1. Acute viral hepatitis B.
It is clinically divided into jaundiced type and non-jaundiced type. The course of acute jaundice type B hepatitis is about 2 to 4 months, and the clinical course can be divided into 3 periods.
(1) Pre-jaundice: The onset can be acute or slow, with non-specific symptoms of infection toxicity such as low-grade fever, peripheral discomfort, fatigue, and joint aches. Digestive system symptoms are highlighted by loss of appetite, nausea, vomiting, abdominal pain, etc.
Extrahepatic lesions and serum sickness-like syndromes may occur in the pre-jaundice period, manifested as: arthralgia and arthritis, urticaria and angioneurotic edema, vascular inflammatory lesions, renal lesions, purpura, plasma membrane inflammation, myocarditis, pancreatitis, etc. The severity and duration of pre-jaundice symptoms can vary greatly, ranging from a few days-2 weeks, or there can be no obvious pre-jaundice, and jaundice as the first symptom.
(2) Jaundice: The initial finding is often a deepening of urine color, followed by sclera and skin yellowing, reaching a peak within 1~2 weeks, reflecting an increase in the concentration of bilirubin in the serum, a lightening of stool color, itching of the skin, etc., and an increase in liver function transaminases. Physical examination may reveal a mildly enlarged liver with soft texture, tenderness and percussion pain, and a few children may have a large spleen. The jaundice period is mostly 2~4 weeks.
(3) Remission period: jaundice subsides, symptoms improve, serum transaminases decrease, and most children recover within 2 weeks to 4 months. However, some patients may become chronic. age at the time of HBV infection is the most important factor affecting chronicity. Among those infected with HBV in the perinatal period and infancy, 90% and 25%-30%, respectively, will develop chronic infection, while only 5%-10% of those infected after age 5 will develop chronic infection.
Acute non-jaundiced hepatitis is more common than jaundice, the symptoms are more symptomatic, or even no obvious symptoms, abnormal liver function, but does not appear jaundice.
2, chronic hepatitis B.
The duration of H BV infection more than 6 months, from the acute hepatitis B delayed and developed into chronic hepatitis, or because of the insidious onset of hepatitis B, to be clinical onset of disease when it has become chronic. Based on serology, virology, biochemical tests and other clinical and ancillary findings in H BV-infected patients, chronic HBV infection can be classified as.
(1) Chronic hepatitis B
(1) HBeAg-positive chronic hepatitis B: serum HBsAg, HBeAg-positive. Anti-HBe negative, HBV DNA positive, ALT persistently or repeatedly elevated, or hepatitis lesions on liver histological examination.
② HBeAg-negative chronic hepatitis B: positive serum HBsAg, persistent negative HBeAg, positive or negative anti-one HBe, positive HBV DNA, persistent or recurrent abnormal ALT, or hepatitis lesions on liver histological examination.
The above two types of chronic hepatitis B can also be further classified as mild, moderate and severe based on biochemical tests and other clinical and ancillary findings.
(2) Carriers
(1) Chronic HBV carriers: Mostly HBsAg, HBeAg and HBV DNA positive individuals in the immune tolerance period, with more than 3 consecutive follow-ups within 1 year showing serum ALT and AST in the normal range and no significant abnormalities in liver histological examination.
Inactive HBsAg carriers: serum HBsAg positive, HBeAg negative, anti-HBe positive or negative, HBV DNA below the minimum detection limit, more than 3 consecutive follow-ups within 1 year, ALT all in the normal range. Liver histology showing Knodell’s Hepatitis Activity Index (HAI) <4< font=""> or mild lesions as determined by other semi-quantitative scoring systems.
(3) Occult chronic hepatitis B
Negative serum HBsAg, but positive HBV DNA in serum and/or liver tissue with clinical manifestations of chronic hepatitis B. In addition to HBV DNA positivity, patients may have positive serum anti-HBs, anti-HBe and/or anti-HBc, but about 20% of patients with occult chronic hepatitis B are negative for serologic markers. Diagnosis requires exclusion of liver injury caused by other viral and non-viral factors.
(iv) Hazards of pediatric hepatitis B
1. Hepatitis B cirrhosis
Hepatitis B cirrhosis is the result of the development of chronic hepatitis B. Its pathology is defined as diffuse liver fibrosis with pseudobullet formation.
①Compensated cirrhosis: generally of Child-Pugh grade A. There is evidence of hepatocyte synthetic dysfunction or portal hypertension (such as hypersplenism and esophagogastric fundic varices) on imaging, biochemistry or hematology, or histology consistent with a diagnosis of cirrhosis without serious complications such as bleeding from ruptured esophagogastric varices, ascites or hepatic encephalopathy.
②Decompensated cirrhosis: Generally of Child-Pugh grade B or C. Patients have had serious complications such as ruptured bleeding from esophagogastric fundic varices, hepatic encephalopathy, and ascites.
The compensated and decompensated stages of cirrhosis can also be subdivided into active or quiescent stages.
2. Hepatocellular carcinoma: It mostly occurs in chronic hepatitis and post-hepatitis cirrhosis, and 82.6% of patients with hepatocellular carcinoma have different degrees of cirrhosis. Hepatitis B virus infection is an independent risk factor for hepatocellular carcinoma.
3. Damage to extra-hepatic organs: such as hepatitis B-related nephritis, hepatitis B-related cardiomyopathy, etc.