Acute fatty liver of pregnancy is a rare condition and occurs in approximately one in 7,000 to one in 15,000 pregnancies. The mortality from acute fatty liver of pregnancy has been reduced significantly to 18%, and is now related primarily to complications, particularly DIC (Disseminated Intravascular Coagulation) and infections. After delivery, most mothers do well, as the stimulus for fatty acid overload is removed. The disease can recur in future pregnancies, with a calculated genetic chance of 25%; the actual rate is lower, however. Mortality of the foetus has also diminished significantly, but still remains 23%, and may be related to the need for premature delivery.

Historically mortality has been high, being in excess of 80%. In recent years the advent of liver transplantation and multidisciplinary intensive care support have improved survival significantly. At present overall short-term survival with transplant is more than 65%.

Several prognostic scoring systems have been devised to predict mortality and to identify who will require an early liver transplant. These include King's College Hospital criteria, MELD score, APACHE II, and Clichy criteria.

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.

Calciphylaxis most commonly occurs in patients with end-stage renal disease who are on hemodialysis or who have recently received a renal (kidney) transplant. Yet calciphylaxis does not occur only in end-stage renal disease patients. When reported in patients without end-stage renal disease, it is called non-uremic calciphylaxis by Nigwekar et al. Non-uremic calciphylaxis has been observed in patients with primary hyperparathyroidism, breast cancer (treated with chemotherapy), liver cirrhosis (due to alcohol abuse), cholangiocarcinoma, Crohn's disease, rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE).

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.

Purpura fulminans is rare and most commonly occurs in babies and small children but can also be a rare manifestation in adults when it is associated with severe infections. For example, Meningococcal septicaemia is complicated by purpura fulminans in 10–20% of cases among children. Purpura fulminans associated with congenital (inherited) protein C deficiency occurs in 1:500,000–1,000,000 live births.

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

Peliosis hepatis is an uncommon vascular condition characterised by multiple, randomly distributed, blood-filled cavities throughout the liver. The size of the cavities usually ranges between a few millimetres and 3 cm in diameter. In the past, it was a mere histological curiosity occasionally found at autopsies, but has been increasingly recognised with wide-ranging conditions from AIDS to the use of anabolic steroids. It also occasionally affects spleen, lymph nodes, lungs, kidneys, adrenal glands, bone marrow, and other parts of gastrointestinal tract.

Peliosis hepatis is often erroneously written "peliosis hepati"ti"s", despite its not being one of the hepatitides. The correct term arises from the Greek "pelios", i.e. discoloured by extravasated blood, livid, and the Latinized genitive case (hepatis) of the Greek "hepar", liver.

Common causes for acute liver failure are paracetamol (acetaminophen) overdose, idiosyncratic reaction to medication (e.g. tetracycline, troglitazone), excessive alcohol consumption (severe alcoholic hepatitis), viral hepatitis (hepatitis A or B — it is extremely uncommon in hepatitis C), acute fatty liver of pregnancy, and idiopathic (without an obvious cause). Reye syndrome is acute liver failure in a child with a viral infection (e.g. chickenpox); it appears that aspirin use may play a significant role. Wilson's disease (hereditary copper accumulation) may infrequently present with acute liver failure.

The condition is typically asymptomatic and is discovered following evaluation of abnormal liver function test. However, when severe, it can manifest as jaundice, hepatomegaly, liver failure, and haemoperitoneum.

Treatment is usually directed towards management of the underlying cause. Withdrawal of azathioprine leads to remission in renal transplant; bacillary peliosis responds to antibiotics. In rare circumstances partial resection of liver or transplant may be required.

A Zahn infarct is a pseudo-infarction of the liver, consisting of an area of congestion with parenchymal atrophy but no necrosis, and usually due to obstruction of a branch of the portal vein. Zahn infarcts are unique in that there is collateral congestion of liver sinusoids that do not include areas of anoxia seen in most infarcts. Fibrotic tissue may develop in the area of the infarct and it could be caused by an occlusive phlebitis in portal vein radicles. Non ischemic infarct of liver with lines of Zahn.

This includes mostly drug-induced hepatotoxicity, (DILI) which may generate many different patterns over liver disease, including

- cholestasis

- necrosis

- acute hepatitis and chronic hepatitis of different forms,

- cirrhosis

- Effects of Acetaminophen (Tylenol)

- other rare disorders like focal nodular hyperplasia, Hepatic fibrosis, peliosis hepatis and veno-occlusive disease.

Liver damage is part of Reye's syndrome.

Due to the rarity of Purpura fulminans and its occurrence in vulnerable patient groups like children research on the condition is very limited and evidence based knowledge is scarce. Currently, there is only one Purpura fulminans related clinical research project, http://www.sapfire-registry.org/, which is registered with clinicaltrials.gov.

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."

In most cases, liver function will return to normal if the offending drug is stopped early. Additionally, the patient may require supportive treatment. In acetaminophen toxicity, however, the initial insult can be fatal. Fulminant hepatic failure from drug-induced hepatotoxicity may require liver transplantation. In the past, glucocorticoids in allergic features and ursodeoxycholic acid in cholestatic cases had been used, but there is no good evidence to support their effectiveness.

An elevation in serum bilirubin level of more than 2 times ULN with associated transaminase rise is an ominous sign. This indicates severe hepatotoxicity and is likely to lead to mortality in 10% to 15% of patients, especially if the offending drug is not stopped (Hy's Law). This is because it requires significant damage to the liver to impair bilirubin excretion, hence minor impairment (in the absence of biliary obstruction or Gilbert syndrome) would not lead to jaundice. Other poor predictors of outcome are old age, female sex, high AST.

The risk factors presently known are:

- Quantity of alcohol taken: Consumption of 60–80g per day (14g is considered one standard drink in the USA, i.e., 1.5 fl oz hard liquor, 5 fl oz wine, 12 fl oz beer; drinking a six-pack of beer daily would be in the middle of the range) for 20 years or more in men, or 20g/day for women significantly increases the risk of hepatitis and fibrosis by 7% to 47%,

- Pattern of drinking: Drinking outside of meal times increases up to 3 times the risk of alcoholic liver disease.

- Gender: Women are twice as susceptible to alcohol-related liver disease, and may develop alcoholic liver disease with shorter durations and doses of chronic consumption. The lesser amount of alcohol dehydrogenase secreted in the gut, higher proportion of body fat in women, and changes in fat absorption due to the menstrual cycle may explain this phenomenon.

- Hepatitis C infection: A concomitant hepatitis C infection significantly accelerates the process of liver injury.

- Genetic factors: Genetic factors predispose both to alcoholism and to alcoholic liver disease. Both monozygotic twins are more likely to be alcoholics and to develop liver cirrhosis than both dizygotic twins. Polymorphisms in the enzymes involved in the metabolism of alcohol, such as ADH, ALDH, CYP4502E1, mitochondrial dysfunction, and cytokine polymorphism may partly explain this genetic component. However, no specific polymorphisms have currently been firmly linked to alcoholic liver disease.

- Iron overload (Hemochromatosis)

- Diet: Malnutrition, particularly vitamin A and E deficiencies, can worsen alcohol-induced liver damage by preventing regeneration of hepatocytes. This is particularly a concern as alcoholics are usually malnourished because of a poor diet, anorexia, and encephalopathy.

Chronic liver diseases like chronic hepatitis, chronic alcohol abuse or chronic toxic liver disease may cause

- liver failure and hepatorenal syndrome

- fibrosis and cirrhosis of liver

Cirrhosis may also occur in primary biliary cirrhosis. Rarely, cirrhosis is congenital.

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.

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 cause can be found in more than 80% of patients.

- Primary Budd–Chiari syndrome (75%): thrombosis of the hepatic vein

- Hepatic vein thrombosis is associated with the following in decreasing order of frequency:

2. Polycythemia vera

1. Pregnancy

2. Postpartum state

3. Use of oral contraceptives

4. Paroxysmal nocturnal hemoglobinuria

5. Hepatocellular carcinoma

6. Lupus anticoagulants

- Secondary Budd–Chiari syndrome (25%): compression of the hepatic vein by an outside structure (e.g. a tumor)

Budd–Chiari syndrome is also seen in infections such as tuberculosis, congenital venous webs and occasionally in inferior vena caval stenosis.

Often, the patient is known to have a tendency towards thrombosis, although Budd–Chiari syndrome can also be the first symptom of such a tendency. Examples of genetic tendencies include protein C deficiency, protein S deficiency, the Factor V Leiden mutation, hereditary anti-thrombin deficiency and prothrombin mutation G20210A. An important non-genetic risk factor is the use of estrogen-containing (combined) forms of hormonal contraception. Other risk factors include the antiphospholipid syndrome, aspergillosis, Behçet's disease, dacarbazine, pregnancy, and trauma.

Many patients have Budd–Chiari syndrome as a complication of polycythemia vera (myeloproliferative disease of red blood cells). Patients suffering from paroxysmal nocturnal hemoglobinuria (PNH) appear to be especially at risk for Budd–Chiari syndrome, more than other forms of thrombophilia: up to 39% develop venous thromboses and 12% may acquire Budd-Chiari.

A related condition is veno-occlusive disease, which occurs in recipients of bone marrow transplants as a complication of their medication. Although its mechanism is similar, it is not considered a form of Budd–Chiari syndrome.

Other toxicologic causes of veno-occlusive disease include plant & herbal sources of pyrrolizidine alkaloids such as Borage, Boneset, Coltsfoot, T'u-san-chi, Comfrey, Heliotrope (sunflower seeds), Gordolobo, Germander, and Chaparral.

Several studies have attempted to predict the survival of patients with Budd–Chiari syndrome. In general, nearly 2/3 of patients with Budd–Chiari are alive at 10 years. Important negative prognostic indicators include ascites, encephalopathy, elevated Child-Pugh scores, elevated prothrombin time, and altered serum levels of various substances (sodium, creatinine, albumin, and bilirubin). Survival is also highly dependent on the underlying cause of the Budd–Chiari syndrome. For example, a patient with an underlying myeloproliferative disorder may progress to acute leukemia, independently of Budd–Chiari syndrome.

The following therapeutic drugs were withdrawn from the market primarily because of hepatotoxicity: Troglitazone, bromfenac, trovafloxacin, ebrotidine, nimesulide, nefazodone, ximelagatran and pemoline.

Laennec's cirrhosis, also known as portal cirrhosis, alcoholic cirrhosis, fatty cirrhosis, or atrophic cirrhosis, is named after René Laennec, a French physician and the inventor of the stethoscope. It is a disease of the liver in which the normal lobular architecture is lost, with fibrosis (scarring) and later nodular regeneration. Laennec's cirrhosis can be associated with inflammatory polyarthritis, most commonly affecting the shoulders, elbows and knees. Osteoporosis, soft tissue swelling in peripheral joints and sometimes calcific periathritis are seen.

In the developed world, Laennec's cirrhosis most commonly affects middle-aged males, typically ages 40–60. This is the most common form of cirrhosis in the U.S. Chronic alcoholism can cause Laennec's cirrhosis.

In areas of the world afflicted with chronic starvation (Africa and Asia), the children are most commonly afflicted.

Unfortunately, response to treatment is not guaranteed. Also, the necrotic skin areas may get infected, and this then may lead to sepsis (i.e. infection of blood with bacteria; sepsis can be life-threatening) in some patients. Overall, the clinical prognosis remains poor.

Acute fatty liver of pregnancy is a rare life-threatening complication of pregnancy that occurs in the third trimester or the immediate period after delivery. It is thought to be caused by a disordered metabolism of fatty acids by mitochondria in the mother, caused by long-chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency. The condition was previously thought to be universally fatal, but aggressive treatment by stabilizing the mother with intravenous fluids and blood products in anticipation of early delivery has improved prognosis.