Research More About Hepatitis X

Do I have Hepatitis X?

• Hepatitis X: Introduction
• Hepatitis X: Diagnostic Testing to confirm diagnosis
• Home Diagnostic Testing
• Alternative diagnoses and misdiagnosis for Hepatitis X
• Treatments for Hepatitis X
• More about Hepatitis X

TopHome Diagnostic Testing

Home medical tests related to Hepatitis X:

• Home Hepatitis Tests
• Home Liver Tests

TopWrongly Diagnosed with Hepatitis X?

The list of other diseases or medical conditions that may be on the differential diagnosis list of alternative diagnoses for Hepatitis X includes:

• Hepatitis A
• Hepatitis B
• Hepatitis C
• Hepatitis D
• Hepatitis E

See the full list of 11 alternative diagnoses for Hepatitis X

TopMore about symptoms of Hepatitis X:

More information about symptoms of Hepatitis X and related conditions:

• Other diseases with similar symptoms and common misdiagnoses
• Tests to determine if these are the symptoms of Hepatitis X
• Symptoms that may be caused by complications of Hepatitis X

Top Other Possible Causes of these Symptoms

Click on any of the symptoms below to see a full list of other causes including diseases, medical conditions, toxins, drug interactions, or drug side effect causes of that symptom.

• Abdominal pain - see all causes of Abdominal pain
• Diarrhea - see all causes of Diarrhea
• Fatigue - see all causes of Fatigue
• Fever - see all causes of Fever
• Flu-like symptoms - see all causes of Flu-like symptoms
• Jaundice - see all causes of Jaundice
• Loss of appetite - see all causes of Poor appetite
• Nausea - see all causes of Nausea
• Vomiting - see all causes of Vomiting
• Yellow eyes - see all causes of Yellow eyes
• Yellow skin - see all causes of Yellow skin

Hepatitis X

Introduction: Hepatitis X

Hepatitis X: Some cases of viral hepatitis cannot be attributed to the hepatitis A, B, C, D, or E viruses. This is called non A...E hepatitis or hepatitis X. Scientists ... more about Hepatitis X.

Hepatitis X: Hepatitis infection by an unknown virus not classified as HepA/B/C/D/E. More detailed information about the symptoms, causes, and treatments of Hepatitis X is available below.

List of symptoms of Hepatitis X:

The list of signs and symptoms mentioned in various sources for Hepatitis X includes the 11 symptoms listed below:

• Flu-like symptoms
• Fever
• Fatigue
• Nausea
• Vomiting
• Loss of appetite
• Abdominal pain
• Diarrhea
• Jaundice
• Yellow eyes
• Yellow skin

Note that Hepatitis X symptoms usually refers to various symptoms known to a patient, but the phrase Hepatitis X signs may refer to those signs only noticable by a doctor.

More ways to research these symptoms: To research other symptoms use the symptom center, or to research causes of more than one symptom in combination, try our multi-symptom search.

Causes of Hepatitis X: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review the full text of medical books online, free, without registration, for more information about the causes of Hepatitis X.

Hepatomegaly: Differential Diagnosis
(In a Page: Signs and Symptoms)

Right heart failure

• Inflammatory disorders, resulting in tender hepatomegaly
  –Hepatitis (viral or drug-induced): Associated with jaundice, fever, nausea, vomiting, fatigue, diarrhea, weight loss
  –Alcoholic liver disease: Associated with liver failure and portal hypertension (e.g., caput medusae, spider angiomata, hemorrhoids, testicular atrophy, ALT is more than two times higher than AST)
• Infiltrative disorders
  –Fatty liver (NASH): Predisposing factors include middle age, obesity, female gender, diabetes, and hyperlipidemia
  –Sarcoidosis: Associated with cough, hilar lymphadenopathy; more common in blacks, women, ages 30–40
  –Hemochromatosis: Iron overload resulting in bronzed skin color, diabetes, abnormal iron panel
  –Wilson's disease: Copper excess resulting in liver failure, lenticular degeneration, and Kayser-Fleischer rings in cornea
• Neoplasms present with focal enlargement, arterial bruit and/or hepatic rub, and constitutional symptoms (e.g., fever, night sweats, weight loss)
  –Metastatic cancer is more common than primary liver cancers (colon, lung, breast)
  –Hepatocellular carcinoma is most common primary liver cancer (often due to chronic hepatitis or cirrhosis)
  –Hepatic adenoma or hepatic cysts
  –Leukemia/lymphoma

• Liver abscess
• Less common causes (“zebras”) include tricuspid regurgitation, Budd-Chiari syndrome, schistosomiasis, amyloidosis, kala-azar (visceral leishmaniasis), and HIV/AIDS

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Jaundice: Differential Diagnosis
(In a Page: Signs and Symptoms)

• Viral hepatitis
  –Fatigue, anorexia, fever, nausea, vomiting, dark urine, light-colored (acholic) loose stools, RUQ pain, hepatomegaly, and/or pruritis

• Alcoholic hepatitis
  –Associated with fever, leukocytosis, and AST:ALT ratio >2

• Nonalcoholic steatohepatitis or nonalchoholic fatty liver disease
  –Associated with obesity, diabetes, hyperlipidemia and medications

• Cholecystitis
  –RUQ pain, fever, leukocytosis
  –Female, fertile, fat, forty
  –Murphy's sign: Pain upon palpation of the
  gallbladder while taking a deep breath

• Drugs and toxins
  –Acetaminophen, alcohol, estrogens, isoniazid, chlorpromazine, erythromycin, nitrofurantoin, rifampin

• Gilbert's syndrome
  
  –Decreased conjugation of bilirubin, especially with dehydration, fasting, infection

Sepsis

Malignancy (liver, pancreas, gallbladder/common bile duct, metastatic)

• Liver infiltration
  –Amyloidosis, lymphoma, sarcoidosis, tuberculosis

Total parenteral nutrition (usually requires at least 2 weeks of therapy)

Intravascular hemolysis

• Cholangitis
  –Charcot's triad of fever, RUQ pain, and jaundice

Sickle cell disease
–Chronic hemolysis, hepatic dysfunction

• Autoimmune hepatitis
  –May mimic viral hepatitis
  –Females >> males, often 10–30 years old
  –Associated with autoimmune disease
  (e.g., RA, UC, Sjögren's syndrome, thyroiditis)

Intrahepatic cholestasis of pregnancy
–Pruritus in third trimester
–Resolves after delivery

Hereditary cholestatic disorders (e.g., Dubin-Johnson syndrome, Rotor syndrome)

Physiologic jaundice of newborn

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Hepatomegaly: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

• Inflammation
  –Most common infections: EBV; hepatitis A, B, C; CMV; TORCH
  –Less common infections: HIV, malaria, amebiasis, tuberculosis, toxocariasis, Borrelia burgdorferi
  –Drugs: Acetaminophen (commonly used in overdoses among adolescents), NSAIDs, isoniazid, sodium valproate, propothiouracil, halothane
  –Toxins: Tyrosinemia, galactosemia, vitamin A toxicity
  –Autoimmune hepatitis
  –Systemic lupus erythematosus

• Inappropriate storage
  –Glycogen storage diseases I–V
  –Lipids: Gaucher disease, Wolman disease, Niemann-Pick disease
  –Fat: Fatty acid oxidation defects, mucopolysaccharidoses
  –Metals: Wilson disease (copper), hemochromatosis (iron)
  –Abnormal proteins: α-1 antitrypsin deficiency (store abnormal protein product)
  –Peroxisomal disease: Zellweger
  –Mucopolysaccharidoses, types I–IV

• Infiltration
  –Hepatoblastoma
  –Hepatocellular carcinoma
  –Hemangioma
  –Histiocytosis
  –Extramedullary hematopoiesis
  –Chronic granulomatous disease
• Vascular congestion
  –Congestive heart failure
  –Budd-Chiari syndrome
  –Veno-occlusive disease
  –Suprahepatic web
• Biliary obstruction
  –Biliary atresia represents the most common cause of pediatric liver transplantation
  –Alagille syndrome
  –Cystic fibrosis
  –Primary sclerosing cholangitis
  –Inspissated bile syndrome
• Miscellaneous
  –Reye syndrome, bile acid synthetic disorder

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Jaundice in Infants – Direct: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

• Bile duct obstruction
  –Biliary atresia: Represents the most frequent cause for liver transplantation in the pediatric patient; prompt diagnosis is crucial, as patient outcome is better if intervention comes before 60 days of life
  –Choledochal cyst
  –Common bile duct gallstone
  –Choledochocele
  –Bile duct stricture
  –Alagille syndrome
  –Caroli disease
  –Congenital hepatic fibrosis

• Neonatal hepatitis
  –Idiopathic hepatitis: Diagnosis of exclusion that should be made only when other causes are excluded; accounts for 60% of patients with neonatal cholestasis
  –Infections: TORCH, hepatitis B, HIV, E. coli, adenovirus, enterovirus, parvovirus B16, tuberculosis, listeriosis, malaria

• Metabolic disorders
  –α-1 antitrypsin deficiency
  –Cystic fibrosis
  –Hypothyroidism
  –Neonatal iron storage disease
  –Amino acids: tyrosinemia
  –Carbohydrates: Galactosemia, fructosemia
  –Lipids: Niemann-Pick, Gaucher, Wolman, cholesterol ester storage disease
  –Mitochondropathies
  –Bile acid synthetic disorders
  –Peroxisomal: Zellweger syndrome
  –Urea cycle defects
• Toxins
  –Total parenteral nutrition
  –Drugs: Trimethaprim-sulfamethoxazole, anticonvulsants
• Miscellaneous
  –Sepsis/hypoperfusion
  –Erythrophagocytic lymphohistiocytosis
  –Extracorporeal membrane oxygenation
  –Trisomy 17, 18, 21
  –Neonatal lupus erythematosus
  –Donohue syndrome
  –Rotor syndrome
  –Dubin-Johnson syndrome
  –Byler disease (PFIC type 1)
  –Cholestasis of North-American Indians
  –Nielsen syndrome

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Jaundice in Infants – Indirect: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

• Icterus neonatorum (physiologic jaundice)
  –The most common form of indirect jaundice in infants under 14 days of age
  –Caused by increased bilirubin production with transient limited conjugation abilities
• Breast-feeding jaundice
  –Occurs in first week of life in 13% of breast-fed infants
  –Secondary to poor volume intake
• Breast-milk jaundice
  –Occurs in about 2% of breast-fed infants after day 7 of life
  –Secondary to glucuronidase in breast milk
• Hematologic: Hemolysis increases bili load
  –Rh incompatability
  –ABO incompatability
  –Glucose-6-phosphate dehydrogenase (G6PD) deficiency
  –Pyruvate kinase deficiency
  –Hereditary spherocytosis
  –Elliptocytosis
  –Thalassemia
  –Polycythemia
• Extravascular blood
  –Cephalohematoma
  –Trauma
  –Swallowed maternal blood
• Endocrinologic
  –Hypothyroidism
  –Maternal diabetes
• Sepsis
• Metabolic
  –Crigler-Najjar I
  –Crigler-Najjar II (Arias syndrome)
  –Crigler-Najjar III
• Cardiopulmonary
  –Congestive heart failure
  –Patent ductus arteriosus
  –Portal vein thrombosis
• Anatomic
  –Pyloric stenosis
  –Duodenal atresia/stenosis
  –Duodenal web
• Drugs
  –Oxytocin
  –Sulfonamides
  –Ceftriaxone
  –Chuen-Lin
• Lucey-Driscoll syndrome

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Treatments of Hepatitis X: Online Medical Books

16 MEDICAL BOOKS ONLINE! Review the full text of medical books online, free, without registration, for more information about the treatments of Hepatitis X.

Hepatomegaly: Treatment
(In a Page: Signs and Symptoms)

• Heart failure: Diuretics, inotropes, and afterload reduction
• Viral hepatitis: Supportive care and antivirals in some chronic cases
• Alcoholic liver disease: Abstinence from alcohol, steroids in severe cases, and possible transplant
• Fatty liver: Treat underlying obesity, diabetes, hyperlipidemia
• Sarcoidosis: Steroids
• Hemochromatosis: Iron removal by weekly phlebotomy for 2–3 years and/or deferoxamine chelation
• Wilson's disease: Copper chelation with D-penicillamine or trientine; may require liver transplantation
• Neoplasms: Resection and chemotherapy
• Abscess or cyst: Antimicrobials, percutaneous drainage, and/or surgical resection
• Amyloidosis: Prednisone and alkylating agents

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Jaundice: Treatment
(In a Page: Signs and Symptoms)

• Discontinue and avoid potentially hepatotoxic medications
• Supportive care for viral hepatitis
• Rehydrate/refeed for Gilbert's syndrome
• Consider steroids in fulminant alcoholic hepatitis
• Cholecystectomy or ERCP with stone removal for obstructing gallstones
• Treat underlying causes of hemolysis or other disorders
• Antibiotics for cholangitis, sepsis
• Hydroxyurea and folate for sickle cell disease, prevent crises by adequate hydration, vaccinating against diseases, and try to prevent other infections

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Hepatomegaly: Treatment
(In A Page: Pediatric Signs and Symptoms)

• Geared towards specific disease
• Cholestasis
  –Ursodeoxycholic acid
  –Supplemental fat soluble vitamins A, D, E, K
• Infections
  –Consider interferon for hepatitis B
  –Consider interferon and ribaviron for hepatitis C
• Toxins
  –Use of NTBC for tyrosinemia
• Metabolic disease
  –Metabolism consultation
  –Often requires specific restricted formulas
• Surgical repair for biliary atresia
  –Kasai portoenterostomy has better outcome if done before 60 days of age
• Mucomyst for acute acetaminophen toxicity
• Immune suppression for autoimmune hepatitis

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Jaundice in Infants – Direct: Treatment
(In A Page: Pediatric Signs and Symptoms)

• Varies by specific disorder

• General medication principles of cholestasis include
  –Promoting bile flow with ursodeoxycholic acid
  –Consider phenobarbital (increases bile excretion)
  –Fat-soluble vitamins including K, D, E
  –Vitamin A is a relative contraindication given hepatotoxicity at high levels

Consider formula with medium chain triglycerides as fat source (does not require bile acids to be absorbed)

Treat underlying disorder
–Kasai portoenterostomy for biliary atresia
–Surgical repair of choledochal cyst
–Special formulas for tyrosinemia
–Lactose free formula for galactosemia (e.g., soy based)
–Remove toxic exposures
–Treat infections
–Treat hypothyroidism

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Jaundice in Infants – Indirect: Treatment
(In A Page: Pediatric Signs and Symptoms)

• Treatment options vary based on level of bilirubin, age of presentation, and cause
  –Goal is prevent levels high enough to cause kernicterus
• Phototherapy involves the use of photon energy to change the structure of bilirubin and permit excretion without glucuronidation
  –Decisions for use are age-based
  –Considered when serum level above 14 mg/dL
• Exchange transfusion should be considered with serum levels above 25 mg/dL
• IVF or breast-feed more frequently to increase volume
  
  
  
• 
  
• Correct endocrine abnormality
• Improve perfusion if cardiac problem
• Correct anatomic abnormality
• Consider enteral binding agents
  –Cholestyramine, charcoal, calcium phosphate
• Crigler-Najjar: Phenobarbital, may need liver transplantation

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Jaundice [Icterus]: Patient counseling
(Professional Guide to Signs & Symptoms (Fifth Edition))

Encourage the patient with a hepatic disorder to decrease his protein intake sharply and increase his intake of carbohydrates. If he has obstructive jaundice, encourage a nutritious, balanced diet (avoiding high-fat foods) and frequent small meals.

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Hepatomegaly: Patient counseling
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Instruct the patient to avoid alcohol. Explain the importance of following the treatment plan to correct or control the underlying disorder as needed. Tell the patient to avoid exposure to people with infections and to maintain good personal hygiene. Explain the importance of pacing activities and having frequent rest periods.

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Jaundice: Patient counseling
(Signs & Symptoms: A 2-in-1 Reference for Nurses)

Encourage the patient with a hepatic disorder to decrease his protein intake sharply and increase his intake of carbohydrates. If he has obstructive jaundice, encourage a nutritious, balanced diet (avoiding high-fat foods) and frequent small meals. Teach the patient ways to reduce pruritus.

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Hepatomegaly: Nursing considerations
(Nursing: Interpreting Signs and Symptoms)

▪ Prepare the patient for liver enzyme, alkaline phosphatase, bilirubin, albumin, and globulin studies to evaluate liver function and for X-rays, a liver scan, celiac arteriography, a computed tomography scan, and ultrasonography to confirm hepatomegaly.

▪ Provide bed rest, relief from stress, and adequate nutrition to help protect liver cells from further damage and to allow the liver to regenerate functioning cells.

▪ Monitor and restrict dietary protein as needed.

▪ Give hepatotoxic drugs or drugs metabolized by the liver in very small doses, if at all.

TopPatient teaching

▪ Explain the underlying disorder and its treatments.

▪ Stress the importance of avoiding alcohol and people with infections.

▪ Discuss the importance of pacing activities and rest periods.

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Jaundice [Icterus]: Nursing considerations
(Nursing: Interpreting Signs and Symptoms)

▪ To decrease pruritus, frequently bathe the patient; apply an antipruritic lotion, such as calamine; and administer diphenhydramine or hydroxyzine.

▪ Prepare the patient for diagnostic tests to evaluate biliary and hepatic function, including laboratory studies (such as urine and fecal urobilinogen, serum bilirubin, liver enzyme, and cholesterol levels; prothrombin time; and a complete blood count), computed tomography, ultrasonography, cholangiography, liver biopsy, and exploratory laparotomy.

TopPatient teaching

▪ Teach the patient appropriate dietary changes.

▪ Discuss ways to reduce pruritis.

▪ Review with the patient prescribed medications and their possible adverse effects.

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Types of Liver Diseases

Alcoholic Liver Disease Alpha-1-Antitrypsin Deficiency Autoimmune Hepatitis Biliary Atresia Budd Chiari Syndrome Cancer of the Gallbladder and Bile Duct Chronic Hepatitis Choledochal cysts Cirrhosis Drug Induced Hepatitis Haemochromatosis Hepatitis A Hepatitis B

Hepatitis C Hepatitis D Hepatitis E Primary Biliary Cirrhosis Primary Sclerosing Cholangitis Liver Diseases & Pregnancy Liver Abscess Liver Adenoma Liver Cancer Tyrosinemia Wilson's Disease

Wilson's Disease

Wilson's Disease

An autosomal recessive disease of copper metabolism. The abnormal gene has been localized to chromosome 13 and is linked to enzyme esterase -D. The overall disease incidence is 1:200000. In this condition the copper excretion in the bile is reduced resulting in accumulation of copper in the liver, resulting in oxidant injury to liver cell mitochondria. The clinical evidence of liver injury is usually detected after 5 years. Deposition of copper in the extrapyramidal system of the brain can result in subtle neurological symptoms in children and frank abnormalities in adults. Clinical presentation varies from asymptomatic copper accumulation (stage-1), enlargement of liver and spleen, abnormal liver enzymes, acute liver failure or liver cirrhosis with protal hypertension (stage-2), asymptomatic copper in central nervous system(stage-3) and frank neurological symptoms (stage-4).

Diagnosis:

Typically Ceruloplasmin is low(<20mg/d1),>100mg/24 hours). False positive reports are common. The copper content of liver is the most reliable test. In wilson's disease the copper content is >250 mic.g/Gm of tissue. Another test that adds to value is to estimate the radioactive copper incorporation in ceruloplasmin, which decreased in Wilson's. In clinical terms the brown rings detected at the junction of the cornea and the iris in the superior aspect of the eye (KF rings) may be difficult to detect among Indians without a slit lamp exam. However these do not appear until mid adolescence and are not unique to Wilson's. Any adolescent with normal alkaline phosphatase and raised enzymes and bilurubin as well as those with acute liver failure with intravascular hemolysis should be strongly suspected of Wilson's disease.

Treatment:

Medical therapy is first line in treatment. Penicillamine-D and trientine dihydrochloride, zinc or tetrathiomolybdate are chelating agents used with success. Oral Zinc has also been proven to have a useful role. It is best to avoid foods rich in copper such as seafood, chocolates or nuts. Indications for liver transplant include- failure to improve either liver or neurological function, acute liver failure or cirrhosis with decompensation of function. Raising enzymes, bilurubin and prothrombin time are poor prognostic signs. Jaundice and ascites also correlated with poor prognosis. Results of liver transplantation is impressive. Complete neurological recovery can be anticipated few months after liver transplant. Early detection and treatment of homozygotes can prevent subsequent need for liver transplant.

Tyrosinemia

Tyrosinemia Type-I

An autosomal recessive disease. The incidence varies form 1:10000 to 1:800 in different geographic areas. Tyrosinemia is diagnosed by demonstrating reduced activity of a vital enzyme FAH (Fumary1 Acetoace hydrogenase) in the blood. Early neonatal screening is essential to diagnose this condition. Lethal liver failure and neurological crises can develop in affected individuals. No FAH activity is discovered in patients with acute failure and up to 20% activity is found in infants with chronic liver failure. Infants usually present with bleeding diathesis due to onset of acute liver failure. The chronic form usually presents after first year. The liver becomes enlarged, coarsely nodular and cirrhotic. At two years of age they have a very high chance of developing liver cell cancer. The neurological consequences could be fatal and include profound weakness and paralysis and respiratory paralysis and respiratory paralysis usually leads to death. Infants can also develop acute/chronic kidney failure.

Treatment is aimed at dietary modification by avoiding Tyrosine, phenylalanine and methionine. A chemical NTBC has been tried to reduce liver injury by toxic metabolites. Dietary modification offers no protection against progression of liver disease and development of cancer. Good outcomes (up to 80%) have been reported after liver transplant for both acute and chronic forms of Tyrosinemia. However complete kidney recovery may not be achieved by liver transplantation.

Liver Cancer

1. What is cancer of liver?
2. Liver Cancer Who's at Risk?
3. What are the symptoms of liver cancer?
4. Screening for hepatocellular cancer (HCC)?
5. What are the diagnosis of liver cancer?
6. Treatment of liver cancer?
7. What is advanced cancer?
8. What is recurrent cancer?
9. What are side effects of treatment?
10. How to control the pain?
11. Support for people with liver cancer.

Cancer of the Liver.
This National Cancer Institute (NCI) booklet has important information about cancer that begins in the liver. It discusses possible causes, symptoms, diagnosis, and treatment of liver cancer. It also has information to help patients cope with this disease. Information specialists at the NCI's Cancer Information Service at 1-800-4-CANCER can help people with questions about cancer and can send NCI publications.

Understanding Cancer
Cancer is a group of many related diseases. All cancers begin in cells, the body's basic unit of life. Cells make up tissues, and tissues make up the organs of the body.

Normally, cells grow and divide to form new cells as the body needs them. When cells grow old and die, new cells take their place.

Sometimes, this orderly process goes wrong. New cells form when the body does not need them, or old cells do not die when they should. These extra cells can form a mass of tissue called a growth or tumor. Tumors can be benign or malignant:

• Benign tumors are not cancer. Usually, doctors can remove them. In most cases, benign tumors do not come back after they are removed. Cells from benign tumors do not spread to tissues around them or to other parts of the body. Most important, benign tumors are rarely a threat to life.
• Malignant tumors are cancer. They are generally more serious and may be life threatening. Cancer cells can invade and damage nearby tissues and organs. Also, cancer cells can break away from a malignant tumor and enter the bloodstream or the lymphatic system. That is how cancer cells spread from the original cancer (the primary tumor) to form new tumors (secondary tumors) in other organs. The spread of cancer is called metastasis. Different types of cancer tend to spread to different parts of the body.

Most primary liver cancers begin in hepatocytes (liver cells). This type of cancer is called hepatocellular carcinoma or malignant hepatoma.

Liver Adenoma

Etiology

• The more common hepatocellular adenoma may be related to contraceptive use.

Epidemiology

• Liver cell adenoma is common in young women and may be related to the use of oral contraceptive medications.
• Bile duct adenomas are quite uncommon and may represent hamartomas or tumors due to developmental aberration.

General Description

• Hepatic adenomas are of two histological types: liver cell and Bile duct type.
• Liver cell adenomas are usually large when detected (25 - 30 centimeters in diameter), while bile duct adenomas are usually small, up to one centimeter in diameter.
• Liver cell adenomas can occur anywhere in the liver tissue, but are quite often seen under the capsule.
• Liver cell adenomas are usually pale to yellow in colour and may be bile stained.
• They are usually well demarcated, but the capsule may not be clearly obvious

Microscopic Appearance

• Histologically, a hepatocellular adenoma is composed of normal looking hepatocytes arranged in sheets and cords.
• Significant evidence of bile deposition may be seen within and between the cells
• Typical portal tracts and central veins are not seen, since the cells are not arranged in a typical lobular pattern.
• Bile duct adenomas are composed of slit - like to circular spaces lined by epithelium that resembles noram bile duct epithelium.
• However, significant vascular supply is a prominent feature.

Clinical features

• Clinically, both liver cell adenimas and bile cell adenomas are noncancerous lesions with little clinical significance.
• However, liver cell adenomas can become large sized during pregnancy, presumably as a result of estrogen stimulation
• Under these circumstances liver cell adenomas can rupture resulting in acute bleeding and peritonitis.

Liver cell adenomas may reduce in size in young women once they stop oral contraceptive ingestion.

Liver Abscess

1. What is liver abscess?
2. What is pathophysiology?
3. What are the causes of liver abscess?
4. What are complications of liver abscess?

Liver Abscess.

Bacterial abscess of the liver is relatively rare. It has been described since the time of Hippocrates (400 BC), with the first published review by Bright appearing in 1936. In 1938, Ochsner’s classical review heralded surgical drainage as the definitive therapy; however, despite the more aggressive approach to treatment, the rate of mortality has remained at 60-80%.

The development of new radiologic techniques, the improvement in microbiologic identification, and the advancement of drainage techniques have decreased mortality rates to 5-30%; yet, the incidence has remained relatively unchanged. Untreated, this infection remains uniformly fatal.

Liver Diseases & Pregnancy

During pregnancy, there are significant normal physiologic changes in liver function studies. These include:

1. A decrease in both the total protein as well albumin.
2. An elevation of the liver dependent clotting factors such as fibrinogen.
3. In addition, there are elevations in the transport proteins produced in the liver such as
ceruloplasmin, transferrin, and sex steroid binding globulin.
4. The alkaline phosphatase will be elevated 2 - 4 times normal.
5. Of note is the fact that the transaminase levels should remain normal during pregnancy. This
has tremendous importance when evaluating the possibility of liver disease in pregnancy.
6. In addition, the bilirubin should stay normal.

However, there are also certain liver conditions that may cause complications in pregnancy. These include:

Hepatitis

The most common liver disease encountered during pregnancy is that of hepatitis. This is no different than in the non - pregnant individual. In some areas around the world such as India, it remains the most common cause of maternal death during pregnancy. It has also been appreciated that the finding of a mother who is a carrier for hepatitis places her foetus at risk in later life of developing both chronic hepatitis and cancer of the liver. It has become accepted clinical practice to screen all patients with a hepatitis surface antigen as a part of their regular parental laboratory work. The diagnosis, evaluation and treatment of hepatitis during pregnancy is no different than in non - pregnant individual.

Cholestatis of Pregnancy

Cholestatis of pregnancy is a condition of unknown cause. It usually arises late in the third trimester of pregnancy. The primary symptom associated with it is extreme itchiness. There may also be mild jaundice (yellowing of the skin due to excess bilirubin). The laboratory evaluation in such patients reveals tremendous increase in alkaline phosphatase to 7-10 times above normal. If the serum bile acids were assayed, it would be found that they are between 10 and 100 times normal. It is this extreme evaluation of bile acids, which is felt to cause the generalized purities. Liver biopsies which have been performed in such patients show simple biliary status without disruption of the hepatocellular architecture.

These changes are completely reversible and return to normal after the pregnancy ends. Cholestatis of pregnancy has no adverse effect on pregnancy and the cure of the problem is the delivery of the foetus, attempts at using ion exchange resins such as cholestyramine to try to lower the serum bile acids have been uniformly unsuccessful due to the tremendous elevation in these bile acids.

Acute Fatty Liver of Pregnancy

A more serious liver disease encountered during pregnancy is that of acute fatty liver. This too, is a condition of unknown cause. It is an extremely rare condition affecting less than 1 in 10,000 patients.

The symptoms are that of a rather sudden onset in the last four weeks of pregnancy of rapidly deepening jaundice, somnolence, and in short order, coma, bleeding dyathosis, and hepatorenal failure. The usual time course form onset of symptoms to hepatorenal failure is approximately 2 weeks. The maternal mortality rate from acute fatty liver of pregnancy approaches 30%. Some similarities to this condition with Reye's syndrome have been suggested. However, there is enough variation in the symptoms and the pathology that such an association is suspect.

The diagnosis of acute fatty liver of pregnancy is usually made upon liver biopsy. The biopsy shows an intense infiltration of all the hepatocytes by fat with a marked disruption of the hepatic architecture. The liver transaminase will be markedly elevated. The alkaline phosphatase will be slightly elevated. The bilirubin is significantly elevated.

It has been recognized as of late that the rapid delivery of the baby will improve the maternal mortality. It has been this understanding which has lead to the improvement in the survival rates from such a condition. There is one case in the literature where, despite the delivery of the baby, it was felt that the disease process had not been reversed and the patient underwent successful liver transplant. There are several cases reported where patients who have survived acute fatty liver of pregnancy have subsequently had an uneventful pregnancy. It has been suggested that there is no increased risk of recurrence. However, the number of such patients is small and it seems premature to advise the margin of safety in subsequent pregnancies.

Primary Sclerosing Cholangitis

Primary Sclerosing Cholangitis (PSC)

PSC mainly affects males and is characterized by chronic inflammation of the bile ducts resulting in stricture formation and obliteration of the duct lumen. In 70% of the patients it is associated with inflammatory bowel disease (IBD).

Presentation and diagnosis:

Jaundice and bacterial cholangitis is a common mode of presentation. Presence of cholangitis indicates imaging of the biliary tree for locating dominant stricture that may require dilatation. Presence of recurrent episodes of cholangitis is in itself an indicator to refer the patient for lliver transplantation even if the synthetic function of the liver is normal. Pruritus is a common presentation. This may be present with normal bilurubin level and in the absence of dominant stricture. Hepatic osteodystrophy, a condition resulting in gross reduction in bone mineral content is common and may lead to fracture in long bone or the spine. 70% of the patients have IBD and colonoscopy is indicated to rule out colonic dysplasia or cancer. Cholangiocarcinoma may complicate PSC and usually results in sudden increase in jaundice, weight loss and serum alkaline phosphatase level. The diagnosis of PSC is primarily by liver biopsy.

Prognosis:

The Mayo clinic model uses age, histology staging, bilurubin level and absence of splenomegaly to prgnosticate outcome. The King's college model uses age, histological grade, hepatomegaly, splenomegaly and serum alkaline phosphatase level. However these are not very useful in clinical situations. Other factors such as nutritional staus, cholangitis and risk of cholangio carcinoma dictate the outcome.

Treatment:

Identification of dominant strictures in the biliary tree needs dilatation and stent placement. Episodes of recurrent cholangitis (biliary tree infection) requires suppressive dose of antibiotics. H1 receptor blockade may alleviate pruritus (itching). Majority of the patients will require liver replacement fairly early. Unlike other chronic liver diseases the indication for listing for lliver transplantation is for recurrent cholangitis, progressive jaundice and nutritional debility than poor synthetic function of the liver.

Primary Biliary Cirrhosis

Primary Biliary Cirrhosis (PBC)

World wide incidence is 4-5 / million (middle age women).
Suspected genetic component in causation (6 fold increase in frequency of DRW8 tissue type among PBC patients).
Other autoimmune diseases such as arthritis, thyroiditis, keratoconjunctivitis, kidney and skin disease occurs with PBC.
Patients present with fatigue and itching and progresses over 10-15 years, presenting with progressive jaundice.

Diagnosis:

Serum alkaline phosphatase is raised.
Serum IgM titer and Cholesterol are raised.
95% have raised Anti mitochondrial antibody titer.
Liver biopsy and histo pathology study will show chronic inflammation of bile ductules around portal tract, granulomatous destruction of bile ducts, liver cell death in early stages and later fibrosis and disappearing bile ducts lead to frank cirrhosis.

Treatment:

Drugs such as Azathioprine, Steroids, Chlorambucil and Cyclosporin can produce biochemical improvement at the cost of bad side effects.
Drugs such as UDCA (Ursodeoxycholic acid) and methotrexate are more promising as they produce biochemical and clinical improvement of symptoms.
No known medical therapy can increase patient survival.
Liver transplantation has the best chance at cure (80% survival at 1 year), all PBC patients with bilurubin > 5 mg/d1 should enroll for liver transplantation.

Prognosis:

Progression of disease stretches over 10 to 15 years.
Older age group, enlarged liver and level of bilurubin correlates with shorter life span
Serum bilurubin level > 2mg/d1 indicates a mean survival of 4 years.
Small percentage can develop recurrent PBC after liver transplantation.

Hepatitis E

1. What is Hepatitis E?
2. What are clinical features of Hepatitis E?
3. What are Epidemiologic features of Hepatitis E?
4. Prevention and control measures of Hepatitis D.

Hepatitis E.

Hepatitis E virus (HEV), the major etiologic agent of enterically transmitted non-A, non-B hepatitis worldwide, is a spherical, non-enveloped, single stranded RNA virus that is approximately 32 to 34 nm in diameter. Based on similar physicochemical and biologic properties, HEV has been provisionally classified in the Caliciviridae family; however, the organization of the HEV genome is substantially different from that of other caliciviruses and HEV may eventually be classified in a separate family.
Hepatitis E - Clinical Features.

Incubation period
Average 40 days
Range 15-60 days

Case-fatality rate
Overall, 1%-3%
Pregnant women, 15%-25%

Illness severity
Increased with age

Chronic sequelae
None identified

Hepatitis D

1. What is Hepatitis D?
2. How is Hepatitis D transmitted?
3. What are clinical features of Hepatitis D?
4. Prevention of Hepatitis D.

Hepatitis D.
HDV is a defective single-stranded RNA virus that requires the helper function of HBV to replicate. HDV requires HBV for synthesis of envelope protein composed of HBsAg, which is used to encapsulate the HDV genome.

Hepatitis D Virus Modes of Transmission.

• Percutanous exposures
  
  • injecting drug use
• Permucosal
  
  • exposures sex contact

Notes:
The modes of HDV transmission are similar to those for HBV, with percutaneous exposures the most efficient. Sexual transmission of HDV is less efficient than for HBV. Perinatal HDV transmission is rare.

Hepatitis C

1. What is Hepatitis C?
2. What is natural history of Hepatitis C?
3. What are clinical features of infection?
4. How is Hepatitis C transmitted?
5. How is Hepatitis C diagnosed?
6. What is the most appropriate approach to diagnose & monitor patients?
7. Treatment & Prevention of Hepatitis C.
8. What is the most effective therapy for Hepatitis C?
9. Which patients with Hepatitis C should be treated?
10. What are the most important areas for future research?

Hepatitis C.
Hepatitis C is a viral infection of the liver which had been referred to as parenterally transmitted "non A, non B hepatitis" until identification of the causative agent in 1989. The discovery and characterization of the hepatitis C virus (HCV) led to the understanding of its primary role in post-transfusion hepatitis and its tendency to induce persistent infection.

HCV is a major cause of acute hepatitis and chronic liver disease, including cirrhosis and liver cancer. Globally, an estimated 170 million persons are chronically infected with HCV and 3 to 4 million persons are newly infected each year. HCV is spread primarily by direct contact with human blood. The major causes of HCV infection worldwide are use of unscreened blood transfusions, and re-use of needles and syringes that have not been adequately sterilized.

No vaccine is currently available to prevent hepatitis C and treatment for chronic hepatitis C is too costly for most persons in developing countries to afford. Thus, from a global perspective, the greatest impact on hepatitis C disease burden will likely be achieved by focusing efforts on reducing the risk of HCV transmission from nosocomial exposures (e.g. blood transfusions, unsafe injection practices) and high-risk behaviours (e.g. injection drug use).

Hepatitis B

1. What is Hepatitis B?
2. History of Hepatitis B virus?
3. Higher Risk Groups.
4. How is Hepatitis B diagnosed?
5. What are signs & symptoms of Hepatitis B?
6. What are Clinical Types?
7. New therapy of Hepatitis B.
8. Hepatitis B Carrier Fact Sheet
9. There are simple ways that hepatitis B carriers can stay healthy.

Hepatitis B.

The disease known as hepatitis B is caused by the infectious Hepatitis B virus (HBV). HBV alone is estimated to have infected 400 million people throughout the globe, making HBV one of the most common human pathogens. Hepatocellular carcinomas (HCC), one of the most common cancers afflicting humans, is primarily caused by chronic HBV infection.. In the last few decades, the correlation between HBV and the development of HCC has been well established. However, the mechanism by which HBV transforms hepatocytes remains elusive. Before HBV can transform a cell, the virus must first infect it. However, the mechanism through which HBV enters hepatocytes has not been resolved despite further understanding of the viral proteins involved. Vaccines are available against HBV, but they may not be 100% effective against all variants of HBV. Furthermore, there is no cure for individuals already infected. Much more research is needed before we fully understand and control the spread of this infectious agent.

The following pages attempt to provide accurate and comprehensible information regarding the various aspects of the hepatitis B virus. Granted, some parts of this site require some scientific background to fully comprehend (i.e. the structural and molecular biology pages), but I have also included a question and answer page for those who feel some information needs clarification. May you find the information you are looking for within.

Hepatitis A

1. What is viral hepatitis A?
2. What are the signs and symptoms of hepatitis A?
3. How is Hepatitis A diagnosed?
4. How can I protect myself?
5. Who can get Hepatitis A?
6. How is Hepatitis A transmitted?
7. What products are available to prevent Hepatitis A infection?
8. When are person protected after receiving Hepatitis A vaccine?
9. Who should receive protection against Hepatitis A before travel?
10. Is immune globulin safe?

Viral Hepatitis A.

Hepatitis (HEP-ah-TY-tis) makes your liver swell and stops it from working right. You need a healthy liver. The liver does many things to keep you alive. The liver fights infections and stops bleeding. It removes drugs and other poisons from your blood. The liver also stores energy for when you need it.

What are the signs and symptoms of hepatitis A?.

Persons with hepatitis A virus infection may not have any signs or symptoms of the disease. Older persons are more likely to have symptoms than children. If symptoms are present, they usually occur abruptly and may include fever, tiredness, loss of appetite, nausea, abdominal discomfort, dark urine, and jaundice (yellowing of the skin and eyes). Symptoms usually last less than 2 months; a few persons are ill for as long as 6 months. The average incubation period for hepatitis A is 28 days (range: 15–50 days). In less than 2% severe liver failure may lead to death unless an emergency liver transplant is done.

Hepatitis A can make you feel like you have the flu.
You might

1. feel tired
2. feel sick to your stomach
3. have a fever
4. not want to eat
5. have stomach pain
6. have diarrhea

Some people have

1. dark yellow urine
2. light-colored stools
3. yellowish eyes and skin

Some people don't have any symptoms. If you have symptoms, or think you might have hepatitis A, go to a doctor. The doctor will test your blood.

Haemochromatosis

Haemochromatosis

Haemochromatosis (HC) also called the 'bronze diabetes' is a disorder in iron metabolism. Iron is an element essential for maintaining good health, particularly for synthesizing haemoglobin, a protein complex present in red blood cells, which carries oxygen. While lack of iron can cause anaemia, too much of it can cause excessive buildup in tissues resulting in damage and disease. In haemochromatosis there is excessive absorption of iron resulting in primary iron overload. This is primarily an inherited disorder. Deposition of body iron may also be caused by excessive destruction of abnormal red cells(eg. Thalasemia major and haemolytic anaemia) and this condition is called secondary haemochromatosis. Primary HC is caused by mutation of the HFE gene which in turn results in excessive iron absorption from the diet. This mutation is known as C282Y. Usually one needs to inherit two sets of the defective gene from each parent to manifest the disease. It is more common amongst the white race where 1 out of 300-400 people are affected. Commonly men in the age group of 30-60 years manifest the symptoms in a slow onset, though children may be affected by a rapid onset of the disease.

Symptoms are usually mild and include fatigue, lethargy and joint pain. Impotence in men and loss of menstruation in women are some of the important early signs.

Multi system organ damage: Liver is usually the site of maximum iron deposition. Liver damage leads to scarring and cirrhosis. Symptoms include jaundice, bleeding, coma, abdominal pain with swelling of the ankles and the abdomen. Excess iron deposit I the heart leads to heart failure and rhythm disturbances. Half the patients develop diabetes due to damage of the pancreas. Rarely thyroid gland dysfunction and neurological disease may manifest. The diagnosis is by the spectrum manifested clinically along with raised serum iron and serum ferritin levels and by liver biopsy.

Treatment: Venesection is a traditional therapy where frequent blood letting is done to reduce the total body iron stores over months. Medicines that chelate iron may also be used. Those with established liver cirrhosis need liver transplantation.

Haemochromatosis

Haemochromatosis

Haemochromatosis (HC) also called the 'bronze diabetes' is a disorder in iron metabolism. Iron is an element essential for maintaining good health, particularly for synthesizing haemoglobin, a protein complex present in red blood cells, which carries oxygen. While lack of iron can cause anaemia, too much of it can cause excessive buildup in tissues resulting in damage and disease. In haemochromatosis there is excessive absorption of iron resulting in primary iron overload. This is primarily an inherited disorder. Deposition of body iron may also be caused by excessive destruction of abnormal red cells(eg. Thalasemia major and haemolytic anaemia) and this condition is called secondary haemochromatosis. Primary HC is caused by mutation of the HFE gene which in turn results in excessive iron absorption from the diet. This mutation is known as C282Y. Usually one needs to inherit two sets of the defective gene from each parent to manifest the disease. It is more common amongst the white race where 1 out of 300-400 people are affected. Commonly men in the age group of 30-60 years manifest the symptoms in a slow onset, though children may be affected by a rapid onset of the disease.

Symptoms are usually mild and include fatigue, lethargy and joint pain. Impotence in men and loss of menstruation in women are some of the important early signs.

Multi system organ damage: Liver is usually the site of maximum iron deposition. Liver damage leads to scarring and cirrhosis. Symptoms include jaundice, bleeding, coma, abdominal pain with swelling of the ankles and the abdomen. Excess iron deposit I the heart leads to heart failure and rhythm disturbances. Half the patients develop diabetes due to damage of the pancreas. Rarely thyroid gland dysfunction and neurological disease may manifest. The diagnosis is by the spectrum manifested clinically along with raised serum iron and serum ferritin levels and by liver biopsy.

Treatment: Venesection is a traditional therapy where frequent blood letting is done to reduce the total body iron stores over months. Medicines that chelate iron may also be used. Those with established liver cirrhosis need liver transplantation.

Drug Induced Hepatitis

1. What is Drug Induced Hepatitis?
2. What are the symptoms of Drug Induced Hepatitis?
3. How is Drug Induced Hepatitis diagnosed?
4. What is the treatment of Drug Induced Hepatitis?
5. What are causes & risks of Drug Induced Hepatitis?
6. Prevention of Drug Induced Hepatitis?

Drug Induced Hepatitis.
Hepatitis is the inflammation of the liver, resulting in liver cell damage and destruction. Drug-induced hepatitis is rare and is caused by toxic exposure to certain medications, vitamins, herbal remedies, or food supplements. Usually, the toxicity occurs after taking the causative agent for several months, or from an overdose of a medication such as acetaminophen. Usually, the agent is discontinued once hepatitis is suspected and is rarely restarted unless it is absolutely essential for treatment.

Cirrhosis

1. What is cirrhosis of liver?
2. What are the causes of cirrhosis?
3. What are the symptoms of cirrhosis?
4. What are the complications of cirrhosis?
5. How is cirrhosis diagnosed?
6. Treatment of cirrhosis of liver?
7. What is impact of cirrhosis?
8. How are the complications of cirrhosis treated?
9. What are the major causes of cirrhosis?
10. What are the symptoms of cirrhosis?

Cirrhosis of the Liver.

The liver, the largest organ in the body, is essential in keeping the body functioning properly. It removes or neutralizes poisons from the blood, produces immune agents to control infection, and removes germs and bacteria from the blood. It makes proteins that regulate blood clotting and produces bile to help absorb fats and fat-soluble vitamins. You cannot live without a functioning liver.

In cirrhosis of the liver, scar tissue replaces normal, healthy tissue, blocking the flow of blood through the organ and preventing it from working as it should. Cirrhosis is the eighth leading cause of death by disease, killing about 25,000 people each year. Also, the cost of cirrhosis in terms of human suffering, hospital costs, and lost productivity is high.

Causes.

Cirrhosis has many causes. In the United States, chronic alcoholism and hepatitis C are the most common causes.

Alcoholic liver disease. To many people, cirrhosis of the liver is synonymous with chronic alcoholism, but in fact, alcoholism is only one of the causes. Alcoholic cirrhosis usually develops after more than a decade of heavy drinking. The amount of alcohol that can injure the liver varies greatly from person to person. In women, as few as two to three drinks per day have been linked with cirrhosis and in men, as few as three to four drinks per day. Alcohol seems to injure the liver by blocking the normal metabolism of protein, fats, and carbohydrates.

Chronic hepatitis C. The hepatitis C virus ranks with alcohol as the major cause of chronic liver disease and cirrhosis in the United States. Infection with this virus causes inflammation of and low grade damage to the liver that over several decades can lead to cirrhosis.

Chronic hepatitis B and D. The hepatitis B virus is probably the most common cause of cirrhosis worldwide, but in the United States and Western world it is less common. Hepatitis B, like hepatitis C, causes liver inflammation and injury that over several decades can lead to cirrhosis. The hepatitis D virus is another virus that infects the liver, but only in people who already have hepatitis B.

Autoimmune hepatitis. This type of hepatitis is caused by a problem with the immune system.

Inherited diseases. Alpha-1 antitrypsin deficiency, haemochromatosis, Wilson's disease, galactosemia, and glycogen storage diseases are among the inherited diseases that interfere with the way the liver produces, processes, and stores enzymes, proteins, metals, and other substances the body needs to function properly.

Nonalcoholic steatohepatitis (NASH). In NASH, fat builds up in the liver and eventually causes scar tissue. This type of hepatitis appears to be associated with diabetes, protein malnutrition, obesity, coronary artery disease, and corticosteroid treatment.

Blocked bile ducts. When the ducts that carry bile out of the liver are blocked, bile backs up and damages liver tissue. In babies, blocked bile ducts are most commonly caused by biliary atresia, a disease in which the bile ducts are absent or injured. In adults, the most common cause is primary biliary cirrhosis, a disease in which the ducts become inflamed, blocked, and scarred. Secondary biliary cirrhosis can happen after gallbladder surgery, if the ducts are inadvertently tied off or injured.

Drugs, toxins, and infections. Severe reactions to prescription drugs, prolonged exposure to environmental toxins, the parasitic infection schistosomiasis, and repeated bouts of heart failure with liver congestion can each lead to cirrhosis.