Simultaneous heterotopia of the gastric mucosa and pancreatic tissue leads to perforation of the small intestine: case report and literature review

Introduction

Background

Heterotopia of gastrointestinal tissue is a relatively rare pathological phenomenon, referring to the growth of certain tissues or cells of the digestive system in areas outside their normal anatomical positions. This condition can occur in any part of the digestive tract (1,2), including the esophagus, stomach, small intestine, large intestine, and associated glands such as the pancreas and liver. Common types of heterotopia include heterotopic gastric mucosa (HGM), heterotopic pancreas (HP), ectopic Brunner’s glands, ectopic sebaceous glands, ectopic salivary glands, ectopic prostate, ectopic thyroid, ectopic renal tissue, and ectopic endometrium. These heterotopic phenomena can lead to a variety of clinical issues (3).

Rationale and knowledge gap

In this case report, we describe the case of a patient with simultaneous dual ectopia of the gastric mucosa and pancreatic tissue leading to perforation of the small intestine. Although there is extensive literature on isolated HGM or HP, the simultaneous presence of both tissues in the same patient and at the same site is exceedingly rare. This condition, termed “double ectopia”, poses unique diagnostic and therapeutic challenges.

Existing literature indicates that solitary HGM or HP is often an incidental, asymptomatic finding. However, when symptomatic, they typically manifest as non-specific abdominal pain, obstruction, bleeding, or intussusception. Cases like the present one, which directly led to jejunal perforation, are exceptionally rare in both domestic and international literature. This severe complication underscores the potential aggressiveness of such lesions. Nevertheless, due to their non-specific clinical presentation, accurate preoperative identification is extremely difficult. Conventional imaging techniques, such as computed tomography (CT) or ultrasound, often struggle to differentiate ectopic tissue from tumors, polyps, or other inflammatory lesions, resulting in a high rate of misdiagnosis. Definitive diagnosis usually relies on intraoperative findings and postoperative histopathological examination.

Objective

Therefore, in addition to providing a detailed description of this case, we also collect and summarize the relevant literature to systematically review and analyze these heterotopic phenomena. Our goal is to further elucidate the etiology, mechanisms, and potential clinical implications of gastrointestinal tissue heterotopia, thereby providing important references for the diagnosis and treatment of similar rare cases. We present this case in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-24-236/rc).

Case presentation

A 16-year-old female (previously completely healthy) was admitted to the emergency department due to upper abdominal pain accompanied by nausea and vomiting for 6 days, along with fever for 4 hours. Initially, she was suspected of having “gastroenteritis”, and on the 2^nd day, she began oral treatment with “cefdinir”. After taking the medication, her symptoms slightly improved. However, on the 5^th day of her illness, her symptoms worsened again, and rebound tenderness was noted in the lower abdomen. Consequently, she underwent abdominal CT and ultrasound examinations, which revealed intestinal dilation within the abdominal cavity (Figure 1A), the accumulation of pelvic fluid, and the presence of gallbladder sludge-like stones. The results revealed a neutrophil count of 11.55×10⁹/L [normal range, (1.8–8.3)×10⁹/L] and a body temperature of 39.3 ℃. The antibiotics were escalated to “cefoperazone and sulbactam”.

Figure 1 Patient’s preoperative CT images along with intraoperative photographs. (A) The patient’s CT scan revealed extensive dilatation of the small intestine. A suspicious edematous area (yellow arrow) was identified in the distal segment of the small intestine, with punctate gas density shadows observed around the mesentery near this area. (B) During laparoscopic exploration, a perforation of the distal small intestine is visible, with continuous leakage of digestive fluid from the perforation and substantial yellow necrotic material adhering to the surrounding. CT, computed tomography.

On the 9^th day of her illness, as her symptoms persisted without relief, she underwent another CT scan, which revealed gas within the abdominal cavity. She was then referred to the general surgery department for treatment. During the laparoscopic exploration in the operating department (Figure 1B), a small intestinal perforation was found approximately 30 cm away from the terminal ileum. The perforation measured about 1.5 cm × 1.5 cm in size, and intestinal fluid oozed out from the perforated site. Surrounding tissue was noted to have yellowish necrotic material, and her appendix appeared congested and edematous. Consequently, the surgeons excised the perforated segment of the small intestine and the inflamed appendix. Postoperative histopathological examination revealed a gray-white raised mass in the mucosa near the perforation measuring 2 cm × 1.5 cm × 0.6 cm. This mass was found to contain ectopic gastric fundic mucosa and pancreatic tissue (Figure 2). The patient had a smooth recovery and was discharged 15 days after the surgery. The patient returned to the outpatient clinic for a follow-up after 6 months and underwent an abdominal CT scan. The results showed that the patient had fully recovered and experienced no discomfort (Figure 3).

Figure 2 The HE-stained image of the submucosal grayish-white nodules near the perforation shows the presence of intestinal absorptive cells, gastric mucosal chief cells, parietal cells, and pancreatic acinar cells simultaneously. (A) Pancreatic acinar cells. (B) Panoramic images show cells from three different tissue sources coexisting simultaneously. (C) Intestinal absorptive cells, gastric mucosal chief cells, and parietal cells. (D) Pancreatic islets and pancreatic duct tissues can be seen within the heterotopic pancreatic tissue. (E) The fragmented structure of small intestinal villi coexists with the heterotopic tissue. (F) The typical structure of small intestinal villi and goblet cells at the resection margin of the mass. Magnification: (A) ×400; (B,D,E) ×40; (C,F) ×200. HE, hematoxylin and eosin.

Figure 3 Clinical timeline. CT, computed tomography; US, ultrasound.

All procedures performed in this study were in accordance with the ethical standards of the Ethics Committee of Qingdao Municipal Hospital Group and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient’s parent for publication of this case and any accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Literature review

A patient with simultaneous gastric mucosa and pancreatic tissue ectopia leading to small bowel perforation is extremely rare, and there are very few reports on such cases. Therefore, we conducted a literature review and analysis based on this condition, examining the characteristics of gastric mucosa ectopia and pancreatic ectopia separately, with a particular focus on the coexistence of both gastric mucosa and pancreatic ectopia.

HGM

HGM refers to the presence of gastric mucosa in an abnormal location outside the stomach. This ectopic tissue is typically found in other parts of the gastrointestinal tract, such as the esophagus (with an incidence of 0.1–13.8%), duodenum (0.5–8.9%), colon, jejunum, ileum, Meckel’s diverticulum, and gallbladder (4-7). However, HGM is most commonly found in the proximal esophagus and is very rare in the small intestine (8); HGM usually occurs only in association with Meckel’s diverticulum. It is worth noting that, compared with typical Meckel’s diverticulum, the incomplete Meckel’s diverticulum may have some differences in structure or function. For example, the diverticulum may not have completely formed a complete blind pouch-like structure, or the heterotopic tissues it contains are incomplete, lacking some typical tissue components. For instance, it may not contain HGM or pancreatic tissue. It is also possible that only a part of the vitelline duct remains, resulting in differences in the morphology and connection mode of the diverticulum compared with the complete type. This diagnosis cannot be excluded in this case.

HGM can be found in individuals of all ages, with an average age at diagnosis of 44.3 years, and a slightly greater incidence in males than in females (9,10). The exact etiology of HGM remains unclear; however, it is widely believed that HGM in the esophagus is a congenital disorder. This condition is believed to be associated with embryonic development. During embryonic development, the columnar epithelium of the esophagus should normally be replaced by stratified squamous epithelium. Incomplete replacement can lead to residual embryonic gastric mucosa remaining in the esophagus.

HGM is typically asymptomatic and is often discovered incidentally during endoscopic examinations or surgical procedures, with an estimated prevalence of 7.8–21.0% in the general population. Symptoms are mostly due to digestive ulcers secondary to gastric acid secretion from the ectopic mucosa. In the small intestine, HGM commonly presents with gastrointestinal bleeding (9,11,12), and certain lesions may lead to intestinal obstruction or intussusception. Furthermore, HGM is believed to be associated with precancerous lesions and malignant tumor development (13-15), particularly when accompanied by intestinal metaplasia, which presents a greater risk. Studies indicate that the incidence of intestinal metaplasia in HGM may be 6.25% (9). Therefore, it is essential to perform biopsies of HGM lesions to confirm this important histological feature, especially in cases involving HGM in the duodenum.

High-radium single-photon emission CT (SPECT)/CT imaging can be utilized for the diagnosis and localization of HGM (16).

In cases where HGM is discovered incidentally and the patient is asymptomatic, no specific treatment is typically needed. However, if the ectopic gastric mucosa exhibits acid-secreting function, resulting in esophageal ulcers, bleeding, or complications related to gastroesophageal reflux disease, acid suppression therapy may be indicated.

HP

HP is a rare congenital disorder characterized by the presence of pancreatic tissue outside of the normal pancreas (17), forming isolated pancreatic tissue that lacks vascular and neural connections to the normal pancreas. There are currently three prevailing theories regarding its pathogenesis: the ectopic theory, the metaplasia theory, and the totipotent cell theory.

• Ectopic theory: this theory is the most widely accepted theory (18-20). Under normal circumstances, during embryonic development, the pancreatic bud develops from the endodermal part of the intestine and is supposed to migrate smoothly to its final position. If this migration process is obstructed, pancreatic tissue may remain in an atypical location.
• Metaplasia theory: the metaplasia theory suggests that the occurrence of HP may be due to the transformation of primitive endodermal cells in other locations during embryonic development into characteristic pancreatic cells. This cellular transition may facilitate the formation of functional pancreatic cells in areas where pancreatic tissue should not exist.
• Totipotent cell theory: totipotent or pluripotent stem cells differentiate in the pancreatic direction under specific conditions, forming structures outside of the pancreas and leading to the occurrence of HP.

HP can be found across all age groups, with an average onset age of 43.5 years and a male-to-female ratio of approximately 0.97. HP can be classified on the basis of its anatomical location, with the most common ectopic sites including the stomach (25–60%), duodenum, jejunum (15–21.7%), ileum (3–6%), and Meckel’s diverticulum (2–6.5%). Other less common and rare sites include the gallbladder, Treitz ligament, colon, spleen, appendix, greater omentum, liver, bile ducts, umbilicus, retroperitoneum, fallopian tubes, lungs, and mediastinum (21-24).

The clinical manifestations of HP vary on the basis of its location and size. Most HP patients typically display no significant symptoms and are often discovered incidentally during endoscopic examinations, with an incidence rate of 0.25% to 0.5% in the general population. Approximately 33% to 47% of HP patients may present with various clinical symptoms, which can be summarized into the following six types:

• Asymptomatic type: patients experience no obvious discomfort, and HP is discovered incidentally during surgery, autopsy, or examinations such as endoscopy or CT.
• Bleeding type: this type presents with gastrointestinal bleeding as the initial symptom. The primary causes include HP inflammation accompanying ulcer formation or direct erosion of blood vessels by pancreatic fluid.
• Ulcer type: when the HP is located in the stomach or duodenum, it may cause abnormal pancreatic fluid secretion or compression of the mucosa, leading to chronic gastritis or peptic ulcers.
• Obstructive type: HP may cause narrowing or obstruction of the lumen due to mass effects or inflammation and ulceration. Symptoms can vary on the basis of the anatomical location.
• Diverticulitis type: HPs located within a diverticulum of the gastrointestinal tract may lead to diverticulitis, which presents with abdominal discomfort, pain, and nausea.
• Tumor type: the incidence of malignant transformation of HP is low, ranging from 0.7% to 1.8% (25). The most common pathological type is ductal adenocarcinoma.

The gross appearance of HP is characterized by raised lesions that vary in shape and size and are covered by villous mucosa, often with a napiform indentation at the apex and tubular openings, exhibiting certain distinctive features. Via a modified Heinrich classification, HP can be categorized into four types (26):

• Type I: composed of typical pancreatic tissue, including acini, ducts, and islet cells;
• Type II: composed of ducts that form small tubular structures;
• Type III: composed solely of acinar tissue of the exocrine pancreas;
• Type IV: this type consists only of endocrine pancreatic cells.

HP lesions in the stomach typically appear as flat or oval shapes on CT images, with a long-to-short diameter ratio exceeding 1.4. In contrast, HPs in soft tissues such as the duodenum and jejunum usually present as round lesions. The MRI findings are similar to those of the native pancreas (27).

Most HP patients are typically asymptomatic. However, for those who have been diagnosed and present with clinical symptoms, conservative medical treatment often proves ineffective. Therefore, the decision to pursue surgical intervention and the timing of such intervention are critical issues.

Simultaneous dual ectopia of the gastric mucosa and pancreatic tissue

We conducted a detailed summary of cases involving simultaneous dual ectopia of the gastric mucosa and pancreatic tissue (Table 1), with results indicating an average age of onset of 25.0 years, ranging from 0.5 to 69 years. The male-to-female ratio for this condition is approximately 5:7, with the sites of occurrence including but not limited to the gastrointestinal tract; all cases were solitary.

Discussion

Currently, the exact pathogenesis of simultaneous dual ectopia of the gastric mucosa and pancreatic tissue remains unclear. However, on the basis of past literature analysis, it may be considered a congenital condition that manifests clinical symptoms at certain times.

Unlike most asymptomatic patients with isolated HGM or HP, patients with simultaneous dual ectopia typically present with severe symptoms (10 out of 12 cases), such as bleeding, intestinal obstruction, and gastrointestinal perforation.

The mechanisms by which the coexistence of gastric mucosa and pancreatic tissue can lead to severe diseases remain unclear, and it is mainly likely due to the interaction of the following mechanisms.

First, the imbalance of acid and alkali can trigger mucosal damage. The parietal cells of the HGM continuously secrete gastric acid, reducing the pH value of the local intestinal fluid to 2.0–3.0, while the normal pH value of the jejunum is 6.0–7.0. This will disrupt the bicarbonate barrier of the intestinal mucosa. In vitro experimental data showed that the activity of Na⁺-K⁺-ATPase in epithelial cells decreased by 40% as a result, and the thickness of the mucus layer was reduced by 60%, causing the intestinal mucosa to be directly exposed to the environment of digestive enzymes (39).

Second, the abnormal activation of pancreatic enzymes will exacerbate tissue damage. Trypsinogen and amylase secreted by pancreatic acinar cells will be abnormally activated in an acidic environment. Trypsin will cleave the tight junction proteins of the intestinal mucosa, leading to a 70% decrease in transepithelial electrical resistance, while amylase will decompose the submucosal glycoprotein and disrupt the extracellular matrix scaffold (40). The activated pancreatic enzymes will also induce the infiltration of neutrophils, release myeloperoxidase, and trigger an oxidative stress cascade reaction (41).

Finally, the combined action of the two will produce a pathophysiological synergistic effect. When the gastric mucosa and pancreatic tissue coexist, an “acid-enzyme damage cycle” will be formed: gastric acid creates conditions for the activation of pancreatic enzymes, and the activated pancreatic enzymes expand the scope of mucosal damage, further exposing more HGM, thus creating a vicious cycle.

Patient perspective

Initially, I only felt a slight pain in my abdomen, but over time, this discomfort gradually intensified. After a period of treatment without any improvement in my symptoms, the doctor conducted a series of tests and informed me that I had a perforation in my small intestine, necessitating surgical intervention. This news hit me like a bolt from the blue, leaving me in a state of shock and fear. The doctor explained that this condition could lead to severe complications and even pose a life-threatening risk.

During the subsequent treatment process, I underwent surgery and faced a long recovery period. After the operation, I learned that the issue was caused by abnormal growth of gastric mucosa and pancreatic tissue, which surprised me greatly. The doctor informed me that this condition is quite rare, and fortunately, I received timely medical attention. In hindsight, it is clear that deciding to proceed with the surgery was both the right and necessary choice.

Conclusions

Once a diagnosis of simultaneous dual ectopia of the gastric mucosa and pancreatic tissue is confirmed, surgical intervention or endoscopic resection should be considered to prevent potential serious complications.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://acr.amegroups.com/article/view/10.21037/acr-24-236/rc

Peer Review File: Available at https://acr.amegroups.com/article/view/10.21037/acr-24-236/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://acr.amegroups.com/article/view/10.21037/acr-24-236/coif). The 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. All procedures performed in this study were in accordance with the ethical standards of the Ethics Committee of Qingdao Municipal Hospital Group and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient’s parent for publication of this case and any accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

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/.

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