Syphilitic hepatitis symptoms. Syphilis is hepatitis. Early syphilitic jaundice

On the contrary, since I witnessed typical arthropathy in severe syphilis of the liver. I once saw a complication of liver syphilis with peritoneal tuberculosis, which is extremely interesting from the point of view of a similar combination with peritoneal tuberculosis.

Diagnosis

The diagnosis of liver syphilis is not always easy or certain. Usually, based on the symptoms of the disease (objective changes in the liver, abdominal dropsy, enlarged spleen), it is possible to recognize liver disease, but its nature often remains in doubt.

First of all, it goes without saying that you should pay attention to the etiological moment. If we are dealing with an undoubted drunkard, then first of all we should assume an ordinary form of cirrhosis.

On the contrary, if the anamnesis indicates syphilis and it is possible to prove the existence of other signs of this disease (bone damage, scars in the pharynx, Wassermann reaction, etc.), then it is certainly more likely to assume syphilitic liver disease. Of the individual signs of liver syphilis, rough irregularities on the surface of the organ are characteristic.

In contrast to the fine granularity with ordinary cirrhosis and sometimes also severe pain in the area of ​​the latter. In addition, it is necessary to take into account that the course of liver syphilis is much longer than the course of ordinary hepatic cirrhosis.

Treatment

Syphilis of the liver and other internal organs is often encountered in practice, but, unfortunately, is rarely diagnosed.

We can safely say that no organ is spared by this fairly common infection, especially the liver, which reacts very subtly to almost all types of acute and chronic infections. According to statistics, syphilis accounts for 7.2% of all liver diseases, which, of course, indicates a relatively high frequency of this disease.

Liver syphilis can be congenital or acquired. Both types can have an acute and chronic course of the disease. An acute course occurs with syphilitic hepatitis, and chronic forms are expressed in the form of syphilitic gummas or in the form of the so-called syphilitic lobular liver, which is a consequence of syphilitic cirrhosis.

Damage to the liver tissue in acquired syphilis can be observed in all three periods of syphilitic infection, but more often it occurs in the secondary and tertiary periods of the pathological process. Certain pathological changes in the liver tissue, characteristic of a syphilitic specific infection, occur mainly due to the penetration and residence of pale spirochetes in the liver tissue for a long time; The possibility of syphilitic intoxication affecting the liver tissue is also not denied.

In the acute period of syphilitic lesions, the process occurs in the form of vulgar infectious hepatitis, when small cell infiltration of the hepatic parenchyma, vasodilation, and exudation occur.

Usually in such cases the liver enlarges, its tissue becomes painful, soft-elastic consistency. In the later stages, due to chronic irritation of the liver tissue by syphilitic poison, the connective tissue grows, which subsequently leads to cirrhotic changes in the organ. Also specific is the formation of single or multiple gummas, which, disintegrating, resorbing, are replaced by connective tissue, which leads to severe deformation of the liver, a decrease in its volume, the formation of a lobulated liver with large constrictions, and sometimes detachment of parts of the liver, which is characteristic of syphilis of this organ. Of course, the described morphological changes and the gradual replacement of its tissue with connective tissue cannot but affect the overall functional ability of this organ. With sharp disturbances in liver function, significant changes occur in the body of patients, which is reflected in the clinical picture of the disease.

Clinical picture

And the symptoms of liver syphilis are quite confusing and do not have characteristic signs characteristic only of syphilis. In the initial, acute period of damage, with the so-called syphilitic hepatitis, there are all the clinical signs of acute infectious hepatitis that are usually observed: a feeling of heaviness, colic, pain in the right hypochondrium, low-grade fever, an increase in the size of the liver, its pain, slight leukocytosis and other morphological and biochemical changes in the blood picture. In such cases, the true etiology of hepatitis can only be determined by a carefully collected anamnesis. If there are anamnestic indications of syphilis, especially with poor and unsystematic treatment, the question becomes clear. In general, for all types of hepatic syphilis, since there are no pathognomonic clinical signs and the disease can be confused with many other liver diseases, a carefully collected history indicating the disease with this disease makes the diagnosis of hepatic syphilis the most likely.

If liver syphilis is suspected, the Wasserman test and other serological tests should be performed. In such cases, positive reactions completely confirm the presence of liver syphilis, and negative reactions do not yet indicate its absence.

With gummous hepatitis, much in the clinical picture depends on the size and number of gummous granulomas in the liver, on the presence of their disintegration or the presence of connective tissue degeneration.

Surgical treatment of liver syphilis

Liver syphilis in all its types is not of great interest to patients, since in most cases it cannot be treated surgically. With the marginal location of deformed, detached parts of the liver, with marginal gummas, one can resort to excision (resection) of parts of the liver, although such resections are unsafe for patients. The more accepted is a conservative-specific method of treatment, which is especially appropriate for syphilitic acute and chronic hepatitis, as well as for liver gummas. The use of conservative treatment is ineffective, almost useless, when the process is over, when the resulting lobular fibrous growths have already led to complete deformation of the liver. Nevertheless, when a diagnosis of liver syphilis is made, systematic antisyphilitic treatment is started.

Etiology. In the early period of the disease, a syphilitic infection can cause acute parenchymal hepatitis, which, however, often occurs from an accidentally introduced Botkin disease virus (“syringe” infection, see Botkin disease). With liver syphilis, a gummous process is more often observed in the tertiary period, with a dense, tuberous liver. As gummas disintegrate, they are replaced by connective tissue with the formation of scars that disfigure the liver (syphilitic lobular liver - hepar lobularis). Late congenital syphilis of the liver is usually characterized by diffuse hepatitis in combination with gummous lesions in the form of numerous small gummas.

Symptoms and course. Acute parenchymal syphilitic hepatitis occurs with symptoms of ordinary hepatitis: jaundice, enlarged and painful liver. The course of this disease is usually longer than Botkin's disease; an accelerated ROE is observed, the number of leukocytes is normal or increased, and fever of a prolonged remitting nature is observed. In diffuse hepatitis with a fine-gummy process, a dense, finely lumpy, painful liver and an enlarged spleen are palpable. If there is a lobulated liver, its surface is hard and uneven. With improper and insufficient treatment, the disease progresses, but is relatively benign. The general condition of the patients remains satisfactory for a long time, liver function is slightly impaired. In the final stage of the disease, jaundice and ascites develop from compression of the bile ducts and portal vein by scar tissue.

Diagnosis. Acute syphilitic hepatitis is differentiated from hepatitis of other etiologies; gummoan and cirrhotic process - with liver cancer and cirrhosis of other origins. Syphilitic hepatitis may be indicated by medical history, a positive Wasserman reaction, clinical features of the course of liver disease and other manifestations of a syphilitic infection in the patient.

Treatment. Specific treatment: penicillin, mercury preparations, bioquinol, iodine; you need to be careful with the use of novarsenol, especially in the presence of jaundice, since novarsenol itself can cause toxic hepatitis (see Acute salvarsan hepatitis). General regimen, diet and nonspecific drug treatment, as for acute parenchymal hepatitis (see)

Prevention. Vigorous antisyphilitic treatment in the initial stages of the disease, as well as prevention, common with chronic hepatitis (see) and salvarsan hepatitis (see). In case of exacerbations of illness, fever, jaundice, the patient is temporarily disabled; during remission, with good health, compensated liver function - limited ability to work: the patient should not overwork and do hard physical work (see Chronic hepatitis).

Many diseases, both viral and bacterial, pose a mortal danger to humans.

Some of them appear almost immediately, while others, on the contrary, do not manifest themselves for a long time. This can lead to the patient learning about a terrible diagnosis when it is too late to do anything. Therefore, it is possible to conduct a preventive anonymous examination to check your health status, in particular, get tested for HIV and hepatitis.

• Testing for HIV
• How to decipher the results?
• How long are the results valid?
• Methods for detecting hepatitis
• ELISA method
• PCR analysis

Testing for HIV

The human immunodeficiency virus was discovered at the end of the last century. It is dangerous because it hardly manifests itself, often until the death of the patient. An HIV test is mandatory in the following cases:

• pregnancy (to avoid the vertical spread of the virus);
• donation (to avoid infection through the blood of other people);
• before carrying out operations.

How is the analysis carried out, where is the blood taken from and is any preparation needed? Blood is taken from the cubital vein on an empty stomach.

In newborns, blood is taken from the umbilical vein. Within 2-10 days, an antibody test is performed, after which a diagnosis is made about the presence or absence of the virus in the body.

How long can blood taken for analysis be stored? At room temperature the shelf life is no more than 12 hours. If you store raw materials in a special refrigerator at a temperature of no more than 8 °C, the period increases to 24 hours. After the specified time, ongoing hemolysis processes may affect the results obtained. The study can also use blood serum, which is obtained by centrifugation. The serum can retain its properties for up to 7 days at a temperature of 4 to 8 °C.

How to decipher the results?

The time period after infection in which reliable results can be obtained is key. The study checks for the presence of antibodies to the Ag p24 protein, which is part of the virus envelope wall. They begin to appear in the blood within 2-4 weeks after infection.

Normally, Ig M Ag p24 and Ig G Ag p24 are absent in the blood. Ig M Ag p24 can be produced within several months after infection, but disappears within a year from the moment of infection. Ig G Ag p24 is produced in the body over the years.

How long are the results valid?

The shelf life of an HIV test is 6 months. This is due to the fact that it is possible to accurately determine the virus only 3 months after infection.

The results are valid only for this period, after which you need to take the test again. This validity period is not relevant during pregnancy - during this period the analysis is carried out monthly.

So, to be sure that there is no disease, a new test is required every 6 months to check for the presence of antibodies in the body.

Methods for detecting hepatitis

The ways of spreading hepatitis B and C are similar to the ways of spreading HIV: sexual and parenteral. These diseases are diagnosed using a test that requires donating blood.

How is hepatitis tested? To test for hepatitis, blood is taken from the antecubital vein on an empty stomach. It is also recommended to refrain from smoking and drinking alcohol for at least 8 hours before donating blood.

The study includes a general blood test and a detailed biochemical test, which allows us to detect the presence of antibodies and markers of hepatitis in the blood.

It takes up to 7 days to receive analysis results. In paid institutions the period is usually no more than 2-3 days.

Hepatitis testing is done in two stages: ELISA and PCR. The second analysis is carried out if the ELISA gives a positive result - both the first time and when repeated.

ELISA method

An enzyme immunoassay shows the presence of the hepatitis virus in the body with a probability of up to 95%. The risk of a false positive or false negative reaction cannot be excluded.

A false positive result is possible in a reaction that occurs in the absence of infection. More often, a false negative result is observed - in the presence of infection, the body does not respond.

Statistics show that obtaining a false negative result is possible in 8% of cases. It is possible in the following cases:

• malignant neoplasms;
• autoimmune pathologies;
• syphilis;
• short period from the moment of infection.

PCR analysis

Polymerase chain reaction is carried out if the enzyme immunoassay gives a positive result. This diagnostic method has been used for more than 15 years and is considered the most reliable.

It is carried out in qualitative and quantitative directions. The qualitative direction involves the determination of fragments of viral RNA in the blood (HCV RNA). Quantitative analysis determines the viral load in the body. In this case, the amount of virus in the blood is determined, which is an important indicator.

A low viral load reduces the risk of transmitting the virus to others and implies a higher effectiveness of treatment. A high viral load, on the contrary, increases the risk of infection and indicates a lower effectiveness of treatment.

How to decipher the result? Decoding the PCR result for the quantitative indicator of the virus is expressed in IU/ml (international units per milliliter of volume). This indicator is accepted throughout the world for standardization purposes. Depending on how many units are detected, the level of virus content is determined.

If the rate is more than 800 IU/ml, this indicates a high viral load. A value of less than 800 IU/ml indicates, on the contrary, a low viral load on the body.

What is the shelf life of a hepatitis test? The biochemical blood test itself has a shelf life of up to 14 days. However, the result of a test for hepatitis is reliable for 6 months from the date of the study. This is due to a window period during which the virus cannot be detected after infection. People who belong to the risk group must undergo the study every six months without fail. If the expiration date of the analysis has expired, a new one is required, since the previous one will no longer be valid.

Prevention and regular examinations help, if not prevent, then identify pathology in the early stages, when treatment will be more effective and simpler.

Syphilitic hepatitis of the liver (liver syphilis) is one of the most common manifestations of visceral syphilis, second in frequency only to syphilitic aortitis and syphilis of the central nervous system. Syphilitic liver lesions of the chronic type are found in sections of one third of all corpses of patients with syphilis. During life, they are recognized only in half of all cases.

Syphilis of the liver is diverse. The most typical form of chronic syphilitic hepatitis of the liver is gummous hepatitis. This form is specific to syphilis, and one that is also characteristic of all other localizations of syphilis. But there are other forms of chronic syphilitic liver damage. Gummy hepatitis is a type of syphilitic interstitial (mesenchymal) hepatitis. It needs to be opposed to syphilitic parenchymal (epithelial) hepatitis and associated hepatitis.

Syphilitic chronic epithelial hepatitis

The disease is based on damage to liver cells of a dystrophic-degenerative nature with a secondary reaction from the mesenchyme.

Syphilotoxic hepatitis can be put in parallel with syphilitic nephrosis or amyloidosis. There, too, we are talking about deep degenerative processes caused by some toxic influences of syphilitic origin, but not by spirochetes directly.

Syphilis can lead to chronic epithelial hepatitis in three ways:

1) as a result of acute hepatitis (“syphilitic jaundice”);

2) as a result of “chronically” acting syphilitic intoxication;

3) as a complication of interstitial gummous hepatitis.

Epithelial hepatitis occurs at any age. At a young age, it is either the result of dystrophic disorders that accompany other manifestations of congenital syphilis (as with lipoid nephrosis), or is combined with congenital interstitial hepatitis. In people aged 20-30 years, chronic epithelial hepatitis is usually the outcome of acute hepatitis (jaundice). At a later age, it develops either as a result of prolonged syphilitic intoxication, or joining gummous hepatitis.

Regarding the pathological picture of this form, it should be emphasized:

1) the intensity of dystrophic changes in liver cells;

2) the severity of the reaction from the reticuloendothelial system (both Kupffer cells and corresponding elements in the spleen and other organs);

3) a relatively high frequency of cases with mixed extra- and intralobular proliferation of connective tissue (often the latter, the insular type, predominates);

4) a relatively weak tendency of the connective tissue of the liver to shrink.

In connection with these features, it is clear that with syphilotoxic hepatitis, the liver retains its increased size longer than with alcoholic cirrhosis.

The specific origin of this type of form is evidenced by individual findings of characteristic manifestations of syphilis in various organs in the form of endarteritis, periarteritis, single gummas, etc., detected during pathological examination.

Clinically, most cases of syphilotoxic hepatitis are quite severe suffering, progressing relatively quickly, previously described as “syphilitic cirrhosis.” In the first stage, there is usually a general malaise, heaviness in the hypochondrium, sometimes itchy skin, poor appetite, and increased nervousness. The liver is enlarged, usually smooth, almost painless. Jaundice appears quite early and varies in intensity. Functional disorders of the liver are more pronounced than with alcoholic hepatitis. The spleen usually enlarges, sometimes even earlier than the liver. It is known that other, extrahepatic, localizations of late syphilis are sometimes accompanied by an enlarged spleen.

In the second stage, the liver becomes denser and somewhat smaller, but usually it retains its increased size and smooth surface for a long time. Collaterals are rarely formed and are weakly expressed. Despite this, ascites appears only in a very late period of the disease and does not reach the degrees that are expressed in portal cirrhosis. These features are due to the low tendency of fibrous liver tissue to shrink.

The bleeding that sometimes appears is not mechanical, but mostly dyscratic in nature and is rarely profuse. Anemia is common and is often macrocytic in nature. A common occurrence is leukopenia. Monocytosis occurs frequently to a severe degree. Damages to the cardiovascular system, nervous system and kidneys are often observed as parallel manifestations of syphilis.

The course of the disease in comparison with other forms of liver syphilis is the least favorable. The disease is usually progressive, the duration of the disease varies between 2 and 5 years. Death most often occurs from liver failure.

Syphilitic chronic mesenchymal (interstitial) hepatitis

The disease is based on the introduction of pale spirochetes into the liver and the development of productive-infiltrative changes there. Spirochetes enter the liver most often through the hepatic artery, as this applies to acquired syphilis. This is understandable, since in general it spreads predominantly hematogenously and since the primary foci that create spirochetemia in acquired syphilis are usually located in the general circulation, outside the portal vein system. The second route, through the portal vein, plays a major role in congenital syphilis (spirochetes enter through the placenta and umbilical vein). With acquired syphilis, this route is of relatively little importance and only with syphilitic foci in the abdominal cavity, primary syphilis of the stomach or spleen, etc., although, of course, the possibility of penetration of spirochetes into the portal blood from the arterial system under any conditions is not excluded. The lymphatic route plays a minimal role (for example, in cases where syphilitic lesions are located in the immediate vicinity of the liver or in the mesenteric or portal lymph nodes).

Gummy hepatitis is usually detected 10-20 years after infection. It is therefore clear that the disease is observed more often in the elderly. However, there are known cases of hepatitis that developed within a year after infection.

This type of hepatitis occurs in syphilis in two forms: in the form of limited gummous hepatitis and in the form of miliary gummous or diffuse interstitial hepatitis.

Focal gummous hepatitis

The pathological picture of focal gummous hepatitis consists of the formation of gummas in the liver, the size of which ranges from a millet grain to an apple. In some cases there are several large gummas, in others there are many small ones.

Gummas are most often located in the peripheral parts of the liver, under the peritoneal layer covering the liver, but they are also found deep in the liver. More often they are found on the upper surface of the liver; on the lower surface they are located mainly in the Spigelian lobe, i.e., near the trunk of the portal vein and the common hepatic duct, and at a certain size they can compress these organs. Sometimes gummas are located along the anterior edge of the liver and protrude into the abdominal cavity.

When examined, gummas look like convex tumors with round or irregular outlines; The color of fresh gums is pink, old ones are whitish-yellowish. Over time, gummas, as a result of wrinkling of the connective tissue included in their composition and encapsulating them, become denser, and in the center of them a curdled mass is formed, which can then calcify and petrify. In other cases, the gumma, undergoing necrosis in the center, softens and suppurates. A dense fibrous tissue like a capsule forms around it.

Histologically, in the initial period of gumma formation, an infiltrate of round cells of blood and local mesenchymal origin (lymphocytes, plasma cells, eosinophils, sometimes giant cells) is found; the number of small vessels around the infiltrate sharply increases. This new vascular formation gives the peripheral layer of the gumma the character of granulation tissue; later, endarteritis and endophlebitis develop, collagen fibers multiply in the peripheral parts and fibrous cords form.

Necrotization of gummas in the center usually occurs after scar tissue has formed around the gummas. In necrotic masses, the contours of blood vessels are sometimes preserved. In the same liver you can find different stages of gumma development. In some patients, fibroblastic and sclerotic processes predominate in the gummous liver, in others - phenomena of gum disintegration; the epithelial tissue of the liver in the areas of gummas undergoes atrophy, in others it is normal. Scars after gummas or around them have a radiant and retracted appearance. Gummy changes, if they develop close to the surface of the liver, are usually accompanied by limited perihepatitis, in the form of thickening of the serous membrane covering the liver: sometimes a number of adhesions with neighboring organs are created around the liver. Large vessels are often changed (endarteritis of the hepatic artery, pylephlebitis of the portal vein). Sometimes lymph nodes affected by syphilis are found in the gates of the liver. The outcome of gummous hepatitis is a syphilitic “lobulated liver”: the organ is furrowed with slits, all in tubercles, disconnected from the rest of the tissue. In some cases, only one lobe is disfigured.

In other organs and tissues there are changes that develop in parallel due to the same infection (aortitis, etc.).

The clinical picture of focal gummous hepatitis can give a wide variety of symptoms and simulate many diseases; it is mistaken for cholelithiasis disease, malaria, stomach or liver cancer, etc. One of the early signs of the disease is pain in the right hypochondrium or in the epigastric region. The pain is quite intense. They are either long-lasting, lasting several hours or days, or acute and short-lived, cramp-like in nature. From time to time they weaken and then strengthen again; Like other syphilis pains, they can get worse at night. The pain usually lasts throughout the entire disease, but sometimes it is limited only to the initial period, and then goes away. They are explained by an inflammatory process that involves the nerve-rich Glissonian capsule and sometimes the peritoneum. In rare cases they are absent.

Another characteristic symptom is fever. The temperature usually fluctuates between 37°C and 38°C, but can periodically rise higher - up to 39°C. It can be irregular, often remitting, and sometimes there are sudden rises for 2-3 days, accompanied by chills. At times, the temperature may be normal for several days, weeks, and occasionally even months. Rise in temperature reflects an active inflammatory process in the liver, which can either worsen and invade new areas of the organ, or subside; The decay and suppuration of gummas explain, in addition to fever, also chills.

The most important and constant sign of the disease is uneven enlargement of the liver. Sometimes large bumps emanating from the liver are already visible to the eye, or the entire liver area bulges out. Often one lobe of the liver enlarges or protrusions are felt on the surface or along the edge of the liver; they can be flat, round, lumpy. There is usually soreness in the area of ​​the protrusions. In the early period, the consistency of the liver is not particularly dense: the gummas themselves are usually denser than the rest of the tissue of the organ. In the later period, the liver becomes smaller and denser, the protrusions can even acquire cartilaginous density. Sometimes, on the contrary, the mounds soften and even acquire the property of swaying. Peritoneal friction noise is sometimes detected above the tubercles.

There is usually no jaundice. Only in rare cases does it appear, sometimes even early, in cases where gummas compress large bile ducts (in this case, jaundice is mechanical in nature and there are no functional disorders of the liver). Jaundice can develop in the late period, when the function of the liver tissue begins to be impaired, urobilinuria appears, disturbances in the synthetic ability of the liver, etc. The spleen in gummous hepatitis is rarely palpable, mainly in the late stage, if portal hypertension develops. Portal hypertension, however, in many cases does not develop, and ascites and collaterals are absent. There may be cases of ascites that develops as a result of compression of the portal vein trunk by gums or scars at the porta hepatis. The composition of the blood has changed little. Only in severe forms there is moderate anemia. Slight leukocytosis is common. The general condition of the patients is initially good. In the later stages, it is disrupted and weight drops.

The outcome of focal gummatous hepatitis in cases with a small number of gummas is favorable: gummas can undergo resorption and scarring. In cases of large changes, severe consequences may develop; portal hypertension with bleeding from the gastrointestinal mucosa, perihepatitis with the transition of the inflammatory process to neighboring organs (pleura, lungs, stomach) and mechanical disorders in them, etc. In the case of suppuration, gummas can serve as a source of purulent diseases of adjacent organs (subphrenic abscess, encysted purulent peritonitis, etc.). Hemorrhages in the liver are possible due to rupture of the vessel. The disease continues for many years, but is difficult to account for (gummas in the liver are sometimes found at autopsy in people who were not expected to have liver disease during their lifetime).

Miliary gummous, or diffuse interstitial, hepatitis

With miliary gummous hepatitis, a uniform enlargement of the liver is observed; its surface is dotted with small whitish plaques or nodules (about the size of a millet grain or smaller). In the later phases of the disease, the liver may shrink. On microscopic examination, the liver is dotted with granulomas, consisting of round mesenchymal elements of local and blood origin (reticuloendothelial elements, lymphocytes, neutrophils, eosinophils), around them there are capillary networks and collagen fibers, later endophlebitis and endarteritis of small vessels are formed. As a result, the center of the lesions becomes necrotic and scars form in place of the granules. Along with this granulomatous form, there is a common form of syphilitic inflammation of the liver. In this case, there is a diffuse infiltration of small cells around the blood vessels throughout the liver.

Infiltrates may also undergo necrotization, resorption, or replacement by scar tissue. Over time, significant fibrosis of the organ forms, resembling annular cirrhosis in the pattern in the sense that the connective tissue multiplies mainly between the lobules (i.e., where granulomas and infiltrates are located adjacent to the vessels). With this form, the spleen is often enlarged with changes in it similar to those observed with cirrhosis of the liver.

The clinical picture of this form of syphilitic hepatitis differs in many respects from that of the epithelial and gummous focal forms.

The first stage is characterized by:

Uniform enlargement of the liver with slight compaction;

Painful phenomena from the liver and its soreness when palpated (however, the pain is not as severe as in the focal form, and is less likely to be paroxysmal in nature);

Increased temperature (but the fever is still not high);

Enlarged spleen (whereas in the focal form the spleen is usually not enlarged);

Absence of jaundice (at the same time, there is no obstructive jaundice, which sometimes develops in a focal form due to compression of the bile ducts by gums);

The absence of functional disorders of the liver (in contrast to chronic syphilitic epithelial hepatitis).

Nutrition, the state of the gastrointestinal tract, the cardiovascular system, and blood composition are disturbed relatively little.

In the second stage, the liver shrinks and becomes denser, symptoms of portal congestion appear, including ascites, health worsens, and patients lose weight.

The outcome of the disease is less favorable than with focal hepatitis, although the course is long. Death occurs from the same reasons as with cirrhosis of the liver in general.

Liver with congenital syphilis

With congenital syphilis, liver damage can be of different types. Pathologically, two forms of congenital liver syphilis are distinguished:

1) flint liver;

2) gummous liver.

The first term refers to the liver, in which there are sharp changes in both the parenchyma and the interstitium in the form of small islands distributed throughout the organ; the liver is enlarged, heavy and dense. The second term refers to gummous hepatitis.

Clinically, hepatitis in early congenital syphilis is distinguished from hepatitis in late congenital syphilis. With early congenital syphilis, in addition to hepatitis, there are other signs that quite clearly depict the general disease (senile appearance of children, cachexia, pemphigus, etc.); children die quickly. With late congenital syphilis, liver damage produces the same syndromes as with acquired syphilis, with some, however, features:

With congenital syphilis, there is a greater tendency to form ascites due to the development of pylephlebitis of the portal zone;

The spleen enlarges more strongly and early;

There are such common stigmata as infantilism, skull deformation, changes in limbs, teeth, keratitis, etc.

“Flint liver” is observed with early syphilis, other forms – with late syphilis.

Diagnosis of syphilitic hepatitis

To recognize chronic syphilitic hepatitis (various forms), the Wasserman reaction, the corresponding history (including family history) and simultaneous damage to other organs by syphilis (aortitis, aortic valve insufficiency, syphilitic disease of the cerebral vessels, tabes of the spinal cord, syphilis of the motor organs, stomach, lungs, etc.), as well as such traces of former syphilitic lesions as radiant scars on the skin and mucous membranes, bone deformation, enlarged lymph nodes, pigmentation disorders, and developmental defects.

If we take together all forms of chronic syphilis of the liver, then the Wasserman reaction turns out to be negative quite often (40% of cases); a negative response is more often obtained with epithelial hepatitis, while with gummous hepatitis the reaction is positive in 80% of cases. Since infection with syphilis sometimes occurs without a primary affect, it is clear that in many cases both the fact of infection and its duration cannot be established.

Parallel damage to other organs should be assessed with reasonable caution when making a diagnosis: sometimes it is due to it, and not due to liver damage, that the Wasserman reaction can be positive. Proving the specificity of extrahepatic lesions by the specificity of the process in the liver and, conversely, the specificity of the process in the liver by damage to other organs, one should keep in mind the possibility of a combination of diseases of different ethnologies. But still, if a patient with liver damage has a positive Wasserman reaction, then the hepatic process should be considered syphilitic, especially in cases where there are no other localizations of syphilis, and even more so when the history and the very nature of the liver disease correspond to a similar etiology.

The effect of antisyphilitic treatment is very important for recognition.

Treatment

Treatment of syphilitic chronic hepatitis should include both nonspecific and specific agents.

Specific drugs include the administration of penicillin derivatives. However, if the patient is allergic to penicillin or the patient’s strain of Treponema pallidum is resistant to penicillin and its derivatives, it is possible, as an alternative treatment, to use drugs such as erythromycin or tetracycline derivatives, as well as cephalosporins.

In case of tertiary syphilis and high resistance of treponema pallidum to antibiotics, in the case of a satisfactory general condition of the patient, bioquinol, miarsenol and novarsenol can be used as additional therapeutic drugs.

Nonspecific treatment of syphilitic hepatitis includes the use of vitamin preparations, adherence to a dietary regimen, etc.

Prevention

Prevention of chronic hepatitis due to syphilis consists, of course, in the general fight against syphilis and vigorous treatment of syphilis after its detection, followed by long-term monitoring with the Wasserman reaction. A huge role in the development of liver damage is played by the absence or insufficiency of timely treatment of syphilis: most patients with tertiary liver syphilis were not treated at all or were clearly insufficiently treated. This especially applies to patients whose syphilitic infection went undetected for a long time.

Health education, clinical examination, etc. are of great importance in the prevention of liver syphilis.

As for congenital syphilis, in addition to general social and preventive measures, mandatory examinations of pregnant women and careful timely treatment of syphilis discovered in them play an important role.

The information presented in this article is intended for informational purposes only and cannot replace professional advice and qualified medical care. If you have the slightest suspicion that you have this disease, be sure to consult your doctor!