BACKGROUND: Asthma remains a leading cause of hospitalization in children. It has been determined that the MDI is equally as effective as nebulized wet aerosol therapy for treatment of acute asthma in adults, and may even work better in children older than 2 years.¹ The authors of this study investigated whether the same relationship holds true in children between the ages of 10 months and 4 years.

POPULATION STUDIED: The investigators enrolled 42 children aged 10 months to 4 years presenting to the emergency department of a large hospital in Israel. Children were not included if they had a history of cardiac disease or chronic respiratory disease (other than asthma), had an altered level of consciousness, or were in respiratory failure. Most subjects were referred from their primary care physicians to the emergency department because of the severity of their presentation.

STUDY DESIGN AND VALIDITY: This study was a randomized controlled double-blind double-dummy clinical trial. Subjects were randomly assigned to 2 groups. Randomization assignment was concealed. The first group received a standard dose of salbutamol (2.5 mg in 1.5 cc of normal saline) by nebulized aerosol therapy along with 4 puffs of placebo by MDI with a spacing device and facemask. The second group received 4 puffs of salbutamol (400 μg) by MDI with spacer and facemask along with 2 mL of normal saline by nebulized aerosol. Clinical scores (respiratory rate, pulse rate, pulse oximetry, wheezing, breath sounds, and retractions) were calculated at baseline and also 15 minutes after the conclusion of each respiratory treatment. Each patient received a total of 3 treatments delivered at 20-minute intervals. The study is well designed. The authors do not mention if any treatments were rendered by the referring physicians before arrival in the emergency department. The presence of antecedent b-agonist therapy could have affected the outcomes. This study was large enough to find a difference in the major outcomes (if one exists) but not to determine whether MDI therapy results in a change in the rate of hospitalization.

OUTCOMES MEASURED: The 2 major outcomes were respiratory rate and the patient’s clinical score. Minor outcomes included pulse rate and room air pulse oximetry. Hospitalization rates between the groups were also compared.

RESULTS: The study groups were similar at baseline. The reduction in respiratory rate and the improvement in patients’ clinical scores were similar between groups. Side effect rates were similar in the 2 groups. A total of 31% required hospitalization, but there was no difference in the rate of hospitalization between groups.

BACKGROUND: Asthma remains a leading cause of hospitalization in children. It has been determined that the MDI is equally as effective as nebulized wet aerosol therapy for treatment of acute asthma in adults, and may even work better in children older than 2 years.¹ The authors of this study investigated whether the same relationship holds true in children between the ages of 10 months and 4 years.

POPULATION STUDIED: The investigators enrolled 42 children aged 10 months to 4 years presenting to the emergency department of a large hospital in Israel. Children were not included if they had a history of cardiac disease or chronic respiratory disease (other than asthma), had an altered level of consciousness, or were in respiratory failure. Most subjects were referred from their primary care physicians to the emergency department because of the severity of their presentation.

STUDY DESIGN AND VALIDITY: This study was a randomized controlled double-blind double-dummy clinical trial. Subjects were randomly assigned to 2 groups. Randomization assignment was concealed. The first group received a standard dose of salbutamol (2.5 mg in 1.5 cc of normal saline) by nebulized aerosol therapy along with 4 puffs of placebo by MDI with a spacing device and facemask. The second group received 4 puffs of salbutamol (400 μg) by MDI with spacer and facemask along with 2 mL of normal saline by nebulized aerosol. Clinical scores (respiratory rate, pulse rate, pulse oximetry, wheezing, breath sounds, and retractions) were calculated at baseline and also 15 minutes after the conclusion of each respiratory treatment. Each patient received a total of 3 treatments delivered at 20-minute intervals. The study is well designed. The authors do not mention if any treatments were rendered by the referring physicians before arrival in the emergency department. The presence of antecedent b-agonist therapy could have affected the outcomes. This study was large enough to find a difference in the major outcomes (if one exists) but not to determine whether MDI therapy results in a change in the rate of hospitalization.

OUTCOMES MEASURED: The 2 major outcomes were respiratory rate and the patient’s clinical score. Minor outcomes included pulse rate and room air pulse oximetry. Hospitalization rates between the groups were also compared.

RESULTS: The study groups were similar at baseline. The reduction in respiratory rate and the improvement in patients’ clinical scores were similar between groups. Side effect rates were similar in the 2 groups. A total of 31% required hospitalization, but there was no difference in the rate of hospitalization between groups.

BACKGROUND: Asthma remains a leading cause of hospitalization in children. It has been determined that the MDI is equally as effective as nebulized wet aerosol therapy for treatment of acute asthma in adults, and may even work better in children older than 2 years.¹ The authors of this study investigated whether the same relationship holds true in children between the ages of 10 months and 4 years.

POPULATION STUDIED: The investigators enrolled 42 children aged 10 months to 4 years presenting to the emergency department of a large hospital in Israel. Children were not included if they had a history of cardiac disease or chronic respiratory disease (other than asthma), had an altered level of consciousness, or were in respiratory failure. Most subjects were referred from their primary care physicians to the emergency department because of the severity of their presentation.

STUDY DESIGN AND VALIDITY: This study was a randomized controlled double-blind double-dummy clinical trial. Subjects were randomly assigned to 2 groups. Randomization assignment was concealed. The first group received a standard dose of salbutamol (2.5 mg in 1.5 cc of normal saline) by nebulized aerosol therapy along with 4 puffs of placebo by MDI with a spacing device and facemask. The second group received 4 puffs of salbutamol (400 μg) by MDI with spacer and facemask along with 2 mL of normal saline by nebulized aerosol. Clinical scores (respiratory rate, pulse rate, pulse oximetry, wheezing, breath sounds, and retractions) were calculated at baseline and also 15 minutes after the conclusion of each respiratory treatment. Each patient received a total of 3 treatments delivered at 20-minute intervals. The study is well designed. The authors do not mention if any treatments were rendered by the referring physicians before arrival in the emergency department. The presence of antecedent b-agonist therapy could have affected the outcomes. This study was large enough to find a difference in the major outcomes (if one exists) but not to determine whether MDI therapy results in a change in the rate of hospitalization.

OUTCOMES MEASURED: The 2 major outcomes were respiratory rate and the patient’s clinical score. Minor outcomes included pulse rate and room air pulse oximetry. Hospitalization rates between the groups were also compared.

RESULTS: The study groups were similar at baseline. The reduction in respiratory rate and the improvement in patients’ clinical scores were similar between groups. Side effect rates were similar in the 2 groups. A total of 31% required hospitalization, but there was no difference in the rate of hospitalization between groups.

BACKGROUND: Because of their beneficial effects on mortality risk and functional status, angiotensin-converting-enzyme (ACE) inhibitors should be prescribed for all patients with heart failure and systolic left ventricular dysfunction unless specific contraindications exist. However, some physicians do not prescribe them because of fear of adverse effects. Angiotensin II type 1 receptor blockers (AT1RBs) may be better tolerated than ACE inhibitors. A secondary analysis of 49 deaths in the original Evaluation of Losartan in the Elderly (ELITE) study, in which the primary end point was the effect of treatment on renal function, showed an unexpected survival benefit for the AT1RB losartan over captopril, an ACE inhibitor. ELITE II was a larger trial designed to confirm whether losartan is superior to captopril in reducing all-cause mortality in elderly heart failure patients.

POPULATION STUDIED: The study included 3152 patients aged 60 years or older with New York Heart Association class II to IV heart failure and an ejection fraction of 40% or less. Most of the patients recruited from the 289 outpatient centers in 46 countries were white men aged older than 65 years who had never received an ACE inhibitor or an AT1RB. Exclusion criteria included previous intolerance or contraindication to either the study drug, systolic blood pressure greater than 90 mm Hg, uncontrolled hypertension, obstructive valvular heart disease, recent cardiac procedure or event, anticipated cardiac surgery, or recent cerebrovascular event.

STUDY DESIGN AND VALIDITY: This study was a prospective randomized double-blind trial funded by the manufacturer of losartan. Designed as an event-driven superiority trial, the study had 90% power to detect a relative 25% difference in all-cause mortality between treatments. At each study center, randomization was stratified on the basis of use of b-blockers. After a single-blind run-in period of 1 to 28 days, 1578 patients were allocated to losartan (12.5 mg titrated to a maximum of 50 mg once daily) and 1574 to captopril (12.5 mg titrated to a maximum of 50 mg 3 times daily). Clinical assessments were done weekly during dose titration and then every 4 months. Periodic laboratory assessments were also performed. The appropriate study design and intention-to-treat analysis were used for this efficacy trial. Neither the patients, those assessing clinical outcomes, nor the drug safety monitoring committee were aware of treatment status. Concealed allocation to treatment group at each study site was assured through central block randomization. The results are only applicable to elderly patients.

OUTCOMES MEASURED: The primary outcome was all-cause mortality, and the secondary end point was the composite of sudden cardiac death or resuscitated cardiac arrest.

RESULTS: Treatment groups were well matched demographically and for confounding variables that might affect response to treatment. Only 1 patient from each group was lost to follow-up during a median follow-up period of 18 months. A total of 280 deaths (17.5%) occurred in the losartan group compared with 250 (15.9%) in the captopril group, with an annual mortality rate of 11.7% and 10.4%, respectively (hazard ratio=1.13; 95.7% confidence interval, 0.95-1.35; P=.16). Neither of these differences was statistically significant, but power may have been an issue. Similarly, there was no significant difference in the composite of sudden death or resuscitated arrests (9.0% vs 7.3%). Fewer patients in the losartan group (excluding those who died) discontinued treatment because of side effects (9.7% vs 14.7%, P <.001).

BACKGROUND: Because of their beneficial effects on mortality risk and functional status, angiotensin-converting-enzyme (ACE) inhibitors should be prescribed for all patients with heart failure and systolic left ventricular dysfunction unless specific contraindications exist. However, some physicians do not prescribe them because of fear of adverse effects. Angiotensin II type 1 receptor blockers (AT1RBs) may be better tolerated than ACE inhibitors. A secondary analysis of 49 deaths in the original Evaluation of Losartan in the Elderly (ELITE) study, in which the primary end point was the effect of treatment on renal function, showed an unexpected survival benefit for the AT1RB losartan over captopril, an ACE inhibitor. ELITE II was a larger trial designed to confirm whether losartan is superior to captopril in reducing all-cause mortality in elderly heart failure patients.

POPULATION STUDIED: The study included 3152 patients aged 60 years or older with New York Heart Association class II to IV heart failure and an ejection fraction of 40% or less. Most of the patients recruited from the 289 outpatient centers in 46 countries were white men aged older than 65 years who had never received an ACE inhibitor or an AT1RB. Exclusion criteria included previous intolerance or contraindication to either the study drug, systolic blood pressure greater than 90 mm Hg, uncontrolled hypertension, obstructive valvular heart disease, recent cardiac procedure or event, anticipated cardiac surgery, or recent cerebrovascular event.

STUDY DESIGN AND VALIDITY: This study was a prospective randomized double-blind trial funded by the manufacturer of losartan. Designed as an event-driven superiority trial, the study had 90% power to detect a relative 25% difference in all-cause mortality between treatments. At each study center, randomization was stratified on the basis of use of b-blockers. After a single-blind run-in period of 1 to 28 days, 1578 patients were allocated to losartan (12.5 mg titrated to a maximum of 50 mg once daily) and 1574 to captopril (12.5 mg titrated to a maximum of 50 mg 3 times daily). Clinical assessments were done weekly during dose titration and then every 4 months. Periodic laboratory assessments were also performed. The appropriate study design and intention-to-treat analysis were used for this efficacy trial. Neither the patients, those assessing clinical outcomes, nor the drug safety monitoring committee were aware of treatment status. Concealed allocation to treatment group at each study site was assured through central block randomization. The results are only applicable to elderly patients.

OUTCOMES MEASURED: The primary outcome was all-cause mortality, and the secondary end point was the composite of sudden cardiac death or resuscitated cardiac arrest.

RESULTS: Treatment groups were well matched demographically and for confounding variables that might affect response to treatment. Only 1 patient from each group was lost to follow-up during a median follow-up period of 18 months. A total of 280 deaths (17.5%) occurred in the losartan group compared with 250 (15.9%) in the captopril group, with an annual mortality rate of 11.7% and 10.4%, respectively (hazard ratio=1.13; 95.7% confidence interval, 0.95-1.35; P=.16). Neither of these differences was statistically significant, but power may have been an issue. Similarly, there was no significant difference in the composite of sudden death or resuscitated arrests (9.0% vs 7.3%). Fewer patients in the losartan group (excluding those who died) discontinued treatment because of side effects (9.7% vs 14.7%, P <.001).

BACKGROUND: Because of their beneficial effects on mortality risk and functional status, angiotensin-converting-enzyme (ACE) inhibitors should be prescribed for all patients with heart failure and systolic left ventricular dysfunction unless specific contraindications exist. However, some physicians do not prescribe them because of fear of adverse effects. Angiotensin II type 1 receptor blockers (AT1RBs) may be better tolerated than ACE inhibitors. A secondary analysis of 49 deaths in the original Evaluation of Losartan in the Elderly (ELITE) study, in which the primary end point was the effect of treatment on renal function, showed an unexpected survival benefit for the AT1RB losartan over captopril, an ACE inhibitor. ELITE II was a larger trial designed to confirm whether losartan is superior to captopril in reducing all-cause mortality in elderly heart failure patients.

POPULATION STUDIED: The study included 3152 patients aged 60 years or older with New York Heart Association class II to IV heart failure and an ejection fraction of 40% or less. Most of the patients recruited from the 289 outpatient centers in 46 countries were white men aged older than 65 years who had never received an ACE inhibitor or an AT1RB. Exclusion criteria included previous intolerance or contraindication to either the study drug, systolic blood pressure greater than 90 mm Hg, uncontrolled hypertension, obstructive valvular heart disease, recent cardiac procedure or event, anticipated cardiac surgery, or recent cerebrovascular event.

STUDY DESIGN AND VALIDITY: This study was a prospective randomized double-blind trial funded by the manufacturer of losartan. Designed as an event-driven superiority trial, the study had 90% power to detect a relative 25% difference in all-cause mortality between treatments. At each study center, randomization was stratified on the basis of use of b-blockers. After a single-blind run-in period of 1 to 28 days, 1578 patients were allocated to losartan (12.5 mg titrated to a maximum of 50 mg once daily) and 1574 to captopril (12.5 mg titrated to a maximum of 50 mg 3 times daily). Clinical assessments were done weekly during dose titration and then every 4 months. Periodic laboratory assessments were also performed. The appropriate study design and intention-to-treat analysis were used for this efficacy trial. Neither the patients, those assessing clinical outcomes, nor the drug safety monitoring committee were aware of treatment status. Concealed allocation to treatment group at each study site was assured through central block randomization. The results are only applicable to elderly patients.

OUTCOMES MEASURED: The primary outcome was all-cause mortality, and the secondary end point was the composite of sudden cardiac death or resuscitated cardiac arrest.

RESULTS: Treatment groups were well matched demographically and for confounding variables that might affect response to treatment. Only 1 patient from each group was lost to follow-up during a median follow-up period of 18 months. A total of 280 deaths (17.5%) occurred in the losartan group compared with 250 (15.9%) in the captopril group, with an annual mortality rate of 11.7% and 10.4%, respectively (hazard ratio=1.13; 95.7% confidence interval, 0.95-1.35; P=.16). Neither of these differences was statistically significant, but power may have been an issue. Similarly, there was no significant difference in the composite of sudden death or resuscitated arrests (9.0% vs 7.3%). Fewer patients in the losartan group (excluding those who died) discontinued treatment because of side effects (9.7% vs 14.7%, P <.001).

BACKGROUND: African Americans experience higher death rates from asthma than whites. Understanding potential differences in how these 2 ethnic groups describe or experience their symptoms during an asthma exacerbation may improve asthma management in African Americans.

POPULATION STUDIED: The investigators studied 40 adult asthmatics with atopy whose baseline asthma therapy consisted of only intermittent b-agonists. Patients were excluded if they used inhaled or oral steroids, theophylline, or antihistamines within 6 weeks of the study. Also, patients were not enrolled if they had hypertension, heart disease, diabetes, malignancy, or immune disorders or if they had used tobacco within the past year or had a cumulative history greater than 10 pack-years. Eight patients were dropped because sufficient airflow obstruction could not be induced; 6 of those were African American. Of the resultant African American group 75% were women, but only 56% of the whites were women.

STUDY DESIGN AND VALIDITY: This study was an experimental protocol, artificially inducing bronchocontriction in otherwise asymptomatic asthmatics. Subjects were given methacholine to induce bronchoconstriction, resulting in a 30% drop in forced expiratory volume in 1 second (FEV1). Two minutes after dosing, subjects described the sensations they experienced in their own words. The descriptions were clustered into general groups for those descriptors used by at least 75% of the group participants. Subjects also rated the severity of breathlessness by visual analog scale (VAS) and by selecting word or number descriptors. This experimental study was tightly controlled to be able to accurately match the symptoms in the 2 ethnic groups. However, this design may not reflect the more complicated and variable patients seen in everyday practice. Also, the study was performed in one geographic area (northern California), and patients in other areas may use a different vocabulary to express their symptoms. Similarly, induced bronchoconstriction may be experienced differently than a natural occurring asthma attack. Also, our ability to generalize the results is frequently limited in qualitative studies such as this one.

OUTCOMES MEASURED: The categories of phrases used to describe the sensation of breathlessness comprised the primary outcome. Symptom severity was a secondary outcome.

RESULTS: Words used to describe the symptoms during airflow obstruction differed between the 2 ethnic groups. African Americans were statistically more likely to use upper airway descriptors to explain their breathlessness: “tight throat,” “voice tight,” “itchy throat,” “tough breath,” and “scared-agitated” were the word clusters most often used. Whites were more apt to use lower airway terms, such as “deep breath,” “out of air,” “aware of breathing,” “hurts to breathe,” and “lightheaded.” No subjects used the traditional medical terminology of “shortness of breath” or “wheezing.” African American subjects rated their baseline breathlessness slightly greater than whites (14.25 vs 11.0 on a 0-100 VAS, P <.04). As expected, severity scores increased as FEV1 decreased. At a 20% reduction, whites reported a greater sense of breathlessness, but there was no difference between the 2 groups at a 30% reduction in FEV1.

BACKGROUND: African Americans experience higher death rates from asthma than whites. Understanding potential differences in how these 2 ethnic groups describe or experience their symptoms during an asthma exacerbation may improve asthma management in African Americans.

POPULATION STUDIED: The investigators studied 40 adult asthmatics with atopy whose baseline asthma therapy consisted of only intermittent b-agonists. Patients were excluded if they used inhaled or oral steroids, theophylline, or antihistamines within 6 weeks of the study. Also, patients were not enrolled if they had hypertension, heart disease, diabetes, malignancy, or immune disorders or if they had used tobacco within the past year or had a cumulative history greater than 10 pack-years. Eight patients were dropped because sufficient airflow obstruction could not be induced; 6 of those were African American. Of the resultant African American group 75% were women, but only 56% of the whites were women.

STUDY DESIGN AND VALIDITY: This study was an experimental protocol, artificially inducing bronchocontriction in otherwise asymptomatic asthmatics. Subjects were given methacholine to induce bronchoconstriction, resulting in a 30% drop in forced expiratory volume in 1 second (FEV1). Two minutes after dosing, subjects described the sensations they experienced in their own words. The descriptions were clustered into general groups for those descriptors used by at least 75% of the group participants. Subjects also rated the severity of breathlessness by visual analog scale (VAS) and by selecting word or number descriptors. This experimental study was tightly controlled to be able to accurately match the symptoms in the 2 ethnic groups. However, this design may not reflect the more complicated and variable patients seen in everyday practice. Also, the study was performed in one geographic area (northern California), and patients in other areas may use a different vocabulary to express their symptoms. Similarly, induced bronchoconstriction may be experienced differently than a natural occurring asthma attack. Also, our ability to generalize the results is frequently limited in qualitative studies such as this one.

OUTCOMES MEASURED: The categories of phrases used to describe the sensation of breathlessness comprised the primary outcome. Symptom severity was a secondary outcome.

RESULTS: Words used to describe the symptoms during airflow obstruction differed between the 2 ethnic groups. African Americans were statistically more likely to use upper airway descriptors to explain their breathlessness: “tight throat,” “voice tight,” “itchy throat,” “tough breath,” and “scared-agitated” were the word clusters most often used. Whites were more apt to use lower airway terms, such as “deep breath,” “out of air,” “aware of breathing,” “hurts to breathe,” and “lightheaded.” No subjects used the traditional medical terminology of “shortness of breath” or “wheezing.” African American subjects rated their baseline breathlessness slightly greater than whites (14.25 vs 11.0 on a 0-100 VAS, P <.04). As expected, severity scores increased as FEV1 decreased. At a 20% reduction, whites reported a greater sense of breathlessness, but there was no difference between the 2 groups at a 30% reduction in FEV1.

BACKGROUND: African Americans experience higher death rates from asthma than whites. Understanding potential differences in how these 2 ethnic groups describe or experience their symptoms during an asthma exacerbation may improve asthma management in African Americans.

POPULATION STUDIED: The investigators studied 40 adult asthmatics with atopy whose baseline asthma therapy consisted of only intermittent b-agonists. Patients were excluded if they used inhaled or oral steroids, theophylline, or antihistamines within 6 weeks of the study. Also, patients were not enrolled if they had hypertension, heart disease, diabetes, malignancy, or immune disorders or if they had used tobacco within the past year or had a cumulative history greater than 10 pack-years. Eight patients were dropped because sufficient airflow obstruction could not be induced; 6 of those were African American. Of the resultant African American group 75% were women, but only 56% of the whites were women.

STUDY DESIGN AND VALIDITY: This study was an experimental protocol, artificially inducing bronchocontriction in otherwise asymptomatic asthmatics. Subjects were given methacholine to induce bronchoconstriction, resulting in a 30% drop in forced expiratory volume in 1 second (FEV1). Two minutes after dosing, subjects described the sensations they experienced in their own words. The descriptions were clustered into general groups for those descriptors used by at least 75% of the group participants. Subjects also rated the severity of breathlessness by visual analog scale (VAS) and by selecting word or number descriptors. This experimental study was tightly controlled to be able to accurately match the symptoms in the 2 ethnic groups. However, this design may not reflect the more complicated and variable patients seen in everyday practice. Also, the study was performed in one geographic area (northern California), and patients in other areas may use a different vocabulary to express their symptoms. Similarly, induced bronchoconstriction may be experienced differently than a natural occurring asthma attack. Also, our ability to generalize the results is frequently limited in qualitative studies such as this one.

OUTCOMES MEASURED: The categories of phrases used to describe the sensation of breathlessness comprised the primary outcome. Symptom severity was a secondary outcome.

RESULTS: Words used to describe the symptoms during airflow obstruction differed between the 2 ethnic groups. African Americans were statistically more likely to use upper airway descriptors to explain their breathlessness: “tight throat,” “voice tight,” “itchy throat,” “tough breath,” and “scared-agitated” were the word clusters most often used. Whites were more apt to use lower airway terms, such as “deep breath,” “out of air,” “aware of breathing,” “hurts to breathe,” and “lightheaded.” No subjects used the traditional medical terminology of “shortness of breath” or “wheezing.” African American subjects rated their baseline breathlessness slightly greater than whites (14.25 vs 11.0 on a 0-100 VAS, P <.04). As expected, severity scores increased as FEV1 decreased. At a 20% reduction, whites reported a greater sense of breathlessness, but there was no difference between the 2 groups at a 30% reduction in FEV1.

Supplement Editor:
Zobair M. Younossi, MD, MPH, FACP, FACG

Contents

Epidemiology and clinical features of hepatitis viruses
Hepatitis A
Hepatitis B
Hepatitis C
Hepatitis D
Hepatitis E
Hepatitis G/GBV-C

Prevention of hepatitis
Hepatitis A and hepatitis E
Hepatitis B and hepatitis D
Hepatitis C
The role of vaccine in patients with chronic liver disease

Diagnostic tests
Hepatitis A
Hepatitis B
Hepatitis C
Hepatitis D
Hepatitis E
Role of liver biopsy in viral hepatitis

Management of acute viral hepatitis
Clinical characteristics of acute viral hepatitis
Treatment of acute viral hepatitis
Progression to chronic viral hepatitis
Fulminant hepatic failure
Therapeutic options and treatment modalities for chronic viral hepatitis
Role of referral to specialist centers
Role of liver transplantation for viral hepatitis
Screening for hepatocellular carcinoma
Treatment recommendations for specific viral etiologies

Managment of special groups
Management issues in pediatric hepatitis
Management issues in pregnancy and birth
Management issues in hemodialysis patients
Managmenet issues for tranplant recipients
Management issues in immunocompromised patients
Managing patients with human immunodeficiency virus
Alcohol and viral hepatitis

References

Supplement Editor:
Zobair M. Younossi, MD, MPH, FACP, FACG

Contents

Epidemiology and clinical features of hepatitis viruses
Hepatitis A
Hepatitis B
Hepatitis C
Hepatitis D
Hepatitis E
Hepatitis G/GBV-C

Prevention of hepatitis
Hepatitis A and hepatitis E
Hepatitis B and hepatitis D
Hepatitis C
The role of vaccine in patients with chronic liver disease

Diagnostic tests
Hepatitis A
Hepatitis B
Hepatitis C
Hepatitis D
Hepatitis E
Role of liver biopsy in viral hepatitis

Management of acute viral hepatitis
Clinical characteristics of acute viral hepatitis
Treatment of acute viral hepatitis
Progression to chronic viral hepatitis
Fulminant hepatic failure
Therapeutic options and treatment modalities for chronic viral hepatitis
Role of referral to specialist centers
Role of liver transplantation for viral hepatitis
Screening for hepatocellular carcinoma
Treatment recommendations for specific viral etiologies

Managment of special groups
Management issues in pediatric hepatitis
Management issues in pregnancy and birth
Management issues in hemodialysis patients
Managmenet issues for tranplant recipients
Management issues in immunocompromised patients
Managing patients with human immunodeficiency virus
Alcohol and viral hepatitis

References

Supplement Editor:
Zobair M. Younossi, MD, MPH, FACP, FACG

Contents

Epidemiology and clinical features of hepatitis viruses
Hepatitis A
Hepatitis B
Hepatitis C
Hepatitis D
Hepatitis E
Hepatitis G/GBV-C

Prevention of hepatitis
Hepatitis A and hepatitis E
Hepatitis B and hepatitis D
Hepatitis C
The role of vaccine in patients with chronic liver disease

Diagnostic tests
Hepatitis A
Hepatitis B
Hepatitis C
Hepatitis D
Hepatitis E
Role of liver biopsy in viral hepatitis

Management of acute viral hepatitis
Clinical characteristics of acute viral hepatitis
Treatment of acute viral hepatitis
Progression to chronic viral hepatitis
Fulminant hepatic failure
Therapeutic options and treatment modalities for chronic viral hepatitis
Role of referral to specialist centers
Role of liver transplantation for viral hepatitis
Screening for hepatocellular carcinoma
Treatment recommendations for specific viral etiologies

Managment of special groups
Management issues in pediatric hepatitis
Management issues in pregnancy and birth
Management issues in hemodialysis patients
Managmenet issues for tranplant recipients
Management issues in immunocompromised patients
Managing patients with human immunodeficiency virus
Alcohol and viral hepatitis

References