Liver mass pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Overview

The exact pathogenesis of a liver mass depends upon the underlying disease. Increased estrogen in hepatic adenoma stimulates hepatocytes via steroid receptors and results vascular ectasia. While in FNH excessive release of growth factors promote growth of small arteries. Some conditions such as hemangioma, hepatic cysts are believed to be as result of genetic abnormality. Precancerous lesions are responsible for HCC, cholangiosarcoma. Hepatic abscess and echinoccosiosis are due to infectious agents.

Pathophysiology

The exact pathogenesis of a liver mass depends upon the underlying disease. The following table summarizes the various causes of liver masses:

Disease	Pathogenesis	Genetics	Associated Conditions	Gross Pathology	Microscopic Pathology
Hepatocellular adenoma	Estrogens cause the transformation of hepatocytes via steroid receptors Results in generalized vascular ectasia	Transcription factor 1 gene (TCF1) Interleukin 6 signal transducer gene (IL6ST) β catenin-1 gene (CTNNB1)	Glycogen storage disease types Ia and III Fanconi anemia Thalassemia Familial adenomatous polyposis Familial diabetes mellitus Hurler disease Galactosemia	Well circumscribed Nonlobulated Smooth and soft White to yellow to brown lesions	Cords of hepatocytes that have a high glycogen and fat content Lack of normal hepatic parenchymal architecture Absence of portal tracts and hepatic veins
Focal nodular hyperplasia	Develop around a preexisting arterial malformation Production of growth factors promote growth of small arteries  Increased perfusion of the adjacent tissue results in peritumoral hyperplasia.	β-catenin gene (CTNNB1) TP53 APC or HNF1α	Klippel-Trénaunay-Weber syndrome	Well-circumscribed Non-encapsulated Central fibrous scar	Hepatic parenchyma arranged in incomplete nodules Fibrous tissue with thick-walled vessels Bile ductular proliferation Cells of chronic inflammation
Hemangioma	Congenital disorder Vascular malformations that enlarge by ectasia  Estrogen and progesterone influence over tumor growth More common in females		Von Hippel Lindau disease	Well-circumscribed Appear red-brown Solitary nodules Less than 5cms	Large cystically dilated vessels Thin walls Intravascular thrombosis Calcifications
Hepatic Cyst	Von Meyenburg complexes separate from biliary tree and dilate to form cyst			Single, unilocular cyst Variable amounts of clear amber fluid (may contain blood, bile, mucus, pus)	Lined by flat / cuboidal epithelium Epithelium rests on thin collagenous wall without spindle cell stroma Degenerative changes include epithelial desquamation, multiloculation, calcification
Lymphangioma	Lymphangioma is caused by either sequestration of Lymph tissue Abnormal budding of lymph vessels Lack of fusion with the venous system, Obstruction of lymph vessels.	Trisomy 13 Tirsomy 18 Trisomy 21	Turner syndrome Noonan syndrome Down syndrome	Grey-white mass Well circumscribed Edematous appearance Variable size (may be massive) Filled with serous fluid Smooth inner lining	Thin walled channels lined by endothelium Intraluminal accumulation of eosinophilic deposits Clusters of intraluminal lymphocytes D2-40 +ve
Angiomyolipoma	Derive from a common progenitor cell that suffered the common second hit mutation. Angiomyolipomas are members of the perivascular epithelioid cells tumor group (PEComas) Composed of variable amounts of three components. Vascular cells Immature smooth muscle cells Fat cells	TSC1 gene TSC2 gene	Von Hippel-Lindau syndrome Tuberous sclerosis	Well circumscribed Uniform yellow mass	Smooth muscles Adipose tissue Abundant blood vessels
Hepatocellular carcinoma	Arises from precancerous lesions.: Genomic alterations Epigenetic modifications Growth factor pathway alterations	p53 PIKCA β-catenin genes ARID1A genes ARID2 genes RB1 genes	HBV infection HCV infection Underlying cirrhotic liver disease Inflammation Necrosis and fibrosis of the liver	Nodular or diffusely infiltrative Pale in relation to surrounding liver or green	Large polygonal tumours cells Graunular eosinophilic cytoplasm Layered dense collagen bundles
Cholangiocarcinoma	The epithelial cell lining the bile ducts are called cholangiocytes. The malignant transformsation of cholangiocytes leads to cholangiocarcinoma. Malignant transformation of cholangiocytes into cholangiocarcinoma include following stages: Hyperplasia Metaplasia Dysplasia Frank carcinoma Progression of malignancy is believed to be due to: Inflammation Obstruction of bile ducts Biliary intraepithelia neoplasia.	ARID1A BAP1 BRAF FGFR2 IDH1 IDH2 KMT2C KRAS PBRM1 PEG3 PTPN3 RNF43 ROBO2 SMAD4 TERT TP53		Mass-forming Nodular lesion or mass in the hepatic parenchyma Gray to gray-white, firm and solid carcinoma Periductal infiltrating Spreading of the carcinoma along the portal tracts with stricture of the affected bile ducts Dilatation of the peripheral bile ducts Intraductal growth types Polypoid or papillary tumor within the variably dilated bile duct lumen Malignant progression of an intraductal papillary neoplasm of the bile duct	Cuboidal or columnar mucin producing cells Dense fibrous(desmoplastic) stroma.
Hepatic abscess	In patients the reticuloendothelial cells (kupffer cells) of liver control the transient portal bacteremia In elderly and immunocompromised the bacteria can overwhelm the kupffer cells and lead to an abscess. Development of pyogenic liver abscess is the result of extension of infection from surrounding organs.			Single or multiple cavities, filled with fowl smelling, creamy yellow necrotic material, usually in right lobe of liver. The abscess may have fibrous capsule which is a centimeter or more thick and gradually merges into the liver parenchyma.	Multiple neutrophilic abscesses with areas of necrosis are seen in the liver parencyma. Suppuration, liquefaction Chronic inflammatory infiltrate consisting of lymphocytes, epithelioid macrophages, eosinophils, and neutrophils.
Parasitic cysts:(Echinococcous)	The transmission of echinococcosisfrom the definitive host to the intermediate host is by ingestion of embryonated eggs passed in the feces. Once the eggs are ingested they hatch in the small intestine and develop into onchospheres. In the small intestine , oncospheres reach various organs by migration through the vascular system and develop into cysts producing protoscolices. The definitive host is infected by ingestion of the organs infected with the cysts.			Cysts tend to be: Filled with clear fluid White appearance Solitary Unilocular	Cyst wall composed of an acellular laminated external layer and a thin, germinal (nucleated) inner layer Brood capsule with protoscoleces inside