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| Fwd: Case: Fever, Arthralgias, and Headache/Hepatitis C/Irbesartan a |
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| THIS WEEK'S TEACHING TOPICS |  | | | | | | | | |
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| EDITOR'S NOTE: Perspective Forum — Residents' Duty Hours and the IOM Report. How has the 80-hour workweek affected patients and residents? In a Perspective article appearing on the Journal Web site today, John Iglehart examines a new report by the Institute of Medicine (IOM) analyzing the 80-hour limit and makes new recommendations. After reading the article, you can vote and comment on this topic. |
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TEACHING TOPIC
1. Case: Fever, Arthralgias, and Headache
CLINICAL PROBLEM-SOLVING, Taken Out of Context, M.P. Thomas and A. Wang, Extract | Full Text | PDF
A 25-year-old woman with a history of depression, mitral-valve prolapse, and migraine headache presented to the emergency department with a three-day history of subjective fever, diffuse arthralgia, and severe generalized headache that was not characteristic of her previous migraines. What is the differential diagnosis?
Clinical Pearls
 Thrombotic Thrombocytopenic Purpura
Clinical manifestations of thrombotic thrombocytopenic purpura are variable. The classic pentad is thrombocytopenia, intravascular hemolysis (microangiopathic hemolytic anemia), neurologic abnormalities, decreased renal function, and fever. However, fever is present infrequently in patients with this disorder. The presence of microangiopathic hemolytic anemia and thrombocytopenia in the absence of another known cause is often considered sufficient to establish the diagnosis and to justify treatment with plasma exchange, which has been shown to improve survival. However, these hematologic findings are not specific for thrombotic thrombocytopenia purpura, and other diagnoses must still be considered, even in the case of an apparently favorable response to treatment.
Infective Endocarditis and Mitral-Valve Prolapse
A predisposing cardiac condition is apparent in approximately half of all cases of infective endocarditis; mitral-valve prolapse is the most frequent underlying cardiac abnormality in infective endocarditis. A common, often benign condition, such as mitral-valve prolapse may be viewed as an irrelevant detail in the presence of more prominent findings reflecting dysfunction of other systems. A diagnostic evaluation must consider the patient's presenting symptoms and signs in the context of predisposing conditions.
Figure 2. Transesophageal Echocardiogram.
| Morning Report Question | | Q: |  |
Are blood cultures always positive in infective endocarditis? | | A: | |
No. “Culture-negative” infective endocarditis, defined as definite infective endocarditis in the absence of positive blood cultures but in the presence of other diagnostic criteria, accounts for approximately 10 to 30% of cases overall and is particularly common when antibiotics are administered before blood cultures have been obtained.
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TEACHING TOPIC
2. Long-Term Therapy for Hepatitis C
ORIGINAL ARTICLE, Prolonged Therapy of Advanced Chronic Hepatitis C with Low-Dose Peginterferon, A.M. Di Bisceglie and Others, Abstract | Full Text | PDF | PPT Slide Set
In patients with chronic hepatitis C who do not have a response to antiviral treatment, the disease may progress to cirrhosis, liver failure, hepatocellular carcinoma, and death. Whether long-term antiviral therapy can prevent progressive liver disease in such patients remains uncertain. In this study by Di Bisceglie and colleagues, long-term therapy with peginterferon at a dose of 90 µg per week for 3.5 years, as compared with no treatment did not reduce the rate of disease progression in patients with chronic hepatitis C and advanced fibrosis.
Table 2. First Primary Outcome in Treated and Control Patients with Noncirrhotic Fibrosis or Cirrhosis at Baseline.
Clinical Pearls
Hepatitis C, Cirrhosis, and Hepatocellular Carcinoma
More than 3 million Americans and 170 million persons worldwide are chronically infected with hepatitis C virus (HCV), which can result in progressive hepatic injury and fibrosis, culminating in cirrhosis and end-stage liver disease. Among adults in the Western world, chronic hepatitis C is a major cause of cirrhosis and a major indication for liver transplantation. Chronic hepatitis C has also contributed to the increasing incidence of hepatocellular carcinoma, for which few satisfactory therapies exist.
Long-Term Peginterferon Therapy
Several reports have suggested that interferon-based therapy in patients with chronic hepatitis C may reduce the risk of hepatocellular carcinoma among those patients with a sustained virologic response. In HALT-C, a large-scale randomized trial, the investigators assessed the effect of interferon on the incidence of hepatocellular carcinoma, and observed that even when maintained for several years, peginterferon therapy does not reduce the incidence of hepatocellular carcinoma in patients with advanced fibrosis and persistent viremia.
| Morning Report Question | | Q: | |
What tests are routinely performed on patients infected with hepatitis C? | | A: | |
Patients with chronic hepatitis C are often routinely and periodically screened with ultrasound and AFP (alpha-fetoprotein) testing to detect hepatocellular carcinoma.
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TEACHING TOPIC
3. Irbesartan in Patients with Heart Failure and Preserved Ejection Fraction
ORIGINAL ARTICLE, Irbesartan in Patients with Heart Failure and Preserved Ejection Fraction, B.M. Massie and Others, Abstract | Full Text | PDF | PPT Slide Set
In this large, randomized trial, treatment with the angiotensin receptor blocker (ARB) irbesartan neither reduced the risk of death or hospitalization for cardiovascular causes among patients who had heart failure with preserved left ventricular ejection fraction, nor improved any of the secondary clinical outcomes, including disease-specific quality of life. These findings contrast with the benefits observed with inhibitors of the renin–angiotensin–aldosterone system, including angiotensin-receptor blockers, in patients with heart failure and a low left ventricular ejection fraction.
Clinical Pearls
Heart Failure with Preserved Ejection Fraction
Approximately half of patients with a diagnosis of heart failure have a normal or near-normal left ventricular ejection fraction. Such patients differ from those with heart failure and a low left ventricular ejection fraction in a number of important ways. Those with preserved left ventricular function tend to be older, female, and to have hypertension rather than ischemia. The rates of death and illness among these patients are high and have not declined, as they have in patients with heart failure and a low left ventricular ejection fraction.
Figure 1. Kaplan–Meier Curves for the Primary Outcome.
Pathophysiology of Heart Failure
Heart failure may be related to a variety of factors, including impairment of left ventricular diastolic dysfunction from myocardial hypertrophy and fibrosis. Other factors include altered myocyte calcium handling, abnormal ventricular-vascular coupling related to decreased vascular compliance, impaired renal handling of salt and fluid, and other as-yet-poorly-characterized abnormalities. In patients with a preserved ejection fraction, the pathophysiologic substrate of a dilated, remodeled heart and clinically evident atherosclerotic disease is less apparent or absent. In this study, in spite of the preponderance of patients with a history of hypertension, only a minority of patients had electrocardiographic evidence of left ventricular hypertrophy.
| Morning Report Questions | | Q: | |
What is the plasma renin activity level in patients with heart failure and a preserved left ventricular ejection fraction as compared with levels in those with a low ventricular ejection fraction? | | A: | |
Available data indicate that plasma renin activity is increased in patients with heart failure and a preserved left ventricular ejection fraction, as compared with control subjects, although levels are lower than in patients who have heart failure with a low left ventricular ejection fraction. Blockage of the renin–angiotensin system has favorable effects in patients with heart failure and a low left ventricular ejection fraction.
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How is body-mass index computed? | | A: | |
Body-mass index is defined as the weight in kilograms divided by the square of the height in meters.
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