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Liver Involvement by Perforated Peptic Ulcer: A Systematic Review

  • Jingjing Jiao1,#  and
  • Lanjing Zhang1,2,3,4,* 
 Author information
Journal of Clinical and Translational Pathology   2021;1(1):2-8

doi: 10.14218/JCTP.2021.00007


Background and Objective

Liver penetration by a confined perforation of peptic ulcer is a rare but severe event. Its clinical and pathological features are unclear.


In total, 41 qualified English publications were identified using the PubMed database and one in-house case.


Among the 42 patients, 20 patients had liver involvement by a perforated duodenal ulcer and 22 by a gastric ulcer. Among the 23 cases of known ulcer histology, 2 ulcers were malignant and were adenocarcinomas in the gastric remnant and the remaining 21 ulcers were confirmed as histologically benign (for frequency of malignancy in duodenal versus gastric ulcers, p = 0.48). The presence of hepatocytes was the clue of diagnosis for 19 cases. The median ages of the patients were 64.5 years (95% Confidence Intervals [CI] 53.40–71.90) for duodenal ulcer and 65.5 years (95% CI: 59.23–70.95) for gastric ulcer, respectively. The male to female ratio was 1.5:1 for duodenal ulcers and 2:1 for gastric ulcers. Patients with liver involvement of a perforated gastric ulcer were more likely to have a larger ulcer (median largest dimension, 4.75 cm versus 2.5 cm, p = 0.014). Female patients with liver involvement of a gastric ulcer were older than male patients (median age 72 versus 60 years, p = 0.045). There were no differences in gender, region (Asia, Europe, America versus others), use of non-steroidal anti-inflammatory drugs (n = 15), H. Pylori positivity (n = 10), possible history of peptic ulcer disease (n = 19) or mortality (n = 32) between duodenal and gastric ulcers.


Careful histologic examination, clinicopathological correlation, and immunohistochemistry are critical to establish the diagnosis and avoid misdiagnosing liver involvement as malignancy.


Duodenal ulcer, Gastric ulcer, Liver penetration, Peptic hepatitis


The classic type of peptic ulcer perforation implies the acute rupture of the stomach or intestinal wall with an out-pouring of gastrointestinal contents and might result in focal or generalized peritonitis. By contrast, the confined perforation of a peptic ulcer is defined as the penetration into and confinement within the tissue of an adjacent structure or organ by peptic ulceration.1 The most common organ involved in the confined perforation is pancreas, followed by gastrohepatic omentum, biliary tract, and liver.2 Peptic ulcer penetration into the liver is a rare complication that is poorly understood.2 Here we identified 41 cases in the English literature and an in-house case, aiming to characterize the clinical and histological features of this entity.

Materials and methods

Case identification and selection

We conducted a comprehensive literature search in PubMed in February 2021. We used the terms of "gastric ulcer AND perforation AND liver", "duodenal ulcer AND perforation AND liver", "peptic ulcer AND perforation AND liver", "gastric ulcer AND penetration AND liver", "duodenal ulcer AND penetration AND liver", "peptic ulcer AND penetration AND liver", “"gastric cancer" AND perforation AND liver”, “"gastric carcinoma" AND perforation AND liver”, “"gastric carcinoma" AND penetration AND liver”, “"gastric carcinoma" AND perforation AND liver”, “"duodenal cancer" AND penetration AND liver”, “"duodenal cancer" AND perforation AND liver”, “"duodenal carcinoma" AND perforation AND liver”, and “"duodenal carcinoma" AND penetration AND liver”. Only original articles were retrieved and reviewed. Additional cases were then identified through the review process. In addition, one in-house case was included.

A case would be selected and included in this study if: (1) it presented cases of gastric ulcer or duodenal ulcer penetration or perforation of the liver with a confirmed diagnosis; and (2) published in a peer-reviewed journal in English. All case selection was performed by author JJ.

Data extraction

The following data were extracted from original articles or pathological report, if available: last name of the first author, publication year, country/region of the corresponding author, age, gender, location of the ulcer, clinical symptoms and signs, histology, endoscopic finding, imaging, ulcer size in largest dimension, laboratory results, outcome, and length of follow-up. All of the case entries were assessed by author JJ.

Statistical analysis

Demographic and clinical parameters were compared between duodenal ulcers and gastric ulcers or between males and females for duodenal ulcers or gastric ulcers using a two-tailed Student’s t-test for continuous variables and Fisher exact or Chi-squared test for categorical variables as indicated. A p-value <0.05 was considered statistically significant. Confidence interval (CI) was calculated using t statistics.


Case collection

Out of 323 articles identified from PubMed by a computerized search in February 2021, 40 publications that presented 41 patients with the liver involved with perforation or penetration of a duodenal or gastric ulcer were identified. With one additional incoming referral case of duodenal ulcer penetration into the liver found at the Princeton Medical Center, Plainsboro, NJ, 42 patients qualified and were included in this series (Fig. 1).

Study flow diagram.
Fig. 1  Study flow diagram.

Clinical features

Among the 42 patients, 20 patients had liver involvement with a perforated duodenal ulcer and 22 patients had liver involvement with a perforated gastric ulcer. Among the 23 cases with known ulcer histology, 2 were malignant and were adenocarcinomas in the gastric remnant,3,4 and the 21 remaining ulcers (11 duodenal and 10 gastric ulcers) were confirmed as histologically benign. However, the frequency of malignant ulcers was not different between duodenal and gastric ulcers (p = 0.48).

For duodenal ulcers, the distribution of patient age was from 21 to 88 years, with a mean of 62.65 and a median of 64.5 years (95% CI: 53.40–71.90). The mean age was 62.75 years for women (21–88 years, median 75 years, 95% CI: 40.77–84.73), and 62.58 years for men (27–85 years, median 60 years, 95% CI: 52.85–72.31) (Fig. 2a). The ratio of male versus female was 1.5:1 (male = 60% and female = 40%). The majority of the duodenal ulcers occurred in the first portion of the duodenum (n = 17), among which 10 cases were located in the anterior wall of the first portion (Fig. 3a). The leading symptom or sign was abdominal pain or tenderness (n = 15), followed by nausea/vomiting/anorexia (n = 11) and gastrointestinal tract (GIT) bleeding (n = 8). The most frequently noticed abnormal lab results were low red blood cell count or hemoglobulin level (n = 9, 90%), followed by leukocytosis (n = 7, 78%) and elevated C-reactive protein (n = 4 (80%)). An abnormal liver function that was defined by elevated aminotransferase, bilirubin, alkaline phosphatase, gamma-glutamyltransferase and reduced albumin, occurred in 50% of duodenal ulcer patients (n = 4). Ten patients had information of possible non-steroidal anti-inflammatory drugs (NSAIDs) use with an equal distribution between with and without NSAIDs use (n = 5, for each). Four cases were positive for H. pylori infection and two were negative. One patient had a previous history of peptic ulcer disease (PUD) and five patients did not have a relevant history.

Distribution of patients’ age for: (a) duodenal ulcer; and (b) and gastric ulcer separated by gender.
Fig. 2  Distribution of patients’ age for: (a) duodenal ulcer; and (b) and gastric ulcer separated by gender.

p-value: comparison between male and female patients by Student t-test.

Anatomical location of: (a) perforated duodenal ulcer; and (b) and gastric ulcer.
Fig. 3  Anatomical location of: (a) perforated duodenal ulcer; and (b) and gastric ulcer.

For gastric ulcers, the distribution of patient age was from 42 to 91 years, with a mean of 65.09 and a median of 65.5 years (95% CI: 59.23–70.95). Female patients were significantly older (p = 0.045) (Fig. 2b). The mean age was 73.29 years for women (55–91 years, median 72 years, 95% CI: 59.66–86.91), and 60.93 years for men (42–80 years, median 60 years, 95% CI: 54.43–67.43). The ratio of male versus female was 2:1 (male = 66.7% and female = 33.3%). The majority of the gastric ulcers occurred in the antrum or pylori region (n = 12), followed by the gastric body (n = 8) (Fig. 3b). The leading symptom/sign was abdominal pain or tenderness (n = 16), followed by GIT bleeding (n = 12) and then nausea/vomiting/anorexia (n = 8). The most frequently noticed abnormal lab results were low red blood cell count or hemoglobulin level (n = 12, 100%), followed by leukocytosis (n = 10, 91%), and elevated alkaline phosphatase (n = 5, 71%). Abnormal liver function occurred in 57% of gastric ulcer patients (n = 8). Two patients had possible NSAIDs use and three did not. Three cases were associated with H. pylori infection and one was not. Eight patients had a previous history of PUD and five patients did not have a relevant history.

The comparison of clinical and demographic characteristics of duodenal and gastric ulcers is given in Table 1. The size of gastric ulcers was significantly larger than duodenal ulcers (median largest dimension = 4.75 cm versus 2.5 cm, p = 0.014); however, all other features were not statistically different between the duodenal and gastric ulcers.

Table 1

Clinical and demographic features of duodenal and gastric ulcers with liver perforation or penetration. Data presented as median (quartile)

Duodenal ulcer (n = 20)Gastric ulcer (n = 22)p-value
Age (years)64.5 (54–81)65.5 (53–73.5)0.64
Ulcer histology
  Malignant/total0/112/12 (16.7%)0.48
  Female/total8/20 (40%)7/21 (33.3%)0.66
  Asia8 (40%)7 (31.8%)
  Europe6 (30%)11 (50%)
  America5 (25%)3 (13.6%)
  Other1 (5%)1 (4.5%)
History of NSAIDs use (n = 15)0.99
  yes5 (50%)2 (40%)
  no5 (50%)3 (60%)
H. Pylori test (n = 10)0.99
  positive4 (66.7%)3 (75%)
  negative2 (33.3%)1 (25%)
Possible history of PUD (n = 19)0.14
  yes1 (16.7%)8 (61.5%)
  no5 (83.3%)5 (38.5%)
Size of ulcer (largest dimension cm) (n = 18)2.5 (1.38–3.20)4.75 (3.25–5.75)0.01
Mortality (n = 32)0.66
  dead2 (13.3%)4 (23.5%)
  alive13 (86.75)13 (76.5%)
Follow-up (days)63 (41.25–225)90 (54–570)0.73

Gross manifestations

Under endoscope or during surgery, a large or giant ulcer (defined as the largest dimension of ≥3 cm for gastric ulcers5 and 2 cm for duodenal ulcer6) was described in 25 patients;7–31 A polypoid or pseudotumoral mass that protruded from the central area of the ulcer bed was mentioned frequently (in 11 cases8,9,13,14,21,24,32–36). Five ulcers had an irregular margin.14,18,22,28,37 In addition, direct gross-examination of the liver tissue was possible under endoscopy.38 One group recently reported a case of duodenal ulcer penetration into the previous hemihepatectomy site due to the detection of a ligature at the ulcer floor.11 Thirteen cases were diagnosed by the direct observation of an ulcer that perforated into the liver during surgery.4,8,12,21,24,26,27,29,33,34,39,40

Radiological manifestations

On radiological imaging, the connection between the stomach or duodenum and the liver was recorded in eight cases,10,22,23,30,39,41–43 which were revealed by the observation of the movement of oral contrast or air bubbles between the two organs or fistula formation on computed tomography (CT), ultrasound or magnetic resonance imaging (MRI). Direct observation of an ulcer that penetrated the liver was observed or suspected in three cases, all by CT.16,17,36 By ultrasound, the target lesion was observed in two cases.14,28 Perforation of a stomach ulcer into the liver with an inflammatory change in the adjacent fat was demonstrated by CT by a brief report.17 Malignancy was radiologically suspected in two cases that included the in-house case.

Histological features

Among the 42 cases, histological features were available in 32 cases. The presence of hepatocyte in biopsy or cytology examination was the clue of diagnosis for 19 cases. Among them, the most frequently observed presentation was peptic hepatitis (hepatocyte with a surrounding inflammatory reaction), which was found in nine cases,10,13,18,22,25,28,31,35,37 and two cases did not have any apparent inflammation9,14 and no information of inflammation was mentioned in five cases.7,19,20,32,36 In the first article that described the features of peptic hepatitis, atypical hepatocytes were demonstrated.10 Other changes in the liver tissue at the site of perforation were reported, which included macro–microvesicular degeneration, pseudoaciner transformation and perisinusoidal fibrosis,15 and fibrotic granulation tissue.16 Eight cases had concurrent liver abscess formation. In addition, one patient in the literature presented with a liver tumor at the site of perforation with an absence of hepatocytes at the gastric ulcer biopsy, which was further confirmed as a nodule of reactive inflammation with no sign of malignancy after surgery.33 The in-house case was first diagnosed as malignancy (adenocarcinoma) in biopsy samples with the presence of atypia and cytoplasmic fat vacuoles that appeared to mimic signet ring cells but was later confirmed as a perforated duodenal ulcer that involved the liver (Fig. 4). The diagnostic pearls (Table 2) were the lobular configuration of large, atypical (hepatocytic) cells, lobular clusters of reactive biliary epithelium, and the CK8/18 and CK7 positive staining pattern of the reactive biliary epithelium. Of note, hepatoid adenocarcinoma of the stomach was positive for CDX-2 and hepatocellular carcinoma and reactive hepatic tissue were not.44

Representative images of biopsy samples from a duodenal ulcer penetration that involved the liver by Hematoxylin & Eosin staining: (a) 200 ×; (b) 40 ×; (c) immunohistochemistry of CK7; (d) arginase; and (e) and CK8/18.
Fig. 4  Representative images of biopsy samples from a duodenal ulcer penetration that involved the liver by Hematoxylin & Eosin staining: (a) 200 ×; (b) 40 ×; (c) immunohistochemistry of CK7; (d) arginase; and (e) and CK8/18.

Biopsy samples showed hepatocyte with: (a) atypia, steatotic change, and inflammation; (b) infiltrating glands; (c) atypical epithelium was positive for CK7 and had a lobular configuration in low-power view (arrows); (d) involved liver parenchyma was positive for arginase (arrowheads); and (e) positive staining in CK8/18 suggestive of a biliary origin and CK8/18 might be confused with hepatoid carcinoma. The presence of biliary epithelium negated the possibility of a hepatoid carcinoma.

Table 2

Diagnostic pearls for differential diagnosis of peptic ulcer with liver perforation or penetration versus hepatocellular carcinoma and hepatoid adenocarcinoma

Peptic ulcer that involves liverHepatoid adenocarcinomaHepatocellular carcinoma, metastatic
Clinical presentationSome, but not all, with history of peptic ulcer; normal serum AFPElevated serum AFPHistory of hepatocellular carcinoma; elevated serum AFP
CytologyBiphasic atypical cells including reactive hepatocytes and bile ductsLarge, atypical cells with abundant eosinophilic cytoplasm (cytoplasmic glycogen and hyaline globules)Similar to that in hepatoid adenocarcinoma
HistologyLobular configuration of the atypical glands (bile ducts), and atypical large polygonal cells (hepatocytes); no bona fide single cellsLack of small glands with cuboidal epithelium (bile ducts); infiltrative pattern; single cells may presentSimilar to that in hepatoid adenocarcinoma
  positiveHepatocytes are positive for CK8/18, arginase, HepPar1 and TTF-1 (cytoplasm) while bile ducts are positive for CK8/18 and CK7Positive for CDX-2, HepPar1, AFP, Glypican 3, CEA and CK19Positive for CK8/18, arginase, HepPar1, Glypican 3 and TTF-1 (cytoplasm);
  negativeBile ducts are negative for arginase, HepPar1 and TTF-1 (cytoplasm) while hepatocytes are negative for CK7Negative for CK7Negative for CDX-2, CK19 (10%+), CK20 (10%+) and CK7


The incidence and prevalence of PUD decreased in recent decades, possibly due to the decrease in H. pylori infection.45 However, PUD complications, which include perforation, remain a substantial healthcare problem.46 PUD perforation had a mortality rate of 5.7%–25%.47–49 In this systematic review, although peptic ulcer perforation/penetration of the liver was a rare event, the mortality rate for duodenal and peptic ulcers were 13.3% and 23.5%, respectively. A better understanding of the disease entity might be warranted for better management of the condition and differential diagnoses.

Compared with the uncomplicated duodenal and gastric ulcers from literature, which had a mean age of 54.3 years (95% CI: 52.8–55.9) and 65.6 years (95% CI: 64.1–67.1),50 patients with liver penetration due to duodenal ulcer were older, with a mean age of 62.65 years (95% CI: 53.40–71.90) and patients with liver penetration duo to gastric ulcer had similar ages, with a mean age of 65.09 years (95% CI: 59.23–70.95). In this analysis of a broad range of publications (from 1880 to 2021), duodenal and gastric ulcers were male predominant, with a male to female ratio from 1.5:1 to 2:1. However, the male predominance in peptic disease has changed.51 There was approximately a three-fold increase in the percentage of women with perforated duodenal ulcer in the last 45 years.52 Recent publications showed that females accounted for more than half of the perforated duodenal and gastric ulcers.49 This analysis showed females with perforated gastric ulcer were significantly older than males, which was consistent with previous reports.49,52

Unlike the free perforation that has the hallmark presentation of the classic triad (sudden onset of abdominal pain, tachycardia, and abdominal rigidity), the presentation of peptic ulcers with liver penetration is largely non-specific with abdominal pain or tenderness being the most frequently reported symptoms or indications, and could be more obscure (e.g., dizziness and weakness29). Abnormal liver function as defined by elevated aminotransferase, bilirubin, alkaline phosphatase, gamma-glutamyl transferase and reduced albumin, occurred in 50% of duodenal ulcers and 57% of gastric ulcers and most of the abnormality, especially the elevated aminotransferase, was mild to moderate, which might explain the local non-specific inflammation in the liver. However, the diagnostic value of liver function tests in cases of liver penetration might be limited. Of note, only 16.7% of perforated duodenal ulcers that involved the liver had a potential previous history of PUD. Although radiological studies might provide diagnostic hints, such as the target sign on ultrasound and the direct observation of a connection between the liver and alimentary tract, endoscopic examination and biopsy played critical roles in establishing the diagnosis and excluding malignancy. Different histological features of the perforation site (inflammation, granulation tissue, fibrosis, and liver abscess) might be determined by the duration of the perforation. With sudden inflammation, liver cells might show atypical features that resemble a carcinoma as first described by Guerrieri et al. in 198710 and the in-house case. Endoscopically, penetration into the liver could frequently appear as a polypoid or pseudotumoral mass that protruded from the central area of the ulcer bed.8,9,13,14,21,24,32–36 This feature, combined with the irregular ulcer ground and margin, the giant ulcer size (average size 5.1 cm for gastric ulcers and 2.4 cm for duodenal ulcers) and clinical features (weight loss and emaciation) always raised the potential for malignancy. However, as indicated by Padda et al.,24 an endoscopic biopsy had the potential risk of inducing active bleeding. For cases that probably require surgical management endoscopic biopsy might be unnecessary.24 A potential iatrogenic free perforation often occurred after endoscopic air inflation, as shown by two case reports included in this analysis.19,36

The limitations of this study include the small sample size and the quality of the case reports, despite being the first systematic review. The risk factors that predisposed for perforation include the use of NSAIDs (including aspirin), smoking and H. Pylori infection.46,53,54 However, among the 42 patients, only 15 had information available on NSAIDs usage and 10 for H. Pylori test results. With a significant amount of missing data, it was difficult to evaluate the risk factors associated with confined peptic ulcer liver perforation or penetration. Therefore, caution should be used when interpreting and applying the related findings.


We summarized the clinical, demographic and histological features of liver involvement by perforated peptic ulcers. Histology examination, either by endoscopic biopsy or by surgical pathology, are required to make the diagnosis. Clinico-pathological correlation and immunohistochemistry are also critical to avoid misdiagnosing liver involvement as malignancy. However, the associated risk factors require further investigation.



peptic ulcer disease


gastrointestinal tract


confidence interval


non-steroidal anti-inflammatory drugs


computed tomography


magnetic resonance imaging



The authors would like to thank the research library of MD Anderson Cancer Center for their help with the retrieval of the articles.

Data sharing statement

No additional data are available.


US and Canadian Academy of Pathology (Ramzi S. Cotran Young Investigator Award, to LZ), and in part by Rutgers Cancer Institute of New Jersey Shared Resource (NCI/NIH, P30CA072720 to LZ).

Conflict of interest

The authors have nothing to disclose.

Authors’ contributions

Study concept and design (LZ), acquisition of data (JJ), analysis and interpretation of data (LZ, JJ), drafting of the manuscript (JJ), critical revision of the manuscript for important intellectual content (LZ, JJ), administrative, technical, or material support, study supervision (LZ).


  1. Haubrich WS, Roth JLA, Bockus HL. The clinical significance of penetration and confined perforation in peptic ulcer disease. Gastroenterology 1953;25(2):173-201 View Article
  2. Norris JR, Haubrich WS. The incidence and clinical features of penetration in peptic ulceration. JAMA 1961;178:386-389 View Article
  3. Qian LM, Ge JG, Huang JM. Rupture of liver abscess following hepatogastric fistula caused by perforation of remnant gastric carcinoma: a case report. Eur Rev Med Pharmacol Sci 2016;20(21):4535-4539
  4. Yuu K, Kawashima H, Toyoda S, Okumura S, Yamamoto K, Mizumura N, et al. Perforated carcinoma in the gastric remnant: a case of conservative treatment prior to successful curative r0 resection. Case Rep Surg 2016;2016:4091952 View Article
  5. Lord R, El-Feki M, Tomos L, Mohammed N, Subramanian V, Rembacken BJ. Giant gastric ulcers: Malignancy yield and predictors from a 10-year retrospective single centre cohort. United European Gastroenterol J 2018;6(7):1000-1006 View Article
  6. Newton EB, Versland MR, Sepe TE. Giant duodenal ulcers. World J Gastroenterol 2008;14(32):4995-4999 View Article
  7. Akyildiz M, Gunsar F, Akay S, Doganavsargil B, Ozütemiz O. Liver penetration of duodenal ulcer. Turk J Gastroenterol 2006;17(4):298-299
  8. Brullet E, Campo R, Calvet X, Gimenez A. Gastric ulcer penetrating to the liver: endoscopic diagnosis. Am J Gastroenterol 1993;88(5):794-795
  9. Goldman IS. Endoscopic diagnosis of hepatic penetration into a gastric ulcer. Am J Gastroenterol 1988;83(5):589-590
  10. Guerrieri C, Waxman M. Hepatic tissue in gastroscopic biopsy: evidence of hepatic penetration by peptic ulcer. Am J Gastroenterol 1987;82(9):890-893
  11. Hayashi H, Kitagawa H, Shoji M, Nakanuma S, Makino I, Oyama K, et al. Duodenal ulcer penetration into the liver at the previous left hemihepatectomy site. Int J Surg Case Rep 2013;4(12):1110-1112 View Article
  12. Jakobsen EB, Friis-Moller A, Friis J. Trichomonas species in a subhepatic abscess. Eur J Clin Microbiol 1987;6(3):296-297 View Article
  13. Jimenez-Perez FJ, Munoz-Navas MA. Endoscopic diagnosis of gastric peptic ulcer penetrating into the liver. Endoscopy 1991;23(2):98-99 View Article
  14. Kayacetin E, Kayacetin S. Gastric ulcer penetrating to liver diagnosed by endoscopic biopsy. World J Gastroenterol 2004;10(12):1838-1840 View Article
  15. Kircali B, Saricam T, Ozakyol A, Vardareli E. Endoscopic biopsy: duodenal ulcer penetrating into liver. World J Gastroenterol 2005;11(21):3329 View Article
  16. Lee SU, Jee SR, Lee HS, Lee SH. Gastric ulcer perforation to the liver diagnosed by endoscopic biopsy. Korean J Gastroenterol 2020;75(5):292-295 View Article
  17. Lesquereux-Martinez L, Alvarez AM, Parada-Gonzalez P, Bustamante-Montalvo M. Gastric ulcer penetrating the liver. Cir Esp 2017;95(1):46 View Article
  18. Martinez-Onsurbe P, Ruiz-Villaespesa A, Gonzalez-Estecha A, Butron-Vila M, de la Iglesia-Ramos M. Cytodiagnosis of gastric ulcer penetration of the liver by examination of endoscopic brushings. Acta Cytol 1991;35(4):464-466
  19. Matsuoka T, Nagai Y, Muguruma K, Yoshikawa K, Higuchi K, Seki S, et al. Liver penetration and gastrobronchial fistula: unusual complication of a peptic ulcer. Am Surg 1995;61(6):492-494
  20. Matsuzaka S, Nagai Y, Hoshi T, Serizawa Y. Visible liver from huge gastric penetration. Intern Med 2018;57(11):1667-1668 View Article
  21. Misra PS, Muscat JL. Endoscopic recognition of duodenal ulcer penetrating to the liver. Gastrointest Endosc 1976;22(3):170-171 View Article
  22. Novacek G, Geppert A, Kramer L, Wrba F, Herbst F, Schima W, et al. Liver penetration by a duodenal ulcer in a young woman. J Clin Gastroenterol 2001;33(1):56-60 View Article
  23. Oka A, Amano Y, Uchida Y, Kagawa K, Tada Y, Kusunoki R, et al. Hepatic penetration by stomal ulcer: rare complication of a peptic ulcer. Endoscopy 2012;44(S 02):E347-348 View Article
  24. Padda SS, Morales TG, Earnest DL. Liver penetration by a duodenal ulcer. Am J Gastroenterol 1997;92(2):352-354
  25. Park RH, Russel RI. Liver penetration by peptic ulcer. Am J Gastroenterol 1988;83(7):793
  26. Silverton R. Palpable masses and peptic ulceration. Med J Aust 1969;2(23):1154-1156 View Article
  27. Solomon LK, Vogiatzis I, Craig E, Campbell FC. Hepatic penetration of a single large duodenal ulcer. Ulster Med J 2005;74(2):134-135
  28. Sperber AD, Fenyves D, Barky Y, Yanai-Inbar I, Levy Y. Penetration of gastric ulcers. Dig Dis Sci 1991;36(5):700-702 View Article
  29. Stylianopoulou L, Bartsokas C, Kalliakmanis V. Gastric ulcer penetration into liver: A case presentation and review of the literature. Clin Case Rep 2021;9(1):282-285 View Article
  30. Venkatesh KR, Halpern A, Riley LB. Penetrating gastric ulcer presenting as a subcapsular liver abscess. Am Surg 2007;73(1):82-84
  31. Whelton MJ, Doyle C, Hyland M. Letter: endoscopic liver biopsy. Lancet 1974;2(7896):1574 View Article
  32. Bosanko NC, Lewis MJ, Chan YS, Winkles CL, Moss M. An example of the healing powers of a human being. BMJ Case Rep 2009;2009:bcr0620080143 View Article
  33. Chau IY, Chen YY, Chau GY. A rare cause of a liver tumor nodule. Gastroenterology 2021;160(3):663-665 View Article
  34. Kypraios D, Fusaroli P, Artuso S, Poli F, Caletti G. Gastric ulcer penetration into the liver mimicking malignancy on endoscopic ultrasound. Endosc Ultrasound 2013;2(2):107-108 View Article
  35. Roberts SH, James OF. Letter: endoscopic liver biopsy. Lancet 1974;2(7893):1395 View Article
  36. Tsai TY, Chen YY, Lee MH. Unusual causes of abdominal pain. Gastroenterology 2014;146(1):e12-13 View Article
  37. Somi MH, Tarzamni MK, Farhang S, Eftekhaar-Sadat AT. Liver mass due to penetration of a silent duodenal ulcer. Arch Iran Med 2007;10(2):242-245
  38. Mimica M. Silent free perforation of duodenal ulcer in an elderly patient presenting with melena: management directed by upper endoscopy and percussion of the liver. Endoscopy 2001;33(4):387 View Article
  39. Mostbeck G, Mallek R, Gebauer A, Tscholakoff D. Hepatic penetration by duodenal ulcer: sonographic diagnosis. J Clin Ultrasound 1990;18(9):726-729
  40. Antia FP, Marker F. Hepatic abscess secondary to duodenal ulcer. Lancet 1955;268(6865):649-650 View Article
  41. Allard JC, Kuligowska E. Percutaneous treatment of an intrahepatic abscess caused by a penetrating duodenal ulcer. J Clin Gastroenterol 1987;9(5):603-606 View Article
  42. Madrazo BL, Hricak H, Sandler MA, Eyler WR. Sonographic findings in complicated peptic ulcer. Radiology 1981;140(2):457-461 View Article
  43. Ono K, Takeda M, Makihata E, Okazaki J, Nagai A. Perforation of a duodenal ulcer into a non-parasitic liver cyst: a rare case of a penetrate hole blockaded with conservative medical management. Intern Med 2014;53(10):1043-1047 View Article
  44. Kwon MJ, Byeon S, Kang SY, Kim KM. Gastric adenocarcinoma with enteroblastic differentiation should be differentiated from hepatoid adenocarcinoma: A study with emphasis on clear cells and clinicopathologic spectrum. Pathol Res Pract 2019;215(9):152525 View Article
  45. Sung JJ, Kuipers EJ, El-Serag HB. Systematic review: the global incidence and prevalence of peptic ulcer disease. Aliment Pharmacol Ther 2009;29(9):938-946 View Article
  46. Lau JY, Sung J, Hill C, Henderson C, Howden CW, Metz DC. Systematic review of the epidemiology of complicated peptic ulcer disease: incidence, recurrence, risk factors and mortality. Digestion 2011;84(2):102-113 View Article
  47. Christensen S, Riis A, Norgaard M, Thomsen RW, Tonnesen EM, Larsson A, et al. Perforated peptic ulcer: use of pre-admission oral glucocorticoids and 30-day mortality. Aliment Pharmacol Ther 2006;23(1):45-52 View Article
  48. Noguiera C, Silva AS, Santos JN, Silva AG, Ferreira J, Matos E, et al. Perforated peptic ulcer: main factors of morbidity and mortality. World J Surg 2003;27(7):782-787 View Article
  49. Thorsen K, Soreide JA, Kvaloy JT, Glomsaker T, Soreide K. Epidemiology of perforated peptic ulcer: age- and gender-adjusted analysis of incidence and mortality. World J Gastroenterol 2013;19(3):347-354 View Article
  50. Groenen MJ, Kuipers EJ, Hansen BE, Ouwendijk RJ. Incidence of duodenal ulcers and gastric ulcers in a Western population: back to where it started. Can J Gastroenterol 2009;23(9):604-608 View Article
  51. Kurata JH, Haile BM, Elashoff JD. Sex differences in peptic ulcer disease. Gastroenterology 1985;88(1 Pt 1):96-100 View Article
  52. Wysocki A, Budzynski P, Kulawik J, Drozdz W. Changes in the localization of perforated peptic ulcer and its relation to gender and age of the patients throughout the last 45 years. World J Surg 2011;35(4):811-816 View Article
  53. Soreide K, Thorsen K, Harrison EM, Bingener J, Moller MH, Ohene-Yeboah M, et al. Perforated peptic ulcer. Lancet 2015;386(10000):1288-1298 View Article
  54. Kurata JH, Nogawa AN. Meta-analysis of risk factors for peptic ulcer. Nonsteroidal antiinflammatory drugs, Helicobacter pylori, and smoking. J Clin Gastroenterol 1997;24(1):2-17 View Article
  • Journal of Clinical and Translational Pathology
  • pISSN 2993-5202
  • eISSN 2771-165X
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Liver Involvement by Perforated Peptic Ulcer: A Systematic Review

Jingjing Jiao, Lanjing Zhang
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