Annals of Internal Medicine is published by the American College of Physicians on the first and third Tuesday of every month. These highlights are not intended to substitute for articles as sources of information. For a copy of an article, call 215-351-2653 or e-mail Angela Collom at firstname.lastname@example.org
Middle-aged Americans Disproportionately Affected by “Silent Epidemic”
Approximately 3.2 million people in the United States are infected with chronic hepatitis C virus (HCV), a leading cause of liver disease, cirrhosis, and death. Chronic hepatitis infection is most prevalent among people born from 1945 through 1965, and most of them do not know they are infected. This population is now reaching the age where they are at risk for HCV-related diseases and premature death. Researchers examined death records from 1999 to 2007 for approximately 22 million people to examine mortality from HBV, HCV, and HIV (for comparison). They found that annual deaths from HCV now exceed those from HIV (15,000 deaths from HCV vs 13,000 deaths from HIV), and deaths from hepatitis B and C are concentrated among middle-aged persons. The authors warn that if policy initiatives do not focus on detection and treatment, then the burden of chronic hepatitis – already at epidemic proportions - will continue to rise. A second article being published in this print issue of Annals of Internal Medicine (early release online November 4, 2011) finds that birth-cohort testing and treatment for HCV is cost-effective, and could save thousands of lives each year. And a third article finds that both universal triple therapy and IL-28B guided triple therapy (treatments proven to increase survival) are cost-effective for treating HCV. The author of an accompanying editorial observes that a national “find-and-treat” policy designed to identify and aggressively treat those diagnosed is the missing piece of the puzzle.
Many people suspect that increasing levels of dietary fructose contribute to obesity, but study results have been mixed. Researchers reviewed two types of published controlled feeding trials to determine the effect of fructose on body weight. In 31 isocaloric trials, participants ate a similar number of calories, but one group ate pure fructose and the other ate nonfructose carbohydrates. In 10 hypercaloric trials, one group consumed their usual diet and the other added excess calories in the form of pure fructose to their usual diets. The researchers found that pure fructose had no effect on weight compared with diets that provided the same calories using nonfructose carbohydrate. Fructose increased weight in diets when the fructose added extra calories compared with the control diets. The researchers conclude that weight gain may be due to extra calories characteristic of high-fructose diets and may not be specific to fructose itself.
Family history is a recognized risk factor for many chronic diseases, including cardiovascular disease. Current guidelines for assessing cardiovascular risk recommend use of a Framingham-based algorithm that takes into account patient age, sex, smoking status, systolic blood pressure, and ratio of total to HDL cholesterol level. This assessment does not routinely include family history information, but physicians may request it at their discretion. Researchers mailed questionnaires about family history to 748 patients in 24 family practices in the United Kingdom to evaluate if taking information about a patient’s family history can improve risk assessment for cardiovascular disease. The researchers found that collecting family history identified nearly 5 percent more high-risk patients who were eligible for targeted prevention than did usual practice procedures. The author of an accompanying editorial writes that the research is promising, but could take effort to implement. Primary care physicians would need a validated method to collect family history; a practical way to collect, enter, and analyze the data; and systems in place to act on the information collected.
Celiac disease is a condition that damages the lining of the small intestine and prevents it from absorbing nutrients from food. The damage is due to a reaction to eating gluten, which is found in wheat, barley, rye, and possibly oats. Patients with celiac disease are diagnosed through specific blood and bowel tests. Some patients without celiac disease can still experience discomfort from eating gluten. Researchers refer to this syndrome as nonceliac gluten sensitivity. The prevalence of nonceliac gluten sensitivity in the general population is supposed to be many times higher than that of celiac disease. The syndrome is characterized by intestinal symptoms (diarrhea, abdominal discomfort, bloating, and flatulence) or extraintestinal symptoms (headache, lethargy, attention-deficit disorder, ataxia, or recurrent oral ulceration). However, some may believe themselves to be food-sensitive, but may withdrawal from gluten unnecessarily. According to the authors, nonceliac gluten sensitivity may only be apparent and caused by the “nocebo” effect of wheat or gluten ingestion. The authors cite cases where patients were formerly on highly restrictive, gluten-free diets and were convinced that it helped to limit their irritable bowel syndrome-like symptoms. According to the authors, few patients have been properly diagnosed. Until a valuable biomarker of nonceliac gluten sensitivity is identified, physicians may want to perform open or single-blind gluten challenge tests on patients complaining of gluten symptoms.