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Chronic hepatitises

Table of contents
Chronic hepatitises
Preliminary diagnosis
Final diagnosis
Treatment, prevention

Chronic hepatitises — inflammatory diseases of a liver of various etiology (viruses, toxic agents, autoimmune processes, etc.) lasting more than 6 months. On kliniko-morphological features allocate 3 main types of chronic hepatitises: chronic persistent hepatitis (CPH), chronic lobulyarny hepatitis (CLH), chronic active hepatitis (CAH). From them HPG and HLG differ in not progressing current. The big liver failure does not develop, portal hypertensia, as a rule, is not observed.

Are transformed to cirrhosis exclusively seldom, most likely in similar cases HAG (see below) in a remission stage which is mistakenly taken for HPG or HLG was observed. HAG proceeds variously, in some cases the big liver failure and portal hypertensia develop. Highly active forms of a disease quite often progress in cirrhosis.

There are no exhaustive data on epidemiology of chronic hepatitises yet. These diseases in the USA about 1 million people have. HAG disease frequency in Sweden makes 1,6 on 100 000 population a year.

It is supposed that chronic persistent hepatitis of a virus etiology develops in 3 — 4 times more often than HAG. Chronic hepatitises of an alcoholic origin take the small place in structure of an alcoholic liver disease. Less often than viral and alcoholic hepatitis chronic hepatitises of a medicinal etiology meet.

Chronic hepatitis men have more often. Only separate types (autoimmune chronic hepatitises) are observed mainly at women. The mass biochemical and immunochemical examinations of the population conducted in the last decade showed that nearly 50% of chronic hepatitises proceed clinically asymptomatically or with the minimum clinical symptomatology. Therefore, at least, in a half of patients the disease is found rather accidentally at mass inspections. Reveal chronic hepatitises at careful inspection had an acute viral hepatitis or HBsAg carriers, and also at the persons having alcoholism or subjected to inspection concerning diseases of other bodies.

Etiology and pathogeny
The bulk of chronic hepatitises is made by diseases of virus.

At 40 — 50% of sick HPG, 70 — 80% of sick HLG and 35% of sick HAG the disease begins with a typical picture of an acute viral hepatitis.

Opening of markers of viruses of hepatitis B expanded possibilities of etiological diagnosis of a viral hepatitis of V. U of many patients having Chronic hepatitis, before carried to cryptogenic, in blood serum hepatitis B virus markers (see also Acute viral hepatitis) by HBeAg, HBsAg, anti-HBc, anti-HBs, anti-HBe were found.

At sick HAG on a current allocate two phases. The first lasting 2 — 10 years (2 — 4 years are more often) is characterized by clinical laboratory signs of high activity of pathological process in a liver and replication of a viral infection (see above). Upon transition of an illness to the second stage the tendency to normalization of clinical laboratory indicators of activity of pathological process in a liver usually appears. Signs of replication are replaced by signs of a persistention of a viral infection, at the time of seroconversion at a small number of patients acute necroses of a liver develop.

At sick HPG and HLG infection persistirovaniye signs are, as a rule, observed, In development of low-active forms of a chronic viral hepatitis the important role belongs to the long persistirovaniye of a virus of hepatitis B proceeding in close contact with the gene device of a hepatocyte. In development also progressed highly active forms of a chronic viral hepatitis the important part is assigned to the replication of a virus which is constantly supporting immunoinflammatory process. More often the long stage of replication of a virus is observed at various defects of both cellular immunity, and humoral. In particular, at sick HAG injury of hepatocytes happens to participation of T lymphocytes. Are present at tissue of a liver surface and nuclear antigen of hepatitis B. In blood serum of these patients various autoantibodies — smooth muscle, mitochondrial, thyroid, etc., and also cell-bound immune complexes circulate. Decrease in a complement at the expense of a gepatodepressiya does cell-bound immune complexes especially aggressive. At a number of patients with a chronic viral hepatitis In superinfection is observed by a hepatitis D virus (or a delta virus). Usually these diseases proceed especially actively and hard.
Also chronic hepatitises of an alcoholic origin are quite often observed.

In development of chronic alcoholic hepatitis the greatest significance is attached to direct toxic action on a liver of alcohol and products of its splitting. Immunopathological reactions are partially connected with education in a liver of an alcoholic hyalin. This protein gives constancy, permanence to pathological process in a liver at a chronic alcoholic disease.

Medicinal chronic hepatitises are caused dopegity, Tubazidum, PASKOM, by nitrofurans, a methotrexate, cytostatic drugs, peleitany, etc.

In 1956 J. R. Mackay, J. J. Tafl and D. Villages of Coweing found in young women a peculiar disease which cornerstone chronic hepatitis with transition to cirrhosis was. The disease reminded hard currency and was called by them lupoid hepatitis. Later this type of chronic hepatitis began to be called autoimmune hepatitis or chronic immune hepatitis.

Emergence since the end of the 50th years of methods of definition of aminotransferases of blood serum and wide use of a puncture biopsy of a liver led to accumulation of new information. These circumstances gave the chance to group of hepatologists in 1967 — 1968 to isolate chronic hepatitises at which the liver is surprised generally in a zone of portal paths, designating them as chronic persistent hepatitises. The chronic hepatitises proceeding as with defeat of portal paths, and actually the segment were opposed to them. It was offered to call these hepatitises "aggressive", and later — "chronic active hepatitises".

In the early seventies N. Popper and soavt. added HLG at which pathological process in a liver is localized generally in actually segment to two main forms of chronic hepatitises though cellular infiltrates meet as well in portal paths.

Thus, modern classification of chronic hepatitises covers three main forms:

CPH (chronic portal hepatitis) — the chronic inflammatory disease of a liver with preferential defeat of portal paths proceeding, as a rule, without the expressed tendency to spontaneous progressing without development of a big liver failure and portal hypertensia. In the absence of repeated injuries of a liver long-term supervision at most of patients reveals subsiding or a tendency to subsiding of pathological process.

HLG — a chronic inflammatory disease of a liver with preferential defeat actually liver segments, partially and portal paths with a frequent tendency to spontaneous subsiding of pathological process. The big liver failure and portal hypertensia is not observed. In the pathogenetic plan represents as if the "stiffened" acute hepatitis. This feature of a disease is so expressed that, according to a number of authors, it can be placed as if between an acute hepatitis and chronic hepatitis.

HAG (chronic aggressive hepatitis, chronic periportal hepatitis, lupoid hepatitis, chronic immune hepatitis) — rather rare general inflammatory disease proceeding with preferential damage of a liver (both a hepatic segment and portal paths, and periportal spaces), which is characterized by the expressed immune disturbances and often spontaneously not calming down activity of pathological process in a liver. Quite often evolyutsinirut in cirrhosis and can come to an end with death as a result of development of a big liver failure or displays of portal hypertensia. It is accepted to allocate two main options of a disease: highly active (progressing) and low-active (slowly progressing). Except these main options, usually isolate two rather rare clinical forms (less than 10 — 15% of sick HAG): lupoid hepatitis, or chronic immune hepatitis, and HAG with a cholestatic syndrome.

Approximate formulation of the diagnosis:
1. HPG of a virus etiology in an aggravation stage.
2. HLG of a virus etiology with a resistant cytolytic syndrome.
3. HAG (a highly active form) of a virus etiology with the expressed disturbance of functions of a liver and initial display of portal hypertensia — a moderate knotty phlebectasia of a gullet.
4. HAG (a low-active form) as a result of intoxication dopegity.

"Cholecystitises   Chronic erosion"