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diseaseCongenital Syphilitic Cirrhosis
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bubble_chart Overview

With the opening up of our country, the infection rate of syphilis spirochetes has shown a resurgence. Due to the application of specific drugs, congenital syphilis is not common, but due to its high mortality rate, it should be taken seriously. Among patients with congenital syphilis, 80% have liver involvement, possibly because the syphilis spirochetes pass through the placenta, enter the umbilical vein, and finally reach the liver. Both congenital syphilis and erythroblast tumor diseases can lead to jaundice, and the two are easily confused, but serological tests for children with congenital syphilis are all positive.

bubble_chart Pathological Changes

The pathological changes of this type of hepatitis resemble those of hepatitis A, featuring ballooning degeneration of hepatocytes, spotty or focal necrosis, and inflammatory cell infiltration in the portal area, primarily lymphocytes and mononuclear macrophages. There is significant gall fel stasis. Electron microscopy observations suggest that the liver cell damage in this disease may be related to a T-cell-mediated immune response.

bubble_chart Clinical Manifestations

The incubation period is 10 to 60 days, with an average of 40 days. According to three domestic epidemiological surveys of hepatitis E, the incubation period is 15 to 75 days, with an average of 36 days. Adult infections mostly manifest as clinical types, while children present as subclinical types. Clinical symptoms and liver function damage are more severe. Generally, it is subclinical. Clinical symptoms and liver function damage are more severe. The onset is usually acute, with jaundice being common. Half of the cases have fever, accompanied by lack of strength, nausea, vomiting, and liver area pain. About one-third experience arthralgia. Common gallbladder stasis symptoms, such as cutaneous pruritus and light-colored stools, are more pronounced than in hepatitis A. Most patients have hepatomegaly, while splenomegaly is less common. Jaundice in most patients subsides in about 2 weeks, with the course of the disease lasting 6 to 8 weeks, and generally does not progress to chronicity. Pregnant women infected with HEV have severe conditions and are prone to liver failure, especially in the advanced stages of pregnancy, with a high mortality rate (10-39%). Late abortion and dead fetus may occur, possibly related to low levels of serum immunoglobulins.

HBsAg-positive individuals with overlapping HEV infection have aggravated conditions and are prone to developing acute severe hepatitis.

bubble_chart Auxiliary Examination

Specific serological etiological examination is the basis for diagnosis.

1. Enzyme-linked immunosorbent assay (ELISA) detects anti-HEV IgM in serum, which is an indicator for the diagnosis of acute hepatitis E. Recombinant or synthetic polypeptides are used as antigens. This method was applied to detect 111 cases of acute hepatitis E in China, with an anti-HEV positive rate of 86.5%. Among 32 patients in the convalescence stage, the anti-HEV positive rate was 6.3%, suggesting that anti-HEV has a short duration, and 63% turned negative 5-6 months after the illness.

2. Western Blot (WB) is more sensitive and specific than ELISA, but the operation is more complex and the detection time is longer.

3. Polymerase Chain Reaction (PCR) is used to detect HEV-RNA in the serum and feces of hepatitis E patients. This method has high sensitivity and specificity, but laboratory contamination during operation can easily lead to false positives.

4. Immunoelectron microscopy (IEM) and immunofluorescence (IF) are used to detect HEV particles and HEV antigen (HEAg) in the feces, gallbladder, and liver tissues of hepatitis E patients. However, both methods require special equipment and techniques, and HEV exists for a short time in liver tissues, gallbladder, and feces, with a low positive rate, making them unsuitable for routine examination.

bubble_chart Diagnosis

The diagnosis should be based on clinical features and liver function tests, with reference to epidemiological data. Exclude infections caused by HAV, HBV, HCV, and other causes of acute liver damage.

bubble_chart Treatment Measures

Proper rest and reasonable nutrition should be the main focus, with selective use of medication as a supplement. Alcohol should be avoided, overexertion should be prevented, and liver-damaging drugs should be avoided. Medication should be kept simple rather than complicated.

1. Early strict bed rest is most important. If symptoms significantly improve, activity can be gradually increased, with the principle of not feeling fatigued. Treatment should continue until symptoms disappear, the isolation period ends, and liver function returns to normal, at which point the patient can be discharged. After 1 to 3 months of rest, the patient can gradually return to work.

2. The diet should be tailored to the patient's taste and consist of easily digestible, light foods. It should include a variety of vitamins, sufficient calories, and an appropriate amount of protein. Fat should not be overly restricted.

3. For patients with reduced food intake or vomiting, a 10% glucose solution of 1000-1500ml with 3g of vitamin C, 400mg of liver-protecting agents, and 8-16U of regular insulin should be administered intravenously once daily. Energy mixtures and 10% potassium chloride can also be added. For those with severe heat, modified Yin Chen Stomach Poria Decoction can be used; for those with both dampness and heat, modified Yin Chen Hao Tang and Wei Ling He Fang can be used; for liver qi depression, Peripatetic Powder can be used; for spleen deficiency with dampness retention, Stomach-Calming Powder can be used. Some advocate for the heavy use of Red Peony Root for deep jaundice, which can be effective. Generally, acute hepatitis can be cured.

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