Hepatitis

Hepatitis is an inflammatory disease of the liver.

Hepatitis acute. Etiology, pathogenesis. The most common cause of acute liver damage in humans is viral hepatitis. Acute hepatitis can also be caused by zinteroviruses, pathogens of intestinal infections, infectious mononucleosis viruses, leptospira, some tropical parasites, septic bacterial infection (see Infectious Diseases; Sepsis). There are also acute toxic hepatitis caused by drugs (inhibitors of MAO-derivatives of hydrazine, PASK, isonicotinic acid derivatives, male fern extract, etc.), industrial poisons (phosphorus, organophosphate insecticides, trinitrotoluene, etc.), fungal poisons of pallid grebe, morels (Muscarine, afalotoxin, etc.). Acute hepatitis can occur as a consequence of radiation (radiation) damage, with extensive body burns, severe infectious diseases, toxicosis of pregnant women. The use of alcohol often predisposes to the development of acute hepatitis. The pathogenesis of acute hepatitis consists either in the direct action of the damaging factor on the hepatic parenchyma, or in immunological disorders that arise in response to primary liver damage, followed by cytolysis of affected and intact hepatocytes. In some cases, the importance of a violation of microcirculation in the liver and intrahepatic cholestasis.

Symptoms, course. In mild cases, acute hepatitis is virtually asymptomatic, only detectable by accidental or targeted examination (for example, in the workplace among persons who are in contact with hepatotropic poisons, in case of household group poisoning with fungi, etc.). In more severe cases (for example, with toxic hepatitis), the clinical symptoms of the disease develop rapidly, often in combination with signs of general intoxication and toxic damage to other organs and systems. At the height of the disease, icteric staining of the skin and mucous membranes, whitish-clayey stools, saturation-dark color ("color of beer") of urine, hemorrhagic phenomena are characteristic. The color of the skin is orange or saffron. However, in mild cases, jaundice is only visible in daylight, the earliest is icteric staining of the sclera and mucosa of the soft palate. Frequent nosebleeds, petechiae; Patients are disturbed by pruritus, bradycardia, oppressed mental state, increased irritability of patients, insomnia and other signs of central nervous system damage are noted.

The liver and spleen are slightly enlarged and slightly painful. With particularly severe lesions and the predominance of necrotic changes in the liver (acute dystrophy), its dimensions may decrease.

Laboratory studies show hyperbilirubinemia (100-300 μmol / L and more), an increase in the activity of a number of serum enzymes: aldolase, aspartate aminotransferase and especially alanine aminotransferase (well above 40 units), lactate dehydrogenase, hypoalbuminemia, hyperglobulinemia (predominantly elevated levels. Indices of protein-sedimentary samples (thymol, sulemic, etc.), the production of fibrinogen, prothrombin, VII, and V coagulation factors is disturbed by the liver, resulting in hemorrhagic phenomena.

Course, complication, prognosis. With timely treatment often comes a full recovery. In some cases, acute hepatitis becomes chronic, and then cirrhosis of the liver. In some cases, acute liver dystrophy develops (see Hepatosis) with a clinic for acute hepatic or hepatic renal failure, from which patients may die.

Differential diagnosis. Of great importance is a carefully collected history, the establishment of the possibility of occupational or household intoxication, the consideration of the epidemiological situation in identifying the nature and cause of the disease. In unclear cases, you should first think about viral hepatitis. The detection of the so-called Australian antigen is characteristic of serum hepatitis B (it is also detected in virus carriers, rarely in other diseases). Mechanical (podpechenochnaya) jaundice arises acutely usually only when the common bile duct is clogged with a stone in cholelithiasis. But in this case the appearance of jaundice is preceded by an attack of biliary colic; Bilirubin in the blood is mostly straight, the stool is discolored. With hemolytic adrenal jaundice, free (indirect) bilirubin is detected in the blood, the stool is intensely colored, and the osmotic resistance of the erythrocytes is usually reduced. In the case of false jaundice (due to the dyeing of the skin with carotene during prolonged and abundant consumption of oranges, carrots, pumpkins), sclera is usually not colored, there is no hyperbilirubinemia.

Treatment. Patients with acute viral hepatitis (and with a suspicion of such), as well as infectious hepatitis of other etiology must be hospitalized in special departments of infectious hospitals, and in the focus of infection, they carry out sanitary and epidemiological measures. Patients with toxic hepatitis are hospitalized in poisoning centers, where they are carried out measures to remove the poison from the body (gastric lavage, etc.), detoxification therapy.

Patients with acute hepatitis appointed bed rest, sparing diet with a restriction of fat and an increase in the carbohydrate content, a large number of fruit juices. In severe cases, especially with severe anorexia and vomiting, 5-10% glucose solution (up to 500 ml) is injected intravenously by a drip method.

When there are signs of congestion or coma with an urgent indication, a massive plasmapheresis is performed. Using a centrifuge or separator, remove 1.5-2 liters of plasma and inject into / 2 liters of fresh frozen plasma. If there is no persistent improvement - clarification of consciousness, an increase in the level of prothrombin, the next day and then repeat the procedure. Daily for 2-3 days or more until the coma is permanently disappearing, 1 -2 liters of fresh frozen plasma should be injected until the blood coagulation system is normal.

The prognosis depends on the etiology of the disease, the severity of liver damage, and the timeliness of treatment.

Prevention of acute hepatitis, taking into account the diversity of their etiological factors, is the strict conduct of sanitary and epidemiological measures, observance of personal hygiene rules, provision of appropriate sanitary and technical supervision at enterprises, preventing the possibility of industrial poisoning by hepatotropic poisons. Do not eat obviously inedible or unknown fungi, as well as edible, but old (which can also cause severe poisoning).

Chronic hepatitis - polyetiological chronic (duration of more than 6 months) lesions of inflammatory-dystrophic liver with moderately expressed fibrosis and mainly preserved lobular structure of the liver. Among chronic liver diseases, chronic hepatitis is the most frequent.

Etiology, pathogenesis. The most important is viral, toxic and toxicoallergic liver damage in viral hepatitis, industrial, domestic, medicinal chronic intoxications (alcohol, chloroform, lead compounds, trinitrotoluene, atophane, aminazine, isoniazid, methyldof, etc.), less often - infectious mononucleosis, herpes viruses , Cytomegaly. Chronic hepatitis is often observed with prolonged septic endocarditis, visceral leishmaniasis, malaria. Chronic cholestatic hepatitis can be caused by prolonged subhepatic cholestasis (due to a stone blockage or scar compression of the common bile duct, cancer of the pancreas head, etc.) in conjunction with the usually joining inflammatory process in the bile ducts and passages, the primary primary toxic or toxico- An allergic lesion of cholangiol. It can also be caused by certain medications (phenothiazine derivatives, methyltestosterone and its analogues, etc.) or occur after a viral hepatitis.

In addition to chronic hepatitis, which is an independent disease (primary hepatitis), there are also chronic non-specific types of hepatitis that occur against the background of chronic infections (tuberculosis, brucellosis, etc.), various chronic diseases of the digestive tract, systemic connective tissue diseases, etc. ( Secondary, or reactive, hepatitis). Finally, in many cases, the etiology of chronic hepatitis remains unclarified.

Pathogenesis: direct action of the atiological factor (virus, hepatotoxic substance) on the hepatic parenchyma, causing dystrophy and necrobiosis of hepatocytes and reactive proliferation of the mesenchyme. One of the pathogenetic mechanisms of the transition of acute viral and toxic hepatitis to chronic and further progression of the latter are specific immunological disorders.

Symptoms, course. Characteristic of an increase in the liver, pain or feeling of heaviness, fullness in the right hypochondrium, dyspeptic phenomena; Less common jaundice, itchy skin, subfebrile condition. Liver enlargement occurs in approximately 95% of patients, but in most cases it is moderate. There is no increase in the spleen or it is slightly enlarged. Pain in the region of the liver is blunt, constant. Frequent loss of appetite, eructation, nausea, poor tolerance of fats, alcohol, flatulence, unstable stool, general weakness, decreased ability to work, hyperhidrosis. In a third of patients, the indistinctly expressed (subcyteric sclera and palate) or moderate jaundice is revealed. Frequent, but nonspecific increase in ESR, dysproteinemia due to a decrease in the concentration of albumins and increase in globulins, predominantly alpha and gamma fractions. Positive results of protein-sedimentary probes - thymol, sulemic, etc. In the blood serum of patients, the content of aminotransferases: ALAT, ASAT and LDH, with difficulty of outflow of bile - alkaline phosphatase was increased. Approximately 50% of patients have mild or moderate hyperbilirubinemia, mainly due to an increase in serum levels of bound (direct) bilirubin. The absorptive ekskretornaya function of the liver is impaired (the half-life of bromsulfalein is prolonged from the blood).

With cholestatic hepatitis, more severe persistent jaundice and laboratory syndrome of cholestasis are usually observed: in the serum the content of alkaline phosphatase, cholesterol, bile acids, bound bilirubin, copper is increased.

Isolate low-active (inactive), benign, persistent and active, aggressive, progressive recurrent hepatitis.

Flow. Low-active (persistent) hepatitis is asymptomatic or with minor symptoms, changes in laboratory parameters are also insignificant. The aggravation of the process is not characteristic.

Chronic active recurrent (aggressive) hepatitis is characterized by severe complaints and bright objective clinical and laboratory signs. Some patients experience systemic auto-allergic manifestations of the disease (polyarthralgia, skin rashes, glomerulonephritis, etc.). Characteristic of frequent relapses of the disease, sometimes occurring under the influence of even minor factors (inaccuracy in diet, overwork, etc.). Frequent relapses lead to significant morphological changes in the liver and the development of cirrhosis. In this regard, the prognosis with active hepatitis is more severe.

Puncture liver biopsy and laparoscopy make it possible to more accurately distinguish these two forms of hepatitis, as well as conduct differential diagnosis with other liver diseases.

Scanning the liver allows you to determine its size; When hepatitis is sometimes observed reduced or uneven accumulation of radioisotope drug in the liver tissue, in some cases, there is an increased accumulation in the spleen.

Differential diagnosis in cases with a vivid clinical picture of diffuse liver damage is primarily to be performed with cirrhosis of the liver. With cirrhosis, the symptoms are more pronounced, the liver is usually much denser than with hepatitis; It can be enlarged, but often reduced in size (atrophic phase of cirrhosis). As a rule, splenomegaly is observed, hepatic signs (vascular telangiectasias, hepatic tongue, hepatic palms) are often revealed, symptoms of portal hypertension may occur. Laboratory tests show significant deviations from the norm of the results of so-called hepatic tests; When puncture biopsy - disorganization of the structure of the liver, a significant proliferation of connective tissue.

Fibrosis of the liver, unlike hepatitis, is usually not accompanied by clinical symptoms and changes in functional liver samples. Anamnesis (the presence of a disease in the past that could cause liver fibrosis), long-term observation of the patient and puncture liver biopsy (in necessary cases) allow him to differentiate from chronic persistent hepatitis.

With fat hepatosis, the liver is usually softer than with chronic hepatitis, the spleen is not enlarged, the puncture biopsy of the liver is crucial in diagnosis.

Differential diagnosis with functional hyperbilirubinemia is based on the features of their clinical picture (mild jaundice with hyperbilirubinemia without bright clinical symptoms and changes in laboratory hepatic samples and puncture liver biopsy). Amyloidosis with predominant hepatic localization, in contrast to chronic hepatitis, is characterized by symptoms and other organ localizations of the process, a positive test with Congo red or methylene blue; The diagnosis is confirmed by puncture liver biopsy. In focal lesions (tumor, cyst, tuberculoma, etc.), the liver is unevenly enlarged, and scanning determines the focus of destruction of the hepatic parenchyma.

Treatment. Patients with chronic persistent and aggressive hepatitis without exacerbation should follow a diet with the exception of spicy, spicy dishes, refractory animal fats, fried foods. Recommended cottage cheese (daily to 100-150 g), mild cheeses, low-fat varieties of fish in boiled form (cod, etc.). In toxic and toxic-allergic hepatitis, it is extremely important to completely stop contact with the relevant toxic substance, with alcoholic hepatitis-taking alcohol, if necessary, treatment for alcoholism is indicated.

With the exacerbation of hepatitis shows hospitalization, bed rest, a more strict, sparing diet with enough protein and vitamins. Assign glucose to 25-30 grams inside, vitamin therapy (especially vitamins B1, B2, B6, B12, nicotinic, folic and ascorbic acid). In order to improve the anabolic processes, anabolic steroid hormones (methandrostenolone by mouth at 15-20 mg / day with a gradual dose reduction or retabolil of 20-50 mg once every 2 weeks) are used. In more acute cases, especially with signs of significant activation of the immunocompetent system, corticosteroid hormones (20-40 mg of prednisone per day) and (or) immunosuppressants are also shown in small doses also in small doses, but for a long time. Treatment with extracts and hydro-lysates of the liver (vitohepat, sireppar and others), but cautiously, since with acute hepatitis, the administration of hepatic hydrolysates can enhance auto-allergic processes and contribute to an even more exacerbation of hepatitis.

In chronic cholestatic hepatitis, the focus should be on identifying and eliminating the cause of cholestasis, in which case one can expect success from treatment activities.

Patients with chronic hepatitis need employment (restriction of heavy physical exertion, exemption from work associated with frequent business trips and not allowing to comply with the diet). Patients with aggressive hepatitis with a rapid progression of the process are transferred to disability III, and in some cases, group II.

Prevention of chronic hepatitis reduces to the prevention of infectious and serum hepatitis, the fight against alcoholism, the exclusion of the possibility of industrial and domestic intoxication with hepatotropic substances, as well as the timely detection and treatment of acute and advanced hepatitis.