Clinical Inquiries

Evidence summary

This answer focuses on the behavioral and sociodemographic factors involved in smoking cessation and does not review the pharmacologic approaches to a successful smoking cessation attempt.

In 1999, 41.3% of current smokers (95% confidence interval [CI], 39.8–42.8) reported quit attempts of at least 1 day during the preceding 12 months.¹ In a 1994 survey of 2000 United Kingdom adults, 70% of smokers reported a desire to quit smoking, and 89% of smokers reported at least 1 quit attempt.² Cochrane Library meta-analyses have found that brief advice from physicians (odds ratio [OR]=1.69; 95% CI, 1.45–1.98), individual counseling or group counseling (OR=1.55; 95% CI, 1.27–1.90), self-help materials (OR=1.23; 95% CI, 1.02–1.49), and nicotine replacement therapy (OR=1.71; 95% CI, 1.60–1.83) enhanced quit rates over a 6-month or greater period.³

However, relapse from smoking cessation is a significant problem. In the 1996 California Tobacco Survey of 4480 Californians, only 15.2% of those who used smoking cessation assistance (self-help, counseling, or nicotine replacement therapy), and 7.0% who used no assistance were abstinent from tobacco in 12 months.⁴

Smoking during the first 2 weeks of an attempt predicts decreased long-term cessation rates. In 2 independent randomized, double-blinded, placebo-controlled studies, 200 subjects were placed on various doses of nicotine replacement (study one: 22-mg nicotine patch for 8 weeks, study two: 22-mg patch for 4 weeks then 11 mg patch for 2 weeks). Of those who remained abstinent during the first 2 weeks while on a patch, 46.2% and 40.9% maintained abstinence at 6 months (OR=4.3 and 23.5, respectively) while abstinent subjects on placebo maintained abstinence at a rate of 43.8% and 30% (OR=9.7 and 18.9, respectively). Conversely, of those who were on a patch and smoked during the first 2 weeks of an attempt, 83.3% and 97.1% were smoking 6 months out while 92.6% and 97.8% of those in the placebo groups who smoked during the first 2 weeks were smoking at 6 months.⁵

In 2 randomized, non-placebo-controlled clinical trials of 200 subjects, 41.3% of smokers placed on nicotine replacement that were abstinent on their quit date and had a low tobacco dependence score (based on the Fagerström Test for Nicotine Dependence) were able to maintain abstinence at the 6-month mark (OR=4.1). Those who smoked on the quit date were 10 times less likely to have long-term success (OR=0.1).⁶

In a retrospective survey of 2000 subjects those with less than 5 previous cessation attempts as well as perceived helpful support from friends had a greater likelihood of successful smoking cessation.⁷ In a retrospective review of socioeconomic factors associated with tobacco cessation among 3575 subjects of the CEASE trial, being a homeowner (OR=1.62) and male gender (OR=1.38) increased likelihood of tobacco cessation at 6 months.⁸ In a retrospective review of 2684 subjects from the Framingham study, women who smoked less that 1 half-pack per day (OR=2.6) and males who were diagnosed with CAD within the past 2 years (OR=1.9) were more likely to maintain abstinence 1 year after the cessation attempt.⁹ The TABLE summarizes results from 5 studies focusing on a variety of factors and their effects on smoking cessation.

Counseling frequency and duration impact smoking cessation. In a meta-analysis of 23 studies, the odds ratio for cessation was 1.3 (95% CI, 1.01–1.6) for minimal counseling (<3 minutes), 1.6 (95% CI, 1.2–2.0) for low-intensity counseling (3 to 10 minutes), and 2.3 (95% CI, 2.0–2.7) for high-intensity counseling (>10 minutes).¹⁰ In a meta-analysis of 35 studies, smoking cessation increased as total contact time for all counseling sessions increased, peaking at 90 minutes (OR=3.0; 95% CI, 2.3–3.8).¹⁰ In a meta-analysis of 45 studies, smoking cessation increased as number of person-to-person counseling sessions increased from 2 to 3 sessions (OR=1.4; 95% CI, 1.1–1.7) to 4 to 8 sessions (OR=1.9; 95% CI, 1.6–2.2) to >8 sessions (OR=2.3; 95% CI, 2.1–3.0).¹⁰

A meta-analysis of 62 studies found no impact of relaxation/breathing techniques, contingency contracting, weight/diet counseling, cigarette fading, or negative affect counseling on smoking cessation.¹⁰ Successful counseling techniques included providing smokers with problem solving skills (OR for successful smoking cessation=1.5; 95% CI, 1.3–1.8), providing intra-treatment social support (OR=1.3; 95% CI, 1.1–1.6), helping smokers obtain extra-treatment social support (OR=1.5; 95% CI, 1.1–2.1), use of rapid smoking (OR=2.0; 95% CI, 1.1–3.5), and use of other “aversive smoking techniques” (OR=1.7; 95% CI, 1.04–2.8).

TABLE
Factors predicting success or failure for a smoking cessation attempt

Recommendations from others

The US Public Health Service Clinical Practice Guideline (2000)¹⁰ supports the following recommendations, based on rigorously conducted meta-analyses: use of office screening systems to identify smokers; physician advice to quit; use of multiple clinician types in smoking cessation counseling; and treatments delivered by telephone counseling, group counseling, and individual counseling, used alone or in combination, as opposed to self-help materials for smoking cessation.

The US Department of Health and Human Services¹¹ recommends that physicians ask and record tobacco-use status and offer smoking cessation advice and treatment at every office visit. They also recommend the “5 A’s” (Ask, Advise, Assess, Assist, and Arrange) for patients who desire smoking cessation and the “5 R’s” motivational intervention (Relevance, Risks, Rewards, Roadblocks, and Repetition) for those who are not ready to quit smoking.

Evidence summary

This answer focuses on the behavioral and sociodemographic factors involved in smoking cessation and does not review the pharmacologic approaches to a successful smoking cessation attempt.

In 1999, 41.3% of current smokers (95% confidence interval [CI], 39.8–42.8) reported quit attempts of at least 1 day during the preceding 12 months.¹ In a 1994 survey of 2000 United Kingdom adults, 70% of smokers reported a desire to quit smoking, and 89% of smokers reported at least 1 quit attempt.² Cochrane Library meta-analyses have found that brief advice from physicians (odds ratio [OR]=1.69; 95% CI, 1.45–1.98), individual counseling or group counseling (OR=1.55; 95% CI, 1.27–1.90), self-help materials (OR=1.23; 95% CI, 1.02–1.49), and nicotine replacement therapy (OR=1.71; 95% CI, 1.60–1.83) enhanced quit rates over a 6-month or greater period.³

However, relapse from smoking cessation is a significant problem. In the 1996 California Tobacco Survey of 4480 Californians, only 15.2% of those who used smoking cessation assistance (self-help, counseling, or nicotine replacement therapy), and 7.0% who used no assistance were abstinent from tobacco in 12 months.⁴

Smoking during the first 2 weeks of an attempt predicts decreased long-term cessation rates. In 2 independent randomized, double-blinded, placebo-controlled studies, 200 subjects were placed on various doses of nicotine replacement (study one: 22-mg nicotine patch for 8 weeks, study two: 22-mg patch for 4 weeks then 11 mg patch for 2 weeks). Of those who remained abstinent during the first 2 weeks while on a patch, 46.2% and 40.9% maintained abstinence at 6 months (OR=4.3 and 23.5, respectively) while abstinent subjects on placebo maintained abstinence at a rate of 43.8% and 30% (OR=9.7 and 18.9, respectively). Conversely, of those who were on a patch and smoked during the first 2 weeks of an attempt, 83.3% and 97.1% were smoking 6 months out while 92.6% and 97.8% of those in the placebo groups who smoked during the first 2 weeks were smoking at 6 months.⁵

In 2 randomized, non-placebo-controlled clinical trials of 200 subjects, 41.3% of smokers placed on nicotine replacement that were abstinent on their quit date and had a low tobacco dependence score (based on the Fagerström Test for Nicotine Dependence) were able to maintain abstinence at the 6-month mark (OR=4.1). Those who smoked on the quit date were 10 times less likely to have long-term success (OR=0.1).⁶

In a retrospective survey of 2000 subjects those with less than 5 previous cessation attempts as well as perceived helpful support from friends had a greater likelihood of successful smoking cessation.⁷ In a retrospective review of socioeconomic factors associated with tobacco cessation among 3575 subjects of the CEASE trial, being a homeowner (OR=1.62) and male gender (OR=1.38) increased likelihood of tobacco cessation at 6 months.⁸ In a retrospective review of 2684 subjects from the Framingham study, women who smoked less that 1 half-pack per day (OR=2.6) and males who were diagnosed with CAD within the past 2 years (OR=1.9) were more likely to maintain abstinence 1 year after the cessation attempt.⁹ The TABLE summarizes results from 5 studies focusing on a variety of factors and their effects on smoking cessation.

Counseling frequency and duration impact smoking cessation. In a meta-analysis of 23 studies, the odds ratio for cessation was 1.3 (95% CI, 1.01–1.6) for minimal counseling (<3 minutes), 1.6 (95% CI, 1.2–2.0) for low-intensity counseling (3 to 10 minutes), and 2.3 (95% CI, 2.0–2.7) for high-intensity counseling (>10 minutes).¹⁰ In a meta-analysis of 35 studies, smoking cessation increased as total contact time for all counseling sessions increased, peaking at 90 minutes (OR=3.0; 95% CI, 2.3–3.8).¹⁰ In a meta-analysis of 45 studies, smoking cessation increased as number of person-to-person counseling sessions increased from 2 to 3 sessions (OR=1.4; 95% CI, 1.1–1.7) to 4 to 8 sessions (OR=1.9; 95% CI, 1.6–2.2) to >8 sessions (OR=2.3; 95% CI, 2.1–3.0).¹⁰

A meta-analysis of 62 studies found no impact of relaxation/breathing techniques, contingency contracting, weight/diet counseling, cigarette fading, or negative affect counseling on smoking cessation.¹⁰ Successful counseling techniques included providing smokers with problem solving skills (OR for successful smoking cessation=1.5; 95% CI, 1.3–1.8), providing intra-treatment social support (OR=1.3; 95% CI, 1.1–1.6), helping smokers obtain extra-treatment social support (OR=1.5; 95% CI, 1.1–2.1), use of rapid smoking (OR=2.0; 95% CI, 1.1–3.5), and use of other “aversive smoking techniques” (OR=1.7; 95% CI, 1.04–2.8).

TABLE
Factors predicting success or failure for a smoking cessation attempt

Recommendations from others

The US Public Health Service Clinical Practice Guideline (2000)¹⁰ supports the following recommendations, based on rigorously conducted meta-analyses: use of office screening systems to identify smokers; physician advice to quit; use of multiple clinician types in smoking cessation counseling; and treatments delivered by telephone counseling, group counseling, and individual counseling, used alone or in combination, as opposed to self-help materials for smoking cessation.

The US Department of Health and Human Services¹¹ recommends that physicians ask and record tobacco-use status and offer smoking cessation advice and treatment at every office visit. They also recommend the “5 A’s” (Ask, Advise, Assess, Assist, and Arrange) for patients who desire smoking cessation and the “5 R’s” motivational intervention (Relevance, Risks, Rewards, Roadblocks, and Repetition) for those who are not ready to quit smoking.

Evidence summary

This answer focuses on the behavioral and sociodemographic factors involved in smoking cessation and does not review the pharmacologic approaches to a successful smoking cessation attempt.

In 1999, 41.3% of current smokers (95% confidence interval [CI], 39.8–42.8) reported quit attempts of at least 1 day during the preceding 12 months.¹ In a 1994 survey of 2000 United Kingdom adults, 70% of smokers reported a desire to quit smoking, and 89% of smokers reported at least 1 quit attempt.² Cochrane Library meta-analyses have found that brief advice from physicians (odds ratio [OR]=1.69; 95% CI, 1.45–1.98), individual counseling or group counseling (OR=1.55; 95% CI, 1.27–1.90), self-help materials (OR=1.23; 95% CI, 1.02–1.49), and nicotine replacement therapy (OR=1.71; 95% CI, 1.60–1.83) enhanced quit rates over a 6-month or greater period.³

However, relapse from smoking cessation is a significant problem. In the 1996 California Tobacco Survey of 4480 Californians, only 15.2% of those who used smoking cessation assistance (self-help, counseling, or nicotine replacement therapy), and 7.0% who used no assistance were abstinent from tobacco in 12 months.⁴

Smoking during the first 2 weeks of an attempt predicts decreased long-term cessation rates. In 2 independent randomized, double-blinded, placebo-controlled studies, 200 subjects were placed on various doses of nicotine replacement (study one: 22-mg nicotine patch for 8 weeks, study two: 22-mg patch for 4 weeks then 11 mg patch for 2 weeks). Of those who remained abstinent during the first 2 weeks while on a patch, 46.2% and 40.9% maintained abstinence at 6 months (OR=4.3 and 23.5, respectively) while abstinent subjects on placebo maintained abstinence at a rate of 43.8% and 30% (OR=9.7 and 18.9, respectively). Conversely, of those who were on a patch and smoked during the first 2 weeks of an attempt, 83.3% and 97.1% were smoking 6 months out while 92.6% and 97.8% of those in the placebo groups who smoked during the first 2 weeks were smoking at 6 months.⁵

In 2 randomized, non-placebo-controlled clinical trials of 200 subjects, 41.3% of smokers placed on nicotine replacement that were abstinent on their quit date and had a low tobacco dependence score (based on the Fagerström Test for Nicotine Dependence) were able to maintain abstinence at the 6-month mark (OR=4.1). Those who smoked on the quit date were 10 times less likely to have long-term success (OR=0.1).⁶

In a retrospective survey of 2000 subjects those with less than 5 previous cessation attempts as well as perceived helpful support from friends had a greater likelihood of successful smoking cessation.⁷ In a retrospective review of socioeconomic factors associated with tobacco cessation among 3575 subjects of the CEASE trial, being a homeowner (OR=1.62) and male gender (OR=1.38) increased likelihood of tobacco cessation at 6 months.⁸ In a retrospective review of 2684 subjects from the Framingham study, women who smoked less that 1 half-pack per day (OR=2.6) and males who were diagnosed with CAD within the past 2 years (OR=1.9) were more likely to maintain abstinence 1 year after the cessation attempt.⁹ The TABLE summarizes results from 5 studies focusing on a variety of factors and their effects on smoking cessation.

Counseling frequency and duration impact smoking cessation. In a meta-analysis of 23 studies, the odds ratio for cessation was 1.3 (95% CI, 1.01–1.6) for minimal counseling (<3 minutes), 1.6 (95% CI, 1.2–2.0) for low-intensity counseling (3 to 10 minutes), and 2.3 (95% CI, 2.0–2.7) for high-intensity counseling (>10 minutes).¹⁰ In a meta-analysis of 35 studies, smoking cessation increased as total contact time for all counseling sessions increased, peaking at 90 minutes (OR=3.0; 95% CI, 2.3–3.8).¹⁰ In a meta-analysis of 45 studies, smoking cessation increased as number of person-to-person counseling sessions increased from 2 to 3 sessions (OR=1.4; 95% CI, 1.1–1.7) to 4 to 8 sessions (OR=1.9; 95% CI, 1.6–2.2) to >8 sessions (OR=2.3; 95% CI, 2.1–3.0).¹⁰

A meta-analysis of 62 studies found no impact of relaxation/breathing techniques, contingency contracting, weight/diet counseling, cigarette fading, or negative affect counseling on smoking cessation.¹⁰ Successful counseling techniques included providing smokers with problem solving skills (OR for successful smoking cessation=1.5; 95% CI, 1.3–1.8), providing intra-treatment social support (OR=1.3; 95% CI, 1.1–1.6), helping smokers obtain extra-treatment social support (OR=1.5; 95% CI, 1.1–2.1), use of rapid smoking (OR=2.0; 95% CI, 1.1–3.5), and use of other “aversive smoking techniques” (OR=1.7; 95% CI, 1.04–2.8).

TABLE
Factors predicting success or failure for a smoking cessation attempt

Recommendations from others

The US Public Health Service Clinical Practice Guideline (2000)¹⁰ supports the following recommendations, based on rigorously conducted meta-analyses: use of office screening systems to identify smokers; physician advice to quit; use of multiple clinician types in smoking cessation counseling; and treatments delivered by telephone counseling, group counseling, and individual counseling, used alone or in combination, as opposed to self-help materials for smoking cessation.

The US Department of Health and Human Services¹¹ recommends that physicians ask and record tobacco-use status and offer smoking cessation advice and treatment at every office visit. They also recommend the “5 A’s” (Ask, Advise, Assess, Assist, and Arrange) for patients who desire smoking cessation and the “5 R’s” motivational intervention (Relevance, Risks, Rewards, Roadblocks, and Repetition) for those who are not ready to quit smoking.

Evidence summary

Approximately 60% of people living in Westernized countries who are older than 60 years will develop diverticulosis of the colon. Colonic diverticuli are thought to develop from an increase in intraluminal pressure. This pressure can be caused by colonic motility abnormalities, but a low-fiber diet can also result in a smaller stool mass and a less distended colon, thereby increasing intraluminal pressure.³

Because of strong epidemiological evidence that people from cultures with high-fiber diets are far less likely to develop diverticulosis than are people who live in cultures of low-fiber diets, it has been assumed that a diet high in fiber can prevent diverticulosis.⁴ Many small, uncontrolled studies have also investigated the effect of high-fiber diets and supplements on symptoms of diverticulosis and prevention of diverticulitis episodes.

One large, prospective study of 47,888 male health professionals gathered baseline dietary information in 1986. In 1990 and 1992, follow-up questionnaires asked the subjects if they had been diagnosed with diverticular disease in the interim, and whether they had symptoms of diverticulitis. The study showed a strong inverse relationship between fruit and vegetable fiber intake and risk of symptomatic diverticular disease. It also demonstrated a direct relationship between fat intake, particularly red meat, and symptomatic diverticular disease. For men in the highest quintile of total fat intake and lowest quintile of total fiber intake, the relative risk (RR) of diverticular disease was 2.35 (95% confidence interval [CI], 1.38–3.98) compared with men in the highest quintile of total fiber intake and lowest quintile of total fat intake. Men in the highest group of red meat intake and lowest quintile of fiber intake had a RR of 3.22 (95% CI, 1.46–7.54) compared with men with the lowest red meat intake and highest dietary fiber intake. In this study, cereal fiber did not reduce the risk of symptomatic diverticular disease.¹

Two small randomized crossover studies evaluated the benefit of dietary fiber supplementation on symptomatic diverticular disease, with conflicting results (TABLE).^5,6 One study found that sterculia gum with an antispasmodic, a high roughage diet, and bran tablets all improved symptomatic diverticular disease, with bran tablets associated with the greatest improvement.⁵ Another study found no significant differences between psyllium, bran, and placebo in reducing symptomatic diverticular disease.⁶ However, the amount of total fiber supplementation for each treatment regimen was less than in other studies.

A small randomized trial of lactulose vs dietary fiber showed both treatments to be effective in alleviating symptoms of diverticular disease.⁷ Two small case series of adults treated with dietary fiber found that fiber alleviated symptoms of diverticular disease,^8,9 and possibly reduced complications of diverticulosis.⁹

We found no studies that investigated the common medical advice to avoid small nuts and seeds, which are thought to cause obstruction of the diverticuli and lead to diverticulitis.

TABLE
Studies on dietary fiber for diverticulosis

Recommendations by others

The American College of Gastroenterology states that it is reasonable to recommend a diet high in fruit and vegetable fiber to patients with uncomplicated diverticulosis.¹⁰

Evidence summary

Approximately 60% of people living in Westernized countries who are older than 60 years will develop diverticulosis of the colon. Colonic diverticuli are thought to develop from an increase in intraluminal pressure. This pressure can be caused by colonic motility abnormalities, but a low-fiber diet can also result in a smaller stool mass and a less distended colon, thereby increasing intraluminal pressure.³

Because of strong epidemiological evidence that people from cultures with high-fiber diets are far less likely to develop diverticulosis than are people who live in cultures of low-fiber diets, it has been assumed that a diet high in fiber can prevent diverticulosis.⁴ Many small, uncontrolled studies have also investigated the effect of high-fiber diets and supplements on symptoms of diverticulosis and prevention of diverticulitis episodes.

One large, prospective study of 47,888 male health professionals gathered baseline dietary information in 1986. In 1990 and 1992, follow-up questionnaires asked the subjects if they had been diagnosed with diverticular disease in the interim, and whether they had symptoms of diverticulitis. The study showed a strong inverse relationship between fruit and vegetable fiber intake and risk of symptomatic diverticular disease. It also demonstrated a direct relationship between fat intake, particularly red meat, and symptomatic diverticular disease. For men in the highest quintile of total fat intake and lowest quintile of total fiber intake, the relative risk (RR) of diverticular disease was 2.35 (95% confidence interval [CI], 1.38–3.98) compared with men in the highest quintile of total fiber intake and lowest quintile of total fat intake. Men in the highest group of red meat intake and lowest quintile of fiber intake had a RR of 3.22 (95% CI, 1.46–7.54) compared with men with the lowest red meat intake and highest dietary fiber intake. In this study, cereal fiber did not reduce the risk of symptomatic diverticular disease.¹

Two small randomized crossover studies evaluated the benefit of dietary fiber supplementation on symptomatic diverticular disease, with conflicting results (TABLE).^5,6 One study found that sterculia gum with an antispasmodic, a high roughage diet, and bran tablets all improved symptomatic diverticular disease, with bran tablets associated with the greatest improvement.⁵ Another study found no significant differences between psyllium, bran, and placebo in reducing symptomatic diverticular disease.⁶ However, the amount of total fiber supplementation for each treatment regimen was less than in other studies.

A small randomized trial of lactulose vs dietary fiber showed both treatments to be effective in alleviating symptoms of diverticular disease.⁷ Two small case series of adults treated with dietary fiber found that fiber alleviated symptoms of diverticular disease,^8,9 and possibly reduced complications of diverticulosis.⁹

We found no studies that investigated the common medical advice to avoid small nuts and seeds, which are thought to cause obstruction of the diverticuli and lead to diverticulitis.

TABLE
Studies on dietary fiber for diverticulosis

Recommendations by others

The American College of Gastroenterology states that it is reasonable to recommend a diet high in fruit and vegetable fiber to patients with uncomplicated diverticulosis.¹⁰

Evidence summary

Approximately 60% of people living in Westernized countries who are older than 60 years will develop diverticulosis of the colon. Colonic diverticuli are thought to develop from an increase in intraluminal pressure. This pressure can be caused by colonic motility abnormalities, but a low-fiber diet can also result in a smaller stool mass and a less distended colon, thereby increasing intraluminal pressure.³

Because of strong epidemiological evidence that people from cultures with high-fiber diets are far less likely to develop diverticulosis than are people who live in cultures of low-fiber diets, it has been assumed that a diet high in fiber can prevent diverticulosis.⁴ Many small, uncontrolled studies have also investigated the effect of high-fiber diets and supplements on symptoms of diverticulosis and prevention of diverticulitis episodes.

One large, prospective study of 47,888 male health professionals gathered baseline dietary information in 1986. In 1990 and 1992, follow-up questionnaires asked the subjects if they had been diagnosed with diverticular disease in the interim, and whether they had symptoms of diverticulitis. The study showed a strong inverse relationship between fruit and vegetable fiber intake and risk of symptomatic diverticular disease. It also demonstrated a direct relationship between fat intake, particularly red meat, and symptomatic diverticular disease. For men in the highest quintile of total fat intake and lowest quintile of total fiber intake, the relative risk (RR) of diverticular disease was 2.35 (95% confidence interval [CI], 1.38–3.98) compared with men in the highest quintile of total fiber intake and lowest quintile of total fat intake. Men in the highest group of red meat intake and lowest quintile of fiber intake had a RR of 3.22 (95% CI, 1.46–7.54) compared with men with the lowest red meat intake and highest dietary fiber intake. In this study, cereal fiber did not reduce the risk of symptomatic diverticular disease.¹

Two small randomized crossover studies evaluated the benefit of dietary fiber supplementation on symptomatic diverticular disease, with conflicting results (TABLE).^5,6 One study found that sterculia gum with an antispasmodic, a high roughage diet, and bran tablets all improved symptomatic diverticular disease, with bran tablets associated with the greatest improvement.⁵ Another study found no significant differences between psyllium, bran, and placebo in reducing symptomatic diverticular disease.⁶ However, the amount of total fiber supplementation for each treatment regimen was less than in other studies.

A small randomized trial of lactulose vs dietary fiber showed both treatments to be effective in alleviating symptoms of diverticular disease.⁷ Two small case series of adults treated with dietary fiber found that fiber alleviated symptoms of diverticular disease,^8,9 and possibly reduced complications of diverticulosis.⁹

We found no studies that investigated the common medical advice to avoid small nuts and seeds, which are thought to cause obstruction of the diverticuli and lead to diverticulitis.

TABLE
Studies on dietary fiber for diverticulosis

Recommendations by others

The American College of Gastroenterology states that it is reasonable to recommend a diet high in fruit and vegetable fiber to patients with uncomplicated diverticulosis.¹⁰

Evidence summary

Streptococcus pneumoniae is the most common cause of community-acquired pneumonia and the second most common cause of bacterial meningitis in the United States.¹ An estimated 40,000 people die annually in the US from pneumococcal infections.¹ Even with antibiotic treatment and intensive care unit support, the mortality of patients with pneumococcal bacteremia approaches 25% to 30%.¹

Because of the importance of this pathogen, it has been the focus of several trials to demonstrate the efficacy of the primary vaccination. To date, 7 meta-analyses have been completed to assess the efficacy of pneumococcal vaccine in adults, with varying results.^2-7 Most recently, a Cochrane Review (updated in 2005)⁸ concluded that “the combined results from randomized studies fail to show that the polysaccharide vaccine is effective in preventing either pneumonia or death.” However, they did recognize that the nonrandomized studies have consistently shown that the polysaccharide vaccine is effective in reducing the more specific outcome of invasive pneumococcal disease (bacteremia and meningitis).

Multiple studies have used measurement of antibody levels to assess the response of patients to the vaccine and for justification of the need for revaccination. However, measurement of antibody levels to pneumococcal serotypes is difficult, inexact, and is only a surrogate marker for the immune status of a patient, which also relies on the overall function of their immune system. Although pneumococcal vaccine is most highly recommended in patients with chronic disease or immunodeficiency, these patients have a poorer initial response rate and a faster decline in antibody levels than younger, immunocompetent recipients of the vaccine.^1,9

A study of pneumococcal strains cultured from hospitalized patients demonstrated a duration of protection against pneumococcal infection that was much longer than that predicted by the shorter duration of antibody levels. The vaccine’s ability to reduce infection (due to serotypes included in the vaccine) lasted for at least 9 years and overall efficacy for preventing infection caused by the serotypes included in the vaccine was 57%.¹

Revaccination is safe; particularly when performed more than 5 years after the initial vaccination. Injection site reactions are more common and more severe in revaccinated persons (rising from 3% to 15% in the immunocompetent patient).¹⁰ Revaccination, however, does not result in increased rates of hospitalization, and few severe reactions have been reported.¹¹

No randomized or prospective trials regarding the clinical efficacy of revaccination have been completed. However, when reviewing the studies of antibody response, several summary conclusions can be made. Among those who were nonresponders to the initial vaccination, revaccination (even repeated revaccination) is not effective in stimulating any significant antibody response.^12-14 Among those who responded to the primary vaccination, revaccination can stimulate a second antibody response—albeit to lower levels and with less duration than after the initial vaccination.^13,15-17 Among those who do respond to revaccination, antibody levels can rapidly decline to undetectable levels in a matter of months, and they may or may not retain protection against disease over time.^14,15 It appears that revaccination recommendations have been based on the safety of the vaccination, concern for patients at risk and reduced antibody levels, rather than on proven clinical utility.

Recommendations from others

The Advisory Committee on Immunization Practices (ACIP) advises that the vaccine be used in “persons with diseases and other conditions predisposing to the development of bacteremic pneumococcal pneumonia” and that “revaccination should not be done at intervals less than five years.” They state "the value of vaccination on the basis of advanced age is not clear at this time.” (Further details may be found at: www.aafp.org/PreBuilt/agecharts_adultimmunization.pdf.)

The American Academy of Family Physicians, American College of Physicians, the American College of Obstetricians and Gynecologists and the American Diabetes Association follow the ACIP recommendations.

Evidence summary

Streptococcus pneumoniae is the most common cause of community-acquired pneumonia and the second most common cause of bacterial meningitis in the United States.¹ An estimated 40,000 people die annually in the US from pneumococcal infections.¹ Even with antibiotic treatment and intensive care unit support, the mortality of patients with pneumococcal bacteremia approaches 25% to 30%.¹

Because of the importance of this pathogen, it has been the focus of several trials to demonstrate the efficacy of the primary vaccination. To date, 7 meta-analyses have been completed to assess the efficacy of pneumococcal vaccine in adults, with varying results.^2-7 Most recently, a Cochrane Review (updated in 2005)⁸ concluded that “the combined results from randomized studies fail to show that the polysaccharide vaccine is effective in preventing either pneumonia or death.” However, they did recognize that the nonrandomized studies have consistently shown that the polysaccharide vaccine is effective in reducing the more specific outcome of invasive pneumococcal disease (bacteremia and meningitis).

Multiple studies have used measurement of antibody levels to assess the response of patients to the vaccine and for justification of the need for revaccination. However, measurement of antibody levels to pneumococcal serotypes is difficult, inexact, and is only a surrogate marker for the immune status of a patient, which also relies on the overall function of their immune system. Although pneumococcal vaccine is most highly recommended in patients with chronic disease or immunodeficiency, these patients have a poorer initial response rate and a faster decline in antibody levels than younger, immunocompetent recipients of the vaccine.^1,9

A study of pneumococcal strains cultured from hospitalized patients demonstrated a duration of protection against pneumococcal infection that was much longer than that predicted by the shorter duration of antibody levels. The vaccine’s ability to reduce infection (due to serotypes included in the vaccine) lasted for at least 9 years and overall efficacy for preventing infection caused by the serotypes included in the vaccine was 57%.¹

Revaccination is safe; particularly when performed more than 5 years after the initial vaccination. Injection site reactions are more common and more severe in revaccinated persons (rising from 3% to 15% in the immunocompetent patient).¹⁰ Revaccination, however, does not result in increased rates of hospitalization, and few severe reactions have been reported.¹¹

No randomized or prospective trials regarding the clinical efficacy of revaccination have been completed. However, when reviewing the studies of antibody response, several summary conclusions can be made. Among those who were nonresponders to the initial vaccination, revaccination (even repeated revaccination) is not effective in stimulating any significant antibody response.^12-14 Among those who responded to the primary vaccination, revaccination can stimulate a second antibody response—albeit to lower levels and with less duration than after the initial vaccination.^13,15-17 Among those who do respond to revaccination, antibody levels can rapidly decline to undetectable levels in a matter of months, and they may or may not retain protection against disease over time.^14,15 It appears that revaccination recommendations have been based on the safety of the vaccination, concern for patients at risk and reduced antibody levels, rather than on proven clinical utility.

Recommendations from others

The Advisory Committee on Immunization Practices (ACIP) advises that the vaccine be used in “persons with diseases and other conditions predisposing to the development of bacteremic pneumococcal pneumonia” and that “revaccination should not be done at intervals less than five years.” They state "the value of vaccination on the basis of advanced age is not clear at this time.” (Further details may be found at: www.aafp.org/PreBuilt/agecharts_adultimmunization.pdf.)

The American Academy of Family Physicians, American College of Physicians, the American College of Obstetricians and Gynecologists and the American Diabetes Association follow the ACIP recommendations.

Evidence summary

Streptococcus pneumoniae is the most common cause of community-acquired pneumonia and the second most common cause of bacterial meningitis in the United States.¹ An estimated 40,000 people die annually in the US from pneumococcal infections.¹ Even with antibiotic treatment and intensive care unit support, the mortality of patients with pneumococcal bacteremia approaches 25% to 30%.¹

Because of the importance of this pathogen, it has been the focus of several trials to demonstrate the efficacy of the primary vaccination. To date, 7 meta-analyses have been completed to assess the efficacy of pneumococcal vaccine in adults, with varying results.^2-7 Most recently, a Cochrane Review (updated in 2005)⁸ concluded that “the combined results from randomized studies fail to show that the polysaccharide vaccine is effective in preventing either pneumonia or death.” However, they did recognize that the nonrandomized studies have consistently shown that the polysaccharide vaccine is effective in reducing the more specific outcome of invasive pneumococcal disease (bacteremia and meningitis).

Multiple studies have used measurement of antibody levels to assess the response of patients to the vaccine and for justification of the need for revaccination. However, measurement of antibody levels to pneumococcal serotypes is difficult, inexact, and is only a surrogate marker for the immune status of a patient, which also relies on the overall function of their immune system. Although pneumococcal vaccine is most highly recommended in patients with chronic disease or immunodeficiency, these patients have a poorer initial response rate and a faster decline in antibody levels than younger, immunocompetent recipients of the vaccine.^1,9

A study of pneumococcal strains cultured from hospitalized patients demonstrated a duration of protection against pneumococcal infection that was much longer than that predicted by the shorter duration of antibody levels. The vaccine’s ability to reduce infection (due to serotypes included in the vaccine) lasted for at least 9 years and overall efficacy for preventing infection caused by the serotypes included in the vaccine was 57%.¹

Revaccination is safe; particularly when performed more than 5 years after the initial vaccination. Injection site reactions are more common and more severe in revaccinated persons (rising from 3% to 15% in the immunocompetent patient).¹⁰ Revaccination, however, does not result in increased rates of hospitalization, and few severe reactions have been reported.¹¹

No randomized or prospective trials regarding the clinical efficacy of revaccination have been completed. However, when reviewing the studies of antibody response, several summary conclusions can be made. Among those who were nonresponders to the initial vaccination, revaccination (even repeated revaccination) is not effective in stimulating any significant antibody response.^12-14 Among those who responded to the primary vaccination, revaccination can stimulate a second antibody response—albeit to lower levels and with less duration than after the initial vaccination.^13,15-17 Among those who do respond to revaccination, antibody levels can rapidly decline to undetectable levels in a matter of months, and they may or may not retain protection against disease over time.^14,15 It appears that revaccination recommendations have been based on the safety of the vaccination, concern for patients at risk and reduced antibody levels, rather than on proven clinical utility.

Recommendations from others

The Advisory Committee on Immunization Practices (ACIP) advises that the vaccine be used in “persons with diseases and other conditions predisposing to the development of bacteremic pneumococcal pneumonia” and that “revaccination should not be done at intervals less than five years.” They state "the value of vaccination on the basis of advanced age is not clear at this time.” (Further details may be found at: www.aafp.org/PreBuilt/agecharts_adultimmunization.pdf.)

The American Academy of Family Physicians, American College of Physicians, the American College of Obstetricians and Gynecologists and the American Diabetes Association follow the ACIP recommendations.

Evidence summary

There are many opinions and recommendations about what constitutes quality health surveillance for children. However, many screening tests for children lack evidence of effectiveness and information on harms.¹ The scope of this question required use of evidence published in high-quality systematic reviews. The US Preventive Services Task Force (USPSTF) provides the most rigorous evidence on which to base recommendations.² Medline was searched for any additional individual studies of interest. The USPSTF has conducted reviews for selected screening tests for children; the TABLE summarizes those with sufficient evidence to recommend them. We identified 1 additional evidence-based recommendation from the Centers for Disease Control and Prevention. This report, based on a systematic review, recommends cystic fibrosis screening in neonates based on moderate benefits and low risks of harm.³

The TABLE summarizes the evidence supporting universal childhood screening for hemoglobinopathies, congenital hypothyroidism, phenylketonuria, and visual defects; and high-risk childhood screening for tuberculosis and lead toxicity. The TABLE also lists the recommendations from the American Academy of Pediatrics (AAP) on frequency and timing of screening as guided by consensus opinion.

The USPSTF recommendations supporting screening for hemoglobinopathies, congenital hypothyroidism, and phenylketonuria are considered standard of care. The USPSTF believes that updating these 1996 recommendations would have little impact on clinical practice.

The USPSTF recommendations supporting vision screening found no direct evidence supporting screening for visual acuity. One fair-quality controlled study (N=3490) showed a decreased prevalence of amblyopia in the screened group and evidence that treatment of amblyotic risk factors prevents amblyopia. A Cochrane review of this topic showed insufficient evidence for visual screening of older (school-aged) children; for amblyopia, no data sufficient for analysis was found.^4,5

The USPSTF recommendation to screen asymptomatic high-risk children for TB is based on the effectiveness of early intervention (14 controlled trials) and the accuracy of the Mantoux test.

TABLE
US Preventive Services Task Force evidence-supported testing for children

The USPSTF document on screening for lead levels is currently being revised and the recommendation may change. Although no controlled studies directly show that screening high-risk children for lead exposure improves clinical outcomes, several lesser-quality studies create a logical path to this conclusion.

The USPSTF finds there is insufficient evidence to recommend for or against performing the following screening tests in children: blood pressure screening; screening for overweight in children and adolescents; and iron deficiency screening in asymptomatic infants. Both Cochrane Systematic Reviews and USPSTF found insufficient evidence to support universal hearing screening, including neonatal hearing screening.⁶ The USPSTF makes no recommendation regarding screening high-risk children for hyperlipidemia.

The USPSTF recommends that the following tests should not be performed in children because there is good evidence that the harms outweigh the benefits: thyroid cancer screening in children and bacteriuria screening in asymptomatic nonpregnant children.

Recommendations from others

There are numerous guidelines recommending various sets of preventive services for children, but there are few evidence-based recommendations. The AAP recommendations can be found in Guidelines for Health Supervision III.⁷ The AAP also publishes policy statements and guidelines in the journal Pediatrics. The American Academy of Family Practice’s (AAFP) recommendations on health supervision can be found at: www.aafp.org/PreBuilt/RCPS_August2005.pdf.

A summary of the AAFP and the AAP recommendations on each of the USPSTF supported tests is in the TABLE. While AAFP and USPSTF recommendations concur, AAP recommendations differ in recommending hearing screening for all newborns, iron deficiency screening at 9 months of age, screening for lipid disorders in children at risk starting at 24 months, and screening urinalysis at age 5 years.

Evidence summary

There are many opinions and recommendations about what constitutes quality health surveillance for children. However, many screening tests for children lack evidence of effectiveness and information on harms.¹ The scope of this question required use of evidence published in high-quality systematic reviews. The US Preventive Services Task Force (USPSTF) provides the most rigorous evidence on which to base recommendations.² Medline was searched for any additional individual studies of interest. The USPSTF has conducted reviews for selected screening tests for children; the TABLE summarizes those with sufficient evidence to recommend them. We identified 1 additional evidence-based recommendation from the Centers for Disease Control and Prevention. This report, based on a systematic review, recommends cystic fibrosis screening in neonates based on moderate benefits and low risks of harm.³

The TABLE summarizes the evidence supporting universal childhood screening for hemoglobinopathies, congenital hypothyroidism, phenylketonuria, and visual defects; and high-risk childhood screening for tuberculosis and lead toxicity. The TABLE also lists the recommendations from the American Academy of Pediatrics (AAP) on frequency and timing of screening as guided by consensus opinion.

The USPSTF recommendations supporting screening for hemoglobinopathies, congenital hypothyroidism, and phenylketonuria are considered standard of care. The USPSTF believes that updating these 1996 recommendations would have little impact on clinical practice.

The USPSTF recommendations supporting vision screening found no direct evidence supporting screening for visual acuity. One fair-quality controlled study (N=3490) showed a decreased prevalence of amblyopia in the screened group and evidence that treatment of amblyotic risk factors prevents amblyopia. A Cochrane review of this topic showed insufficient evidence for visual screening of older (school-aged) children; for amblyopia, no data sufficient for analysis was found.^4,5

The USPSTF recommendation to screen asymptomatic high-risk children for TB is based on the effectiveness of early intervention (14 controlled trials) and the accuracy of the Mantoux test.

TABLE
US Preventive Services Task Force evidence-supported testing for children

The USPSTF document on screening for lead levels is currently being revised and the recommendation may change. Although no controlled studies directly show that screening high-risk children for lead exposure improves clinical outcomes, several lesser-quality studies create a logical path to this conclusion.

The USPSTF finds there is insufficient evidence to recommend for or against performing the following screening tests in children: blood pressure screening; screening for overweight in children and adolescents; and iron deficiency screening in asymptomatic infants. Both Cochrane Systematic Reviews and USPSTF found insufficient evidence to support universal hearing screening, including neonatal hearing screening.⁶ The USPSTF makes no recommendation regarding screening high-risk children for hyperlipidemia.

The USPSTF recommends that the following tests should not be performed in children because there is good evidence that the harms outweigh the benefits: thyroid cancer screening in children and bacteriuria screening in asymptomatic nonpregnant children.

Recommendations from others

There are numerous guidelines recommending various sets of preventive services for children, but there are few evidence-based recommendations. The AAP recommendations can be found in Guidelines for Health Supervision III.⁷ The AAP also publishes policy statements and guidelines in the journal Pediatrics. The American Academy of Family Practice’s (AAFP) recommendations on health supervision can be found at: www.aafp.org/PreBuilt/RCPS_August2005.pdf.

A summary of the AAFP and the AAP recommendations on each of the USPSTF supported tests is in the TABLE. While AAFP and USPSTF recommendations concur, AAP recommendations differ in recommending hearing screening for all newborns, iron deficiency screening at 9 months of age, screening for lipid disorders in children at risk starting at 24 months, and screening urinalysis at age 5 years.

Evidence summary

There are many opinions and recommendations about what constitutes quality health surveillance for children. However, many screening tests for children lack evidence of effectiveness and information on harms.¹ The scope of this question required use of evidence published in high-quality systematic reviews. The US Preventive Services Task Force (USPSTF) provides the most rigorous evidence on which to base recommendations.² Medline was searched for any additional individual studies of interest. The USPSTF has conducted reviews for selected screening tests for children; the TABLE summarizes those with sufficient evidence to recommend them. We identified 1 additional evidence-based recommendation from the Centers for Disease Control and Prevention. This report, based on a systematic review, recommends cystic fibrosis screening in neonates based on moderate benefits and low risks of harm.³

The TABLE summarizes the evidence supporting universal childhood screening for hemoglobinopathies, congenital hypothyroidism, phenylketonuria, and visual defects; and high-risk childhood screening for tuberculosis and lead toxicity. The TABLE also lists the recommendations from the American Academy of Pediatrics (AAP) on frequency and timing of screening as guided by consensus opinion.

The USPSTF recommendations supporting screening for hemoglobinopathies, congenital hypothyroidism, and phenylketonuria are considered standard of care. The USPSTF believes that updating these 1996 recommendations would have little impact on clinical practice.

The USPSTF recommendations supporting vision screening found no direct evidence supporting screening for visual acuity. One fair-quality controlled study (N=3490) showed a decreased prevalence of amblyopia in the screened group and evidence that treatment of amblyotic risk factors prevents amblyopia. A Cochrane review of this topic showed insufficient evidence for visual screening of older (school-aged) children; for amblyopia, no data sufficient for analysis was found.^4,5

The USPSTF recommendation to screen asymptomatic high-risk children for TB is based on the effectiveness of early intervention (14 controlled trials) and the accuracy of the Mantoux test.

TABLE
US Preventive Services Task Force evidence-supported testing for children

The USPSTF document on screening for lead levels is currently being revised and the recommendation may change. Although no controlled studies directly show that screening high-risk children for lead exposure improves clinical outcomes, several lesser-quality studies create a logical path to this conclusion.

The USPSTF finds there is insufficient evidence to recommend for or against performing the following screening tests in children: blood pressure screening; screening for overweight in children and adolescents; and iron deficiency screening in asymptomatic infants. Both Cochrane Systematic Reviews and USPSTF found insufficient evidence to support universal hearing screening, including neonatal hearing screening.⁶ The USPSTF makes no recommendation regarding screening high-risk children for hyperlipidemia.

The USPSTF recommends that the following tests should not be performed in children because there is good evidence that the harms outweigh the benefits: thyroid cancer screening in children and bacteriuria screening in asymptomatic nonpregnant children.

Recommendations from others

There are numerous guidelines recommending various sets of preventive services for children, but there are few evidence-based recommendations. The AAP recommendations can be found in Guidelines for Health Supervision III.⁷ The AAP also publishes policy statements and guidelines in the journal Pediatrics. The American Academy of Family Practice’s (AAFP) recommendations on health supervision can be found at: www.aafp.org/PreBuilt/RCPS_August2005.pdf.

A summary of the AAFP and the AAP recommendations on each of the USPSTF supported tests is in the TABLE. While AAFP and USPSTF recommendations concur, AAP recommendations differ in recommending hearing screening for all newborns, iron deficiency screening at 9 months of age, screening for lipid disorders in children at risk starting at 24 months, and screening urinalysis at age 5 years.

Evidence summary

The evaluation of treatments of nongenital warts is confounded by the propensity of simple warts to disappear spontaneously. Approximately two thirds of warts resolved without therapy over a 2-year period, according to 1 study in an institutional population.¹ Since adverse effects from treatment, such as pain and scarring, can occur, patients should be educated as to options of therapy (or no therapy).²

Seventeen studies of cryotherapy with between 30 and 400 patients show cure rates ranging from 29% to 87%, although most did not have placebo arms. Pooled data from 69 patients in 2 small studies did not show a benefit between the cryotherapy and nontreatment arms,³ although there were very low cure rates from cryotherapy in 1 study and high spontaneous remission rates in the other. Longer freeze times seem to improve cryotherapy cure rates but also cause increased blistering and pain.⁴

One randomized controlled trial of 61 patients showed cure rates of 85% with duct tape vs 60% with cryotherapy.⁵ Duct tape therapy had the advantages of reduced cost and less pain.

Although pulsed dye laser has efficacy in various studies, no evidence favors it over cryotherapy or cantharidin.⁶ Treatment with CO₂ laser and Er:Yag laser had an efficacy of 52% to 100%. However, many of these studies were small, poorly randomized, and had no placebo control. The potential hazard of aerosolized virus particles from these therapies has not been evaluated.⁷

Two recent reviews also found that cryotherapy is similar in efficacy to salicylic acid, and reported that other nonpharmacologic treatments lack evidence.^2,8

Recommendations from others

The American Academy of Dermatology states that “in children, warts can disappear without treatment over a period of several months to several years. However, warts that are bothersome, painful, or rapidly multiplying should be treated.”⁹ Nonpharmacologic treatments recommended include cryotherapy, electrosurgery, “cutting,” and lasers.

Evidence summary

The evaluation of treatments of nongenital warts is confounded by the propensity of simple warts to disappear spontaneously. Approximately two thirds of warts resolved without therapy over a 2-year period, according to 1 study in an institutional population.¹ Since adverse effects from treatment, such as pain and scarring, can occur, patients should be educated as to options of therapy (or no therapy).²

Seventeen studies of cryotherapy with between 30 and 400 patients show cure rates ranging from 29% to 87%, although most did not have placebo arms. Pooled data from 69 patients in 2 small studies did not show a benefit between the cryotherapy and nontreatment arms,³ although there were very low cure rates from cryotherapy in 1 study and high spontaneous remission rates in the other. Longer freeze times seem to improve cryotherapy cure rates but also cause increased blistering and pain.⁴

One randomized controlled trial of 61 patients showed cure rates of 85% with duct tape vs 60% with cryotherapy.⁵ Duct tape therapy had the advantages of reduced cost and less pain.

Although pulsed dye laser has efficacy in various studies, no evidence favors it over cryotherapy or cantharidin.⁶ Treatment with CO₂ laser and Er:Yag laser had an efficacy of 52% to 100%. However, many of these studies were small, poorly randomized, and had no placebo control. The potential hazard of aerosolized virus particles from these therapies has not been evaluated.⁷

Two recent reviews also found that cryotherapy is similar in efficacy to salicylic acid, and reported that other nonpharmacologic treatments lack evidence.^2,8

Recommendations from others

The American Academy of Dermatology states that “in children, warts can disappear without treatment over a period of several months to several years. However, warts that are bothersome, painful, or rapidly multiplying should be treated.”⁹ Nonpharmacologic treatments recommended include cryotherapy, electrosurgery, “cutting,” and lasers.

Evidence summary

The evaluation of treatments of nongenital warts is confounded by the propensity of simple warts to disappear spontaneously. Approximately two thirds of warts resolved without therapy over a 2-year period, according to 1 study in an institutional population.¹ Since adverse effects from treatment, such as pain and scarring, can occur, patients should be educated as to options of therapy (or no therapy).²

Seventeen studies of cryotherapy with between 30 and 400 patients show cure rates ranging from 29% to 87%, although most did not have placebo arms. Pooled data from 69 patients in 2 small studies did not show a benefit between the cryotherapy and nontreatment arms,³ although there were very low cure rates from cryotherapy in 1 study and high spontaneous remission rates in the other. Longer freeze times seem to improve cryotherapy cure rates but also cause increased blistering and pain.⁴

One randomized controlled trial of 61 patients showed cure rates of 85% with duct tape vs 60% with cryotherapy.⁵ Duct tape therapy had the advantages of reduced cost and less pain.

Although pulsed dye laser has efficacy in various studies, no evidence favors it over cryotherapy or cantharidin.⁶ Treatment with CO₂ laser and Er:Yag laser had an efficacy of 52% to 100%. However, many of these studies were small, poorly randomized, and had no placebo control. The potential hazard of aerosolized virus particles from these therapies has not been evaluated.⁷

Two recent reviews also found that cryotherapy is similar in efficacy to salicylic acid, and reported that other nonpharmacologic treatments lack evidence.^2,8

Recommendations from others

The American Academy of Dermatology states that “in children, warts can disappear without treatment over a period of several months to several years. However, warts that are bothersome, painful, or rapidly multiplying should be treated.”⁹ Nonpharmacologic treatments recommended include cryotherapy, electrosurgery, “cutting,” and lasers.

Evidence summary

EBV-specific antibody tests. A validating cohort study assessed the sensitivity and specificity of 6 commercial test kits for detection of Epstein-Barr virus-specific antibodies (EBVCA and EBNA). The study compared antibody levels in 139 serum specimens from patients with recent primary EBV infections (confirmed by both a positive heterophile antibody test and an EBV antibody pattern compatible with recent infection) and in 40 specimens from healthy normal controls. The average sensitivity of the antibody tests was 97% (95%–99%) and average specificity was 94% (86%–100%).¹

TABLE
Comparison of various tests for infectious mononucleosis

Heterophile antibody tests. Two validating cohort studies assessed the accuracy of several commercially available test kits for the detection of heterophile antibodies (eg, “Mono spot” tests). The first compared 6 kits using either a latex agglutination or a solid-phase assay against a “gold standard” of serologic verification for 53 serum samples from primary EBV infection, 26 samples from EBV immune patients, and 21 samples from healthy donors.² Serologic verification used immunoflourescence to determine: the absence of IgG but presence of IgM, the presence of IgG but absence of IgM, or the absence of both antibodies (respectively) against EBVCA. The second study used a similar method to test 6 more heterophile kits using blood samples from 140 patients.¹ The sensitivity of heterophile antibody testing is lower in children under 12 (25%–50%) and early in the illness (25% false-negative rate in first week).³

PCR assay for EBV DNA. Another validating cohort study evaluated PCR testing for EBV DNA among children (average age 9 years, 4 months), 28 with infectious mononucleosis, 25 who were EBV seronegative, and 26 who were seropositive. Children with acute infectious mononucleosis were diagnosed by symptoms, >10% atypical lymphocytes, and a positive heterophile antibody test. The PCR found a sensitivity and specificity of 75% and 98% at 1 week.⁴ Testing earlier, especially in children, is expected to decrease the sensitivity due to the lower maturity of the immune system response.

Lymphocyte and atypical lymphocyte count. A validating cohort study compared peripheral blood samples in 181 patients aged >16 years with a clinical diagnosis of infectious mononucleosis confirmed by a positive heterophile antibody test with those from 181 similar patients with a negative test. An increased percentage of lymphocytes and atypical lymphocytes were associated with higher sensitivity and specificity for infectious mononucleosis.⁵

Recommendations from others

In the appropriate clinical situation, the Centers for Disease Control and Prevention recommends verifying the diagnosis of infectious mononucleosis with a CBC and heterophile antibody test. If the heterophile test result is negative, additional testing such as EBV DNA tests may be necessary.⁶

Evidence summary

EBV-specific antibody tests. A validating cohort study assessed the sensitivity and specificity of 6 commercial test kits for detection of Epstein-Barr virus-specific antibodies (EBVCA and EBNA). The study compared antibody levels in 139 serum specimens from patients with recent primary EBV infections (confirmed by both a positive heterophile antibody test and an EBV antibody pattern compatible with recent infection) and in 40 specimens from healthy normal controls. The average sensitivity of the antibody tests was 97% (95%–99%) and average specificity was 94% (86%–100%).¹

TABLE
Comparison of various tests for infectious mononucleosis

Heterophile antibody tests. Two validating cohort studies assessed the accuracy of several commercially available test kits for the detection of heterophile antibodies (eg, “Mono spot” tests). The first compared 6 kits using either a latex agglutination or a solid-phase assay against a “gold standard” of serologic verification for 53 serum samples from primary EBV infection, 26 samples from EBV immune patients, and 21 samples from healthy donors.² Serologic verification used immunoflourescence to determine: the absence of IgG but presence of IgM, the presence of IgG but absence of IgM, or the absence of both antibodies (respectively) against EBVCA. The second study used a similar method to test 6 more heterophile kits using blood samples from 140 patients.¹ The sensitivity of heterophile antibody testing is lower in children under 12 (25%–50%) and early in the illness (25% false-negative rate in first week).³

PCR assay for EBV DNA. Another validating cohort study evaluated PCR testing for EBV DNA among children (average age 9 years, 4 months), 28 with infectious mononucleosis, 25 who were EBV seronegative, and 26 who were seropositive. Children with acute infectious mononucleosis were diagnosed by symptoms, >10% atypical lymphocytes, and a positive heterophile antibody test. The PCR found a sensitivity and specificity of 75% and 98% at 1 week.⁴ Testing earlier, especially in children, is expected to decrease the sensitivity due to the lower maturity of the immune system response.

Lymphocyte and atypical lymphocyte count. A validating cohort study compared peripheral blood samples in 181 patients aged >16 years with a clinical diagnosis of infectious mononucleosis confirmed by a positive heterophile antibody test with those from 181 similar patients with a negative test. An increased percentage of lymphocytes and atypical lymphocytes were associated with higher sensitivity and specificity for infectious mononucleosis.⁵

Recommendations from others

In the appropriate clinical situation, the Centers for Disease Control and Prevention recommends verifying the diagnosis of infectious mononucleosis with a CBC and heterophile antibody test. If the heterophile test result is negative, additional testing such as EBV DNA tests may be necessary.⁶

Evidence summary

EBV-specific antibody tests. A validating cohort study assessed the sensitivity and specificity of 6 commercial test kits for detection of Epstein-Barr virus-specific antibodies (EBVCA and EBNA). The study compared antibody levels in 139 serum specimens from patients with recent primary EBV infections (confirmed by both a positive heterophile antibody test and an EBV antibody pattern compatible with recent infection) and in 40 specimens from healthy normal controls. The average sensitivity of the antibody tests was 97% (95%–99%) and average specificity was 94% (86%–100%).¹

TABLE
Comparison of various tests for infectious mononucleosis

Heterophile antibody tests. Two validating cohort studies assessed the accuracy of several commercially available test kits for the detection of heterophile antibodies (eg, “Mono spot” tests). The first compared 6 kits using either a latex agglutination or a solid-phase assay against a “gold standard” of serologic verification for 53 serum samples from primary EBV infection, 26 samples from EBV immune patients, and 21 samples from healthy donors.² Serologic verification used immunoflourescence to determine: the absence of IgG but presence of IgM, the presence of IgG but absence of IgM, or the absence of both antibodies (respectively) against EBVCA. The second study used a similar method to test 6 more heterophile kits using blood samples from 140 patients.¹ The sensitivity of heterophile antibody testing is lower in children under 12 (25%–50%) and early in the illness (25% false-negative rate in first week).³

PCR assay for EBV DNA. Another validating cohort study evaluated PCR testing for EBV DNA among children (average age 9 years, 4 months), 28 with infectious mononucleosis, 25 who were EBV seronegative, and 26 who were seropositive. Children with acute infectious mononucleosis were diagnosed by symptoms, >10% atypical lymphocytes, and a positive heterophile antibody test. The PCR found a sensitivity and specificity of 75% and 98% at 1 week.⁴ Testing earlier, especially in children, is expected to decrease the sensitivity due to the lower maturity of the immune system response.

Lymphocyte and atypical lymphocyte count. A validating cohort study compared peripheral blood samples in 181 patients aged >16 years with a clinical diagnosis of infectious mononucleosis confirmed by a positive heterophile antibody test with those from 181 similar patients with a negative test. An increased percentage of lymphocytes and atypical lymphocytes were associated with higher sensitivity and specificity for infectious mononucleosis.⁵

Recommendations from others

In the appropriate clinical situation, the Centers for Disease Control and Prevention recommends verifying the diagnosis of infectious mononucleosis with a CBC and heterophile antibody test. If the heterophile test result is negative, additional testing such as EBV DNA tests may be necessary.⁶

Evidence summary

IUDs are an effective and safe form of contraception. However, many clinicians have questions about the true contraindications to IUD use in the following situations.

Infection. IUDs do not increase the risk of complications among immunosuppressed HIV-positive women.¹ IUD insertion does not increase the risk of PID for women with gonorrhea or chlamydia infection compared with infected nonusers.² In one study, having multiple sexual partners was not associated with an increased risk of PID unless those partners carry specific infections, such as gonorrhea or chlamydia.³

In the US, approximately 1 in 1000 women develop PID after IUD insertion.³ Bacterial vaginosis may increase dysmenorrhea for women with IUDs (34.8 vs 13.9%, P=.03).⁴ In an observational study, all of 7 women with actinomyces who had IUDs removed remained negative for actinomyces after insertion of a new IUD.⁵

Nulliparity and infertility. Nulliparous women have increased rates of discomfort with IUD placement (17.8% vs 8.8%) and may have an increased risk of expulsion (up to 18.5% in one study, compared with less than 5.7% for all IUD users).⁶ Short-term (≤3.5 years) IUD use by nulliparous women was not associated with decreased fertility in a case-control study;⁷ however, 1 cohort study demonstrated lower fertility with use of a copper IUD for longer periods: hazard ratio (HR): 0.69 (95% confidence interval [CI], 0.497–0.97) for 42–78 months; HR=0.50 (95% CI, 0.34–0.73) for >78 months.⁸

Uterine anomalies. Significant uterine enlargement can increase the risk of IUD expulsion (0 vs 4 women [13%]; P=.04 in 1 retrospective cohort study).⁹ There are case reports of IUD failure and uterine perforation among women with anomalies that distort the uterine cavity.^10,11

Other. Some contraindications to IUD use, such as concurrent pregnancy, are obvious. Other common sense contraindications might include insertion by patients with recent postpartum endometritis, gynecologic malignancy, genital bleeding of unknown cause, and gestational trophoblastic disease.

Recommendations from others

Manufacturer product labeling lists a number of contraindications. The American College of Obstetrics and Gynecology and the World Health Organization have similar but generally less restrictive lists of contraindications to IUD placement (TABLE).

TABLE
Contraindications to IUD placement

Evidence summary

IUDs are an effective and safe form of contraception. However, many clinicians have questions about the true contraindications to IUD use in the following situations.

Infection. IUDs do not increase the risk of complications among immunosuppressed HIV-positive women.¹ IUD insertion does not increase the risk of PID for women with gonorrhea or chlamydia infection compared with infected nonusers.² In one study, having multiple sexual partners was not associated with an increased risk of PID unless those partners carry specific infections, such as gonorrhea or chlamydia.³

In the US, approximately 1 in 1000 women develop PID after IUD insertion.³ Bacterial vaginosis may increase dysmenorrhea for women with IUDs (34.8 vs 13.9%, P=.03).⁴ In an observational study, all of 7 women with actinomyces who had IUDs removed remained negative for actinomyces after insertion of a new IUD.⁵

Nulliparity and infertility. Nulliparous women have increased rates of discomfort with IUD placement (17.8% vs 8.8%) and may have an increased risk of expulsion (up to 18.5% in one study, compared with less than 5.7% for all IUD users).⁶ Short-term (≤3.5 years) IUD use by nulliparous women was not associated with decreased fertility in a case-control study;⁷ however, 1 cohort study demonstrated lower fertility with use of a copper IUD for longer periods: hazard ratio (HR): 0.69 (95% confidence interval [CI], 0.497–0.97) for 42–78 months; HR=0.50 (95% CI, 0.34–0.73) for >78 months.⁸

Uterine anomalies. Significant uterine enlargement can increase the risk of IUD expulsion (0 vs 4 women [13%]; P=.04 in 1 retrospective cohort study).⁹ There are case reports of IUD failure and uterine perforation among women with anomalies that distort the uterine cavity.^10,11

Other. Some contraindications to IUD use, such as concurrent pregnancy, are obvious. Other common sense contraindications might include insertion by patients with recent postpartum endometritis, gynecologic malignancy, genital bleeding of unknown cause, and gestational trophoblastic disease.

Recommendations from others

Manufacturer product labeling lists a number of contraindications. The American College of Obstetrics and Gynecology and the World Health Organization have similar but generally less restrictive lists of contraindications to IUD placement (TABLE).

TABLE
Contraindications to IUD placement

Evidence summary

IUDs are an effective and safe form of contraception. However, many clinicians have questions about the true contraindications to IUD use in the following situations.

Infection. IUDs do not increase the risk of complications among immunosuppressed HIV-positive women.¹ IUD insertion does not increase the risk of PID for women with gonorrhea or chlamydia infection compared with infected nonusers.² In one study, having multiple sexual partners was not associated with an increased risk of PID unless those partners carry specific infections, such as gonorrhea or chlamydia.³

In the US, approximately 1 in 1000 women develop PID after IUD insertion.³ Bacterial vaginosis may increase dysmenorrhea for women with IUDs (34.8 vs 13.9%, P=.03).⁴ In an observational study, all of 7 women with actinomyces who had IUDs removed remained negative for actinomyces after insertion of a new IUD.⁵

Nulliparity and infertility. Nulliparous women have increased rates of discomfort with IUD placement (17.8% vs 8.8%) and may have an increased risk of expulsion (up to 18.5% in one study, compared with less than 5.7% for all IUD users).⁶ Short-term (≤3.5 years) IUD use by nulliparous women was not associated with decreased fertility in a case-control study;⁷ however, 1 cohort study demonstrated lower fertility with use of a copper IUD for longer periods: hazard ratio (HR): 0.69 (95% confidence interval [CI], 0.497–0.97) for 42–78 months; HR=0.50 (95% CI, 0.34–0.73) for >78 months.⁸

Uterine anomalies. Significant uterine enlargement can increase the risk of IUD expulsion (0 vs 4 women [13%]; P=.04 in 1 retrospective cohort study).⁹ There are case reports of IUD failure and uterine perforation among women with anomalies that distort the uterine cavity.^10,11

Other. Some contraindications to IUD use, such as concurrent pregnancy, are obvious. Other common sense contraindications might include insertion by patients with recent postpartum endometritis, gynecologic malignancy, genital bleeding of unknown cause, and gestational trophoblastic disease.

Recommendations from others

Manufacturer product labeling lists a number of contraindications. The American College of Obstetrics and Gynecology and the World Health Organization have similar but generally less restrictive lists of contraindications to IUD placement (TABLE).

TABLE
Contraindications to IUD placement

Evidence summary

Screening for hyperlipidemia using total cholesterol and low-density lipoprotein (LDL) cholesterol is recommended for adults after the age of 35 years for men and 45 years for women.¹ Younger adults (men aged 20–35 and women aged 20–45) should be screened for lipid disorders if they have other risk factors for CVD.¹

Children with heterozygous familial hypercholesterolemia, an autosomal dominant disorder with a prevalence of 1 in 500, are at increased risk of cardiovascular morbidity and mortality in adulthood. One quarter of males with familial hyper-cholesterolemia suffer fatal coronary heart disease (CHD) by age 50 years.²

The use of statins by children with familial hypercholesterolemia for up to 2 years is safe and lowers LDL cholesterol.³ Longer use by children has not been studied, so no comment can be made about long-term safety and decreased CHD morbidity and mortality.

One systematic review and cost-effectiveness analysis investigated the appropriateness and cost-effectiveness of screening methods for familial hypercholesterolemia beginning at the age of 16 years.⁴ The authors identified potential screening strategies from 6 cross-sectional studies and applied these to a decision analysis. Screening of first-degree relatives of those with familial hypercholesterolemia was most effective in detecting cases of familial hypercholesterolemia (number needed to screen [NNS]=3; cost per case detected=$232; cost per life-year gained=$5397).

Universal screening of all 16-year-olds was also cost-effective (cost per life-year gained=$4839), but resulted in a much larger NNS and cost of detection (NNS=1365, cost per case detected=$16,999). The authors concluded that case finding through screening of first-degree relatives was the most cost-effective strategy overall.

In contrast to children affected with familial hypercholesterolemia, the relationship of blood cholesterol levels in children without familial hypercholesterolemia to CHD later in life has not been established. A paucity of data exists that links lowering of cholesterol in childhood with reduced CHD morbidity and mortality in adulthood. Therefore, the benefits of detecting and treating childhood hyperlipidemia without familial hypercholesterolemia are not known. Despite the lack of patient-oriented outcomes research in this area, 2 guidelines recommend screening all children for hyperlipidemia.^5,9

Three studies investigated the use of various recommended screening indicators in identifying children with hyperlipidemia. The first was a control cohort from a case-control study that applied the National Cholesterol Education Program (NCEP) guidelines for screening in children⁵ to 501 US males less than 20 years old, and examined the effectiveness of using the recommended 2 major screening indicators (family history of premature cardiovascular disease and parent cholesterol >240 mg/dL) plus 5 discretionary indicators (high-fat/high-cholesterol diet, hypertension, obesity, smoker, steroid/medication).⁶ If all major and discretionary indicators were applied to the cohort, 96% of the children with LDL greater than 130 mg/dL were identified. However, the individual positive predictive values (PPV; probability of having LDL >130 when a child had a screening indicator) ranged from 6.8% to 20.6%.

The 2 other studies used a cross-sectional design to evaluate family history of premature cardiovascular disease and hyperlipidemia screening indicators in 4183 grade-school children in Taiwan⁷ and 2217 youths in Quebec.⁸ Family history performed poorly as a mechanism for identifying children with hypercholesterolemia (total cholesterol >200 mg/dL; LDL >130 mg/dL) (PPV <12.5%⁷, PPV=7.7%⁸). More than 75% of the children in the Taiwan study would have been missed using family history as a screen. Both studies concluded that family history as a screening indicator is insensitive and inaccurate, and no more useful than general population screening.

Recommendations from others

Neither the American Academy of Family Physicians or the US Preventive Services Task Force makes a recommendation about screening for hyperlipidemia in this age group.

The American Academy of Pediatrics recommends screening children aged 2 years or older whose parents or grandparents had coronary atherosclerosis at age 55 or younger (defined by diagnostic coronary arteriography, myocardial infarction, angina pectoris, peripheral vascular disease, cerebrovascular disease, or sudden cardiac death). They also advocate screening children of a parent with an elevated blood cholesterol level (total cholesterolra 240 mg/dL or higher) and those whose parental history is unobtainable.⁹

Evidence summary

Screening for hyperlipidemia using total cholesterol and low-density lipoprotein (LDL) cholesterol is recommended for adults after the age of 35 years for men and 45 years for women.¹ Younger adults (men aged 20–35 and women aged 20–45) should be screened for lipid disorders if they have other risk factors for CVD.¹

Children with heterozygous familial hypercholesterolemia, an autosomal dominant disorder with a prevalence of 1 in 500, are at increased risk of cardiovascular morbidity and mortality in adulthood. One quarter of males with familial hyper-cholesterolemia suffer fatal coronary heart disease (CHD) by age 50 years.²

The use of statins by children with familial hypercholesterolemia for up to 2 years is safe and lowers LDL cholesterol.³ Longer use by children has not been studied, so no comment can be made about long-term safety and decreased CHD morbidity and mortality.

One systematic review and cost-effectiveness analysis investigated the appropriateness and cost-effectiveness of screening methods for familial hypercholesterolemia beginning at the age of 16 years.⁴ The authors identified potential screening strategies from 6 cross-sectional studies and applied these to a decision analysis. Screening of first-degree relatives of those with familial hypercholesterolemia was most effective in detecting cases of familial hypercholesterolemia (number needed to screen [NNS]=3; cost per case detected=$232; cost per life-year gained=$5397).

Universal screening of all 16-year-olds was also cost-effective (cost per life-year gained=$4839), but resulted in a much larger NNS and cost of detection (NNS=1365, cost per case detected=$16,999). The authors concluded that case finding through screening of first-degree relatives was the most cost-effective strategy overall.

In contrast to children affected with familial hypercholesterolemia, the relationship of blood cholesterol levels in children without familial hypercholesterolemia to CHD later in life has not been established. A paucity of data exists that links lowering of cholesterol in childhood with reduced CHD morbidity and mortality in adulthood. Therefore, the benefits of detecting and treating childhood hyperlipidemia without familial hypercholesterolemia are not known. Despite the lack of patient-oriented outcomes research in this area, 2 guidelines recommend screening all children for hyperlipidemia.^5,9

Three studies investigated the use of various recommended screening indicators in identifying children with hyperlipidemia. The first was a control cohort from a case-control study that applied the National Cholesterol Education Program (NCEP) guidelines for screening in children⁵ to 501 US males less than 20 years old, and examined the effectiveness of using the recommended 2 major screening indicators (family history of premature cardiovascular disease and parent cholesterol >240 mg/dL) plus 5 discretionary indicators (high-fat/high-cholesterol diet, hypertension, obesity, smoker, steroid/medication).⁶ If all major and discretionary indicators were applied to the cohort, 96% of the children with LDL greater than 130 mg/dL were identified. However, the individual positive predictive values (PPV; probability of having LDL >130 when a child had a screening indicator) ranged from 6.8% to 20.6%.

The 2 other studies used a cross-sectional design to evaluate family history of premature cardiovascular disease and hyperlipidemia screening indicators in 4183 grade-school children in Taiwan⁷ and 2217 youths in Quebec.⁸ Family history performed poorly as a mechanism for identifying children with hypercholesterolemia (total cholesterol >200 mg/dL; LDL >130 mg/dL) (PPV <12.5%⁷, PPV=7.7%⁸). More than 75% of the children in the Taiwan study would have been missed using family history as a screen. Both studies concluded that family history as a screening indicator is insensitive and inaccurate, and no more useful than general population screening.

Recommendations from others

Neither the American Academy of Family Physicians or the US Preventive Services Task Force makes a recommendation about screening for hyperlipidemia in this age group.

The American Academy of Pediatrics recommends screening children aged 2 years or older whose parents or grandparents had coronary atherosclerosis at age 55 or younger (defined by diagnostic coronary arteriography, myocardial infarction, angina pectoris, peripheral vascular disease, cerebrovascular disease, or sudden cardiac death). They also advocate screening children of a parent with an elevated blood cholesterol level (total cholesterolra 240 mg/dL or higher) and those whose parental history is unobtainable.⁹

Evidence summary

Screening for hyperlipidemia using total cholesterol and low-density lipoprotein (LDL) cholesterol is recommended for adults after the age of 35 years for men and 45 years for women.¹ Younger adults (men aged 20–35 and women aged 20–45) should be screened for lipid disorders if they have other risk factors for CVD.¹

Children with heterozygous familial hypercholesterolemia, an autosomal dominant disorder with a prevalence of 1 in 500, are at increased risk of cardiovascular morbidity and mortality in adulthood. One quarter of males with familial hyper-cholesterolemia suffer fatal coronary heart disease (CHD) by age 50 years.²

The use of statins by children with familial hypercholesterolemia for up to 2 years is safe and lowers LDL cholesterol.³ Longer use by children has not been studied, so no comment can be made about long-term safety and decreased CHD morbidity and mortality.

One systematic review and cost-effectiveness analysis investigated the appropriateness and cost-effectiveness of screening methods for familial hypercholesterolemia beginning at the age of 16 years.⁴ The authors identified potential screening strategies from 6 cross-sectional studies and applied these to a decision analysis. Screening of first-degree relatives of those with familial hypercholesterolemia was most effective in detecting cases of familial hypercholesterolemia (number needed to screen [NNS]=3; cost per case detected=$232; cost per life-year gained=$5397).

Universal screening of all 16-year-olds was also cost-effective (cost per life-year gained=$4839), but resulted in a much larger NNS and cost of detection (NNS=1365, cost per case detected=$16,999). The authors concluded that case finding through screening of first-degree relatives was the most cost-effective strategy overall.

In contrast to children affected with familial hypercholesterolemia, the relationship of blood cholesterol levels in children without familial hypercholesterolemia to CHD later in life has not been established. A paucity of data exists that links lowering of cholesterol in childhood with reduced CHD morbidity and mortality in adulthood. Therefore, the benefits of detecting and treating childhood hyperlipidemia without familial hypercholesterolemia are not known. Despite the lack of patient-oriented outcomes research in this area, 2 guidelines recommend screening all children for hyperlipidemia.^5,9

Three studies investigated the use of various recommended screening indicators in identifying children with hyperlipidemia. The first was a control cohort from a case-control study that applied the National Cholesterol Education Program (NCEP) guidelines for screening in children⁵ to 501 US males less than 20 years old, and examined the effectiveness of using the recommended 2 major screening indicators (family history of premature cardiovascular disease and parent cholesterol >240 mg/dL) plus 5 discretionary indicators (high-fat/high-cholesterol diet, hypertension, obesity, smoker, steroid/medication).⁶ If all major and discretionary indicators were applied to the cohort, 96% of the children with LDL greater than 130 mg/dL were identified. However, the individual positive predictive values (PPV; probability of having LDL >130 when a child had a screening indicator) ranged from 6.8% to 20.6%.

The 2 other studies used a cross-sectional design to evaluate family history of premature cardiovascular disease and hyperlipidemia screening indicators in 4183 grade-school children in Taiwan⁷ and 2217 youths in Quebec.⁸ Family history performed poorly as a mechanism for identifying children with hypercholesterolemia (total cholesterol >200 mg/dL; LDL >130 mg/dL) (PPV <12.5%⁷, PPV=7.7%⁸). More than 75% of the children in the Taiwan study would have been missed using family history as a screen. Both studies concluded that family history as a screening indicator is insensitive and inaccurate, and no more useful than general population screening.

Recommendations from others

Neither the American Academy of Family Physicians or the US Preventive Services Task Force makes a recommendation about screening for hyperlipidemia in this age group.

The American Academy of Pediatrics recommends screening children aged 2 years or older whose parents or grandparents had coronary atherosclerosis at age 55 or younger (defined by diagnostic coronary arteriography, myocardial infarction, angina pectoris, peripheral vascular disease, cerebrovascular disease, or sudden cardiac death). They also advocate screening children of a parent with an elevated blood cholesterol level (total cholesterolra 240 mg/dL or higher) and those whose parental history is unobtainable.⁹

Evidence summary

In areas where tuberculosis is prevalent, the World Health Organization recommends BCG vaccination at birth, without booster doses, to prevent childhood complications of TB infection;¹ however, the vaccine’s efficacy is known to be inconsistent. Though BCG vaccine given at birth can decrease the risk of miliary TB and TB meningitis among children, estimates of its effectiveness in preventing adult pulmonary TB range widely from 0% to 80%.¹

Though prior BCG vaccination increases the risk of a reactive PPD, this effect is also known to be inconsistent. A 2002 meta-analysis showed that the person’s age at the time of their BCG vaccination and the years since vaccination influence the relative risk of a positive PPD (TABLE). The highest relative risk of a positive PPD occurred among patients who received BCG vaccination after infancy and within 15 years of the PPD testing. This same meta-analysis also examined the significance of the size of the PPD response; a subset of 4 studies showed that equal proportions of BCG vaccinated and unvaccinated patients had indurations of 14 mm or more.²

BCG vaccine may confound PPD readings, but several studies indicate that PPD can still be a useful screening tool for tuberculosis infection after vaccination. A Brazilian case-control study found that reactions by those BCG recipients later exposed to TB were significantly greater than those with no TB exposure.³ The study noted that 47.5% of exposed children (defined as those with a household contact) had PPD readings of >10 mm, compared with just 3.6% of control children. In a Quebec cohort of 1198 foreign-born children and young adults, prior BCG vaccination could account for 50% of PPDs with induration of 5 to 9 mm, but only 4% of reactions 10 mm or greater. This study also showed that patients from countries with a high or moderate incidence of TB were more likely to have reactive PPDs than those from countries of low incidence, suggesting that exposure to TB accounts for some of the positive PPDs.⁴

Where it is available, the QuantiFERON-TB Gold test may be used in place of, or in addition to, the PPD for patients who are known to have received a BCG vaccine. This blood test detects interferon-gamma in the serum of people sensitized to Mycobacterium tuberculosis. Because the test is specific to proteins found in M tuberculosis, there is no cross-reactivity with BCG. A Japanese study of 216 BCG-vaccinated individuals showed interferon-gamma assays to be 98.1% specific. The same study reported 89.0% sensitivity for the combination of 2 interferon-gamma assays among 118 TB culture-confirmed individuals.⁵ A published report estimated the cost to the health care system per patient tested by a single interferon-gamma release assay as $33.67, compared with approximately $11 for PPD testing.⁶

TABLE
PPD reactions >10 mm when BCG was given during and after infancy

Recommendations from others

While the US Preventive Services Task Force (USPSTF) does not make a specific recommendation regarding PPD readings after BCG vaccine, it does recommend screening high-risk populations. The USPSTF further notes that reactions >10 mm should not be attributed to prior BCG vaccine.⁷

The Centers for Disease Control and Prevention (CDC) and American Thoracic Society joint statement recommends against altering guidelines for testing and interpretation among BCG recipients.⁸ In 2005, the CDC recommended the QuantiFERON-TB Gold test be used under the same indications as the PPD, noting its potential benefit among those previously immunized with BCG.⁹

Evidence summary

In areas where tuberculosis is prevalent, the World Health Organization recommends BCG vaccination at birth, without booster doses, to prevent childhood complications of TB infection;¹ however, the vaccine’s efficacy is known to be inconsistent. Though BCG vaccine given at birth can decrease the risk of miliary TB and TB meningitis among children, estimates of its effectiveness in preventing adult pulmonary TB range widely from 0% to 80%.¹

Though prior BCG vaccination increases the risk of a reactive PPD, this effect is also known to be inconsistent. A 2002 meta-analysis showed that the person’s age at the time of their BCG vaccination and the years since vaccination influence the relative risk of a positive PPD (TABLE). The highest relative risk of a positive PPD occurred among patients who received BCG vaccination after infancy and within 15 years of the PPD testing. This same meta-analysis also examined the significance of the size of the PPD response; a subset of 4 studies showed that equal proportions of BCG vaccinated and unvaccinated patients had indurations of 14 mm or more.²

BCG vaccine may confound PPD readings, but several studies indicate that PPD can still be a useful screening tool for tuberculosis infection after vaccination. A Brazilian case-control study found that reactions by those BCG recipients later exposed to TB were significantly greater than those with no TB exposure.³ The study noted that 47.5% of exposed children (defined as those with a household contact) had PPD readings of >10 mm, compared with just 3.6% of control children. In a Quebec cohort of 1198 foreign-born children and young adults, prior BCG vaccination could account for 50% of PPDs with induration of 5 to 9 mm, but only 4% of reactions 10 mm or greater. This study also showed that patients from countries with a high or moderate incidence of TB were more likely to have reactive PPDs than those from countries of low incidence, suggesting that exposure to TB accounts for some of the positive PPDs.⁴

Where it is available, the QuantiFERON-TB Gold test may be used in place of, or in addition to, the PPD for patients who are known to have received a BCG vaccine. This blood test detects interferon-gamma in the serum of people sensitized to Mycobacterium tuberculosis. Because the test is specific to proteins found in M tuberculosis, there is no cross-reactivity with BCG. A Japanese study of 216 BCG-vaccinated individuals showed interferon-gamma assays to be 98.1% specific. The same study reported 89.0% sensitivity for the combination of 2 interferon-gamma assays among 118 TB culture-confirmed individuals.⁵ A published report estimated the cost to the health care system per patient tested by a single interferon-gamma release assay as $33.67, compared with approximately $11 for PPD testing.⁶

TABLE
PPD reactions >10 mm when BCG was given during and after infancy

Recommendations from others

While the US Preventive Services Task Force (USPSTF) does not make a specific recommendation regarding PPD readings after BCG vaccine, it does recommend screening high-risk populations. The USPSTF further notes that reactions >10 mm should not be attributed to prior BCG vaccine.⁷

The Centers for Disease Control and Prevention (CDC) and American Thoracic Society joint statement recommends against altering guidelines for testing and interpretation among BCG recipients.⁸ In 2005, the CDC recommended the QuantiFERON-TB Gold test be used under the same indications as the PPD, noting its potential benefit among those previously immunized with BCG.⁹

Evidence summary

In areas where tuberculosis is prevalent, the World Health Organization recommends BCG vaccination at birth, without booster doses, to prevent childhood complications of TB infection;¹ however, the vaccine’s efficacy is known to be inconsistent. Though BCG vaccine given at birth can decrease the risk of miliary TB and TB meningitis among children, estimates of its effectiveness in preventing adult pulmonary TB range widely from 0% to 80%.¹

Though prior BCG vaccination increases the risk of a reactive PPD, this effect is also known to be inconsistent. A 2002 meta-analysis showed that the person’s age at the time of their BCG vaccination and the years since vaccination influence the relative risk of a positive PPD (TABLE). The highest relative risk of a positive PPD occurred among patients who received BCG vaccination after infancy and within 15 years of the PPD testing. This same meta-analysis also examined the significance of the size of the PPD response; a subset of 4 studies showed that equal proportions of BCG vaccinated and unvaccinated patients had indurations of 14 mm or more.²

BCG vaccine may confound PPD readings, but several studies indicate that PPD can still be a useful screening tool for tuberculosis infection after vaccination. A Brazilian case-control study found that reactions by those BCG recipients later exposed to TB were significantly greater than those with no TB exposure.³ The study noted that 47.5% of exposed children (defined as those with a household contact) had PPD readings of >10 mm, compared with just 3.6% of control children. In a Quebec cohort of 1198 foreign-born children and young adults, prior BCG vaccination could account for 50% of PPDs with induration of 5 to 9 mm, but only 4% of reactions 10 mm or greater. This study also showed that patients from countries with a high or moderate incidence of TB were more likely to have reactive PPDs than those from countries of low incidence, suggesting that exposure to TB accounts for some of the positive PPDs.⁴

Where it is available, the QuantiFERON-TB Gold test may be used in place of, or in addition to, the PPD for patients who are known to have received a BCG vaccine. This blood test detects interferon-gamma in the serum of people sensitized to Mycobacterium tuberculosis. Because the test is specific to proteins found in M tuberculosis, there is no cross-reactivity with BCG. A Japanese study of 216 BCG-vaccinated individuals showed interferon-gamma assays to be 98.1% specific. The same study reported 89.0% sensitivity for the combination of 2 interferon-gamma assays among 118 TB culture-confirmed individuals.⁵ A published report estimated the cost to the health care system per patient tested by a single interferon-gamma release assay as $33.67, compared with approximately $11 for PPD testing.⁶

TABLE
PPD reactions >10 mm when BCG was given during and after infancy

Recommendations from others

While the US Preventive Services Task Force (USPSTF) does not make a specific recommendation regarding PPD readings after BCG vaccine, it does recommend screening high-risk populations. The USPSTF further notes that reactions >10 mm should not be attributed to prior BCG vaccine.⁷

The Centers for Disease Control and Prevention (CDC) and American Thoracic Society joint statement recommends against altering guidelines for testing and interpretation among BCG recipients.⁸ In 2005, the CDC recommended the QuantiFERON-TB Gold test be used under the same indications as the PPD, noting its potential benefit among those previously immunized with BCG.⁹

Evidence summary

Fractures within 1.5 cm of the fifth metatarsal tuberosity, without extension distal to the fourth-fifth intermetatarsal articulation, occurring with less than 2-week symptom prodrome and without a history of previous fracture, are defined as “acute Jones’ fractures” (FIGURE). In a recent RCT by Mologne et al,¹ 37 active-duty military personnel with acute Jones’ fractures were randomized to either 8 weeks of no weight-bearing in a short leg casting, followed by a walking cast or hard-soled shoe until clinical union; or to early outpatient intramedullary screw fixation followed by no weight-bearing for 2 weeks, then weight-bearing as tolerated in a hard-soled shoe until clinical union. Screw fixation significantly reduced both time to clinical union and time to return to sports—by nearly 50% when compared with non-weightbearing short leg casting. Furthermore, at 26 weeks the casting group saw a significant 44% failure rate compared with only 5% in the surgical group (number needed to treat [NNT]=2.6). Six patients in the surgical group had mild discomfort from the screw head, and 3 needed the screw to be removed. Generalization of the results was limited by the mostly male military population.

The rates and times of union with short leg casting vary over a wide range in the research literature. The casting group in the RCT above had union rates of 56% and median time to union of 14.5 weeks (lower and upper quartile range, 10.5–18.5).¹ A prospective registry of 68 consecutive acute Jones’ fractures in primarily young military service members showed a 72% union rate with non-weightbearing short leg casting with average time to union of 21.2 weeks.² A heterogeneous group of 5 retrospective follow-up studies of short leg casting reported wide ranges in union rates of 72% to 100%, and in time to healing of 7 weeks to 21 months.^3-7 These studies varied in average age, sex, and athletic ability of their samples as well as type of immobilization and weight-bearing status during treatment.

Tuberosity avulsion fractures are proximal fifth metatarsal styloid fractures resulting from a forceful pull of the lateral band of the long plantar ligament or the peroneus brevis tendon during ankle inversion. A 12-week RCT in 89 consecutive patients presenting to an emergency department with fifth metatarsal tuberosity avulsion fractures compared a nonrigid, soft Jones’ dressing consisting of alternating layers of cast padding and elastic bandages with a rigid short leg casting.⁸ The Jones’ dressing had a significant 28% reduction in time to return to pre-injury levels of activity. Other outcomes—time in treatment modality, time to radiographic healing, and functional foot score—were not different between intervention groups. Validity was limited by the 32% lost to follow-up rate.

FIGURE
Acute fracture of the fifth metatarsal

Recommendations from others

We were unable to locate any consensus statements or clinical guidelines regarding the treatment of Jones’ fractures.

DeLee and Drez’s Orthopaedic Sports Medicine recommends immobilization in a cast or below-the-knee boot with strict non-weightbearing for at least 6 weeks for acute Jones’ fractures.⁹ It recommends surgical treatment, followed by 6 weeks of cast immobilization, then progression to weight bearing based on radiographic findings, for nonoperative treatment failures or with desire to return high-performance athletes to activity.

In Fracture Management for Primary Care, the authors recommend posterior splinting and non-weightbearing with crutches for acute Jones’ fractures, followed by non-weightbearing short leg casting application at 3 to 5 days from injury.¹⁰ After a minimum of 6 to 8 weeks of casting, they recommend options of 4 additional weeks of casting or internal fixation for clinical or radiographic nonunion.

For tuberosity avulsion fractures, the authors recommend use of a firm-soled shoe for 4 to 8 weeks. For patients with discomfort at an initial 4- to 7-day follow-up, they give an option of using a walking short leg casting for 2 weeks, with follow-up every 2 to 4 weeks until clinical healing.

Evidence summary

Fractures within 1.5 cm of the fifth metatarsal tuberosity, without extension distal to the fourth-fifth intermetatarsal articulation, occurring with less than 2-week symptom prodrome and without a history of previous fracture, are defined as “acute Jones’ fractures” (FIGURE). In a recent RCT by Mologne et al,¹ 37 active-duty military personnel with acute Jones’ fractures were randomized to either 8 weeks of no weight-bearing in a short leg casting, followed by a walking cast or hard-soled shoe until clinical union; or to early outpatient intramedullary screw fixation followed by no weight-bearing for 2 weeks, then weight-bearing as tolerated in a hard-soled shoe until clinical union. Screw fixation significantly reduced both time to clinical union and time to return to sports—by nearly 50% when compared with non-weightbearing short leg casting. Furthermore, at 26 weeks the casting group saw a significant 44% failure rate compared with only 5% in the surgical group (number needed to treat [NNT]=2.6). Six patients in the surgical group had mild discomfort from the screw head, and 3 needed the screw to be removed. Generalization of the results was limited by the mostly male military population.

The rates and times of union with short leg casting vary over a wide range in the research literature. The casting group in the RCT above had union rates of 56% and median time to union of 14.5 weeks (lower and upper quartile range, 10.5–18.5).¹ A prospective registry of 68 consecutive acute Jones’ fractures in primarily young military service members showed a 72% union rate with non-weightbearing short leg casting with average time to union of 21.2 weeks.² A heterogeneous group of 5 retrospective follow-up studies of short leg casting reported wide ranges in union rates of 72% to 100%, and in time to healing of 7 weeks to 21 months.^3-7 These studies varied in average age, sex, and athletic ability of their samples as well as type of immobilization and weight-bearing status during treatment.

Tuberosity avulsion fractures are proximal fifth metatarsal styloid fractures resulting from a forceful pull of the lateral band of the long plantar ligament or the peroneus brevis tendon during ankle inversion. A 12-week RCT in 89 consecutive patients presenting to an emergency department with fifth metatarsal tuberosity avulsion fractures compared a nonrigid, soft Jones’ dressing consisting of alternating layers of cast padding and elastic bandages with a rigid short leg casting.⁸ The Jones’ dressing had a significant 28% reduction in time to return to pre-injury levels of activity. Other outcomes—time in treatment modality, time to radiographic healing, and functional foot score—were not different between intervention groups. Validity was limited by the 32% lost to follow-up rate.

FIGURE
Acute fracture of the fifth metatarsal

Recommendations from others

We were unable to locate any consensus statements or clinical guidelines regarding the treatment of Jones’ fractures.

DeLee and Drez’s Orthopaedic Sports Medicine recommends immobilization in a cast or below-the-knee boot with strict non-weightbearing for at least 6 weeks for acute Jones’ fractures.⁹ It recommends surgical treatment, followed by 6 weeks of cast immobilization, then progression to weight bearing based on radiographic findings, for nonoperative treatment failures or with desire to return high-performance athletes to activity.

In Fracture Management for Primary Care, the authors recommend posterior splinting and non-weightbearing with crutches for acute Jones’ fractures, followed by non-weightbearing short leg casting application at 3 to 5 days from injury.¹⁰ After a minimum of 6 to 8 weeks of casting, they recommend options of 4 additional weeks of casting or internal fixation for clinical or radiographic nonunion.

For tuberosity avulsion fractures, the authors recommend use of a firm-soled shoe for 4 to 8 weeks. For patients with discomfort at an initial 4- to 7-day follow-up, they give an option of using a walking short leg casting for 2 weeks, with follow-up every 2 to 4 weeks until clinical healing.

Evidence summary

Fractures within 1.5 cm of the fifth metatarsal tuberosity, without extension distal to the fourth-fifth intermetatarsal articulation, occurring with less than 2-week symptom prodrome and without a history of previous fracture, are defined as “acute Jones’ fractures” (FIGURE). In a recent RCT by Mologne et al,¹ 37 active-duty military personnel with acute Jones’ fractures were randomized to either 8 weeks of no weight-bearing in a short leg casting, followed by a walking cast or hard-soled shoe until clinical union; or to early outpatient intramedullary screw fixation followed by no weight-bearing for 2 weeks, then weight-bearing as tolerated in a hard-soled shoe until clinical union. Screw fixation significantly reduced both time to clinical union and time to return to sports—by nearly 50% when compared with non-weightbearing short leg casting. Furthermore, at 26 weeks the casting group saw a significant 44% failure rate compared with only 5% in the surgical group (number needed to treat [NNT]=2.6). Six patients in the surgical group had mild discomfort from the screw head, and 3 needed the screw to be removed. Generalization of the results was limited by the mostly male military population.

The rates and times of union with short leg casting vary over a wide range in the research literature. The casting group in the RCT above had union rates of 56% and median time to union of 14.5 weeks (lower and upper quartile range, 10.5–18.5).¹ A prospective registry of 68 consecutive acute Jones’ fractures in primarily young military service members showed a 72% union rate with non-weightbearing short leg casting with average time to union of 21.2 weeks.² A heterogeneous group of 5 retrospective follow-up studies of short leg casting reported wide ranges in union rates of 72% to 100%, and in time to healing of 7 weeks to 21 months.^3-7 These studies varied in average age, sex, and athletic ability of their samples as well as type of immobilization and weight-bearing status during treatment.

Tuberosity avulsion fractures are proximal fifth metatarsal styloid fractures resulting from a forceful pull of the lateral band of the long plantar ligament or the peroneus brevis tendon during ankle inversion. A 12-week RCT in 89 consecutive patients presenting to an emergency department with fifth metatarsal tuberosity avulsion fractures compared a nonrigid, soft Jones’ dressing consisting of alternating layers of cast padding and elastic bandages with a rigid short leg casting.⁸ The Jones’ dressing had a significant 28% reduction in time to return to pre-injury levels of activity. Other outcomes—time in treatment modality, time to radiographic healing, and functional foot score—were not different between intervention groups. Validity was limited by the 32% lost to follow-up rate.

FIGURE
Acute fracture of the fifth metatarsal

Recommendations from others

We were unable to locate any consensus statements or clinical guidelines regarding the treatment of Jones’ fractures.

DeLee and Drez’s Orthopaedic Sports Medicine recommends immobilization in a cast or below-the-knee boot with strict non-weightbearing for at least 6 weeks for acute Jones’ fractures.⁹ It recommends surgical treatment, followed by 6 weeks of cast immobilization, then progression to weight bearing based on radiographic findings, for nonoperative treatment failures or with desire to return high-performance athletes to activity.

In Fracture Management for Primary Care, the authors recommend posterior splinting and non-weightbearing with crutches for acute Jones’ fractures, followed by non-weightbearing short leg casting application at 3 to 5 days from injury.¹⁰ After a minimum of 6 to 8 weeks of casting, they recommend options of 4 additional weeks of casting or internal fixation for clinical or radiographic nonunion.

For tuberosity avulsion fractures, the authors recommend use of a firm-soled shoe for 4 to 8 weeks. For patients with discomfort at an initial 4- to 7-day follow-up, they give an option of using a walking short leg casting for 2 weeks, with follow-up every 2 to 4 weeks until clinical healing.