Computed tomography characteristics of hepatic involvement secondary to tuberculous peritonitis: a case series
Letter to the Editor

Computed tomography characteristics of hepatic involvement secondary to tuberculous peritonitis: a case series

Ke-Xin Li1#, Jing-Liang Liu2#, Ying Pu1, Min Qi1, Jia-Lu Wei1, Xu-Wen Fu3, Xiang Li1

1Department of Radiology, Kunming Third People’s Hospital, Yunnan Clinical Medical Center for Infectious Diseases, Kunming, China; 2Department of Radiology, The People’s Hospital of Lincang, Lincang, China; 3Department of Clinical Pharmacy, Kunming Third People’s Hospital, Yunnan Clinical Medical Center for Infectious Diseases, Kunming, China

#These authors contributed equally to this work.

Correspondence to: Xiang Li, MM. Department of Radiology, Kunming Third People’s Hospital, Yunnan Clinical Medical Center for Infectious Diseases, No. 319 of Wujing Street, Guandu District, Kunming 650041, China. Email: lixianglxlxiang@126.com; Xu-Wen Fu, MB. Department of Clinical Pharmacy, Kunming Third People’s Hospital, Yunnan Clinical Medical Center for Infectious Diseases, No. 319 of Wujing Street, Guandu District, Kunming 650041, China. Email: xuwen_fufxw@outlook.com.

Submitted Sep 24, 2025. Accepted for publication Jan 20, 2026. Published online Feb 11, 2026.

doi: 10.21037/qims-2025-2059

Introduction

Tuberculosis (TB) is an infectious disease caused by Mycobacterium tuberculosis that can affect multiple organ systems and continues to represent a major global public health challenge. In 2023, approximately 10.8 million new TB cases were reported worldwide. China, recognized as a high-burden country, accounted for an estimated 740,000 new cases and 27,000 deaths (1).

Hepatic tuberculosis (HTB) constitutes a rare form of extrapulmonary tuberculosis (EPTB). The relatively low incidence of HTB is attributed to the phagocytic function of Kupffer cells within the liver. In non-immunosuppressed populations, HTB represents approximately 0.4% of all TB cases (2) and 1–3.5% of EPTB cases (2,3). In contrast, regions with a high prevalence of human immunodeficiency virus (HIV) infection demonstrate an increased incidence of HTB (4), leading to renewed attention in both clinical and public health contexts.

The pathogenesis of HTB primarily involves hematogenous dissemination, though direct invasion from adjacent lesions can also occur (5,6). Perihepatic peritoneal TB is closely associated with tuberculous peritonitis (TP) (7), but the mechanisms of progression to hepatic involvement are not well characterized. Therefore, we conducted a single-center, retrospective case series to explore and describe this potential progression by analyzing the clinical and serial computed tomography (CT) imaging data of patients with TP who subsequently developed HTB at Kunming Third People’s Hospital between December 2019 and October 2024. Their clinical courses and CT findings were evaluated to describe the radiological features that suggest contiguous progression from TP to HTB.

Methods

This retrospective case series was conducted at Kunming Third People’s Hospital and approved by the Institutional Review Board. We reviewed the medical records of patients diagnosed with TP between December 2019 and October 2024. The diagnosis of TP was established based on the following composite criteria: (I) clinical presentation with ascites, fever, or abdominal pain; (II) imaging findings suggestive of peritoneal involvement (nodularity, thickening, omental caking, or lymphadenopathy); (III) ascitic fluid analysis showing lymphocytic exudate with elevated adenosine deaminase (ADA) levels (>40 U/L) or positive mycobacterial culture/polymerase chain reaction (PCR); and (IV) exclusion of other causes (malignancy, pyogenic infection, etc.). Patients with microbiological/histological confirmation (ascites culture, biopsy) were classified as definite TB, whereas those meeting clinical imaging criteria with therapeutic response were classified as probable TB. For hepatic lesions, the diagnosis of tuberculous involvement was based on the following criteria: (I) temporal association with known TP (lesions appearing during or after TP diagnosis); (II) contiguous anatomical relationship with peritoneal disease (direct extension from perihepatic peritoneum or along Glisson’s capsule); (III) imaging characteristics [hypodense lesions on CT, T2 hyperintensity on magnetic resonance imaging (MRI), peripheral enhancement, or restricted diffusion]; and (IV) exclusion of alternative diagnoses (pyogenic abscess, fungal infection, malignancy, drug-induced injury) based on clinical context, laboratory findings, and imaging evolution. Given the retrospective nature and lack of pathological confirmation, these lesions were classified as “presumed tuberculous involvement” rather than definite TB. All patients received and were documented to be adherent to standard first-line anti-TB therapy [HRZE (isoniazid, rifampin, pyrazinamide, and ethambutol) regimen] throughout the observation period, as assessed by direct questioning and pill counts during follow-up visits. No changes to the core therapeutic regimen were made in response to the development of the new hepatic lesions.

Measurement of CD4+ and CD8+ T-lymphocyte counts was not part of a standardized protocol for all patients with TP at our institution during the study period. Instead, these tests were performed at the discretion of the treating physicians, typically in patients presenting with more severe clinical manifestations, signs of immunosuppression, or for baseline assessment prior to considering corticosteroid therapy.

Image acquisition

All contrast-enhanced CT examinations included arterial, portal venous, and delayed phases. The timing for each phase was determined using a bolus-tracking technique, with the arterial phase triggered 5–8 seconds after the attenuation in the abdominal aorta at the level of the celiac artery reached 100 Hounsfield units (HU). This typically resulted in scan initiation at 25–35 seconds (arterial phase), 60–70 seconds (portal venous phase), and 150–180 seconds (delayed phase) after the start of contrast injection. A weight-based dose of 1.5 mL/kg body weight of iodinated contrast medium (Loversol, Jiangsu Hengrui, Lianyungang, China) was administered intravenously at a flow rate of 3.0–3.5 mL/s via a power injector, followed by a 20-mL saline flush. Axial images were reconstructed with a slice thickness of 1.25 mm for multiplanar reformation (MPR) and review.

Image analysis

CT images were independently reviewed by two radiologists (with 10 years of experience in abdominal imaging) who were blinded to the clinical course and timing of the scans during the initial assessment. Discrepancies were resolved by consensus with a third senior radiologist (with over 15 years of experience). The following imaging features were prospectively evaluated for both the peritoneum and the hepatic lesions:

Location and distribution

Site of peritoneal thickening (e.g., perihepatic, omental, parietal) and location of hepatic lesions (segmental distribution relative to Couinaud’s classification).

Morphology and attenuation

Size (long-axis diameter in mm), shape (nodular, fusiform, irregular), and attenuation (hypodense, isodense, hyperdense relative to hepatic parenchyma) on unenhanced and contrast-enhanced phases.

Enhancement characteristics

Pattern of enhancement was specifically categorized as: (I) rim enhancement (peripheral enhancement with central hypodensity); (II) homogeneous enhancement; (III) heterogeneous enhancement (further specified as septal, nodular, or without a specific pattern); (IV) transient hepatic attenuation difference (THAD). The presence of a “capsular breach”—defined as loss of the linear hypodense plane between a perihepatic lesion and the hepatic parenchyma—and direct continuity between perihepatic collections and hepatic nodules were specifically assessed.

Temporal evolution

The sequential changes on serial CT scans were meticulously recorded, including the initial appearance of perihepatic peritoneal thickening, subsequent development of perihepatic loculated fluid collections, and the eventual formation of hepatic parenchymal nodules, along with their evolution in size and enhancement pattern over time.

Case presentation

Case 1

A 22-year-old male was admitted to Kunming Third People’s Hospital on 24 December 2019 with a 20-day history of abdominal distension. The patient had initially presented to a local facility, where an abdominal CT revealed massive ascites. Laparoscopic peritoneal biopsy demonstrated chronic granulomatous inflammation consistent with TP.

On admission, physical examination revealed abdominal distension, diffuse tenderness, and positive shifting dullness. Laboratory findings were shown in Table 1.

Table 1

Abdominal symptoms, laboratory findings, and time to hepatic involvement in seven patients

Case Abdominal symptoms WBC NEU LYM ESR CRP ALB PAB CD4 CD8 T-SPOT Time
1 Abdominal distension Low Normal Normal High High Low Normal Low Normal Positive 3 months
2 Abdominal distension, abdominal pain Low Normal Low Normal Normal Low Normal Low Low Positive 3 months
3 Abdominal pain Normal Normal Low High High Low Low Low Low Positive 3 months
4 None Low Low Normal Normal Normal Low Normal Low Normal Positive 7 months
5 Abdominal distension, abdominal pain Normal Normal Low High High Low Low Low Low Positive 3 months
6 Abdominal pain, diarrhea Normal Normal Low High High Low Low Low Low Positive 1.5 months
7 None Normal Normal Low High High Low Low Low Normal Positive 4 months

Time, time from initial presentation to CT demonstrating of hepatic lesions. ALB, serum albumin level; CD4, CD4+ T-cell count; CD8, CD8+ T-cell count; CRP, C-reactive protein; ESR, erythrocyte sedimentation rate; LYM, lymphocyte count; NEU, neutrophil count; PAB, serum prealbumin level; WBC, white blood cell count.

A chest CT on December 26, 2019, showed no abnormalities. Abdominal CT demonstrated thickening and enhancement of the peritoneum and omentum, mild perihepatic peritoneal thickening with enhancement, and both free and loculated ascites (Figure 1A,1B). A diagnosis of TP was established, and treatment with HRZE regimen in combination with corticosteroid therapy, was initiated. The patient was discharged on 18 January 2020.

Figure 1 Contrast-enhanced abdominal CT in a 22-year-old male with TP. (A,B) Portal venous phase images obtained on 26 December 2019 show mild perihepatic peritoneal thickening and enhancement (white arrow). (C,D) Portal venous phase images obtained on 10 March 2020 demonstrate marked progression of perihepatic peritoneal thickening (white arrows) with new heterogeneously enhancing nodular lesions in the left and right hepatic lobes (hollow white arrows). CT, computed tomography; TP, tuberculous peritonitis.

During continuation of anti-TB therapy, a follow-up CT was conducted on 10 March 2020 (Figure 1C,1D).

Case 2

A 45-year-old female was admitted to Kunming Third People’s Hospital on 24 June 2020 with a 2-month history of abdominal distension and pain. The symptoms had occurred spontaneously, without identifiable precipitating factors, and had intermittently resolved.

On admission, physical examination revealed a soft abdomen with periumbilical tenderness and positive shifting dullness. The results of laboratory investigations are demonstrated in Table 1.

Chest and abdominal CT were performed on 29 June 2020 (Figure 2A). The patient was diagnosed with both secondary pulmonary TB and TP. Anti-TB therapy with HRZE regimen combined with corticosteroid therapy was initiated. The patient was discharged on 8 July 2020.

Figure 2 Contrast-enhanced abdominal CT in a 45-year-old female with secondary pulmonary TB and TP. (A) Portal venous phase image on 29 June 2020 showing left pleural effusion, ascites, perihepatic peritoneal thickening and enhancement (white arrow), and rim-enhancing loculated fluid in the perihepatic space. (B) Portal venous phase image on 30 September 2020 demonstrating left pleural effusion and ascites, marked progression of perihepatic peritoneal thickening (white arrow), enlarged perihepatic loculated fluid, and a new heterogeneously enhancing nodule in the right anterior hepatic lobe (hollow white arrow). (C) Portal venous phase image on 3 February 2021 showing further progression of perihepatic peritoneal thickening (white arrow) and enlargement of the heterogeneously enhancing nodule in the right anterior hepatic lobe (hollow white arrow). CT, computed tomography; TB, tuberculosis; TP, tuberculous peritonitis.

During continuation of anti-TB therapy, follow-up CT was conducted on 30 September 2020 (Figure 2B). A repeat CT was scheduled on 3 February 2021 (Figure 2C).

Case 3

A 23-year-old male was admitted to Kunming Third People’s Hospital on 30 July 2020 with a 1-week history of fever, cough, and abdominal pain. The patient had experienced a fever of unknown etiology one week prior, with a maximum temperature of 39.1 ℃, accompanied by paroxysmal dry cough, abdominal distension, and fatigue. On admission, physical examination revealed a soft abdomen with diffuse tenderness without rebound pain. Laboratory findings are presented in Table 1.

Chest and abdominal CT were performed on 20 August 2020 (Figure 3A,3B). The diagnoses were (I) secondary pulmonary TB, (II) TP, (III) TB lymphadenitis of abdominal lymph nodes, and (IV) renal TB. Anti-TB treatment with the HRZE regimen in combination with corticosteroid anti-inflammatory therapy was initiated. The patient was discharged on 11 September 2020.

Figure 3 Contrast-enhanced abdominal CT in a 23-year-old male with secondary pulmonary TB, TP, abdominal lymph node TB, and renal TB. (A,B) Portal venous phase images on 20 August 2020 showing marked peritoneal and omental thickening with enhancement, and significant perihepatic peritoneal thickening and enhancement (white arrows). (C,D) Portal venous phase images on 13 November 2020 demonstrating localized perihepatic peritoneal thickening (white arrows) with new heterogeneously enhancing nodules in the posterior segment of the right hepatic lobe and in the left hepatic lobe (hollow white arrows). CT, computed tomography; TB, tuberculosis; TP, tuberculous peritonitis.

During continuation of anti-TB therapy, a follow-up CT was conducted on 23 September 2020. A repeat CT was scheduled on 13 November 2020 (Figure 3C,3D).

Case 4

A 17-year-old female was admitted on 27 January 2024 with a 3-day history of fever and headache during ongoing anti-TB therapy of 3 months’ duration. She had been hospitalized locally with fever 3 months earlier. A chest CT at that time revealed right pleural effusion, and a thoracoscopic pleural biopsy demonstrated chronic granulomatous inflammation with caseous necrosis, consistent with pleural TB. The HRZE regimen was initiated.

At 3 days before admission, fever recurred with a maximum temperature of 38.0 ℃. On admission, physical examination recorded a body temperature of 38.3 ℃ and diminished breath sounds in the right lower lung. The laboratory findings are included in Table 1.

Chest and abdominal CT were conducted on 30 January 2024 (Figure 4A,4B). The diagnoses were as follows: (I) secondary pulmonary TB and (II) TP. The HRZE regimen with adjunctive corticosteroid anti-inflammatory treatment was continued. Follow-up CT scans were conducted on 20 August 2024 (Figure 4C,4D).

Figure 4 Contrast-enhanced abdominal CT in a 17-year-old female with secondary pulmonary TB and TP. (A,B) Portal venous phase images on 30 January 2024, showing perihepatic peritoneal thickening and enhancement (white arrow in B) with focal nodular changes (white arrow in A). (C,D) Portal venous phase images on 20 August 2024 demonstrating improvement of the nodular perihepatic peritoneal thickening (C) with a new heterogeneously enhancing nodule in the posterior segment of the right hepatic lobe (hollow white arrow in D). CT, computed tomography; TB, tuberculosis; TP, tuberculous peritonitis.

Case 5

A 51-year-old female was admitted on 1 February 2024 with a 6-month history of abdominal distension, abdominal pain, and intermittent low-grade fever, with exacerbation of symptoms during the preceding month. Six months earlier, abdominal distension and pain of unknown etiology, accompanied by occasional low-grade fever (maximum temperature 37.8 ℃) had developed. No medical evaluation was pursued until 1 month before admission, when the abdominal distension worsened. Abdominal ultrasound revealed massive ascites, and CT demonstrated irregular peritoneal thickening. Laparoscopic peritoneal biopsy indicated granulomatous inflammation with positive TB DNA.

On physical examination, coarse breath sounds were present bilaterally, with abdominal distension, absence of abdominal tenderness, and no rebound pain. The results of laboratory testing are shown in Table 1.

Chest and abdominal CT were performed on 23 February 2024 (Figure 5A,5B). The patient was diagnosed with secondary pulmonary TB and TP. The patient received an HRZE regimen with corticosteroid anti-inflammatory therapy, which resulted in symptomatic improvement. The patient was discharged on 1 March 2024.

Figure 5 Contrast-enhanced abdominal CT in a 51-year-old female with secondary pulmonary TB and TP. (A,B) Portal venous phase images on 23 February 2024 showing peritoneal and omental thickening with enhancement (white arrow in A), nodular perihepatic peritoneal thickening and enhancement (hollow white arrow in A, white arrow in B), and compression with congestion of the adjacent hepatic parenchyma (hollow white arrow in B). (C,D) Portal venous phase images on 28 May 2024 demonstrating marked progression of perihepatic peritoneal thickening (white arrows) with new heterogeneously enhancing nodular lesions in the left and right hepatic lobes (hollow white arrows). CT, computed tomography; TB, tuberculosis; TP, tuberculous peritonitis.

During ongoing anti-TB therapy, the patient was readmitted on 28 May 2024 due to recurrent abdominal pain. Chest and abdominal CT scans were scheduled (Figure 5C,5D).

Case 6

A 21-year-old male was admitted with a 1-year history of intermittent diarrhea and a 3-month history of abdominal pain, cough, and dyspnea, which had worsened with fever during the preceding month. Intermittent diarrhea had initially developed 1 year earlier, without systematic treatment. Three months before admission, cough (predominantly dry) and dyspnea developed. Thoracentesis had been performed at another hospital, and the pleural fluid culture was positive for M. tuberculosis. Treatment with the HRZE regimen was initiated, and the patient was discharged. One month before admission, a fever developed, with a maximum recorded temperature of 38.5 ℃.

On physical examination, diminished breath sounds were noted in the right lung, along with abdominal distension and positive shifting dullness. The results of laboratory investigations are displayed in Table 1.

Chest CT and abdominal CT were conducted on 3 September 2024 (Figure 6A,6B).

Figure 6 Contrast-enhanced abdominal CT in a 21-year-old male with pleural TB and TP. (A,B) Portal venous phase images on 3 September 2024 showing perihepatic peritoneal thickening and enhancement with rim-enhancing loculated fluid in the perihepatic space (white arrows). (C,D) Portal venous phase images on 22 October 2024 demonstrating marked progression of perihepatic peritoneal thickening (white arrows) with multiple new round heterogeneously enhancing nodules in the right and left hepatic lobes (hollow white arrows). CT, computed tomography; TB, tuberculosis; TP, tuberculous peritonitis.

The patient was diagnosed with pleural TB and TP. The HRZE regimen with adjunctive corticosteroid therapy was continued, leading to symptomatic improvement, and the patient was discharged on 22 September 2024.

During ongoing anti-TB therapy, a follow-up CT was conducted on 22 October 2024 (Figure 6C,6D).

Case 7

A 20-year-old male was admitted on 6 September 2024 with a 20-day history of cough, expectoration, and fever. Intermittent fever, cough, and expectoration of unknown etiology had developed 20 days earlier, with a maximum recorded temperature of 40 ℃. The sputum was white and viscous and was accompanied by dyspnea. At a local hospital, empirical antibiotic therapy (details unavailable) resulted in improvement of fever, but cough and expectoration persisted.

On physical examination, coarse breath sounds were noted bilaterally. The abdomen was soft, without tenderness or rebound tenderness. The results of laboratory investigations are presented in Table 1.

Chest and abdominal CT were performed on 6 September 2024 (Figure 7A). The patient was diagnosed with subacute miliary pulmonary TB and TP. Treatment with the HRZE regimen was initiated, resulting in symptomatic improvement, and the patient was discharged on 30 September 2024.

Figure 7 Non-contrast chest CT in a 20-year-old male with subacute miliary pulmonary TB and TP. (A) Image on 6 September 2024 showing marked peritoneal thickening adjacent to the left hepatic lobe (white arrow). (B) Image on 29 November 2024 demonstrating marked peritoneal thickening adjacent to the left hepatic lobe with loculated perihepatic fluid (white arrow). (C) Image on 18 January 2025 showing enlarged loculated fluid adjacent to the left hepatic lobe (white arrow). (D) Image on 18 January 2025 demonstrating a new hypodense nodular lesion in the left hepatic lobe (hollow white arrow). CT, computed tomography; TB, tuberculosis; TP, tuberculous peritonitis.

Follow-up CT scans were performed on 25 October 2024, 29 November 2024, and 18 January 2025 (Figure 7B-7D).

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration and its subsequent amendments. Written informed consent was provided by the patients for publication of the article and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

The timeline of radiological findings, anti-TB therapy details, and clinical outcomes in 7 patients with TP is presented in Table 2.

Table 2

Timeline of radiological findings, anti-tuberculosis therapy details, and clinical outcomes in 7 patients with TP

Case Age (y)/gender Baseline CT examination (findings and date) Perihepatic collection (timing & CT features) Hepatic nodules (timing, location, & CT features) Nodule size evolution Anti-TB regimen & DST Adherence & clinical status at nodule appearance Aspiration microbiology (perihepatic fluid) Resolution/persistence & therapy adjustment Corresponding figure panels
1 22/M 26 Dec 2019: mild perihepatic peritoneal thickening/enhancement; free/loculated ascites; no nodules Not explicitly reported (progression to thickening directly) 3 months (10 Mar 2020): new heterogeneously enhancing nodules in left/right hepatic lobes Not specified HRZE (2 months) → INH + RIF (4 months); DST not performed Good (100% doses); clinically improved (abdominal distension resolved, no fever) No aspiration performed Persistent at 6-month follow-up; no therapy adjustment (paradoxical reaction suspected) 1A, 1B (baseline); 1C, 1D (nodules)
2 45/F 29 Jun 2020: perihepatic peritoneal thickening/enhancement; rim-enhancing loculated perihepatic fluid; left pleural effusion; ascites; no nodules Baseline (Jun 29, 2020): rim-enhancing loculated perihepatic fluid; enlarged at 3 months (Sep 30, 2020) 3 months (30 Sep 2020): new heterogeneously enhancing nodule in right anterior hepatic lobe; enlarged at 8 months (Feb 3, 2021) Enlarged (8 vs. 3 months) HRZE (2 months) → INH + RIF (7 months, prolonged); DST not performed Good (95% doses); clinically stable (fever resolved, mild abdominal discomfort persisted) Routine bacterial/fungal culture (−); TB PCR (+), TB culture (+) (M. tuberculosis) Persistent at 12-month follow-up; therapy prolonged (6–9 months) due to slow radiological response 2A (baseline); 2B (3 months); 2C (8 months)
3 23/M 20 Aug 2020: marked peritoneal/omental thickening/enhancement; significant perihepatic peritoneal thickening/enhancement; no nodules Not explicitly reported (localized thickening at 3 months) 3 months (13 Nov 2020): new heterogeneously enhancing nodules in posterior segment of right hepatic lobe + left hepatic lobe Not specified HRZE (2 months) → INH + RIF (4 months); DST performed (baseline), susceptible to all first-line drugs Excellent (100% doses); clinically improved (weight gain, abdominal tenderness resolved) No aspiration performed Partially resolved at 9-month follow-up (nodule size reduced by 50%); no therapy adjustment (paradoxical reaction confirmed) 3A, 3B (baseline); 3C, 3D (nodules)
4 17/F 30 Jan 2024: perihepatic peritoneal thickening/enhancement with focal nodular changes; no hepatic nodules Not explicitly reported (thickening improved at 7 months) 7 months (20 Aug 2024): new heterogeneously enhancing nodule in posterior segment of right hepatic lobe Not specified HRZE (2 months) → INH + RIF (4 months); DST not performed Good (90% doses); clinically stable (no recurrent symptoms, normal inflammatory markers) No aspiration performed Persistent at 6-month follow-up; no therapy adjustment 4A, 4B (baseline); 4C, 4D (nodules)
5 51/F 23 Feb 2024: peritoneal/omental thickening/enhancement; nodular perihepatic peritoneal thickening/enhancement; hepatic parenchymal compression/congestion; no nodules Not explicitly reported (progression to marked thickening) 3 months (28 May 2024): new heterogeneously enhancing nodular lesions in left/right hepatic lobes Not specified HRZE (2 months) → INH + RIF (6 months, prolonged); DST performed, susceptible to first-line drugs Fair (85% doses); clinically stable (controlled blood glucose, no TB-related symptoms) No aspiration performed Resolved at 15-month follow-up; therapy prolonged (6→8 months) due to comorbid diabetes 5A, 5B (baseline); 5C, 5D (nodules)
6 21/M 3 Sep 2024: perihepatic peritoneal thickening/enhancement; rim-enhancing loculated perihepatic fluid; no nodules Baseline (Sep 3, 2024): Rim-enhancing loculated perihepatic fluid 1 month (22 Oct 2024): multiple new round heterogeneously enhancing nodules in right/left hepatic lobes Not specified HRZE (2 months) → INH + RIF
(4 months); DST not performed		 Excellent (100% doses); clinically improved (fever/night sweats resolved) Routine bacterial/fungal culture (−); TB PCR (+) Resolved at 8-month follow-up; no therapy adjustment (paradoxical reaction) 6A, 6B (baseline); 6C, 6D (nodules)
7 20/M 6 Sep 2024: marked peritoneal thickening adjacent to left hepatic lobe; no nodules or perihepatic fluid 2 months (Nov 29, 2024): loculated perihepatic fluid adjacent to left hepatic lobe; enlarged at 4 months
(18 Jan 2025)		 4 months (18 Jan 2025): new hypodense nodular lesion in left hepatic lobe Not specified HRZE (2 months) → INH + RIF (4 months); DST performed, susceptible to all first-line drugs Good (95% doses); clinically stable (mild abdominal pain, no systemic symptoms) Routine bacterial/fungal culture (−); TB PCR (−), TB culture (−) Persistent at 5-month follow-up; percutaneous drainage of perihepatic fluid (Jan 25, 2025); no regimen change 7A (baseline); 7B (2 months); 7C, 7D (4 months)

Anti-TB regimens follow WHO guidelines (standard 6-month course: 2 months HRZE, followed by 4 months INH + RIF). Adherence was assessed via patient self-report and pill counts: excellent (100%), good (90–99%), fair (80–89%). Paradoxical reaction was defined as radiological progression with clinical stability/improvement, good adherence, and no evidence of drug resistance/superinfection. Follow-up duration range: 5–15 months (median: 9 months). CT, computed tomography; DST, drug susceptibility testing; HRZE, isoniazid + rifampin + pyrazinamide + ethambutol; INH, isoniazid; PCR, polymerase chain reaction; RIF, rifampin; TB, tuberculosis; TP, tuberculous peritonitis.

Discussion

TP, a diffuse peritoneal infection and a frequent EPTB manifestation, can develop via direct extension, lymphatic, or hematogenous dissemination (8,9). Compared with pulmonary TB, HTB exhibits distinct epidemiological, pathological, and pathophysiological characteristics (10). HTB is generally considered a result of hematogenous dissemination of M. tuberculosis to the liver. At present, no standardized radiological classification system for HTB has been established. Some reports have categorized HTB into miliary, large nodular, perihepatic peritoneum, and tuberculous cholangitis types (11), whereas others have proposed classifications including miliary, granulomatous hepatitis, nodular, tuberculous cholangitis, and hilar mass types (2).

In the former classification, the perihepatic peritoneum type refers to TB limited to the perihepatic peritoneum without parenchymal involvement. The perihepatic peritoneum corresponds to the visceral peritoneum (12). However, CT lacks the resolution to reliably distinguish visceral from parietal peritoneum due to intrinsic density limitations and lesion characteristics. Consequently, whether TB of the perihepatic peritoneum should be classified as HTB or TP remains controversial.

Findings from the present case series, based on longitudinal CT follow-up, supported the hypothesis that involvement of the perihepatic parietal peritoneum and/or perihepatic peritoneum may progress to hepatic parenchymal involvement. This observation warrants consideration of the hypothesis that clinical awareness of such patients needs to be enhanced and close radiological monitoring should be carried out. The temporal pattern of lesion evolution observed in our series—namely, the development of new hepatic lesions despite general improvement in systemic symptoms and other sites of tuberculous involvement under effective therapy—invites comparison with a paradoxical reaction (PR) or immune reconstitution inflammatory syndrome (IRIS). PR/IRIS is a well-recognized phenomenon characterized by the clinical or radiological worsening of pre-existing lesions or the appearance of new lesions attributable to the recovered immune system’s heightened inflammatory response to persistent mycobacterial antigens. Our cases share key features with PR/IRIS, including the timing (within months of treatment initiation) and the context of effective therapy (as evidenced by improving pulmonary/peritoneal disease and the absence of rifampicin resistance). However, the presentation of PR/IRIS as discrete, new parenchymal nodules arising from a serosal site is not a classic manifestation, which more commonly involves the worsening of existing lymph nodes or meningeal lesions. Therefore, although PR/IRIS remains a plausible contributing mechanism, the unique radiologic progression—from peritoneal thickening to perihepatic loculation and finally to parenchymal nodule formation—more strongly suggests a process of direct contiguous spread that became radiologically apparent as the systemic inflammatory milieu was controlled by therapy. The subsequent resolution of all lesions on follow-up imaging without treatment modification further supports this interpretation. However, the absence of pathological confirmation and the retrospective nature of this analysis preclude definitive conclusions regarding the underlying immunopathogenesis.

TP has been described in three pathological patterns: exudative, adhesive, and caseous. The exudative type is characterized by peritoneal congestion and edema, often leading to the development of ascites, which may become loculated. The adhesive type involves fibrous adhesions among the peritoneum, mesentery, and bowel loops. The caseous type is characterized by the presence of caseous necrosis. These patterns may coexist within the same individual and can transform from one type to another over time (8).

In the present cases, the majority of patients initially demonstrated diffuse thickening of the perihepatic peritoneum along with peritoneal and omental involvement, accompanied by ascites, consistent with the exudative pattern. During anti-TB therapy, these lesions evolved into localized hepatic peritoneal thickening with fusiform hypodense collections in the perihepatic space, exhibiting rim enhancement on contrast-enhanced imaging. Such radiological features are consistent with adhesive or caseous pathological changes. With disease progression, tuberculous involvement of the perihepatic parietal peritoneum or perihepatic peritoneum extended into the hepatic parenchyma, forming hypodense nodules with heterogeneous enhancement on CT. It is also important to acknowledge that CT alone may be insufficient for definitive diagnosis in many real-world cases. When diagnostic uncertainty persists despite CT follow-up, contrast-enhanced MRI (including diffusion-weighted imaging [DWI] for restricted diffusion) can provide superior soft-tissue characterization and may better demonstrate the necrotic core and enhancing rim of tuberculomas. Furthermore, ultrasound-guided aspiration of perihepatic collections or hepatic lesions for microbiological or pathological confirmation should be considered, especially for lesions that progress paradoxically or exhibit atypical features (6).

Notably, in the absence of pathological confirmation, it is crucial to consider alternative diagnoses for the newly developed hepatic nodules. Pyogenic abscesses typically present with more pronounced systemic toxicity, marked rim enhancement, and the “cluster” sign; the absence of intralesional gas in our cases further argues against this common alternative. Fungal infections (e.g., candidiasis) are less common in non-severely immunocompromised hosts and often manifest as numerous, small, scattered microabscesses, a pattern distinct from the larger, contiguous subcapsular nodules observed here. Furthermore, the differential diagnosis must include primary liver malignancies, particularly hepatocellular carcinoma (HCC). As highlighted in recent literature, the imaging features of HTB can closely mimic those of HCC, including arterial phase hyperenhancement and washout appearance, leading to frequent misdiagnosis (13). In our series, the heterogeneous enhancement pattern of the hepatic nodules could indeed raise suspicion for HCC. However, the immediate subcapsular location, direct continuity with perihepatic peritoneal disease, and the evolution characterized by development under therapy and subsequent stabilization or resolution without specific anti-tumor treatment are more indicative of an infectious/inflammatory process such as tuberculoma. Lymphoma and metastatic disease usually demonstrate more pronounced and homogeneous enhancement or a “target” appearance. The absence of a known primary malignancy in our relatively young patient cohort, coupled with the strong temporal and spatial association of the hepatic lesions with the progression of adjacent TP, provided the most plausible basis for diagnosing presumed hepatic tuberculoma.

An interesting observation in this case series was the consistent presence of hypoalbuminemia and reduced CD4+ T-lymphocyte counts among the identified patients. It is important to note, however, that in the absence of a comparator group of TP patients without hepatic involvement, these parameters cannot be definitively established as specific risk factors for contiguous progression. Rather, hypoalbuminemia and lymphopenia are well-recognized markers of systemic inflammatory response and chronic disease severity in TB and other advanced infections (14-16). Therefore, their presence in this cohort most likely reflects the overall severity of the systemic tuberculous disease in these particular patients, all of whom had extensive TP, and in some cases, concurrent pulmonary or pleural involvement. The aforementioned selection bias in lymphocyte subset testing further reinforces the likelihood that this cohort represents a more severely ill subset of TP patients (17,18). Whether such disease severity itself creates a milieu permissive for local contiguous spread, or whether these immunological and nutritional deficits are merely concomitant features, cannot be determined from our data; investigation in future controlled studies is warranted.

Our study has several important limitations. First, the diagnosis of hepatic tuberculous involvement was presumptive rather than histologically confirmed, as none of the patients underwent liver biopsy due to the clinical context (already receiving anti-TB therapy, coagulopathy, or small lesion size). Although the temporal and anatomical contiguity strongly support the proposed mechanism of contiguous spread, the absence of microbiological or histological validation remains a significant gap. Second, the retrospective design and small sample size limit the generalizability of our findings. Third, the composite diagnostic criteria for TP, although clinically accepted, may include patients with other granulomatous conditions. These limitations underscore the hypothesis-generating nature of our observations and highlight the need for prospective studies with pathological correlation to validate this imaging pattern.

Conclusions

This case series describes a temporal and spatial pattern of radiological progression from TP to presumed hepatic involvement. This progression was observed in a cohort of patients who frequently presented with common features of severe systemic illness, such as hypoalbuminemia and lymphopenia. CT findings typically demonstrate heterogeneously enhancing nodules at the hepatic margin, often arising within approximately 3 months. However, the inferential nature of the hepatic diagnosis, based on imaging evolution and clinical context without pathological confirmation, must be emphasized. The contiguous hepatic involvement/lesions adjacent to perihepatic TP may occur and have a recognizable temporal-anatomic CT pattern; confirmation and exclusion of alternative causes remain essential.

Acknowledgments

None.

Footnote

Funding: This study was supported by Kunming Science and Technology Planning Project (No. 2024-1-NS-0032); Yunnan Province High-Level Health and Technical Talent Training Program (No. H2024076) and Kunming Municipal Health Science and Technology Talent Training Program (No. 2024-SW(Leader)-26).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-2059/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 institutional and/or national research committee(s) and with the Helsinki Declaration and its subsequent amendments. Written informed consent was obtained from the patients or their legal guardians. for publication of the article and 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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Cite this article as: Li KX, Liu JL, Pu Y, Qi M, Wei JL, Fu XW, Li X. Computed tomography characteristics of hepatic involvement secondary to tuberculous peritonitis: a case series. Quant Imaging Med Surg 2026;16(3):254. doi: 10.21037/qims-2025-2059

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