Chronic Hepatitis C With Hepatic Coma

How Is Viral Hepatitis Prevented

Prevention of hepatitis involves measures to avoid exposure to the viruses, using immunoglobulin in the event of exposure, and vaccines. Administration of immunoglobulin is called passive protection because antibodies from patients who have had viral hepatitis are given to the patient. Vaccination is called active protection because killed viruses or non-infectious components of viruses are given to stimulate the body to produce its own antibodies.

Avoidance of exposure to viruses

Prevention of viral hepatitis, like any other illness, is preferable to reliance upon treatment. Taking precautions to prevent exposure to another individual’s blood , semen , and other bodily secretions and waste will help prevent the spread of all of these viruses.

Use of immunoglobulins

Immune serum globulin is human serum that contains antibodies to hepatitis A. ISG can be administered to prevent infection in individuals who have been exposed to hepatitis A. ISG works immediately upon administration, and the duration of protection is several months. ISG usually is given to travelers to regions of the world where there are high rates of hepatitis A infection and to close or household contacts of patients with hepatitis A infection. ISG is safe with few side effects.

Hepatitis A

Individuals at increased risk of acquiring hepatitis A are:

Some local health authorities or private companies may require hepatitis A vaccination for food handlers.

Hepatitis B

Hepatitis B vaccine is recommended for:

Diagnosis Of Chronic Hepatitis

• Liver test results compatible with hepatitis

• Viral serologic tests

• Possibly autoantibodies, immunoglobulins, alpha-1 antitrypsin level, and other tests

• Occasionally biopsy

• Serum albumin, platelet count, and prothrombin time/international normalized ratio

recommendations for testing, managing, and treating hepatitis C virus infection and the U.S. Preventive Services Task Forces clinical guideline Hepatitis C Virus Infection in Adolescents and Adults: Screening.)

Chronic hepatitis is suspected in patients with any of the following:

• Suggestive symptoms and signs

• Incidentally noted elevations in aminotransferase levels

• Previously diagnosed acute hepatitis

In addition, to identify asymptomatic patients, the CDC recommends testing of all adults 18 years at least once.

Baseline Predictors Of Child

Male sex , platelet count lower than 100,000/L , increased international normalized ratio , presence of esophageal varices , history of HCC and history of decompensation were significantly associated with C-P class worsening at univariate analysis. At multivariate analysis, male sex , platelet count lower than 100,000/L and increased INR resulted independently associated with C-P class worsening. HIV coinfection was not associated with the C-P class worsening both at univariate and at multivariate analysis .

Table 4 – Baseline factors associated with Child-Pugh class worsening following viral eradication. Univariate and multivariate analysis

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Hepatitis C Can Be Invisible

There may be few symptoms after initial HCV infection. Many people with hepatitis C dont even know they have the life-threatening disease.

HCV attacks the liver. Many people exposed develop a chronic infection after initial infection with HCV. Chronic HCV infection slowly causes inflammation and damage in the liver. Sometimes the condition may not be diagnosed for 20 or 30 years.

• yellow discoloration in eyes and skin
• swelling in legs
• abnormal blood tests, such as bilirubin, albumin, and coagulation parameters
• enlarged veins in the esophagus and upper stomach that may bleed
• impaired mental function due to buildup of toxins
• infection of the abdominal lining and ascites
• combined kidney and liver failure

A liver biopsy will show scarring, which can confirm the presence of cirrhosis in people with HCV.

Lab tests and a physical exam may be enough for your doctor to diagnose advanced liver disease without a biopsy.

Less than a quarter of people with HCV will develop cirrhosis. But, certain factors can increase your risk of cirrhosis, including:

• alcohol use
• infection with HCV and another virus
• high levels of iron in the blood

Anyone with chronic HCV infection should avoid alcohol. Cirrhosis can also accelerate in people older than 45 as fibrosis and scarring increase. Aggressively treating HCV infection in younger people may help prevent progression to cirrhosis.

Its important to stay healthy if you have cirrhosis. Be sure to keep all immunizations up to date, including:

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Life Expectancy Among Patients With Chronic Hepatitis C Virus Infection And Cirrhosis

by The JAMA Network Journals

Patients with chronic hepatitis C virus infection and advanced fibrosis or cirrhosis who attained sustained virological response had survival comparable with that of the general population, whereas patients who did not attain SVR had reduced survival, according to a study in the November 12 issue of JAMA.

Almost three million people in the United States are chronically infected with the hepatitis C virus . The life expectancy of patients with chronic HCV infection is reduced compared with the general population, largely attributable to the development of cirrhosis, liver failure and cancer. Studies have shown that the risk of all-cause death is lower among patients with chronic HCV infection and advanced hepatic fibrosis if sustained virological response is attained, but comparisons have been limited to those without SVR, according to background information in the article.

In total, 530 patients were followed for a median of 8.4 years follow-up was complete in 454 patients , 192 of whom attained SVR. Thirteen patients with SVR died, resulting in a cumulative 10-year overall survival of 91.1 percent, which did not differ significantly from the age- and sex-matched general population. In contrast, 100 patients without SVR died. The cumulative 10-year survival was 74.0 percent, which was significantly lower compared with the matched general population.

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Chronic Hepatitis C Infection With Hepatic Coma

Approved by: Maulik P. Purohit MD, MPH

Hepatitis C Infection is a viral infection that causes inflammation and injury to the liver.

The topic Chronic Hepatitis C Infection with Hepatic Coma you are seeking is a synonym, or alternative name, or is closely related to the medical condition Hepatitis C Infection.

What Is Acute Fulminant Hepatitis

Rarely, individuals with acute infections with HAV and HBV develop severe inflammation, and the liver fails . These patients are extremely ill with the symptoms of acute hepatitis already described and the additional problems of confusion or coma , as well as bruising or bleeding . In fact, up to 80% of people with acute fulminant hepatitis can die within days to weeks therefore, it is fortunate that acute fulminant hepatitis is rare. For example, less than 0.5% of adults with acute infection with HBV will develop acute fulminant hepatitis. This is even less common with HCV alone, although it becomes more frequent when both HBV and HCV are present together.

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Chronic Hepatitis B And C

There are specific antiviral treatments for chronic hepatitis B Treatment Hepatitis B is a common cause of chronic hepatitis. Patients may be asymptomatic or have nonspecific manifestations such as fatigue and malaise. Diagnosis is by serologic testing. Without treatment… read more and antiviral treatments for chronic hepatitis C Treatment Hepatitis C is a common cause of chronic hepatitis. It is often asymptomatic until manifestations of chronic liver disease occur. Diagnosis is confirmed by finding positive anti-HCV and positive… read more .

In chronic hepatitis due to HBV, prophylaxis for contacts of patients may be helpful. No vaccination is available for contacts of patients with HCV infection.

Corticosteroids and immunosuppressants should be avoided in chronic hepatitis B and C because these drugs enhance viral replication. If patients with chronic hepatitis B have other disorders that require treatment with corticosteroids, immunosuppressive therapies, or cytotoxic chemotherapy, they should be treated with antiviral drugs at the same time to prevent a flare or reactivation of hepatitis B or acute liver failure due to hepatitis B. A similar situation with hepatitis C being activated or causing acute liver failure has not been described.

Hcv And Changes In Metabolic Pathways

On proton magnetic resonance spectroscopy, metabolic abnormalities of choline/creatine ratio in basal ganglia and white matter have been detected in patients with histologically proven mild hepatitis C with respect to both healthy volunteers and chronic hepatitis B patients, suggesting a role for HCV itself in affecting cerebral functions. Moreover, significant correlations have been reported between cognitive dysfunction and HCV replication and between degree of impairment and the choline/creatine ratio in the basal ganglia and white matter in contrast to what is commonly observed in hepatic encephalopathy, a higher content in cerebral choline has been recorded in these patients. Although the exact significance of elevated choline in the white matter remains uncertain, it may be implicated in glial activation secondary to oxidative stress a similar mechanism has been suggested for chronic fatigue syndrome in HIV infection.

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Genotyping And Serotyping Of Hcv

Hepatitis C genotyping is helpful in defining the epidemiology of hepatitis C, but on an individual patient basis, genotyping is crucial in regard to treatment recommendations and duration. Genotyping is based on sequence analysis by sequencing or reverse hybridization. Although viral load can vary within a 0.5- to 1-log range, HCV genotype does not change during the course of infection. In case of suspected superinfection, another genotype might rarely be detected. For reliable genotyping, 5URT alone is insufficient, including parts of the core sequence enhance genotyping reliability. Sequencing of NS5b is the gold standard.

Serotyping is the only other option to test for the type of HCV in cases of remote infection. This, however, is relevant for epidemiologic studies only and is not used clinically.

Andrea D. Branch, in, 2004

Hcv And Direct Neuroinvasion

Since HCV core and non-structural NS3 and NS5A proteins have been found to activate macrophages/microglia as well as astrocytes of infected patients, HCV proteins have been hypothesized to have a role in inducing neurotoxicity. HCV core protein has been described to mediate neuronal injury by suppression of neuronal autophagy and through immune activation. Specifically, HCV core protein has been demonstrated to activate both toll-like receptor 2 signaling and extracellular signal-related kinase neurotoxicity has been described to result from prolonged TLR2-mediated activation of ERK.

Brain microvascular endothelial cells have been recently demonstrated to support HCV tropism and replication. HCV has been shown to induce apoptosis in these cells, leading to changes in the permeability of the blood brain barrier, microglia activation, and diffusion of pro-inflammatory cytokines into the CNS.

However, evidence for an association between HCV neuroinvasion and neuropsychiatric disorders is currently scarce indeed, replication of quasispecies occurs at a very low level within the CNS and HCV RNA is almost undetectable in cerebrospinal fluid finally, a poor correlation between viral load and clinical manifestations has been reported.

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Hcv Infection And Peripheral Neuropathy Disorders

In contrast to the brain, there is currently no evidence for peripheral nerves as permissive sites for HCV replication however, a wide variety of motor, sensory or sensorimotor mono- or polyneuropathies has been described during chronic HCV infection. Most peripheral neuropathies have been reported in patients with HCV-related mixed cryoglobulinemia, with prevalence up to 86% of cases. In particular, a sensory motor peripheral neuropathy has been found in up to 30% of HCV-positive cryoglobulinemic patients. Such neuropathy is the consequence of ischemic nerve changes, secondary to small-vessel vasculitis or necrotizing arteritis of medium-sized vessels. Frequently, the clinical onset is sub-acute as a distal, symmetric, sensory or sensorimotor polyneuropathy, although asymmetrical sensory impairment has also been reported. Small fiber sensory polyneuropathy , a painful condition mainly characterized by burning feet and tingling, is the most frequent neuropathy observed in patients with mild cryoglobulinemia syndrome, whereas the so called large fiber sensory neuropathy has been described less frequently. HCV-associated restless legs syndrome has also been reported as expression of SFSN. SFSN may later evolve in LFSN. LFSN symptoms include sensory loss, paresthesias, numbness, and cramps.

Diagnosis And Severity Rating

Overt hepatic encephalopathy is diagnosed based on clinical findings and by excluding other causes of altered mental status. The most common disorders to consider in the differential diagnosis of overt hepatic encephalopathy are medication-related adverse effects, severe electrolyte disorders , uremia, systemic infection, central nervous system infection, psychiatric disorders, alcohol-related disorders , hypoglycemia, hypercapnia, nonconvulsive epilepsy, and intracranial bleeding or stroke. As part of the diagnostic process, the clinician should categorize the type and severity of the overt hepatic encephalopathy. For most individuals, the West Haven criteria is considered the gold standard for categorizing the severity of overt hepatic encephalopathy it grades the severity of the hepatic encephalopathy based on a clinical assessment, with a score ranging from grade 0 to grade 4 . The Glasgow Coma Scale, however, may be more useful in persons with severe encephalopathy and a marked alteration in mental status . The diagnosis of minimal hepatic encephalopathy requires specific psychometric testing.

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What Is Chronic Viral Hepatitis

Patients infected with HBV and HCV can develop chronic hepatitis. Doctors define chronic hepatitis as hepatitis that lasts longer than 6 months. In chronic hepatitis, the viruses live and multiply in the liver for years or decades. For unknown reasons, these patients’ immune systems are unable to eradicate the viruses, and the viruses cause chronic inflammation of the liver. Chronic hepatitis can lead to the development over time of extensive liver scarring , liver failure, and liver cancer. Liver failure from chronic hepatitis C infection is the most common reason for liver transplantation in the U.S. Patients with chronic viral hepatitis can transmit the infection to others with blood or body fluids as well as infrequently by transmission from mother to newborn.

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Prognosis For Chronic Hepatitis

Prognosis for patients with chronic hepatitis is highly variable and often depends on the cause and availability of treatment.

Chronic hepatitis caused by a drug often regresses completely when the causative drug is withdrawn.

Without treatment, cases caused by HBV can resolve , progress rapidly, or progress slowly to cirrhosis over decades. Resolution often begins with a transient increase in disease severity and results in seroconversion from hepatitis B e antigen to antibody to hepatitis B e antigen . Coinfection with HDV causes the most severe form of chronic HBV infection without treatment, cirrhosis develops in up to 70% of patients with coinfection.

Untreated chronic hepatitis due to HCV causes cirrhosis in 20 to 30% of patients, although development may take decades and varies because it is often related to a patient’s other risk factors for chronic liver disease, including alcohol use and obesity.

Chronic autoimmune hepatitis usually responds to therapy but sometimes causes progressive fibrosis and eventual cirrhosis.

Chronic HBV infection increases the risk of hepatocellular carcinoma Hepatocellular Carcinoma Hepatocellular carcinoma usually occurs in patients with cirrhosis and is common in areas where infection with hepatitis B and C viruses is prevalent. Symptoms and signs are usually nonspecific… read more . The risk is also increased in other liver disorders , but usually when cirrhosis or advanced fibrosis has developed.

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