Key prevention strategies for cirrhosis are population-wide interventions to reduce alcohol intake (through pricing strategies, public health campaigns, and personal counseling), programs to reduce the transmission of viral hepatitis, and screening of relatives of people with hereditary liver diseases.

Little is known about factors affecting cirrhosis risk and progression. Research has suggested that coffee consumption appears to help protect against cirrhosis.

People with ascites due to cirrhosis are at risk of spontaneous bacterial peritonitis.

Hallmark of the disease is thrombosis/sclerosis of branches of portal vein. Vessels formed are often termed as mesangiosinusoids or periportal cavernoma.

It is characterized by 'obliterative portovenopathy', which leads to various problems such as portal hypertension, massive splenomegaly, and variceal bleeding. It is estimated that about 85% of people with NCPF have repeated episodes of variceal bleeding.

Mortality is indirect and caused by complications. After cholangitis occurs, patients typically die within 5–10 years.

Mild disease has a risk of death of about 10% while moderate disease has a risk of death of 20%. When it occurs as a result of bone marrow transplant and multiorgan failure is present, the risk of death is greater than 80%.

The prognosis for people with ALD depends on the liver histology as well as cofactors, such as concomitant chronic viral hepatitis. Among patients with alcoholic hepatitis, progression to liver cirrhosis occurs at 10–20% per year, and 70% will eventually develop cirrhosis. Despite cessation of alcohol use, only 10% will have normalization of histology and serum liver enzyme levels. As previously noted, the MDF has been used to predict short-term mortality (i.e., MDF ≥ 32 associated with spontaneous survival of 50–65% without corticosteroid therapy, and MDF 11) and 90-day (MELD > 21) mortality. Liver cirrhosis develops in 6–14% of those who consume more than 60–80 g of alcohol daily for men and more than 20 g daily for women. Even in those who drink more than 120 g daily, only 13.5% will suffer serious alcohol-related liver injury. Nevertheless, alcohol-related mortality was the third leading cause of death in 2003 in the United States. Worldwide mortality is estimated to be 150,000 per year.

The prevalence of FLD in the general population ranges from 10% to 24% in various countries. However, the condition is observed in up to 75% of obese people, 35% of whom progress to NAFLD, despite no evidence of excessive alcohol consumption. FLD is the most common cause of abnormal liver function tests in the United States. "Fatty livers occur in 33% of European-Americans, 45% of Hispanic-Americans, and 24% of African-Americans."

The condition is usually congenital, but sporadic cases have also been reported. It may be associated with other congenital defects, commonly with autosomal recessive polycystic kidney disease, the most severe form of PKD. Some suggest that these two conditions are one disorder with different presentation.

The disease is typically progressive, leading to fulminant liver failure and death in childhood, in the absence of liver transplantation. Hepatocellular carcinoma may develop in PFIC-2 at a very early age; even toddlers have been affected.

Severe protein deficiency can cause Laennec's cirrhosis.

Two causes have been identified. The first is malnutrition, or, more specifically, protein deprivation. This is seen in starving children who have insufficient supplies of protein and therefore manufacture insufficient amounts of lipoproteins. They develop fatty livers: it is presumed that if they survive, cirrhosis will develop.

Chronic alcoholism can cause Laennec's cirrhosis. Whether or not alcohol alone can produce fatty nutritional cirrhosis has been debated for decades. Current evidence is that it can. If so, the condition should be renamed "alcoholic cirrhosis". Those who do not subscribe to the "alcohol-as-a-poison" school state that the changes to be described are the result of malnutrition common to alcoholics. They argue that alcoholics, in a sense, are no different from those in a state of chronic protein deprivation — both have protein deprivations.

Treatment is directed largely to removing the cause, or, where that is impossible, to modifying its effects. Thus, therapy aimed at improving right heart function will also improve congestive hepatopathy. True nutmeg liver is usually secondary to left-sided heart failure causing congestive right heart failure, so treatment options are limited.

The intrahepatic shunts found in large dog breeds are passed on in a simple autosomal recessive way, while the extrahepatic shunts of the small breeds are inherited on a polygenic basis.

Embryogenically, congenital hepatic fibrosis is due to malformation of the duct plate, a round structure appearing in the eighth week of gestation that is formed by primitive hepatocytes, which differentiate into cholangiocytes. Congenital hepatic fibrosis usually presents in adolescent or young adulthood, but onset of signs and symptoms can range from early childhood through mid-life. Clinical features may vary but commonly include Cholangitis, hepatomegaly and signs of portal hypertension.

Caroli disease is typically found in Asia, and diagnosed in persons under the age of 22. Cases have also been found in infants and adults. As medical imaging technology improves, diagnostic age decreases.

The serum bilirubin level is an indicator of the prognosis of PBC, with levels of 2–6 mg/dL having a mean survival time of 4.1 years, 6–10 mg/dL having 2.1 years and those above 10 mg/dL having a mean survival time of 1.4 years.

After liver transplant, the recurrence rate may be as high as 18% at 5 years, and up to 30% at 10 years. There is no consensus on risk factors for recurrence of the disease.

Complications of PBC can be related to chronic cholestasis or cirrhosis of the liver. Chronic cholestasis leads to osteopenic bone disease and osteoporosis, alongside hyperlipidaemia and vitamin deficiencies.

Patients with PBC have an increased risk of hepatocellular carcinoma compared to the general population, as is found in other cirrhotic patients. In patients with advanced disease, one series found an incidence of 20% in men and 4% in women.

Causes can include pancreatitis, cirrhosis, diverticulitis, and cholangiocarcinoma. It is also a known complication of splenectomy.

Portal vein thrombosis, previously known as Cauchois–Eppinger–Frugoni syndrome, is a form of venous thrombosis affecting the hepatic portal vein, which can lead to portal hypertension and reduction in the blood supply to the liver.

NAFLD can also be caused by some medications (drug-induced illness):

- Amiodarone

- Antiviral drugs (nucleoside analogues)

- Aspirin rarely as part of Reye's syndrome in children

- Corticosteroids

- Methotrexate

- Tamoxifen

- Tetracycline

Signs and symptoms of portal hypertension include:

In addition, a widened portal vein as seen on a CT scan or MRI may raise the suspicion about portal hypertension. A cutoff of 13 mm is widely used in this regard, but the diameter is often larger than this is in normal individuals as well.

Portal hypertension is hypertension (high blood pressure) in the hepatic portal system – made up of the portal vein and its branches, that drain from most of the intestines to the liver. Portal hypertension is defined as a hepatic venous pressure gradient. Cirrhosis (a form of chronic liver failure) is the most common cause of portal hypertension; other, less frequent causes are therefore grouped as non-cirrhotic portal hypertension. When it becomes severe enough to cause symptoms or complications, treatment may be given to decrease portal hypertension itself or to manage its complications.

Native American men have a high prevalence of non-alcoholic fatty liver disease. Two genetic mutations for this susceptibility have been identified, and these mutations provided clues to the mechanism of NASH and related diseases.

Polymorphisms (genetic variations) in the single-nucleotide polymorphisms (SNPs) T455C and C482T in APOC3 are associated with fatty liver disease, insulin resistance, and possibly hypertriglyceridemia. 95 healthy Asian Indian men and 163 healthy non-Asian Indian men around New Haven, Connecticut were genotyped for polymorphisms in those SNPs. 20% homogeneous wild both loci. Carriers of T-455C, C-482T, or both (not additive) had a 30% increase in fasting plasma apolipoprotein C3, 60% increase in fasting plasma triglyceride and retinal fatty acid ester, and 46% reduction in plasma triglyceride clearance. Prevalence of non-alcoholic fatty liver disease was 38% in carriers, 0% wild (normal). Subjects with fatty liver disease had marked insulin resistance.

There is a 2-3:1 male-to-female predilection in primary sclerosing cholangitis. PSC can affect men and women at any age, although it is commonly diagnosed in the fourth decade of life, most often in the presence of inflammatory bowel disease (IBD). PSC progresses slowly and is often asymptomatic, so it can be present for years before it is diagnosed and before it causes clinically significant consequences. There is relatively little data on the prevalence and incidence of primary sclerosing cholangitis, with studies in different countries showing annual incidence of 0.068–1.3 per 100,000 people and prevalence 0.22–8.5 per 100,000; given that PSC is closely linked with ulcerative colitis, it is likely that the risk is higher in populations where UC is more common. In the United States, an estimated 29,000 individuals have PSC.

Nodular regenerative hyperplasia is a form of liver hyperplasia associated with portal hypertension.

Nodular regenerative hyperplasia (NRH) is a rare liver condition characterized by a widespread benign transformation of the hepatic parenchyma into small regenerative nodules. NRH may lead to the development of non-cirrhotic portal hypertension. There are no published systematic population studies on NRH and our current knowledge is limited to case reports and case series. NRH may develop "via" autoimmune, hematological, infectious, neoplastic, or drug-related causes. It is associated with rheumatoid arthritis, Felty syndrome, myeloproliferative disorders, liver, kidney and bone marrow transplantation, cytotoxic drugs like azathioprine, mercaptopurine, thioguanine, antiretroviral drugs for HIV like didanosine and vitamin A. The disease is usually asymptomatic, slowly or non-progressive unless complications of portal hypertension develop. Accurate diagnosis is made by histopathology, which demonstrates diffuse micronodular transformation without fibrous septa. Lack of perinuclear collagen tissue distinguishes NRH from typical regenerative nodules in the cirrhotic liver. While the initial treatment is to address the underlying disease, ultimately the therapy is directed to the management of portal hypertension. The prognosis of NRH depends on both the severity of the underlying illness and the prevention of secondary complications of portal hypertension. In this review we detail the epidemiology, pathogenesis, diagnosis, management, and prognosis of NRH.

It can be a complication of azathioprine therapy.

Congestive hepatopathy, also known as nutmeg liver and chronic passive congestion of the liver, is liver dysfunction due to venous congestion, usually due to congestive heart failure. The gross pathological appearance of a liver affected by chronic passive congestion is "speckled" like a grated nutmeg kernel; the dark spots represent the dilated and congested hepatic venules and small hepatic veins. The paler areas are unaffected surrounding liver tissue. When severe and longstanding, hepatic congestion can lead to fibrosis; if congestion is due to right heart failure, it is called cardiac cirrhosis.