OVERVIEW
Some hepatitis virus-infected patients may have manifestations of rheumatologic immune diseases, such as arthralgia and/or arthritis, skin rash, etc. Autoantibodies, such as rheumatoid factor (RF), antinuclear antibodies, anti-smooth muscle antibodies, cryoglobulins, and antithyroid peroxidase antibodies, can be detected in some of the patients. The production of autoantibodies is related to hepatitis virus infection of B lymphocytes and molecular mimicry mechanisms, and the autoimmune response is related to the severity and duration of the disease.
Etiology
There are currently two main theories about the mechanisms by which hepatitis virus infection triggers an autoimmune response, namely molecular mimicry and bypass activation. Hepatitis virus infection can indeed lead to a range of autoimmune-mediated pathologies.
Symptoms
Multiple joint involvement with joint pain and or swelling, often wandering.
Hepatitis B virus infection can cause rheumatoid-like clinical manifestations such as joint swelling and pain and rash, often occurring early in the disease. Hepatitis C virus is associated with primary mixed cryoglobulinemia, and in a few patients, hepatitis C, primary mixed cryoglobulinemia, rash, and arthritis may be present.
Examination
1. Blood count and sedimentation
Platelet and leukocyte decreases are common, and a few patients have normochromic anemia with an occasional decrease in reticulocytes. Erythrocyte sedimentation rate increases.
2. Urine routine
Proteinuria, hematuria, tubular urine can be seen; in patients with renal tubular acidosis, urine pH>6.6, urobilin and urobilinogen can be positive.
3. Blood biochemical examination
Aminotransferases are often significantly increased, sometimes higher than glutamic aminotransferase, serum bilirubin is often elevated. Albumin decreases, globulin increases, and the ratio of albumin to globulin is inverted. Prothrombin time is often prolonged, and gamma globulin is markedly elevated on protein electrophoresis. In the inactive phase, liver function tests may improve or be within normal limits, and alkaline phosphatase may be elevated. Blood sodium and potassium may be low in those with severe edema or on diuretics for a longer period of time; in those with chronic renal failure, blood sodium and potassium are elevated. Blood NPN (non-protein nitrogen) and urea nitrogen (BUN) are elevated, and creatinine is elevated. In patients with renal tubular acidosis, blood calcium, blood phosphorus, blood potassium is low, and blood chloride is high.
4. Immunological examination
Some patients can detect autoantibodies, such as rheumatoid factor (RF), antinuclear antibody, anti-smooth muscle antibody, cryoglobulin, and anti-thyroid peroxidase antibody.
Diagnosis
Diagnosis can be confirmed on the basis of etiology, clinical manifestations and laboratory tests.
Complications
Arthritis, nephropathy, polyarteritis nodosa and systemic vasculitis may be combined.
Treatment
During the active stage, hospitalization and bed rest are required. It is advisable to eat a diet that is easy to digest, rich in vitamins and enough calories, and appropriate activities can be carried out when the condition improves. It is not easy to eat too much, and the principle is to maintain normal nutritional status and body weight. Eating too much and moving too little can lead to obesity and hyperlipidemia, even fatty liver.
1. Hepatitis B virus-associated arthritis has no specific treatment, and the course of the disease is often self-limiting. Non-steroidal anti-inflammatory drugs can reduce joint symptoms.
2. Interferon α2b is preferred for patients with hepatitis C. Interferon α2b is effective in some cases of hepatitis C virus-associated cryoglobulinemia, and immunosuppressants can be used to treat treatment-failed cryoglobulinemia.