Successful treatment of laparoscopic surgery in treating acute diffuse peritonitis due to drug-induced acute liver injury: a case description

Introduction

Acute liver failure (ALF) is primarily attributed to drug-induced liver injury (DILI), exhibiting an incidence rate ranging from 14 to 19 cases per 100,000 individuals (1). The list of clinical medications linked to DILI is perpetually expanding, with the incidence of DILI exhibiting an annual uptrend (2). Since the diagnosis of DILI hinges on the exclusion of other potential causes, progress in both prevention and treatment has remained limited (1). Emergency laparotomy is frequently performed in instances of acute diffuse peritonitis, owing to its potentially life-threatening characteristics (3). Laparoscopy offers significant advantages due to its extensive applicability in both diagnosing and managing acute abdominal conditions (4,5). Nevertheless, there is no published research on the application of laparoscopic surgery for treating acute DILI complicated by diffuse peritonitis. In the case detailed herein, the patient was effectively treated via laparoscopic abdominal drainage following a diagnosis of acute diffuse peritonitis. The intraoperative images and liver biopsy pathology confirmed the presence of DILI.

Case presentation

A 27-year-old male, with no prior history of liver or kidney disorders, alcohol intake, food and medication allergies, or coronavirus disease 2019 (COVID-19) infection within the past 28 days, was admitted to the gastroenterology department. He presented with fever and upper abdominal distension for 2 days following the consumption of hot pot. He experienced chills, fever, dizziness, and fatigue, without having measured his body temperature. Subsequently, he experienced intermittent episodes of abdominal distension and discomfort in the upper abdomen, accompanied by nausea. There were no visible signs of vomiting or diarrhea. He self-administered three bags of GanMaoLingKeLi [999] [total 1.2 g N-acetyl-para-aminophenol (APAP); 999 Pharmaceutical, Shenzhen, China], along with six tablets of New Contech (total 3 g APAP; Shanghai Johnson & Johnson Pharmaceutical, Shanghai, China) over 12 hours. Additionally, he took three ibuprofen extended-release capsules (total 0.9 g ibuprofen; Pfizer, New York, NY, USA) within 24 hours. Although his fever subsided and the abdominal pain significantly alleviated after the medication was administered, he later experienced a resurgence of fever, chills, and intermittent upper abdominal discomfort the following day. Laboratory analyses uncovered abnormal indicators of both infection and liver damage (Table 1), whereas markers for viral hepatitis were observed to remain within normal limits. 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 patient for publication of this article and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

His physical examination results were as follows: body temperature of 38.2 ℃, heart rate of 121 bpm, soft abdominal muscles, tenderness in the mid and upper abdomen as well as the right upper quadrant, absence of hepatic percussion pain, negative shifting dullness, normal bowel sounds, no edema in both lower limbs, and normal digital rectal examination. The following treatments were administered: 2 g of cefoperazone-sulbactam for injection every 8 hours, 1.2 g of glutathione for injection administered once daily, and 40 mL of glycyrrhizin for injection given once daily.

Re-evaluation of the laboratory tests indicated that both the infection and liver function deterioration had intensified compared to the prior assessment (Table 1). Further examinations uncovered the following insights: electrocardiogram (ECG) showed evidence of sinus tachycardia at 111 beats per minute, coupled with T-wave alterations in the inferior wall. Furthermore, the color Doppler ultrasonography of the urinary system revealed no significant abnormalities. The computed tomography (CT) plain scan detected edema of the hepatoduodenal ligament, a minor accumulation of fluid within the abdominal-pelvic cavity, and a slight presence of fluid in the right thoracic cavity (Figure 1A).

Figure 1 Abdominal and thoracic CT. (A) Day 0: a small amount of fluid in the right thoracic cavity (A-1), a small amount of fluid in the abdominal cavity (A-2), edema of the hepatoduodenal ligament (A-3), a small amount of fluid in the pelvic cavity (A-4). (B) Day 3: an increased amount of pleural effusion compared to before (B-1), an increased amount of abdominal effusion compared to before (B-2), edema of the hepatoduodenal ligament (B-3), an increased amount of pelvic effusion compared to before (B-4). (C) Day 3: a significant reduction in pleural effusion (C-1), a significant reduction in abdominal effusion (C-2), reduced edema of the hepatoduodenal ligament (C-3), a significant reduction in pelvic effusion (C-4). The red triangle indicates the location of fluid accumulation (pleural, abdominal, or pelvic effusion) or edema of the hepatoduodenal ligament (corresponding to the abnormal findings described in each subfigure). CT, computed tomography.

After 2 days of hospitalization, his symptoms exhibited no signs of improvement. These included a persistent fever of 39.1 ℃, heart rate of 100 beats per minute, a mere 280 mL of urine output over 24 hours, and continuous chest tightness. The advanced abdominal CT scan revealed a significant escalation in both abdominal pelvic effusion and pleural effusion, as evidenced by a comparison with prior imaging outcomes (Figure 1B). In sharp contrast, an abdominal CT plain scan on the third day post-surgery revealed a significant reduction in both abdominal and pleural effusions, compared to preoperative levels (Figure 1C).

The general surgeon’s physical examination, conducted post-consultation, unveiled the following observations: widespread abdominal muscle rigidity, localized tenderness, and pronounced rebound pain, predominantly concentrated in the right upper quadrant. There was also a positive tapping sensation in the hepatic region, suspicious positive shifting dullness, and yellowish-brown fluid retrieved via diagnostic abdominal paracentesis (Figure 2A). An emergency laparoscopic exploration was conducted following the general surgeon’s suspicion of acute diffuse peritonitis.

Figure 2 Photos of diagnostic abdominal paracentesis and the operation; liver biopsy. (A) Ascites is yellowish-brown fluid obtained through diagnostic abdominal paracentesis. (B) 2,000 mL of yellow effusion in the abdominal pelvic cavity. (C) Dark yellow effusion in right upper quadrant of the abdomen. (D) Hepatic stasis and edema. (E) Essentially normal gallbladder (black triangle) and mild edema of the hepatoduodenal ligament (green triangle). (F) Hepatocyte swelling in the center of the hepatic lobules with focal hepatocyte necrosis was observed. (G) Mild cholestasis was observed in hepatocytes and bile ducts. (H) The infiltration of lymphocytes, neutrophils, and eosinophils in the portal area was accompanied by partial bile duct injury and occlusion (hematoxylin-eosin stain, ×40).

The intraoperative findings were as follows: 2,000 m: of yellow effusion was observed, along with dark yellow effusion in the right upper quadrant of the abdomen (Figure 2B,2C). Additionally, there was pus fur accompanied by scattered white miliary deposits on the liver surface. The liver exhibited signs of congestion and edema (Figure 2D). The gallbladder appeared essentially normal, whereas the hepatoduodenal ligament showed mild edema (Figure 2E). No perforation in the digestive tract was identified during the dissection of the hepatoduodenal ligament, and the remaining organs presented normal appearances. Consequently, the surgeon collected ascites samples for bacterial culture, routine biochemical analysis, amylase evaluation, and chyle examination. Additionally, a segment of liver tissue was excised for pathological examination. Following the evacuation of peritoneal fluid, drainage tubes were subsequently placed into the right subhepatic space and the pelvic cavity, respectively. Concurrently, right thoracic closed drainage was executed to remove light yellow pleural fluid. The operation lasted 118 minutes. Following surgery, he was administered 0.5 g of imipenem and cilastatin for injection every 8 hours to prevent infection. Additionally, he received 1.2 g of glutathione for injection daily to protect hepatic function, 0.2 g of magnesium isoglycyrrhizinate for injection daily to further support hepatic function, and 12.5 g of human albumin infusion once a day to supplement albumin levels. He experienced positive outcomes on the first day post-operation. These included a stable body temperature, improved liver function indicators (Table 1), the removal of 600 mL of yellow fluid from the abdominal drainage tube, and the extraction of 700 mL of light-yellow fluid from the thoracic drainage tube. The thoracic drainage tube was removed on the 4th day post-surgery, whereas the abdominal drainage tube was extracted on the 6th day following the procedure. On the third day after the operation, both the peritoneal effusion and the pleural effusion were significantly reduced compared to before the operation (Figure 1C). On the 10th day, both infection and liver function tests returned normal, thereby facilitating the patient’s discharge on the 14th day post-surgery. Both aerobic and anaerobic blood bacterial cultures were negative. The ascitic fluid analysis, which encompassed culture, routine tests, amylase, and chylous tests, was also negative, with the exception of a positive Rivalta test. Additionally, the liver biopsy pathology revealed acute DILI (Figure 2F-2H). The patient was advised to avoid APAP and non-steroidal anti-inflammatory drugs (NSAIDs) in the future and was scheduled for regular liver function follow-up. At the 3-month postoperative visit, his liver function remained normal.

Discussion

DILI can result from a wide range of prescription and over-the-counter medications. Over 1,000 medications and herbal supplements can lead to DILI (1), and the incidence of DILI has been rising rapidly in recent years (6). LiverTox, sponsored by the National Institutes of Health, serves as the definitive resource on DILI. This website offers comprehensive information on more than 1,200 medications that have the potential to cause liver damage. Individuals with DILI often exhibit no initial symptoms and are frequently diagnosed only after an abnormal liver function test is detected during a routine physical examination (7). The primary clinical manifestations of DILI may include fatigue, anorexia, nausea, discomfort in the upper right abdomen, and dark urine. DILI should be considered if abnormal liver function occurs concurrently with the aforementioned conditions (7). Alanine transaminase (ALT) levels may exceed 100 times the upper limit of normal (ULN) during the acute onset of DILI, but there is no specific diagnostic indicator for DILI (1,8). DILI is an exclusive diagnosis that relies on a thorough patient history and meticulous utilization of blood tests, hepatobiliary imaging, and liver biopsy. Diagnostic calculations based on clinical scoring systems can currently be used for clinical diagnosis. For example, when diagnosing acute DILI, the liver biochemical threshold should meet one of the following criteria: (Ⅰ) ALT is more than 5 times the ULN; (Ⅱ) alkaline phosphatase (ALP) is greater than 2 times the ULN; (Ⅲ) ALT is greater than 3 times the ULN and total bilirubin (TBil) is greater than 2 times the ULN (6). In our case, the patient’s ALT was greater than 5 times the ULN (Table 1).

DILI is divided into three types: direct injury, specific injury, and indirect injury (1). The direct injury is caused by drugs that are inherently toxic to the liver. The direct injury is common, predictable, and dose-dependent. It usually has a short incubation period, occurring within one to 5 days of intentional or accidental overdose of high or ultra-high therapeutic doses (1). The most common pattern of direct DILI is an elevation in serum enzymes without jaundice, such as elevated levels ALT or ALP (7). Severe liver damage will manifest as signs of liver failure, including coagulation dysfunction, hyperammonemia, and coma within a few days. Large doses of acetaminophen, aspirin, niacin, amiodarone, and many anti-tumor drugs can cause acute liver necrosis, which can be fatal (9). No reports of acute diffuse peritonitis caused by acute DILI were found in the relevant literature, and no reports of laparoscopic surgery being used in the treatment of such cases were found.

The primary cause of venous obstruction syndrome is typically acute drug-induced damage to the endothelial cells lining the blood vessels (1). This injury can result in the obstruction of venous blood flow and subsequent liver damage. Affected patients will experience abdominal pain, liver enlargement, and weight gain, which are often followed by the onset of jaundice. The condition can rapidly progress to liver failure. Histological examination of the liver typically reveals dilatation of the hepatic sinuses, erythrocyte extravasation, and necrosis of the central hepatocytes (1).

APAP is metabolized by the liver and is a widely used antipyretic and analgesic drug (8). It is the most common drug that causes liver failure (8), and it is also used to create animal models of ALF (9). Although the use of APAP in therapeutic doses may be considered safe, it can predictably cause liver damage in humans or animal models when given at sufficiently high doses (7,8). At present, the number of cases of acute DILI caused by APAP is increasing, and in some cases, liver transplantation is necessary (8). Guidelines for the diagnosis and treatment of APAP-induced DILI have been developed (7,9).

Ibuprofen, which causes one in 100,000 cases of DILI, is one of the most commonly used and safest NSAIDs (10). However, it is responsible for the majority of DILI cases (29%) caused by NSAIDs in Spain (11). Common adverse reactions to ibuprofen include rash (56%), fever (56%), jaundice (50%), choluria (39%), vomiting (39%), and abdominal pain (22%) (10). Additionally, the absolute risk of vascular and gastrointestinal complications is higher than that of liver injury (10). No reports of severe DILI caused by normal doses of ibuprofen were found in the PubMed and Ovid databases. Zoubek et al. (11) found 22 cases of DILI caused by ibuprofen through a literature search. Although the incidence is extremely low, the occurrence of DILI caused by ibuprofen may be related to taking excessive doses of ibuprofen or using other NSAIDs at the same time (11,12). Severe cases include severe hypersensitivity reactions, such as toxic epidermal necrolysis or Stevens-Johnson syndrome, as well as ALF with 60% of cases requiring liver transplantation (10,12). The patients who take drugs containing both APAP and ibuprofen orally at the same time are more likely to develop acute DILI and severe liver damage.

To date, no reliable diagnostic methods with demonstrated safety and efficacy have been established for DILI. Laparoscopy is not mandatory for the diagnosis and treatment of DILI (3). Liver biopsy evaluation of DILI is not mandatory, but its results may be helpful in certain cases where DILI is suspected (8). The clinical use of liver biopsy to diagnose DILI is infrequent (8). It is commonly used to distinguish DILI from other diseases, such as autoimmune hepatitis. The clinical need for continued use or re-use of suspected drugs, persistent elevation or deterioration of liver function indicators, and continued use or re-exposure to related drugs are also taken into consideration for a liver biopsy (8). The microscopic manifestations of DILI on liver biopsy include hepatocyte necrosis, cholestasis, steatosis, bile duct injury or disappearance, and lymphocyte or eosinophilic infiltration (10,13). Histological changes vary at different stages of DILI (10,13). Liver biopsy can always be accurately performed during laparoscopy or exploratory laparotomy. Fortunately, during the laparoscopic procedure performed on this patient, we identified hepatic abnormalities and subsequently obtained a liver biopsy. In this case, a direct-view biopsy obtained accurate results (Figure 2F-2H), which were beneficial for the patient’s diagnosis and treatment.

Complications of acute liver injury include hepatic encephalopathy, bleeding tendency, infection, and ascites, which is the primary complication (2). Infection is a prevalent complication among patients with liver failure, with spontaneous bacterial peritonitis (SBP) being the most frequent type. Ascites can be categorized into two distinct types: exudative and leaky (14). The positive Rivalta test for ascites in this case suggested the likelihood of inflammation. DILI-induced acute generalized peritonitis in this case likely involves two interconnected pathophysiological pathways. First, hepatic exudate-mediated peritoneal inflammation: severe DILI causes hepatocyte necrosis and stretching of the liver capsule, triggering the release of inflammatory exudate (containing necrotic hepatocytes, cytokines, and chemokines) from the liver surface. This exudate accumulates in the peritoneal cavity, directly stimulating peritoneal mesothelial cells and activating local inflammatory responses (e.g., increased vascular permeability, leukocyte recruitment). Second, systemic inflammatory mediator amplification: DILI-induced hepatocyte injury elevates systemic levels of proinflammatory cytokines, including tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). These cytokines further amplify peritoneal inflammation, leading to widespread peritoneal hyperemia, edema, and exudation—ultimately progressing to acute generalized peritonitis. This mechanism aligns with prior reports that severe liver injury can induce peritoneal inflammation via exudate release and cytokine dysregulation (1,13). Experts concur that laparoscopic peritoneal biopsy is the prevailing gold standard for determining the underlying cause of exudative peritonitis. Acute peritonitis commonly serves as a frequent cause of surgical acute abdomen (4), and acute diffuse peritonitis is a potentially life-threatening condition that necessitates exploratory laparotomy (15). With the progression of laparoscopic surgery and the growing proficiency of surgeons in this domain, there has been a heightened exploration into employing laparoscopic techniques for the treatment of unexplained ascites (14) and diffuse peritonitis (4).

Laparoscopic surgery for peritonitis has been shown to be safer and more feasible, particularly in terms of early surgical outcomes, when compared to traditional open surgery. The literature consistently reports a high accuracy rate for laparoscopic exploration, reaching as high as 98% (5). Although abdominal irrigation during laparoscopic surgery can be challenging due to intestinal dilation, which can reduce the space available for the surgery and result in unintentional inhalation of tissue into the suction tube (3), the utilization of laparoscopic surgery for treating peritonitis-related conditions, such as peptic ulcer perforation, appendicitis, cholecystitis, small intestinal obstruction, and colonic disorders, is becoming increasingly widespread (15). When patients have acute conditions, emergency surgery is very crucial (15). Compared to the drawbacks of exploratory laparotomy, such as limited visual clarity, insufficient peritoneal drainage, increased risk of infection, prolonged procedure duration, postoperative adhesions, and resultant complications, laparoscopic surgery presents numerous benefits. These benefits encompass a comprehensive visualization of the surgical field and expedited postoperative recovery, particularly for obese patients (4,5,14,15). Laparoscopy also offers a detailed and magnified view of the peritoneal cavity, enabling the surgeon to procure biopsy specimens for histological diagnosis (14).

Based on this case and published evidence, we propose the following indications and contraindications for laparoscopic surgery in DILI-complicated acute generalized peritonitis.

Indications

• Clinical suspicion of DILI-complicated peritonitis requiring both peritoneal drainage and liver biopsy for diagnosis/treatment.
• Stable hemodynamics (systolic blood pressure ≥90 mmHg, heart rate <120 bpm) without refractory shock.
• No severe organ dysfunction preoperatively [e.g., partial pressure of arterial oxygen/fraction of inspired oxygen (PaO₂/FiO₂) ≥300 mmHg, serum creatinine <176.8 µmol/L].
• Absence of absolute contraindications to laparoscopic surgery (listed below).

Contraindications

• Severe cardiopulmonary dysfunction (e.g., acute myocardial infarction within 3 months, severe chronic obstructive pulmonary disease with respiratory failure) unable to tolerate pneumoperitoneum.
• Severe coagulopathy (prothrombin time >20 seconds, platelet count <50×10⁹/L) with high bleeding risk.
• Severe peritoneal adhesion (e.g., history of ≥2 abdominal surgeries) precluding safe pneumoperitoneum establishment.
• Hemodynamic instability (refractory shock despite fluid resuscitation) requiring emergent open surgery.

Notably, laparoscopic surgery is not a first-line option for uncomplicated DILI or SBP. For uncomplicated DILI, liver biopsy can be performed percutaneously; for SBP, antibiotic therapy is the mainstay. Laparoscopic surgery should only be considered when DILI is complicated by peritonitis and meets the above indications.

Conclusions

DILI is an uncommon but significant liver disease, the frequency of which depends on the dosage frequency and the likelihood of DILI. In order to reduce the risk of adverse reactions, it is recommended that liver function indicators are monitored while taking APAP and ibuprofen. Genetic screening can be employed when necessary, and public health education on safe drug use should be enhanced. Due to the absence of specific diagnostic indicators for DILI, a liver biopsy is instrumental in providing additional diagnostic evidence for suspected cases. In this instance, acute diffuse peritonitis resulting from DILI was effectively managed through laparoscopic exploration and abdominal drainage. Although we successfully cured this patient via laparoscopic surgery, laparoscopy is not an essential procedure for the diagnosis and treatment of DILI and SBP. In some cases, it is even unsuitable, such as for patients with severe cardiopulmonary insufficiency who cannot tolerate pneumoperitoneum, coagulation dysfunction, or multiple organ dysfunction. Moreover, laparoscopic surgery has certain drawbacks, including prolonged operation time, increased medical costs, high requirements for surgeons’ technical skills, and the loss of manual tactile sensation. Therefore, in the treatment of this patient, we ultimately chose laparoscopy on the premise of fully evaluating other alternative measures as well as the advantages and disadvantages of laparoscopy, and achieved favorable results. We present this case hoping to provide assistance for the diagnosis and treatment of subsequent similar patients and offer new ideas for the management of difficult and complicated cases. Long-term follow-up and patient education on avoiding hepatotoxic drugs are essential to prevent recurrence.

Acknowledgments

None.

Footnote

Funding: None.

Conflicts of Interest: Both authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-554/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 patient for publication of this 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/.

References

1. Hoofnagle JH, Björnsson ES. Drug-Induced Liver Injury - Types and Phenotypes. N Engl J Med 2019;381:264-73. [Crossref] [PubMed]
2. Yasuda K, Asou M, Asakawa T, Araki M. Ascites management by cell-free concentrated ascites reinfusion therapy during recovery from drug-induced acute liver injury: a case report. J Med Case Rep 2020;14:192. [Crossref] [PubMed]
3. Yasui K, Ishiguro S, Komatsu S, Matsumura T, Komaya K, Saito T, Arikawa T, Kaneko K, Sano T. Novel approach to intraoperative peritoneal lavage with an extracorporeal stirring method in laparoscopic surgery for generalized peritonitis: Preliminary results. Asian J Endosc Surg 2020;13:89-94. [Crossref] [PubMed]
4. Rahman MS, Banna HU, Hasan MN, Jumman M. Advantage of laparoscopic peritoneal toileting in acute peritonitis with unclear etiology: A case report with inspiring outcome (with video). Int J Surg Case Rep 2020;72:285-9. [Crossref] [PubMed]
5. Agha RA, Borrelli MR, Farwana R, Koshy K, Fowler AJ, Orgill DP. SCARE Group. The SCARE 2018 statement: Updating consensus Surgical CAse REport (SCARE) guidelines. Int J Surg 2018;60:132-6. [Crossref] [PubMed]
6. European Association for the Study of the Liver. EASL Clinical Practice Guidelines: Drug-induced liver injury. J Hepatol 2019;70:1222-61. [Crossref] [PubMed]
7. Navarro VJ, Senior JR. Drug-related hepatotoxicity. N Engl J Med 2006;354:731-9. [Crossref] [PubMed]
8. Chalasani NP, Maddur H, Russo MW, Wong RJ, Reddy KRPractice Parameters Committee of the American College of Gastroenterology. ACG Clinical Guideline: Diagnosis and Management of Idiosyncratic Drug-Induced Liver Injury. Am J Gastroenterol 2021;116:878-98. [Crossref] [PubMed]
9. Larson AM, Polson J, Fontana RJ, Davern TJ, Lalani E, Hynan LS, Reisch JS, Schiødt FV, Ostapowicz G, Shakil AO, Lee WMAcute Liver Failure Study Group. Acetaminophen-induced acute liver failure: results of a United States multicenter, prospective study. Hepatology 2005;42:1364-72. [Crossref] [PubMed]
10. Zoubek ME, Lucena MI, Andrade RJ, Stephens C. Systematic review: ibuprofen-induced liver injury. Aliment Pharmacol Ther 2020;51:603-11. [Crossref] [PubMed]
11. Zoubek ME, González-Jimenez A, Medina-Cáliz I, Robles-Díaz M, Hernandez N, Romero-Gómez M, Bessone F, Hallal H, Cubero FJ, Lucena MI, Stephens C, Andrade RJ. High Prevalence of Ibuprofen Drug-Induced Liver Injury in Spanish and Latin-American Registries. Clin Gastroenterol Hepatol 2018;16:292-4. [Crossref] [PubMed]
12. Roales-Gómez V, Molero AI, Pérez-Amarilla I, Casabona-Francés S, Rey-Díaz-Rubio E, Catalán M, Vanaclocha F, Colina F. DRESS syndrome secondary to ibuprofen as a cause of hyperacute liver failure. Rev Esp Enferm Dig 2014;106:482-6.
13. Tian QJ, Zhao XY, Wang Y, Wee A, Soon GST, Gouw ASH, Li M, Yang RY, Wang L, Wang QY, Duan WJ, Wang Y, Wang XM, Kong YY, Ou XJ, You H, Jia JD. Histologic pattern is better correlated with clinical outcomes than biochemical classification in patients with drug-induced liver injury. Mod Pathol 2019;32:1795-805. [Crossref] [PubMed]
14. Quoc Ai D, Thi Thuy Hang H, Que Son T. Laparoscopic surgery for the diagnosis of abdominal effusion in the modern era of imaging - a retrospective study in a low-to-middle-income country. Ann Med Surg (Lond) 2023;85:407-11. [Crossref] [PubMed]
15. Yeom JH, Lee JH, Song JS, Lee MH, Kim MG. Extending the Indication for Laparoscopic Surgery in Patients With Pan-Peritonitis. Surg Laparosc Endosc Percutan Tech 2019;29:120-5. [Crossref] [PubMed]