Intrahepatic HDAg positive only transiently

Introduction Acute hepatitis D, one of the clinical diagnoses of hepatitis D virus, refers to simultaneous HDV/HBV infection. The incubation period is 4 to 20 weeks. The clinical manifestations and biochemical characteristics are similar to those of acute hepatitis B alone, which may include fatigue, loss of appetite, jaundice and liver swelling and pain. Some patients have two peaks of transaminase. Due to the short time of acute hepatitis B HBV, HDV infection often ends with the disappearance of HBV, so HDAg in the liver is only transiently positive, serum anti-HDIgM is transiently elevated with low titer, and then secondary anti-HD IgG appears. . The majority of HDV/HBV infections have a good prognosis. The risk of developing chronic hepatitis is no higher than that of HBV infection alone. A few patients can develop severe hepatitis.

Cause

(1) Causes of the disease

The intact HDV particles are spherical, 35 to 37 nm in diameter, contain HDV RNA and HDAg, and have a shell of HBsAg. HDV RNA is the genome of HDV, consisting of 1679 to 1683 nucleotides, which is single-stranded, circular, and can be folded into a non-branched rod-like structure. HDV-RNA has 9 coding regions (ORFs) and ORF5 encodes HDAg. HDAg is a nuclear protein that allows the body to induce anti-HDIgM and anti-HDIgG. Anti-HDIgM appeared earlier, generally positive in the early stage of acute HDV infection, and the recovery period gradually disappeared. The sustained high titer of anti-HDIgM suggested chronic disease. Anti-HD IgG appeared later, and it was found to be positive for many years and low titer after 3 to 8 weeks after onset. Anti-HD IgG was elevated during disease activity. Current infections often show anti-HDIgM positive, while previous infections are anti-HDIgM negative and anti-HDIgG positive. Anti-HD is not a neutralizing antibody and can still be infectious when positive.

HDV infection significantly inhibits the synthesis of HBV DNA. Serological tests have shown that HDAg appears to be consistent with a decrease in HBV DNA in serum, and that as HDAg expression increases, HBV DNA decreases. At the peak of HDAg expression, HBV DNA often disappeared, but with the appearance of HDAg-negative and anti-HD, HBV DNA returned to its original level. It has been previously thought that the assembly of HDV relies on the synthesis of HBsAg, and its replication and expression also require the assistance of HBV or other hepadnaviruses. In vitro transfection assays have demonstrated that HDV-RNA replication and HDAg expression do not require the help of hepadnaviruses. HDV itself can be done independently, but in the formation of intact HDV, it must be provided by a hepadnavirus.

(two) pathogenesis

Clinical and animal experiments showed that after HDV infection, liver function damage was directly proportional to serum and intrahepatic HDAg titer. In situ hybridization was used to detect the distribution of HDV RNA in liver cells in areas with obvious damage to liver cells. Therefore, HDV is considered to be directly Caused by liver cell damage. Some scholars have also found that patients with chronic hepatitis B or HBsAg overlap with HDV infection, and the clinical manifestations vary from normal to mild inflammation to severe hepatic necrosis, accompanied by heavier inflammatory cell infiltration in the portal area, suggesting hepatitis D. In addition to the direct cytotoxicity of HDV, the pathogenesis is related to the host's immune response.

an examination

Related inspection

MRI examination of liver, gallbladder, pancreas and spleen by liver, gallbladder and spleen

Acute hepatitis D

Refers to HDV/HBV infection at the same time. The incubation period is 4 to 20 weeks. The clinical manifestations and biochemical characteristics are similar to those of acute hepatitis B alone, which may include fatigue, loss of appetite, jaundice and liver swelling and pain. Some patients have two peaks of transaminase. Due to the short time of acute hepatitis B HBV, HDV infection often ends with the disappearance of HBV, so HDAg in the liver is only transiently positive, serum anti-HDIgM is transiently elevated with low titer, and then secondary anti-HD IgG appears. . The majority of HDV/HBV infections have a good prognosis. The risk of developing chronic hepatitis is no higher than that of HBV infection alone. A few patients can develop severe hepatitis.

2. Chronic hepatitis D

It refers to the overlap of HDV infection on the basis of the original chronic HBV infection, and its clinical course mainly depends on the status of HBV infection and the degree of liver damage during HDV infection. Can have the following performance.

(1) Self-limiting hepatitis D: The general clinical symptoms are not serious, and the course of disease is short. It can also manifest as typical acute HBsAg-positive hepatitis, and has a tendency to self-limiting recovery. After HBV carriers were infected with HDV, HDAg first appeared in the liver, followed by HDAgemia, and serum anti-HDIgM and IgG were positively converted. Once HDV is cleared, anti-HDIgM decreases, while anti-HD IgG maintains high levels for several years. Only a small number of patients with overlapping infections have recovered from this self-limiting condition, and most of them are prone to develop chronic hepatitis.

(2) Chronic progressive hepatitis D: When chronic hepatitis B or HBsAg carriers are infected with HDV, they often show clinical deterioration, or similar acute hepatitis attacks in the chronic process. HDAg in the nucleus of the liver cells continued to be positive, but serum HDAg only transiently appeared, and anti-HDIgM and anti-HD IgG showed high titers and did not decrease. The most common histological change is chronic hepatitis or cirrhosis. The age of the HDV-positive cirrhosis group was much younger than that of the HDV-negative group, indicating that HDV-positive hepatitis is more likely to evolve into cirrhosis.

(3) HDV and severe hepatitis: Govindarajan reported that of the 71 patients with acute severe hepatitis, 24 (33.8%) had HDV markers in the serum, while in the control group, 118 patients with common acute jaundice hepatitis B, only 5 (4.2%) had HDV mark. Li Qifen reported 36 cases (34.3%) of 105 cases of HDV/HBV double infection in severe hepatitis. Other authors have also found similar situations, suggesting that overlapping HDV infections in severe hepatitis should be taken seriously.

For patients with hepatitis B and HBsAg who are significantly fluctuating or progressively deteriorating, and for patients with severe hepatitis, the possibility of simultaneous or overlapping HDV infection should be considered. The diagnosis depends on laboratory tests.

1. Acute HDV/HBV infection: Patients with acute hepatitis, except for acute HBV infection markers, serum anti-HDIgM positive, anti-HDIgG low titer positive; or serum and/or intrahepatic HDAg, HDV-RNA positive.

2. HDV/HBV overlap infection: chronic hepatitis B patients or chronic HBsAg carriers, serum HDV-RNA and/or HDAg-positive; or anti-HDIgM and anti-HD IgG high titer positive; or intrahepatic HDV-RNA and (or) HDAg positive.

Differential diagnosis

The disease is easy to distinguish from liver diseases such as hepatitis A, hepatitis C, and drug-induced liver disease.

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