Hepatocellular and gastric carcinoma associated with familial polyposis coli

LaFerla, Godfrey; Kaye, S. B.; Crean, G. P.

doi:10.1002/jso.2930380107

Cited by 20 publications

(6 citation statements)

References 13 publications

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“…This increased risk may be attributable to the high background risk of gastric cancer in the Korean population. Only a few cases of gastric cancer have been reported in Western FAP patients [9][10][11]. In this series, with a median of five years of followup, no patient with or without a gastric adenoma was diagnosed with gastric cancer.…”

Section: Discussionmentioning

confidence: 67%

Gastric Adenomas in Familial Adenomatous Polyposis Are Common, But Subtle, and Have a Benign Course

Ngamruengphong¹,

Boardman²,

Heigh³

et al. 2013

American Journal of Gastroenterology

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Background: Patients with familial adenomatous polyposis (FAP) are known to have an increased risk for gastric adenomas. The clinical features of gastric adenomas in FAP have not been well characterized, and there is a lack of standardized approaches to the management of these lesions. Aims: To study the endoscopic appearance, risk factors, clinical course, and response to therapy of gastric adenomas in patients with FAP. Methods: We retrospectively reviewed the records of 97 patients with FAP who underwent esophagogastroduodenoscopy (EGD) at Mayo Clinic (Florida, Rochester and Arizona) between 2004 and 2013. Results: Nine patients (9%) had biopsy-proven gastric adenomas. Adenomas were located in the antrum (five patients), in the body and fundus in the setting of background fundic gland polyps (FGP) (three patients), and in the body not associated with FGP (one patient). Adenoma size was 3-40 mm and the number of adenomas per patient ranged from one to 20. Adenomas in the antrum were flat and subtle, whereas those in the gastric body or fundus were polypoid and difficult to differentiate from the cystic FGPs seen in patients with FAP. The performing endoscopists reported difficulty with identifying adenomas, and six patients had at least one EGD within the previous three years where gastric adenomas were not reported. Adenomas were classified as tubular in eight patients and tubulovillous in one patient. High grade dysplasia was noted in one patient. After a median follow-up of 63 months (interquartile range: 20-149 months), no patient in our entire cohort (with or without gastric adenomas) developed gastric cancer. The patients in whom gastric adenoma developed, compared to those without gastric adenoma, were more likely to be younger [36 ± 12 vs. 48 ± 15 years, p = 0.02], have concomitant chronic gastritis [22% vs. 0%, p = 0.008], and have desmoid tumors [5 (56%) vs. 19 (22%), p = 0.04]. Conclusions: Gastric adenomas are not uncommon in patients with FAP and are often difficult to identify endoscopically. Endoscopists should have a high degree of suspicion for gastric adenomas in these patients and a low threshold to biopsy. Given the benign clinical course, recommended initial management is conservative with endoscopic therapy and periodic surveillance.

show abstract

Section: Discussionmentioning

confidence: 67%

Gastric Adenomas in Familial Adenomatous Polyposis Are Common, But Subtle, and Have a Benign Course

Ngamruengphong¹,

Boardman²,

Heigh³

et al. 2013

American Journal of Gastroenterology

View full text Add to dashboard Cite

show abstract

“…This increased risk may be attributable to the high background risk of gastric cancer in the Korean population. Only a few cases of gastric cancer have been reported in Western FAP patients [9-11]. In this series, with a median of five years of follow-up, no patient with or without a gastric adenoma was diagnosed with gastric cancer.…”

Section: Discussionmentioning

confidence: 78%

Gastric adenomas in familial adenomatous polyposis are common, but subtle, and have a benign course

Ngamruengphong

Boardman

Heigh

et al. 2014

Hered Cancer Clin Pract

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BackgroundPatients with familial adenomatous polyposis (FAP) are known to have an increased risk for gastric adenomas. The clinical features of gastric adenomas in FAP have not been well characterized, and there is a lack of standardized approaches to the management of these lesions.AimsTo study the endoscopic appearance, risk factors, clinical course, and response to therapy of gastric adenomas in patients with FAP.MethodsWe retrospectively reviewed the records of 97 patients with FAP who underwent esophagogastroduodenoscopy (EGD) at Mayo Clinic (Florida, Rochester and Arizona) between 2004 and 2013.ResultsNine patients (9%) had biopsy-proven gastric adenomas. Adenomas were located in the antrum (five patients), in the body and fundus in the setting of background fundic gland polyps (FGP) (three patients), and in the body not associated with FGP (one patient). Adenoma size was 3–40 mm and the number of adenomas per patient ranged from one to 20. Adenomas in the antrum were flat and subtle, whereas those in the gastric body or fundus were polypoid and difficult to differentiate from the cystic FGPs seen in patients with FAP. The performing endoscopists reported difficulty with identifying adenomas, and six patients had at least one EGD within the previous three years where gastric adenomas were not reported. Adenomas were classified as tubular in eight patients and tubulovillous in one patient. High grade dysplasia was noted in one patient. After a median follow-up of 63 months (interquartile range: 20–149 months), no patient in our entire cohort (with or without gastric adenomas) developed gastric cancer. The patients in whom gastric adenoma developed, compared to those without gastric adenoma, were more likely to be younger [36 ± 12 vs. 48 ± 15 years, p = 0.02], have concomitant chronic gastritis [22% vs. 0%, p = 0.008], and have desmoid tumors [5 (56%) vs. 19 (22%), p = 0.04].ConclusionsGastric adenomas are not uncommon in patients with FAP and are often difficult to identify endoscopically. Endoscopists should have a high degree of suspicion for gastric adenomas in these patients and a low threshold to biopsy. Given the benign clinical course, recommended initial management is conservative with endoscopic therapy and periodic surveillance.

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“…Rarely, liver cancer occurs in association with conditions that have a genetic, congenital or metabolic origin. HCC has been rarely documented in familial polyposis coli [34], ataxia telangiectasia [35], familial cholestatic cirrhosis, congenital hepatic fibrosis, neurofibromatosis, situs inversus and the fetal alcohol syndrome [29,36].…”

Section: Genetic and Congenital Abnormalitiesmentioning

confidence: 99%

Epidemiology and carcinogenesis of hepatocellular carcinoma

Leong

2005

HPB

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The incidence of hepatocellular carcinoma (HCC) shows marked variation worldwide but the magnitude of this tumor is reflected by the occurrence of at least 1 million new cases annually and the uniformly dismal outlook with median survivals of <25 months after resection and <6 months with symptomatic treatment. The strikingly uneven distribution of this tumor parallels the prevalence of hepatitis B infection with rising incidence in western countries attributed to hepatitis C infection. Chronic hepatitis and cirrhosis constitute the major preneoplastic conditions in the majority of HCCs and may be related to other etiologic agents such as environmental chemical carcinogens including nitrites, hydrocarbons, solvents, organochlorine pesticides, and the chemicals in processed foods, cleaning agents, cosmetics and pharmaceuticals, as well as plant toxins such as anatoxins produced by fungi that cause spoilage of grain and food in the tropics. Genetic diseases such as genetic hematochromatosis, Wilson's disease, alpha-1-antitrypsin deficiency, and the inborn errors of metabolism including hereditary tyrosinemia and hepatic porphyria, are known to be associated with HCC. Numerous genetic alterations and the modulation of DNA methylation are recognized in HCC and it is likely that these genetic and epigenetic changes combine with factors involved in chronic hepatocyte destruction and regeneration to result in neoplastic growth and multiple molecular pathways may be involved in the production of subsets of hepatocellular tumors.

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Hepatocellular and gastric carcinoma associated with familial polyposis coli

Cited by 20 publications

References 13 publications

Gastric Adenomas in Familial Adenomatous Polyposis Are Common, But Subtle, and Have a Benign Course

Gastric Adenomas in Familial Adenomatous Polyposis Are Common, But Subtle, and Have a Benign Course

Gastric adenomas in familial adenomatous polyposis are common, but subtle, and have a benign course

Epidemiology and carcinogenesis of hepatocellular carcinoma

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