Hepatic Hemangiomas: Background, Pathophysiology, Epidemiology

Sections

Overview

Background

Hemangioma is the most common benign tumor affecting the liver.^[1]Hepatic hemangiomas are mesenchymal in origin and usually are solitary. Some authorities consider them to be benign congenital hamartomas. Hemangiomas are composed of masses of blood vessels that are atypical or irregular in arrangement and size.

The etiology of these lesions remains unknown, although oral contraceptives and steroids may accelerate the growth of a hemangioma. Whether or not these drugs actually induce the formation of the hemangioma is unclear.

Pathophysiology

Although no definite familial or genetic mode of inheritance has been described, Moser et al reported a large family of Italian origin in which 3 female patients in 3 successive generations had large symptomatic hepatic hemangiomas.^[2]The authors postulated that restriction of the disease to the female sex could be explained by sex-dependent differences in penetrance, the expression of a presumed liver-hemangioma gene, or the production of proliferative factors, such as female sex hormones.

Several pharmacologic agents have been postulated to promote tumor growth. Steroid therapy,^[3]estrogen therapy, and pregnancy^[4]can increase the size of an already existing hemangioma. One study prospectively evaluated 94 women with hepatic hemangiomas, with a mean follow-up period of 7.3 years (range, 1-17 y).^[5]An increase in the size of the hemangiomas was seen in 23% of women who received hormonal therapy as opposed to 10% of control subjects (P=0.05). Hemangiomas have also been reported in pregnant women following ovarian stimulation therapy with clomiphene citrate and human chorionic gonadotropin.^[6]

Epidemiology

United States data

The reported incidence of hepatic hemangiomas is approximately 2%. The prevalence rate at necropsy is as high as 7.4%. The widespread use of noninvasive abdominal imaging modalities has led to increased detection of asymptomatic lesions in vivo.

Sex- and age-related demographics

Women, especially with a history of multiparity, are affected more often than men. The female-to-male ratio is 4-6:1.

Hepatic hemangiomas can occur at all ages, but most are diagnosed in individuals aged 30-50 years. Female patients often present at a younger age and with larger tumors.

Hepatic hemangiomas may be seen in infancy. They have also been detected prenatally in a growing fetus.^{[7, 8]}

Prognosis

Overall, a patient with a hepatic hemangioma has an excellent prognosis. Malignant transformation has not been described.

Complications

Complications depend on the size and location of the tumor. It needs to be emphasized that the following complications are rarely described:

Rupture with resultant hemoperitoneum: Rarely, large tumors rupture spontaneously or after blunt trauma. Patients may present with signs of circulatory shock and hemoperitoneum.
Intratumoral bleeding
Compression of bile ducts and nearby arteries and veins: One case has been reported of lower extremity edema caused by compression of the inferior vena cava by a cavernous hemangioma of the caudate lobe of the liver.
Gastric compression: Early satiety, nausea, and vomiting may occur when large lesions compress the stomach, producing gastric outlet obstruction.
Hemobilia
High-output congestive heart failure

Clinical Presentation

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Media Gallery

Hemangioma of the liver as seen on ultrasound. Courtesy of Wikimedia Commons/James Heilman, MD (https://commons.wikimedia.org/wiki/File:Hemangiomaliver.PNG).
Hepatic hemangioma. (a): Transverse sonogram of left lobe of liver presenting a typical hyperechogenic hemangioma. (b) and (c): Two different hypoechogenic liver lesions suspected to be atypical hemangioma, subsequently confirmed by computed tomography scanning. Courtesy of BMC Gastroenterology, PMID: 2150493.
Hepatic hemangioma. Moderately (a) and heavily (b) T2-weighted magnetic resonance images show typical bright lesions. Courtesy of BMC Gastroenterology, PMID: 2150493.
Hepatic hemangioma. (A) On plain computed tomography (CT) scan, an oval, low-density lesion with clear boundaries and central liquefactive necrosis is seen). (B) and (C): CT-enhanced scans show nodular enhancement at the edges of the lesion during the early arterial phase, and a higher density than the normal liver, appearing as the “fast out, slow in” sign. Courtesy of PLoS One, PMID: 26287964.

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Author

David C Wolf, MD, FACP, FACG, AGAF, FAASLD Medical Director of Liver Transplantation, Westchester Medical Center; Professor of Clinical Medicine, Division of Gastroenterology and Hepatobiliary Diseases, Department of Medicine, New York Medical College

David C Wolf, MD, FACP, FACG, AGAF, FAASLD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Salix; Gilead; Abbvie; Intercept; Merck.

Coauthor(s)

Unnithan V Raghuraman, MD, FACG, FACP, FRCP Consulting Staff, Department of Gastroenterology, St John Medical Center

Unnithan V Raghuraman, MD, FACG, FACP, FRCP is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Additional Contributors

Vivek V Gumaste, MD Associate Professor of Medicine, Mount Sinai School of Medicine of New York University; Adjunct Clinical Assistant, Mount Sinai Hospital; Director, Division of Gastroenterology, City Hospital Center at Elmhurst; Program Director of GI Fellowship (Independent Program); Regional Director of Gastroenterology, Queens Health Network

Vivek V Gumaste, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association

Disclosure: Nothing to disclose.

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