What is liver hemangioma and what causes it?

Although hepatic hemangioma is a benign tumor, it is very harmful and cannot be ignored. People with vascular malformations are generally prone to this disease. Some hepatic hemangiomas are true tumors. In addition, experts believe that hormones are also related to the occurrence of hepatic hemangiomas.

Hepatic hemangioma is a benign tumor of the liver. The most common type is hepatic cavernous hemangioma. Cavernous hemangioma is usually solitary and mostly occurs in the right lobe of the liver; about 10% are multiple and can be distributed in one lobe or both sides of the liver. Hemangiomas appear as dark red or bluish-purple cystic bulges in the liver. Lobulated or nodular, soft, compressible, and most are clearly demarcated from adjacent tissues. The patient generally has no symptoms.

1. One possibility is vascular malformation.

Its growth is due to the expansion of sinusoids under the action of blood flow. The sinusoids have complete endothelial cells, abundant elastic fibers underneath, fibroblasts and smooth muscle cells in the middle membrane layer, and extremely rich and widely distributed collagen fibers in the interstitium, resulting in unclear boundaries between the inner, middle and outer membrane layers and disordered arrangement of elastic fibers. Collagen fibers can fill the sinusoid cavity, and endothelial cells swell to varying degrees, even semi-detached or detached; red blood cells can infiltrate into the interstitium in large quantities, thus confirming that hepatic hemangioma is an arterial malformation of the hepatic artery terminal.

2. The second view is that hepatic hemangioma is a true tumor.

Its growth is due to the formation of new vascular tissue. Hormones play an important role in the formation of new vascular tissue. It is speculated that steroids act on the microstructure of the vascular wall, which is a part of the cavernous blood vessels. The possible mechanism is that steroids such as prednisone inhibit the biosynthesis of collagen in the vascular wall.

On the other hand, steroids have the effect of stimulating or promoting angiogenesis. It has been reported that sex hormones can promote the proliferation and migration of vascular endothelial cells and even form capillary-like structures.

Clinical studies have also confirmed that there is a certain correlation between female hormones and the growth of hepatic hemangiomas. A long-term follow-up survey showed that 12.7% of female patients with hepatic hemangioma had tumor enlargement during the follow-up period, but only 6.3% had significant enlargement. In 22.7% of those receiving hormone therapy, the diameter of their hepatic hemangioma increased, twice that of the control group. All of the above indicate that the growth and recurrence of hepatic hemangioma are closely related to sex hormones, exogenous such as oral contraceptives, and endogenous such as pregnancy. That is, pregnancy or oral contraceptives can accelerate tumor growth or cause recurrence after cure.

It has also been reported that the positive expression rate of vascular endothelial growth factor (VEGF) in hepatic hemangioma is as high as 78%. The higher the VEGF expression,

The more vigorous the proliferation of endothelial cells, the more likely hepatic hemangiomas should be considered as neoplasms. However, the true mechanism of hormones in the occurrence and development of hepatic hemangioma is still unknown. We need to conduct in-depth research to provide a theoretical basis for the clinical drug treatment of hepatic hemangioma.