Hepatitis virus-related rheumatism

Introduction to hepatitis virus related rheumatism Hepatitis virus-associated rheumatism refers to chronic active hepatitis caused by hepatitis virus, also known as chronic progressive hepatitis. It is a systemic inflammatory disease caused by immune mechanism and mainly caused by liver damage. It is characterized by: 1 typical histological changes of liver disease; 2 in addition to liver lesions, there are many systemic damage features; An immunological abnormality. Among the currently known hepatitis A, B, C, D, E, and G hepatitis viruses, the first five types may be associated with chronic extrahepatic tissue and organ damage, but the most prominent type B (HBV), type C ( HCV), D-type (HDV), type A (HAV) and type E (HEV) followed. Hepatitis G virus has not been successfully isolated in China, and no case reports. Saint et al (1953) first discovered a progressive inflammatory disease with poor prognosis, with early manifestation of infectious hepatitis, and named it chronic active hepatitis. Joske (1955) stressed that the development of viral hepatitis is related to the phenomenon of lupus cells, suggesting that this chronic liver disease should be named after "lupus-like hepatitis", but it is now completely certain that this liver disease is completely different from systemic lupus erythematosus liver disease. Saint et al (1953) first discovered a progressive inflammatory disease with poor prognosis, with early manifestations of infectious hepatitis and named it chronic active hepatitis. Joske (1955) emphasized the development of viral hepatitis and lupus cells. Related to the phenomenon, it is proposed that this chronic liver disease should be named after "lupus-like hepatitis", but it is now completely certain that this liver disease is completely different from systemic lupus erythematosus liver disease. basic knowledge The proportion of illness: 0.003% Susceptible people: no specific population Mode of infection: 1, faecal transmission 2, iatrogenic infection 3, transfusion transmission 4, sexual transmission 5, droplet transmission Complications: ascites chronic nephritis nodular polyarteritis chronic renal failure myocarditis aplastic anemia

Hepatitis virus related rheumatism etiology

(1) Causes of the disease

1. Hepatitis A virus (HAV) is a ribonucleic acid (RNA), many of which are similar to intestinal microribonucleic acid viruses. It belongs to the family of microriboviridae. The enterovirus belongs to the T2 type. The virus is 27-32 nm in diameter and is symmetric. Tetrahedron, two kinds of hollow and solid particles can be seen under electron microscope. The former has no nucleic acid, the stain can be transparent, the latter contains nucleic acid, and the staining is not transparent. The two are immunologically indistinguishable, using formalin, chlorine, ultraviolet light. It can be inactivated by heating at 98 ° C for one minute.

2. Hepatitis B virus (HBV) is a deoxyribonucleic acid (DNA) virus observed by electron microscopy with spherical particles (22 nm in diameter), columnar or tubular particles (22 nm in diameter, about 230 nm in length) and Dane particles (42 to 45 nm in diameter). ), it consists of a complete hepatitis B virus from the outer shell and the inner core. The virus particles can be divided into half-full type, partially semi-full type and hollow type. The latter two types are defect variants. The disease has three antigen-antibody systems, namely type B. Hepatitis 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), Hepatitis B The core antibody (Anti-HBC), the complete HBV-DNA genome consists of 3200-3300 nitrogen-containing base pairs, which are circular, and some double-stranded small-molecule DNA contains a long chain (negative chain) and a short chain. (Positive chain), the complete long chain has a constant length except for the fixed point, and the length of the incomplete short chain is not constant. The nucleotide sequence of the negative strand has four open coding regions, respectively named S. C, P, and X regions, each with a start codon and a stop codon, each region has a different Sex.

3. Hepatitis C virus (HCV) is a flavivirus with a diameter of 50-60 nm. The outer shell contains lipids and is sensitive to chloroform. The molecular weight is 13724~13733D.

4. Hepatitis D virus (HDV) is a defective virus with a diameter of 35 to 37 nm. The outside is surrounded by a shell with HBsAg. It contains hepatitis D antigen (HDAg) and HDV-RNA, and the positive and negative of HDV-RNA. The nucleotide strands carry genetic information and can be expressed separately. The open reading frame 5 (ORF5) located in the genomic complementary strand encodes a polypeptide consisting of 215 amino acids, HDAg, which is a nuclear protein that is heat resistant. And acid, but easy to be inactivated by proteases and bases, HDV assembly must rely on the synthesis of HBsAg, its replication and expression must also have the presence of HBV, so HDV and HBV are mixed infection, it is easy to cause chronic HBV infection However, the chronic synergistic effect of HDV on HBV infection is unclear, and it has been confirmed that HDV alone rarely causes disease alone.

5. Hepatitis E virus (HEV) is a new genus of the circoviridae family. It is a ring-shaped particle (30-32 nm in diameter), has no outer shell, has rounded protrusions and gaps, and the viral genome is 8.51 KD. Double RNA virus, about 7600 nucleotides, was confirmed by molecular cloning technology. HEV from different regions of the world is a single strain. The gene combination has three partially overlapping open reading frames (ORFs), which are ORF1 coding non-structural Protein; ORF2 encodes a protein with seven antigenic determinants; ORF3 encodes a protein with a high amino acid content, possibly synthesizing a nucleocapsid protein.

(two) pathogenesis

It is believed that after hepatitis virus, especially hepatitis B virus infection, hepatocyte damage and extrahepatic lesions are caused by the body's immune response to the virus. The immune response includes antiviral immunity and autoimmunity against hepatocytes. The former refers to the virus. Cellular and humoral immunity of antigens, the latter being an immune response against self-target antigens due to functional coordination disorders between T cells and B cells.

1. Cellular immune defect

Cellular immunodeficiency is a factor in the persistence of viral antigens and repeated replication and reproduction in host cells, leading to chronic viral infections. Clinical practice has confirmed that immunization of killer T cells with HBsAg on the surface of hepatocytes infected with hepatitis B virus The reaction not only destroys the liver cells, but also stimulates the autoimmune reaction, causing the liver cells of patients with chronic active hepatitis to be repeatedly destroyed. At present, most scholars believe that the liver cell damage of chronic active hepatitis is closely related to lymphocyte toxicity. It is caused by the immune response of sensitized lymphocytes to HBsAg or liver-specific lipoprotein (LSP) on the surface of hepatocytes. This immunopathological response may also be directed to normal hepatocyte membrane antigens, not to hepatitis B virus infection. Hepatocytes, some HBsAg-negative patients with cytotoxicity, T cell subset imbalance and inhibitory T cell function decline, are the main cause of HBsAg-negative autoimmune chronic active hepatitis.

2. Humoral immune factors Alberti

When only 1/3 of HBsAg-positive patients were discovered in 1977, T cells had cytotoxic effects on target cells wrapped with HBsAg, and the cytotoxicity index was significantly lower than that of acute hepatitis, indicating that the pathogenesis of chronic active hepatitis is not a Cellular immunity can explain, it also involves humoral immunity and other factors. The pathogenic effect of humoral immunity is mainly several antigen-antibody complexes associated with hepatitis B virus, ie, HBsAg-anti-HBS, HBeAg-resistant HBE and HBcAg-anti-HBC three antigen-antibody systems are also involved in the inflammatory response of other autoantigen-antibody immune complexes.

The immune complexes formed in the body after hepatitis B virus infection can be divided into intracellular and extracellular. The former antigen is mostly the virus and its related antigen, and most of them exist in the blood circulation (ie, CIC), the latter antigens are mostly HBsAg, HBcAg or LSP, located on the surface of the cell membrane, but also in the cytoplasm and in the nucleus. After the formation of various properties of CIC, the fate depends mainly on the size of the complex, regardless of the CIC of the large particles. Combined with complement or not, it is eventually phagocytized by liver Kupffer cells, but small particles of CIC are not easily phagocytosed. 19SCIC can also be deposited on the vascular basement membrane through the increased permeability of the intima, mediated by complement. Damaged tissues, complexes of HBsAg, HBcAg and cell membrane LSP in hepatocytes can not only lyse cells by binding to complement, but also cause hepatocyte damage through antibody-dependent cell-mediated cytotoxicity. Chronic active hepatitis is now available. A brief summary of the mechanisms by which various immune complexes cause tissue damage is presented below (Table 1):

3. Immunomodulation and genetic factors

Eddleston's immunomodulatory theory has received increasing attention. The theory emphasizes the coordination of T cells and B cells, organically harmonizing cellular immunity, humoral immunity, and immune responses to viral and autoimmune antigens, including the number of T cells and B cells. And the coordination of functions and coordination is an important basis for the production of autoimmune reactions. In addition, there are substances such as E-rosette inhibitor (RIF), liver extract (LEX) and low-density lipoprotein, which have molecular immunomodulatory effects in the host serum. RIF is released by hepatocyte synthesis and plays a regulatory role in the immune regulatory system. Its presence is closely related to the chronic hepatitis. LEX is released by hepatocytes and can inhibit lymphocytes against PHA and allogeneic cells. Stimulation response and DNA synthesis, therefore, it is believed that LEX has a cytotoxic effect on inhibiting host effector lymphocytes, and the presence of low-density lipoprotein also affects the occurrence of chronic active hepatitis, because it can affect inhibitory T cell function, inhibition T cells (Ts cells) are 9 times more sensitive than TH cells, and these molecular regulators must pass through the cells. Immune regulation plays a role, therefore, the role of cellular immune regulation is more important, the host has inhibitory macrophages, inhibitory B cells and inhibitory T cells, which not only can interfere with molecular immune regulation, and The immunomodulatory effect can be amplified by inhibiting the inhibitory factor secreted by the cell itself. Therefore, during hepatocyte injury, the two can interact with each other. In addition to the persistence of the viral antigen and immune dysregulation, the inhibitory T cell function is also associated with Related to genetic factors, it has been found during genetic immunization studies that there is a structure on T cells that is not controlled by the Ig gene and is controlled by the HLA-D site on human chromosome 6, which may be related to T cells. It has been associated with specific antigen receptors. It has been found that a variety of autoimmune diseases are associated with alleles on HLA. The incidence of HLA-AT and B8 is significantly increased in chronic active hepatitis. It has been confirmed that HBsAg is negative or positive. Chronic active hepatitis, the frequency of HLA-B8 is very high, especially HBsAg-negative chronic active hepatitis, HLA-B8 frequency is higher, organ specific itself The immune diseases are all B8-associated diseases. In recent years, foreign countries have reported that the active antigens associated with HLA in Caucasians are A1, B8, DW3 and DRW3; the Japanese are A1, B13, BW22 and Haplotype A9, BW35, etc. are associated with chronic active hepatitis. The above results indicate that HLA-A and B antigens are different in different races associated with chronic active hepatitis, indicating that HLA-A and B antigens are not completely The direct cause of chronic active hepatitis.

In summary, the process of a series of immunopathological reactions, such as chronic active hepatitis tissue damage, may be:

1T, B cell dysfunction.

2 cytotoxic effects of effector cells.

3 Injury caused by hepatitis B virus immune complex.

4 the presence of autoantigens, where LSP is the primary target antigen,

The involvement of 5 and cellular immune regulatory systems,6 is related to certain HLA antigen genes to varying degrees.

4. Drug-induced chronic active hepatitis

May be related to drug allergy or poisoning, foreign reports using phenolphthalein catharsis drugs can cause the disease; after stopping the drug, it will be improved, and then relapsed with medication, there are also reports of isoniazid, methyldopa, etc. can cause the disease, However, it is rare in China to cause this disease caused by drugs.

5. Pathology

(1) Liver tissue changes: mainly around the lobular changes, with the characteristics of portal peripheral hepatitis.

1 active period: liver cells have obvious degeneration, swelling, silkworm-like necrosis, a small piece of distribution, also known as "fragmented necrosis", severe sub-macro necrosis, accompanied by obvious "cholecystosis", leaflets The remaining liver cells are often arranged in adenoids, isolated or surrounded by slender fibers, causing destruction of the hepatic lobule structure, collapse of the reticular fiber scaffold, inflammatory cell infiltration in the portal area, often accompanied by small bile duct hyperplasia and fibrous tissue hyperplasia. The jaundice is often accompanied by obvious "cholestatic", the inflammation in the portal area is gradually enlarged, and finally the restriction plate of the liver lobule is also destroyed.

2 quiescent period: hepatocyte degeneration, necrosis is reduced, but the plate destruction still exists, hepatocyte regeneration is obvious, pseudo-lobule formation, reticular fibers and collagen fibers in the portal area and necrotic foci increase, and develop into the liver parenchyma, forming Bridge or star fibrosis, inflammatory cell infiltration in the portal area, small bile duct hyperplasia is still obvious, and there are piles of distributed multinucleated giant cells, which are granulomatous changes, so some cases can eventually evolve into cirrhosis.

(2) Changes in extrahepatic tissue: In addition to changes in liver tissue, this disease can also invade multiple organ systems in the body.

1 Kidney: The kidney of this patient may be changed by glomerulonephritis, especially membranous glomerulonephritis.

2 vascular: In recent years, it has been confirmed that HBsAg-positive chronic active hepatitis may be associated with nodular polyarteritis. Pathological examination shows fibrin necrosis and perivascular inflammation on the wall of small arteries. Immunofluorescence shows different degrees on the vessel wall. The deposition of HBsAg, IgM, IgG and C3 suggests that immune complexes may be the cause of vascular damage.

3 joints and skin: some patients may develop arthritis, some of them may have cryoprecipitate in serum, containing C3 ~ C5, IgG, IgM immune complex, and some patients may have joint synovitis, but inflammatory cells are very Less, electron microscopy found that there are 4 × 10-9mm ~ 6 × 10-9mm particles 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, lymph nodes and spleen hair growth centers can be seen active, and the spleen arterioles wall is transparently degenerated. Immunofluorescence proves that there are HBsAg deposition in the above tissues, accompanied by IgG, IgM, occasional viruses, immunoglobulins. , immune complex formed by complement.

Hepatitis virus related rheumatism prevention

The main point of prevention is to prevent hepatitis B virus infection. The promotion and application of hepatitis B vaccine is the most important. It is necessary to promote all kinds of medical and preventive injections one by one.

Hepatitis virus related rheumatism complications Complications ascites chronic nephritis nodular polyarteritis chronic renal failure myocarditis aplastic anemia

Can be progressive enlargement, severe ascites can occur, and there is bleeding tendency, joint cavity effusion, chronic nephritis, nodular polyarteritis, chronic renal failure, myocarditis, pericarditis, reduction of whole blood, aplastic anemia.

Hepatitis virus-associated rheumatic symptoms Common symptoms Hepatic dysfunction, weakness, spider, liver, palm, hemorrhage, upper abdominal discomfort, jaundice, oral ulcer, facial butterfly, erythema diarrhea

Both sexes can occur, HBsAg-positive people are more males, male to female ratio is 9:1, while HBsAg-negative females are more females, male to female ratio is 1:4, HBsAg-positive chronic active hepatitis is older, More common in 40 to 50 years old, HBsAg-negative chronic active hepatitis is more common in 30 to 40 years old. This disease is often characterized by early symptoms of gastrointestinal symptoms, but some patients start with extrahepatic symptoms first, and HBsAg-negative patients with extrahepatic Symptoms are more common.

1. Liver disease performance

Divided into light and heavy, light patients with slow progress, common symptoms are weakness, loss of appetite, right upper quadrant discomfort and liver pain, abdominal distension, diarrhea, weight loss, low fever, dizziness and insomnia, etc., no jaundice, in addition to the above In addition to symptoms, there may be persistent or progressive jaundice, pigmentation of the skin, dark complexion, visible spider mites on the face, neck, chest and arms, liver palm and subcutaneous hemorrhage, liver often swollen, hard texture There are tenderness and sneezing pain, the spleen can be touched, and even progressive swelling, severe cases can also have ascites, lower extremity edema, and bleeding tendency to subcutaneous hemorrhage, gum bleeding, nose bleeding, uterine bleeding, gastrointestinal Bleeding is common.

2. Extrahepatic manifestations

(1) joint symptoms: the affected joints appear as multiple or single joints, symmetry or asymmetry, migratory or persistent redness, swelling, heat, pain and dysfunction, may be associated with joint effusion, but No joint deformation was found, and the main cause of joint symptoms was that the immune complex activates complement and causes a local inflammatory response.

(2) Renal lesions: characterized by mesangial proliferative nephritis, focal nephritis or nephrotic syndrome. When nodular polyarteritis occurs in this disease, the renal lesions progress progressively and can gradually develop into chronic nephritis. Lead to chronic renal failure, accompanied by high blood pressure and electrolyte imbalance in the body, renal tubular involvement may occur when renal tubular acidosis.

(3) Sjogren's syndrome.

(4) Nodular polyarteritis: caused by HBsAg-anti-HBS complex, its clinical manifestations are unexplained fever, polyarthritis or joint pain, myalgia, rash, urticaria, central nervous system and peripheral neuropathy , high blood pressure, blood eosinophilia, azotemia, abnormal liver function.

(5) heart disease: manifested as myocarditis, pericarditis, conduction block and coronary insufficiency, etc., can cause palpitations, dyspnea, angina pectoris-like chest pain, and occasionally A-S syndrome and myocardial infarction.

(6) changes in the blood system: qualitative and quantitative changes, volume changes are more common, including leukopenia, thrombocytopenia, whole blood reduction and aplastic anemia, qualitative changes are less common, such as the emergence of atypical lymphocytes, Giant erythrocytosis, shortened red blood cell life and hemolytic anemia.

(7) Skin changes: In addition to visible skin spider mites, skin pruritus, desquamation, pigmentation, telangiectasia, pattern, purple lines, acne, scleroderma, skin sagging, facial butterfly erythema Allergic to sunlight and drugs, nodular erythema, erythema multiforme, alopecia and body hair reduction, etc. It is currently believed that some specific rashes are caused by skin allergic vasculitis, and skin lesions are directly related to liver diseases, so it is called For "hepatic-skin syndrome", mucosal lesions manifest as oral ulcers, mainly in three forms: 1 niacin deficiency stomatitis; 2 ulcerated ulcers; 3 scattered shallow ulcers on the congested oral mucosa.

(8) Neurological diseases: In addition to hepatic encephalopathy, central nervous system abnormalities such as epileptiform convulsions, increased intracranial pressure, subarachnoid hemorrhage, mild hemiplegia with low partial sensation, and extrapyramidal balance Obstruction and cranial nerve palsy, peripheral nervous system damage has peripheral neuritis, sensory and motor nerves can be involved, can also be expressed as a combination of single neuronitis, asymmetrical distribution, nervous system damage is caused by circulating immune complex deposition Caused by, but cellular immune damage also plays an important role in neurological pathology.

(9) Endocrine and metabolic abnormalities: Metabolic disorders are mainly abnormal glucose metabolism, and some may be characterized by hypoglycemia and diabetes, the latter having polydipsia, polyphagia, polyuria, weight loss and diabetes.

(10) Pulmonary lesions: may be characterized by interstitial pneumonia, severe cough, prolonged unhealed, but less, chest pain is obvious, pleural effusion may occur during the deterioration of the disease.

Hepatitis virus related rheumatism examination

1. Blood routine and erythrocyte sedimentation rate: platelet and leukocyte reduction are more common, a few patients have positive pigmented anemia, and occasionally reticulocytes fall.

2. Urine routine: proteinuria, hematuria, tubular urine can be seen; urine pH is greater than 6.6 in patients with renal tubular acidosis, urinary bilirubin and urobilinogen can be positive, and the sedimentation rate of erythrocyte sedimentation rate increases.

3. Biochemical examination: transaminase often continues to increase significantly, sometimes aspartate aminotransferase is higher than alanine aminotransferase, serum bilirubin is often elevated, flocculation test continues to be positive, albumin is reduced, globulin is elevated, and albumin and globulin ratio is inverted. Prothrombin time is prolonged. Protein electrophoresis shows that gamma globulin is significantly elevated, and sulfonium bromide is obviously retained. In the inactive phase, liver function test can be improved or in the normal range, alkaline phosphatase can be elevated.

Patients with severe edema or taking diuretics for a long time, blood sodium, blood potassium can be low; patients with chronic renal failure, elevated blood sodium and potassium, blood NPN, BUN increased, creatinine increased, renal tubular acidosis The patient's blood calcium, blood phosphorus, blood potassium is low, blood chlorine is high.

4. Immunological examination

(1) Specific immunological examination:

1 Hepatitis A: A.HAV-IgM antibody: It is currently the most reliable and sensitive method for diagnosing acute hepatitis A. HAV-IgM positive indicates acute HAV infection, B.HAV or other antigen: detected in feces HAV or its antigen can be regarded as acute infection, and C.HAV-RNA can be detected by HAV-RNA in liver tissue and other tissues. This method is sensitive and rapid.

2 Hepatitis B: HBsAg, anti-HBS, HBeAg, anti-HBE, HBcAg, anti-HBC can be detected by various methods. It is of great significance for judging the presence or absence of hepatitis B infection. DNA-p and PHSA receptors are determined. It is of great value to determine the presence or absence of HBV replication in patients with hepatitis B. High titer anti-HBC-IgM positive 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. And in-phase radioimmunoassay can be used to study the localization of pre-S antigen in hepatocytes in patients with acute and chronic hepatitis B. In liver tissues with HBV replication, pre-S1 and pre-S2 of HBsAg are often included, and anti-pre-S1 and anti-sera can be determined in serum. In the former S2, the former appears in the incubation period, and the latter appears before the virus replication is terminated. Therefore, the anti-pre-S1 positive can be used as an early diagnostic indicator of acute hepatitis B, and the anti-pre-S2 can be used as an indicator of hepatitis recovery.

3 Hepatitis C: Hepatitis C is often diagnosed by the exclusion of type A, type B, type E and other viruses (CMV, EBV). Serum anti-HCV-IgM and/or HCV-RNA are positive and can be diagnosed.

4 hepatitis D: Serological diagnosis of hepatitis D depends on anti-HDV-IgM positive, or HDAg or HD-V cDNA hybridization positive; HDAg-positive or HD-V cDNA hybridization positive in liver tissue can be confirmed.

5 Hepatitis E: The diagnosis of hepatitis E depends on serum anti-HEV-IgM-positive or immunoelectron microscopy to see 30-32 nm virus particles in the feces.

(2) Non-specific immune examination:

1 Immunoglobulin test: IgG was significantly elevated, IgM and IgA were mild to moderately elevated, and their elevation was parallel to the increase of polyclonal gamma globulin, and its increase or decrease meant that the condition deteriorated or resolved.

2 Cellular immunoassay: Most patients have different degrees of cellular immunoassay. For example, the E rosette test can reduce the PHA lymphocyte transformation test, and the cellular immunity is reduced in parallel with the degree of chronic disease.

3 Complement assay: total complement (CH50), C3 reduction seen in most patients.

4 autoantibodies: A. rheumatoid factor (IgM-RF) positive rate is 10% to 20%, B. antinuclear antibody positive rate is as high as 20% to 50%, C. anti-smooth muscle antibody positive rate is 40% to 80% , D. anti-mitochondrial antibody positive rate is 10% to 50%, E. anti-DNA antibody positive rate is 30% to 40%, F. lupus cell positive rate is 10% to 20%, G.ENA antibody is 20% to 50% Positive, most of them are SSA/Ro, SSB/La positive, a few are SSA/Ro, SSB/La, RNP/Sm are positive.

5. X-ray inspection

Interstitial fibrosis can be seen in the lungs, the lung texture is reticulated, and there may be a small amount of pleural effusion, pleural thickening, pericardial effusion and myocarditis.

6. ECG examination

Multiple sinus tachycardia can occur, and many other arrhythmias, myocarditis, left ventricular hypertrophy, and low voltage can also occur.

Diagnosis and identification of hepatitis virus related rheumatism

Diagnostic criteria

The diagnosis of this disease is based on:

1 has a history of hepatitis, the course of the disease is close to or more than one year.

2 Frequent or repeated symptoms such as fatigue, liver pain and bloating, general health and labor capacity decline.

3 liver is accompanied by texture changes and tenderness.

4 There is no other reason to explain progressive splenomegaly or spider mites, liver palm and so on.

5 liver function tests are repeated or persistent abnormalities.

Most of the 6HBsAg assays are positive. Although some cases have obvious symptoms and signs, and the liver function test can still be normal, it can cause difficulties in diagnosis. Therefore, it is necessary to observe the condition dynamically, comprehensive clinical manifestations, auxiliary examinations, pathology and other aspects. The material can be diagnosed if it is considered comprehensively.

Chronic active hepatitis can be divided into two types according to the detection of serum HBsAg:

1HBsAg positive chronic active hepatitis.

2HBsAg-negative chronic active hepatitis (ie, lupus-like hepatitis or autoimmune hepatitis).

Differential diagnosis

Acute hepatitis

The onset is very similar to the disease. The prognosis of acute hepatitis is good. It rarely improves after 10 weeks. The disease often has multiple systemic damage symptoms. The flocculation test and globulin are persistently positive. There are autoantibodies in the serum. Identification, liver biopsy if necessary.

2. Chronic persistent hepatitis

The clinical, biochemical and even histopathological changes of mild cases or remission cases of this disease are similar to those of chronic persistent hepatitis. It is necessary to follow up for a long time, accumulate more clinical, biochemical, immunological data, and conduct comprehensive analysis to make judgments. The main identification of the two is shown in Table 3.

3. Autoimmune diseases

The disease sometimes needs to be differentiated from autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis. Although systemic lupus erythematosus has multiple systemic damage, the clinical and pathological changes of the liver are different from those of chronic active hepatitis. If necessary, liver puncture can be used for identification. Sm antibody is found in serum. It is a characteristic finding of systemic lupus erythematosus. If chronic active hepatitis is positive for joint symptoms and rheumatoid factor, it must be differentiated from rheumatoid arthritis. However, the latter generally has no active liver disease, and the disease sometimes overlaps with rheumatoid arthritis.

4. Primary biliary cirrhosis

More common in women aged 40 to 60 years, in the early stage of the disease, even in the early stage of jaundice, there is generalized itching, hypercholesterolemia, alkaline phosphatase significantly increased, etc., most cases of mitochondrial antibodies are positive, and these manifestations are rare, in addition, the original The biliary cirrhosis of the biliary cirrhosis is less effective than the immunosuppressive agents such as hormones.

5. Hepatolenticular degeneration (Wilson's disease)

Is an autosomal dominant hereditary disease, often with nervous system manifestations, sometimes clinical manifestations can be similar to this disease, but 90% of patients with hepatolenticular degeneration can be seen in the cornea KF ring, serum ceruloplasmin, blood copper and There is an increase in urinary copper, but no serum and cellular immune abnormalities.

6. A history of useful drugs for drug liver disease, such as phenolphthalein, methyldopa, etc., the onset is generally slow, gastrointestinal symptoms are mild, often accompanied by allergic manifestations, such as rash, high eosinophil count, The specific lymphocyte transformation test was positive and HBsAg was negative.

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