Peliosis hepatis is a rare vascular disorder characterized by blood-filled cystic dilations of liver sinusoids. Spaces formed by sinusoidal endothelial damage and/or hepatocyte necrosis fill with blood. Immunosuppression (AIDS, organ transplantation), anabolic steroids, azathioprine, tamoxifen, and Bartonella henselae infection (bacillary peliosis) are major risk factors. Most cases are asymptomatic and incidental. In severe cases, risk of spontaneous rupture and hemorrhage exists. Lesions may be diffusely distributed or form focal nodular masses.
Age Range
20-60
Peak Age
40
Gender
Male predominant
Prevalence
Rare
Two main pathogenetic mechanisms are proposed in peliosis hepatis: (1) Phlebectatic type — damage to sinusoidal endothelial cells with disruption of endothelial barrier causes sinusoids to dilate and fill with blood. Endothelial damage can be toxic (anabolic steroids, azathioprine), infectious (Bartonella henselae — creates cavernous spaces by endothelial cell proliferation), or immunological (HIV-related endothelial dysfunction). (2) Parenchymal type — spaces formed by hepatocyte necrosis fill with blood, no endothelial lining. Enhancement pattern reflects the vascular nature of lesions: centripetal filling (hemangioma-like) or early homogeneous enhancement (blood flow through sinusoidal spaces between hepatocytes). In chronic cases, fibrosis may develop.
The combination of T2 hyperintensity (vascular spaces), T1 hyperintense areas consistent with hemorrhage, and hemangioma-like but irregular centripetal filling on dynamic contrast imaging in multiple hepatic lesions in the setting of immunosuppression or drug use (anabolic steroids, azathioprine) is the signature finding of peliosis hepatis.
Multiple hypodense or isodense lesions, sizes ranging from millimeters to several centimeters. Distribution may be diffuse. Hyperdense areas may be seen in large lesions due to internal hemorrhage.
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Multiple hypodense/isodense lesions are seen in the liver, and peliosis hepatis should be considered in the clinical context.
Enhancement pattern is variable: (1) Early globular peripheral enhancement → centripetal filling (hemangioma-like), (2) early homogeneous enhancement, or (3) no enhancement (thrombotic spaces). Pattern depends on the vascular anatomy and thrombosis status of the lesion.
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Variable enhancement pattern is seen in the lesions, with some showing peripheral globular enhancement and others early homogeneous fill-in.
Centripetal filling on delayed phase — hemangioma-like delayed homogeneous enhancement is seen in some lesions. Thrombotic or organized bloody spaces may remain non-enhancing.
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Centripetal filling is observed in some lesions on delayed phase, reflecting vascular nature consistent with peliosis hepatis.
Hypointense or isointense signal on T1 — fluid signal of blood-filled spaces. T1 hyperintensity (methemoglobin) in lesions with hemorrhage. In diffuse peliosis, liver parenchyma may show heterogeneous T1 signal.
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Lesions show variable signal on T1, with hyperintense areas consistent with hemorrhage seen in some lesions.
Hyperintense signal on T2 — high free water content of blood-filled vascular spaces. Similar to T2 hyperintensity of hemangioma but may be more heterogeneous (areas of organized blood and fibrosis).
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Lesions show hyperintense signal on T2, consistent with fluid content of vascular spaces.
Heterogeneous echotexture — hypoechoic or hyperechoic lesions, in diffuse peliosis the liver parenchyma has heterogeneous appearance. Hepatomegaly may accompany. US findings are non-specific.
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Heterogeneous echotexture and hepatomegaly are seen in the liver parenchyma, and peliosis hepatis is considered in the clinical context; contrast-enhanced MRI is recommended for further characterization.
Criteria
Sinusoidal endothelium preserved but dilated — regular endothelium-lined spaces. More common form.
Distinct Features
More regular enhancement pattern (hemangioma-like centripetal filling). Less hemorrhage risk. Common in drug-related (anabolic steroids) cases. Regression possible with drug discontinuation.
Criteria
Spaces without endothelial lining from hepatocyte necrosis — irregularly bordered, blood-filled lacunae.
Distinct Features
More irregular enhancement pattern. Higher hemorrhage and rupture risk (no endothelial barrier). More common in immunosuppression (AIDS) related cases. Worse prognosis.
Criteria
Peliosis due to Bartonella henselae infection — bacteria induces endothelial cell proliferation creating cavernous spaces. AIDS patients + cat contact is typical context.
Distinct Features
Dramatic regression with antibiotic therapy (doxycycline, erythromycin) — diagnostic and therapeutic test. Splenic peliosis may coexist. Bacilli can be demonstrated by Warthin-Starry stain. May coexist with cutaneous bacillary angiomatosis.
Distinguishing Feature
Hemangioma shows homogeneous light-bulb bright signal on T2 and regular centripetal enhancement. Peliosis T2 signal is more heterogeneous (hemorrhagic products) and enhancement is more irregular. Hemangioma lacks immunosuppression/drug context. Hemangioma is usually solitary or few while peliosis is usually multiple.
Distinguishing Feature
Angiosarcoma has much more aggressive rapid progression, hepatomegaly, and spontaneous rupture (hemoperitoneum). Angiosarcoma tends to form dominant mass, peliosis shows more diffuse distribution. Thorotrast/vinyl chloride exposure should be investigated in angiosarcoma. Biopsy is required for definitive differential.
Distinguishing Feature
Hepatic lymphoma shows multiple hypodense lesions but enhancement is minimal or absent (enhancement is present in peliosis). B symptoms, lymphadenopathy, and splenomegaly are more common in lymphoma. Hemorrhage findings on T1 are not expected in lymphoma. LDH and β2-microglobulin elevation supports lymphoma.
Distinguishing Feature
Simple cyst has water density (0-15 HU), does not enhance, and has thin smooth wall. Peliosis lesions have blood density (30-50 HU), show enhancement, and have irregular margins. Clinical context (immunosuppression) supports peliosis.
Urgency
routineManagement
conservativeBiopsy
Not NeededFollow-up
6-monthPeliosis hepatis is asymptomatic in most cases and treatment is directed at correcting the underlying cause. In drug-related cases (anabolic steroids, azathioprine, tamoxifen), lesions may regress with discontinuation of the responsible drug. In bacillary peliosis (Bartonella henselae), antibiotic therapy (doxycycline 100 mg twice daily, minimum 3 months) is curative. Immunosuppression control (HIV treatment, transplant patients) is important. In severe cases, risk of spontaneous rupture and hemoperitoneum exists (5-10%) — embolization or surgery may be needed for large lesions. Biopsy is generally risky due to vascular nature and should be avoided — clinical context + imaging is usually sufficient. 6-month US or MRI follow-up is recommended.
May regress with treatment of underlying cause (drug withdrawal, reduced immunosuppression). Risk of spontaneous rupture and hemoperitoneum exists. Biopsy should be performed cautiously due to bleeding risk. Hepatic failure may develop in severe cases.