Multiple Inflammatory and Serum Amyloid A Positive Telangiectatic Hepatic Adenomas with Glycogenated Nuclei Arising in a Background of Nonalcoholic Steatohepatitis
Kiat H. Lim1
, Stephen C. Ward2
, Sasan Roayaie3
, Emil Cohen4
, Myron Schwartz3
, M. Isabel Fiel2
, Swan N. Thung2
1Department of Pathology, Singapore General Hospital, Singapore
2Department of Pathology, The Mount Sinai Medical Center, New York, New York
3Division of Hepatobiliary Surgery, Department of Surgery, The Mount Sinai Medical Center, New York, New York
4Department of Radiology, The Mount Sinai Medical Center, New York, New York
The authors describe multiple telangiectatic or inflammatory adenomas in a 53-year-old woman with steatohepatitis who presented with acute right upper quadrant abdominal pain. Magnetic resonance imaging revealed 6 lesions consistent with multiple hepatic adenomas, 2 of which showed hemorrhage. She underwent right lobectomy and nonanatomical segment 2 liver resections and seven nodules ranging in size from 1.0 to 5.0 cm were identified. All nodules contained portal-like structures and ductular reaction, features seen in focal nodular hyperplasia, as well as significant inflammation, telangiectatic sinusoids and immunoreactivity for serum amyloid A, placing them according to a recently described classification systems as telangiectatic or inflammatory adenomas. The diffuse positivity of the serum amyloid A staining results in this case suggests an important diagnostic role of this stain in smaller tissue samples, such as in core biopsy specimens.
2
Wanless I R, Albrecht S, Bilbao J et al..
Multiple focal nodular hyperplasia of the liver associated with vascular malformations of various organs and neoplasia of the brain: a new syndrome.
Mod Pathol.
1989;
2
456-462
3
Nguyen B N, Flejou J-F, Terris B et al..
Focal nodular hyperplasia of the liver: a comprehensive pathologic study of 305 lesions and recognition of new histologic forms.
Am J Surg Pathol.
1999;
23
1441-1463
4
Bioulac-Sage P, Reboiussou S, Cunha A S et al..
Clinical, morphologic and molecular features defining so-called telangiectatic focal nodular hyperplasia of the liver.
Gastroenterology.
2005;
128
1211-1218
5
Bioulac-Sage P, Rebouissou S, Thomas C et al..
Hepatocellular adenoma subtype classification using molecular markers and immunohistochemistry.
Hepatology.
2007;
46
740-748
6
Paradis V, Champault A, Ronot M et al..
Telangiectatic adenoma: an entity associated with increased body mass index and inflammation.
Hepatology.
2007;
46
140-146
7
Zucman-Rossi J, Benhamouche S, Godard C et al..
Differential effects of inactivated Axin 1 and activated beta-catenin mutations in human hepatocellular carcinomas.
Oncogene.
2007;
26
774-780
9
Peterfy C G, Rosenthall L.
Large telangiectatic focal nodular hyperplasia presenting with normal radionuclide studies: case report.
J Nucl Med.
1990;
31
2037-2039
10
Haber M, Rueben A, Oliveiro P et al..
Multiple focal nodular hyperplasia of the liver associated with hemihyperthrophy and vascular malformations.
Gastroenterology.
1995;
108
1256-1262
13
Kim H-S, Kim Y A, Kim C J et al..
Telangiectatic focal nodular hyperplasia of the liver: a case detected at birth.
J Korean Med Sci.
2003;
18
746-750
14
Zucman-Rossi J, Jeannot E, Nhieu J T et al..
Genotype-phenotype correlation in hepatocellular adenoma: a new classification and relationship with HCC.
Hepatology.
2006;
43
515-524
15
Yamagata K, Oda N, Kaisaki P J et al..
Mutations in the hepatocyte nuclear factor-1alpha gene in maturity-onset diabetes of the young (MODY3).
Nature.
1996;
384
458-460
16
Bacq Y, Jacquemin E, Balabaud C et al..
Familial liver adenomatosis associated with hepatocytes nuclear factor 1alpha inactivation.
Gastroenterology.
2003;
125
1470-1475
17
Reznik Y, Dao T, Coutant R et al..
Hepatocyte nuclear factor-1 alpha gene inactivation: cosegregation between liver adenomatosis and diabetes phenotypes in two maturity-onset diabetes of the young (MODY3) families.
J Clin Endocrinol Metab.
2004;
89
1476-1480
