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Hepatitis virus-associated rheumatic disease

  Hepatitis virus-associated rheumatic diseases refer to chronic active hepatitis caused by hepatitis viruses, also known as chronic progressive hepatitis. It is a systemic inflammatory disease mainly involving liver damage, caused by immune mechanisms. Its characteristics include: ① Typical histological changes in liver disease; ② In addition to liver lesions, there are also features of multi-system damage; ③ Multiple immunological abnormalities. Among the currently known types of hepatitis viruses (A, B, C, D, E, G), the first five types can be accompanied by chronic extrahepatic tissue and organ damage, with type B (HBV) being the most prominent, followed by type C (HCV), type D (HDV), type A (HAV), and type E (HEV) in descending order. Type G hepatitis virus has not been successfully isolated in China, and there are no case reports. Saint et al. (1953) first discovered a progressive inflammatory disease with poor prognosis, characterized by infectious hepatitis as an early manifestation, and named it chronic active hepatitis. Joske (1955) emphasized that the progressive development of viral hepatitis is related to lupus cell phenomenon, thus proposing to name this chronic progressive liver disease as 'lupoid hepatitis', but it has now been completely confirmed that this liver disease is completely different from the liver disease of systemic lupus erythematosus. Saint et al. (1953) first discovered a progressive inflammatory disease with poor prognosis, characterized by infectious hepatitis as an early manifestation, and named it chronic active hepatitis. Joske (1955) emphasized that the progressive development of viral hepatitis is related to lupus cell phenomenon, thus proposing to name this chronic progressive liver disease as 'lupoid hepatitis', but it has now been completely confirmed that this liver disease is completely different from the liver disease of systemic lupus erythematosus.

 

Table of contents

1. What are the causes of hepatitis virus-related rheumatic diseases
2. What complications can hepatitis virus-related rheumatic diseases easily lead to
3. What are the typical symptoms of hepatitis virus-related rheumatic diseases
4. How should hepatitis virus-related rheumatic diseases be prevented
5. What kind of laboratory tests need to be done for hepatitis virus-related rheumatic diseases
6. Dietary taboos for patients with hepatitis virus-related rheumatic diseases
7. Conventional methods of Western medicine for the treatment of hepatitis virus-related rheumatic diseases

1. What are the causes of hepatitis virus-related rheumatic diseases

  First, the cause of the disease

  1. Hepatitis A virus (HAV):It is a ribonucleic acid virus (RNA), many of its characteristics are similar to those of enteric micro ribonucleic acid viruses, belonging to the family of micro ribonucleic acid viruses, genus Enterovirus type T2, virus diameter 27-32nm,呈symmetric icosahedron. Under electron microscopy, hollow and solid particles can be seen, the former without nucleic acid, which can be stained and permeable, and the latter containing nucleic acid, which cannot be stained and permeable. There is no difference between the two in immunology. It can be inactivated by formaldehyde, chlorine, ultraviolet light, and heating to 98℃ for one minute.

  2. Hepatitis B virus (HBV):It is a deoxyribonucleic acid (DNA) virus. Electron microscopy shows spherical particles (diameter 22nm), rod-like or tubular particles (diameter 22nm, about 230nm in length), and Dane particles (diameter 42-45nm). It consists of a complete hepatitis B virus composed of a shell and a core. The virus particles can be classified into semi-full, partially semi-full, and hollow types, with the latter two types being defective variants. This disease has three antigen-antibody systems, namely, hepatitis B surface antigen (HBsAg), hepatitis B surface antibody (Anti-HBS), hepatitis B E antigen (HBeAg), hepatitis B E antibody (Anti-HBE), hepatitis B core antigen (HBcAg), and hepatitis B core antibody (Anti-HBC). The complete HBV-DNA genome is composed of 3200-3300 nitrogenous base pairs and is circular, with some double-stranded small molecular DNA containing one long strand (negative strand) and one short strand (positive strand). The complete long strand has a constant length except for gaps at fixed points, while the length of the incomplete short strand is not constant. The nucleotide sequence of the negative strand has four open coding regions, named S, C, P, and X regions, each carrying a start codon and a stop codon, and each region has different characteristics.

  3. Hepatitis C virus (HCV):It belongs to the Flaviviridae family, with a diameter of 50-60nm, a lipid-containing capsid, and is sensitive to chloroform, with a molecular weight of 13724-13733D.

  4. Hepatitis D virus (HDV):It is a defective virus with a diameter of 35-37nm. The outer part is wrapped in a capsid with HBsAg, and the inner part contains hepatitis D antigen (HDAg) and HDV-RNA. Both strands of the HDV-RNA have genetic information and can be expressed independently. The open reading frame 5 (ORF5) located on the complementary strand of the genome can encode a polypeptide consisting of 215 amino acids, namely HDAg. HDAg is a nuclear protein that is heat and acid-resistant but easily inactivated by proteases and alkali. The assembly of HDV must depend on the synthesis of HBsAg, and its replication and expression also require the presence of HBV. Therefore, HDV and HBV are commonly co-infected simultaneously, which is why it is easy to lead to chronic HBV infection. However, the synergistic effect of HDV on chronic HBV infection is not yet clear, and it has been confirmed that HDV alone rarely causes disease.

  5. Hepatitis E virus (HEV):It belongs to a new genus of the Circoviridae family, with circular particles (diameter of 30-32nm), no capsid, with circular protuberances and notches. The viral genome is an 8.51KD single-stranded and double-stranded RNA virus, with about 7600 nucleotides. The HEV from different regions of the world has been confirmed to be a single strain by molecular cloning technology. The genome has three overlapping open reading frames (ORF), which encode non-structural proteins for ORF1, proteins with 7 antigenic determinants for ORF2, and proteins with a high content of base amino acids for ORF3, which may synthesize nucleocapsid proteins.

  Mechanism of Disease

  Currently, it is believed that the liver cell damage and extrahepatic lesions caused by hepatitis virus infection, especially hepatitis B virus, are due to the body's immune response to the virus. The immune response includes antiviral immunity and autoimmune response to liver cells. The former refers to cell-mediated and humoral immunity to viral antigens, while the latter is an immune response against self-target antigens caused by dysfunction in the functional coordination between T cells and B cells.

  1. Deficiency in cell-mediated immunity:Deficiency in cell-mediated immunity is a factor that allows viral antigens to persist, replicate, and reproduce repeatedly within host cells, leading to chronic viral infection. Clinical practice has confirmed that the immune response of cytotoxic T cells to HBsAg on the surface of liver cells infected with hepatitis B virus not only can destroy liver cells but also can elicit autoimmune reactions, causing liver cells of patients with chronic active hepatitis to be repeatedly destroyed. Most scholars currently believe that the liver cell damage in chronic active hepatitis is closely related to lymphocytic toxicity, which is caused by the immune response of sensitized lymphocytes to HBsAg or liver-specific lipoprotein (LSP) on the surface of liver cells. This immune pathological reaction may also be directed against normal liver cell membrane antigens rather than against liver cells infected with hepatitis B virus. The positive cytotoxic response in some HBsAg-negative patients, imbalance in T cell subsets, and decreased function of suppressive T cells are the main reasons for the formation of HBsAg-negative autoimmune chronic active hepatitis.

  2. Factors of humoral immunity:When Alberti discovered it in 1977, only 1/3 of the patients were HBsAg positive. T cells had cytotoxic effects on target cells wrapped with HBsAg, and the cytotoxic index was significantly lower than that of acute hepatitis, indicating that the pathogenesis of chronic active hepatitis cannot be explained by a single cell-mediated immunity, but also involves humoral immunity and other factors. The pathogenic effect of humoral immunity is mainly related to several antigen-antibody complexes associated with hepatitis B virus, namely, the three major antigen-antibody systems related to HBsAg-anti-HBs, HBeAg-anti-HBe, and HBcAg-anti-HBC, as well as the inflammatory reactions related to other autoantigen-antibody immune complexes.

  The immune complexes formed in the body after infection with hepatitis B virus can be divided into intracellular and extracellular types according to their location. The antigens of the former are mostly the virus and its related antigens, which are mostly present in the blood circulation (i.e., CIC), while the antigens of the latter are mostly HBsAg, HBcAg, or LSP, located on the cell membrane surface, and can also be located in the cytoplasm and nucleus. After the formation of various types of CIC, their fate mainly depends on the size of the complex. Large particle CIC are eventually engulfed by Kupffer cells in the liver regardless of whether they are bound to complement or not, but small particle CIC are not easily engulfed and cleared, among which 19SCIC can even cross the increased permeability of the vascular endothelium and deposit on the vascular basement membrane, causing tissue damage through complement-mediated pathways. The immune complexes such as HBsAg, HBcAg in the liver cells and LSP on the cell membrane, not only can dissolve cells by binding to complement, but also can lead to liver cell damage through antibody-dependent cell-mediated cytotoxicity. The following is a brief summary of the mechanisms by which various immune complexes causing tissue damage in chronic active hepatitis are listed as follows:

  3. Immune regulation and genetic factors:Eddleston's theory of immune regulation is gaining increasing attention. This theory emphasizes the coordinated action of T cells and B cells, organically integrating cellular immunity, humoral immunity, and immune responses to viral antigens and autoantigens. The disorder of the number of T cells and B cells and the coordination of their functions is an important basis for the production of autoimmune reactions. In addition, there are substances with molecular immune regulatory effects in the host serum, such as E-rosette inhibitory factor (RIF), liver extract (LEX), and low-density lipoprotein. RIF is synthesized and released by liver cells and plays a feedback regulatory role in the immune regulatory system, and its presence is closely related to the chronicity of hepatitis. LEX is released after liver cell injury and can inhibit the stimulatory response of lymphocytes to PHA and allogeneic cells as well as DNA synthesis, therefore, it is believed that LEX has a cytotoxic effect on host effector lymphocytes. The presence of low-density lipoprotein also affects the occurrence of chronic active hepatitis, as it can affect the function of suppressor T cells, and the sensitivity of suppressor T cells (Ts cells) to it is 9 times higher than that of TH cells. These molecular regulatory factors must act through cellular immune regulation. Therefore, the role played by cellular immune regulation is more important. The body has suppressor macrophages, suppressor B cells, and suppressor T cells, which can not only interact with molecular immune regulation but also expand the immune regulatory effect by inhibiting the suppressive factors secreted by the cells themselves. Therefore, both can influence each other during the process of liver cell injury. The low function of suppressor T cells is not only related to the persistence of viral antigens and immune disorders but also related to genetic factors. In the process of genetic immune research, it has been found that there is a structure on T cells that is not controlled by Ig genes but is controlled by the HLA-D locus on chromosome 6 of humans. This may be related to the presence of specific antigen receptors on T cells. It has now been found that various autoimmune diseases are related to HLA alleles, and the incidence of HLA-AT and B8 in chronic active hepatitis is significantly increased. It has been confirmed that regardless of the negative or positive HBsAg status of chronic active hepatitis, the frequency of HLA-B8 is very high, especially in HBsAg-negative chronic active hepatitis, the frequency of HLA-B8 is even higher. Organ-specific autoimmune diseases all belong to B8-associated diseases. In recent years, it has been reported abroad that in white people, chronic active hepatitis is associated with antigens A1, B8, DW3, and DRW3; in Japanese people, A1, B13, BW22, and haplotype A9, BW35 are associated with chronic active hepatitis. The above results show that the HLA-A and B antigens associated with chronic active hepatitis in different ethnic groups are not the same, which indicates that HLA-A and B antigens themselves are not the direct cause of chronic active hepatitis.

  In summary, the process that leads to a series of immune pathological reactions causing tissue damage in chronic active hepatitis may include: ①Disorder of T and B cell function. ②Cytotoxic effect of effector cells. ③Damage caused by hepatitis B virus immune complexes. ④The presence of autoantigens, among which LSP is the main target antigen. ⑤Participation of molecular and cellular immune regulatory systems. ⑥To varying degrees, related to certain HLA antigen genetic genes.

  4. Drug-induced chronic active hepatitis:It may be related to drug allergy or poisoning. Overseas reports indicate that phenolphthalein-type cathartic drugs can cause this disease; the condition improves after discontinuation of the drug, and recurrence occurs upon re-administration. Additionally, some reports suggest that isoniazid, methyldopa, and others can cause the disease. However, in China, it is rare for the disease to be caused by drugs.

  5. Pathology

  

  ①Period of activity: Liver cells show obvious变性, swelling, and蚕噬状necrosis, distributed in small patches, also known as

  ② Quiescent phase: The degeneration and necrosis of liver cells are reduced, but the limit plate destruction still exists, and the regeneration of liver cells is obvious, with the formation of pseudo-lobules. The reticular fibers and collagen fibers in the portal area and necrotic foci increase and develop into the liver parenchyma, forming bridging or star-shaped fibrosis. There is infiltration of inflammatory cells in the portal area, and the proliferation of small bile ducts is still obvious, with a large number of multinucleated giant cells distributed in clusters, showing granulomatous changes, so some cases may eventually evolve into liver cirrhosis.

  (2) Extrahepatic tissue changes: This disease can invade multiple organ systems of the body in addition to changes in liver tissue.

  ① Kidney: The kidneys of patients with this disease may show glomerulonephritis changes, especially membranous glomerulonephritis.

  ② Vascular: In recent years, it has been confirmed that chronic active hepatitis with HBsAg positivity may be complicated with nodular polyarteritis, and pathological examination shows necrosis of the walls of small arteries and perivascular inflammation. Immunofluorescence examination shows that HBsAg, IgM, IgG, and C3 are deposited to varying degrees on the vascular wall, thus suggesting that immune complexes may be the cause of vascular injury.

  ③ Joints and skin: Some patients may develop arthritis, and some patients may have cold precipitates in the serum, containing C3-C5, IgG, and IgM immune complexes. Some patients may have synovitis of the joints, but there are few inflammatory cells. Electron microscopy finds particles of 4×10-9mm to 6×10-9mm in the synovial cells. The pathological changes of skin lesions are non-specific inflammation, which is also caused by immune complexes.

  ④ Lymph nodes and spleen: Under the microscope, it can be seen that the lymph nodes and spleen germinal centers are active, and the walls of the splenic small arteries undergo hyaline degeneration. Immunofluorescence proves that HBsAg is deposited in the above tissues, accompanied by IgG, IgM, and occasionally immune complexes formed by viruses, immunoglobulins, and complement.

2. What complications are easily caused by hepatitis virus-related rheumatism

  It may be complicated with progressive enlargement, and severe cases may present with ascites, along with bleeding tendency, joint effusion, chronic nephritis, nodular polyarteritis, chronic renal failure, myocarditis, pericarditis, thrombocytopenia, and aplastic anemia.

  Due to the action of systemic or local factors, fluid leaks from the blood vessels and lymphatic vessels into the peritoneal cavity, resulting in ascites. Hypoproteinemia, sodium and water retention, inactivation of antidiuretic hormone and aldosterone, portal hypertension, hepatic vein obstruction, peritoneal inflammation, and malignant tumors are all important factors causing ascites. The related symptoms of ascites: when a patient has a small amount of ascites [300-500 milliliters (ml)], there may be no obvious discomfort and it is not easy to be noticed; when there is moderate amount of ascites (500-3000mL), there may be a feeling of abdominal distension, with an abdominal外形 of swelling; during physical examination, there may be a mobile dullness. When there is a large amount of ascites (more than 3000mL), it may manifest as respiratory difficulty and lower limb edema. Ascites caused by different diseases often show different accompanying symptoms and signs, such as fever, jaundice, anemia, enlargement of the liver and spleen, heart failure, and other symptoms and signs.

3.. What are the typical symptoms of rheumatoid diseases related to hepatitis viruses

  Both sexes can be affected, with more males than females among HBsAg-positive cases, with a male-to-female ratio of 9:1, while HBsAg-negative cases are more common in females, with a male-to-female ratio of 1:4. HBsAg-positive chronic active hepatitis occurs at an older age, most commonly between 40 and 50 years old, while HBsAg-negative chronic active hepatitis is more common between 30 and 40 years old. This disease is often manifested by gastrointestinal symptoms as an early sign, but some patients may present with extrahepatic symptoms first, and HBsAg-negative patients are more likely to present with extrahepatic symptoms.

  First, liver disease manifestations

  They are divided into mild and severe types. The mild type has a slow progression of the disease, common symptoms include weakness, decreased appetite, discomfort in the upper right abdomen and dull pain in the liver area, abdominal distension, diarrhea, weight loss, low fever, dizziness, and insomnia, and jaundice is rare. In severe cases, in addition to the above symptoms, there may be persistent or progressive jaundice, hyperpigmentation of the skin, dark complexion, and spider veins on the face, neck, chest, and arms. There may be liver palms and subcutaneous hemorrhagic spots. The liver is often enlarged, with a harder texture and tenderness, and may have percussion pain. The spleen may be palpable, even progressively enlarged. The severe type may also present with ascites, lower limb edema, and a tendency to bleed, with subcutaneous hemorrhage, gingival bleeding, nosebleed, uterine bleeding, and gastrointestinal bleeding being common.

  Second, extrahepatic manifestations

  1. Joint symptoms:Affected joints may present as multiple or single joints, showing symmetry or asymmetry, migratory or persistent redness, swelling, heat, pain, and dysfunction. They may be accompanied by joint effusion, but joint deformation has not been found. The main cause of joint symptoms is the activation of complement by immune complexes, leading to local inflammatory reactions.

  2. Renal lesions:Characterized by membranous proliferative nephritis, focal nephritis, or nephrotic syndrome. When polyarteritis nodosa occurs in this disease, the renal lesions progress progressively and may gradually develop into chronic nephritis, eventually leading to chronic renal failure. It is also accompanied by hypertension and electrolyte imbalance in the body. Renal tubular acidosis may occur when renal tubules are involved.

  3. Sjögren's syndrome.

  4. Polyarteritis nodosa:Caused by the HBsAg-anti-HBs complex, its clinical manifestations include fever of unknown origin, polyarthritis or joint pain, myalgia, rash, urticaria, central and peripheral nervous system lesions, hypertension, increased eosinophilic granulocytes, azotemia, and abnormal liver function.

  5. Heart disease:Manifested as myocarditis, pericarditis, conduction block, and coronary insufficiency, which can cause palpitations, dyspnea, angina-like chest pain, occasionally leading to Adams-Stokes syndrome and myocardial infarction.

  6. Changes in the blood system:There are changes in both quality and quantity, with quantitative changes more common, including leukopenia, thrombocytopenia, anemia, and aplastic anemia, and qualitative changes are less common, such as the appearance of atypical lymphocytes, increased megaloblastic erythrocytes, shortened red blood cell lifespan, and hemolytic anemia, etc.

  7. Skin changes:In addition to visible skin spider nevi, there may also be pruritus, desquamation, hyperpigmentation, dilatation of capillaries, patterns, purpura, acne, scleroderma, skin ptosis, facial butterfly-shaped erythema, allergic to sunlight and drugs, nodular erythema, polymorphic erythema, alopecia, and reduction of body hair, etc. Currently, it is believed that some specific rashes are caused by cutaneous allergic angiitis. Skin lesions are directly related to liver disease, therefore, it is called 'liver-skin syndrome'. Mucosal lesions manifest as oral ulcers, mainly in three forms: ① Nicotinic acid deficiency-like stomatitis; ② Aphthous ulcer; ③ Scattered superficial ulcers appear on the congested oral mucosa.

  8. Nervous system lesions:In addition to hepatic encephalopathy, there may also be central nervous system abnormalities, such as epilepsy-like seizures, increased intracranial pressure, subarachnoid hemorrhage, mild hemiparesis with hypoesthesia on one side, extrapyramidal system balance disorders, and cranial nerve palsy, etc. Peripheral nervous system damage includes peripheral neuritis, both sensory and motor nerves can be involved, and it can also manifest as complex mononeuritis, showing asymmetric distribution. Nervous system damage is caused by the deposition of circulating immune complexes, but the cytotoxic effect of cell immunity also plays an important role in nervous system lesions.

  9. Endocrine and metabolic abnormalities:Metabolic disorders are mainly characterized by abnormal glucose metabolism, some may manifest as hypoglycemia attacks and diabetes, the latter with polydipsia, polyphagia, polyuria, weight loss, and glycosuria.

  10. Pulmonary lesions:It can manifest as interstitial pneumonia, with severe cough, persistent and refractory, but with little phlegm, marked chest pain, and pleural effusion can occur during the period of deterioration.

4. How to prevent rheumatoid diseases related to hepatitis virus

  The focus of prevention is to prevent hepatitis B virus infection, the popularization and application of hepatitis B vaccine is the most important, and vigorous promotion of various medical and preventive injections should be one needle and one tube per person. Vigorously promote safe injections (including needles for acupuncture), and strictly disinfect medical instruments such as dental instruments and endoscopes. Medical personnel should wear gloves when contacting the blood, body fluids, and secretions of patients, in accordance with the principles of standard prevention in hospital infection management, strictly prevent iatrogenic transmission. In the service industry, instruments such as hairdressing, shaving, foot care, puncture, and tattooing should also be strictly disinfected. Pay attention to personal hygiene, do not share items such as razors and toothbrushes. Conduct correct sex education; if the sexual partner is HBsAg positive, hepatitis B vaccine should be administered; for those with multiple sexual partners, regular checks should be conducted, and management should be strengthened, and a condom should be used during sexual intercourse. For pregnant women with HBsAg positivity, amniocentesis should be avoided, and delivery time should be shortened to ensure the integrity of the placenta, and to minimize the opportunity for newborns to be exposed to maternal blood.

5. What laboratory tests are needed for hepatitis virus-associated rheumatoid diseases

  One. Blood routine and erythrocyte sedimentation rate:Decreased platelet and white blood cell counts are common, with a few patients having normochromic anemia, and occasionally, reticulocyte counts may decrease.

  Two. Urinalysis:Proteinuria, hematuria, and cast urine may be present; in patients with renal tubular acidosis, urine pH may be greater than 6.6, and urobilinogen and urobilin may be positive, with an increased erythrocyte sedimentation rate.

  Three. Biochemical examination:Alanine aminotransferase (ALT) levels often remain significantly elevated, sometimes with aspartate aminotransferase (AST) levels higher than ALT levels. Serum bilirubin levels are often elevated, and flocculation tests remain positive. Albumin levels decrease, globulin levels increase, and the albumin-globulin ratio is inverted. Prothrombin time is often prolonged, and protein electrophoresis shows a marked increase in gamma globulin. Sodium bromophenolate retention is significant. During the non-activity period, liver function tests may improve or be within normal limits, and alkaline phosphatase levels may increase.

  Serum sodium and potassium may be low in severe edema or in those who have taken diuretics for a long time; in patients with chronic renal failure, serum sodium and potassium levels may be elevated, along with increased blood NPN, BUN, creatinine, and in patients with renal tubular acidosis, blood calcium, phosphorus, and potassium levels may be low, while blood chloride levels may be high.

  Four. Immunological examination

  1. Specific immune examination

  (1) Hepatitis A: A. HAV-IgM antibody: It is currently recognized as the most reliable and sensitive method for diagnosing acute hepatitis A. Positive HAV-IgM indicates acute HAV infection. B. HAV or other antigens: The detection of HAV or its antigens in feces can be considered as an acute infection. C. HAV-RNA can be detected by the detection of HAV-RNA in liver tissue and other tissues, which is sensitive and rapid.

  (2) Hepatitis B: Various methods can be used to detect HBsAg, anti-HBs, HBeAg, anti-HBe, HBcAg, anti-HBC in serum, which is of great significance in determining the presence of hepatitis B infection. DNA-p and PHSA receptor assays are of great value in determining whether HBV replication is present in patients with hepatitis B. High-titer anti-HBC-IgM positivity is conducive to the diagnosis of acute hepatitis B. Some people have obtained the pre-S1 and pre-S2 genes of HBsAg by genetic engineering methods, and tissue chemistry and homologous radioimmunoassay can be used to study the localization of pre-S antigen in liver cells in patients with acute and chronic hepatitis B. In liver tissue with HBV replication, there are often pre-S1 and pre-S2 of HBsAg, and anti-pre-S1 and anti-pre-S2 can be detected in serum. The former appears in the incubation period, and the latter appears before the virus replication stops. Therefore, anti-pre-S1 positivity can be used as an early diagnostic indicator for acute hepatitis B, and anti-pre-S2 can be used as an indicator of hepatitis recovery.

  (3) Hepatitis C: Hepatitis C is often diagnosed by excluding hepatitis A, B, E, and other viruses (CMV, EBV), with positive serum anti-HCV-IgM and/or HCV-RNA confirming the diagnosis.

  (4) Hepatitis D: The serological diagnosis of hepatitis D relies on positive anti-HDV-IgM, or HDAg or HD-VcDNA hybridization; HDAg positivity or HD-VcDNA hybridization positivity in liver tissue can confirm the diagnosis.

  (5) Hepatitis E: The diagnosis of hepatitis E depends on the positivity of serum anti-HEV-IgM or the presence of 30-32nm viral particles in the feces observed by immunoelectron microscopy.

  2. Non-specific immunity tests

  (1) Immunoglobulin detection: Significant elevation of IgG, mild to moderate elevation of IgM and IgA, their elevation is parallel to the elevation of polyclonal gamma globulin, and their elevation or decrease means the deterioration or remission of the disease.

  (2) Cellular immunity test: The cellular immunity test of most patients shows varying degrees of reduction, such as the E-rosette test and the PHA lymphocyte transformation test, which can be reduced. The reduction of cellular immunity is parallel to the degree of chronicity of the disease.

  (3) Complement determination: Total complement (CH50), C3 is reduced in most patients.

  (4) Autoantibodies: A. The positivity rate of rheumatoid factor (IgM-RF) is 10% to 20%, B. The positivity rate of antinuclear antibody is as high as 20% to 50%, C. The positivity rate of antismooth muscle antibody is 40% to 80%, D. The positivity rate of anti-mitochondrial antibody is 10% to 50%, E. The positivity rate of anti-DNA antibody is 30% to 40%, F. The positivity rate of lupus cells is 10% to 20%, G. The positivity rate of ENA antibody is 20% to 50%, most of which are SSA/Ro, SSB/La positive, a few are SSA/Ro, SSB/La, and RNP/Sm are all positive.

  Fifth, X-ray examination

  Interstitial fibrosis can be seen in the lungs, the pulmonary vessels are reticulated, and there may be a small amount of pleural effusion, pleural thickening, pericardial effusion, and changes in myocarditis.

  Sixth, electrocardiogram (ECG) examination

  Sinus tachycardia often occurs, and other various arrhythmias, myocarditis, left ventricular hypertrophy, low voltage, etc., may also occur.

6. Dietary taboos for patients with hepatitis virus-related rheumatoid diseases

  What foods should be avoided for patients with hepatitis virus-related rheumatoid diseases

  1. Reduce the intake of sour and salty foods: For example, peanuts, white wine, sugar, and chicken, duck, fish, meat, eggs, etc.

  2. Reduce the intake of sweets.

  3. Reduce the intake of high-fat and high-cholesterol foods: For example, milk, fatty meat, fried foods, etc.

  (The above information is for reference only, please consult a doctor for details.)

 

7. Conventional methods of Western medicine for treating rheumatoid diseases related to hepatitis virus

  First, treatment

  1. General treatment:During the active stage, hospitalization and bed rest are required, and easy-to-digest, vitamin-rich, and sufficient-calorie diets should be consumed. After the condition improves, appropriate activities can be performed. Eating too much should be avoided to maintain normal nutritional status and weight. Overeating and lack of movement can lead to obesity and hyperlipidemia, even fatty liver.

  2. General treatment:Including liver-protecting drugs, immunosuppressants, and immunomodulators.

  (1) Liver-protecting drugs: There are two types, chemical drugs and traditional Chinese medicine preparations.

  ①Chemical drugs: A large amount of vitamin C, inosine, vitamin B6, and complex phosphatase can be used. For those with long-term elevated transaminases accompanied by disorders of glucose metabolism, insulin-glucose therapy can be tried; for those with disorders of fat metabolism, inositol can be used. Silymarin (Yiganling) 6 tablets per day, taken in three doses, can not only improve liver function but also inhibit liver fibrosis, with good efficacy.

  ②Herbal medicine preparations: There are many kinds of herbal medicines effective for the treatment of this disease. The following lists several effective preparations:

  A. Scutellaria baicalensis tablet: It is a flavonoid effective component extracted from the root of Scutellaria baicalensis, with the effects of clearing heat, detoxifying, anti-inflammatory, and anti-allergic. The side effects are only mild gastrointestinal reactions. 2 tablets each time, 3 times a day, suitable for patients with long-term elevated transaminases with low increase range.

  B. Schisandra: It is now known that its effective ingredients are Schisandrin A, B, C, and D, which have a good effect on reducing transaminases, but the long-term efficacy is poor, and there is often a rebound phenomenon in transaminases after discontinuation of the drug. Some patients may experience mild stomachache, acid regurgitation, and discomfort in the upper abdomen after taking the drug, and the addition of alkaline drugs can reduce gastrointestinal reactions. This drug is not suitable for cases of chronic active ulcer and fat metabolism disorder. The dose is 2 capsules of Schisandrin ester twice a day, each containing 2 grains; 3 tablets of Schisandrin tablets each time, 3 times a day.

  C. Sediophilus: The active ingredient is Sedophyllin, which has the effects of clearing heat, promoting diuresis, and detoxification. The long-term efficacy of this drug is not ideal, and there may be a rebound phenomenon in transaminases after discontinuation of the drug, so it is necessary to discontinue the drug slowly to avoid the rebound of transaminases. The dose is 2 tablets each time, 3 times a day.

  (2) Immunosuppressants:

  ①Glucocorticoids: Have non-specific anti-inflammatory and immunosuppressive effects. Due to the suppression of antibody production in the body by hormones, it may lead to HBsAg carrier state and other side effects, so it should be strictly controlled. The indications are: A. Negative HBsAg, severe autoimmune response with multiple organ system damage. B. Histologically confirmed chronic active hepatitis with obvious clinical symptoms, continuous elevation of transaminases for 10 weeks and increased gamma globulin. The dose of hormones should generally be small or moderate, 20-40mg of prednisone or prednisolone per day, taken in 3-4 divided doses. After the condition is relieved, the dose can be gradually reduced to maintenance dose. 5-10mg of prednisone or prednisolone per day. A course of treatment is 6 months to 1 year or more.

  ②Azathioprine: A derivative of mercaptopurine (6-mercaptopurine) with the action of blocking DNA synthesis, thereby inhibiting the proliferation of immunoglobulins and T cells. The indications for the use of this drug are: A. Severe reaction after the use of hormones. B. Concurrent diabetes that is not suitable for the use of hormones. C. Inability to control symptoms with the use of hormones alone. The initial dose is 1.5mg/kg per day, and regular blood counts, liver function, and renal function tests should be performed during the medication period. Currently, it is widely advocated to use it in combination with hormones, with 50mg of azathioprine plus 30mg of prednisolone daily. After the efficacy is shown, prednisolone should be reduced to maintenance dose, 10mg per day, or 50mg of azathioprine plus 10mg of prednisolone, which has the same efficacy as 20mg of prednisolone.

  ③D-penicillamine: A sulfur-containing amino acid with the function of inhibiting pathological humoral immune response, and can also reduce liver tissue damage caused by immune complexes under the participation of complement. It can be administered by increasing the dose, starting with 100mg each time, 3 times a day, and then gradually increasing the dose, about 300mg per week, until the maximum maintenance dose of 900-1200mg per day. After the liver function improves, the dose can be gradually reduced, 3 times a day, 100-200mg each time, for 6-9 months as a course of treatment.

  ④ Other: Chloroquine 0.25g per time, 2 times a day, 2-4 weeks as a course of treatment, with poor efficacy and significant side effects.

  (3) Immune enhancers: They can restore the body's cellular immune function to normal levels, clear the virus, and thus restore the condition. The existing immune enhancers include immune ribonucleic acid, transfer factor, levamisole, and Yunzhi Gan Tai Granule. They are described as follows:

  ① Immune ribonucleic acid (abbreviated as IRNA): It is divided into two major categories, specific and non-specific. Specific immune ribonucleic acid is the hepatitis B immune ribonucleic acid prepared from the spleen and lymph nodes of horses and sheep with passive immunity, which mainly acts to transmit specific immune information, that is, to transfer the specific immune function from the immune ribonucleic acid extracted from the immune animals with HBsAg to humans, in order to enhance the specific immune function of humans, enhance the body's immune function, clear HBsAg, and terminate the chronic infection state of hepatitis B. The dosage is 1-2mg per time, injected 1-2 times a week, subcutaneously around the axillary or inguinal lymph nodes, and 4-6 months as a course of treatment. It is reported that the efficacy rate is more than 60%.

  The non-specific immunoribonucleic acid extracted from the peripheral leukocytes and spleen leukocytes of normal people has been used to treat chronic active hepatitis with positive HBsAg. After application, more than 80% of patients' lymphocyte transformation test, E-rosette test, skin delayed hypersensitivity test and other cell immune indicators increased, but the rate of HBsAg conversion to negative was low. The dosage is 3mg per time, once a week. It is injected subcutaneously on the inner side of the upper arm below the armpit, and 4-6 months as a course of treatment.

  ② Transfer factor: It is divided into two types, specific and non-specific. Abroad, the efficacy of specific transfer factor in the treatment of chronic active hepatitis is basically negative. China mostly uses non-specific transfer factor prepared from mixed leukocytes of normal people, and the T cell function of most patients can be increased after application. Some patients may experience transient exacerbation of liver function after taking the medicine, which may be due to the improvement of cellular immunity of the body, indirectly promoting humoral immune function of B cells. If the symptoms are not significantly exacerbated, it can be continued to use, and the liver function can still be normal. The dosage is once a week, 1-2U per time, injected subcutaneously on the inner side of the upper arm, and 20-30 weeks as a course of treatment.

  ③ Levamisole: It has the effects of promoting macrophage phagocytic function and enhancing T cell immune function. The dosage is 150mg per day, taken twice a day. The efficacy of this drug is not ideal and can be used in combination with hormones. It has good efficacy for chronic active hepatitis with negative HBsAg.

  ④ Yunzhi Gan Tai Granule: It is a Chinese proprietary medicine with strong immune-enhancing effects. It has good hypolipidemic effects, improves liver function rapidly, and is a non-specific T cell immune enhancer. The dosage is 5g per time, 3 times a day, and a course of treatment lasts for 3 months.

  (4) Other: It has been reported abroad that interferon inducers have certain efficacy for chronic active hepatitis with positive HBsAg, and currently in China, polyinosinic acid (PolyI∶C) is mainly used to induce the production of endogenous interferon. Interferon can make virus-infected cells produce antiviral proteins, affect the transcription and translation during virus replication, and inhibit the synthesis of viral proteins. The general dosage is 0.5-1mg each time, twice a week, and two weeks as one course. Two to four courses can be judged for efficacy. Preliminary findings show that HBsAg of patients can turn negative, and transaminases can decrease to normal. The administration of high doses of vitamin C during treatment can enhance the efficacy of interferon inducers by 3 times.

  Cyclosporin and tacrolimus have been successfully used in patients who are ineffective to hormone treatment.

  (5) Symptomatic treatment: As chronic active hepatitis is a multisystemic disease, in addition to systemic treatment, symptomatic treatment should be carried out in a timely manner when symptoms caused by extrinsic system damage are severe.

  ① Joint symptoms: Non-hormonal anti-inflammatory analgesics such as aspirin and ibuprofen can be given in appropriate doses, and the dosage should be small.

  ② When myocarditis is severe, in addition to systemic treatment, appropriate drugs for nourishing the myocardium, such as coenzyme A and adenosine triphosphate, should be given according to circumstances.

  ③ Chronic renal failure: appropriate antihypertensive treatment should be carried out, and drugs to correct acidosis, reduce blood potassium levels, and promote protein synthesis should be given.

  ④ When anemia is severe, appropriate blood transfusion and medication to stimulate bone marrow should be given.

  ⑤ When there is a significant tendency to hemorrhage, a larger dose of vitamin K can be given.

  ⑥ Other: Once infection occurs, effective anti-infection treatment should be carried out in a timely manner. During the period of immunosuppressive therapy, infections are mostly opportunistic infections, the causative agents are mostly Gram-negative bacilli, so appropriate drugs should be used. In addition, timely and proper treatment is required for hepatic coma.

  II. Prognosis

  It varies due to different causes and severity of the disease. Mild cases may resolve into chronic persistent hepatitis, severe cases may develop into liver cirrhosis, and liver cancer may occasionally be found. Patients with negative HBsAg after treatment have a good prognosis.

  Factors affecting prognosis include alcoholism, heavy physical labor, secondary infection, improper medication, untimely treatment, and incomplete treatment.

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