Isolated hepatic tuberculoma: A case report and review of the literature

Abstract

BACKGROUND

Hepatic tuberculosis (TB) is an uncommon form of extrapulmonary TB resulting from Mycobacterium tuberculosis infection of the liver. Its incidence is higher among immunocompromised individuals, including those with human immunodeficiency virus infection. However, its occurrence is rarely observed in immunocompetent individuals and remains less broadly documented. The nonspecific clinical manifestations of hepatic TB frequently complicate diagnosis, resulting in frequent misdiagnosis and inappropriate treatment.

CASE SUMMARY

This case report presents a 29-year-old immunocompetent man with epigastric pain. No evidence of pulmonary or gastrointestinal TB was found, and systemic symptoms such as fever or fatigue were absent. Hepatic TB was confirmed through histopathological examination and molecular testing using endoscopic ultrasound-guided fine-needle aspiration biopsy (EUS-FNA). Symptoms resolved completely following an antitubercular therapy, with follow-up evaluation confirming clinical cure.

CONCLUSION

In liver space occupying lesions, the possibility of TB should be considered. When other methods fail to identify the cause, obtaining liver tissue through EUS-FNA enables definitive diagnosis.

Key Words: Hepatic tuberculosis; Hepatic tuberculoma; Endoscopic ultrasound-guided fine needle aspiration; Granuloma; Case report

Core Tip: This case report describes a young immunocompetent man with primary hepatic tuberculosis, presenting as an isolated caudate lobe lesion without extrahepatic involvement. Clinical manifestation was atypical, characterized solely by abdominal pain. Radiological findings mimicked a malignant tumor. The final diagnosis was confirmed through endoscopic ultrasound-guided fine-needle aspiration biopsy (EUS-FNA) and polymerase chain reaction. Both blood and liver tissue tuberculosis spot tests were negative, so it should not be solely relied upon for diagnosis. This case highlights the crucial role of EUS-FNA in obtaining diagnosis and successful treatment, emphasizing its value when imaging can not provide a clear diagnosis.

INTRODUCTION

The incidence of tuberculosis (TB) is higher in people with compromised immune function[1]. Among its extrapulmonary forms, hepatic TB is an uncommon manifestation, resulting from dissemination of Mycobacterium tuberculosis (Mtb) to the liver[2]. Although abundant Kupffer cells in the liver usually phagocytose pathogens during early infection, clinically evident TB remains uncommon. Nonspecific clinical manifestations and overlapping imaging findings often lead to misdiagnosis. Early diagnosis is crucial, as most patients respond favorably to antitubercular therapy. Herein, we present a case of isolated TB in an immunocompetent patient without pulmonary or ileocecal involvement to improve the clinical awareness of this condition.

CASE PRESENTATION

Chief complaints

A 29-year-old man was admitted with a 5-day history of epigastric pain. The patient was 177 cm tall and weighed 72 kg.

History of present illness

The patient had previously visited another hospital for treatment. Liver ultrasound showed a dilated common bile duct, which was considered to be a negative stone. No special treatment was given. The patient experienced nausea, acid reflux, and abdominal distension. The symptoms were aggravated by fatty food intake and partially alleviated by nocturnal eating. Since symptom onset, the patient had been maintained on a liquid diet and reported constipation, reduced physical strength, and stable body weight, while remaining in generally satisfactory condition.

History of past illness

The patient denied any history of hypertension, diabetes, coronary heart disease, or infectious diseases such as hepatitis B, TB, human immunodeficiency virus infection, or schistosomiasis. He also reported no history of significant trauma or any known drug/food allergies. The patient had no long-term medication history.

Personal and family history

The patient reported no relevant family history but disclosed a personal history of tobacco and alcohol use.

Physical examination

The body temperature was normal (36.2 °C). Vital signs were stable, with blood pressure at 125/78 mmHg, pulse at 74 bpm, and respiratory rate at 20 breaths/minute. No jaundice or lymphadenopathy was observed. Chest percussion showed clear lung fields. Abdominal examination revealed no hepatosplenomegaly on palpation and normal bowel sounds (4 times/minute), and no edema or other abnormal signs were observed.

Laboratory examinations

Laboratory test results showed the following: Alanine aminotransferase 295 U/L (normal range: 0-41 U/L), aspartate aminotransferase 170 U/L (0-40 U/L), total bilirubin 27.1 μmol/L (0-26 μmol/L), direct bilirubin 17.7 μmol/L (0-8.0 μmol/L), alkaline phosphatase 186 U/L (40-130 U/L), γ-glutamyl transpeptidase 202 U/L (10-71 U/L), lactate dehydrogenase 239 U/L (135-225 U/L), negative hepatitis B virus markers, negative carcinoembryonic antigen, elevated C-reactive protein level 85.5 mg/L (< 1 mg/L), erythrocyte sedimentation rate 14 mm/hour (0.00-15.00 mm/hour), hemoglobin 144.0 g/L (130.0-175.0 g/L), and negative blood culture for anaerobic and aerobic bacteria. Table 1 summarizes the key liver function test results during the clinical course.

Table 1 Laboratory findings of the liver function in the clinical course.

Test	Unit	2022			2023		2024
		January 16	May 10	September 6	March 10	November 16	December 25
T-Bil	mg/dL	1.59	0.58	0.80	0.42	0.55	0.51
AST	IU/L	170	13	14	13	15	36
ALT	IU/L	295	14	12	10	15	70
γ-GTP	IU/L	202	32	30	26	22	22
LDH	IU/L	239	160	168	158	188	194
ALP	IU/L	186	71	70	64	61	69
Cr	mg/dL	NP	0.76	0.80	0.79	0.78	0.89
CRP	mg/dL	2.52	NP	NP	NP	NP	NP
Plt	104/μL	NP	NP	19.3	19.8	20.3	22.3

T-Bil: Total bilirubin; AST: Aspartate aminotransferase; ALT: Alanine transaminase; γ-GTP: γ-glutamyl transpeptidase; LDH: Lactate dehydrogenase; ALP: Alkaline phosphatase; Cr: Creatine; CRP: C-reactive protein; Plt: Platelet; NP: Not performed.

Imaging examinations

Chest computed tomography (CT) indicated bilateral pleural thickening and adhesion without additional abnormalities. Abdominal ultrasound revealed a hypoechoic mass (50.5 mm × 25.5 mm) in segment S1 of the liver encircling the portal vein. The larger size measured by ultrasound, as compared to CT and magnetic resonance imaging (MRI), may be attributed to the technique's sensitivity in capturing the surrounding perifocal edema or inflammatory reaction along with the core lesion itself[3]. Abdominal CT demonstrated a slightly hypoechoic lesion approximately 20 mm in diameter within the caudate lobe. Magnetic resonance cholangiopancreatography identified an abnormal signal focus (approximately 28 mm) in the caudate lobe, accompanied by bile duct stenosis and enlarged hepatic hilar lymph nodes. The observed stenosis corresponded to the cholestasis revealed by liver function tests on January 16, 2022. It is noteworthy that it left untreated, this condition could progress to obstruction, but significant improvement was achieved post-treatment. Abdominal MRI further confirmed enhancing signal foci in the caudate lobe alongside prominently enlarged and enhanced lymph nodes in the hepatic hilum (Figure 1). The timeline of key imaging findings and corresponding lesion characteristics are detailed in Table 2. Table 3 summarizes the diagnosis and treatment process of this case, outlining the chronological steps from initial presentation to final diagnosis and therapy initiation.

Figure 1 Computed tomography and magnetic resonance imaging images of the liver. A: Sagittal plane showing lesions in the caudal lobe region (arrow); B: Axial position of lesions in the caudal lobe region (arrow); C: Coronal view showing lesions in the caudal lobe region and enlarged lymph nodes below the caudal lobe (arrow); D: Multiple enlarged lymph nodes in the portal space; E: Lesion in caudal lobe region (T1 sequence) (arrow); F: Multiple enlarged lymph nodes in the portal space on T1 sequence (slightly prolonged T2 signal nodules, partially fused) (arrow); G: Caudal lobe region lesion (T2 sequence); H: Multiple enlarged lymph nodes in the portal space on T2 sequence (slightly prolonged T2 signal nodules, partially fused) (arrow); I: Lesion in the caudal lobe region on the enhanced sequence, appearing as a circular enhancement (coronal plane) (arrow); J: Enlarged lymph nodes in the portal space with high signal intensity on diffusion-weighted imaging (arrow).

Table 2 Timeline of imaging findings and lesion characteristics.

Date	Modality	Lesion size	Imaging features
January 17, 2022	MRCP	Approximately 28 mm	Abnormal signal focus in the caudate lobe, associated with bile duct stenosis and proximal biliary dilation. Enlarged hilar lymph nodes
January 18, 2022	Abdominal CT	Approximately 20 mm	Subtle hypodense lesion in the caudate lobe with mild enhancement. Enlarged lymph nodes in the hepatic hilum and retroperitoneum with ring enhancement
January 20, 2022	Abdominal MRI	Approximately 26 mm	Irregular, mixed-signal foci in the caudate lobe with mildly prolonged T1/T2 signals, diffusion restriction, and ring enhancement. Markedly enlarged and enhanced lymph nodes in the hepatic hilum
January 24, 2022	Abdominal ultrasound	50.5 mm × 25.5 mm	Hypoechoic mass in liver segment I (S1), with internal hyperechoic changes, seen encircling the portal vein

MRI: Magnetic resonance imaging; CT: Computed tomography; MRCP: Magnetic resonance cholangiopancreatography.

Table 3 Diagnosis and treatment process of this case.

Date	Action	Outcome
January 16, 2022	Hospital admission	Admitted with a 5-day history of epigastric pain
January 16-18, 2022	Initial laboratory and imaging investigations	Elevated liver enzymes (ALT 295 U/L AST170U/L). CT/MRCP identified a 20-28 mm hypodense lesion in the caudate lobe with enlarged, rim-enhancing lymph nodes
January 20, 2022	Abdominal MRI with contrast	Confirmed irregular mixed-signal foci in the caudate lobe
January 24, 2022	EUS-FNA	Tissue samples obtained from the liver lesion and adjacent lymph nodes
January 24, 2022	Cytological examination report	Specimen showed necrotic background with lymphocytes, multinucleated giant cells, and epithelioid cells
January 26, 2022	Gene-Xpert (MTB/RIF)	Mycobacterium tuberculosis DNA detected (low levels). No rifampicin resistance detected
January 27, 2022	Antitubercular therapy initiated	Standard HRZE regimen initiated (isoniazid, rifampin, ethambutol, pyrazinamide)
January 28, 2022	Pathological and genetic	Histopathology confirmed granulomatous inflammation with necrosis. TB RT-PCR was positive
January 30, 2022	Hospital discharge	Discharged in stable condition on anti-TB medications
May 10, 2022	Outpatient follow-up visits	The treatment compliance was good, and no significant adverse reactions were reported. Ultrasound showed a 2.5 cm × 1.7 cm slightly hypoechoic area in the caudate lobe of the liver; Another 1.5 cm × 1.2 cm slightly high echo area can be seen
Monthly	Outpatient follow-up visits	Good treatment compliance with no significant adverse effects reported
November 17, 2023	Final imaging follow-up	Ultrasound confirmed complete resolution of the liver lesion, indicating clinical cure
November, 2023	Completion of anti-TB therapy	Total treatment duration: 22 months

TB: Hepatic tuberculosis; RT-PCR: Reverse transcription-polymerase chain reaction; HRZE: Isoniazid, rifampicin, pyrazinamide, and ethambutol; CT: Computed tomography; MRCP: Magnetic resonance cholangiopancreatography; MRI: Magnetic resonance imaging; EUS-FNA: Endoscopic ultrasound-guided fine-needle aspiration biopsy; ALT: Alanine transaminase.

FINAL DIAGNOSIS

For histopathological evaluation, an endoscopic ultrasound-guided liver biopsy was performed on January 24, 2022 (Figure 2). The procedure used a linear Olympus echoendo-scope (GF-UCT 240) and a 22G needle (EchoTip Ultra, Cook Medical) to target the hypoechoic lesion in the caudate lobe. The modified wet-suction technique was employed: The stylet was removed, the needle lumen was pre-flushed with saline, and aspiration was then performed using a 5-mL syringe with pre-applied negative pressure. Each pass consisted of 20 to-and-fro needle movements within the target, for a total of four passes. Cytological examination revealed a necrotic background with abundant lymphocytes, multinucleated giant cells, and epithelioid cells (Figure 3). Histopathological examination revealed caseating granulomas, a hallmark feature of TB. Subsequent analysis of the specimens demonstrated a positive acid-fast bacilli (AFB) stain, and detection of Mtb DNA by Xpert MTB/RIF Ultra assay targeting the IS6110 gene, with no rifampicin resistance identified. The collective findings—characteristic granulomatous morphology, positive AFB stain, and molecular confirmation—establish a definitive diagnosis of TB.

Figure 2 Endoscopic ultrasound-guided fine-needle aspiration biopsy procedure. A: Ultrasound image of the liver (S1 segment) showing a lesion characterized by low-level echoes, measuring approximately 50.5 mm × 25.5 mm (arrow). Internal changes, including high-intensity echoes, were observed within the lesion. It was observed that the lesion surrounded the portal vein and its confluence and was in proximity to the lower segment of the hepatic portal vein. The surrounding low-intensity lymph nodes appear dispersed; B and C: Ultrasound-guided puncture at the lesion site (arrow); D: Perifocal lymph node puncture (arrow).

Figure 3 Pathological images of liver biopsy specimens (× 100). Scattered granulomatous nodules with small areas of focal necrosis observed within the lesion tissue.

TREATMENT

The patient was started on standard daily oral quadruple antitubercular therapy, consisting of rifampicin (0.45 g, 6.25 mg/kg), isoniazid (0.3 g, 4.17 mg/kg), ethambutol (0.75 g, 10.42 mg/kg), and pyrazinamide (0.75 g, 10.42 mg/kg). During the treatment period, close monitoring of patient compliance through monthly outpatient visits showed good compliance. Through a series of liver function tests and symptom investigations, no significant adverse reactions were observed throughout the process, especially drug induced toxic reactions.

OUTCOME AND FOLLOW-UP

The patient maintained stable vital signs throughout the treatment course, with regular monthly outpatient visits confirming full treatment adherence. The decision to extend anti-TB treatment to a total of two years was based on guideline recommendations, which allow for modification of treatment duration according to individual response, due to the slow regression observed on serial imaging[4]. The medication regimen was well tolerated without significant hepatic or renal toxicity. Serial imaging revealed a gradual regression of the liver lesion. After anti-TB treatment, the anti-TB medications were discontinued. Follow-up ultrasound on November, 2023 confirmed complete resolution of the lesion, indicating clinical cure. The patient reported complete relief of abdominal pain, no obvious discomfort, normal appetite and bowel habits, and physical activity returning to pre-disease levels, indicating good functional recovery.

DISCUSSION

TB is one of the most common chronic infectious diseases in Asia and Africa, primarily presenting as pulmonary TB. Hepatic TB is a rare condition and frequently manifests as a secondary infection following primary involvement of other organs, particularly the lungs or intestines. Hepatic TB develops when Mtb disseminates to the liver via hematogenous or lymphatic routes[5]. Clinically, it often presents with nonspecific symptoms, necessitating differentiation from common hepatic pathologies, including liver metastases, hepatocellular carcinoma, and liver abscesses[6]. The intrinsic defenses of the liver, including abundant macrophages and CD8+ T cells with potent phagocytic and regenerative capacities, alongside the inhibitory effect of bile on Mtb growth, hinder the possibility of typical (TB) lesion formation[7]. These factors collectively contribute to the rarity of hepatic TB, which remains predominantly reported in case reports rather than large clinical series.

Compared with previously reported cases in the literature, the present case shares similarities but also exhibits distinct differences. Compared with previous reports on solitary hepatic tuberculoma, our patient was young and immunocompetent, presented with local abdominal pain but lacked systemic symptoms such as fever, and had no history of TB or evidence of pulmonary or intestinal involvement. CT imaging demonstrated a hypodense lesion in the caudate lobe of the liver (Figure 1A-C), along with an enlarged and increased number of lymph nodes in the hepatic hilum and retroperitoneum exhibiting ring-like enhancement (Figure 1D, F, H, and J). Owing to the challenging anatomical location of the lesion, percutaneous biopsy was not feasible; therefore, an EUS-FNA was performed (Figure 2). Histopathological analysis of the obtained tissue revealed scattered granulomatous inflammation with focal necrosis areas (Figure 3). A positive Mtb genetic test confirmed the diagnosis of hepatic TB. However, the tuberculosis spot test (T-SPOT) results of blood and liver are negative, indicating that in some isolated cases, T-SPOT may be negative, so it should not be solely relied upon for diagnosis. Although immunological tests, such as the tuberculin skin test and interferon-γ release assays, provide diagnosis information, their inability to distinguish latent infection from active disease limits their diagnostic specificity and sensitivity in hepatic tuberculoma[8]. This underscores the limitation of relying solely on immunological tests for diagnosis in such atypical presentations and highlights the critical role of histopathology and molecular confirmation.

Clinical manifestations and physical signs of hepatic TB are nonspecific and may include low-grade fever, night sweats, right upper quadrant abdominal pain, weight loss, hepatomegaly, and jaundice[9]. Laboratory tests may reveal anemia and elevated erythrocyte sedimentation rate and C-reactive protein levels[10], alongside mild liver function abnormalities. The primary pathological changes in hepatic TB are chronic granulomas, which may present as caseous necrosis, liquefactive necrosis, fibrosis, or calcification at different disease stages[11]. These changes reflect the host immune response to Mtb[12]. Radiological manifestations of hepatic TB also vary according to the underlying pathological status.

A literature review indicates that hepatic TB can be sonographically classified into the following four types: Diffuse, mass-forming, abscess, and calcific lesions. Owing to the nonspecific clinical and imaging features, hepatic TB is often misdiagnosed or overlooked in clinical practice. Establishing diagnostic criteria based on common sonographic patterns may facilitate recognition. Ultrasound examination may reveal lesions with variable echogenicity, including hypoechoic, mixed, anechoic, and hyperechoic patterns with acoustic shadows. In early granulomatous lesions without caseous or liquefactive necrosis, contrast-enhanced ultrasound often shows arterial-phase hyperenhancement with delayed-phase washout. If caseous or liquefactive necrosis develops, the necrotic area typically shows no enhancement in any phase, while the surrounding tissue may exhibit arterial- or portal-venous-phase nodular or rim enhancement owing to inflammatory cell infiltration or fibrosis[13]. Ultrasound also facilitates lesion localization and characterization and provides real-time guidance for targeted biopsy, improving sampling accuracy and reducing the risks associated with blind puncture[13].

In this case, ultrasound revealed a hypoechoic mass in the S1 segment of the liver, measuring approximately 50.5 mm × 25.5 mm, with internal hyperechoic changes, consistent with caseous necrosis. On non-contrast CT, hepatic TB lesions typically appear as hypodense areas. CT typically shows little or no arterial-phase enhancement with mild portal-venous-phase enhancement in granulomatous lesions. In early granuloma stages, perilesional inflammation may result in congestion and edema, appearing as a “halo sign” on post-contrast images. This reactive border, which is often incorporated into the hypoechoic area visualized by ultrasound but may not be fully captured by CT, likely accounts for the larger lesion size measured on ultrasonography[3]. In cases with caseous or liquefactive necrosis, rim enhancement or complete absence of enhancement may be observed, occasionally accompanied by peripheral parenchymal perfusion abnormalities[14]. On MRI, early granulomas exhibit T1 and T2 hyperintensities, while fibrotic stages demonstrate low signal on T1- and T2-weighted sequences. Post-contrast enhancement may appear at the margins or be entirely absent[15]. The MRI findings in this case demonstrated irregular, mixed, mildly T1- and T2-prolonged signal foci in the caudate lobe, consistent with that of the granulomatous stage of hepatic TB.

The imaging differential diagnosis of hepatic tuberculoma mainly includes hepatocellular carcinoma, intrahepatic cholangiocarcinoma, hepatic lymphoma, and other benign and malignant hepatic tumors. This overlap frequently contributes to misdiagnosis and even unnecessary surgical resection[16]. Hepatocellular carcinoma frequently manifests as marked arterial-phase enhancement with rapid washout in the portal-venous and delayed phases. This is often in the setting of cirrhosis; elevated alpha-fetoprotein levels are important ancillary diagnostic indicators[17]. Intrahepatic cholangiocarcinoma presents as an irregularly shaped hypodense mass with heterogeneous enhancement on contrast-enhanced imaging, often accompanied by bile duct dilatation[18]. Liver lymphoma presents with variable imaging features, commonly appearing as low- or iso-dense masses with minimal enhancement after contrast administration, and it is frequently associated with enlarged extrahepatic lymph nodes[19].

Histopathological examination of needle biopsy specimens remains the gold standard for diagnosing and differentiating hepatic TB[20]. Simultaneously, a molecular test for Mtb further confirms the diagnosis. The definitive diagnosis in our case, achieved through EUS-FNA, directly led to the initiation of successful antitubercular therapy, thereby avoiding an unnecessary surgical intervention. This sequence underscores the critical causal link between obtaining adequate tissue for histology and polymerase chain reaction (PCR) and achieving a favorable non-surgical outcome.

But as a single-case study from a single institution, it lacks the statistical power to establish generalizable conclusions about disease prevalence or treatment efficacy. The diagnostic approach was influenced by the lesion’s anatomical location in the caudate lobe (Figure 1A-C), which made EUS-FNA (Figure 2) the preferred biopsy method over percutaneous approaches. This selection bias limits comparisons with cases where different biopsy techniques were employed. A summary of findings from other case reports of liver TB is provided in Table 4[5,21-32].

Table 4 Summary of case reports of liver tuberculosis.

No.	Ref.	Age	Immune status	Lesion location	Diagnostic method	IGRA result	Treatment duration	Outcome
1	Chen et al[21], 2003	56	Hepatitis C-related liver cirrhosis and end-stage renal disease	Liver segments IV, V	Ultrasound-guided biopsy	Not mentioned	Isoniazid, rifampicin, pyrazinamide, ethambutol for 6 months	Good recovery, asymptomatic at 1-year follow-up
2	Culafic et al[22], 2005	57	Immunocompetent	Liver segments III, IV and peritoneum	Laparoscopic biopsy	Not mentioned	Isoniazid, rifampicin and pyrazinamide for 12 months	Good recovery
3	Köksal et al[23], 2006	48	Diabetes mellitus	Posterior segment of right hepatic lobe	Ultrasound-guided percutaneous biopsy	Not mentioned	Isoniazid, rifampicin for 9 months; morphine floxacin, ethambutol for 3 months	Cure, abscess reduced in size
4	Kharrasse et al[5], 2014	44	Benign gastroesophageal reflux disease	Hepatic SVIII segment	Liver biopsy	Not mentioned	Isoniazid, rifampicin, ethambutol, and pyrazinamide for 2 months, then isoniazid, rifampicin, and ethambutol for 4 months	Good recovery
5	Zhang et al[24], 2014	30	Hepatitis B history, pulmonary tuberculosis	Liver (multiple nodules)	CT-guided fine needle aspiration biopsy	Not mentioned	Rifampicin, isoniazid, pyrazinamide, ethambutol, plus prednisone and dioxacin for 1 year	Recovery, weight gain, normal CT at 6 months
6	Liao et al[25], 2015	40	Immunocompetent	Lung and liver	CT-guided percutaneous biopsy of the lung and liver	Not mentioned	INH, RFP, PZA, EMB (HRZE)	Symptoms relieved
7	Dawani et al[26], 2018	32	Immunocompetent	Liver and spleen	Ultrasound-guided fine needle aspiration biopsy	Quantiferon-TB test negative	Anti-tuberculous therapy for 6 months	Recovery, weight gain, ultrasound normal at 15-month follow-up
8	Ai et al[27], 2018	45	Immunocompetent	Liver (multiple masses)	Next-generation sequencing of liver tissue and ultrasound-guided biopsy	T-SPOT, TB positive	Rifampicin, isoniazid, ethambutol, pyrazinamide, levofloxacin	Symptom resolution, asymptomatic at 8-week follow-up
9	Liang et al[28], 2018	58	Immunocompetent	Pancreas and liver	CT-guided fine needle aspiration biopsy of hepatic lesion	Not mentioned	Rifampicin, isoniazid, pyrazinamide, ethambutol for 2 months, then rifampicin and isoniazid for 4 months	Symptom resolution, asymptomatic at 2-year follow-up
10	Haque et al[29], 2019	58	Immunocompetent	Liver and gallbladder region	Peroperative frozen section biopsy	Not mentioned	Anti-tuberculous treatment for 1 year	Improvement, symptoms disappeared, weight gain
11	Pang et al[30], 2019	15	Immunocompetent	Hilar region of the liver	Postoperative pathological examination	The results of TBAB and T-SPOT were negative	Systemic anti tuberculosis treatment, a total of 6 months	Symptoms disappeared completely
12	Alsaif et al[31], 2021	47	Immunocompetent	Liver (HCC and tuberculosis co-existing)	CT-guided biopsy	Not mentioned	Rifampicin, isoniazid, ethambutol, levofloxacin; duration not specified	Clinical improvement, fever resolved, tumor not resected
13	Hao et al[32], 2023	38	Hepatitis B history, hepatobiliary adenocarcinoma	Liver	Postoperative pathology	Not mentioned	Standard antituberculous treatment for 1 year	Recovery well
14	Hao et al[32], 2023	51	Immunocompetent	Liver	Laparoscopic biopsy	Not mentioned	Rifampicin, isoniazid, pyrazinamide, ethambutol for 2 months, then rifampicin and isoniazid for 4 months	Abdominal pain resolved, good outcome

IGRA: Interferon-gamma release assay; INH: Isoniazid; RFP: Rifampicin; PZA: Pyrazinamide; EMB: Ethambutol; HRZE: Isoniazid, rifampicin, pyrazinamide, ethambutol; CT: Computed tomography; T-SPOT: Enzyme-linked immunospot assay for T cells for Mycobacterium tuberculosis infection; TB: Tuberculosis.

CONCLUSION

The clinical presentations and signs of hepatic TB are often nonspecific. EUS-FNA is a safe and highly effective diagnostic tool. In this case, histopathological and molecular examination confirmed TB despite negative T-SPOT results. If histological assessment reveals hepatocyte swelling, architecture distortion, epithelioid cells, or Langhans giant cells[33], further differentiation from malignant tumors is essential. Molecular testing for Mtb nucleic acids should be performed concurrently to confirm the diagnosis. In similar cases, tissue sampling should not be delayed, and prompt initiation of antitubercular therapy is essential for successful outcomes as early diagnosis and treatment are associated with a favorable prognosis. However, untreated hepatic TB may lead to severe complications, including liver failure, hepatic rupture, or secondary infections. Additionally, outcomes can significantly worsen in patients with underlying cirrhosis or immunosuppression, in whom disease progression can be rapid[34]. Figure 4[4,35] summarizes the diagnosis and treatment process of liver TB based on current guidelines and relevant case reports.

Figure 4 Diagnosis and treatment process of hepatic tuberculosis. ALP: Alkaline Phosphatase; BDLLfxC: Bedaquiline, delamanid, linezolid, levofloxacin, cycloserine; BPaLM: Bedaquiline, pretomanid, linezolid, moxifloxacin; CRP: C-Reactive protein; CT: Computed tomography; DR-TB: Drug-resistant tuberculosis; DS-EPTB: Drug-susceptible extrapulmonary tuberculosis; ESR: Erythrocyte sedimentation rate; EUS-FNA: Endoscopic ultrasound-guided fine-needle aspiration; GGT: Gamma-glutamyl transferase; IGRA: Interferon-gamma release assay; LC-aNAAT: Lipoarabinomannan-capture nucleic acid amplification test; MRI: Magnetic resonance imaging; MTB: Mycobacterium tuberculosis; Pre XDR-TB: Pre-extensively drug-resistant tuberculosis; TBST: Tuberculin skin test; US: Ultrasonography; RIF Ultra: Rifampicin ultra; H: Isoniazid; R: Rifampicin; Z: Pyrazinamide; E: Ethambutol; P: Protionamide; M: Moxifloxacin.