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Benign liver tumors

Benign tumors are masses of cells that can’t invade neighboring tissues or organs, and therefore are usually defined as non-cancerous. Benign liver tumors are actually pretty common, and typically don't cause any serious complications, and there are three major types: cavernous hemangiomas, focal nodular hyperplasias, and hepatocellular adenomas. Cavernous hemangiomas are the most common form and are these masses or swelling of the endothelial cells in blood vessels of the liver that, when we check it out on histology, they form these huge vascular spaces that sort of look like a system of caves. In other words, instead of blood flowing through a tube, the blood goes into a giant cavern with endothelial cells randomly sprinkled throughout. Although these vascular spaces look huge on histology, most patients have relatively small lesions, usually less than about 1.5 cm, and therefore don’t have any symptoms; in more rare cases, with larger lesions, patients may develop symptoms and in very rare cases, experience rupture and intraperitoneal bleeding. Finding and diagnosing these hemangiomas can be done through several imaging techniques like ultrasound, CT scans, and MRI. The second most common type of benign liver tumor is a focal nodular hyperplasia, or FNH. These are like these localized (focal) aggregates (nodular) of rapidly reproducing liver cells (hyperplasia). FNH is actually the most common non-blood vessel-related benign tumor in the liver and are seen slightly more in women than men, but can happen at any age. Basically this is a loosely used term to describe when nodules or aggregations of seemingly benign hepatocytes are found in the liver. Ultimately, we don’t really know why these form, but it’s thought that they could be a response to vascular injury of some kind that leads the hepatocytes to ramp up reproduction and form these aggregates of cells. Another reason it’s thought to be a result of vascular injury is that there’s almost always an abnormally large blood vessel in the center, with smaller branches radiating out into the periphery. And further supporting the injury hypothesis, is that there’s almost always a characteristic gross finding of centralized fibrous scar tissue produced by stellate cells. On histology you’ll often see this fibrous tissue as well, sometimes called fibrous septae, which means wall or separation. Diagnosis is usually done by CT scan looking for these masses of cells, in almost all cases, though, focal nodular hyperplasias are found incidentally during some other exam. Unless associated with pain, these benign tumors are typically left alone. Alright, another type of benign hepatocyte tumor, one that’s a lot more rare, are hepatic adenomas. These are tumors thought to be made up of liver epithelial cells, and often develop in an otherwise healthy liver. Usually these hepatocytes are enlarged, non-functional, and contain more glycogen and lipids than normal. The tissue around them is usually highly vascularized and usually both bile ducts and portal areas are absent. Again, like focal nodular hyperplasias, we don’t really know why they form, but one important distinction is that these are highly associated with the use of estrogen-based drugs, especially oral contraceptives, but also other anabolic steroids. Before the introduction of birth control, or oral contraceptives (or OCPs for short), hepatic adenomas were rarely reported and have increased along with increasing OCP use over time, and are associated more with higher-dosed regimens. And, the introduction of lower-dose OCPs has resulted in a reduction in cases. That said, how estrogen influences the development of hepatic adenomas is unclear. One theory is that estrogen might bind to estrogen receptors on the hepatocytes themselves and cause conversion of the hepatocytes into hepatic adenoma cells, though it probably has a lot to do with genetic predisposition or specific genetic mutations in combination with estrogen-based therapies. Along with OCPs, genetic glycogen storage diseases, particularly von Gierke’s disease, are also highly associated with hepatic adenomas, patients with von Gierke’s disease have liver cells that can’t generate glucose from glycogen through gluconeogenesis. What isn’t clear is why or how this deficiency tends to lead to hepatic adenomas. Although less common than the other forms of benign tumors, hepatic adenomas are more likely to rupture and lead to internal bleeding, especially during pregnancy. If patients with adenomas are using OCPs and stop or reduce their dosage, the adenomas usually tend to regress, likewise for patients with von Gierke’s disease, managing their diet—like their glucose, insulin, and glucagon levels, has led to improvement and even resolution of the adenomas.