Hepatocellular adenoma risk factors: Difference between revisions

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{{CMG}};{{AE}} {{ZAS}}
{{CMG}};{{AE}} {{ZAS}}
==Overview==
==Overview==
The most important [[risk factor]] in the development of [[hepatocellular adenoma]] is the use of [[Oral contraceptive|oral contraceptive medications]]. Other [[Risk factor|risk factors]] include [[Glycogen storage disease|glycogen storage diseases]], [[familial adenomatous polyposis]], [[Klinefelter's syndrome]], [[metabolic syndrome]], [[obesity]], long term use of [[anabolic]] [[androgenic]] [[steroids]], [[vascular disorders]] such as [[portal vein]] [[agenesis]], [[Budd-Chiari syndrome]] and [[hereditary hemorrhagic telangiectasia]].
The most important [[risk factor]] for the development of hepatocellular adenoma is the use of [[Oral contraceptive|oral contraceptive medications]]. Other [[Risk factor|risk factors]] include [[Glycogen storage disease|glycogen storage diseases]], [[familial adenomatous polyposis]], [[Klinefelter's syndrome]], [[metabolic syndrome]], [[obesity]], long term use of [[anabolic]] [[androgenic]] [[steroids]], [[vascular disorders]] such as [[portal vein]] [[agenesis]], [[Budd-Chiari syndrome]], and [[hereditary hemorrhagic telangiectasia]].


==Hepatocellular adenoma risk factors==
==Risk Factors==
* The most important [[risk factor]] in the development of [[hepatocellular adenoma]] is use of [[Oral contraceptive|oral contraceptive medications]].<ref>{{Cite journal
* The most important [[risk factor]] for the development of hepatocellular adenoma is the use of [[Oral contraceptive|oral contraceptive medications]], such as:<ref>{{Cite journal
  | author = [[L. Rosenberg]]
  | author = [[L. Rosenberg]]
  | title = The risk of liver neoplasia in relation to combined oral contraceptive use
  | title = The risk of liver neoplasia in relation to combined oral contraceptive use
Line 17: Line 17:
  | pmid = 1651205
  | pmid = 1651205
}}</ref>
}}</ref>
:*[[Drospirenone and Ethinyl estradiol]]
:*[[Drospirenone and Ethinyl estradiol]]
:*[[Norethindrone acetate and Ethinyl estradiol]]
:*[[Norethindrone acetate and Ethinyl estradiol]]
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:*[[Norgestrel and Ethinyl estradiol]]
:*[[Norgestrel and Ethinyl estradiol]]
:* The risk is proportional to:<ref name="pmid18333188">{{cite journal| author=Barthelmes L, Tait IS| title=Liver cell adenoma and liver cell adenomatosis. | journal=HPB (Oxford) | year= 2005 | volume= 7 | issue= 3 | pages= 186-96 | pmid=18333188 | doi=10.1080/13651820510028954 | pmc=PMC2023950 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18333188  }} </ref>
:* The risk is proportional to:<ref name="pmid18333188">{{cite journal| author=Barthelmes L, Tait IS| title=Liver cell adenoma and liver cell adenomatosis. | journal=HPB (Oxford) | year= 2005 | volume= 7 | issue= 3 | pages= 186-96 | pmid=18333188 | doi=10.1080/13651820510028954 | pmc=PMC2023950 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18333188  }} </ref>
::* [[Hormone|Hormonal]] [[dose]]
:* [[Hormone|Hormonal]] [[dose]]
::* Duration of [[medication]]
:* Duration of [[medication]]
* Other [[Risk factor|risk factors]] include:<ref name="pmid18333188">{{cite journal| author=Barthelmes L, Tait IS| title=Liver cell adenoma and liver cell adenomatosis. | journal=HPB (Oxford) | year= 2005 | volume= 7 | issue= 3 | pages= 186-96 | pmid=18333188 | doi=10.1080/13651820510028954 | pmc=PMC2023950 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18333188  }} </ref><ref>{{Cite journal
* Other [[Risk factor|risk factors]] include:<ref name="pmid18333188">{{cite journal| author=Barthelmes L, Tait IS| title=Liver cell adenoma and liver cell adenomatosis. | journal=HPB (Oxford) | year= 2005 | volume= 7 | issue= 3 | pages= 186-96 | pmid=18333188 | doi=10.1080/13651820510028954 | pmc=PMC2023950 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18333188  }} </ref><ref>{{Cite journal
  | author = [[U. Beuers]], [[W. O. Richter]], [[M. M. Ritter]], [[B. Wiebecke]] & [[P. Schwandt]]
  | author = [[U. Beuers]], [[W. O. Richter]], [[M. M. Ritter]], [[B. Wiebecke]] & [[P. Schwandt]]
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:* [[Familial adenomatous polyposis]]
:* [[Familial adenomatous polyposis]]


==Risk factors for malignant transformation==
===Risk Factors for Malignant Transformation===
The [[risk factor]] for [[malignant transformation]] of [[Hepatocellular adenoma|hepatic adenoma]] to [[hepatocellular carcinoma]] is:<ref name="pmid25786843">{{cite journal| author=Aamann L, Schultz N, Fallentin E, Hamilton-Dutoit S, Vogel I, Grønbæk H| title=[Hepatocellular adenoma - new classification and recommendations]. | journal=Ugeskr Laeger | year= 2015 | volume= 177 | issue= 12 | pages=  | pmid=25786843 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25786843  }} </ref>
[[risk factor|Risk factors]] for the [[malignant transformation]] of hepatocellular adenoma to [[hepatocellular carcinoma]] include:<ref name="pmid25786843">{{cite journal| author=Aamann L, Schultz N, Fallentin E, Hamilton-Dutoit S, Vogel I, Grønbæk H| title=[Hepatocellular adenoma - new classification and recommendations]. | journal=Ugeskr Laeger | year= 2015 | volume= 177 | issue= 12 | pages=  | pmid=25786843 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25786843  }} </ref>
 
:* Gender (men)
:* Gender (men)
:* Size (> 8 cm)
:* Size (> 8 cm)
:* Subtype (''[[beta-catenin]]''-activated [[Hepatocellular adenoma|HCA]])
:* Sub-type (''[[beta-catenin]]''-activated hepatocellular adenoma)


==References==
==References==

Latest revision as of 21:07, 20 August 2019

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Zahir Ali Shaikh, MD[2]

Overview

The most important risk factor for the development of hepatocellular adenoma is the use of oral contraceptive medications. Other risk factors include glycogen storage diseases, familial adenomatous polyposis, Klinefelter's syndrome, metabolic syndrome, obesity, long term use of anabolic androgenic steroids, vascular disorders such as portal vein agenesis, Budd-Chiari syndrome, and hereditary hemorrhagic telangiectasia.

Risk Factors

Risk Factors for Malignant Transformation

Risk factors for the malignant transformation of hepatocellular adenoma to hepatocellular carcinoma include:[6]

  • Gender (men)
  • Size (> 8 cm)
  • Sub-type (beta-catenin-activated hepatocellular adenoma)

References

  1. L. Rosenberg (1991). "The risk of liver neoplasia in relation to combined oral contraceptive use". Contraception. 43 (6): 643–652. PMID 1651205. Unknown parameter |month= ignored (help)
  2. 2.0 2.1 Barthelmes L, Tait IS (2005). "Liver cell adenoma and liver cell adenomatosis". HPB (Oxford). 7 (3): 186–96. doi:10.1080/13651820510028954. PMC 2023950. PMID 18333188.
  3. U. Beuers, W. O. Richter, M. M. Ritter, B. Wiebecke & P. Schwandt (1991). "Klinefelter's syndrome and liver adenoma". Journal of clinical gastroenterology. 13 (2): 214–216. PMID 1851773. Unknown parameter |month= ignored (help)
  4. N. S. Alshak, J. Cocjin, L. Podesta, R. van de Velde, L. Makowka, P. Rosenthal & S. A. Geller (1994). "Hepatocellular adenoma in glycogen storage disease type IV". Archives of pathology & laboratory medicine. 118 (1): 88–91. PMID 8285839. Unknown parameter |month= ignored (help)
  5. S. Bala, P. H. Wunsch & W. G. Ballhausen (1997). "Childhood hepatocellular adenoma in familial adenomatous polyposis: mutations in adenomatous polyposis coli gene and p53". Gastroenterology. 112 (3): 919–922. PMID 9041254. Unknown parameter |month= ignored (help)
  6. Aamann L, Schultz N, Fallentin E, Hamilton-Dutoit S, Vogel I, Grønbæk H (2015). "[Hepatocellular adenoma - new classification and recommendations]". Ugeskr Laeger. 177 (12). PMID 25786843.


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