Hepatitis D

　　The pathogenesis and immunity of hepatitis D virus (HDV) are not yet clear. It is generally believed that HDV has a direct cytopathic effect on liver cells. HDV is a defective single-stranded negative-chain RNA virus and must depend on hepatitis B virus (HBV) and other hepatotropic DNA viruses to provide a coat in order to replicate. HDV exists in the nuclei of liver cells and serum of HDV-infected individuals with positive HBsAg, mainly replicating within liver cells. HDV is prone to mutation, and after human infection with HDV, the synthesis of HBV-DNA can be significantly suppressed. The appearance of HDAg is consistent with the decrease of HBV-DNA in serum. With the negative conversion of HDAg and the appearance of anti-HD, HBV-DNA returns to the original level. It is mainly transmitted through blood transfusion and blood products, similar to the transmission mode of hepatitis B. HDV infection is common in HBV carriers, and sporadic HDV infection can also be seen. After the co-infection of HDV and HBV, it can promote the aggravation of liver damage and is prone to develop into chronic active hepatitis, liver cirrhosis, and severe hepatitis.

　　The clinical manifestations of hepatitis D patients depend on the original HBV infection status. The incubation period is 4 to 20 weeks.Common symptoms include decreased appetite, abdominal distension, aversion to greasy food,. Nausea, vomiting, and easy fatigue.. Hepatitis D is prone to complications such as liver cirrhosis, chronic active hepatitis, and severe hepatitis.

　　The clinical manifestations of hepatitis D after infection with HDV depend on the original HBV infection status. The incubation period is 4 to 20 weeks.Common symptoms include decreased appetite, abdominal distension, aversion to greasy food,. Nausea, vomiting, and easy fatigue.Some patients may have jaundice of the sclera or skin, fever, hidden pain in the liver area, liver enlargement, and tenderness. Some patients may develop spider angiomas and liver palms. The disease. . There are the following two types:.

　　1. Simultaneous infection with HDV and HBV

　　Simultaneous infection with HDV and HBV is seen in patients without a history of HDV infection, and the clinical manifestation is acute hepatitis D. The clinical symptoms are similar to acute hepatitis B, and there are two peaks of bilirubin and ALT elevation during the course of the disease. HBsAg appears first in the serum, followed by the positivity of HDAg in the liver. In the acute phase, the positivity of HDAg in the serum persists for a few days before turning negative, followed by the positivity of anti-HDIgM, which has a short duration and low titer. Anti-HDIgG is negative.

　　2. HDV and HBV superinfection

　　The clinical manifestations of HDV and HBV superinfection are diverse, ranging from acute hepatitis to chronic hepatitis and severe hepatitis. It is more common in chronic HBV carriers, and the symptoms are mainly determined by whether the patient was a chronic HBsAg carrier before the HDV infection or a chronic liver disease patient with HBV. If the patient is a HBsAg carrier, after infection with HDV, the symptoms will resemble acute HBsAg-positive hepatitis, but with negative anti-HBVIgM, which is more severe than a simple HBV infection. If the patient has chronic liver disease with HBV, due to the persistent infection of HBV and the continuous replication of HDV, the existing liver tissue lesions may worsen, and it may manifest as an acute hepatitis attack or accelerate the development of chronic active liver disease and liver cirrhosis. Therefore, when encountering chronic hepatitis B, if the original condition is stable and the symptoms suddenly worsen, even leading to liver failure, it is very similar to severe hepatitis, and it should be considered as a possible superinfection with HDV.

　　The condition of hepatitis D is often related to the infection mode of the hepatitis D virus, which includes co-infection and superinfection. Prevention should start from these two aspects.

　　1. Co-infection

　　Simultaneous infection with both HDV and HBV may lead to two types of conditions:

　　1. Acute D hepatitis virus-related hepatitis. Its clinical and biochemical characteristics are similar to those of simple hepatitis B, with mild symptoms and not severe liver tissue damage. HDV in the liver appears only transiently, and the disease often presents as self-limiting.

　　2. Fulminant hepatitis. If a large amount of HDV is infected at one time, it can lead to a relatively serious outcome. Clinical symptoms and liver damage are severe, with a high mortality rate.

　　2. Overlapping infection

　　Infection with HDV on the basis of chronic HBV, the classification is as follows:

　　1. Self-limiting hepatitis. Generally, clinical symptoms are not severe, the course is short, and there is a tendency to self-limit and recover. Hepatitis B surface antigen carriers are the target of D hepatitis virus attack.

　　2. Chronic progressive D hepatitis. This is the deterioration of chronic hepatitis B or the progression of asymptomatic hepatitis B virus carriers to progressive active hepatitis. The condition is severe, with progressive development, which can lead to liver cirrhosis with poor prognosis.

　　For D hepatitis tests, the detection of D hepatitis virus antigen (HDAg) and D hepatitis virus antibody (anti-HD) in serum is generally performed using enzyme-linked immunosorbent assay (ELISA). In addition, immunohistochemistry can be used to detect HDAg in liver tissue, and HDVcDNA probes can be used to detect HDV-RNA in serum. This method has high sensitivity and can improve the detection rate of serum HDV.

　　1. Liver function tests

　　Liver function tests include bilirubin, turmeric turbidity test, AST, ALT, A/G, prothrombin time, and serum protein electrophoresis.

　　2. Specific serological etiological examination

　　Specific serological etiological examination includes HBsAg, anti-HBs, HBeAg, anti-HBe, anti-HBc, and anti-HBcIgM. If conditions permit, HBV-DNA, DNA-p, Pre-S1, Pre-S2, and other tests can be performed. In situ hybridization technology is used to detect HBV-DNA within the liver.

　　With the increasing incidence of D hepatitis in China year by year, the treatment of D hepatitis is receiving more and more attention from people. However, there is still no satisfactory treatment for the D hepatitis virus to date, so lifestyle adjustments have received widespread attention from patients. Below, let's understand the pros and cons of D hepatitis food therapy in detail:

　　1. What is good for D hepatitis patients to eat?

　　1. Ensure an adequate supply of calories, with an appropriate amount being 8400-10500 kilojoules (2000-2500 calories) per day.

　　2. Carbohydrates can generally account for 60-70% of total calories.

　　3. Promote the repair and regeneration of liver cells, and increase the supply of protein, which should generally account for 15% of total calories. It is especially important to ensure a certain amount of high-quality protein, such as animal protein and soy products.

　　4. Ensure the supply of vitamins. B vitamins such as vitamin B1, vitamin B2, niacin, and vitamin C play an important role in improving symptoms. In addition to choosing foods rich in these vitamins, it is also possible to take various vitamin preparations orally.

　　5. Ensure an adequate supply of liquid. Drinking more juice, rice gruel, honey water, watermelon juice, and other beverages can accelerate the excretion of toxins and ensure the normal metabolic function of the liver.

　　6. Prioritize the intake of high-quality protein foods such as fish, lean meat, eggs, dairy products, and soy products.

　　7. Increase the intake of fresh vegetables and fruits.

　　Secondly, what foods should dengue patients avoid?

　　1. The high-calorie therapy for hepatitis advocated in the past in dengue food therapy is not advisable, because although high-calorie intake can improve clinical symptoms, it can ultimately lead to fatty liver, which can worsen the condition, so the disadvantages outweigh the benefits.

　　2. The high-sugar diet used in the past should be corrected, because high-sugar diet, especially excessive glucose, fructose, and sucrose, can affect the appetite of patients, worsen gastrointestinal bloating, increase fat storage in the body, and are prone to obesity and fatty liver. The supply of carbohydrates should mainly be through staple foods.

　　3. Avoid fried, baked, and other strongly刺激性 food, limit foods high in nitrogen extracts such as meat soup and chicken soup, to reduce the burden on the liver.

　　4. Strictly prohibit alcohol consumption.

　　5. Be cautious with spicy and other刺激性 food.

　　Through the introduction of dengue food therapy, it can serve as a guide for dengue patients in their daily life. Don't lose heart if you get hepatitis, be positive about treatment, and at the same time adjust your lifestyle, cooperate with the treatment of the disease, and believe that it will definitely have a positive effect on the condition.

　　Dengue hepatitis, also known as delta hepatitis, is an infectious disease caused by the delta hepatitis virus and other hepatotropic DNA viruses such as hepatitis B virus. It is mainly transmitted through blood transfusion and blood products, similar to the mode of transmission of hepatitis B. After HDV and HBV co-infection, it can promote the aggravation of liver damage and is prone to develop into chronic active hepatitis, liver cirrhosis, and severe hepatitis.

　　There is no effective treatment for HDV infection, the key is prevention. Clinical treatment mainly focuses on liver protection and symptomatic treatment. Antiviral drugs such as interferon mainly interfere with the synthesis of HBV-DNA, but have no inhibitory effect on the synthesis of HDV-RNA. If HBV replication decreases, it can increase the synthesis of HDV-RNA. Immune modulators have also not shown improvement. Similar to Hepatitis B. Acute hepatitis is generally treated with symptomatic supportive treatment based on reasonable diet and rest. Chronic hepatitis should be treated with antiviral and immune modulatory therapy in addition to general liver protection treatment.