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Esophageal varix

MedGen UID:
5027
Concept ID:
C0014867
Disease or Syndrome
Synonym: Esophageal varices
SNOMED CT: Esophageal varix (28670008); OV - Esophageal varices (28670008); Esophageal varices (28670008)
 
HPO: HP:0002040
Monarch Initiative: MONDO:0001221

Definition

Extreme dilation of the submucusoal veins in the lower portion of the esophagus. [from HPO]

Term Hierarchy

Conditions with this feature

Cholesteryl ester storage disease
MedGen UID:
40266
Concept ID:
C0008384
Disease or Syndrome
Deficiency of lysosomal acid lipase causes 2 distinct phenotypes in humans: Wolman disease (WOLD; 620151) and cholesteryl ester storage disease (CESD). WOLD is an early-onset fulminant disorder of infancy with massive infiltration of the liver, spleen, and other organs by macrophages filled with cholesteryl esters and triglycerides. Death occurs early in life. CESD is a milder, later-onset disorder with primary hepatic involvement by macrophages engorged with cholesteryl esters. This slowly progressive visceral disease has a wide spectrum of involvement ranging from early onset with severe cirrhosis to later onset of more slowly progressive hepatic disease with survival into adulthood (summary by Du et al., 2001).
Glycogen storage disease, type IV
MedGen UID:
6642
Concept ID:
C0017923
Disease or Syndrome
The clinical manifestations of glycogen storage disease type IV (GSD IV) discussed in this entry span a continuum of different subtypes with variable ages of onset, severity, and clinical features. Clinical findings vary extensively both within and between families. The fatal perinatal neuromuscular subtype presents in utero with fetal akinesia deformation sequence, including decreased fetal movements, polyhydramnios, and fetal hydrops. Death usually occurs in the neonatal period. The congenital neuromuscular subtype presents in the newborn period with profound hypotonia, respiratory distress, and dilated cardiomyopathy. Death usually occurs in early infancy. Infants with the classic (progressive) hepatic subtype may appear normal at birth, but rapidly develop failure to thrive; hepatomegaly, liver dysfunction, and progressive liver cirrhosis; hypotonia; and cardiomyopathy. Without liver transplantation, death from liver failure usually occurs by age five years. Children with the non-progressive hepatic subtype tend to present with hepatomegaly, liver dysfunction, myopathy, and hypotonia; however, they are likely to survive without progression of the liver disease and may not show cardiac, skeletal muscle, or neurologic involvement. The childhood neuromuscular subtype is rare and the course is variable, ranging from onset in the second decade with a mild disease course to a more severe, progressive course resulting in death in the third decade.
Wilson disease
MedGen UID:
42426
Concept ID:
C0019202
Disease or Syndrome
Wilson disease is a disorder of copper metabolism that can present with hepatic, neurologic, or psychiatric disturbances, or a combination of these, in individuals ranging from age three years to older than 50 years; symptoms vary among and within families. Liver disease includes recurrent jaundice, simple acute self-limited hepatitis-like illness, autoimmune-type hepatitis, fulminant hepatic failure, or chronic liver disease. Neurologic presentations include movement disorders (tremors, poor coordination, loss of fine-motor control, chorea, choreoathetosis) or rigid dystonia (mask-like facies, rigidity, gait disturbance, pseudobulbar involvement). Psychiatric disturbance includes depression, neurotic behaviors, disorganization of personality, and, occasionally, intellectual deterioration. Kayser-Fleischer rings, frequently present, result from copper deposition in Descemet's membrane of the cornea and reflect a high degree of copper storage in the body.
Cholestasis-pigmentary retinopathy-cleft palate syndrome
MedGen UID:
208652
Concept ID:
C0795969
Disease or Syndrome
MED12-related disorders include the phenotypes of FG syndrome type 1 (FGS1), Lujan syndrome (LS), X-linked Ohdo syndrome (XLOS), Hardikar syndrome (HS), and nonspecific intellectual disability (NSID). FGS1 and LS share the clinical findings of cognitive impairment, hypotonia, and abnormalities of the corpus callosum. FGS1 is further characterized by absolute or relative macrocephaly, tall forehead, downslanted palpebral fissures, small and simple ears, constipation and/or anal anomalies, broad thumbs and halluces, and characteristic behavior. LS is further characterized by large head, tall thin body habitus, long thin face, prominent nasal bridge, high narrow palate, and short philtrum. Carrier females in families with FGS1 and LS are typically unaffected. XLOS is characterized by intellectual disability, blepharophimosis, and facial coarsening. HS has been described in females with cleft lip and/or cleft palate, biliary and liver anomalies, intestinal malrotation, pigmentary retinopathy, and coarctation of the aorta. Developmental and cognitive concerns have not been reported in females with HS. Pathogenic variants in MED12 have been reported in an increasing number of males and females with NSID, with affected individuals often having clinical features identified in other MED12-related disorders.
Joubert syndrome with oculorenal defect
MedGen UID:
340930
Concept ID:
C1855675
Disease or Syndrome
Classic Joubert syndrome (JS) is characterized by three primary findings: A distinctive cerebellar and brain stem malformation called the molar tooth sign (MTS). Hypotonia. Developmental delays. Often these findings are accompanied by episodic tachypnea or apnea and/or atypical eye movements. In general, the breathing abnormalities improve with age, truncal ataxia develops over time, and acquisition of gross motor milestones is delayed. Cognitive abilities are variable, ranging from severe intellectual disability to normal. Additional findings can include retinal dystrophy, renal disease, ocular colobomas, occipital encephalocele, hepatic fibrosis, polydactyly, oral hamartomas, and endocrine abnormalities. Both intra- and interfamilial variation are seen.
Cirrhosis, familial
MedGen UID:
350049
Concept ID:
C1861556
Disease or Syndrome
Cirrhosis in which no causative agent can be identified.
COG6-congenital disorder of glycosylation
MedGen UID:
766144
Concept ID:
C3553230
Disease or Syndrome
CDG2L is an autosomal recessive multisystem disorder apparent from birth or early infancy. It is characterized by poor growth, gastrointestinal and liver abnormalities, delayed psychomotor development, hypotonia, recurrent infections, hematologic abnormalities, increased bleeding tendency, and hyperhidrosis or hyperkeratosis. More variable features include nonspecific dysmorphic facial features and cardiac septal defects. The disorder often results in death in infancy or the first years of life (summary by Rymen et al., 2015). For a general discussion of CDGs, see CDG1A (212065) and CDG2A (212066).
Vasculitis due to ADA2 deficiency
MedGen UID:
854497
Concept ID:
C3887654
Disease or Syndrome
Adenosine deaminase 2 deficiency (DADA2) is a complex systemic autoinflammatory disorder in which vasculopathy/vasculitis, dysregulated immune function, and/or hematologic abnormalities may predominate. Inflammatory features include intermittent fevers, rash (often livedo racemosa/reticularis), and musculoskeletal involvement (myalgia/arthralgia, arthritis, myositis). Vasculitis, which usually begins before age ten years, may manifest as early-onset ischemic (lacunar) and/or hemorrhagic strokes, or as cutaneous or systemic polyarteritis nodosa. Hypertension and hepatosplenomegaly are often found. More severe involvement may lead to progressive central neurologic deficits (dysarthria, ataxia, cranial nerve palsies, cognitive impairment) or to ischemic injury to the kidney, intestine, and/or digits. Dysregulation of immune function can lead to immunodeficiency or autoimmunity of varying severity; lymphadenopathy may be present and some affected individuals have had lymphoproliferative disease. Hematologic disorders may begin early in life or in late adulthood, and can include lymphopenia, neutropenia, pure red cell aplasia, thrombocytopenia, or pancytopenia. Of note, both interfamilial and intrafamilial phenotypic variability (e.g., in age of onset, frequency and severity of manifestations) can be observed; also, individuals with biallelic ADA2 pathogenic variants may remain asymptomatic until adulthood or may never develop clinical manifestations of DADA2.
Adams-Oliver syndrome 5
MedGen UID:
863407
Concept ID:
C4014970
Disease or Syndrome
Adams-Oliver syndrome (AOS) is characterized by aplasia cutis congenita (ACC) of the scalp and terminal transverse limb defects (TTLD). ACC lesions usually occur in the midline of the parietal or occipital regions, but can also occur on the abdomen or limbs. At birth, an ACC lesion may already have the appearance of a healed scar. ACC lesions less than 5 cm often involve only the skin and almost always heal over a period of months; larger lesions are more likely to involve the skull and possibly the dura, and are at greater risk for complications, which can include infection, hemorrhage, or thrombosis, and can result in death. The limb defects range from mild (unilateral or bilateral short distal phalanges) to severe (complete absence of all toes or fingers, feet or hands, or more, often resembling an amputation). The lower extremities are almost always more severely affected than the upper extremities. Additional major features frequently include cardiovascular malformations/dysfunction (23%), brain anomalies, and less frequently renal, liver, and eye anomalies.
Adams-Oliver syndrome 6
MedGen UID:
908556
Concept ID:
C4225271
Disease or Syndrome
Adams-Oliver syndrome (AOS) is characterized by aplasia cutis congenita (ACC) of the scalp and terminal transverse limb defects (TTLD). ACC lesions usually occur in the midline of the parietal or occipital regions, but can also occur on the abdomen or limbs. At birth, an ACC lesion may already have the appearance of a healed scar. ACC lesions less than 5 cm often involve only the skin and almost always heal over a period of months; larger lesions are more likely to involve the skull and possibly the dura, and are at greater risk for complications, which can include infection, hemorrhage, or thrombosis, and can result in death. The limb defects range from mild (unilateral or bilateral short distal phalanges) to severe (complete absence of all toes or fingers, feet or hands, or more, often resembling an amputation). The lower extremities are almost always more severely affected than the upper extremities. Additional major features frequently include cardiovascular malformations/dysfunction (23%), brain anomalies, and less frequently renal, liver, and eye anomalies.
Portal hypertension, noncirrhotic
MedGen UID:
934702
Concept ID:
C4310735
Disease or Syndrome
Cerebroretinal microangiopathy with calcifications and cysts 2
MedGen UID:
1390862
Concept ID:
C4479220
Disease or Syndrome
Dyskeratosis congenita and related telomere biology disorders (DC/TBD) are caused by impaired telomere maintenance resulting in short or very short telomeres. The phenotypic spectrum of telomere biology disorders is broad and includes individuals with classic dyskeratosis congenita (DC) as well as those with very short telomeres and an isolated physical finding. Classic DC is characterized by a triad of dysplastic nails, lacy reticular pigmentation of the upper chest and/or neck, and oral leukoplakia, although this may not be present in all individuals. People with DC/TBD are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome or acute myelogenous leukemia, solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis. Other findings can include eye abnormalities (epiphora, blepharitis, sparse eyelashes, ectropion, entropion, trichiasis), taurodontism, liver disease, gastrointestinal telangiectasias, and avascular necrosis of the hips or shoulders. Although most persons with DC/TBD have normal psychomotor development and normal neurologic function, significant developmental delay is present in both forms; additional findings include cerebellar hypoplasia (Hoyeraal Hreidarsson syndrome) and bilateral exudative retinopathy and intracranial calcifications (Revesz syndrome and Coats plus syndrome). Onset and progression of manifestations of DC/TBD vary: at the mild end of the spectrum are those who have only minimal physical findings with normal bone marrow function, and at the severe end are those who have the diagnostic triad and early-onset BMF.
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.
Retinitis pigmentosa 89
MedGen UID:
1710499
Concept ID:
C5394552
Disease or Syndrome
Retinitis pigmentosa-89 (RP89) is characterized by classic features of RP as well as features of ciliopathy, including postaxial polydactyly and renal and hepatic disease. Onset of symptoms is within the first decade of life (Cogne et al., 2020). For a general phenotypic description and discussion of genetic heterogeneity of RP, see 268000.
COACH syndrome 1
MedGen UID:
1769861
Concept ID:
C5435651
Disease or Syndrome
Any COACH syndrome in which the cause of the disease is a variation in the TMEM67 gene.
Rajab interstitial lung disease with brain calcifications 1
MedGen UID:
1750003
Concept ID:
C5436276
Disease or Syndrome
Rajab interstitial lung disease with brain calcifications-1 (RILDBC1) is an autosomal recessive multisystem disorder with a highly variable phenotype. Most patients present in infancy or early childhood with poor growth and interstitial lung disease, which may lead to death. Some may also have liver, skeletal, and renal abnormalities, and most have intracranial calcifications on brain imaging. Some may have early impaired motor development, but most have normal cognitive development (summary by Xu et al., 2018). Genetic Heterogeneity of Rajab Interstitial Lung Disease with Brain Calcifications Also see Rajab interstitial disease with brain calcifications-2 (RILDBC2; 619013), caused by mutation in the FARSA gene (602918).
Portal hypertension, noncirrhotic, 2
MedGen UID:
1794158
Concept ID:
C5561948
Disease or Syndrome
Noncirrhotic portal hypertension-2 (NCPH2) is an autosomal recessive disorder characterized by signs of liver dysfunction that become apparent in the first decades of life. Affected individuals have jaundice, hyperbilirubinemia, pancytopenia, including neutropenia, lymphopenia, and thrombocytopenia, hepatosplenomegaly, and esophageal varices. Some patients may have recurrent infections or features suggestive of an immunodeficiency. Liver biopsy is notable for the absence of cirrhosis and the presence of nodular regeneration. Liver sinusoidal endothelial cells (LSECs) have abnormal expression of CD34 (142230) (summary by Drzewiecki et al., 2021). For a discussion of genetic heterogeneity of NCPH, see 617068.
Neurodevelopmental disorder with hypotonia and dysmorphic facies
MedGen UID:
1794184
Concept ID:
C5561974
Disease or Syndrome
Neurodevelopmental disorder with hypotonia and dysmorphic facies (NEDHYDF) is characterized by global developmental delay and hypotonia apparent from birth. Affected individuals have variably impaired intellectual development, often with speech delay and delayed walking. Seizures are generally not observed, although some patients may have single seizures or late-onset epilepsy. Most patients have prominent dysmorphic facial features. Additional features may include congenital cardiac defects (without arrhythmia), nonspecific renal anomalies, joint contractures or joint hyperextensibility, dry skin, and cryptorchidism. There is significant phenotypic variability in both the neurologic and extraneurologic manifestations (summary by Tan et al., 2022).
Biliary, renal, neurologic, and skeletal syndrome
MedGen UID:
1794200
Concept ID:
C5561990
Disease or Syndrome
Biliary, renal, neurologic, and skeletal syndrome (BRENS) is an autosomal recessive complex ciliopathy with multisystemic manifestations. The most common presentation is severe neonatal cholestasis that progresses to liver fibrosis and cirrhosis. Most patients have additional clinical features suggestive of a ciliopathy, including postaxial polydactyly, hydrocephalus, retinal abnormalities, and situs inversus. Additional features of the syndrome may include congenital cardiac defects, echogenic kidneys with renal failure, ocular abnormalities, joint hyperextensibility, and dysmorphic facial features. Some patients have global developmental delay. Brain imaging typically shows dilated ventricles, hypomyelination, and white matter abnormalities, although some patients have been described with abnormal pituitary development (summary by Shaheen et al., 2020 and David et al., 2020).
Cholestasis, progressive familial intrahepatic, 8
MedGen UID:
1794255
Concept ID:
C5562045
Disease or Syndrome
Progressive familial intrahepatic cholestasis-8 (PFIC8) is an autosomal recessive disorder characterized by cholestasis and high gamma-glutamyltransferase presenting in the infantile period (summary by Unlusoy Aksu et al., 2019). For a general phenotypic description and a discussion of genetic heterogeneity of PFIC, see PFIC1 (211600).
Pulmonary fibrosis and/or bone marrow failure syndrome, telomere-related, 8
MedGen UID:
1841132
Concept ID:
C5830496
Disease or Syndrome
Telomere-related pulmonary fibrosis and/or bone marrow failure syndrome-8 (PFBMFT8) is an autosomal dominant disorder characterized by the onset of progressive pulmonary fibrosis in adulthood. Some affected individuals have signs of bone marrow failure, such as thrombocytopenia, or liver dysfunction, including hepatopulmonary syndrome. Other features of dyskeratosis congenita, including premature graying of the hair, may be observed. Telomeres are shortened compared to controls (Kelich et al., 2022). For a discussion of genetic heterogeneity of telomere-related pulmonary fibrosis and/or bone marrow failure, see PFBMFT1 (614742).

Professional guidelines

PubMed

Kang Y, Park S, Kim S, Han SJ, Koh H
Clin Res Hepatol Gastroenterol 2021 Jan;45(1):101437. Epub 2020 May 13 doi: 10.1016/j.clinre.2020.04.007. PMID: 32417223
Goral V, Yılmaz N
Medicina (Kaunas) 2019 Jul 3;55(7) doi: 10.3390/medicina55070335. PMID: 31277322Free PMC Article
Korda D, Deák PÁ, Kiss G, Gerlei Z, Kóbori L, Görög D, Fehérvári I, Piros L, Máthé Z, Doros A
Transplant Proc 2017 Sep;49(7):1530-1534. doi: 10.1016/j.transproceed.2017.06.015. PMID: 28838434

Recent clinical studies

Etiology

Hong Y, Yu Q, Mo F, Yin M, Xu C, Zhu S, Lin J, Xu G, Gao J, Liu L, Wang Y
J Int Med Res 2023 Oct;51(10):3000605231200371. doi: 10.1177/03000605231200371. PMID: 37818651Free PMC Article
Yang W, Li L, Feng X, Cheng H, Ge X, Bao Y, Huang L, Wang F, Liu C, Chen X, Mo Z, Yang X
Commun Biol 2022 May 2;5(1):405. doi: 10.1038/s42003-022-03351-7. PMID: 35501403Free PMC Article
Goral V, Yılmaz N
Medicina (Kaunas) 2019 Jul 3;55(7) doi: 10.3390/medicina55070335. PMID: 31277322Free PMC Article
Guo YW, Miao HB, Wen ZF, Xuan JY, Zhou HX
World J Gastroenterol 2017 Nov 21;23(43):7746-7755. doi: 10.3748/wjg.v23.i43.7746. PMID: 29209115Free PMC Article
Korda D, Deák PÁ, Kiss G, Gerlei Z, Kóbori L, Görög D, Fehérvári I, Piros L, Máthé Z, Doros A
Transplant Proc 2017 Sep;49(7):1530-1534. doi: 10.1016/j.transproceed.2017.06.015. PMID: 28838434

Diagnosis

Hong Y, Yu Q, Mo F, Yin M, Xu C, Zhu S, Lin J, Xu G, Gao J, Liu L, Wang Y
J Int Med Res 2023 Oct;51(10):3000605231200371. doi: 10.1177/03000605231200371. PMID: 37818651Free PMC Article
Kang TW, Kim M, Kim YK, Kim SH, Sinn DH, Kim K
Clin Imaging 2018 Jan-Feb;47:18-24. Epub 2017 Aug 10 doi: 10.1016/j.clinimag.2017.08.004. PMID: 28818763
Korda D, Deák PÁ, Kiss G, Gerlei Z, Kóbori L, Görög D, Fehérvári I, Piros L, Máthé Z, Doros A
Transplant Proc 2017 Sep;49(7):1530-1534. doi: 10.1016/j.transproceed.2017.06.015. PMID: 28838434
Kettner M, Ramsthaler F, Schnabel A
J Forensic Sci 2010 May;55(3):842-4. Epub 2010 Jan 25 doi: 10.1111/j.1556-4029.2009.01284.x. PMID: 20102472
Trenkner SW, Levine MS, Laufer I, Glick SN
AJR Am J Roentgenol 1983 Jul;141(1):43-4. doi: 10.2214/ajr.141.1.43. PMID: 6602526

Therapy

Hong Y, Yu Q, Mo F, Yin M, Xu C, Zhu S, Lin J, Xu G, Gao J, Liu L, Wang Y
J Int Med Res 2023 Oct;51(10):3000605231200371. doi: 10.1177/03000605231200371. PMID: 37818651Free PMC Article
Yang W, Li L, Feng X, Cheng H, Ge X, Bao Y, Huang L, Wang F, Liu C, Chen X, Mo Z, Yang X
Commun Biol 2022 May 2;5(1):405. doi: 10.1038/s42003-022-03351-7. PMID: 35501403Free PMC Article
Goral V, Yılmaz N
Medicina (Kaunas) 2019 Jul 3;55(7) doi: 10.3390/medicina55070335. PMID: 31277322Free PMC Article
Guo YW, Miao HB, Wen ZF, Xuan JY, Zhou HX
World J Gastroenterol 2017 Nov 21;23(43):7746-7755. doi: 10.3748/wjg.v23.i43.7746. PMID: 29209115Free PMC Article
Korda D, Deák PÁ, Kiss G, Gerlei Z, Kóbori L, Görög D, Fehérvári I, Piros L, Máthé Z, Doros A
Transplant Proc 2017 Sep;49(7):1530-1534. doi: 10.1016/j.transproceed.2017.06.015. PMID: 28838434

Prognosis

Hong Y, Yu Q, Mo F, Yin M, Xu C, Zhu S, Lin J, Xu G, Gao J, Liu L, Wang Y
J Int Med Res 2023 Oct;51(10):3000605231200371. doi: 10.1177/03000605231200371. PMID: 37818651Free PMC Article
Pham JT, Kalantari J, Ji C, Chang JH, Kiang SC, Jin DH, Tomihama RT
AJR Am J Roentgenol 2020 Nov;215(5):1247-1251. Epub 2020 Sep 9 doi: 10.2214/AJR.19.22460. PMID: 32901570
Zhang CX, Xu XY, Wang L, Huang M, Li L
Ultrasound Med Biol 2014 Sep;40(9):2058-63. Epub 2014 Jun 17 doi: 10.1016/j.ultrasmedbio.2014.03.017. PMID: 24951299
Lee JY, Kim TY, Jeong WK, Kim Y, Kim J, Kim KW, Kim YH, Sohn JH
Dig Dis Sci 2014 Sep;59(9):2333-43. Epub 2014 Apr 11 doi: 10.1007/s10620-014-3149-8. PMID: 24723070
De BK, Ghoshal UC, Das AS, Nandi S, Mazumder DN
Indian J Gastroenterol 1998 Jan;17(1):10-2. PMID: 9465505

Clinical prediction guides

Hong Y, Yu Q, Mo F, Yin M, Xu C, Zhu S, Lin J, Xu G, Gao J, Liu L, Wang Y
J Int Med Res 2023 Oct;51(10):3000605231200371. doi: 10.1177/03000605231200371. PMID: 37818651Free PMC Article
Pham JT, Kalantari J, Ji C, Chang JH, Kiang SC, Jin DH, Tomihama RT
AJR Am J Roentgenol 2020 Nov;215(5):1247-1251. Epub 2020 Sep 9 doi: 10.2214/AJR.19.22460. PMID: 32901570
Lee JY, Kim TY, Jeong WK, Kim Y, Kim J, Kim KW, Kim YH, Sohn JH
Dig Dis Sci 2014 Sep;59(9):2333-43. Epub 2014 Apr 11 doi: 10.1007/s10620-014-3149-8. PMID: 24723070
Kettner M, Ramsthaler F, Schnabel A
J Forensic Sci 2010 May;55(3):842-4. Epub 2010 Jan 25 doi: 10.1111/j.1556-4029.2009.01284.x. PMID: 20102472
Van Stiegmann G, Goff JS
Gastrointest Endosc 1988 Mar-Apr;34(2):113-7. doi: 10.1016/s0016-5107(88)71274-2. PMID: 3259195

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