Mycobacterium tuberculosis (TB) is the causative agent of TB, a chronic granulomatous illness. This disease is prevalent in low-income countries, posing a significant global health challenge. Gastrointestinal TB is one of the three forms. The disease can mimic other intra-abdominal conditions, leading to delayed diagnosis owing to the absence of specific symptoms. While gastric outlet obstruction (GOO) remains a frequent complication, its incidence has declined with the advent of proton pump inhibitors and Helicobacter pylori eradication therapy. Gastroduodenal TB can cause upper gastrointestinal hemorrhage, obstruction, and malignancy-like tumors.

A 23-year-old male presented with recurrent epigastric pain, distension, nausea, vomiting, and weight loss, prompting a referral to a gastroenterologist clinic. Endoscopic examination revealed distorted gastric mucosa and signs of chronic inflammation. However, treatment was interrupted, possibly owing to vomiting or comorbidities such as human immunodeficiency virus infection or diabetes. Subsequent surgical intervention revealed a dilated stomach and diffuse thickening of the duodenal wall. Resection revealed gastric wall effacement with TB.

Primary gastric TB is rare, frequently leading to GOO. Given its rarity, suspicions should be promptly raised when encountering relevant symptoms, often requiring surgical intervention for diagnosis and treatment.

Tuberculosis (TB) is a chronic granulomatous disease caused by aerobic bacteria Mycobacterium TB[1,2].

Its global incidence is high in low-income nations, posing a significant health concern. TB has high morbidity and mortality rates despite its status as a treatable disease[3]. Abdominal TB ranks as the third most common extrapulmonary form[4].

Gastrointestinal TB (GI–TB) is one of the three forms of abdominal TB. The other types include visceral, peritoneal, and tuberculous lymphadenopathy[5].

Mycobacterium TB enters the gastrointestinal system via hematogenous spread, ingestion of contaminated sputum, or direct dissemination from infected adjacent lymph nodes and fallopian tubes[6,7].

Diagnosing abdominal TB is often hindered by the absence of distinct clinical signs and symptoms, leading to delayed identification because the disease can mimic other intra-abdominal pathologies[8,9].

Correcting the general status of patients with a confirmed diagnosis of GOO, administering intravenous fluids to correct an electrolyte imbalance, and performing gastric decompression by inserting a nasogastric tube are all essential to the initial management of these patients[10]. The most common causes of gastric outlet obstruction (GOO) are peptic ulcer disease (PUD) and gastric cancer. However, the frequency of GOO owing to PUD has declined since the development of proton pump inhibitors and Helicobacter eradication therapy.

Gastric bezoars, pancreatitis-related fluid collection, caustic ingestion, massive gastric polyps, Crohn's disease, and complications following gastric surgery contribute to GOO[11].

Gastroduodenal TB (GD-TB) presents with various manifestations, including upper gastrointestinal hemorrhage, obstruction, and gastric or periampullary tumors suggestive of malignancy[12].

Similar to our patient, most individuals with GD-TB exhibit signs of GOO, often attributed not only to intrinsic duodenal lesions but also to extrinsic compression by tuberculous lymph nodes[13].

Here, we present a case of GD-TB-associated GOO in a previously healthy 23-year-old patient who exhibited no signs of pulmonary TB.

Primary GD-TB.

A decision was made to relieve the obstruction surgically. Intraoperatively, the following findings were noted: Dilation of the stomach and diffuse wall thickening of the duodenum, along with multiple enlarged mesenteric lymph nodes (located at the lesser curvature, transverse colon mesentery, small bowel mesentery, paraduodenal area, and interaortocaval region). Subsequently, antrectomy and Roux-en-Y reconstruction with gastrojejunostomy were performed, along with lymph node dissection (Figure 2).

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Figure 2 Intraoperative finding. A-C: An intense inflammatory mass causing duodenal obstruction alongside multiple pathologic lymph nodes observed in the mesenteric and paraduodenal regions; D: Resected distal gastric and dissected lymph nodes.

The pathology report from the resected distal part of the antrum and lymph nodes revealed findings indicative of gastric TB, characterized by effacement of the gastric wall architecture and numerous caseating granulomatous inflammation. Specifically, the distal margins displayed positivity for granulomatous inflammation. Additionally, 12 Lymph nodes exhibited suppurative and non-suppurative granulomatous inflammation, further supporting the TB diagnosis. Periodic Acid-Schiff stain stains yielded negative results for fungal hyphae. These findings were consistent with GD-TB (Figure 3). Notably, cytology analysis for Acid Fast Bacteria staining and Gene Xpert testing were not pursued owing to the absence of peritoneal ascites detected during the operation.

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Figure 3 Histopathology. A: Granulomatous inflammation and giant cells on the serosal surface; B: Lymph node parenchyma with effacement of multiple large tuberculoid necrotizing granuloma; C: Lymph node parenchyma with effacement of large tuberculoid necrotizing granuloma (thick arrows) epithelioid histiocytes (thin arrows) peripheral lymphocytes (triangles); D: Lymph node with tuberculoid necrotizing granuloma (thick arrows) and Langerhans giant cells (thin arrows) and peripheral lymphocytes (triangles).

The postoperative course was uneventful, and the patient was discharged from the hospital following successful tolerance of full enteral feeding. Plans were made for follow-up visits at the polyclinic and referral to a TB center to initiate anti-tubercular treatment. Currently, the patient is adhering to the anti-tubercular medication regimen well and has experienced no adverse effects.

GI–TB most frequently affects the ileocecal area, with the colon and jejunum following closely after. A total of 64% of GI–TB cases are caused by jejunal and ileocecal TB[14]. However, the esophagus, stomach, and duodenum are rarely affected. The duodenum and gastric are the primary sites of involvement for gastric TB.

Primary and isolated stomach TB is exceptionally rare, documented only in very few cases in the literature. A total of 0.4%–2% of all GI–TB cases are associated with primary gastric TB, while 2%–2.5% are associated with primary duodenal TB[15].

Several factors contribute to the low frequency of gastric TB, including the bactericidal properties of gastric acid, the presence of thick and intact gastric mucosa, and the absence of lymphoid structures in the gastric mucosa[14,16]. Treatment with H2 blockers increases the likelihood of involvement of the lesser curvature and pylorus in gastric TB, often presenting as ulcerating lesions[5]. Manifestations such as pyloric stenosis, miliary tubercles, and hypertrophic variations may also occur[14]. Gastric TB is frequently associated with TB lymphadenitis, as observed in cases where peripancreatic lymph nodes are involved, alongside visible ulcerative lesions in the prepyloric region.

The third part of the duodenum is commonly affected in cases of primary duodenal TB.

Both intrinsic and extrinsic factors can contribute to duodenal involvement[17]. Extrinsic involvement is most prevalent and is often related to lymphadenopathy in the duodenum's C-loop. Intrinsic variations may manifest as ulcerative, hypertrophic, or ulcer hypertrophic forms, potentially leading to fistula or stricture formation.

Various modalities contribute to GI–TB involvement, including ingestion of contaminated milk or food (primary TB), ingestion of contaminated sputum (secondary TB), hematogenous spread from a distant TB focus, or contiguous dissemination from infected neighboring foci via the lymphatic channels[18,19]. Given the absence of evidence of extra-abdominal TB in our case, we believe the infection to be primary gastric TB involving the peripancreatic lymph node.

GD-TB presents with nonspecific clinical characteristics commonly associated with weight loss, epigastric pain, and fever. In certain cases, GOO may be the presenting feature. Gastric TB may also mimic lymphoma or carcinoma, complicating the differential diagnosis. A study by Rao et al[12] conducted at a single center in India reported that among 23 patients with histologically confirmed GD-TB, vomiting (60.8%) and epigastric pain (56.5%) were the most prevalent presenting symptoms, with characteristics of GOO observed in 61% of cases (14 patients)[12]. While two patients had pyloric stenosis, the remaining twelve experienced obstruction owing to duodenal stricture. Additionally, out of the 23 patients studied, four had diabetes mellitus, and none were human immunodeficiency virus-positive. Similar to this study, our patient presented with vomiting, epigastric pain, and early satiety, suggestive of GOO.

The lack of specific clinical symptoms and diagnostic indicators often leads to underdiagnosis of GD-TB.

Histopathological examination of gastroduodenal biopsy specimens obtained via endoscopy remains the gold standard for diagnosing GD-TB. However, owing to the submucosal nature of granulomatous lesions, they are often challenging to identify, even in biopsy samples. A review revealed that granulomas were detected in only seven out of 27 patients who underwent endoscopic biopsy for duodenal TB[20].

Similarly, Rao et al[12] reported positive biopsies in their study in only 2 out of 20 patients.

Complications of GD-TB may include GOO, hemorrhage, and perforation, which can significantly increase morbidity[11].

As outlined in a review by Rao et al[12], in cases of TB-related GOO, truncal vagotomy and gastrojejunostomy (with or without feeding jejunostomy) were performed in twelve out of fourteen patients[12].

While abdominal TB can affect individuals of any age, there is a significant predominance among women, particularly those between the ages of 25 and 45[21]. In patients with GD-TB presenting with obstruction or mass, the yield of endoscopic biopsy is typically low[22,23].

Dyspeptic symptoms suggestive of gastric lesions often lead to suspicion of peptic ulcer, while weight loss may prompt consideration of gastric cancer as the primary diagnosis.

Up to 20% of patients undergoing examinations may exhibit evidence of pulmonary TB on chest X-ray[24], and duodenal bulb deformity may be detected during upper gastrointestinal endoscopy[25]. Because ulcerated lesions predominantly reside in the submucosa, conventional endoscopic biopsies often yield poor results and rarely uncover granulomas[21].

Although preoperative diagnosis of duodenal TB is exceedingly rare[17,26], Debi et al[14] have demonstrated that an endoscopic ultrasound is a valuable modality for characterizing lesions and obtaining samples for cytological confirmation[1]. In cases where histological diagnosis cannot be established by other means, intraoperative fine-needle aspiration cytology may be employed to obtain samples from the affected duodenal section[27].

Most lesions diagnosed with TB before surgery respond well to appropriate antitubercular treatment and may not require surgical intervention[28]. Antituberculosis medication therapy is the cornerstone of medical treatment for gastric TB. However, surgery becomes necessary for patients experiencing severe GOO owing to hypertrophic TB, with antituberculosis medication therapy following surgery[29].

In cases of GOO, gastrojejunostomy is preferred over pyloroplasty owing to the severe fibrosis around the pyloroduodenal junction, which may compromise the safety of pyloroplasty.

This study adheres to the surgical case report guidelines 2016 criteria[30].

Primary gastric TB is rare and often poses a diagnostic challenge, particularly when it presents as GOO. In regions where TB is prevalent, heightened suspicion is warranted. Surgery is often essential for diagnosis and treatment.