Ectopic liver tissue on the gallbladder: A Preferred Reporting Items for Systematic Reviews and Meta-analyses guided systematic review

Abstract

BACKGROUND

Ectopic liver tissue (ELT) is a rare congenital anomaly characterized by hepatic parenchyma located outside the native liver without anatomical continuity. The gallbladder surface or its mesentery represents the most frequent intra-abdominal location, where ELT is typically discovered incidentally during cholecystectomy or other abdominal procedures. Although most lesions are clinically silent and histologically benign, ELT may exhibit structural and metabolic vulnerabilities related to aberrant vascular and biliary drainage, predisposing it to complications such as torsion, ischemia, and, rarely, malignant transformation. Owing to its rarity, available evidence is largely limited to case reports and small series, resulting in heterogeneous terminology, inconsistent reporting, and uncertainty regarding true incidence, clinicopathological features, and optimal surgical management.

AIM

To systematically synthesize the available literature on ELT associated with the gallbladder, with particular emphasis on demographic characteristics, anatomical features, clinical presentation, diagnostic modalities, surgical management, histopathological findings, and the potential risk of malignant transformation.

METHODS

This systematic review adhered to Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines and was registered in International Prospective Register of Systematic Reviews (No. CRD420251114781). A literature search was conducted in PubMed, MEDLINE, Scopus, Web of Science, and Google Scholar for studies published up to August 1, 2025, without language restrictions. Search terms combined free-text and Medical Subject Headings terms such as “accessory liver lobe”, “ectopic liver tissue”, “hepatic choristoma”, and related phrases specific to the gallbladder. Studies reporting ELT located on the gallbladder were included. Data extraction covered demographics, anatomical site, clinical features, diagnostics, surgical approach, histopathology, and malignancy potential. Two reviewers independently extracted data and assessed study quality, resolving discrepancies by consensus.

RESULTS

A total of 97 articles containing 121 cases of ELT located on the gallbladder surface or its mesentery meeting the aforementioned criteria were analyzed. Additionally, three new cases from our study bring the total to 124 patients. Among them, 82 were female, 38 were male, and 4 had no available sex data. Their ages ranged from 5 days to 91 years among 119 patients; this information was unavailable for the remaining 5 patients. Surgical indications varied, with 52 patients undergoing surgery for cholelithiasis and associated conditions, 23 for acute cholecystitis and related diseases, 10 for presumed chronic cholecystitis, and the remaining patients for various other indications. Laparoscopic cholecystectomy was performed in 85 patients, open cholecystectomy in 18, and various other surgical or diagnostic procedures in 21 patients, histopathological evaluation revealed that ELT exhibited normal hepatic architecture in most cases (n = 106), while 10 patients presented with histopathological abnormalities such as steatohepatitis, cirrhosis, and hepatocellular carcinoma (n = 3). Histopathological details of the ELT tissue could not be obtained for the remaining 8 patients.

CONCLUSION

ELT is a rare congenital anomaly often detected incidentally during surgery. This review represents the first comprehensive and detailed systematic analysis in the literature focusing on gallbladder-associated ELT. Although the risk of malignant transformation remains uncertain, reported histopathological abnormalities including hepatocellular carcinoma highlight the need for careful evaluation.

Key Words: Liver; Gallbladder; Ectopic liver tissue; Hepatic choristoma; histopathological features; Hepatocellular carcinoma

Core Tip: Ectopic liver tissue (ELT) associated with the gallbladder is an uncommon congenital anomaly, most often detected incidentally during cholecystectomy. Evidence regarding its clinical relevance, optimal management, and malignant potential remains fragmented due to reliance on isolated case reports. This Preferred Reporting Items for Systematic Reviews and Meta-analyses-guided systematic review synthesizes data from 97 published articles and additional cases to clarify demographic features, anatomical characteristics, surgical approaches, and histopathological outcomes of gallbladder-associated ELT. Although most lesions exhibit normal hepatic architecture, reported cases of hepatocellular carcinoma underscore the importance of recognition and complete excision with histopathological evaluation when ELT is encountered intraoperatively.

INTRODUCTION

Ectopic liver tissue (ELT), also known as hepatic choristoma, is a rare congenital anomaly characterized by the presence of functional liver parenchyma outside the main hepatic structure. ELT differs from accessory liver, which retains a hepatic connection[1-4], whereas ELT lacks any direct anatomical continuity with the main liver[5-7]. Accessory liver and ELTs were first described by Morgagni in 1767 and Corsy in 1922, respectively[1,8-11]. The incidence of ELT has been reported to range between 0.09% and 0.47%, with the gallbladder being the most common intra-abdominal site of occurrence[12,13]. This condition is typically asymptomatic and often detected incidentally during abdominal surgeries, laparoscopic procedures, or autopsie[1,9,13-15]. However, in some cases, ELT may present with complications such as torsion, ischemia, hepatocellular carcinoma (HCC), or compression of adjacent structures, leading to significant clinical consequences[16,17].

The embryological origin of ELT remains a subject of debate, with several theories proposed to explain its development. It has been suggested that accessory liver lobes most commonly occur in the wall of the gallbladder, under the surface of the liver, and at sites such as the gastrohepatic ligament, umbilical cord, adrenal glands, pancreas, pylorus, diaphragm, and splenic capsule when a portion of the pars hepatica is displaced during embryogenesis[1,18-20]. Some hypotheses suggest that it results from the displacement or migration of hepatic precursor cells during embryogenesis, while others propose that ELT originates from the formation and subsequent detachment of an accessory hepatic lobe. Additionally, the entrapment of hepatocyte-destined mesenchyme in various locations during embryogenesis has been suggested as a contributing factor[1,21,22]. Despite its structural similarity to native liver tissue, ELT often lacks complete vascular and biliary connections, which may impair its metabolic integration. This incomplete functional architecture has been hypothesized to create a microenvironment that could potentially predispose ELT to malignant transformation, although definitive evidence confirming an intrinsically increased oncogenic risk remains limited[1,16,18,23].

Histologically, ELT resembles normal liver tissue, exhibiting typical lobular architecture with portal structures and central veins. However, due to its ectopic nature, it is prone to metabolic dysfunctions such as steatosis, hemosiderosis, cholestasis, cirrhosis, and neoplastic changes[1,8,11,13], particularly HCC[23-25]. Some studies suggest that the risk of HCC in gallbladder-associated ELT cases may be lower than in other ectopic locations due to differences in embryological origin and exposure to carcinogens[1,5,15,17,23]. However, Granek et al[26] reported that HCC has been observed in approximately 3% of gallbladder-associated ELT cases, with some diagnosed in the presence of a normal native liver, indicating a potential malignant risk even in the absence of pre-existing hepatic disease. However, cases of HCC arising within ELT have been documented, underscoring the need for careful evaluation and monitoring.

The diagnosis of ELT is often challenging due to its rarity and asymptomatic nature. Preoperative imaging studies such as ultrasound (US), computed tomography (CT), or magnetic resonance imaging (MRI) may occasionally detect ELT, but in most cases, it is identified intraoperatively[11,13]. Surgical management remains the primary approach, with complete resection recommended to prevent potential complications. When ELT is identified during laparoscopic cholecystectomy, careful dissection is crucial to avoid vascular injury or bile leakage, as its vascular supply may arise from the cystic artery, hepatic parenchyma, or mesenteric vessels[2,6,7,15].

Given the clinical and surgical implications of ELT, further research is needed to clarify its pathogenesis, optimize diagnostic protocols, and establish evidence-based management guidelines. By consolidating available data, this systematic review aims to enhance the understanding of ELT, assess its clinical significance, and provide insights into effective treatment strategies.

MATERIALS AND METHODS

Protocol registration

This systematic review was prospectively registered in the International Prospective Register of Systematic Reviews (No. CRD420251114781) and conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines to ensure methodological rigor and transparency[27]. The study selection process is outlined in a Preferred Reporting Items for Systematic Reviews and Meta-analyses flow diagram (Figure 1). The diagram ensured transparency and reproducibility in study selection.

Figure 1 Preferred Reporting Items for Systematic Reviews and Meta-analyses flow diagram showing the identification, screening, eligibility, and inclusion of studies.

Literature search strategy

A comprehensive search was performed in PubMed, MEDLINE, Web of Science, Scopus, and Google Scholar, covering studies published from database inception through August 1, 2025. No language or publication status restrictions were applied. The search strategy combined Medical Subject Headings (MeSH) terms and free-text keywords, including: “ectopic liver tissue”, “accessory liver lobe”, “aberrant liver tissue”, “hepatic choristoma”, “ectopic liver nodule”, “heterotopic liver”, and “gallbladder”. Boolean operators (AND/OR) were used to optimize sensitivity. Database-specific search strategies were structured as follows: PubMed: [“Ectopic Liver” (MeSH) OR “Liver, Accessory” (MeSH) OR “ectopic liver” (title/abstract) OR “ectopic liver tissue” (title/abstract) OR “hepatic choristoma” (title/abstract) OR “heterotopic liver” (title/abstract) OR “accessory liver” (title/abstract) OR “aberrant liver” (title/abstract)] AND [“Gallbladder” (MeSH) OR “gallbladder” (title/abstract) OR “gallbladder wall” (title/abstract)]. Web of Science: TableTopic Search = (“ectopic liver” OR “accessory liver” OR “hepatic choristoma” OR “heterotopic liver” OR “aberrant liver”) AND (“gallbladder” OR “gallbladder wall”). Scopus: TITLE-ABS-KEY (“ectopic liver” OR “accessory liver” OR “hepatic choristoma” OR “heterotopic liver” OR “aberrant liver”) AND (“gallbladder” OR “gallbladder wall”). Google Scholar: (“ectopic liver” OR “accessory liver” OR “hepatic choristoma” OR “heterotopic liver” OR “aberrant liver”) AND (“gallbladder” OR “gallbladder wall”). Boolean operators (AND/OR) were used to optimize search sensitivity. Backward citation tracking involved reviewing reference lists of included articles, while forward citation tracking used tools such as Scopus and Google Scholar to identify newer studies citing the included articles. Search results were imported into EndNote 21 for duplicate removal and reference management.

Eligibility criteria

Studies were included if they reported human cases of ELT located on the gallbladder serosa or mesentery, regardless of patient age, sex, or geographic region. Eligible study designs included case reports, case series, and observational studies with extractable individual patient data. Exclusion criteria included: (1) ELT located within the gallbladder lumen which refers to tissue arising inside the cavity rather than on the serosal surface; (2) Animal or preclinical studies; (3) Insufficient data for extraction; (4) Inaccessible full texts; and (5) Duplicate publications of the same cases.

Data extraction

Two reviewers independently extracted data using a predefined Excel spreadsheet. Extracted variables included publication details (author, year, country), patient demographics (age, sex), clinical presentation, diagnostic modality, surgical indication, management options (laparoscopic/open), intraoperative findings, histopathological characteristics (e.g., hepatocyte morphology, fibrosis, steatosis, dysplasia, malignancy), and postoperative outcomes. Missing data were coded as “not available”, and attempts were made to contact corresponding authors for clarification when needed.

Risk of bias assessment

The methodological quality of included studies was assessed using the Joana Briggs Institute Critical Appraisal Checklists for case reports and case series. Two reviewers independently evaluated each study, resolving discrepancies through discussion. Appraisal domains included patient history, diagnostic assessment, intervention, outcome clarity, and completeness of reporting. Responses were categorized as “yes”, “no”, or “not available”.

Statistical analysis

Due to the rarity of gallbladder-associated ELT and variability in reporting, meta-analysis was not feasible. Data were synthesized descriptively. Continuous variables were summarized as median (interquartile range), while categorical data were reported as n (%). Descriptive results were organized into comprehensive summary tables (Tables 1 and 2).

Table 1 Demographic and clinical characteristics of reported cases of ectopic liver tissue on the gallbladder.

Ref.	Year	Country	Language	Age	Sex	History of liver disease	Preliminary diagnosis
Emral[96]	2025	Türkiye	English	34	Female	No	Cholelithiasis
Wan et al[99]	2025	China	English	40	Female	Chronic liver disease	Liver cancer
Jain et al[97]	2025	United States	English	36	Female	No	Gallbladder polyp
				57	Female	No	Chronic calculous cholecystitis + malignancy
Touati et al[98]	2024	Tunisia	English	45	Female	No	Cholelithiasis
Zhang and Zheng[3]	2025	China	English	51	Female	No	Gallbladder polyp
Xu et al[4]	2024	United States	English	52	Male	Hepatosteatosis	Biliary dyskinesia + gallbladder polyp
				35	Female	No	Acute calculous cholecystitis
Imamura et al[5]	2024	Japan	English	40	Male	NA	Cholelithiasis
Ferjaoui et al[6]	2024	Tunisia	English	60	Female	No	Cholelithiasis
Echeverry-Gutiérrez et al[7]	2024	Mexico	English	34	Male	No	Chronic calculous cholecystitis
Zhang et al[28]	2023	Australia	English	36	Female	No	Cholelithiasis
Öğüt et al[29]	2023	Türkiye	English	44	Female	No	Acute calculous cholecystitis
Nakajima et al[17]	2023	Japan	English	74	Male	Alcoholic liver disease	Acute calculous cholecystitis + choledocholithiasis
Hussein Al-Janabi et al[30]	2023	Syria	English	40	Male	No	Chronic calculous cholecystitis
				52	Male	No	NA
Arora and Kalra[31]	2023	India	English	60	Male	No	Acute calculous cholecystitis
Yildirim et al[32]	2022	Türkiye	English	51	Female	No	Cholelithiasis
Hanaki and Miyatani[33]	2022	Japan	English	60	Male	No	Acute calculous cholecystitis
Goyal and Vikas[34]	2022	India	English	NA	Female	No	Cholelithiasis
Çağlar[35]	2022	Türkiye	Turkish	38	Female	No	Cholelithiasis
Sarı et al[36]	2021	Türkiye	English	45	Male	No	Cholelithiasis
				41	Female	No	Cholelithiasis + choledocholithiasis
Rakka et al[37]	2021	Belgium	English	40	Female	No	Cholelithiasis
Moshref and Alotaibi[38]	2021	Saudi Arabia	English	47	Male	No	Acute on chronic calculous cholecystitis
Healy and Harris[39]	2021	Australia	English	61	Male	Cirrhosis	NA
Kachi et al[9]	2020	Lebanon	English	62	Female	No	Cholelithiasis
				44	Female	No	Cholelithiasis
Avdaj et al[13]	2020	Kosovo	English	47	Female	No	Chronic calculous cholecystitis
Akbulut et al[1]	2020	Türkiye	English	25	Female	No	Living liver donor
				45	Female	Cirrhosis	Cirrhosis
Yüksel et al[40]	2019	Türkiye	English	34	Female	No	Acute calculous cholecystitis
Pandit et al[41]	2019	Nepal	English	30	Female	No	Biliary pancreatitis calculous
Mannan et al[42]	2019	Saudi Arabia	English	38	Female	NA	Acute calculous cholecystitis
Isa et al[24]	2019	Bahrain	English	42	Female	No	Cholelithiasis
Granek et al[26]	2019	Australia	English	36	Male	No	Acute calculous cholecystitis
Baral et al[43]	2019	United States	English	67	Female	No	Cholelithiasis
Topcu et al[14]	2018	Türkiye	English	64	Female	No	Cholelithiasis
				70	Female	No	Pancreatic cancer
Lodha et al[44]	2018	India	English	50	Male	NA	Kidney tumor
Greenberg et al[45]	2018	United States	English	52	Female	Hepatosteatosis	Cholelithiasis
Burke et al[46]	2018	Ireland	English	30	Female	NA	Cholelithiasis
Weber-Alvarez et al[15]	2017	Mexico	English	37	Female	NA	Acute calculous cholecystitis
Termos et al[47]	2017	Kuwait	English	73	Female	No	Gallbladder cancer
Galimov et al[48]	2017	Russia	Russian	70	Male	NA	Acute calculous cholecystitis
Yahya et al[49]	2016	Libya	English	45	Female	NA	Acute calculous cholecystitis
				45	Female	NA	Cholelithiasis
				35	Female	NA	Cholelithiasis
				20	Male	NA	Penetrating abdominal injury
Mani et al[50]	2016	United States	English	56	Male	Hepatosteatosis	Acute calculous cholecystitis
Longjam et al[51]	2016	India	English	42	Female	NA	Cholelithiasis
Leena[52]	2016	India	English	25	Male	NA	Autopsy
Kostov and Kobakov[53]	2016	Bulgaria	English	49	Male	Rectum cancer liver metastasis	Rectum cancer liver metastasis
Karaca et al[10]	2016	Türkiye	English	43	Female	No	Cholelithiasis
Jaboury[54]	2016	Australia	English	22	Female	NA	Cholelithiasis
Ito et al[19]	2016	Japan	English	59	Female	No	Cholelithiasis
Handra-Luca[55]	2016	France	English	68	Female	NA	Cholelithiasis
				56	Female	NA	Cholelithiasis
Aslan and Akkas[56]	2016	Türkiye	English	49	Female	NA	Chronic calculous cholecystitis
Yankol et al[57]	2015	Türkiye	English	30	Male	No	Living liver donor
Smyth et al[58]	2015	Australia	English	77	Female	No	Cholelithiasis
Hussein et al[59]	2015	Lebanon	English	49	Female	No	Acute calculous cholecystitis
Bal et al[2]	2015	Türkiye	English	51	Female	NA	Biliary pancreatitis calculous
Abhilash et al[60]	2015	India	English	45	Female	NA	Acute calculous cholecystitis
Terakawa et al[61]	2014	Japan	Japanese	33	Female	No	Cholelithiasis
Pulle et al[62]	2014	India	English	43	Female	NA	Cholelithiasis
Arslan et al[12]	2014	Türkiye	English	59	Female	No	Cholelithiasis
Yajima et al[63]	2013	Japan	Japanese	73	Female	No	Cholelithiasis
Sirasanagandla et al[64]	2013	India	English	62	Male	NA	Autopsy
Öztürk et al[65]	2013	Türkiye	Turkish	35	Female	No	Cholelithiasis
Martinez et al[11]	2013	Brazil	English	37	Female	NA	Cholelithiasis
Khan et al[66]	2013	India	English	32	Female	NA	Cholelithiasis
Hassan et al[67]	2013	India	English	32	Female	No	Chronic calculous cholecystitis
Sözen et al[68]	2012	Türkiye	Turkish	40	Female	NA	Cholelithiasis
Patel et al[69]	2011	United Kingdom	English	21	Female	NA	Cholelithiasis
Karaman et al[25]	2012	Türkiye	English	63	Male	NA	Cholelithiasis
Mallya et al[100]	2012	India	English	36	Female	No	Living liver donor
Nagar et al[70]	2011	United States	English	25	Female	No	Abdominal pain + cystic mass
Dettmer et al[71]	2011	Switzerland	English	91	Female	No	Acute calculous cholecystitis
Catani et al[72]	2011	Italy	English	72	Female	No	Acute calculous cholecystitis
				83	Female	No	Cholelithiasis
Ateş et al[73]	2010	Türkiye	Turkish	64	Female	No	Acute calculous cholecystitis
				49	Male	NA	Cholelithiasis
Triantafyllidis et al[21]	2009	Greece	English	56	Female	NA	Cholelithiasis
Sánchez et al[74]	2009	Mexico	Spanish	36	Male	NA	Chronic calculous cholecystitis
Kyeong et al[75]	2008	South Korea	English	66	Female	NA	Cholelithiasis
Soto et al[76]	2007	United States	English	32	Female	NA	Cholelithiasis
Malhas et al[77]	2007	United Kingdom	English	39	Female	NA	Cholelithiasis
				42	Male	Hepatosteatosis	Cholelithiasis
Koh and Hunt[78]	2007	Australia	English	60	Female	NA	Acute calculous cholecystitis
Beltran et al[79]	2007	Chile	English	33	Female	NA	Cholelithiasis
				27	Male	NA	Gastric cancer
				35	Male	NA	Pancreatic pseudocyst
				47	Male	No	Cholelithiasis
Wang and Liu[80]	2006	China	Chinese	38	Male	NA	Gallbladder polyp
Ngowe Ngowe et al[81]	2006	Cameroun	French	46	Female	No	Acute calculous cholecystitis
Ikeda et al[82]	2006	Japan	English	70	Male	Chronic liver disease	Cirrhosis + hepatocellular carcinoma
Lundy et al[83]	2005	United States	English	38	Female	NA	Liver cancer
Leone et al[16]	2004	Italy	English	54	Female	No	Gallbladder cancer
Sakarya et al[84]	2002	Turkey	English	NA	NA	NA	NA
Griniatsos et al[88]	2002	United Kingdom	English	39	Female	NA	Acute calculous cholecystitis
				49	Male	NA	Cholelithiasis
Acar et al[86]	2002	Turkey	English	55	Female	NA	Cholelithiasis
Arakawa et al[23]	1999	Japan	English	48	Male	Alcoholic liver disease	Autopsy
Hamdani and Baron[87]	1994	United States	English	49	Male	Cirrhosis	Primer sclerosing cholangitis
Ohbuchi et al[88]	1993	Japan	Japanese	64	Female	No	Gallbladder polyp
Boyle et al[89]	1992	United States	English	44	Female	No	Acute calculous cholecystitis
Watanabe et al[22]	1989	Japan	English	37	Male	Cystic liver lesion	Cystic liver lesion
				56	Male	Cirrhosis	Alcoholic liver disease
				71	Female	Cirrhosis	Cirrhosis
				64	Female	Cirrhosis	Cirrhosis
Tejada and Danielson[90]	1989	United States	English	43	Male	NA	Cholelithiasis + hereditary spherocytosis
Fellbaum et al[91]	1987	Austria	German	34	Female	NA	Cholelithiasis
Natori et al[92]	1986	Japan	English	56	Female	No	Cholelithiasis
Ashby[93]	1969	United Kingdom	English	42	Male	NA	Duodenal ulcer
Bassis and Izenstark[94]	1956	United States	English	5 days	Male	NA	Autopsy
				NA	NA	NA	Chronic calculous cholecystitis
				NA	NA	NA	Chronic calculous cholecystitis
				NA	NA	NA	Chronic calculous cholecystitis
Thorsness[95]	1941	United States	English	63	Female	NA	Autopsy
Cullen[8]	1925	United States	English	33	Female	No	Jaundice
Our case 1				58	Male	No	Acute calculous cholecystitis
Our case 2				30	Female	No	Living liver donor
Our case 3				41	Female	No	Cholelithiasis

NA: Not available.

Table 2 Radiological, surgical, and histopathological findings in reported cases of ectopic liver tissue on the gallbladder.

Ref.	Radiologic tools	Lesion sizes (mm)	Surgical procedure	Histopathological findings of ELT	Histopathological findings of gallbladder specimens
Emral[96]	US	10	LC	ELT	NA
Wan et al[99]	US + CT + MRI	15	Cholecystectomy (radical)	HCC	Chronic calculous cholecystitis
Jain et al[97]	NA	20	Cholecystectomy (which?)	ELT	Normal gallbladder
	CT	18	OC	ELT	Chronic calculous cholecystitis
Touati et al[98]	US	10	LC	ELT	Chronic calculous cholecystitis
Zhang and Zheng[3]	US	10	LC (3-port)	ELT	NA
Xu et al[4]	US + HIDA	9	LC	Steatohepatitis	Chronic calculous cholecystitis
	US	17	LC	ELT	Acute on chronic calculous cholecystitis
Imamura et al[5]	NA	10	LC	ELT	NA
Ferjaoui et al[6]	US	20	LC	ELT	Chronic calculous cholecystitis
Echeverry-Gutiérrez et al[7]	US	20	LC	ELT	NA
Zhang et al[28]	US	NA	LC	ELT	NA
Öğüt et al[29]	US	15	LC	No excise	Chronic calculous cholecystitis
Nakajima et al[17]	CT	10	OC	HCC	Necrotic cholecystitis
Hussein Al-Janabi et al[30]	US	10	LC	ELT	NA
	NA	13	LC	ELT	NA
Arora and Kalra[31]	US	NA	LC	ELT	Chronic calculous cholecystitis
Yildirim et al[32]	US	10	LC	ELT	Cholelithiasis + cholesterolosis
Hanaki and Miyatani[33]	CT	8	LC	ELT	Acute cholecystitis cholelithiasis
Goyal and Vikas[34]	US	NA	LC	ELT	Chronic calculous cholecystitis
Çağlar[35]	US	20	LC	ELT	NA
Sarı et al[36]	US	16	LC	ELT	NA
	ERCP	8	LC	ELT	NA
Rakka et al[37]	US	20	LC	ELT	NA
Moshref and Alotaibi[38]	US	12	LC	ELT	Chronic calculous cholecystitis
Healy and Harris[39]	Laparoscopy	NA	LC	Micronodular cirrhosis	NA
Kachi et al[9]	NA	5	LC	ELT	NA
	US	10	LC	ELT	NA
Avdaj et al[13]	US	NA	LC	ELT	NA
Akbulut et al[1]	CT + MRI	15	Donor hepatectomy	ELT	Normal gallbladder
	CT	NA	LT	Cirrhosis	Chronic calculous cholecystitis
Yüksel et al[40]	US	17	LC	ELT	Chronic calculous cholecystitis
Pandit et al[41]	US + MRCP	35	LC	ELT	NA
Mannan et al[42]	US	50	LC	ELT	NA
Isa et al[24]	US	NA	LC	ELT	NA
Granek et al[26]	US	19	LC	ELT	NA
Baral et al[43]	US	30	LC	ELT	NA
Topcu et al[14]	US	15	OC	ELT	NA
	US + CT + MRI	80	Whipple procedure	ELT	NA
Lodha et al[44]	US + CT	20	Lap nephrectomy	No excise	NA
Greenberg et al[45]	US + CT	30	LC	ELT	NA
Burke et al[46]	US	NA	LC	ELT	NA
Weber-Alvarez et al[15]	US	10	LC	ELT	Acute on chronic calculous cholecystitis
Termos et al[47]	US + CT	30	LC	ELT	NA
Galimov et al[48]	US	6	LC	ELT	Phlegmonous cholecystitis (cholelithiasis)
Yahya et al[49]	NA	NA	LC	ELT	NA
	US	NA	LC	ELT	NA
	US	60	LC	ELT	NA
	NA	NA	Diagnostic laparoscopy	ELT	NA
Mani et al[50]	CT	NA	LC	ELT	NA
Longjam et al[51]	US	12	LC	ELT	Chronic calculous cholecystitis
Leena[52]	Autopsy	15	Autopsy	NA	NA
Kostov and Kobakov[53]	NA	35	OC	ELT	Hydatid cyst on gallbladder wall
Karaca et al[10]	US	15	LC	ELT	NA
Jaboury[54]	NA	NA	LC	ELT	NA
Ito et al[19]	US + CT + MRI	15	LC	ELT	NA
Handra-Luca[55]	US	5	LC	ELT	Chronic calculous cholecystitis
	US	11	LC	ELT	Chronic calculous cholecystitis
Aslan and Akkas[56]	US	8	LC	ELT	NA
Yankol et al[57]	US + CT + MRCP	15	Donor hepatectomy	ELT	NA
Smyth et al[58]	US	20	LC	ELT	Chronic calculous cholecystitis
Hussein et al[59]	CT	NA	LC	ELT	NA
Bal et al[2]	US + ERCP	20	LC	ELT	Chronic calculous cholecystitis
Abhilash et al[60]	US	10	LC	ELT	Chronic calculous cholecystitis
Terakawa et al[61]	US + CT + MRCP	12	LC	ELT	NA
Pulle et al[62]	US	20	LC	ELT	Chronic calculous cholecystitis
Arslan et al[12]	US	20	LC	ELT	NA
Yajima et al[63]	US + CT	6	LC	ELT	NA
Sirasanagandla et al[64]	NA	20	Autopsy	ELT	NA
Öztürk et al[65]	US	20	LC	ELT	NA
Martinez et al[11]	US	30	LC	ELT	Chronic calculous cholecystitis
Khan et al[66]	NA	NA	LC	Fatty change	Chronic calculous cholecystitis
Hassan et al[67]	US	10	LC	ELT	Chronic calculous cholecystitis
Sözen et al[68]	US	8	LC	ELT	NA
Patel et al[69]	US	26	LC	ELT	NA
Karaman et al[25]	US	11	LC	ELT	NA
Mallya et al[100]	NA	15	Donor hepatectomy	ELT	NA
Nagar et al[70]	US + CT + MRCP	45	LC	ELT	Localized cholecystitis
Dettmer et al[71]	CT	15	LC	ELT	Acute cholecystitis cholelithiasis)
Catani et al[72]	US	15	LC	ELT	NA
	US	14	LC	ELT	NA
Ateş et al[73]	NA	15	LC	ELT	NA
	US	15	LC	ELT	NA
Triantafyllidis et al[21]	US	15	LC	ELT	Chronic calculous cholecystitis
Sánchez et al[74]	US	30	LC	ELT	NA
Kyeong et al[75]	CT	10	LC	ELT	Chronic calculous cholecystitis
Soto et al[76]	US	8	LC	ELT	NA (cholelithiasis)
Malhas et al[77]	US	NA	LC	ELT	NA
	US	NA	LC	ELT	NA
Koh and Hunt[78]	NA	15	LC	ELT	NA
Beltran et al[79]	US	17	LC	ELT	NA
	US + CT	7	OC + gastrectomy	ELT	NA
	US + CT	18	OC	ELT	NA
	US	12	LC	ELT	Chronic calculous cholecystitis
Wang and Liu[80]	US	11	LC	ELT	Chronic calculous cholesterol polyps)
Ngowe Ngowe et al[81]	US	30	OC	ELT	Chronic calculous cholecystitis
Ikeda et al[82]	US + CT	NA	OC + segment V resection	Steatohepatitis	NA
Lundy et al[83]	US + CT	30	LC	ELT	NA
Leone et al[16]	US + CT	90	OC	HCC	NA
Sakarya et al[84]	NA	NA	LC	NA	NA
Griniatsos et al[88]	US	10	LC	ELT	NA
	US	15	LC	ELT	NA
Acar et al[86]	US	14	OC	ELT	Papillary epithelial hyperplasia
Arakawa et al[23]	Autopsy	15	Autopsy	Alcoholic cirrhosis	NA
Hamdani and Baron[87]	US + CT + MRI	30	LT	ELT	NA
Ohbuchi et al[88]	US	5	LC	ELT	NA
Boyle et al[89]	US	20	OC	ELT	Chronic calculous cholecystitis
Watanabe et al[22]	CT	5	Diagnostic laparoscopy	Biliary microhamartoma	NA
	Laparoscopy	8	Diagnostic laparoscopy	NA	NA
	Laparoscopy	6	Diagnostic laparoscopy	NA	NA
	US + CT	10	Diagnostic laparoscopy	NA	NA
Tejada and Danielson[90]	US	11	OC + splenectomy	ELT	Chronic calculous cholecystitis
Fellbaum et al[91]	NA	5	OC	ELT	Chronic calculous cholecystitis
Natori et al[92]	CT	12	OC + excision	ELT	Chronic calculous cholecystitis
Ashby[93]	NA	10	OC + excision	ELT	NA
Bassis and Izenstark[94]	NA	8	Autopsy	ELT	NA
	NA	15	OC	ELT	Chronic calculous cholecystitis
	NA	10	OC	ELT	Chronic calculous cholecystitis
	NA	6	OC	ELT	Chronic calculous cholecystitis
Thorsness[95]	Autopsy	5	Autopsy	ELT	NA
Cullen[8]	NA	12	Excision	NA	NA
Our case 1	US + CT	25	LC	ELT	Chronic calculous cholecystitis
Our case 2	US + CT + MRI	8	Donor hepatectomy	ELT	Chronic calculous cholecystitis
Our case 3	US	13	LC	ELT	Chronic calculous cholecystitis

US: Ultrasonography; CT: Computed tomography; MRI: Magnetic resonance imaging; HIDA: Hepatobiliary iminodiacetic acid; ERCP: Endoscopic retrograde cholangiopancreatography; MRCP: Magnetic resonance cholangiopancreatography; NA: Not available; LC: Laparoscopic cholecystectomy; OC: Open cholecystectomy; LT: Liver transplantation; ELT: Ectopic liver tissue; HCC: Hepatocellular carcinoma.

RESULTS

A total of 97 articles including 121 patients, published between January 1925 and August 2025, met the inclusion criteria in our literature search using the PubMed, MEDLINE, Google Scholar, and Google databases[1-17,19,21-26,28-100]. Additionally, three new cases from our study bring the total to 124 patients. The distribution of published cases by country was as follows: Turkey (n = 19), United States (n = 14), Japan (n = 11), India (n = 11), Australia (n = 6), United Kingdom (n = 4), Mexico (n = 3), China (n = 3), Italy (n = 2), Lebanon (n = 2), Saudi Arabia (n = 2), Tunisia (n = 2), Austria (n = 1), Bahrain (n = 1), Belgium (n = 1), Brazil (n = 1), Bulgaria (n = 1), Cameroun (n = 1), Chile (n = 1), France (n = 1), Greece (n = 1), Ireland (n = 1), Kosovo (n = 1), Kuwait (n = 1), Libya (n = 1), Nepal (n = 1), Russia (n = 1), South Korea (n = 1), Switzerland (n = 1), Syria (n = 1). The language distribution of the articles was as follows: English (n = 85), Turkish (n = 4), Japanese (n = 3), French (n = 1), German (n = 1), Chinese (n = 1), Russian (n = 1), and Spanish (n = 1). Full-text access was obtained for all articles including analysis.

Apart from the 97 articles presented above, four studies related to ELT located on the gallbladder were excluded from this review. In the study by Svane and Knudtzon[101], two cases of ELT located on the gallbladder surface were reported; however, the article was not accessible in any form and therefore could not be included. Beltrán et al[102] published a case in Spanish, but since the same case was also published in English in the same year, the Spanish article was excluded. Although the preprint version by Wan et al[103] was available online on Research Square in 2023, the version published in 2025[99] was included in the article. Finally, in the German article by Eiserth[104], three cases related to the gallbladder were mentioned, but due to insufficient clarity, these cases were also not included in the review.

Among the 124 reported patients including our 3 cases, 82 were female, 38 were male, and 4 had no available sex data. The ages ranged from 5 days to 91 years, with age data missing for 5 patients. Excluding the 5-day-old infant, for the 118 adult patients with available age data, the median age was 45 years, with a range of 20-91 years and an interquartile range of 36-58 years.

Among 124 patients, underlying liver disease was absent in 59 cases, while 16 patients were identified with specific conditions: Cirrhosis (n = 6), hepatosteatosis (n = 4), alcoholic liver disease (n = 2), chronic liver disease (n = 2), rectal carcinoma with liver metastasis (n = 1), and cystic liver lesion (n = 1). For the remaining 49 patients, information on liver disease was not available.

Surgical indications and preliminary diagnoses were reported as follows: The most common indication was cholelithiasis (n = 52), including one case with choledocholithiasis and one with hereditary spherocytosis. Acute cholecystitis was the second most frequent (n = 22), one case also associated with choledocholithiasis. Suspected chronic cholecystitis accounted for 10 cases, including one with a suspicion of malignancy. Gallbladder-originating masses or polyps were seen in 6 patients, two of which were initially suspected to be gallbladder cancer. Cirrhosis was reported in 4 patients, including one with suspected HCC. ELT was identified during autopsy in 5 cases. Four cases were incidentally discovered during surgery for living liver donation. In 3 patients, the surgical indication was not specified. The remaining 18 patients had diverse indications, including liver cancer (n = 2), biliary pancreatitis (n = 2), and single cases of abdominal pain with a cystic mass, acute on chronic cholecystitis, alcoholic liver disease, biliary dyskinesia with gallbladder polyp, cystic liver lesion, duodenal ulcer, gastric cancer, jaundice, kidney tumor, pancreatic cancer, pancreatic pseudocyst, penetrating abdominal injury, primary sclerosing cholangitis, and rectal carcinoma with liver metastasis.

The diagnostic evaluation of ELT across reported cases involved a wide spectrum of modalities. US was the most frequently employed imaging technique (n = 63). US + CT was used in 11 cases. CT alone was performed in 10 cases. US + CT + MRI (n = 5), Autopsy (n = 3), laparoscopy (n = 3), and US + CT + magnetic resonance cholangiopancreatography (n = 3) were less common. Single cases were reported for CT + MRI (n = 1), US + magnetic resonance cholangiopancreatography (n = 1), US + endoscopic retrograde cholangiopancreatography (n = 1), endoscopic retrograde cholangiopancreatography alone (n = 1), and US + hepatobiliary iminodiacetic acid (n = 1). In 21 cases, no specific preoperative diagnostic workup was reported.

Surgical approaches were diverse: 85 patients underwent laparoscopic cholecystectomy (one of them with a three-port technique), 18 patients underwent open cholecystectomy (including segment V resection in one, splenectomy in one, and gastrectomy in one), 5 patients underwent autopsy, 5 patients underwent diagnostic laparoscopy, 4 patients underwent donor hepatectomy, 2 patients underwent liver transplantation, 1 patient underwent laparoscopic nephrectomy, 1 patient underwent radical cholecystectomy, 1 patient underwent excision, 1 patient underwent cholecystectomy without a specified technique, and 1 patient underwent a Whipple procedure. Among 105 patients, the ELT lesion size was measured, with a median diameter of 15 mm (minimum-maximum: 1.1-90 mm; Q1-Q3: 10-20 mm). In the remaining 19 patients, lesion size data were not available.

Among 124 patients, histopathological outcomes were as follows: ELT with normal liver architecture (n = 106), data not available (n = 6), not excised (n = 2), HCC (n = 3), steatohepatitis (n = 2), alcoholic cirrhosis (n = 1), biliary microhamartoma (n = 1), cirrhosis (n = 1), fatty change (n = 1), and micronodular cirrhosis (n = 1). A detailed summary of the demographic, clinical, and histopathological characteristics is provided in Tables 1 and 2. In addition, intraoperative images of our three cases included in this study are presented in Figure 2.

Figure 2 Intraoperative image. A: From case 1, showing ectopic liver tissue (ELT) attached to the gallbladder wall; B: From case 2, demonstrating pedunculated ELT being dissected from the gallbladder serosa; C: From case 3, demonstrating a broad-based ELT attached to the gallbladder serosa (orange arrow: ELT, blue arrow: Gallbladder, purple: Pericholecystic adhesions).

DISCUSSION

Terminology and definitions

ELT is a rare congenital anomaly characterized by the presence of functional liver parenchyma outside the primary hepatic structure, lacking direct anatomical continuity with the native liver. ELT can be categorized based on its anatomical presentation: (1) Solitary ectopic liver, a completely separate hepatic tissue with no connection to the main liver, commonly found on the gallbladder, hepatic ligaments, or peritoneal surfaces[1,22,59]; (2) Microscopic ectopic liver, consisting of small hepatic foci embedded within another organ, such as the gallbladder wall[56,86]; (3) Accessory liver lobe, a larger hepatic mass connected to the native liver via a vascular stalk[1,57,64]; and (4) Small accessory hepatic nodules, weighing 10-30 g and partially attached to the native liver[19,56]. These classifications assist in differentiating developmental anomalies and guide appropriate management strategies[21,47,54,85]. It is crucial to distinguish ELT from accessory liver tissue, as these two entities are often confused in the literature[54,59,86]. Accessory liver tissue, also known as an accessory liver lobe, maintains vascular and biliary connections to the main liver and represents a developmental duplication of hepatic tissue[16,19,42,51,57]. In contrast, ELT is entirely separate, lacking metabolic function due to impaired vascularization and bile drainage, which increases its risk of malignant transformation[11,43,47,58]. While accessory liver lobes are often incidental findings with little clinical significance[16-18,49,54], ELT poses distinct risks, particularly when associated with HCC[56,64,99]. Given these distinctions, accurate classification of ELT is essential for appropriate clinical management[7,36,51]. A conceptual schematic overview summarizing the proposed pathophysiological mechanisms of gallbladder-associated ELT is illustrated in Figure 3.

Figure 3 Conceptual schematic overview of gallbladder-associated ectopic liver tissue illustrating anatomical location, proposed microenvironmental stressors (impaired vascularization and biliary drainage), and potential progression to hepatocellular carcinoma. HCC: Hepatocellular carcinoma.

Incidence and clinical relevance

Determining the true incidence of ELT is challenging due to its asymptomatic nature and incidental diagnosis during surgical procedures or autopsy[9,13,15,37,40]. Reported incidences range from 0.24% to 0.47%, with the gallbladder being the most common location[12,13]. A review of 5500 autopsies found ELT in only 0.05% of cases, with gallbladder involvement in just three instances[1,12,15,104]. Additionally, a laparoscopic study involving 1060 procedures identified ELT attached to the gallbladder in three cases (0.47%)[15,22]. While these findings highlight the rarity of ELT, advancements in laparoscopic and robotic surgery may improve detection rates in the future.

Theories of development and pathogenesis

Several theories have been proposed to explain the embryological development of ELT[49,54,56,60]. The most widely accepted hypotheses include the migration or displacement of hepatocyte precursor cells during embryogenesis, the formation of an accessory liver lobe followed by regression of its connection to the native liver, and the entrapment of hepatic tissue during diaphragm or umbilical ring closure[19,47,56,59,60]. Additionally, dorsal budding of hepatic tissue before pleuroperitoneal canal closure has been suggested as a contributing factor[43,56,60,85]. The variability in ELT size and location supports the notion that multiple mechanisms, rather than a single etiologic factor, may contribute to its development[16,36,42].

Size variability and histological features

The size of ELT varies significantly, ranging from microscopic foci to several centimeters in diameter[7,23,43,56,86]. In cases without HCC, the average reported size is 17.8 mm, although some lesions can grow larger[16,19,36,51,57,71]. Histologically, ELT resembles normal liver tissue, displaying regular lobules, central veins, and normal portal structures[19,21,42,47,60]. However, some cases exhibit architectural abnormalities, such as the absence of the classical hexagonal lobule pattern[7,54,59,64]. Like native liver tissue, ELT can undergo fatty changes, hemosiderosis, cholestasis, cirrhosis, hepatitis, or even malignant transformation into HCC[1,11,43,57]. In this study, which included data from 105 patients with available lesion size, the median dimension of gallbladder-associated ELT was reported as 15 mm, indicating that in 50% of patients the lesion size ranged between 10 mm and 20 mm.

Vascular supply and surgical considerations

The vascular supply of ELT is not well documented, but three primary vascular patterns have been described: (1) An artery originating from the cystic artery[78]; (2) A vascular pedicle arising from the liver parenchyma[2]; and (3) Vascular structures embedded within a mesentery extending from the liver to the ectopic tissue[72]. Identifying the vascular supply is crucial to prevent intraoperative complications, such as hemorrhage or ischemia[2,40,43]. Surgeons should also be aware of potential biliary drainage abnormalities, which may impact postoperative outcomes[1,64]. In the present study, it was observed that in most cases the ELT was excised concurrently with cholecystectomy. However, in a few cases, since alternative surgical procedures were planned, only the presence of the lesion was reported, and the ELT was left intact as no cholecystectomy was performed. In one study, even though cholecystectomy was carried out, the ectopic tissue was not resected. In our view, whenever surgery involving the hepatobiliary system is planned, the potential risk of complications necessitates the resection of ectopic tissue. Although no established consensus exists, we recommend that in all patients undergoing gallbladder surgery, such ectopic tissues adjacent to the gallbladder should be respected and submitted for histopathological examination.

Association with HCC

ELT has been linked to HCC in multiple case reports and small retrospective studies. However, the exact prevalence and risk factors remain a subject of debate[11,49,54,64]. While some studies indicate that ELT is at a higher risk for malignant transformation due to impaired bile drainage, reduced vascular supply[1,5-7], and limited metabolic capacity[36,47,51], others argue that the incidence of HCC in ELT is comparable to that in normal liver tissue[12,15,28,37,42].

Several studies have reported cases of HCC arising in ELT without underlying cirrhosis, suggesting that ELT may be predisposed to malignant transformation independent of classic hepatocarcinogenic factors[1,4,19,30,54,56]. This contrasts with HCC in native liver tissue, where cirrhosis is often a key predisposing factor[6,22,47,59]. A review of ELT-associated HCC cases demonstrated that a significant proportion developed malignancy without preexisting cirrhosis, raising questions about the molecular[5,7,11] and genetic mechanisms driving carcinogenesis in ectopic hepatic tissue[17,49,71]. Additionally, variations in ELT location may influence the risk of HCC. Some studies suggest that ELT located outside the gallbladder, particularly in the peritoneal cavity or retroperitoneum, may have a higher risk of malignant transformation compared to ELT attached to the gallbladder[1,4,36,43,52]. However, statistical analyses remain inconclusive, with no definitive evidence confirming a higher malignancy risk based on ELT location alone[1,57].

The heterogeneity in reported malignant risk may partly reflect methodological limitations inherent to the ELT literature. Most available data derive from isolated case reports and small retrospective series, predisposing to publication bias, as malignant cases are more likely to be reported. In addition, variations in diagnostic criteria, inconsistent documentation of underlying liver status, and limited follow-up durations further complicate risk estimation. These factors may explain why some studies suggest an elevated malignant potential, whereas others report a risk comparable to native hepatic tissue.

From a molecular standpoint, hepatocarcinogenesis in ELT is presumed to share core oncogenic events with conventional HCC, including telomerase reactivation through telomerase reverse transcriptase promoter mutations, activation of the Wnt/β-catenin signaling pathway (catenin beta 1 alterations), and TP53-associated cell-cycle dysregulation[105-107]. However, unlike intrahepatic HCC, ELT typically lacks the background of chronic cirrhosis or sustained viral hepatitis. Instead, its aberrant microenvironment may play a central role. Incomplete vascularization and impaired biliary drainage may predispose ELT to chronic hypoxia and bile stasis, promoting oxidative stress, DNA damage, and pro-inflammatory signaling cascades. Activation of hypoxia-inducible factors and persistent regenerative stimuli may create a pro-carcinogenic milieu despite the absence of traditional risk factors. Although direct molecular profiling data in ELT-associated HCC remain limited, these mechanisms suggest that microenvironmental stressor factors may converge on canonical hepatocarcinogenic pathways[1,106].

From a clinical perspective, the detection of HCC in ELT is often incidental, either through imaging studies performed for unrelated reasons or during histopathological examination of resected gallbladders[5,12,14,15]. Given the rarity of ELT-associated HCC, there are no standardized screening or management protocols[1,18,19,47]. Some researchers advocate for prophylactic resection of ELT, particularly in patients with risk factors for HCC[5,17,18,49,54], while others suggest a more conservative approach with regular monitoring via imaging and serum biomarkers[1,4,28,36]. In the present study, HCC was identified in ELT in 3 out of 124 patients with gallbladder-associated lesions. Notably, among these three cases, one patient had no documented underlying liver disease, whereas the remaining two had pre-existing hepatic conditions (alcohol-related liver disease and chronic liver disease, respectively). This heterogeneity suggests that malignant transformation in ELT may occur both in the presence and absence of classical hepatocarcinogenic backgrounds. Therefore, it remains challenging to determine whether ELT itself confers an intrinsically increased oncogenic susceptibility or whether systemic hepatic risk factors contribute in selected cases. This finding underscores the necessity of not overlooking ELT and highlights the importance of subjecting all excised tissues to thorough histopathological examination.

In a previously published systematic review conducted by our group investigating the development of HCC in ELT regardless of localization, we identified 55 cases of HCC reported across 53 studies[106]. The most common sites of ectopic HCC were the subphrenic space (20.0%), peritoneum (12.7%), retroperitoneum (10.9%), pancreas (10.9%), and the surface or lumen of the gallbladder (9.1%). Interestingly, the majority of these patients tested negative for viral markers of liver disease and had no evidence of underlying hepatic pathology, suggesting that tumorigenesis in ELT may follow a distinct biological pattern.

Building upon these findings, further research, including larger case series and molecular studies, is needed to clarify the oncogenic potential of ELT and to determine whether specific surveillance or treatment strategies are warranted. Future investigations should prioritize prospective case registration and targeted molecular profiling, particularly focusing on telomerase reverse transcriptase promoter mutations, catenin beta 1-mediated Wnt/β-catenin activation, TP53 alterations, and hypoxia-inducible signaling pathways. Comparative genomic analyses between ELT-associated HCC and intrahepatic HCC may help determine whether ELT follows a distinct oncogenic trajectory. Understanding the role of genetic mutations, microenvironmental factors, and cellular pathways in ELT-associated carcinogenesis may provide insights into HCC pathophysiology more broadly and inform future clinical management guidelines.

Limitations

This review is limited by the nature of the available evidence, which predominantly consists of case reports and small series with heterogeneous reporting quality and incomplete data. Publication and language biases are likely despite broad database coverage. Misclassification between accessory liver and true ELT, and between serosal vs intraluminal locations, may have occurred due to variable terminology and diagnostic criteria across studies. Because of clinical and methodological heterogeneity, quantitative meta-analysis and pooled risk estimation (including precise malignancy risk) were not feasible. Finally, most ELT diagnoses were made intraoperatively, which may underrepresent asymptomatic lesions detectable only by standardized imaging protocols.

CONCLUSION

ELT associated with the gallbladder is an uncommon developmental anomaly that is most often identified intraoperatively. In this Preferred Reporting Items for Systematic Reviews and Meta-analyses-guided systematic review of 97 articles plus three new cases (total 124 patients), ELT typically measured in the sub-centimeter to centimeter range (median 15 mm) and most specimens displayed normal hepatic architecture; however, histopathological abnormalities were documented and HCC was identified in three patients. These findings indicate that, although the absolute malignant risk remains low and uncertain, ELT should not be disregarded when encountered. When technically feasible and safe, concurrent excision during cholecystectomy with submission for histopathological evaluation is reasonable, with careful attention to potential variant vascular or biliary anatomy. As detection increases with modern imaging and minimally invasive surgery, standardized reporting and management algorithms are needed. Future work should focus on prospective registries and molecular profiling to clarify oncogenic risk and guide surveillance or treatment strategies.

ACKNOWLEDGEMENTS

During the preparation of this work, the authors used ChatGPT (OpenAI, San Francisco, CA, United States; version GPT-5.2.) in order to improve the readability and language of the manuscript. After using these tools, the authors reviewed and edited the content as needed and take full responsibility for the content of the publication.