constipation (Malczyk & Ośięcimska, 2017). The origin of these gastrointestinal symptoms in AN is not yet fully understood (Kress et al., 2018). Many of these symptoms will persist, even after renutrition. At disease onset, given the presence of these gastrointestinal symptoms, the clinical presentation of AN can be similar to other primary gastrointestinal diseases, such as coeliac disease, irritable bowel syndrome or inflammatory bowel disease (IBD) (Mitchell & Crow, 2006). Using information about the onset of gastrointestinal symptoms and the eating habits as well as information about the quality of the symptoms can help identify the aetiology (Kress et al., 2018). The interrelationships between AN and certain gastrointestinal diseases seem complex. Research suggests that gastro intestinal (GI) symptoms can pre-dispose to disordered eating (Conviser et al., 2018; Kaluski et al., 2008; Wiklund et al., 2019), which can then

evolve into a full threshold ED (Chamay-Weber et al., 2005). A Swedish cohort was found to have bi-directional associations between AN and IBD (Hedman et al., 2019), as has a review of case studies, finding the co-existence of AN and Crohn's disease being the most common (Ilzarbe et al., 2017). In a Danish sample aged 8–32 years, a significant risk of IBD was seen after a diagnosis of AN (Relative Risk [RR] for Crohn's disease = 1.60; RR for Ulcerative Colitis = 1.66) (Larsen et al., 2021). A bi-directional association has also been found between coeliac disease and AN (Mårild et al., 2017). However, a genome wide association study completed by Tylee et al. (2018) found no association between Crohn's disease or Ulcerative Colitis and AN.

There is currently an increased interest in the scientific community regarding gut microbiome, particularly the ‘gut-brain axis’, which relates to ‘interaction between the gut microbiome and behaviour’ (Seitz et al., 2019). There is a clear relationship between gut microbiome and inflammation (Seitz et al., 2019). Multiple studies have been performed in the recent years to evaluate gut microbiome in AN. Results are mixed, with the clinical significance still unclear (Seitz et al., 2019).

Faecal calprotectin (fCP), a marker of inflammation detected in the faeces, is a sensitive measure of colonic inflammation that has been increasingly used in recent years, mainly for the clinical assessment of IBD (Stríz & Trebichavský, 2004). fCP is a calcium-binding protein belonging to the S-100 protein family that is released primarily by neutrophil granulocytes (Li et al., 2015). Calprotectin is produced in significant amounts in white blood cells. It is found predominantly in the cytoplasm of neutrophils, is released upon neutrophil cell death or damage (Ross et al., 2022) and is resistant to enzymatic degradation and therefore can be readily detected in bodily fluids such as faeces (Ross et al., 2022; Tøn et al., 2000). As the mucosal barrier is altered in intestinal inflammation, white cells could cross the intestinal wall
(D'Incà et al., 2007). Elevation of fCP occurs in a wide array of gastrointestinal conditions including colitis and malignancy, and although it is a sensitive measure of inflammation, it is not specific for any single condition (Summerton et al., 2002; Theede et al., 2015).

This study aimed to describe levels of fCP in patients diagnosed and admitted with AN, and to describe factors in patients with AN that may be associated with an elevated fCP. We hypothesise that fCP may be elevated in patients with AN secondary to an underlying inflammatory process due to malnutrition and changes in intestinal permeability (IP), and that patients with more severe disease may have higher levels of fCP.

## 2 | MATERIALS AND METHODS

A research assistant recruited patients in two periods, between July 2014 and July 2015, as well as between July 2018 and July 2019, during their hospitalisation for AN in a large University Pediatric Hospital. All patients with a diagnosis of restrictive AN as per the DSM-5 criteria who were admitted during the recruitment period were eligible for inclusion in this study. All patients who consented to be in the study were included. No specific exclusion criteria were applied, as to not reduce the sample size further. fCP was measured between 7 and 10 days after hospitalisation and was reported in µg/g. In case of elevated calprotectin level, a control was performed. The samples were stored at -20 C and transported in batches on ice to an affiliated hospital laboratory. Extraction and ELISA assay analysis was performed in the laboratory, which then provided electronic results to our team. Normal values for fCP in healthy individuals in our centre are <50 µg/g stool. We therefore used a cut off at 50 µg/g stool.

Information was gathered on the following covariates, as these factors can characterise the severity of the patients' AN, as well as comorbidities, in the following categories:

1. Information related to the course of AN, including minimum and maximum weight and body mass index (BMI = weight (kg)/height (m)$^2$), rapidity of under-nutrition and weight loss, duration of disease, pubertal status (pre- or post-menarche) and duration of amenorrhoea.

2. The clinical characteristics upon admission: age (months), weight, height, BMI, minimum heart rate (bpm) and blood pressure (mmHg) during the first 3 days of hospitalisation.

3. Presence or absence of gastrointestinal symptoms and medication at the time of hospitalisation.

Anthropometric measurements (i.e. BMI) were expressed in kg/m$^2$ and as the standard deviation (SD) according to the World Health Organization growth chart.

The characteristics of participants with normal and abnormal fCP were compared using two-sample *t*-tests (for continuous variables) and fisher's exact tests (for categorical or dichotomous variables). A narrative summary detailing the clinical presentation and characteristics of patients with abnormal fCP was provided. The study was approved by the hospital Ethics Review Board (2017-1253) and informed consent was provided by all study participants.

## 3 | RESULTS

Eight patients were recruited during both recruitment periods. Study participants had a median age of 187 months [166; 195.5], median BMI 14.9 kg/m$^2$ [13.9; 17.3] with a -2.165 [-2.32; -1.09] SD and a duration of illness of 9 months [7; 11.5]. The number of hospitalisations in the included participants ranged between one and five. All participants' characteristics at the time of hospital admission are detailed in Table 1.

Five patients (62%) had no GI symptoms, and three patients (38%) reported non-specific GI symptoms, such as constipation and post-prandial pain. Three patients received medications for an associated comorbidity (juvenile arthritis, depression, hypothyroidism) (Table 2).

Of the eight patients, three had normal calprotectin levels (38%), four had high levels (50%), and one (12%) had a level just above normal (Table 2). For abnormal results, calprotectin level controls showed similar results.

Patients with an abnormal fCP seemed more likely to have a longer duration of disease compared to patients with a normal fCP (median 13 vs. 8 months *p* = 0.2). Characteristics of patients with a normal and abnormal fCP were otherwise similar. Of note, one patient had a fCP result just above normal and was excluded from these analyses (patient 5).

The next section provides insight on clinical background and characteristics of patients with elevated fCP.

### 3.1 | Patient 1

A 17-year-old girl was admitted for sinus bradycardia. Her past medical history was significant for asthma, mild constipation, an unspecified anxiety disorder, an unspecified depressive disorder, and a mild traumatic brain injury 6 months earlier. She was diagnosed with anorexia 2 years prior and had never been hospitalised. She took no medication. She had amenorrhoea for the last
<table><caption>TABLE 1 Characteristics of all patients included in the study: course of AN.</caption><thead><tr><th>Patients</th><th>Age (months)</th><th>BMI kg/m²</th><th>BMI (SD)</th><th>Duration of the illness (months)</th><th>Number of hospitalisations</th></tr></thead><tbody><tr><td>1</td><td>208</td><td>17.4</td><td>-1.23</td><td>19</td><td>1</td></tr><tr><td>2</td><td>194</td><td>14.9</td><td>-2.15</td><td>7</td><td>5</td></tr><tr><td>3</td><td>179</td><td>18.1</td><td>-0.69</td><td>10</td><td>1</td></tr><tr><td>4</td><td>160</td><td>13.3</td><td>-2.35</td><td>16</td><td>5</td></tr><tr><td>5</td><td>154</td><td>17.3</td><td>-0.5</td><td>7</td><td>2</td></tr><tr><td>6</td><td>189</td><td>12.9</td><td>-2.92</td><td>10</td><td>2</td></tr><tr><td>7</td><td>185</td><td>14.1</td><td>-2.32</td><td>6</td><td>2</td></tr><tr><td>8</td><td>200</td><td>14.9</td><td>-2.18</td><td>8</td><td>4</td></tr></tbody></table>

Note: White lines: patients with abnormal fCP level, light grey line: patient with fCP level just above normal, dark grey lines: patients with normal fCP level.
Abbreviations: AN, anorexia nervosa; BMI, body mass index; fCP, faecal calprotectin.

<table><caption>TABLE 2 Characteristics of all patients included in the study: clinical status.</caption><thead><tr><th>Patients</th><th>GI symptoms</th><th>Comorbidities</th><th>Treatment at admission</th><th>Blood pressure</th><th>Pulse</th><th>Faecal calprotectin</th></tr></thead><tbody><tr><td>1</td><td>Vague postprandial abdominal pain</td><td>Depression at the beginning</td><td>None</td><td>92/51</td><td>41</td><td>124</td></tr><tr><td>2</td><td>None</td><td></td><td>None</td><td>71/41</td><td>41</td><td>243</td></tr><tr><td>3</td><td>None</td><td></td><td>None</td><td>73/43</td><td>36</td><td>438</td></tr><tr><td>4</td><td>Constipation</td><td>Juvenile arthritis</td><td>Naproxen, methotrexate, folic acid</td><td>75/58</td><td>55</td><td>423</td></tr><tr><td>5</td><td>None</td><td></td><td>None</td><td>86/54</td><td>36</td><td>52</td></tr><tr><td>6</td><td>None</td><td></td><td>None</td><td>72/42</td><td>42</td><td>&lt;17</td></tr><tr><td>7</td><td>None</td><td></td><td>Olanzapine</td><td>82/49</td><td>42</td><td>20</td></tr><tr><td>8</td><td>Constipation</td><td>Hypothyroidism</td><td>Lansoprazole, Polyethylene glycol</td><td>75/44</td><td>43</td><td>37</td></tr><tr><td></td><td>Vague epigastric pain</td><td></td><td></td><td></td><td></td><td></td></tr><tr><td></td><td>Gastroesophageal reflux</td><td></td><td>Levothyroxine</td><td></td><td></td><td></td></tr></tbody></table>

Note: White lines: patients with abnormal fCP level, light grey line: patient with fCP level just above normal, dark grey lines: patients with normal fCP level.
Abbreviations: fCP, faecal calprotectin; GI, gastro intestinal.

4 months. She was hospitalised for 8 days, and her BMI went from 17.31 to 17.61 kg/m². Her minimal weight was 46 kg. fCP was performed 8 days after the admission and was elevated at 124 µg/g. She had gained 700 g as of that day. She complained of palpitations with a normal electrocardiogram and nonspecific postprandial abdominal fullness, which was resolved with the resolution of constipation. She denied any purging behaviour, such as vomiting or laxative use.

## 3.2 | Patient 2

A 16-year-old girl was admitted because of sinus bradycardia. Her past medical history was significant for mild constipation. She was diagnosed with anorexia

7 months prior to her hospital stay and had never been hospitalised. She took no medication. She had amenorrhoea for 5 months prior to her hospitalisation. She was hospitalised for 2 months, and her BMI went from 14.91 to 17.51 kg/m². Her minimal weight was 39.1 kg. fCP was performed 10 days after admission and was elevated at 243 µg/g. She had gained 2.7 kg as of that day. She complained of no physical or gastrointestinal symptoms during her stay. She denied any purging behaviour, such as vomiting or laxative use.

## 3.3 | Patient 3

A 14-year-old girl was hospitalised for sinus bradycardia. She had no significant past medical history except for AN
diagnosed a year prior her hospital stay and constipation secondary to her ED. She had never been hospitalised before. She took no medication. She had amenorrhoea for the past 7 months before her hospitalisation. She was hospitalised for 1 month and her BMI went from 18.1 to 18.7 kg/m². Her minimal weight was 51.7 kg. Upon admission, she had acute renal insufficiency, which resolved a month after admission. Her renal work-up was normal. She also complained of constipation. She had an episode of rectal bleeding with a positive hematest, caused by an anal fissure. An abdominal ultrasound was normal. fCP performed 9 days after the admission was elevated at 438 µg/g. She had gained 500 g as of that day. She denied any other gastrointestinal complaints or any purging behaviour, such as vomiting or laxative use.

## 3.4 | Patient 4

A 13-year-old girl, with a past medical history significant for juvenile idiopathic arthritis, a left solitary kidney and growth stunting, was admitted for AN. She had been hospitalised five times for AN and had been diagnosed 2 years prior to this hospital stay. She was premenarchal. She took Methotrexate 25 mg once per week, Folate 5 mg every other day, and Naproxen 250 mg twice a day by mouth. She discontinued her Naproxen 3 weeks prior to her admission. She was also prescribed Lansoprazole 30 mg by mouth every day. She was hospitalised for 2 months, and her BMI went from 13.3 to 15 kg/m². Her minimal weight was 28.3 kg. During her hospital stay, she complained of significant abdominal pain and constipation. Anti-transglutaminase and a hydrogen breath test were negative. However, fCP, performed 10 days after the admission, was elevated at 423 µg/g. She had gained 2.5 kg as of that day. It was repeated a month later and was still elevated at 466 µg/g. She had gained 3.5 kg as of that day. A colonoscopy and an esophagogastroduodenoscopy with biopsies were performed and were normal. She had no gastrointestinal complaints on discharge.

## 3.5 | Patient 5

A 12-year-old girl was admitted because of sinus bradycardia. She had no significant past medical history except for AN diagnosed 9 months prior. She had been hospitalised for AN once before. She took no medication. On arrival, she had mild acute renal insufficiency, which resolved in the first week of her hospital stay. She was premenarchal. She was hospitalised for 2 months, and her BMI went from 16.8 to 18.11 kg/m². Her minimal weight was 34.4 kg. fCP was performed 7 days after

admission and was slightly elevated at 52 µg/g. She had gained 1 kg as of that day. She complained of no physical or gastrointestinal symptoms during her hospital stay. She denied any purging behaviour, such as vomiting or laxative use.

# 4 | DISCUSSION

Although a small sample of patients was included in this study, it demonstrates that abnormal levels of fCP can be seen in patients diagnosed with AN and with severe malnutrition. Further, patients with an abnormal fCP were more likely to have a lengthier course of disease. This is aligned with what has been reported previously on the impact of food deprivation and restriction on the epithelial gut barrier.

A few studies have explored the relationship between the gastrointestinal tract and AN and described possible changes in IP in patients with AN. IP is defined by the capacity of the components of the intestinal lumen to cross the tight junctions between the epithelial cells (Jésus et al., 2014). Although it has been investigated in patients with AN, studies have shown inconsistent results, with some reporting an increase and others reporting a decrease in IP. In animal, studies agree that depleted states induce alterations of IP and digestive ability (Genton et al., 2015). In human, studies are contradictory. For example, Monteleone et al. (2022) reported a decrease of means of the lactulose/mannitol (LA/MA) test and Kleppe et al. (2004) reported a decreased in zonulin serum concentration in favour of a decrease in IP. On the other hand, Grigioni et al. (2022) reported an increased urinary LA/MA ratio in patients with AN when compared to controls, that may indicate an increased IP.

The intestinal barrier function is strongly associated with microbiome. Intestinal microbes secrete substrates and metabolites that are essential for metabolism and appetite, and thus have an influence on eating behaviour (van de Wouw et al., 2017). An alteration in the microbiome has been hypothesised to play a role in the pathophysiology of AN (Pascal et al., 2017) and changes in the microbiota have been associated with weight gain (Mack et al., 2016). In a recent systematic review by Carbone et al. (2020), authors reported that intestinal microbial diversity in AN patient was lower compared to healthy controls and suggested that it could interfere with nutrient absorption and calorie intake. They concluded that an increased gut permeability due to microbial change in AN could result in systemic inflammation. In a more recent review (Dhopatkar et al., 2023), studies investigating the gut microbiome in AN indicate significant dysbiosis in AN compared with controls. But results
are contradictory as well as for Alpha diversity or abundances of individual bacteria. Nutritional treatment, in general, reduced dysbiosis seen in pre-treatment AN, with an increase in gut microbiota associated with anti-inflammatory properties such as Roseburia and Faecalibacterium. The increase in inflammation related to the microbiota could be a primary hypothesis of elevation of fCP in our patients.

fCP can be used as a marker of local inflammation in patients (Duman et al., 2015). An elevated fCP in patients with chronic gastrointestinal complaints usually leads to an endoscopy in order to rule out IBD (Heida et al., 2017). fCP levels have also been associated with IBD disease activity. There is no accepted normal reference range in the paediatric population, especially since fCP is suspected to vary with age (Li et al., 2015). However, some studies have proposed a threshold of 50 µg/g in adolescents, similarly to adults. While highly sensitive for gastrointestinal inflammation, an important limitation of fCP is its specificity, estimated between 0.6 and 0.68. The number of false positive results is thus considerable (Heida et al., 2017). In our cases, we must consider the possibility that the elevated results were related to a false positive result, as we do not have a significant sample number.

The varying daily excretion, liver cirrhosis, the use of aspirin and NSAIDs are one amongst many factors that have been linked to an elevation of fCP (Carroccio et al., 2003). Two of the patients included in our study took some medication that could have an influence on the fCP elevation, such as lansoprazole and naproxen.

In this preliminary study, we have demonstrated that an elevation of the fCP in AN is possible. We then hypothesise that it could be associated with an alteration of the patient's microbiome and gut permeability, which could lead to gastrointestinal inflammation. After a thorough review of the patients' files, only the duration of the disease was found correlated with the level of elevation. More than the extent of weight loss or the intensity of undernutrition, it appears to alter the integrity of the gastrointestinal barrier, increasing fCP.

## 4.1 | Strengths and limits

The limits of the study are mostly related to the sample size, which is smaller than what was expected, and can therefore not allow us to draw statistically significant conclusions related to our findings. Although our team wished to have a stronger sample size, the reluctance of patients to provide stool samples strongly impacted the study size. Increasing the recruitment period did not have

the desired effect of reaching more patients. It can however allow us to raise hypothesis and give the opportunity for further research. Moreover, there are limitations regarding patients' characteristics. Indeed, our patients are all female. This was not a purposeful choice made by the team. AN being a predominantly female disease, up to 90%, it was difficult to obtain a sample that contained males in such a small study size (Morris & Twaddle, 2007). Few of our patients reported GI symptoms (3/8) while these symptoms are common in AN-related malnutrition. It is possible that patients without constipation are more likely to donate stools for research. We may have selected patients with a particular microbiota that does not cause constipation but would increase inflammation, as shown by the increase in the fcalprotectin.

There are also limits related to the calprotectin, being widely variable with age, with cut-offs varying in different centres, as well as its low specificity. Many factors in our patients' history were also associated with higher values of calprotectin, as mentioned previously.

## AUTHOR CONTRIBUTIONS

Conceptualization was made by Chantal Stheneur, Pierre-Philippe Piché-Renaud and Christophe Faure, including methodology (Chantal Stheneur and Christophe Faure). Validation was provided by Dina Moubayed, Danielle Taddeo, Olivier Jamoulle and Jean-Yves Frappier. Dina Moubayed conducted the investigation, data curation, and writing (original draft preparation), with support from Pierre-Philippe Piché-Renaud and Camille Provost. Supervision was provided by Chantal Stheneur; All authors have read and agreed to the published version of the manuscript.

## ACKNOWLEDGEMENTS

Dr. Stephanie Proulx-Cabana who offered support and guidance. Material support from the biochemistry department of Maisonneuve-Rosemont Hospital was provided. Financial support came from the division of adolescent medicine of CHU Sainte-Justine. The authors have no financial relationship relevant to this article to disclose.

## CONFLICT OF INTEREST STATEMENT

The authors have no relevant financial or non-financial interests to disclose.

## DATA AVAILABILITY STATEMENT

The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.
ORCID

Dina Moubayed https://orcid.org/0000-0002-6113-1106

Chantal Stheneur https://orcid.org/0000-0002-1171-5998

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**How to cite this article:** Moubayed, D., Piché-Renaud, P.-P., Provost, C., Faure, C., Taddeo, D., Jamoulle, O., Frappier, J.-Y., & Stheneur, C. (2023). Faecal calprotectin: Marker of intestinal inflammatory process in anorexia nervosa? A preliminary study. *European Eating Disorders Review*, **31**(5), 709-716. https://doi.org/10.1002/erv.2983