Hepatitis

Hepatitis is inflammation and damage of the liver tissue by various etiological agents, including both infekctious and non-infectious causes. The most common infectious agents include viruses – viral hepatitis, less often bacteria (eg. leptospira). Non-infectious causes include toxins, drug abuse, or for exapmle autoimmune diseases. The cell damage is a result of either a direct cytotoxic effect (toxin-mediated necrosis) or the body's response to the harmful agents (viral hepatitis). The clinical picture is very diverse and includes an asymptomatic course, nausea, abdominal pain, jaundice and liver failure, depending on the extent of the ongoing necrosis and the liver tissue infiltration by inflammatory cells.

Types
Hepatitis can be classified according to several different criteria.
 * According to the clinical course, we divide it into
 * acute (if it lasts less than 6 months),
 * chronic (if it does not subside after 6 months);
 * according to histological criteria (the extent of the ongoing fibrotic changes and the reconstruction of the lobar architecture of the liver tissue)
 * according to the cause into
 * infectious,
 * toxic,
 * autoimmune,
 * hereditary diseases associated with hepatitis.

Infectious hepatitis
Infectious hepatitis is caused by either viruses, which can be further divided into hepatotropic (hepatitis A-E virus) and nonhepatototropic, or into RNA and DNA viruses, or by bacteria and fungi.
 * Viral agents include:
 * RNA viruses, the most common hepatotoropic viruses are HAV, HCV, HDV, HEV (these viruses replicate mainly in the liver and cause inflammatory degenerative changes) and nonhepatotropic include for example the yellow fever virus and the coxsackie virus;
 * The most common DNA viruses are: HBV, Ebstein Barrové virus - EBV, Cytomegalovirus -CMV and Herpesvirus - HSV.
 * Bacterial agents include Leptospira (Weil´s disease), Brucella, Rickettsia (Q fever), Salmonella (abdominal typfus)

Non-ifectious hepatitis
Non-ifectious hepatitis is caused by liver damage from external influences or as a result of an already existing autoimmune disease. The causes include:


 * alcohol,
 * drug abuse – paracetamol, halothane,
 * poisoning – fungi and other toxins,
 * autoimmune causes (for autoimmune hepatitis, we determine the following antibodies: antinuclear (ANA), antimitochondrial (AMA), liver membrane antibodies (LMA) and other;
 * metabolic diseases (eg. Wilson´s disease)

Acute hepatitis
The most common cause of acute hepatitis is alcohol damage and viral hepatitis. Toxic damage, paracetamol and halothane and many others are also common causes of acute hepatitis.

Chronic hepatitis
Chronic hepatitis has manifestations that do not subside after 6 monthsí (laboratory and histopathological changes persist for more than 6 months - eg increased liver tests, especially ALT, AST). Of the viral hepatitis, the ones that turn chronic most often are:
 * hepatitis C (85-90% of the total number of symptomatic courses),
 * hepatitis D (which only occurs when co-infected with HBV)
 * hepatitis B, which becomes chronic in 10-15% of cases.

Besides viral hepatitis, these can also cause chronic hepatitis:
 * autoimmune causes,
 * autoimmune hepatitis
 * primary sclerosing cholangitis,
 * primary biliary cirrhosis
 * alkoholic hepatitis,
 * drug abuse and
 * metabolic diseases. The most common are:
 * α1-antitrypsine deficiency
 * Wilson´s disease
 * Hemochromatosis.

Unlike in acute hepatitis, the cause is more difficult to diagnose in chronic hepatitis. One can only speculate whether it is an autoimmune cause, drug damage, antibody-negative hepatitis, etc. For this reason, a biopsy is very often indicated.

Clinics
Patients usually complain about decreased performance, fatigue, loss of appetite, arthralgia and intermittent diarrhea. The liver is palpably sensitive. Patients with low inflammatory activity in the liver tissue may also have an asymptomatic course. There is a temporary acute flare-up of the chronic course – during this inflammatory flare-up there is jaundice, the liver is enlarged and palpable. The spleen may also be enlarged. Typically,in the biopsy we find an inflammatory activity in the liver tissue, as well as impaired metabolic function of the liver - menstrual disorders, including amenorrhoea, in men testicular atrophy, gynecomastia and lack of secondary hair. Immunopathological reactions may occur – especially type III. immunopathological reaction, when antibody complexes with viral components are formed, in which case the hepatitis is accompanied by extrahepatic diseases such as cryoglobulinemia, Panarteriitis nodosa, glomerulonefritis, polyarteritis nodosa, and other.

Metabolic liver diseases
Metabolic liver disease refers to the damage of the liver due to its important role in metabolism. It can be a disorder of the metabolism of lipids, carbohydrates, amino acids, urea, metals, porphyrins or a disorder of the transport of bile pigments. Hereditary and congenital metabolic disorders:

Hereditary disorders of lipid metabolism: Wolman's disease and cholesterol storage disease, Niemann-Pick complex, Gaucher's disease, abetalipoproteinemia, β-oxidation disorders

Hereditary disorders of carbohydrate metabolism: glycogenosis, galactosemia, hereditary flucose intolerance

Hereditary disorders of amino acid metabolism: tyrosinemia and defects in branched-chain amino acid metabolism

Congenital disorders of urea metabolism

Congenital disorders of metal metabolism: hemochromatosis, Wilson´s disease

Congenital disorders of porphyrin metabolism: hepatic porfyria

dědičné poruchy transportu žlučových barviv.

Clinical picture
Hepatitis occurs with varying intensity of clinical manifestations.


 * inapparent infection
 * This form is completely asymptomatic.
 * Abortive form
 * Short-term illness with [influenza]] or dyspepsia. It is often accompanied by a slight increase

of aminotransferases.
 * Icteric form
 * Anicteric form
 * It is the most common in all types of hepatitis.
 * Cholestatic form
 * Reminiscent of obstructive jaundice.
 * Malignant or fulminant form
 * Liver failure, development of a hepatic coma with high mortality.

The course
The course of hepatitis is divided into 3 stages.

Stage of liver failure
This stage usually lasts 2-8 weeks (if it is longer, it is prolonged hepatitis).

Stage of reconvalescence
We most often encounter functional disorders of various parts of the GIT. It is, for example, anorexia, a feeling of fullness after a meal, constipation or diarrhea, pressure under the ribs. Quite often there can be pain in the liver area. These are posthepatic heparalgias (adhesions between the capsule and the peritoneum). They usually disappear within a few months

Laboratory tests
The first biochemical change that we notice in the laboratory examination is an increase in aminotransferases. This change is already visible in the prodromal stage.

In acute hepatitis ALT rises more than AST. The dynamics of ALT and AST values ​​help assess the course of the disease and the prognosis.

Persistent levels after jaundice may indicate possible chronicity. Rise after recovery is called a relapse. In prolonged and chronic hepatitis, we observe changes in the protein electrophoresis. A decrease of albumin and an increase of gamma globulins. There are also viral markers – viz dále.

Anamnesis

 * family history – liver disease, bile duct disease, familiar hyperbilirubinemia, hemolytic conditions,
 * personal history – neonatal jaundice…,
 * Reasons for accidentally detected high aminotransferases in a healthy child:
 * laboratory mistake – old or hemolyzed blood (new sample will decide),
 * incipient acute hepatitis – markers,
 * liver damage from another infection,
 * drug damage to the liver,
 * diseases of thebile ducts or the pancreas – ALP, GMT, amylase,
 * diseases of other organs with AST or ALT – myocardium, muscles,
 * hepatic steatosis – diabetes, obesity, disorders of lipid metabolism, thyreopathy.

Acute hepatitis therapy
Hospitalization in the infectiousward – isolation, for the purpose of a quick and comprehensive diagnosis and for the observance of the rest regime. Antiviral therapy is not performed, the basis is rest and a diet (an exception is HCV, where early administration of interferone α reduces the likelihood of transition to chronicity).

Diet
Physical activity is not recommended in the acute phase, it is harmful. When it comes to diet, excessive protein intakce or fat reduction is unnecessary. Substances formed from the burning of fats and alcohol are harmful, which is why we avoid them. We make sure that the patient does not take hepatotoxic drugs. Hepatoprotective drugs (sylimarin – Flavobion) do not significantly affect the course.

The patient is discharged when the problems of the subject disappear (jaundice) and after the enzymes fall to a double standard. We monitor the patient even after the dicharge. The first check-up is 2-3 weeks after. Palpation and liver tests are appropriate during the first check-up. The condition for returning to school is the normalization of animotransferases and the regression of jaundice.

After Hepatitis A we see the disappearance of IgM antiVHA.

After Hepatitis B we see the disappearance of HBsAg.

In Hepatitis C it is useful to ensure that the viral DNA disappeared from the serum by PCR.

Related articles

 * Viral hepatitis
 * Viral hepatitis/case report
 * Chronic non-infectious liver diseases
 * Liver cirrhosis • Portal hypertension • Liver failure (pediatrics) • Liver failure • Liver tests

Literature