Report of Meckel Diverticulum Mimicking Stricturing Crohn's Disease in an Adolescent Boy

Abstract

Inflammatory bowel disease, specifically Crohn's disease (CD), can present with hematochezia, iron deficiency anemia, intestinal obstruction, elevated fecal calprotectin often overlapping with other conditions. We report a 16-year-old adolescent boy with presumed stricturing CD whose anti-tumor necrosis factor therapy failed to respond. Persistent iron deficiency anemia and elevated fecal calprotectin prompted reevaluation imaging, raising concerns for the Meckel diverticulum. Surgical resection resulted in resolution of anemia. This case highlights the importance of reassessing a diagnosis in refractory cases. Providers should consider the Meckel diverticulum as a diagnosis that can mimic CD especially if the course is refractory to treatment.

INTRODUCTION

Crohn's disease (CD), a type of inflammatory bowel disease (IBD), is a chronic relapsing and remitting condition affecting any part of the gastrointestinal tract, leading to hematochezia, iron deficiency anemia, abdominal pain, and weight loss.¹ While 87% of children present with the inflammatory phenotype at diagnosis, however, some may present with a stricturing and/or penetrating phenotype.²

Iron deficiency anemia, elevated fecal calprotectin, and intestinal strictures raise a concern for CD; however, the Meckel diverticulum can present with a similar constellation of findings.^3,4 The Meckel diverticulum is a congenital anomaly resulting from incomplete obliteration of the vitelline duct during fetal development.⁴ It typically presents in early childhood with painless rectal bleeding, with complications including intussusception, obstruction, and perforation.⁴ We report a case of the Meckel diverticulum presenting as an intestinal stricture in an adolescent boy, initially misdiagnosed as structuring small bowel CD. The Meckel diverticulum can present at any age and should be considered when patients’ conventional IBD therapies fail to respond.⁴

CASE REPORT

A 16-year-old adolescent boy presented with hematochezia and a 4-year history of iron deficiency anemia, requiring regular blood and iron transfusions. At age 12, initial endoscopy was macroscopically normal, though pathology confirmed the presence of numerous Helicobacter-like organisms in gastric biopsies. Anthropometrics remained within normal limits.

Despite Helicobacter pylori eradication, hematochezia continued. At age 14, 2 repeat endoscopies showed no macroscopic or microscopic evidence of inflammation. Magnetic resonance enterography (MRE) demonstrated no bowel wall thickening, but capsule endoscopy identified ulcers at the distal terminal ileum. A presumptive diagnosis of CD was made, and 5-aminosalicylic acid therapy was initiated. Symptoms persisted after 1 year of treatment, and hemoglobin dropped as low as 6.6 g/dL. Serum albumin, inflammatory markers (C-reactive protein and erythrocyte sedimentation rate), and platelet counts remained normal, though fecal calprotectin was elevated (212–551 μg/g; normal < 50 μg/g) (Table 1).

Table 1.

Laboratory test parameters throughout clinical course

	Diagnosis of H. pylori (1)	Repeat endoscopy (2)	Capsule endoscopy (3)	Leading up to transfer	Upon transfer (4)	After resection	2 yr follow-up (5)
Hgb (g/dL)	8.7	7.4	7.3	7.9	8.5	14.8	15.5
HCT (%)	31.1	25.7	27.0	26.9	30.4	47.3	45.5
Platelets (×103/mcL)	401	399	371	255	237	325	297
Albumin (gm/dL)	4.6	4.4	4.6	4.3	3.5	4.3	3.9
CRP (mg/dL)	<0.1	<0.3		<0.3	2.2	<0.40	<0.5
ESR (mm/h)	4	7			25	2	2
FCP (µg/g)	254	275	494	551	208		53

Of note, laboratory test results were grouped to the nearest event outlined in the timeline. Numbers in brackets correspond to the closest significant event.

Those values in bold are outside the normal reference range. Those boxes left blank represent missing values.

CRP, C-reactive protein; ESR, erythrocyte sedimentation rate; FCP, fecal calprotectin; HCT, hematocrit; Hgb, hemoglobin.

Four months later, he presented to a quaternary care facility with epigastric pain and lightheadedness. Hemoglobin was 5.8 g/dL and inflammatory markers were elevated (C-reactive protein: 2.2 mg/dL, erythrocyte sedimentation rate: 25 mm/h). Repeat MRE demonstrated focal mural thickening and luminal narrowing of the ileum. Double balloon retrograde enteroscopy (DBE) revealed scattered shallows erosions and a distal ileal stricture; however, histopathology again showed no evidence of acute or chronic inflammation. Given the stricture, therapy was escalated to intravenous corticosteroids and infliximab for presumed stricturing CD.

One month later, he returned with diarrhea and nocturnal stooling. Repeat imaging confirmed a persistent small bowel stricture. After rereview with a fellowship-trained pediatric abdominal radiologist, the differential was broadened to include the Meckel diverticulum (Figure 1). Following shared decision making with the family, diagnostic laparoscopy was performed. A large Meckel diverticulum with a feeding vessel was identified just proximal to the terminal ileum (Figure 2). Histology confirmed a true diverticulum containing all layers of the small bowel wall with focal areas containing ectopic gastric-type mucosa, consistent with the Meckel diverticulum (Figure 2).

Figure 1.

(A) Axial contrast-enhanced computed tomography image through the pelvis shows a short segment of bowel wall thickening and luminal narrowing (arrows). An adjacent bowel loop is dilated (*). Findings were interpreted as suspicious for stricturing Crohn's disease. (B) and (C) Similar findings were present on follow-up magnetic resonance enterography, including focal luminal narrowing and postcontrast hyperenhancement (arrows). The dilated bowel loop appeared fecalized containing stool-like material.

Figure 2.

(A) Gross photograph of a resected small intestine segment with a 10.5 cm diverticulum (arrows) terminating in a blind pouch. The opened specimen shows a 1.5 cm circumferential linear ulceration (white arrow) corresponding to a stricture. Proximal and distal margins are marked by black and white asterisks, respectively. (B) Ileal biopsy 2 months earlier demonstrates preserved villous and crypt architecture without inflammatory epithelial lesions (hematoxylin and eosin [H&E], 4×). (C) Resected diverticulum shows transition to gastric heterotopic mucosa (black asterisk) with mucosal erosion (H&E, 4×). (D) High-power view highlights gastric mucosa morphology (H&E, 40×). (E) Low-power view shows ulceration, ectopic gastric mucosa, fibrosis, and muscular thickening, consistent with stricture (H&E, 4×).

Following resection, symptoms resolved, infliximab was discontinued, and colonoscopy at 3 months was normal. Fecal calprotectin normalized to 53 μg/g at 2 years (Figure 3). Hemoglobin, inflammatory markers, albumin, and platelets normalized (Table 1).

Figure 3.

Timeline of events of the patient's clinical course. EGD, esophagogastroduodenoscopy; H. pylori, Helicobacter pylori; MRE, magnetic resonance enterography.

DISCUSSION

We present an adolescent boy with persistent anemia, hematochezia, and an intestinal stricture who was treated for CD before exploratory laparoscopy revealed a Meckel diverticulum. The stricture most likely developed secondary to chronic mucosal inflammation and fibrosis caused by acid secretion from the ectopic gastric mucosa, a finding characteristic of the Meckel diverticulum (Figure 2), while the remaining terminal ileum and colon showed no evidence of mucosal chronicity.

Although 90%–96% of individuals with the Meckel diverticulum remain asymptomatic, complications including bowel perforation, volvulus, and intussusception can occur.^4–6 Misdiagnosis of the Meckel diverticulum as CD has been documented in the literature, though pediatric cases are uncommon.^6–14 To date, only 3 case reports describe preadolescent patients, initially suspected of CD who were later found to have the Meckel diverticulum (Table 2).^12,14,15 Our case differs from previously reported pediatric cases of the Meckel diverticulum mimicking CD in several respects. First, the diagnostic course in our patient spanned 4 years, considerably longer than in previous reports, reflecting how persistent and convincing an IBD picture this presentation can generate. Moreover, to our knowledge, this is the first reported case in which DBE was used in the diagnostic evaluation. The stricture and erosions visualized on DBE reinforced the diagnosis of CD in our patient, and without this modality, repeat imaging may have been pursued more promptly. Finally, unlike in other reported cases, our patient's early history of H. pylori infection may have contributed to the delayed reconsideration of the diagnosis.

Table 2.

Pediatric cases of the Meckel diverticulum mimicking Crohn's disease

Publication	Age (yr), sex	Initial clinical history and symptoms	Laboratory test results and fecal calprotectin	Method of diagnosis	Treatment of IBD
Kang et al11	8, male	Three months of pallor and weakness. Capsule endoscopy showing diffuse erythematous mucosa in distal ileum. Ongoing symptoms 4 yr later (melena, syncope)	Hgb 7.7 g/dL Albumin 4.5 g/dL CRP 0.04 mg/dL ESR 6 mm/h FCP > 2,000 μg/g	CTA revealed an enhancing stricture connected to distal ileum. Small bowel barium study noting concern for a possible Meckel diverticulum. Exploratory laparoscopy with resection followed	Oral Mesalamine
Hedge et al15	6, male	Two months of recurrent hematochezia. Imaging suggesting Crohn's disease. Diagnosed with Meckel diverticulum on exploratory laparotomy. CTE was completed noting mesenteric fat stranding, thickened loops of small bowel. Suspected microperforation or microabscesses	CRP 9.6 mg/dL ESR 17 mm/hr	MRE was suggested of perforated Meckel diverticulitis that led to exploratory laparoscopy with resection	None
Mendoza Alvarez et al16	11, male	Six weeks of periumbilical pain, 2 wk nonbloody diarrhea and fever. Infliximab was started. CT with concerns of a phlegmon with worsening symptoms	Hgb 9.9 g/dL Albumin 2.5 g/dL CRP 221 mg/L FCP > 1,250 ug/g	A technetium-99 m scan was obtained that led to exploratory laparoscopy with resection	Infliximab

CRP, C-reactive protein; CT, computed tomography; CTA, computed tomography angiography; CTE, computed tomography enterography; ESR, erythrocyte sedimentation rate; FCP, fecal calprotectin; HCT, hematocrit; Hgb, hemoglobin.

Despite a presumed stricture on DBE, therapy was escalated to infliximab in the absence of supporting histopathology. This decision was made based on imaging and endoscopic findings that were considered sufficient to characterize the disease as stricturing CD. Stricturing CD can present with radiographic and endoscopic findings without definitive histologic changes, given the patchy nature of the disease; this discordance has been reported previously.^17,18 The patient's age and the chronicity of symptoms may have contributed to the initial exclusion of the Meckel diverticulum from the initial differential diagnosis. Nonetheless, the absence of histologic evidence of IBD across multiple endoscopies should have prompted earlier broadening of the differential. We highlight this as a key teaching point: an ongoing refractory case without supportive histopathology should prompt consideration of alternative diagnoses.

The persistently elevated fecal calprotectin in this case warrants discussion. Fecal calprotectin, a cytosolic protein primarily found in neutrophils, macrophages, and monocytes, is a nonspecific marker of gastrointestinal inflammation used primarily to differentiate IBD from functional disorders.¹⁹ In pediatric IBD, fecal calprotectin has high sensitivity (90%) but modest specificity (60%–75%) and elevated levels can result from gastroenteritis, H. pylori infections, polyps, neoplasms, and as illustrated in this study, the Meckel diverticulum.²⁰ Moreover, fecal calprotectin can be less reliable for small bowel disease.^21,22 One systematic review reported a sensitivity range of 43%-100% for small bowel disease compared with 67%–100% in colon disease IBD while other reports confirm that fecal calprotectin may be as elevated for small bowel disease.^21,22 In this patient, the elevation was likely driven by mucosal ulceration from acid-secreting heterotopic gastric mucosa rather than IBD. In contrast, serum markers are also commonly used to evaluate inflammation and have clinical utility in monitoring clinical disease activity, however our patient’s values were normal. In addition, hypoalbuminemia is an important marker of enteropathy and intestinal inflammation, present in about one-fifth of patients, which our patient did have.²³ These discordant findings should prompt consideration of an alternative diagnosis.

This case highlights the importance of including the Meckel diverticulum in the differential when clinical, endoscopic, and histologic findings are incongruent and patient’s conventional IBD therapy fails to respond. Given the significant implications of initiating systemic immunosuppression, such as infliximab, clinicians should consider the Meckel diverticulum before escalating treatment in patients in an uncertain CD diagnosis.

DISCLOSURES

Author contributions: M. Maccani, C. Bartel, and N. Zeky conceptualized and drafted the initial manuscript, and critically reviewed and revised the manuscript. OF Lopez-Nunez, A. Garrison, JR Dillman provided clinical expertise and critically reviewed and revised the manuscript. J. Dhaliwal conceptualized, assisted in drafting the manuscript, and provided oversight for the crafting of this case report manuscript. She critically reviewed and revised the manuscript. All authors approved the final manuscript as submitted and agree to be accountable for all aspects of the work. N. Zeky is the article guarantor.

Financial disclosure: None to report.

Informed consent was obtained for this case report.

ABBREVIATIONS:

CD

Crohn's disease

DBE

double balloon retrograde enteroscopy

IBD

inflammatory bowel disease

MRE

magnetic resonance enterography