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Eating disorder or disordered eating: undiagnosed inflammatory bowel disease mimicking eating disorder
  1. Rachel Elizabeth Harris,
  2. Rachel Tayler,
  3. Richard K Russell
  1. Department of Paediatric Gastroenterology, Hepatology and Nutrition, Royal Hospital for Children Glasgow, Glasgow, UK
  1. Correspondence to Dr Rachel Elizabeth Harris, Department of Paediatric Gastroenterology, Hepatology and Nutrition, Royal Hospital for Children Glasgow, Glasgow G51 4TF, UK; rachel.harris16{at}


We describe the case of a patient with ongoing weight loss, low mood and previously undisclosed gastrointestinal (GI) symptoms initially diagnosed with an eating disorder and subsequently diagnosed with ulcerative colitis over a year following initial presentation. This patient exhibited disordered eating secondary to the worsening symptoms of undiagnosed inflammatory bowel disease (IBD) and had altered her eating habits to reduce the diarrhoea and rectal bleeding she was experiencing, contributing to significant weight loss.The implications of a delayed diagnosis of IBD or incorrect diagnosis of eating disorder are severe both physically and psychologically. We discuss factors in the assessment of patients which may raise suspicion of organic GI disease such as IBD—an important differential diagnosis in those with non-specific GI symptoms and suspected eating disorder—and highlight baseline investigations which should be performed to ensure a diagnosis of IBD is not missed in these patients.

  • general paediatrics
  • inflammatory bowel disease
  • paediatric gastroenterology
  • ulcerative colitis
  • eating disorder

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Case report

An 11-year-old patient was admitted with minimal oral intake, low mood and no evidence of distorted body image. She denied any abdominal pain or vomiting and “could not remember” her last bowel motion. Her weight was 30.5 kg (Z score −1.45), height 149.5 cm (Z score +0.1) and body mass index (BMI) 13.6 (Z score −2.63). White cell count was elevated (14.8×109/L), with other investigations within normal range (table 1).

Table 1

Timeline of events

The patient was diagnosed with an eating disorder and was cared for jointly by the medical and child and adolescent mental health service (CAMHS) teams. She remained an inpatient to establish nasogastric (NG) feeding and monitor for refeeding syndrome. Notably during this admission, stool charting was not undertaken and bowel output was not recorded alongside oral intake. The patient was discharged and NG-fed for 6 weeks. Over the subsequent year she was followed up by the CAMHS team. Fluoxetine was commenced and subsequently discontinued due to improvement in mood. She was also prescribed ferrous fumarate for iron deficiency.

A year later the patient was referred by her general practitioner to general paediatrics with chronic abdominal pain. Fluoxetine was recommenced after CAMHS team review finding low mood, obsessive concerns surrounding food hygiene (in particular, food making her ‘ill’) and ongoing weight loss.

Her weight was 33 kg (Z score −2.01), height 153.2 cm (Z score −0.39) and BMI 14.1 (Z score −2.72). She reported intermittent right-sided abdominal pain but denied any other gastrointestinal (GI) symptoms. Blood test (table 1) revealed C reactive protein (CRP) of 17 mg/L and her erythrocyte sedimentation rate (ESR) was 22 mm/hour. Tissue transglutaminase (TTG) and stool for Helicobacter pylori were negative. Faecal calprotectin was grossly elevated at 1533 μg/g. The patient was referred to paediatric gastroenterology.

On gastroenterology review the patient was pale, thin and very withdrawn. Abdominal examination revealed a fullness in the right iliac fossa. She divulged that her abdominal pain was associated with eating and she was passing stool six times daily, including nocturnally, with blood in most stools. These symptoms had been occurring since her initial presentation 16 months previously; however, the patient had not reported these due to significant anxiety. At this time the team felt that this presentation represented undiagnosed Crohn’s disease (CD), with small bowel involvement suspected due to marked weight loss.

The patient underwent endoscopy which revealed marked colonic ulceration and erythema worst in the rectum to sigmoid, consistent with a diagnosis of left-sided ulcerative colitis (UC). Histopathology confirmed this suspicion.

This patient exhibited disordered eating secondary to undiagnosed inflammatory bowel disease (IBD). She had altered her eating habits to reduce the diarrhoea and rectal bleeding associated with evolving UC, contributing to significant weight loss and leading to the diagnostic suspicion of small bowel CD. Her reluctance to disclose her symptoms and low mood led to the initial diagnosis of eating disorder and significantly delayed diagnosis of IBD for more than a year.

The patient was commenced on rectal and oral 5-aminosalicylic acid, which improved all symptoms and resulted in significant weight gain. A significant change in the patient’s mood was noted immediately post-diagnosis; she had disclosed that she ‘thought she was going to die’ and had been internalising very significant worries concerning her symptoms. Her UC diagnosis had relieved her of a substantial psychological burden. The patient is currently receiving follow-up from the paediatric IBD team, having been discharged from CAMHS and fluoxetine discontinued.

Subsequently the patient’s twin was diagnosed with UC, having come forward with undisclosed symptoms of 18 months’ duration following the diagnosis of her sister. The above delay in referral to gastroenterology services had impacted on the disease course of not one, but two patients.


It can be difficult to discern between organic and psychosomatic causes of GI symptoms. Patients may have a primary GI disorder with resulting disordered eating, or a primary eating disorder with consequent GI sequelae, and both may present with non-specific symptoms such as abdominal pain, nausea, vomiting, altered bowel habit, anorexia, weight loss and growth failure on a spectrum of severity. Patients may withhold symptoms as evidenced in the case above, and furthermore the onset of IBD may be insidious, leading to diagnostic uncertainty and delay. The implications of this or of an incorrect diagnosis of eating disorder are serious—growth failure, acute deterioration of symptoms, increased morbidity/complications and serious psychological associations, as demonstrated in this case. We highlight elements of patient assessment which may aid in differentiating IBD from suspected eating disorder as a cause of non-specific GI symptoms.


Direct questioning for nocturnal abdominal pain or stooling, chronic diarrhoea, blood in stools, unexplained fever, or family history of organic GI or autoimmune disease should be undertaken, and positive history should prompt further investigation. Opportunities for observation of the patient and their symptoms, such as during inpatient admission, should be used where possible to minimise the risk of possible undisclosed symptoms and to maximise diagnostic efficacy. Tools such as fluid, food and stool charting may be employed to facilitate this.

Lack of distorted body image should also raise suspicion of organic GI disease in patients with suspected eating disorder. In a case series of four female patients aged 13–37 initially diagnosed with an eating disorder and all later diagnosed with CD, all were noted to have non-specific GI symptoms, but none had any evidence of distorted body image, as in the case above.1 With risk of eating disorder highest in patients aged 13–17, our patient’s younger age should also have triggered further investigation.2


Localised abdominal tenderness, fullness or mass should prompt further investigation.1 Examination of the buccal mucosa and the perianal area is important to identify local disease such as tagging, fissuring or ulceration. Perianal disease is present in approximately 15% of children with CD at diagnosis.3

Laboratory tests

Baseline blood tests should be performed in patients presenting with persistent GI symptoms, including full blood count (FBC), albumin, ESR and CRP. Results of one or more of these tests will show abnormalities in around 80% of cases of undiagnosed IBD.4 Normal laboratory values however do not exclude IBD, and the presence of a high index of suspicion should warrant further investigation regardless. In one study of 526 children with newly diagnosed IBD, <5% of those with moderate/severe disease had normal markers (haemoglobin, ESR, albumin and platelets), but 21% of cases of mild CD and 54% of cases of mild UC had normal blood markers.5

Stool samples should be collected to exclude infection as a cause of symptoms. Faecal calprotectin is a marker of intestinal inflammation which is a useful adjunct to the aforementioned blood tests. In a study of 48 children newly diagnosed with IBD, faecal calprotectin was found to be raised at diagnosis in 96%, making it more likely to be abnormal at diagnosis than commonly measured blood markers. In combination blood tests and faecal calprotectin are almost universally abnormal in patients with undiagnosed IBD.4 Figure 1 demonstrates a schemata for investigation.

Figure 1

Diagnostic pathways in IBD. Patients displaying features consistent with IBD should be fast-tracked for specialist review. Adapted from Kammermeier J et al.3 CRP, C reactive protein; ESR, erythrocyte sedimentation rate; IBD, inflammatory bowel disease; MRE, magnetic resonance enterography; VCE, video capsule endoscopy.


  • It is crucial to rule out organic causes of GI symptoms in patients with suspected eating disorder, and also to consider that such patients may not disclose symptoms.

  • The implications of a delayed diagnosis of IBD or incorrect diagnosis of eating disorder are severe physically and psychologically.

  • Early symptom recognition and appropriate baseline investigations may lead to prompt diagnosis and initiation of management, reducing morbidity and potentially serious sequelae.

  • Although not currently recommended in the National Institute for Health and Care Excellence guidelines for recognition of eating disorder,2 all teenagers with suspected eating disorder should have FBC, ESR, CRP, liver function tests, TTG and faecal calprotectin performed to avoid future missed cases of organic disease.

  • Normal laboratory results do not rule out organic disease; where a high index of suspicion is present, further investigation should always be undertaken.



  • Contributors REH prepared the manuscript, with comments and review from all authors. RKR and RT provided critical review of the manuscript. All authors have approved the draft.

  • Funding REH’s Clinical Research Fellow role at the Royal Hospital for Children, Glasgow, is supported by Catherine McEwan Foundation. RKR is supported by an NHS Research Scotland senior fellowship award.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Patient consent for publication Obtained.

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