Pseudocirrhosis without chemotherapy

Case contributed by Michael P Hartung
Diagnosis certain


New onset liver failure. Recently diagnosed inflammatory breast cancer.

Patient Data

Age: 40 years
Gender: Female

Diffusely abnormal liver with heterogeneous echotexture and nodular contour. No discrete mass. 

Diffusely abnormal liver with multinodular appearance and infiltrative, low-attenuation soft tissue. Enlargement of the right hepatic lobe. 

Medium ascites. Peritoneal enhancement and subtle nodularity. Bilateral ovarian masses. 

Liver (Random) Biopsy:

  • Metastatic breast carcinoma
  • ER/PR/HER2 positive

Sections of non-neoplastic liver reveals hepatic parenchyma containing intact bile ducts. There in no portal inflammation noted. Scattered lobular inflammation is seen. The parenchyma is notable for cholestasis with feathery degeneration of hepatocytes with rosette formation in areas of cholestasis. Mallory-Denk bodies, excess iron storage and hepatocellular protein globules are absent. Some of the hepatocytes appears to have a "small cell change"-like appearance with some areas exhibiting hepatic cord atrophy, while other areas have the appearance of hypertrophy.  These changes likely represent findings secondary to mass effect and possible outflow obstruction. A trichrome-stained slide reveals focal periportal pericellular fibrosis. In situ hybridization for EBV encoded RNA (EBER) is negative.

Case Discussion

Pseudocirrhosis most often is used to describe the morphologic changes of cirrhosis developing in patients with metastatic breast cancer after chemotherapy. It has also been described in other malignancies and in patients who have NOT received chemotherapy, as in this case.

However, in my literature search, I did not find any actual case reports with images of pseudocirrhosis without chemotherapy, indicating that this is actually quite rare. 

The pathophysiology of pseudocirrhosis can be due to scarring/capsular retraction following chemotherapy, desmoplastic reaction due to infiltrative active tumor, and nodular regenerative hyperplasia.1

In this case, the pathology report supports cholestatic liver injury, mass effect/outflow obstruction, and pericellular fibrosis as the cause of this appearance. 

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