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.

The causes of intrahepatic cholestasis of pregnancy are still not fully understood. Hormones and genetic factors are likely to be important in the pathogenesis of the disease. A number of features of the disease suggest a link to hormones:

- ICP occurs in the third trimester at the time when hormone levels are at their highest.

- Twin and triplet pregnancies, which are associated with higher hormone levels, show a higher incidence of ICP.

- ICP resolves quickly after delivery, when placental hormone production ceases.

- Older high-dose estrogen oral contraceptive pills could cause features of ICP.

Treatment with progesterone in the third trimester of pregnancy has been shown to be associated with the development of ICP, and levels of metabolites of progesterone, particularly sulfated progesterone, are higher in patients with ICP than unaffected women, suggesting that progesterone also has a role in ICP.

"Breastfeeding jaundice" or "lack of breastfeeding jaundice," is caused by insufficient breast milk intake, resulting in inadequate quantities of bowel movements to remove bilirubin from the body. This leads to increased enterohepatic circulation, resulting in increased reabsorption of bilirubin from the intestines. Usually occurring in the first week of life, most cases can be ameliorated by frequent breastfeeding sessions of sufficient duration to stimulate adequate milk production.

Prolonged hyperbilirubinemia (severe jaundice) can result in chronic bilirubin encephalopathy (kernicterus). Quick and accurate treatment of neonatal jaundice helps to reduce the risk of neonates developing kernicterus.

Infants with kernicterus may have a fever or seizures. High pitched crying is an effect of kernicterus. Scientists used a computer to record and measure cranial nerves 8, 9 and 12 in 50 infants who were divided into two groups equally depending upon bilirubin concentrations. Of the 50 infants, 43 had tracings of high pitched crying.

Exchange transfusions performed to lower high bilirubin levels are an aggressive treatment.

Yellow discoloration of the skin, especially on the palms and the soles, but not of the sclera or inside the mouth is due to carotenemia—a harmless condition.

"Pre-hepaticular" jaundice is caused by anything which causes an increased rate of hemolysis (breakdown of red blood cells). Unconjugated bilirubin comes from the breakdown of the heme pigment found in red blood cells' hemoglobin. The increased breakdown of red blood cells leads to an increase in the amount of unconjugated bilirubin present in the blood and deposition of this unconjugated bilirubin into various tissues can lead to a jaundiced appearance. In tropical countries, severe malaria can cause jaundice in this manner. Certain genetic diseases, such as sickle cell anemia, spherocytosis, thalassemia, pyruvate kinase deficiency, and glucose 6-phosphate dehydrogenase deficiency can lead to increased red cell lysis and therefore hemolytic jaundice. Commonly, diseases of the kidney, such as hemolytic uremic syndrome, can also lead to coloration.

In jaundice secondary to hemolysis, the increased production of bilirubin leads to the increased production of urine-urobilinogen. Bilirubin is not usually found in the urine because unconjugated bilirubin is not water-soluble, so, the combination of increased urine-urobilinogen with no bilirubin (since, unconjugated) in urine is suggestive of hemolytic jaundice.

Laboratory findings include:

- Urine: no bilirubin present, urobilinogen > 2 units (i.e., hemolytic anemia causes increased heme metabolism; exception: infants where gut flora has not developed).

- Serum: increased unconjugated bilirubin.

- Kernicterus is associated with increased unconjugated bilirubin not carried by albumin. Newborns are especially vulnerable to this due to increased permeability of the blood brain barrier.

The distinction between complications of hepatitis X and symptoms of hepatitis X is often obscure. While jaundice (yellow discoloration of the skin or whites of the eyes due to an increase of bile pigments in the blood), is a symptom of hepatitis, it is also a complication. Further complications that may arise include hyperpigmentation, renal (kidney) failure, and CSF xanthochromia. Liver disease is another fatal complication of hepatitis X. This could potentially lead to abdominal pain, hepatomegaly, splenomegaly, chest pain, and an altered bowel habit.

There has been no specific drug therapy developed for hepatitis, with the exception of hepatitis C. Patients are advised to rest in the early stages of the illness, and to eat small, high-calorie, high-protein meals in order to battle anorexia. Larger meals are more easily tolerated in the morning, for patients often experience nausea later in the day. Although high-protein meals are recommended, protein intake should be reduced if signs of precoma — lethargy, confusion, and mental changes — develop.

In acute viral hepatitis, hospitalization is usually required only for patients with severe symptoms (severe nausea, vomiting, change in mental status, and PT greater than 3 seconds above normal) or complications. If the patient experiences continuous vomiting and is unable to maintain oral intake, parenteral nutrition may be required.

In order to relieve nausea and also prevent vomiting, antiemetics (diphenhydramine or prochlorperazine) may be given 30 minutes before meals. However, phenothiazines have a cholestatic effect and should be avoided. The resin cholestyramine may be given only for severe pruritus.

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.

The mechanism of hepatomegaly consists of vascular swelling, inflammation (due to the various causes that are infectious in origin) and deposition of (1) non-hepatic cells or (2) increased cell contents (such due to iron in hemochromatosis or hemosiderosis and fat in fatty liver disease)

North American Indian childhood cirrhosis (NAIC) is a disease in humans that can affect Ojibway-Cree children in northwestern Quebec, Canada. The disease is due to an autosomal recessive abnormality of the "CIRH1A" gene, which codes for cirhin.

NAIC is a ribosomopathy. An R565W mutation of "CIRH1A" leads to partial impairment of cirhin interaction with NOL11.

Initial transient neonatal jaundice advances over time to biliary cirrhosis with severe liver fibrosis. Eventually, liver failure occurs, and requires liver transplantation.

Hepatomegaly is the condition of having an enlarged liver. It is a non-specific medical sign having many causes, which can broadly be broken down into infection, hepatic tumours, or metabolic disorder. Often, hepatomegaly will present as an abdominal mass. Depending on the cause, it may sometimes present along with jaundice.

Banti's syndrome (also known as Banti's disease), named for is Guido Banti., is a chronic congestive enlargement of the spleen resulting in premature destruction of the red blood cells by the spleen.

Untreated, the disease has a mortality rate upwards of 90%. Cats treated in the early stages can have a recovery rate of 80–90%. Left untreated, the cats usually die from severe malnutrition or complications from liver failure. Treatment usually involves aggressive feeding through one of several methods.

Cats can have a feeding tube inserted by a veterinarian so that the owner can feed the cat a liquid diet several times a day. They can also be force-fed through the mouth with a syringe. If the cat stops vomiting and regains its appetite, it can be fed in a food dish normally. The key is aggressive feeding so the body stops converting fat in the liver. The cat liver has a high regeneration rate and the disease will eventually reverse assuming that irreparable damage has not been done to the liver.

The best method to combat feline hepatic lipidosis is prevention and early detection. Obesity increases the chances of onset. In addition, if a cat stops eating for 1–2 days, it should be taken to a vet immediately. The longer the disease goes untreated, the higher the mortality rate.

Liver disease (also called hepatic disease) is a type of damage to or disease of the liver.

Ischemic hepatitis can be caused by a number of reasons (that lead to low blood pressure) including:

- Abnormal heart rhythm

- Heart failure

- Infection

- Profuse bleeding

- Blood clots (hepatic artery after surgery)

Several analyses have found a significantly decreased risk of coronary artery disease (CAD) in individuals with GS.

Specifically, people with mildly elevated levels of bilirubin (1.1 mg/dl to 2.7 mg/dl) were at lower risk for CAD and at lower risk for future heart disease. These researchers went on to perform a meta-analysis of data available up to 2002, and confirmed the incidence of atherosclerotic disease (hardening of the arteries) in subjects with GS had a close and inverse relationship to the serum bilirubin. This beneficial effect was attributed to bilirubin IXα which is recognized as a potent antioxidant, rather than confounding factors such as high-density lipoprotein levels.

This association was also seen in long-term data from the Framingham Heart Study. Moderately elevated levels of bilirubin in people with GS and the (TA)/(TA) genotype were associated with one-third the risk for both coronary heart disease and cardiovascular disease as compared to those with the (TA)/(TA) genotype (i.e. a normal, nonmutated gene locus).

Platelet counts and MPV are decreased in patients with Gilbert's Syndrome. The elevated levels of bilirubin and decreasing levels of MPV and CRP in Gilbert's syndrome patients may have an effect on the slowing down of the atherosclerotic process.

The enzymes that are defective in GS - UDP glucuronosyltransferase 1 family, polypeptide A1 (UGT1A1) - are also responsible for some of the liver's ability to detoxify certain drugs. For example, Gilbert's syndrome is associated with severe diarrhea and neutropenia in patients who are treated with irinotecan, which is metabolized by UGT1A1.

While paracetamol (acetaminophen) is not metabolized by UGT1A1, it is metabolized by one of the other enzymes also deficient in some people with GS. A subset of people with GS may have an increased risk of paracetamol toxicity.

In the 80 percent of the cases where there is no virus identified as the cause.

Infants with neonatal hepatitis caused by the cytomegalovirus, rubella or the hepatitis A, B, and C viruses may transmit the infection to others who come in close contact with the infant.

These infected infants should not come into contact with pregnant women because of the possibility that the woman will transmit the virus to her unborn child.

One of the reasons a cat may stop eating is separation anxiety and the emotional stress that results. Moving, gaining or losing housemates or pets, going on vacation, or prolonged boarding are all common situations that pet owners report just prior to the onset of the disease, but it may develop without these conditions existing. Obesity is known to increase the risk of hepatic lipidosis; however, there is no known "official" cause of the disease. Severe anorexia usually precedes the onset of the disease. When the cat has no energy from eating, the liver must metabolize fat deposits in the body into usable energy to sustain life. The cat liver, however, is poor at metabolizing fat, causing a buildup of fat in the cells of the liver, leading to fatty liver. At this point the disease can be diagnosed; however, it will often not be diagnosed, and many animals are euthanized due to improper or no diagnosis.

People of Northern European and Iberian ancestry are at the highest risk for A1AD. Four percent carry the PiZ allele; between 1 in 625 and 1 in 2000 are homozygous.

Another study detected a frequency of 1 in 1550 individuals and a gene frequency of 0.026. The highest prevalence of the PiZZ variant was recorded in the northern and western European countries with mean gene frequency of 0.0140.

The mechanism of ischemic hepatitis depends on the etiopathogenetic origin, be it a cardiomyopathy, cardiac tamponade, trauma, or bleeding. Usually ischemic hepatitis reveals itself after a hypotensive event with increase levels of aminotransferase, hypotension is thought to be one of the primary insults in ischemic hepatitis.

α-antitrypsin deficiency has been associated with a number of diseases:

- Cirrhosis

- COPD

- Pneumothorax

- Asthma

- Granulomatosis with polyangiitis

- Pancreatitis

- Gallstones

- Bronchiectasis

- Pelvic organ prolapse

- Primary sclerosing cholangitis

- Autoimmune hepatitis

- Emphysema, predominantly involving the lower lobes and causing bullae

- Secondary membranoproliferative glomerulonephritis

- Cancer

- Hepatocellular carcinoma (liver)

- Bladder carcinoma

- Gallbladder cancer

- Lymphoma

- Lung cancer