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All patients with abnormal liver function should be carried out specific treatment. Application of immunosuppressive therapy has not yet extended the life of PBC patients reported that ursodeoxycholic acid (UDCA) although not reduce the demand for liver transplantation in patients, but can be an overall improvement in serum biochemical parameters of cholestasis, delaying the need for liver transplant patients time, and may prolong life.
1. Ursodeoxycholic acid damage caused by hydrophobic bile acid retention in the liver cells may be the main reason for the progress of PBC lesions. UDCA can promote the PBC, primary sclerosing cholangitis patients with intrahepatic bile from the liver into the bile duct cells, thereby reducing the intracellular levels of hydrophobic bile acids, play a role in protecting the cell membrane. UDCA also has also immunomodulatory effects. UDCA therapy can significantly improve biochemical markers of cholestasis patients, delaying the occurrence of portal hypertension in patients and reduce the incidence of esophageal varices, but it did not reduce the probability of variceal bleeding, and fatigue, itching of the effects are not sure Osteoporosis is invalid. Even if the long-term use PBC UDCA can not delay the progression of the disease still needs to end the sexual development of liver transplantation. UDCA amount or one-time Dayton clothing graded the same effect, but the latter seems a better clinical compliance. UDCA rare side effects,


mainly diarrhea. There are several joint a small sample of ammonia chatter pyridine UDCA, colchicine alkaline, or information prednisone PBC and found that the effect of combination therapy is not better than UDCA alone. Recommendations: PBC progress extremely variable, of asymptomatic patients in the study showed that the survival rate compared with the same surname other people the same age is lower. Asymptomatic patients, and UDCA treatment response is not sure. UDCA on liver function of patients return to normal liver function than those who never change the effect. So the best choice for liver dysfunction associated with PBC, UDCA treatment of patients with application of the dose 13 ~ 15mg/kg/d, or one ton service points. If both the application of cholestyramine, the two should be an interval of 4 hours or more.

Primary biliary cirrhosis (PBC) is a progressive destruction of intrahepatic bile ducts and cholestasis in chronic unexplained as the main feature of the disease.
Pathogenesis
Primary biliary cirrhosis through four typical stages of development, occurrence of a normal bile duct inflammation and erosion associated with chip interval and interlobular bile duct damage, granulomas can also be found. , bile duct hyperplasia occurred then, the portal area began to be destroyed, inflammation spto the liver, bile duct hyperplasia and fibrosis around the portal vein. bile duct hyperplasia and inflammation of the lower fibers of the cable is connected with the portal area, -band apparent cholestasis and Mallory hyaline. , appears hard, rules, significant regeneration of bile stained summary, the formation of cirrhosis. If there is no granuloma and bile duct lesions characteristic is difficult to be of primary biliary cirrhosis and other types of cirrhosis of the liver to distinguish. With histological of the problem is between the above-mentioned period of significant overlap, especially in stage , , and the stage may not reflect the clinical status (such as a stage disease patients may have no clinical manifestations).
Symptoms and signs
Although primary biliary cirrhosis among men and women in all age groups can occur in medical education. Net but more than 90% collected in 35 to 70-year-old female patient, and often latent disease. About 50% of asymptomatic patients discovered only in the routine examination of serum biochemical abnormalities. In about 50% of patients, skin itching and / or unexplained fatigue is the initial symptom, and may occur in the months or even years before other clinical manifestations. About 50% of the patients liver enlargement, hard, but no tenderness; 25% of patients enlarged spleen; about 15% of the patients also appear yellow skin tumors and macular tumors; 10% of the patients over calm pigment; 20% patients with jaundice, and progress over time, in combination with other symptoms. Other possible clinical manifestations include clubbing, metabolic bone disease (such as osteoporosis), peripheral neuropathy, renal tubular moderate steatorrhea (due to the secretion of cholestasis and pancreatic dysfunction caused.) As the disease progress, all the features and complications of cirrhosis of the liver can occur. Often associated with primary biliary cirrhosis autoimmune diseases (such as rheumatoid arthritis, scleroderma, Sjogren's syndrome and autoimmune thyroiditis.)
Laboratory
The disease early laboratory findings showed features of cholestasis, and alkaline phosphatase, and accompanied by


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