Symptoms which can return over the following month include:

- Flu-like symptoms

- Fatigue

- Fever

- Abdominal pain

- Strong headaches similar to migraines

- Nausea

- Vomiting

- Diarrhea

- Lack of concentration

- Appetite loss

- Depression

- Jaundice, a yellowing of the skin or whites of the eyes

- Sharp pains in the right-upper quadrant of the abdomen

- Weight loss

The primary symptom is yellowish discoloration of the white part of the eyes and skin in a newborn baby. Other symptoms may include excess sleepiness or poor feeding.

A bilirubin level more than 34 μmol/l (2 mg/dL) may be visible. For the feet to be affected level generally must be over 255 μmol/l (15 mg/dL).

The main sign of jaundice is a yellowish discoloration of the white area of the eye and the skin. Urine is dark in colour.

Slight increases in serum bilirubin are best detected by examining the sclerae, which have a particular affinity for bilirubin due to their high elastin content. The presence of scleral icterus indicates a serum bilirubin of at least 3 mg/dL.

The conjunctiva of the eye are one of the first tissues to change color as bilirubin levels rise in jaundice. This is sometimes referred to as "scleral icterus". However, the sclera themselves are not "icteric" (stained with bile pigment) but rather the conjunctival membranes that overlie them. The yellowing of the "white of the eye" is thus more properly termed "conjunctival icterus". The term "icterus" itself is sometimes incorrectly used to refer to jaundice that is noted in the sclera of the eyes; however, its more common and more correct meaning is entirely synonymous with jaundice.

Hyperbilirubinemia, more precisely hyperbilirubinemia due to the unconjugated fraction, may cause bilirubin to accumulate in the gray matter of the central nervous system, potentially causing irreversible neurological damage leading to a condition known as kernicterus. Depending on the level of exposure, the effects range from clinically unnoticeable to severe brain damage and even death. Newborns are especially vulnerable to hyperbilirubinemia-induced neurological damage and therefore must be carefully monitored for alterations in their serum bilirubin levels.

Neonatal jaundice is a yellowish discoloration of the white part of the eyes and skin in a newborn baby due to high bilirubin levels. Other symptoms may include excess sleepiness or poor feeding. Complications may include seizures, cerebral palsy, or kernicterus.

In many cases there is no specific underlying disorder (physiologic). In other cases it results from red blood cell breakdown, liver disease, infection, hypothyroidism, or metabolic disorders (pathologic). A bilirubin level more than 34 μmol/l (2 mg/dL) may be visible. Concerns, in otherwise healthy babies, occur when levels are greater than 308 μmol/L (18 mg/dL), jaundice is noticed in the first day of life, there is a rapid rise in levels, jaundice lasts more than two weeks, or the baby appears unwell. In those with concerning findings further investigations to determine the underlying cause are recommended.

The need for treatment depends on bilirubin levels, the age of the child, and the underlying cause. Treatments may include more frequent feeding, phototherapy, or exchange transfusions. In those who are born early more aggressive treatment tends to be required. Physiologic jaundice generally lasts less than seven days. The condition affecting over half of babies in the first week of life. Of babies that are born early about 80% are affected.

Most women with this condition present in third trimester with itching without a rash. Typically, the itching is localized to the palms of the hands and soles of the feet but can be anywhere on the body.

Hallmarks of ICP include the following symptoms:

Most common:

- Itching, in particular but not limited to that of the palms of the hands and soles of the feet, without presence of a rash

- Itching that increases in the evening

- Itching that does not respond favorably to anti-histamines or other anti-itch remedies

- Often, elevated LFT results as well as serum bile acid counts

Less common:

- Darker urine

- Lighter stools

- Increased clotting time (due to possibly associated vitamin K deficiency)

- Fatigue

- Increased nausea

- Decrease in appetite

- Jaundice

- Upper right quadrant pain

It is important to note that not all ICP sufferers have all of the above symptoms. For example, Jaundice only occurs in relatively small subset of cases, and in some cases abnormal lab results were not seen until 15 weeks or more after the onset of symptoms.

Hepatitis X often goes undiagnosed by doctors due to the difficulty in detecting the virus, which can only be detected with a double-blood test. These tests are often painful and are not usually administered by doctors. Usually by the time symptoms reveal themselves it is too late to stop the virus which terminates with sterility in the patient.

Symptoms having to do with hepatomegaly can include several, among them the individual may experience some weight loss, poor appetite and lethargy (jaundice and bruising may also be present)

Intrahepatic cholestasis of pregnancy (ICP), also known as obstetric cholestasis, cholestasis of pregnancy, jaundice of pregnancy, and prurigo gravidarum, is a medical condition in which cholestasis occurs during pregnancy. It typically presents with troublesome itching and can lead to complications for both mother and fetus.

Pruritus (itching) has long been considered to be a common symptom of pregnancy. The vast majority of times, itching is a minor annoyance caused by changes to the skin, especially that of the abdomen. However, there are instances when itching is a symptom of ICP. This is usually most intense on the palms of the hands, and the soles of the feet, but can be widespread.

ICP occurs most commonly in the third trimester, but can begin at any time during the pregnancy.

Acute fatty liver of pregnancy (or hepatic lipidosis of pregnancy) usually manifests in the third trimester of pregnancy, but may occur any time in the second half of pregnancy, or in the puerperium, the period immediately after delivery. On average, the disease presents during the 35th or 36th week of pregnancy. The usual symptoms in the mother are non-specific including nausea, vomiting, anorexia (or lack of desire to eat) and abdominal pain; excessive thirst may be the earliest symptom without overlap with otherwise considered normal pregnancy symptoms; however, jaundice and fever may occur in as many as 70% of patients.

In patients with more severe disease, pre-eclampsia may occur, which involves elevation of blood pressure and accumulation of fluid (termed oedema). This may progress to involvement of additional systems, including acute renal failure, hepatic encephalopathy, and pancreatitis. There have also been reports of diabetes insipidus complicating this condition.

Many laboratory abnormalities are seen in acute fatty liver of pregnancy. Liver enzymes are elevated, with the AST and ALT enzymes ranging from minimal elevation to 1000 IU/L, but usually staying in the 300-500 range. Bilirubin is almost universally elevated. Alkaline phosphatase is often elevated in pregnancy due to production from the placenta, but may be additionally elevated. Other abnormalities may include an elevated white blood cell count, hypoglycemia, elevated coagulation parameters, including the international normalized ratio, and decreased fibrinogen. Frank disseminated intravascular coagulation, or DIC, may occur in as many as 70% of people.

Abdominal ultrasound may show fat deposition in the liver, but, as the hallmark of this condition is microvesicular steatosis (see pathology below), this is not seen on ultrasound. Rarely, the condition can be complicated by rupture or necrosis of the liver, which may be identified by ultrasound.

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.

Gilbert's syndrome produces an elevated level of unconjugated bilirubin in the bloodstream, but normally has no serious consequences. Mild jaundice may appear under conditions of exertion, stress, fasting, and infections, but the condition is otherwise usually asymptomatic. Severe cases are seen by yellowing of the skin tone and yellowing of the sclera in the eye.

GS has been reported to possibly contribute to an accelerated onset of neonatal jaundice, especially in the presence of increased red blood cell destruction due to diseases such as G6PD deficiency. This situation can be especially dangerous if not quickly treated, as the high bilirubin causes irreversible neurological disability in the form of kernicterus.

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.

Enlargement of spleen, ascites, jaundice, and the result of destruction of various blood cells by spleen – anemia, leukopenia, thrombocytopenia, gastrointestinal bleeding – may constitute the presenting symptoms.

Gilbert's syndrome (GS) is a mild liver disorder in which the liver does not properly process bilirubin. Many people never have symptoms. Occasionally a slight yellowish color of the skin or whites of the eyes may occur. Other possible symptoms include feeling tired, weakness, and abdominal pain.

Gilbert's syndrome is due to a mutation in the UGT1A1 gene which results in decreased activity of the bilirubin uridine diphosphate glucuronosyltransferase enzyme. It is typically inherited in an autosomal recessive pattern and occasionally in an autosomal dominant pattern depending on the type of mutation. Episodes of jaundice may be triggered by stress such as exercise, menstruation, or not eating. Diagnosis is based on higher levels of unconjugated bilirubin in the blood without either signs of other liver problems or red blood cell breakdown.

Typically no treatment is needed. If jaundice is significant phenobarbital may be used. Gilbert's syndrome affects about 5% of people in the United States. Males are more often diagnosed than females. It is often not noticed until late childhood to early adulthood. The condition was first described in 1901 by Augustin Nicolas Gilbert.

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.

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.

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.

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

Feline hepatic lipidosis, also known as feline fatty liver syndrome, is one of the most common forms of liver disease of cats. The disease officially has no known cause, though obesity is known to increase the risk. The disease begins when the cat stops eating from a loss of appetite, forcing the liver to convert body fat into usable energy. If this process continues for too long, fat builds up in the cells of the liver, and the disease has officially onset. Prognosis varies depending on the stage of the disease, with both a high recovery and mortality rate at different stages. The disease is reversible through intense feeding. Treatment may involve the insertion of a temporary feeding tube to ensure adequate caloric intake for cats that have stopped eating as a result of this disease.

Various systems are affected.

- CNS abnormalities – microcephaly, mental retardation, spasticity, epilepsy, periventricular calcification

- Eye – choroidoretinitis and optic atrophy

- Ear – sensorineural deafness

- Liver – hepatosplenomegaly and jaundice due to hepatitis

- Lung – pneumonitis (interstitial pneumonitis)

- Heart – myocarditis

- Thrombocytopenic purpura, haemolytic anaemia

- Late sequelae in individuals asymptomatic at birth – hearing defects and reduced intelligence

Neonatal hepatitis is a form of hepatitis that affects the fetuses and neonates.

People who develop ischemic hepatitis may have weakness, fatigue, mental confusion, and low urine production (oliguria). A small percentage of affected people may develop hepatic coma. Jaundice can occur, but is rare and transient, as is actual loss of function of the liver.

Symptoms of alpha-1 antitrypsin deficiency include shortness of breath, wheezing, rhonchi, and rales. The patient's symptoms may resemble recurrent respiratory infections or asthma that does not respond to treatment. Individuals with A1AD may develop emphysema during their thirties or forties even without a history of significant smoking, though smoking greatly increases the risk for emphysema. A1AD causes impaired liver function in some patients and may lead to cirrhosis and liver failure (15%).

In newborns, alpha-1 antitrypsin deficiency has indicators that include early onset jaundice followed by prolonged jaundice. It is a leading indication for liver transplantation in newborns.

Initially, the symptoms of biliary atresia are indistinguishable from those of neonatal jaundice, a usually harmless condition commonly seen in infants. Distinctive symptoms of biliary atresia are usually evident between one and six weeks after birth. Infants and children with biliary atresia develop progressive cholestasis, a condition in which bile is unable to leave the liver and builds up inside of it. When the liver is unable to excrete bilirubin through the bile ducts in the form of bile, bilirubin begins to accumulate in the blood, causing symptoms. These symptoms include yellowing of the skin, itchiness, poor absorption of nutrients (causing delays in growth), pale stools, dark urine, and a swollen abdomen. Eventually, cirrhosis with portal hypertension will develop. If left untreated, biliary atresia can lead to liver failure. Unlike other forms of jaundice, however, biliary-atresia-related cholestasis mostly does not result in kernicterus, a form of brain damage resulting from liver dysfunction. This is because in biliary atresia, the liver, although diseased, is still able to conjugate bilirubin, and conjugated bilirubin is unable to cross the blood–brain barrier.