Cirrhosis is a disease polietiologic. The ratio of each etiological factors in different countries and geographical areas varies, depending on the socio-economic conditions, nutrition peculiarities.
To date, proved the leading role epidemic of hepatitis a in the Genesis of cirrhosis. According to the materials of many researchers (E. M. Tareev, 1958, 1964, 1965; M, Malkov, 1957; E. N. Ter-Grigorova, 1950, 1963; M. A. Yasinovka, 1958; X. X. Mansurov, 1959-1963; Kalk, 1954, and others), Botkin's disease causes 50-60% of progressive chronic hepatitis and liver cirrhosis.
Having examined during 1951-1968, 820 patients with cirrhosis of the liver, 469 (57,2%) of them we have established a causal relationship of this disease with previously transferred epidemic hepatitis.
History 540 patients with cirrhosis epidemic hepatitis, mentioned in 5 times more likely than 500 persons with no signs of liver disease (Century, Smagin, 1966). The guilt of hepatitis virus in the development of cirrhosis of the liver, including in some cases where indications previously transferred epidemic hepatitis was absent, to some extent confirmed virological research, though the latter are not specific to the epidemic of hepatitis. M. A. Yasinovka (1957) observed a positive reaction of binding complement, on J. K. Himmelfarb 80% of patients with chronic hepatitis or cirrhosis. In. A. Simonov and others (1968), in parallel examining tissue culture infectious agents isolated from patients epidemic hepatitis and liver, spleen and blood of patients with cirrhosis found that irregular cytopathogene changes in the studied crops were similar in both cases. Similar data obtained M. A. Slancevite and D. B. Golubev (1968), who used intrusion method chick embryo and tissue cultures. Gitnick and others (1970), who examined 31 people with chronic active liver disease, discovered Australia antigen in 3 patients with cirrhosis who have no history of previously deferred hepatitis. These patients are no blood transfusion and was not applied hepatotoxic drugs.
Malnutrition, mainly protein deficit, specific amino acids, vitamins (B12, B6 and E), is a frequent cause of cirrhosis in some colonial countries, or more recently used to be legitimate.
With protein and vitamin a deficiency is associated with the so-called kwashiorkor, which the children weaned from the breast and contained mostly on carbohydrate nutrition. The disease is characterized by severe malnutrition, fatty degeneration of the liver, progressing to cirrhosis. It is widespread in tropical countries.
In our conditions the factor of malnutrition is endogenous in origin and is associated with chronic enterocolitis and some infections (X. X. Mansurov, 1954, 1963).
It is recognized that alcohol abuse creates relative and absolute failure lipotropic agents and leads to fatty liver with the possible subsequent development of cirrhosis. Recent studies carried out by using electron microscopy and entomologicheskij methods indicate a direct toxic effect of alcohol on the liver cells (Schiff, 1964; Thaler, 1962; Foulk, 1968; Phillips, 1968).
Alcoholism as an independent etiological factor at present is rarely the cause of cirrhosis. But this fact should not be considered a reason for rehabilitation of alcohol, as abuse creates conditions conducive to the other hepatotropic influences the outcome in liver cirrhosis.
Many researchers overestimated the value of malaria as a factor causing cirrhosis. E. M. Tareev and M. K. Kulmatov (1958), who investigated using a biopsy of the liver of patients with severe malaria splenomegaly and to repeat these studies after recovery from this disease, have not found the notorious malaria cirrhosis. Similar conclusions have been drawn X. X. Mansurov (1963) and Sherlock (1959).
The idea of the meaning of granulomatosis (brucellosis, tuberculosis, syphilis, sarcoidosis) as factors leading to the development of cirrhosis in the last decade has changed significantly. Most researchers shared the opinion that as a result of these diseases occur fibrosis, not cirrhosis of the liver (with E. M. Tareev, 1958, 1966; X. X. Mansurov, 1963; Sherlock, 1955; Popper and Schaffner, 1957). However, in severe and prolonged cases of brucellosis may develop true cirrhosis (I. Century Davydov, 1956; McCulIough, Eisele, 1951).
Currently, the majority of researchers recognized that the development of cirrhosis when syphilis is possible only due to congenital its forms. Acquired same syphilis can lead to scar deformations of the liver without rebuilding its parenchyma (the so-called lobed liver - hepar lobatum), which is often treated by the doctors as syphilis cirrhosis. In patients with syphilis cirrhosis last usually develops due to other hepatotropic effects, the most often - syringe hepatitis (Popper, Schaffner, 1957; E. M. Tareev, 1966; Sherlock, 1955, 1968).
Toxic agents with long-term or large exposure may cause liver cirrhosis. This effect have carbon tetrachloride, trinitrotoluene, arsenic, phosphorus, chlorinated naphthalenes, chloroform and poisons plant origin - opulently heliotrope, weeds Senetio and Crota-laria, mushrooms Amantia phalloides (E. M. Tareev, 1958, 1966; M. N. Khanin, 1959, 1968; N. X. Abdullayev, 1968; Foulk, 1963). The specific weight of toxic agents among the causes of cirrhosis small.
Toxic-allergic hepatitis and cirrhosis may develop on the basis of individual intolerance of certain substances, including drugs, such as Tofan, anti-convulsants (dilantin), tuberculostatic (PAS), sulfanilamida, antibiotics, chlorpromazine.
Cirrhosis of the liver, when developing autoimmunization diseases that have no specific etiology, for example in nonspecific ulcerative colitis, can also be considered as allergic (3. A. Bondar, 1966, 1968; E. M. Tareev, 1966; Foulk, 1963; Klatskin, 1963).
The value of obstruction of the biliary tract and inflammation (cholangitis) as the reasons for the development of biliary cirrhosis currently, no doubt.
Principal causes, such as opisthorchiasis, bilharzia (schistosomiasis), can cause cirrhosis of the liver, it should be considered in the areas of dissemination of parasites.
Still no consensus on whether really cirrhosis changes that occur in the liver, with chronic heart failure. Popper and Schaffner (1957), Saphir (1958), V. N. Fadeeva (1968), specially studied this question, argue that the restructuring of the architectonics of the liver, according to morphological criteria of cirrhosis of the liver, is rare, and, with a few exceptions, only when constrictive pericarditis the same or at long tricuspid insufficiency. In other cases of chronic heart stagnation develops "stagnant" fibrosis. Changes in the liver, similar congestive fibrosis can occur and the violation of the outflow of blood through the system of the hepatic veins due to full or partial blocking (so-called syndrome of Budd - Chiari).

The majority of authors (with E. N. Ter-Grigorova, 1963, 1968; Sherlock, 1955, 1968, and others) reject the possibility splenorenal mechanism of the development of cirrhosis and believe that a simultaneous suffering of the spleen and liver is the result of a parallel impact of the same pathogenic factor on both organs.
Approximately a quarter of the patients the cause of cirrhosis of the liver can not be established. Often cirrhosis can be caused by the combined effect of several hepatotropic factors, and the priority of one of them is often impossible.
Among these reasons there is no factor that would necessarily caused by chronic progressive disease of the liver. Moreover, the impact of each of them relatively seldom realized in this way. So, the most common cause of cirrhosis of the liver-epidemic hepatitis, - has an outcome in chronic hepatitis b 7-9%, and in cirrhosis of the liver - in 1-3% of cases. Of the 2500 patients epidemic hepatitis, observed by us, the outcome in chronic hepatitis installed 9.3%, and 2.8% of the cases objectively we tracked during 12 years of follow-up development of cirrhosis. P. A. Grigor'ev and N. P. Kukina (1963), watching over 1000 patients epidemic hepatitis, lead, respectively 2,8 1,4%.
What are the conditions that determine the possibility of developing a chronic progressive disease of the liver caused by one or the other hepatotropic agent?
E. M. Tareev (1958, 1966), Kalzalka and others (1949), Siede (1958) assign the leading place the severity and duration of primary hepatotropic impact, particularly viral infections. Our monitoring shows that 78.3% of the liver cirrhosis, which developed because of the epidemic of hepatitis, owe their origin to the severe and prolonged the past, although the development of cirrhosis were observed clinically mild and Busselton during this hepatitis.
Undoubtedly, has a value and changing reactivity caused by the preceding and accompanying hepatotropic factor (in particular, epidemic hepatitis) effects, such as alcoholism, chronic colitises, diseases of the biliary tract, malnutrition, infections; inadequate treatment, premature return to a regular diet and work in the convalescence period (N. , Lupu and others, 1962; Century, Smagin, 1958, 1966).
The value of constitutionally-genetic factors in the Genesis of chronic hepatitis and liver cirrhosis is still unclear. Many described the family cases not be viewed as solid evidence of the hereditary nature of the disease, because in such cases it is possible impact on the family members of the same hepatotropic factor, in particular transplacental transmission of HBV from mother to fetus (Bodin, Newns, 1953; E. I. Ter-Grigorova, 1964, 1968).
However, hereditary basis of some forms of chronic liver disease such as gepatolentikuliarnaya degeneration, to a certain extent - hemochromatosis, currently installed (Osborn and others, 1963; Powell, 1963; Sherlock, 1967; A. M. Shaposhnikov, 1968). A number of unusual reactions to drugs, sometimes leading to liver cirrhosis caused by hereditary deficiency of certain enzyme systems. These circumstances strongly encourage to study the value of genotype for development and the most common forms of chronic liver disease.
It is possible that the outcome of the primary hepatotropic intervention in chronic progressive disease of the liver, in addition to the above conditions as determined and inherited enzyme abnormalities.