Benign liver neoplasms encompass a variety of liver lesions, each with distinct pathologic, radiographic, and molecular characteristics. These include hemangioma, focal nodular hyperplasia, hepatocellular adenoma, and other less commonly seen lesions (Table 57-1). Benign liver lesions occur in up to 20% of the population and far surpass the incidence of malignant liver lesions. With the increased utilization of cross-sectional imaging, these tumors are being identified more frequently. Benign liver lesions are usually asymptomatic and are generally observed. Surgical intervention is warranted in symptomatic patients, cases where malignancy cannot be excluded, or if there is a potential for malignant transformation or associated complications (Fig. 57-1). Liver lesions with equivocal imaging characteristics can lead to diagnostic uncertainty resulting in important therapeutic ramifications. As a result, a thorough understanding of benign liver neoplasms is necessary to more accurately and appropriately screen patients for expectant management versus surgical intervention.
TABLE 57-1BENIGN LIVER LESIONS ||Download (.pdf) TABLE 57-1 BENIGN LIVER LESIONS
| Hepatocelullar adenoma |
| Focal nodular hyperplasia |
| Nodular regenerative hyperplasia |
| Bile duct adenoma |
| Hemangioma |
| Lipoma |
| Leiomyoma |
| Peliosus hepatis |
| Hamartoma |
| Simple cyst |
| Biliary cystadenoma |
| Abscess |
| Focal fatty infiltration |
Treatment algorithm for solitary liver lesions. CT, computed tomography; MRI, magnetic resonance imaging.
Epidemiology and Etiology
Hepatic hemangiomas are the most common benign tumor of the liver, affecting up to 20% of the population.1,2 Hemangiomas occur predominantly in females (60%-80%) and typically present in the third to fifth decades of life.3-5 Hemangiomas may be isolated to the liver or associated with systemic syndromes.6 In nearly 50% of patients, hepatic hemangiomas are multifocal.7
The etiology of hepatic hemangiomas is poorly defined. They are thought to arise either as congenital lesions that enlarge due to vascular ectasia or as vascular enlargement from previously normal hepatic vasculature. The blood supply of hepatic hemangiomas is derived from the hepatic artery. Commonly seen characteristics suggest a role of estrogens in their pathogenesis. These include female predominance, increase in size during pregnancy, and change in size while taking oral contraceptive pills (OCPs), as well as association of estrogen replacement therapy with hemangioma recurrence.8-10 The association of hormones and hemangioma does, however, remains controversial. For example, a case-control study showed no association between liver hemangioma and a history of OCP use.11 However, Glinkova et al. performed a prospective evaluation of 94 women with 181 hemangiomas and concluded that hormone therapy increased the risk of hemangioma enlargement.7 Although the association of hormone therapy and hepatic hemangioma pathogenesis remains poorly understood, hepatic hemangioma patients with nonphysiologic exposure to sex hormones warrant serial close observation.
Grossly, cavernous hemangiomas are soft, compressible, blood ...