<unk>  is a form of liver hyperplasia associated with portal hypertension.<unk>  <unk>  is a rare liver condition characterized by a widespread benign transformation of the hepatic parenchyma into small<unk>  nodules.<unk>  may lead to the development of non-cirrhotic portal hypertension. There are no published systematic population studies on<unk>  and our current knowledge is limited to case reports and case series.<unk>  may develop via autoimmune, hematological, infectious, neoplastic, vascular, or drug-related causes. It is associated with rheumatoid arthritis, Felty syndrome, myeloproliferative disorders, hereditary hemorrhagic telangiectasia (HHT, Osler–Weber–Rendu syndrome), liver, kidney and bone marrow transplantation, cytotoxic drugs like azathioprine, mercaptopurine, thioguanine, antiretroviral drugs for HIV like didanosine and vitamin A. There is also association between<unk>  and platinum-based drugs, such as chemotherapy with oxaliplatin. The disease is usually asymptomatic, slowly or non-progressive unless complications of portal hypertension develop. Accurate diagnosis is made by histopathology, which demonstrates diffuse micronodular transformation without fibrous septa. Lack of perinuclear collagen tissue distinguishes<unk>  from typical<unk>  nodules in the cirrhotic liver. While the initial treatment is to address the underlying disease, ultimately the therapy is directed to the management of portal hypertension. The prognosis of<unk>  depends on both the severity of the underlying illness and the prevention of secondary complications of portal hypertension. In this review we detail the epidemiology, pathogenesis, diagnosis, management, and prognosis of<unk> . Feathery degeneration is seen in PBC It can be a complication of azathioprine therapy.
Nodular regenerative hyperplasia
Nodular sclerosis
Xanthogranulomatous inflammation
Atypical small acinar proliferation
Focal nodular hyperplasia
Follicular hyperplasia
Gandy–Gamna nodules
Ground glass hepatocyte