Hepatitis chronic disease

Carroll KM, Ball SA, Nich C, et al Targeting behavioral therapies to enhance naltrexone treatment of opioid dependence. Arch Gen Psychiatry 38 755-761, 2001 Centers for Disease Control and Prevention Recommendation for prevention and control of hepatitis (virus (HCV) infection and HCV-related chronic disease. MMWR Recommendations and Reports 47(RR19) l-39, 1998 Charney DS, Steinberg DE, Kleber HD, et al The clinical use of clonidine in abrupt withdrawal from methadone. Arch Gen Psychiatry 38 1273-1277, 1981 Charney D S, Heninger OR, Kleber H D The combined use of clonidine and naltrexone as a rapid, safe, and effective treatment of abrupt withdrawal from methadone. Am J Psychiatry 143 831-837, 1986... 

Antibodies against HCV (anti-HCV) in the blood indicate infection with the HCV. If the infection persists for more than 6 months and viral replication is confirmed by HCV RNA levels, then the person has chronic hepatitis C. Chronic disease may be due to an ineffective host immune system against the HCV. Cytotoxic T lymphocytes are ineffective in eradicating the HCV, thus allowing persistent damage to hepatic cells. Therefore, immunocompromised individuals are less likely to eliminate HCV.12... 

Only 10% to 15% of patients have acute hepatitis C that resolves without any further sequelae.10 In more than 85% of cases, hepatitis C develops into a chronic disease. Approximately 70% of chronic HCV cases progress to mild, moderate, or severe hepatitis. While the natural history of the progression to cirrhosis is not clear, it is estimated that 10% to 20% of cases may take up to 20 to 40 years from the time of exposure to advance from fibrosis to cirrhosis.10 Fifteen to twenty percent of patients infected with HCV develop complications associated with cirrhosis. Once cirrhosis is confirmed, the rate of developing hepatocellular carcinoma increases to 1% to 4% per year.10 The estimated death rate from HCV infection is 1.8 deaths per 100,000 persons per year.12,15... 

Patients with viral hepatitis B, C, and D may develop chronic disease leading to ESLD. Treatment is only available for chronic liver disease associated with HBV, HCV, and HDV.20,21... 

Centers for Disease Control and Prevention. Recommendations for prevention and control of hepatitis C virus (HCV) infection and HCV-related chronic disease. MMWR Recomm Rep 1998 47(RR-19) l-39. 

This patient has the subjective symptoms of weight loss, decreased appetite, shortness of breath, and cough. Abnormal laboratory values include elevated temperature, decreased hemoglobin and hematocrit, and decreased CD4 count. Chest x-ray shows diffuse interstitial infiltrates bilaterally. Physical exam reveals thrush. The assessment is possible AIDS with CD4 count of 150 cells/mm3, thrush, a respiratory illness (possibly Pneumocystis jiroveci pneumonia), and anemia of chronic disease. He also has a history of hepatitis B, hypertension, and GERD (on famotidine), poor adherence to his anti hypertensive medications, and likely has an irregular daily regimen due to his occupation as a truck driver. 

It has been well documented that the anaemia of chronic disease, ACD, results in a lowering of various haematological parameters. Several mediators are involved, among them histamine, serotonin, bradykinin, prostaglandins and, as found more recently, cytokines and nitric oxide. ACD is a parameter of systemic autoimmune disorders. The severe inflammatory stimuli lead to several systemic changes, mediated by inflammation-associated cytokines, e.g. IL-6, IL-1 TNFa, TGF beta that regulate hepatic synthesis of the acute phase proteins. 

Chronic disease Moderate/severe renal or hepatic impairment, CHF, cirrhosis... 

Because of its antiviral and anticancer effects, IFN-a is used in the treatment of hepatitis and various forms of cancer, such as Kaposi s sarcoma, non-Hodgkin s lymphoma, and hairy cell leukemia. Exhibit 4.8 describes the treatment of hepatitis C with IFN- . IFN-jS is used for treating multiple sclerosis, a chronic disease of the nervous system. The medical application of IFN-y is for cancer, AIDS, and leprosy. 

Lack of access to medicines and inappropriate doses result in serious morbidity and mortality, particularly for childhood infections and chronic diseases, such as hypertension, diabetes, epilepsy and mental disorders. Inappropriate use and over-use of medicines waste resources - often out-of-pocket payments by patients - and result in significant patient harm in terms of poor patient outcomes and adverse drug reactions. Furthermore, over-use of antimicrobials is leading to increased antimicrobial resistance and non-sterile injections to the transmission of hepatitis, HIV/AIDS and other blood-borne diseases. Finally, irrational over-use of medicines can stimulate inappropriate patient demand, and lead to reduced access and attendance rates due to medicine stock-outs and loss of patient confidence in the health system. 

Hepatitis C virus (HCV) is an RNA virus that is a common cause of parenterally acquired viral hepatitis chronic infection follows acute infection in 80% to 85% of cases. Although liver disease resulting from chronic HCV infection is only slowly progressive, HCV is the most common cause of chronic liver disease in the United States, the most common etiology for hepatocellular carcinoma, and the leading indication for liver transplantation [34-36]. 

Acute or chronic diseases that affect liver architecture or function markedly affect hepatic metabolism of some drugs. 

Swertia pseudochinensis Dang Yao (whole plant) Swertiamarin, swertisin, methyl-bellidifolin, homoorentin, methyl-swertianin, isovitexin, bellidifolin, decussatin, swertifrancheside.33 Choleretic, improve hepatic function. Treat acute icteric hepatitis, chronic liver disease. 

Liver cirrhosis is among the top 10 causes of death in the Western world. The disease occurs after chronic damage to hepatic cells, mainly hepatocytes, which can be caused by viral hepatitis, chronic alcohol abuse or toxic injury, biliary disease, and metabolic liver disorders [64], Liver cirrhosis is characterized by an abnormal deposition of connective tissue in the liver, which hampers the normal functions of the liver. Other features of the disease are general tissue damage, chronic inflammation, and the conversion of normal liver architecture into structurally abnormal nodules. Secondary to these anatomical changes are disturbances in the liver function and in the hemodynamics leading to portal hypertension and intrahepatic shunting [39, 64, 103],... 

It is less likely in other forms of liver disease, such as acute hepatitis and cirrhosis. Cirrhosis may actually protect against atherosclerosis [5, 8, 9]. The reasons for this are not clear. Secondary hypercholesterolaemia frequently occurs in cholestatic conditions, but usually does not require treatment [10]. Other risk factors for hyperlipidaemia and cardiovascular disease should be assessed, as their presence may independently indicate a need for medical intervention [9]. In PBC, patients with severe, chronic disease do not appear to have an increased cardiovascular risk as a result of their hypercholesterolaemia this may be due to the presence of cirrhosis. In contrast, in less severe PBC... 

Classification The classification of the hepatobiliary enzymes essential for enzyme diagnostics is based on their characteristic nature - i. e. excretory, secretory and indicator enzymes, (s. tab. 5.5) They are located predominantly within the liver cells and the biliary ducts as well as within the hepatic lobules. The speed of enzyme elimination does not depend on the blood enzyme levels, but follows an exponential curve. This allows the computation of the half-life of enzymes within the plasma, which is not influenced either by gender or age and is a typical enzyme characteristic. The velocity of enzyme elimination is largely constant, (s. tab. 5.5) However, in chronic diseases of the liver, it is known, for example, that GPT is usually eliminated faster than GOT despite its longer half-life. 

Liver diseases severe acute (necrotic) hepatitis, chronic hepatitis, chronic alcoholic liver damage, liver cirrhosis, cardiac liver, liver abscess, liver tumours and liver metastases, toxic liver damage, etc. A severe and, above all, constant reduction in ChE activity (e. g. < 500 U/1) is usually suggestive of an unfavourable prognosis and the foreseeable moment of liver death . 

Williams, S.J., Farrell, G.C. Serial antipyrine clearance studies defect altered hepatic metabolic function during spontaneous and interferon-induced changes in chronic hepatitis B disease activity. Hepatology 1989 10 192-197... 

Criteria The therapeutic agents should meet the following criteria (7.) as far as possible, they should have no side effects or interactions, (2.) the adjuvant effects should be proven or at least deemed plausible by biochemical and/or pharmacological studies, and (i.) the additional cost should be justifiable and within certain limits. Because of their merely adjuvant modes of action, such substances must be used long-term (>2 years) to obtain positive effects in chronic hepatitis -as is also necessary with other chronic diseases. 

Fundamentally, treatment of cirrhosis should begin during its chronic precursory stages, i. e. chronic hepatitis or chronic cholangitis. A chronic disease confirmed by detailed diagnostics usually still responds to effective treatment measures, which are, however, of no help once the cirrhotic stage has been reached. 

Alcoholism affects about 10% of the drinking population and alcohol (ethanol) abuse has been implicated in at least 20% of admissions to general hospitals. This chronic disease exhibits high mortality due to a wide variety of factors. Ethanol produces effects in virtually every organ system. The biochemical effects of ethanol are due to increased production of NADH that decreases the [NAD ]/[NADH] ratio in the cytoplasm of liver cells at least tenfold from the normal value of about 1000. Increased production of lactate and inhibition of gluconeo-genesis (Chapter 15) result. The hyperuricemia associated with ethanol consumption has been attributed to accelerated turnover of adenine nucleotides and their catabolism to uric acid (Chapter 27). Alcohol increases hepatic fatty acid and triacylglycerol synthesis and mobilization of fat from adipose tissue, which can lead to fatty liver, hepatitis, and cirrhosis. These effects are complicated by a deficiency of B vitamins and protein. 

There is epidemiologic evidence to suggest an increased prevalence of duodenal ulcers in patients with certain chronic diseases, but the pathophysiologic mechanisms of these associations are uncertain. A strong association exists in patients with systemic mastocytosis, multiple endocrine neoplasia type 1, chronic pulmonary diseases, chronic renal failure, kidney stones, hepatic cirrhosis, and ai-antitrypsin deficiency. An association may exist in patients with cystic fibrosis, chronic pancreatitis, Crohn s disease, coronary artery disease, polycythemia vera, and hyperparathyroidism. 

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