A 21-year-old woman, resident of urban North India, presented to our tertiary care hospital with one month of low-grade, intermittent fever and mild right hypochondriac abdominal discomfort described as a dragging sensation. The illness was insidious, accompanied by profound anorexia and unintentional weight loss. Notably, there was no history of cough, urinary symptoms, jaundice, night sweats, or changes in bowel habits.

On examination, the patient was thin-built (BMI 16.8 kg/m²) and pale, without peripheral lymphadenopathy or icterus. Abdominal palpation revealed hepatomegaly without guarding or tenderness. Systemic examination was otherwise unremarkable except for signs of protein-energy malnutrition. Initial laboratory investigations (Table 1(Tab. 1)) revealed normocytic anemia (Hb 7.4 g/dL), elevated liver enzymes predominantly in a cholestatic pattern-markedly elevated alkaline phosphatase (907 U/L) and γ-glutamyl transpeptidase (542 U/L)-with mildly elevated bilirubin and AST. Over the subsequent weeks, there was a fluctuating but persistent pattern of deranged liver biochemistry. Viral serologies for hepatitis B, C, and HIV were negative. Autoimmune workup, including antinuclear antibody (ANA) testing by immunofluorescence, was also negative. Ultrasonography of the abdomen showed hepatomegaly (15 cm), a thickened gallbladder wall, mild ascites, and splenomegaly. Chest X-ray was unremarkable except for mild cardiomegaly and blunting of the right costophrenic angle. Echocardiography revealed a mild circumferential pericardial effusion and mild pulmonary artery hypertension.

Due to persistently worsening liver function and no clear etiology, a contrast-enhanced CT of the abdomen was performed (Figure 1a(Fig. 1)), revealing significant hepatomegaly (19 cm), periportal cuffing, and enlarged periportal lymph nodes with a thickened gallbladder wall but no biliary dilatation. In view of diagnostic uncertainty, the patient was referred to the Department of Gastroenterology for further evaluation. Following multidisciplinary discussion and informed consent, she underwent a percutaneous ultrasound-guided liver biopsy along with fine-needle aspiration cytology (FNAC) of periportal lymph nodes.

Histopathological examination of the liver biopsy (Figure 1b(Fig. 1)) revealed non-caseating and caseating granulomas composed of epithelioid cells and Langhans-type multinucleated giant cells. Special staining with Ziehl-Neelsen (ZN) confirmed the presence of acid-fast bacilli (AFB), consistent with Mycobacterium tuberculosis infection. Periodic acid-Schiff (PAS) stain and Congo red stain for amyloid were negative, ruling out fungal or amyloid-related pathologies.

The diagnosis of hepatic tuberculosis with diffuse granulomatous inflammation and intrahepatic cholestasis was established. The patient was initiated on a standard four-drug anti-tubercular therapy (ATT) regimen: isoniazid (5 mg/kg/day), rifampicin (10 mg/kg/day), pyrazinamide (25 mg/kg/day), and ethambutol (15 mg/kg/day), along with supportive nutrition therapy and pyridoxine.

Over the ensuing 4 weeks, the patient demonstrated significant clinical improvement with resolution of fever, increased appetite, and weight gain. Follow-up investigations at 4 and 8 weeks revealed progressive normalization of liver function parameters, as shown in Table 2(Tab. 2). Repeat ultrasonography at 3 months showed regression of hepatosplenomegaly and disappearance of ascites.

A 20-year-old woman with no significant past medical history presented to our outpatient department with complaints of dull epigastric pain persisting for two months. The pain was described as intermittent, non-radiating, and poorly localized, without clear aggravating or relieving factors. She also reported profound anorexia and unintended weight loss of approximately 6 kg during the same period.

There was no associated history of nausea, vomiting, hematemesis, melena, or altered bowel habits. Importantly, she denied any fever, respiratory symptoms, or constitutional complaints such as night sweats. There was no personal or family history of tuberculosis, and she had not received Bacillus Calmette-Guérin (BCG) vaccination in childhood. The patient was not on any medications and had no history of immunosuppression or contact with a known TB patient.

On clinical examination, she appeared pale and undernourished, with a BMI of 17.2 kg/m². Mild epigastric tenderness was noted on deep palpation, without palpable mass or organomegaly. There was no lymphadenopathy, ascites, or peripheral stigmata of chronic illness. Cardiopulmonary and neurological examinations were within normal limits.

Initial laboratory investigations revealed microcytic anemia with hemoglobin of 7.1 g/dL, while leukocyte counts and differential were within normal limits. Liver and renal function panels were unremarkable. ESR was elevated at 22 mm/h, and the Mantoux test was strongly positive at 15 mm. Viral serologies for HIV, hepatitis B, and C were negative.

Ultrasonography of the abdomen revealed thickening of the gastric wall, predominantly in the pyloric and antral regions. This finding prompted a contrast-enhanced CT (CECT) scan of the abdomen, which showed circumferential thickening of the gastric body and antrum with mild perigastric stranding and subcentimetric lymphadenopathy. These findings raised differential considerations of gastric lymphoma, infiltrative carcinoma, or granulomatous disease.

Upper gastrointestinal endoscopy was performed, revealing thickened, velvety gastric folds in the body and antrum, without ulceration or bleeding. No mass lesion or obstruction was visualized. Endoscopic biopsy was inconclusive due to superficial sampling. Subsequently, an endoscopic ultrasound (EUS) was conducted, revealing homogeneous thickening of the third layer of the gastric wall (muscularis propria) without nodal involvement or serosal breach. EUS-guided fine-needle aspiration cytology (FNAC) was performed from the thickened gastric wall.

Cytological analysis of the aspirate demonstrated multiple epithelioid cell granulomas with central necrosis and surrounding lymphoplasmacytic infiltrate (Figure 2a, b(Fig. 2)). Occasional Langhans-type giant cells were observed. The final diagnosis of isolated gastric tuberculosis was made.

The patient was initiated on first-line anti-tubercular therapy (isoniazid, rifampicin, pyrazinamide, and ethambutol) , along with pyridoxine and iron supplementation for anemia. Nutritional rehabilitation with high-protein diet and oral supplements was also implemented.

Over the course of 12 weeks, the patient demonstrated progressive clinical recovery. She reported complete resolution of abdominal pain and gained 10 kg in body weight. Repeat endoscopy at 3 months showed marked reduction in gastric wall thickening and normalization of the mucosal folds. Follow-up laboratory testing demonstrated a rise in hemoglobin to 11.6 g/dL, normalized ESR, and improved nutritional markers.

A 48-year-old man presented to our outpatient clinic with a primary complaint of progressive dysphagia to solid foods over the preceding two months. Initially intermittent, the dysphagia had become persistent and was associated with vague, non-radiating retrosternal and epigastric discomfort. He denied odynophagia, regurgitation, vomiting, or symptoms suggestive of gastroesophageal reflux.

No history of cough for six weeks, without hemoptysis, diurnal variation, or positional influence. The patient also reported unintended weight loss (approx. 5 kg), reduced appetite, and low-grade evening fevers. There were no prior episodes of TB, nor a history of close contact with a TB patient. He had no history of dyspepsia, abdominal pain, altered bowel habits, or systemic features like joint pain or rash. There was no history of substance abuse or long-term medication use.

Physical examination revealed a BMI of 21.5 kg/m². There was no pallor, or lymphadenopathy or clubbing. Chest auscultation was unremarkable breath sounds over the right upper lung field. Cardiovascular and abdominal examinations were unremarkable.

Initial laboratory evaluation (Table 3(Tab. 3)) revealed hemoglobin of 13.0 g/dL, total leukocyte count of 7500/mm³ with a normal differential, and ESR of 65 mm/hr. Liver and renal function tests were within normal limits. Mantoux test was positive (10 mm). Viral markers for HIV, hepatitis B, and C were negative.

In view of persistent dysphagia, an esophagogastroduodenoscopy (EGD) was performed, revealing discrete ulcerated lesions in the esophagus at 25, cm from the incisors (Figure 1(Fig. 1)). The ulcers were shallow, irregular, and surrounded by hyperemic mucosa. No strictures or mass lesions were observed. Biopsies were taken from the ulcer margins. A contrast-enhanced computed tomography (CT) scan of the chest revealed short segment circumferential thickening of the esophageal wall,. Additionally, multiple enlarged Pretracheal , subcranial regions.

Histopathological analysis of esophageal biopsy (Figure 3(Fig. 3)) revealed hyperplastic squamous epithelium with focal erosions dense infiltration of inflammatory cells subepithelial granulomatous inflammation comprising epithelioid cells, Langhans giant cells, and lymphocytic infiltrates (Figure 3(Fig. 3)). Overall feature suggestive of Chronic Granulomatous esophagitis Although AFB staining was negative, the combination of granulomatous inflammation, positive Mantoux test, and suggestive radiologic features clinched the diagnosis of esophageal tuberculosis.

The patient was initiated on a four-drug anti-tubercular therapy (isoniazid 5 mg/kg, rifampicin 10 mg/kg, pyrazinamide 25 mg/kg, and ethambutol 15 mg/kg daily), along with pyridoxine. Nutritional support and cough suppression were also instituted. Clinical improvement was observed within four weeks, with resolution of fever and weight stabilization. At the 8-week mark, a repeat EGD demonstrated near-complete mucosal healing with resolution of esophageal ulcers (Figure 4(Fig. 4)). A follow-up CT chest confirmed radiologic clearance of pulmonary lesions. Laboratory markers also normalized (Table 4(Tab. 4)), and the patient remained asymptomatic on ATT.

A 24-year-old male from western Uttar Pradesh presented with persistent non-bilious vomiting for over one month, associated with dull upper abdominal pain and early satiety. He reported progressive postprandial fullness and weight loss of nearly 5 kg over two months. There was no history of fever, hematemesis, melena, dysphagia, odynophagia, altered bowel habits, alcohol use, NSAID intake, or prior anti-tubercular therapy. He denied any history of chronic cough, contact with a tuberculosis case, or prior gastrointestinal illness. He had sought treatment from a local practitioner and was prescribed a proton-pump inhibitor and anti-emetics, with no symptomatic improvement. On presentation, he appeared mildly dehydrated but was afebrile, with stable vital signs. Abdominal examination revealed a soft but distended epigastrium with visible succussion splash; there was no palpable mass or organomegaly. Digital rectal examination was unremarkable.

Laboratory investigations revealed microcytic anemia (hemoglobin 9.1 g/dL, MCV 78 fL), normal total leukocyte and platelet counts, and preserved liver and renal function. Serum amylase, lipase, calcium, and electrolytes were within normal range. HIV, HBsAg, and anti-HCV serologies were negative. Erythrocyte sedimentation rate (ESR) was mildly elevated (38 mm/hr), while C-reactive protein was normal.

An upper gastrointestinal endoscopy revealed circumferential mucosal edema and thickening at the D1-D2 junction, causing significant luminal narrowing and stasis of gastric contents suggestive of partial gastric outlet obstruction. No ulcer or mass lesion was seen. Multiple biopsies were taken from the affected area.Contrast-enhanced CT of the abdomen revealed concentric mural thickening of the proximal duodenum, with multiple enlarged periduodenal and mesenteric lymph nodes exhibiting central necrosis. There was no pulmonary lesion or abdominal ascites. Histopathological examination showed chronic granulomatous inflammation with caseous necrosis, consistent with tuberculosis. Ziehl-Neelsen staining revealed occasional acid-fast bacilli. No dysplasia or malignancy was noted (Figure 4a, b(Fig. 4)).

The patient was diagnosed with isolated duodenal tuberculosis causing partial gastric outlet obstruction. He was initiated on standard weight-based anti-tubercular therapy (isoniazid, rifampicin, pyrazinamide, and ethambutol). Nutritional support was provided with a liquid diet. Over the next six weeks, his symptoms improved significantly, and he regained 2.5 kg. A follow-up endoscopy at 8 weeks showed partial resolution of the duodenal narrowing, and therapy was continued for six months with complete clinical resolution. Under 30 cases have been reported on Duodenal tuberculosis and this forms an extremely rare entity. Other cases reviewed are compiled in Supplementary table 1.

Always consider hepatic TB in patients from endemic regions presenting with fever, hepatomegaly, and a cholestatic liver profile, especially if initial imaging is non-diagnostic.

These cases underscore the continued burden of extrapulmonary TB even in immunocompetent adults without pulmonary disease. Delayed diagnosis due to nonspecific symptoms and diagnostic inertia can lead to complications requiring invasive interventions. Our findings support the integration of early tissue diagnosis-particularly liver biopsy and EUS-guided sampling-into diagnostic pathways in endemic settings. In resource-limited regions, clinical suspicion combined with empirical ATT may be warranted when histology is suggestive, even if microbiologic confirmation is lacking.

Liver: High vascularity and reticuloendothelial function make it a filtration site, yet primary involvement is rare due to robust immune surveillance.

The authors declare that no funds, grants, or other support were received during the preparation of this manuscript.

The authors did not receive support from any organization for the submitted work.

The authors declare they have no financial interests.

AI tools were used solely for language refinement and stylistic editing, without any role in data generation, analysis, interpretation, or figure creation.

AY, YS: Conceptualization, supervision, validation, writing-original draft, visualization, project administration, writing - review & editing.