Peliosis hepatis complicated by portal hypertension following renal transplantation

Abstract

Peliosis hepatis (PH) is a vascular lesion of the liver that mimics a hepatic tumor. PH is often associated with underlying conditions, such as chronic infection and tumor malignancies, or with the use of anabolic steroids, immunosuppressive drugs, and oral contraceptives. Most patients with PH are asymptomatic, but some present with abdominal distension and pain. In some cases, PH may induce intraperitoneal hemorrhage and portal hypertension. This study analyzed a 46-year-old male who received a transplanted kidney nine years prior and had undergone long-term immunosuppressive therapy following the renal transplantation. The patient experienced progressive abdominal distention and pain in the six months prior to this study. Initially, imaging studies revealed multiple liver tumor-like abnormalities, which were determined to be PH by pathological analysis. Because the hepatic lesions were progressively enlarged, the patient suffered from complications related to portal hypertension, such as intense ascites and esophageal varices bleeding. Although the patient was scheduled to undergo liver transplantation, he suffered hepatic failure and died prior to availability of a donor organ.

Keywords: Liver neoplasm; Peliosis hepatis; Portal hypertension; Renal failure; Renal transplantation.

Figure 1

Abdominal ultrasound showing multiple hyperechoic or mixed echoic tumors in the bilateral lobes of liver (arrows). Minimal ascites was also detected. A: One mixed echoic tumor (arrows) at segment 3, left portal vein (PV); B: One mixed echoic tumor (marked) at segment 5; C: One hyperechoic tumor at segment 5, right hepatic vein (HV), minimal ascites also detected; D: One hyperechoic tumor (arrows) at segment 5 near the main portal trunk.

Figure 2

Liver dynamic computed tomography showing multiple liver tumors. A: Hypodense liver tumors before contrast injection; B: Heterogeneous enhancement in the arterial phase and portal venous phase after contrast injection; C: Follow-up computed tomography showing increased size of the hepatic lesion; D: Massive ascites observed at 4 mo after the follow-up.

Figure 3

Microscopic analysis of liver biopsy specimens showing sinusoidal dilatation with red blood cell-filled cysts without endothelial lining cells. A: 100 × magnification of hematoxylin-eosin stained biopsy specimens; B: 400 × magnification of A; C, D: Immunohistochemistry analysis of CD31 (C) and CD34 (D) in liver biopsy specimens showing diffuse positive staining in the sinusoid endothelial cells; E: Ki-67 staining of liver biopsy specimens. The cell proliferative Ki-67 stain index was within 20%-40%, indicating active cell proliferation in the tissue.