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Hepatic cysts

MedGen UID:
82761
Concept ID:
C0267834
Disease or Syndrome
Synonym: Liver cysts
SNOMED CT: Hepatic cyst (85057007); Cyst of liver (85057007); Liver cyst (85057007)
 
HPO: HP:0001407

Definition

A cystic lesion located in the liver. [from NCI]

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
  • Hepatic cysts

Conditions with this feature

Cranioectodermal dysplasia 1
MedGen UID:
96586
Concept ID:
C0432235
Disease or Syndrome
Cranioectodermal dysplasia (CED) is a ciliopathy with skeletal involvement (narrow thorax, shortened proximal limbs, syndactyly, polydactyly, brachydactyly), ectodermal features (widely spaced hypoplastic teeth, hypodontia, sparse hair, skin laxity, abnormal nails), joint laxity, growth deficiency, and characteristic facial features (frontal bossing, low-set simple ears, high forehead, telecanthus, epicanthal folds, full cheeks, everted lower lip). Most affected children develop nephronophthisis that often leads to end-stage kidney disease in infancy or childhood, a major cause of morbidity and mortality. Hepatic fibrosis and retinal dystrophy are also observed. Dolichocephaly, often secondary to sagittal craniosynostosis, is a primary manifestation that distinguishes CED from most other ciliopathies. Brain malformations and developmental delay may also occur.
Orofaciodigital syndrome I
MedGen UID:
307142
Concept ID:
C1510460
Disease or Syndrome
Oral-facial-digital syndrome type I (OFD1) is usually male lethal during gestation and predominantly affects females. OFD1 is characterized by the following features: Oral (lobulated tongue, tongue nodules, cleft of the hard or soft palate, accessory gingival frenulae, hypodontia, and other dental abnormalities). Facial (widely spaced eyes or telecanthus, hypoplasia of the alae nasi, median cleft or pseudocleft upper lip, micrognathia). Digital (brachydactyly, syndactyly, clinodactyly of the fifth finger; duplicated hallux [great toe]). Kidney (polycystic kidney disease). Brain (e.g., intracerebral cysts, agenesis of the corpus callosum, cerebellar agenesis with or without Dandy-Walker malformation). Intellectual disability (in ~50% of individuals).
Polysyndactyly-cardiac malformation syndrome
MedGen UID:
337895
Concept ID:
C1849719
Congenital Abnormality
Syndrome with characteristics of polysyndactyly, hexadactyly (duplication of the first toe) and complex cardiac malformation (including atrial and ventricular septal defect, single ventricle, aortic dextroposition, or dilation of the right heart). It has been described in six patients from three unrelated families. Other manifestations were present in some patients (i.e. facial dysmorphism, hepatic cysts).
Meckel syndrome, type 6
MedGen UID:
382942
Concept ID:
C2676790
Disease or Syndrome
Because of their serious health problems, most individuals with Meckel syndrome die before or shortly after birth. Most often, affected infants die of respiratory problems or kidney failure.\n\nOther signs and symptoms of Meckel syndrome vary widely among affected individuals. Numerous abnormalities of the brain and spinal cord (central nervous system) have been reported in people with Meckel syndrome, including a group of birth defects known as neural tube defects. These defects occur when a structure called the neural tube, a layer of cells that ultimately develops into the brain and spinal cord, fails to close completely during the first few weeks of embryonic development. Meckel syndrome can also cause problems with development of the eyes and other facial features, heart, bones, urinary system, and genitalia.\n\nMeckel syndrome is a disorder with severe signs and symptoms that affect many parts of the body. The most common features are enlarged kidneys with numerous fluid-filled cysts; an occipital encephalocele, which is a sac-like protrusion of the brain through an opening at the back of the skull; and the presence of extra fingers and toes (polydactyly). Most affected individuals also have a buildup of scar tissue (fibrosis) in the liver.
Polycystic kidney disease 2
MedGen UID:
442699
Concept ID:
C2751306
Disease or Syndrome
Autosomal dominant polycystic kidney disease (ADPKD) is generally a late-onset multisystem disorder characterized by bilateral kidney cysts, liver cysts, and an increased risk of intracranial aneurysms. Other manifestations include: cysts in the pancreas, seminal vesicles, and arachnoid membrane; dilatation of the aortic root and dissection of the thoracic aorta; mitral valve prolapse; and abdominal wall hernias. Kidney manifestations include early-onset hypertension, kidney pain, and kidney insufficiency. Approximately 50% of individuals with ADPKD have end-stage kidney disease (ESKD) by age 60 years. The prevalence of liver cysts increases with age and occasionally results in clinically significant severe polycystic liver disease (PLD), most often in females. Overall, the prevalence of intracranial aneurysms is fivefold higher than in the general population and further increased in those with a positive family history of aneurysms or subarachnoid hemorrhage. There is substantial variability in the severity of kidney disease and other extra-kidney manifestations.
Polycystic kidney disease, adult type
MedGen UID:
461191
Concept ID:
C3149841
Disease or Syndrome
Autosomal dominant polycystic kidney disease (ADPKD) is generally a late-onset multisystem disorder characterized by bilateral kidney cysts, liver cysts, and an increased risk of intracranial aneurysms. Other manifestations include: cysts in the pancreas, seminal vesicles, and arachnoid membrane; dilatation of the aortic root and dissection of the thoracic aorta; mitral valve prolapse; and abdominal wall hernias. Kidney manifestations include early-onset hypertension, kidney pain, and kidney insufficiency. Approximately 50% of individuals with ADPKD have end-stage kidney disease (ESKD) by age 60 years. The prevalence of liver cysts increases with age and occasionally results in clinically significant severe polycystic liver disease (PLD), most often in females. Overall, the prevalence of intracranial aneurysms is fivefold higher than in the general population and further increased in those with a positive family history of aneurysms or subarachnoid hemorrhage. There is substantial variability in the severity of kidney disease and other extra-kidney manifestations.
Asphyxiating thoracic dystrophy 4
MedGen UID:
462535
Concept ID:
C3151185
Disease or Syndrome
Short-rib thoracic dysplasia (SRTD) with or without polydactyly refers to a group of autosomal recessive skeletal ciliopathies that are characterized by a constricted thoracic cage, short ribs, shortened tubular bones, and a 'trident' appearance of the acetabular roof. SRTD encompasses Ellis-van Creveld syndrome (EVC) and the disorders previously designated as Jeune syndrome or asphyxiating thoracic dystrophy (ATD), short rib-polydactyly syndrome (SRPS), and Mainzer-Saldino syndrome (MZSDS). Polydactyly is variably present, and there is phenotypic overlap in the various forms of SRTDs, which differ by visceral malformation and metaphyseal appearance. Nonskeletal involvement can include cleft lip/palate as well as anomalies of major organs such as the brain, eye, heart, kidneys, liver, pancreas, intestines, and genitalia. Some forms of SRTD are lethal in the neonatal period due to respiratory insufficiency secondary to a severely restricted thoracic cage, whereas others are compatible with life (summary by Huber and Cormier-Daire, 2012 and Schmidts et al., 2013). There is phenotypic overlap with the cranioectodermal dysplasias (Sensenbrenner syndrome; see CED1, 218330). For a discussion of genetic heterogeneity of short-rib thoracic dysplasia, see SRTD1 (208500).
Nephronophthisis 13
MedGen UID:
482242
Concept ID:
C3280612
Disease or Syndrome
The nephronophthisis (NPH) phenotype is characterized by reduced renal concentrating ability, chronic tubulointerstitial nephritis, cystic renal disease, and progression to end-stage renal disease (ESRD) before age 30 years. Three age-based clinical subtypes are recognized: infantile, juvenile, and adolescent/adult. Infantile NPH can present in utero with oligohydramnios sequence (limb contractures, pulmonary hypoplasia, and facial dysmorphisms) or postnatally with renal manifestations that progress to ESRD before age 3 years. Juvenile NPH, the most prevalent subtype, typically presents with polydipsia and polyuria, growth retardation, chronic iron-resistant anemia, or other findings related to chronic kidney disease (CKD). Hypertension is typically absent due to salt wasting. ESRD develops at a median age of 13 years. Ultrasound findings are increased echogenicity, reduced corticomedullary differentiation, and renal cysts (in 50% of affected individuals). Histologic findings include tubulointerstitial fibrosis, thickened and disrupted tubular basement membrane, sporadic corticomedullary cysts, and normal or reduced kidney size. Adolescent/adult NPH is clinically similar to juvenile NPH, but ESRD develops at a median age of 19 years. Within a subtype, inter- and intrafamilial variability in rate of progression to ESRD is considerable. Approximately 80%-90% of individuals with the NPH phenotype have no extrarenal features (i.e., they have isolated NPH); ~10%-20% have extrarenal manifestations that constitute a recognizable syndrome (e.g., Joubert syndrome, Bardet-Biedl syndrome, Jeune syndrome and related skeletal disorders, Meckel-Gruber syndrome, Senior-Løken syndrome, Leber congenital amaurosis, COACH syndrome, and oculomotor apraxia, Cogan type).
Renal-hepatic-pancreatic dysplasia 1
MedGen UID:
811626
Concept ID:
C3715199
Disease or Syndrome
Any renal-hepatic-pancreatic dysplasia in which the cause of the disease is a mutation in the NPHP3 gene.
Renal-hepatic-pancreatic dysplasia 2
MedGen UID:
815764
Concept ID:
C3809434
Disease or Syndrome
RHPD2 is an autosomal recessive multisystemic disorder with severe abnormalities apparent in utero and often resulting in fetal death or death in infancy. The main organs affected include the kidney, liver, and pancreas, although other abnormalities, including cardiac, skeletal, and lung defects, may also be present. Affected individuals often have situs inversus. The disorder results from a defect in ciliogenesis and ciliary function, as well as in cell proliferation and epithelial morphogenesis; thus, the clinical manifestations are highly variable (summary by Grampa et al., 2016). For a discussion of genetic heterogeneity of renal-hepatic-pancreatic dysplasia, see RHPD1 (208540).
Polycystic kidney disease 3 with or without polycystic liver disease
MedGen UID:
854672
Concept ID:
C3887964
Disease or Syndrome
Autosomal dominant polycystic kidney disease (ADPKD) is generally a late-onset multisystem disorder characterized by bilateral kidney cysts, liver cysts, and an increased risk of intracranial aneurysms. Other manifestations include: cysts in the pancreas, seminal vesicles, and arachnoid membrane; dilatation of the aortic root and dissection of the thoracic aorta; mitral valve prolapse; and abdominal wall hernias. Kidney manifestations include early-onset hypertension, kidney pain, and kidney insufficiency. Approximately 50% of individuals with ADPKD have end-stage kidney disease (ESKD) by age 60 years. The prevalence of liver cysts increases with age and occasionally results in clinically significant severe polycystic liver disease (PLD), most often in females. Overall, the prevalence of intracranial aneurysms is fivefold higher than in the general population and further increased in those with a positive family history of aneurysms or subarachnoid hemorrhage. There is substantial variability in the severity of kidney disease and other extra-kidney manifestations.
Senior-Loken syndrome 8
MedGen UID:
905171
Concept ID:
C4225376
Disease or Syndrome
Any Senior-Loken syndrome in which the cause of the disease is a mutation in the WDR19 gene.
Polycystic liver disease 2
MedGen UID:
934736
Concept ID:
C4310769
Disease or Syndrome
PCLD2 is an autosomal dominant disease characterized by the presence of multiple liver cysts resulting from structural changes in the biliary tree during development. Abnormal biliary structures may be present early in life, but they usually remain asymptomatic until cyst growth initiates during adulthood. In advanced stages, patients may develop massively enlarged livers, which cause a spectrum of clinical features and complications. Genetic studies suggest that an accumulation of somatic hits in cyst epithelium determines the rate of cyst formation. A subset of patients (28-35%) may develop kidney cysts that are usually incidental findings and do not result in clinically significant renal disease (review by Cnossen and Drenth, 2014). For a discussion of genetic heterogeneity of polycystic liver disease, see PCLD1 (174050).
Immunoskeletal dysplasia with neurodevelopmental abnormalities
MedGen UID:
1381460
Concept ID:
C4479452
Disease or Syndrome
Polycystic kidney disease 4
MedGen UID:
1621793
Concept ID:
C4540575
Disease or Syndrome
Autosomal recessive polycystic kidney disease (ARPKD) belongs to a group of congenital hepatorenal fibrocystic syndromes and is a cause of significant renal and liver-related morbidity and mortality in children. The majority of individuals with ARPKD present in the neonatal period with enlarged echogenic kidneys. Renal disease is characterized by nephromegaly, hypertension, and varying degrees of renal dysfunction. More than 50% of affected individuals with ARPKD progress to end-stage renal disease (ESRD) within the first decade of life; ESRD may require kidney transplantation. Pulmonary hypoplasia resulting from oligohydramnios occurs in a number of affected infants. Approximately 30% of these infants die in the neonatal period or within the first year of life from respiratory insufficiency or superimposed pulmonary infections. With neonatal respiratory support and renal replacement therapies, the long-term survival of these infants has improved to greater than 80%. As advances in renal replacement therapy and kidney transplantation improve long-term survival, it is likely that clinical hepatobiliary disease will become a major feature of the natural history of ARPKD. In addition, a subset of individuals with this disorder are identified with hepatosplenomegaly; the renal disease is often mild and may be discovered incidentally during imaging studies of the abdomen. Approximately 50% of infants will have clinical evidence of liver involvement at diagnosis although histologic hepatic fibrosis is invariably present at birth. This can lead to progressive portal hypertension with resulting esophageal or gastric varices, enlarged hemorrhoids, splenomegaly, hypersplenism, protein-losing enteropathy, and gastrointestinal bleeding. Other hepatic findings include nonobstructed dilatation of the intrahepatic bile ducts (Caroli syndrome) and dilatation of the common bile duct, which may lead to recurrent or persistent bacterial ascending cholangitis due to dilated bile ducts and stagnant bile flow. An increasing number of affected individuals surviving the neonatal period will eventually require portosystemic shunting or liver transplantation for complications of portal hypertension or cholangitis. The classic neonatal presentation of ARPKD notwithstanding, there is significant variability in age and presenting clinical symptoms related to the relative degree of renal and biliary abnormalities.
Polycystic liver disease 3 with or without kidney cysts
MedGen UID:
1646969
Concept ID:
C4693472
Disease or Syndrome
PCLD3 is an autosomal dominant disorder characterized by the development of multiple liver cysts that usually becomes apparent in adulthood. Liver cysts range in size and number, and the clinical severity is variable. Most patients also have a few renal cysts, but they do not result in significant renal disease or renal failure (summary by Besse et al., 2017). For a discussion of genetic heterogeneity of polycystic liver disease, see PCLD1 (174050).
Polycystic liver disease 4 with or without kidney cysts
MedGen UID:
1644991
Concept ID:
C4693479
Disease or Syndrome
PCLD4 is an autosomal dominant disease characterized by adult-onset of liver cysts arising from the bile duct epithelium. Some patients may develop a few kidney cysts, but these are often incidental and do not result in renal failure (summary by Cnossen et al., 2014). For a discussion of genetic heterogeneity of polycystic liver disease, see PCLD1 (174050).
Polycystic kidney disease 6 with or without polycystic liver disease
MedGen UID:
1648469
Concept ID:
C4748044
Disease or Syndrome
Autosomal dominant polycystic kidney disease (ADPKD) is generally a late-onset multisystem disorder characterized by bilateral kidney cysts, liver cysts, and an increased risk of intracranial aneurysms. Other manifestations include: cysts in the pancreas, seminal vesicles, and arachnoid membrane; dilatation of the aortic root and dissection of the thoracic aorta; mitral valve prolapse; and abdominal wall hernias. Kidney manifestations include early-onset hypertension, kidney pain, and kidney insufficiency. Approximately 50% of individuals with ADPKD have end-stage kidney disease (ESKD) by age 60 years. The prevalence of liver cysts increases with age and occasionally results in clinically significant severe polycystic liver disease (PLD), most often in females. Overall, the prevalence of intracranial aneurysms is fivefold higher than in the general population and further increased in those with a positive family history of aneurysms or subarachnoid hemorrhage. There is substantial variability in the severity of kidney disease and other extra-kidney manifestations.
Autoinflammation, immune dysregulation, and eosinophilia
MedGen UID:
1750270
Concept ID:
C5436572
Disease or Syndrome
Autoinflammation, immune dysregulation, and eosinophilia (AIIDE) is an autosomal dominant disorder characterized by onset of severe atopic dermatitis and chronic gastrointestinal inflammation, mainly involving the colon, in infancy or early childhood. Affected individuals tend to have asthma and food or environmental allergies, as well as poor overall growth with short stature. Severe liver involvement has also been reported (Takeichi et al., 2021). Laboratory studies show increased eosinophils with normal or increased IgE levels, as well as evidence of a hyperactive immune state, including increased erythrocyte sedimentation rate and C-reactive protein. Treatment with JAK inhibitors, such as ruxolitinib and tofacitinib, results in dramatic clinical improvement (summary by Gruber et al., 2020).

Professional guidelines

PubMed

Spahiu L, Behluli E, Grajçevci-Uka V, Liehr T, Temaj G
J Mother Child 2022 Mar 1;26(1):118-123. Epub 2023 Feb 22 doi: 10.34763/jmotherandchild.20222601.d-22-00034. PMID: 36803942Free PMC Article
European Association for the Study of the Liver. Electronic address: easloffice@easloffice.eu; European Association for the Study of the Liver
J Hepatol 2022 Oct;77(4):1083-1108. Epub 2022 Jun 18 doi: 10.1016/j.jhep.2022.06.002. PMID: 35728731
Shimizu T, Yoshioka M, Kaneya Y, Kanda T, Aoki Y, Kondo R, Takata H, Ueda J, Kawano Y, Hirakata A, Matsushita A, Taniai N, Mamada Y, Yoshida H
J Nippon Med Sch 2022 Mar 11;89(1):2-8. Epub 2021 Sep 14 doi: 10.1272/jnms.JNMS.2022_89-115. PMID: 34526451

Recent clinical studies

Etiology

Wang Z, Bian H, Li J, Xu J, Fan H, Wu X, Cao Y, Guo B, Xu X, Wang H, Zhang L, Zhou H, Fan J, Ren Y, Geng Y, Feng X, Li L, Wei L, Zhang X
Lancet Digit Health 2023 Nov;5(11):e754-e762. Epub 2023 Sep 26 doi: 10.1016/S2589-7500(23)00136-X. PMID: 37770335
Masyuk TV, Masyuk AI, LaRusso NF
Annu Rev Pathol 2022 Jan 24;17:251-269. Epub 2021 Nov 1 doi: 10.1146/annurev-pathol-042320-121247. PMID: 34724412Free PMC Article
Yang F, Qian Z, Sun F, Chen K, Fan L, Duan J, Wang Q, Asakawa T, Zheng S
J Laparoendosc Adv Surg Tech A 2021 Mar;31(3):314-319. Epub 2020 Jun 18 doi: 10.1089/lap.2019.0829. PMID: 32552410
Lee-Law PY, van de Laarschot LFM, Banales JM, Drenth JPH
Curr Opin Gastroenterol 2019 Mar;35(2):65-72. doi: 10.1097/MOG.0000000000000514. PMID: 30652979
van de Laarschot LFM, Drenth JPH
Biochim Biophys Acta Mol Basis Dis 2018 Apr;1864(4 Pt B):1491-1497. Epub 2017 Aug 4 doi: 10.1016/j.bbadis.2017.08.003. PMID: 28782656

Diagnosis

Reizine E, Mulé S, Luciani A
Radiol Clin North Am 2022 Sep;60(5):755-773. Epub 2022 Jul 4 doi: 10.1016/j.rcl.2022.05.005. PMID: 35989043
Armutlu A, Quigley B, Choi H, Basturk O, Akkas G, Pehlivanoglu B, Memis B, Jang KT, Erkan M, Erkan B, Balci S, Saka B, Bagci P, Farris AB, Kooby DA, Martin D, Kalb B, Maithel SK, Sarmiento J, Reid MD, Adsay NV
Am J Surg Pathol 2022 Sep 1;46(9):1219-1233. Epub 2022 Jul 4 doi: 10.1097/PAS.0000000000001930. PMID: 35778790
European Association for the Study of the Liver. Electronic address: easloffice@easloffice.eu; European Association for the Study of the Liver
J Hepatol 2022 Oct;77(4):1083-1108. Epub 2022 Jun 18 doi: 10.1016/j.jhep.2022.06.002. PMID: 35728731
Shimizu T, Yoshioka M, Kaneya Y, Kanda T, Aoki Y, Kondo R, Takata H, Ueda J, Kawano Y, Hirakata A, Matsushita A, Taniai N, Mamada Y, Yoshida H
J Nippon Med Sch 2022 Mar 11;89(1):2-8. Epub 2021 Sep 14 doi: 10.1272/jnms.JNMS.2022_89-115. PMID: 34526451
Marrero JA, Ahn J, Rajender Reddy K; Americal College of Gastroenterology
Am J Gastroenterol 2014 Sep;109(9):1328-47; quiz 1348. Epub 2014 Aug 19 doi: 10.1038/ajg.2014.213. PMID: 25135008

Therapy

Vardakostas D, Damaskos C, Garmpis N, Antoniou EA, Kontzoglou K, Kouraklis G, Dimitroulis D
Eur Rev Med Pharmacol Sci 2018 Mar;22(5):1387-1396. doi: 10.26355/eurrev_201803_14484. PMID: 29565498
Zarzour JG, Porter KK, Tchelepi H, Robbin ML
Abdom Radiol (NY) 2018 Apr;43(4):848-860. doi: 10.1007/s00261-017-1402-2. PMID: 29167944
Wijnands TF, Görtjes AP, Gevers TJ, Jenniskens SF, Kool LJ, Potthoff A, Ronot M, Drenth JP
AJR Am J Roentgenol 2017 Jan;208(1):201-207. Epub 2016 Nov 8 doi: 10.2214/AJR.16.16130. PMID: 27824501
Masyuk TV, Masyuk AI, LaRusso NF
Curr Drug Targets 2017;18(8):950-957. doi: 10.2174/1389450116666150427161743. PMID: 25915482Free PMC Article
Wüthrich RP, Mei C
Expert Opin Pharmacother 2014 Jun;15(8):1085-95. Epub 2014 Mar 28 doi: 10.1517/14656566.2014.903923. PMID: 24673552

Prognosis

Wang Z, Bian H, Li J, Xu J, Fan H, Wu X, Cao Y, Guo B, Xu X, Wang H, Zhang L, Zhou H, Fan J, Ren Y, Geng Y, Feng X, Li L, Wei L, Zhang X
Lancet Digit Health 2023 Nov;5(11):e754-e762. Epub 2023 Sep 26 doi: 10.1016/S2589-7500(23)00136-X. PMID: 37770335
Aziz H, Hamad A, Afyouni S, Kamel IR, Pawlik TM
J Gastrointest Surg 2023 Sep;27(9):1963-1970. Epub 2023 May 23 doi: 10.1007/s11605-023-05709-6. PMID: 37221388
Yang F, Qian Z, Sun F, Chen K, Fan L, Duan J, Wang Q, Asakawa T, Zheng S
J Laparoendosc Adv Surg Tech A 2021 Mar;31(3):314-319. Epub 2020 Jun 18 doi: 10.1089/lap.2019.0829. PMID: 32552410
Wüthrich RP, Mei C
Expert Opin Pharmacother 2014 Jun;15(8):1085-95. Epub 2014 Mar 28 doi: 10.1517/14656566.2014.903923. PMID: 24673552
Lantinga MA, Gevers TJ, Drenth JP
World J Gastroenterol 2013 Jun 21;19(23):3543-54. doi: 10.3748/wjg.v19.i23.3543. PMID: 23801855Free PMC Article

Clinical prediction guides

Wang Z, Bian H, Li J, Xu J, Fan H, Wu X, Cao Y, Guo B, Xu X, Wang H, Zhang L, Zhou H, Fan J, Ren Y, Geng Y, Feng X, Li L, Wei L, Zhang X
Lancet Digit Health 2023 Nov;5(11):e754-e762. Epub 2023 Sep 26 doi: 10.1016/S2589-7500(23)00136-X. PMID: 37770335
Boerrigter MM, Te Morsche RHM, Venselaar H, Pastoors N, Geerts AM, Hoorens A, Drenth JPH
Genes (Basel) 2023 Aug 19;14(8) doi: 10.3390/genes14081652. PMID: 37628703Free PMC Article
Wijnands TF, Görtjes AP, Gevers TJ, Jenniskens SF, Kool LJ, Potthoff A, Ronot M, Drenth JP
AJR Am J Roentgenol 2017 Jan;208(1):201-207. Epub 2016 Nov 8 doi: 10.2214/AJR.16.16130. PMID: 27824501
Masyuk TV, Masyuk AI, LaRusso NF
Dig Dis 2015;33(3):420-5. Epub 2015 May 27 doi: 10.1159/000371696. PMID: 26045278Free PMC Article
Lantinga MA, Gevers TJ, Drenth JP
World J Gastroenterol 2013 Jun 21;19(23):3543-54. doi: 10.3748/wjg.v19.i23.3543. PMID: 23801855Free PMC Article

Recent systematic reviews

Furumaya A, van Rosmalen BV, de Graeff JJ, Haring MPD, de Meijer VE, van Gulik TM, Verheij J, Besselink MG, van Delden OM, Erdmann JI; Dutch Benign Liver Tumor Group
HPB (Oxford) 2021 Jan;23(1):11-24. Epub 2020 Aug 20 doi: 10.1016/j.hpb.2020.07.005. PMID: 32830070
Bernts LHP, Echternach SG, Kievit W, Rosman C, Drenth JPH
Surg Endosc 2019 Mar;33(3):691-704. Epub 2018 Oct 17 doi: 10.1007/s00464-018-6490-8. PMID: 30334152Free PMC Article
Wijnands TF, Görtjes AP, Gevers TJ, Jenniskens SF, Kool LJ, Potthoff A, Ronot M, Drenth JP
AJR Am J Roentgenol 2017 Jan;208(1):201-207. Epub 2016 Nov 8 doi: 10.2214/AJR.16.16130. PMID: 27824501
Leombroni M, Buca D, Celentano C, Liberati M, Bascietto F, Gustapane S, Marrone L, Manzoli L, Rizzo G, D'Antonio F
Ultrasound Obstet Gynecol 2017 Aug;50(2):167-174. Epub 2017 Jul 9 doi: 10.1002/uog.17244. PMID: 27553859
Moorthy K, Mihssin N, Houghton PW
Ann R Coll Surg Engl 2001 Nov;83(6):409-14. PMID: 11777137Free PMC Article

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