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What are the indications for urodynamic testing in older adults with incontinence?
Urodynamic testing is indicated for older adults with incontinence when the underlying cause remains unclear (Grade of Recommendation: B, based on multiple well designed, but inconsistent, randomized controlled trials [RCTs]). Simple cystometry—specifically, measuring post void residual and bladder capacity—is helpful in the evaluation of urinary incontinence when the cause has remained unclear. It may also offer benefit when surgery is under consideration, when there is a history of genitourinary surgery, or when a conservative therapeutic trial has not had an adequate response (Grade of Recommendation: C, based on a small number of RCTs, retrospective cohort studies and systemic reviews).
Evidence summary
Current studies regarding urodynamic testing in older adults with incontinence are limited by multiple factors, including inherent gender bias, poor reproducibility, and small study populations. Moreover, the lack of a reference standard has contributed to difficulty in assessing outcome measures. No published study to date has convincingly supported a role for advanced urodynamic testing (leak point pressure measurement, pressure flow studies, electromyelography, etc.) in the evaluation of routine urinary incontinence. Simple cystometry, (measuring post-void residuals and determining bladder capacity), has proved particularly useful in detecting abnormalities of detrusor compliance and contractility, especially when the cause of incontinence is unclear.1,2
One well designed retrospective cohort study of 950 women found that the positive predictive value of clinical symptoms in urinary incontinence alone (74% in the context of a 53% prevalence of incontinence) was not accurate enough to rely on for decisions about surgery.3 This study supports the need for urodynamic evaluation in most women prior to surgical incontinence treatment.
Another recent small RCT (n=87) found that, of patients with previous genitourinary surgery or more severe stress incontinence, about one quarter were more likely to have their management revised after urodynamic studies.4 Patients who demonstrated little or no improvement during the first few months of conservative treatment also ran a higher risk of misdiagnosis. Despite these findings, no difference in treatment outcomes was detected for women randomized to urodynamic testing.
Two additional RCTs suggest that, despite the wide use of urodynamic testing, reproducibility is limited and may lack sufficient sensitivity and specificity to identify underlying pathology.5,6 Specific concerns raised in these studies included test-retest variation, as well as concerns about possible interpretation error of urodynamic testing.
Recommendations from others
In its 1996 Clinical Practice Guideline Update, the Agency for Healthcare Research and Quality (AHRQ) recommended a focused history and targeted examination (including urinalysis and post-void residual measurement) in order to detect reversible causes of urinary incontinence.1 The guideline stresses that urodynamic testing is invasive and expensive, and it should be reserved for those situations when the patient desires such evaluation and the information gathered would potentially change management. Although AHRQ considers this guideline too old to direct current medical practice, we found little recent evidence to refute these recommendations.
TABLE
Indications for urodynamic evaluation in older adults
| Unclear diagnosis and inability to develop a reasonable treatment plan based on basic diagnostic evaluation. |
| Consideration of surgical intervention, particularly if previous surgery failed or the patient is a high surgical risk. |
| Patient dissatisfaction after an adequate therapeutic trial or desire to pursue further therapy |
| Table adapted from Reference 1. |
Clinical Commentary by John Gazewood, MD, at http://www.fpin.org.
1. Fantyl JA, Newman DK, Colling J, DeLancey JOL, Keeys C, Loughery R, et al. No. 2, 1996 Update AHCPR Publication No. 96-0682. Public Health Service, Agency for Health Care Policy and Research, Rockville, MD.
2. Ouslander JG, Leach GE, Staskin DR. Prospective evaluation of an assessment strategy for geriatric urinary incontinence. J Am Geriatr Soc 1989;37(8):706-14.
3. Weidner AC, Myers ER, Evan R, Visco AG, Cundiff GW, Bump RC. Which women with stress incontinence require urodynamic evaluation? Am J Obstet Gynecol 2001;184:20-7.
4. Holtedahl K, Verelst M, Schiefloe A, Hunskaar S. Usefulness of urodynamic examination in female urinary incontinence—lessons from a population-based, randomized, controlled study of conservative treatment. Scand J Urol Nephrol 2000;34:169-74.
5. Lose G, Thyssen H. Neurourol Urodynamics 1996;15:302-3.
6. Sorensen S, Gregersen H, Sorenson SM. Long term reproducibility of urodynamic investigations in healthy fertile females. Scand J Urol Nephrol 1988;114:35-41.
Urodynamic testing is indicated for older adults with incontinence when the underlying cause remains unclear (Grade of Recommendation: B, based on multiple well designed, but inconsistent, randomized controlled trials [RCTs]). Simple cystometry—specifically, measuring post void residual and bladder capacity—is helpful in the evaluation of urinary incontinence when the cause has remained unclear. It may also offer benefit when surgery is under consideration, when there is a history of genitourinary surgery, or when a conservative therapeutic trial has not had an adequate response (Grade of Recommendation: C, based on a small number of RCTs, retrospective cohort studies and systemic reviews).
Evidence summary
Current studies regarding urodynamic testing in older adults with incontinence are limited by multiple factors, including inherent gender bias, poor reproducibility, and small study populations. Moreover, the lack of a reference standard has contributed to difficulty in assessing outcome measures. No published study to date has convincingly supported a role for advanced urodynamic testing (leak point pressure measurement, pressure flow studies, electromyelography, etc.) in the evaluation of routine urinary incontinence. Simple cystometry, (measuring post-void residuals and determining bladder capacity), has proved particularly useful in detecting abnormalities of detrusor compliance and contractility, especially when the cause of incontinence is unclear.1,2
One well designed retrospective cohort study of 950 women found that the positive predictive value of clinical symptoms in urinary incontinence alone (74% in the context of a 53% prevalence of incontinence) was not accurate enough to rely on for decisions about surgery.3 This study supports the need for urodynamic evaluation in most women prior to surgical incontinence treatment.
Another recent small RCT (n=87) found that, of patients with previous genitourinary surgery or more severe stress incontinence, about one quarter were more likely to have their management revised after urodynamic studies.4 Patients who demonstrated little or no improvement during the first few months of conservative treatment also ran a higher risk of misdiagnosis. Despite these findings, no difference in treatment outcomes was detected for women randomized to urodynamic testing.
Two additional RCTs suggest that, despite the wide use of urodynamic testing, reproducibility is limited and may lack sufficient sensitivity and specificity to identify underlying pathology.5,6 Specific concerns raised in these studies included test-retest variation, as well as concerns about possible interpretation error of urodynamic testing.
Recommendations from others
In its 1996 Clinical Practice Guideline Update, the Agency for Healthcare Research and Quality (AHRQ) recommended a focused history and targeted examination (including urinalysis and post-void residual measurement) in order to detect reversible causes of urinary incontinence.1 The guideline stresses that urodynamic testing is invasive and expensive, and it should be reserved for those situations when the patient desires such evaluation and the information gathered would potentially change management. Although AHRQ considers this guideline too old to direct current medical practice, we found little recent evidence to refute these recommendations.
TABLE
Indications for urodynamic evaluation in older adults
| Unclear diagnosis and inability to develop a reasonable treatment plan based on basic diagnostic evaluation. |
| Consideration of surgical intervention, particularly if previous surgery failed or the patient is a high surgical risk. |
| Patient dissatisfaction after an adequate therapeutic trial or desire to pursue further therapy |
| Table adapted from Reference 1. |
Clinical Commentary by John Gazewood, MD, at http://www.fpin.org.
Urodynamic testing is indicated for older adults with incontinence when the underlying cause remains unclear (Grade of Recommendation: B, based on multiple well designed, but inconsistent, randomized controlled trials [RCTs]). Simple cystometry—specifically, measuring post void residual and bladder capacity—is helpful in the evaluation of urinary incontinence when the cause has remained unclear. It may also offer benefit when surgery is under consideration, when there is a history of genitourinary surgery, or when a conservative therapeutic trial has not had an adequate response (Grade of Recommendation: C, based on a small number of RCTs, retrospective cohort studies and systemic reviews).
Evidence summary
Current studies regarding urodynamic testing in older adults with incontinence are limited by multiple factors, including inherent gender bias, poor reproducibility, and small study populations. Moreover, the lack of a reference standard has contributed to difficulty in assessing outcome measures. No published study to date has convincingly supported a role for advanced urodynamic testing (leak point pressure measurement, pressure flow studies, electromyelography, etc.) in the evaluation of routine urinary incontinence. Simple cystometry, (measuring post-void residuals and determining bladder capacity), has proved particularly useful in detecting abnormalities of detrusor compliance and contractility, especially when the cause of incontinence is unclear.1,2
One well designed retrospective cohort study of 950 women found that the positive predictive value of clinical symptoms in urinary incontinence alone (74% in the context of a 53% prevalence of incontinence) was not accurate enough to rely on for decisions about surgery.3 This study supports the need for urodynamic evaluation in most women prior to surgical incontinence treatment.
Another recent small RCT (n=87) found that, of patients with previous genitourinary surgery or more severe stress incontinence, about one quarter were more likely to have their management revised after urodynamic studies.4 Patients who demonstrated little or no improvement during the first few months of conservative treatment also ran a higher risk of misdiagnosis. Despite these findings, no difference in treatment outcomes was detected for women randomized to urodynamic testing.
Two additional RCTs suggest that, despite the wide use of urodynamic testing, reproducibility is limited and may lack sufficient sensitivity and specificity to identify underlying pathology.5,6 Specific concerns raised in these studies included test-retest variation, as well as concerns about possible interpretation error of urodynamic testing.
Recommendations from others
In its 1996 Clinical Practice Guideline Update, the Agency for Healthcare Research and Quality (AHRQ) recommended a focused history and targeted examination (including urinalysis and post-void residual measurement) in order to detect reversible causes of urinary incontinence.1 The guideline stresses that urodynamic testing is invasive and expensive, and it should be reserved for those situations when the patient desires such evaluation and the information gathered would potentially change management. Although AHRQ considers this guideline too old to direct current medical practice, we found little recent evidence to refute these recommendations.
TABLE
Indications for urodynamic evaluation in older adults
| Unclear diagnosis and inability to develop a reasonable treatment plan based on basic diagnostic evaluation. |
| Consideration of surgical intervention, particularly if previous surgery failed or the patient is a high surgical risk. |
| Patient dissatisfaction after an adequate therapeutic trial or desire to pursue further therapy |
| Table adapted from Reference 1. |
Clinical Commentary by John Gazewood, MD, at http://www.fpin.org.
1. Fantyl JA, Newman DK, Colling J, DeLancey JOL, Keeys C, Loughery R, et al. No. 2, 1996 Update AHCPR Publication No. 96-0682. Public Health Service, Agency for Health Care Policy and Research, Rockville, MD.
2. Ouslander JG, Leach GE, Staskin DR. Prospective evaluation of an assessment strategy for geriatric urinary incontinence. J Am Geriatr Soc 1989;37(8):706-14.
3. Weidner AC, Myers ER, Evan R, Visco AG, Cundiff GW, Bump RC. Which women with stress incontinence require urodynamic evaluation? Am J Obstet Gynecol 2001;184:20-7.
4. Holtedahl K, Verelst M, Schiefloe A, Hunskaar S. Usefulness of urodynamic examination in female urinary incontinence—lessons from a population-based, randomized, controlled study of conservative treatment. Scand J Urol Nephrol 2000;34:169-74.
5. Lose G, Thyssen H. Neurourol Urodynamics 1996;15:302-3.
6. Sorensen S, Gregersen H, Sorenson SM. Long term reproducibility of urodynamic investigations in healthy fertile females. Scand J Urol Nephrol 1988;114:35-41.
1. Fantyl JA, Newman DK, Colling J, DeLancey JOL, Keeys C, Loughery R, et al. No. 2, 1996 Update AHCPR Publication No. 96-0682. Public Health Service, Agency for Health Care Policy and Research, Rockville, MD.
2. Ouslander JG, Leach GE, Staskin DR. Prospective evaluation of an assessment strategy for geriatric urinary incontinence. J Am Geriatr Soc 1989;37(8):706-14.
3. Weidner AC, Myers ER, Evan R, Visco AG, Cundiff GW, Bump RC. Which women with stress incontinence require urodynamic evaluation? Am J Obstet Gynecol 2001;184:20-7.
4. Holtedahl K, Verelst M, Schiefloe A, Hunskaar S. Usefulness of urodynamic examination in female urinary incontinence—lessons from a population-based, randomized, controlled study of conservative treatment. Scand J Urol Nephrol 2000;34:169-74.
5. Lose G, Thyssen H. Neurourol Urodynamics 1996;15:302-3.
6. Sorensen S, Gregersen H, Sorenson SM. Long term reproducibility of urodynamic investigations in healthy fertile females. Scand J Urol Nephrol 1988;114:35-41.
Evidence-based answers from the Family Physicians Inquiries Network
What are effective strategies for reducing the risk of steroid-induced osteoporosis?
Calcium, in combination with vitamin D, prevents bone loss and is recommended in all patients. (Grade of recommendation: A, based on systematic reviews of randomized controlled trials [RCTs]). Alendronate and risedronate prevent fractures and should be considered for all patients at increased risk of fracture (5 mg of prednisone or equivalent, daily for longer than 3 months). (Grade of recommendation: A, based on RCTs) Replacement of sex hormones in hypogonadal patients prevents bone loss and increases bone mineral density (BMD). (Grade of recommendation: A for women, based on RCTs; B for men, based on one randomized, crossover trial.) Calcitonin prevents bone loss for up to 1 year. (Grade of recommendation: A, based on systematic review.)
Evidence summary
A systematic review of 5 RCTs (N=274) confirmed clinically and statistically significant prevention of bone loss at the lumbar spine for patients receiving glucocorticoids who also received calcium (500–1000 mg daily) and vitamin D (400–800 IU) daily.1 A systematic review found that patients receiving steroids longer than 3 months gained bone mass when placed on a bisphosphonate.2 A two-year RCT of 208 patients receiving steroids who also received alendronate or placebo demonstrated an incidence of vertebral fracture of 0.7% and 6.8% (NNT=16; RRR=90%; ARR = 5.9%; P= .026), respectively.3 A 48-week RCT involving 477 patients receiving steroids who also received alendronate or placebo demonstrated a 2.3% and 3.7% in incidence of vertebral fracture, respectively (RRR = 38%; ARR = 1.4%; P= NS).4 A 1-year RCT of 184 men on or off steroids using risedronate found an 82.4% decreased incidence of vertebral fractures compared with those who received placebo (NNT = 5; P= .008).5
In hypogonadal patients, several small studies have shown that replacement of sex hormones (estrogen in women and testosterone in men) increases lumbar spine BMD (women 2% and 3–4%; men 5%; all P< .05). Fracture reduction and risk of long-term use were not studied.6-8 In a systematic review of 9 RCTs, including 441 patients, calcitonin preserved bone mass in the lumbar spine but not the femoral neck during the first year of steroid therapy. Lumbar spine BMD values with calcitonin were significantly higher than with placebo at 6 and 12 months, but were similar at 24 months.9
Recommendations from others
The American College of Rheumatology recommends calcium and vitamin D be offered to all patients initiating a regimen of prednisone 5 mg/d or its equivalent with expected duration of longer than 3 months. Bisphosphonates should be prescribed for all patients starting steroids and for patients receiving steroids with a T-score less than -1.0; however they should be used with caution in pre-menopausal women.8 A leading researcher states the rank order for prevention is a bisphosphonate followed by a vitamin D metabolite or hormone replacement.10
Clinical Commentary by Michael Fisher, MD, at http://www.fpin.org.
1. Homik J, Suarez-Almazor ME, Shea B, Cranny A, et al. Cochrane Database Syst Rev. Issue 2, 2002.
2. Blair MM, Carson DS, Barrington R. J Fam Pract 2000;49:839-48.
3. Adachi JD, Saag KG, Delmas PD, Liberman UA, et al. Arthritis Rheum 2001;44:202-11.
4. Saag KG, Emkey R, Schnitzer TJ, Brown JP, et al. N Engl J Med 1998;339:292-9.
5. Reid DM, Adami S, Devogelaer JP, Chines AA. Calcif Tissue Int 2001;69:242-7.
6. Kung AW, Chan TM, Lau CS, Wong RW, et al. Rheumatology 1999;38:1239-44.
7. Reid IR, Wattie DJ, Evans MC, Stapleton JP. Arch Intern Med 1996;156:1173-7.
8. American College of Rheumatology Ad Hoc Committee on Glucocorticoid-Induced Osteoporosis. Arthritis Rheum 2001;44:1496-503.
9. Cranney A, Welch V, Adachi JD, Homik J, et al. Cochrane Database Syst Rev. Issue 2, 2002.
10. Sambrook PN. Ann Acad Med Singapore 2002;31:48-53.
Calcium, in combination with vitamin D, prevents bone loss and is recommended in all patients. (Grade of recommendation: A, based on systematic reviews of randomized controlled trials [RCTs]). Alendronate and risedronate prevent fractures and should be considered for all patients at increased risk of fracture (5 mg of prednisone or equivalent, daily for longer than 3 months). (Grade of recommendation: A, based on RCTs) Replacement of sex hormones in hypogonadal patients prevents bone loss and increases bone mineral density (BMD). (Grade of recommendation: A for women, based on RCTs; B for men, based on one randomized, crossover trial.) Calcitonin prevents bone loss for up to 1 year. (Grade of recommendation: A, based on systematic review.)
Evidence summary
A systematic review of 5 RCTs (N=274) confirmed clinically and statistically significant prevention of bone loss at the lumbar spine for patients receiving glucocorticoids who also received calcium (500–1000 mg daily) and vitamin D (400–800 IU) daily.1 A systematic review found that patients receiving steroids longer than 3 months gained bone mass when placed on a bisphosphonate.2 A two-year RCT of 208 patients receiving steroids who also received alendronate or placebo demonstrated an incidence of vertebral fracture of 0.7% and 6.8% (NNT=16; RRR=90%; ARR = 5.9%; P= .026), respectively.3 A 48-week RCT involving 477 patients receiving steroids who also received alendronate or placebo demonstrated a 2.3% and 3.7% in incidence of vertebral fracture, respectively (RRR = 38%; ARR = 1.4%; P= NS).4 A 1-year RCT of 184 men on or off steroids using risedronate found an 82.4% decreased incidence of vertebral fractures compared with those who received placebo (NNT = 5; P= .008).5
In hypogonadal patients, several small studies have shown that replacement of sex hormones (estrogen in women and testosterone in men) increases lumbar spine BMD (women 2% and 3–4%; men 5%; all P< .05). Fracture reduction and risk of long-term use were not studied.6-8 In a systematic review of 9 RCTs, including 441 patients, calcitonin preserved bone mass in the lumbar spine but not the femoral neck during the first year of steroid therapy. Lumbar spine BMD values with calcitonin were significantly higher than with placebo at 6 and 12 months, but were similar at 24 months.9
Recommendations from others
The American College of Rheumatology recommends calcium and vitamin D be offered to all patients initiating a regimen of prednisone 5 mg/d or its equivalent with expected duration of longer than 3 months. Bisphosphonates should be prescribed for all patients starting steroids and for patients receiving steroids with a T-score less than -1.0; however they should be used with caution in pre-menopausal women.8 A leading researcher states the rank order for prevention is a bisphosphonate followed by a vitamin D metabolite or hormone replacement.10
Clinical Commentary by Michael Fisher, MD, at http://www.fpin.org.
Calcium, in combination with vitamin D, prevents bone loss and is recommended in all patients. (Grade of recommendation: A, based on systematic reviews of randomized controlled trials [RCTs]). Alendronate and risedronate prevent fractures and should be considered for all patients at increased risk of fracture (5 mg of prednisone or equivalent, daily for longer than 3 months). (Grade of recommendation: A, based on RCTs) Replacement of sex hormones in hypogonadal patients prevents bone loss and increases bone mineral density (BMD). (Grade of recommendation: A for women, based on RCTs; B for men, based on one randomized, crossover trial.) Calcitonin prevents bone loss for up to 1 year. (Grade of recommendation: A, based on systematic review.)
Evidence summary
A systematic review of 5 RCTs (N=274) confirmed clinically and statistically significant prevention of bone loss at the lumbar spine for patients receiving glucocorticoids who also received calcium (500–1000 mg daily) and vitamin D (400–800 IU) daily.1 A systematic review found that patients receiving steroids longer than 3 months gained bone mass when placed on a bisphosphonate.2 A two-year RCT of 208 patients receiving steroids who also received alendronate or placebo demonstrated an incidence of vertebral fracture of 0.7% and 6.8% (NNT=16; RRR=90%; ARR = 5.9%; P= .026), respectively.3 A 48-week RCT involving 477 patients receiving steroids who also received alendronate or placebo demonstrated a 2.3% and 3.7% in incidence of vertebral fracture, respectively (RRR = 38%; ARR = 1.4%; P= NS).4 A 1-year RCT of 184 men on or off steroids using risedronate found an 82.4% decreased incidence of vertebral fractures compared with those who received placebo (NNT = 5; P= .008).5
In hypogonadal patients, several small studies have shown that replacement of sex hormones (estrogen in women and testosterone in men) increases lumbar spine BMD (women 2% and 3–4%; men 5%; all P< .05). Fracture reduction and risk of long-term use were not studied.6-8 In a systematic review of 9 RCTs, including 441 patients, calcitonin preserved bone mass in the lumbar spine but not the femoral neck during the first year of steroid therapy. Lumbar spine BMD values with calcitonin were significantly higher than with placebo at 6 and 12 months, but were similar at 24 months.9
Recommendations from others
The American College of Rheumatology recommends calcium and vitamin D be offered to all patients initiating a regimen of prednisone 5 mg/d or its equivalent with expected duration of longer than 3 months. Bisphosphonates should be prescribed for all patients starting steroids and for patients receiving steroids with a T-score less than -1.0; however they should be used with caution in pre-menopausal women.8 A leading researcher states the rank order for prevention is a bisphosphonate followed by a vitamin D metabolite or hormone replacement.10
Clinical Commentary by Michael Fisher, MD, at http://www.fpin.org.
1. Homik J, Suarez-Almazor ME, Shea B, Cranny A, et al. Cochrane Database Syst Rev. Issue 2, 2002.
2. Blair MM, Carson DS, Barrington R. J Fam Pract 2000;49:839-48.
3. Adachi JD, Saag KG, Delmas PD, Liberman UA, et al. Arthritis Rheum 2001;44:202-11.
4. Saag KG, Emkey R, Schnitzer TJ, Brown JP, et al. N Engl J Med 1998;339:292-9.
5. Reid DM, Adami S, Devogelaer JP, Chines AA. Calcif Tissue Int 2001;69:242-7.
6. Kung AW, Chan TM, Lau CS, Wong RW, et al. Rheumatology 1999;38:1239-44.
7. Reid IR, Wattie DJ, Evans MC, Stapleton JP. Arch Intern Med 1996;156:1173-7.
8. American College of Rheumatology Ad Hoc Committee on Glucocorticoid-Induced Osteoporosis. Arthritis Rheum 2001;44:1496-503.
9. Cranney A, Welch V, Adachi JD, Homik J, et al. Cochrane Database Syst Rev. Issue 2, 2002.
10. Sambrook PN. Ann Acad Med Singapore 2002;31:48-53.
1. Homik J, Suarez-Almazor ME, Shea B, Cranny A, et al. Cochrane Database Syst Rev. Issue 2, 2002.
2. Blair MM, Carson DS, Barrington R. J Fam Pract 2000;49:839-48.
3. Adachi JD, Saag KG, Delmas PD, Liberman UA, et al. Arthritis Rheum 2001;44:202-11.
4. Saag KG, Emkey R, Schnitzer TJ, Brown JP, et al. N Engl J Med 1998;339:292-9.
5. Reid DM, Adami S, Devogelaer JP, Chines AA. Calcif Tissue Int 2001;69:242-7.
6. Kung AW, Chan TM, Lau CS, Wong RW, et al. Rheumatology 1999;38:1239-44.
7. Reid IR, Wattie DJ, Evans MC, Stapleton JP. Arch Intern Med 1996;156:1173-7.
8. American College of Rheumatology Ad Hoc Committee on Glucocorticoid-Induced Osteoporosis. Arthritis Rheum 2001;44:1496-503.
9. Cranney A, Welch V, Adachi JD, Homik J, et al. Cochrane Database Syst Rev. Issue 2, 2002.
10. Sambrook PN. Ann Acad Med Singapore 2002;31:48-53.
Evidence-based answers from the Family Physicians Inquiries Network
Should we treat elevated cholesterol in elderly patients?
HMG-CoA reductase inhibitors, or statins, have been shown to decrease all-cause mortality in individuals aged 65 and older with known coronary heart disease (CHD) and elevated cholesterol levels. (Grade of recommendation: A, based on randomized controlled trials.) The clinical benefit of statin use in older persons without known CHD, however, is uncertain. Decisions about testing for lipid levels and treatment should include discussions with the patient about the potential benefits and risks of treatment, taking into account the individual’s overall risk of CHD. (Grade of recommendation: C, based on extrapolations from cohort studies.)
Evidence summary
Two randomized controlledtrials and 1 cohort study demonstrated a decrease in all-cause mortality in individuals aged 65 and older with known CHD by treating elevated cholesterol levels with either pravastatin or simvastatin.1-3 The overall decrease in absolute risk of death was similar (range, 4.1%–6.2%; numbers needed to treat [NNT] = 17–25). The LIPID trial demonstrated a reduction in CHD-related death (relative risk [RR] = 0.76; 95% CI, 0.62–0.93; NNT = 37) and myocardial infarctions (RR = 0.74; 95% CI, 0.60–0.91; NNT = 36) in elderly patients taking pravastatin 40 mg once daily for 6 years compared with placebo.3
Unfortunately, no comparable evidence is available to guide practitioners in their care of older patients without known CHD. A 1993 report on results of the Framingham study showed the association between all-cause mortality and cholesterol level only in individuals younger than 50 years.4 Two other cohort studies showed an association between elevated cholesterol levels and increased CHD mortality.5,6 It is unclear whether all-cause or CHD mortality is the better outcome to measure.
The best available evidence addressing the benefit of lowering lipid levels in persons with elevated cholesterol but without CHD is from the West of Scotland Coronary Prevention study, which included patients aged 45 to 64 years.7 This study showed a 0.5% reduction in CHD mortality (NNT = 200) and a 0.9% reduction in all-cause mortality (NNT = 111). Neither reduction reached statistical significance.
Several reports have demonstrated that statins safely and effectively lower cholesterol levels in patients aged 65 and older.1-3,8,9 Moreover, statins do not decrease health-related quality of life.10 Approximately 1% to 4% of those who take statins experience side effects, including abnormal liver function, arthralgias, myalgias, rash, sinusitis, and diarrhea.
Recommendations from others
The National Cholesterol Education Program published its updated guidelines in 2001, lending support for statin treatment of elevated low-density lipoprotein cholesterol levels in selected men aged 65 or older and women aged 75 or older without CHD.11 The target low-density lipoprotein level varied from 100 to 160 mg/dL depending on presence of other cardiac risk factors. The recommendation emphasized lifestyle changes, noninvasive testing for subclinical atherosclerosis, and consideration of treatment for individuals with extensive subclinical disease or multiple risk factors, rather than focusing merely on chronological age.
Clinical Commentary by Nicholas Solomos, MD, at http://www.fpin.org.
1. Pedersen TR, Wilhelmsen L, Faergeman O, et al. Am J Cardiol 2000;86:257-62.
2. Miettinen TA, Pyorala K, Olsson AG, et al. Circulation 1997;96:4211-8.
3. Hunt D, Young P, Simes J, et al. Ann Intern Med 2001;134:931-40.
4. Kronmal RA, Cain KC, Ye Z, et al. Arch Intern Med 1993;153:1065-73.
5. Rubin SM, Sidney S, Black DM, et al. Ann Intern Med 1990;113:916-20.
6. American College of Physicians. Clinical Guideline: Part 1. Ann Intern Med 1996;124:515-7.
7. Shepherd J, Cobbe SM, Ford I, et al. N Engl J Med 1995;333:1301-7.
8. Chan P, Lee CB, Lin TS, et al. Am J Hypertens 1995;8:1099-104.
9. Chan P, Huang TY, Tomlinson B, et al. J Clin Pharmacol 1997;37:496-501.
10. Santanello NC, Barber BL, Applegate WB, et al. J Am Geriatr Soc 1997;45:8-14.
11. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection. Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Bethesda, MD: National Institutes of Health, National Heart, Lung, and Blood Institute; May 2001. NIH publication 01-3670. Available at: http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3_rpt.htm.
HMG-CoA reductase inhibitors, or statins, have been shown to decrease all-cause mortality in individuals aged 65 and older with known coronary heart disease (CHD) and elevated cholesterol levels. (Grade of recommendation: A, based on randomized controlled trials.) The clinical benefit of statin use in older persons without known CHD, however, is uncertain. Decisions about testing for lipid levels and treatment should include discussions with the patient about the potential benefits and risks of treatment, taking into account the individual’s overall risk of CHD. (Grade of recommendation: C, based on extrapolations from cohort studies.)
Evidence summary
Two randomized controlledtrials and 1 cohort study demonstrated a decrease in all-cause mortality in individuals aged 65 and older with known CHD by treating elevated cholesterol levels with either pravastatin or simvastatin.1-3 The overall decrease in absolute risk of death was similar (range, 4.1%–6.2%; numbers needed to treat [NNT] = 17–25). The LIPID trial demonstrated a reduction in CHD-related death (relative risk [RR] = 0.76; 95% CI, 0.62–0.93; NNT = 37) and myocardial infarctions (RR = 0.74; 95% CI, 0.60–0.91; NNT = 36) in elderly patients taking pravastatin 40 mg once daily for 6 years compared with placebo.3
Unfortunately, no comparable evidence is available to guide practitioners in their care of older patients without known CHD. A 1993 report on results of the Framingham study showed the association between all-cause mortality and cholesterol level only in individuals younger than 50 years.4 Two other cohort studies showed an association between elevated cholesterol levels and increased CHD mortality.5,6 It is unclear whether all-cause or CHD mortality is the better outcome to measure.
The best available evidence addressing the benefit of lowering lipid levels in persons with elevated cholesterol but without CHD is from the West of Scotland Coronary Prevention study, which included patients aged 45 to 64 years.7 This study showed a 0.5% reduction in CHD mortality (NNT = 200) and a 0.9% reduction in all-cause mortality (NNT = 111). Neither reduction reached statistical significance.
Several reports have demonstrated that statins safely and effectively lower cholesterol levels in patients aged 65 and older.1-3,8,9 Moreover, statins do not decrease health-related quality of life.10 Approximately 1% to 4% of those who take statins experience side effects, including abnormal liver function, arthralgias, myalgias, rash, sinusitis, and diarrhea.
Recommendations from others
The National Cholesterol Education Program published its updated guidelines in 2001, lending support for statin treatment of elevated low-density lipoprotein cholesterol levels in selected men aged 65 or older and women aged 75 or older without CHD.11 The target low-density lipoprotein level varied from 100 to 160 mg/dL depending on presence of other cardiac risk factors. The recommendation emphasized lifestyle changes, noninvasive testing for subclinical atherosclerosis, and consideration of treatment for individuals with extensive subclinical disease or multiple risk factors, rather than focusing merely on chronological age.
Clinical Commentary by Nicholas Solomos, MD, at http://www.fpin.org.
HMG-CoA reductase inhibitors, or statins, have been shown to decrease all-cause mortality in individuals aged 65 and older with known coronary heart disease (CHD) and elevated cholesterol levels. (Grade of recommendation: A, based on randomized controlled trials.) The clinical benefit of statin use in older persons without known CHD, however, is uncertain. Decisions about testing for lipid levels and treatment should include discussions with the patient about the potential benefits and risks of treatment, taking into account the individual’s overall risk of CHD. (Grade of recommendation: C, based on extrapolations from cohort studies.)
Evidence summary
Two randomized controlledtrials and 1 cohort study demonstrated a decrease in all-cause mortality in individuals aged 65 and older with known CHD by treating elevated cholesterol levels with either pravastatin or simvastatin.1-3 The overall decrease in absolute risk of death was similar (range, 4.1%–6.2%; numbers needed to treat [NNT] = 17–25). The LIPID trial demonstrated a reduction in CHD-related death (relative risk [RR] = 0.76; 95% CI, 0.62–0.93; NNT = 37) and myocardial infarctions (RR = 0.74; 95% CI, 0.60–0.91; NNT = 36) in elderly patients taking pravastatin 40 mg once daily for 6 years compared with placebo.3
Unfortunately, no comparable evidence is available to guide practitioners in their care of older patients without known CHD. A 1993 report on results of the Framingham study showed the association between all-cause mortality and cholesterol level only in individuals younger than 50 years.4 Two other cohort studies showed an association between elevated cholesterol levels and increased CHD mortality.5,6 It is unclear whether all-cause or CHD mortality is the better outcome to measure.
The best available evidence addressing the benefit of lowering lipid levels in persons with elevated cholesterol but without CHD is from the West of Scotland Coronary Prevention study, which included patients aged 45 to 64 years.7 This study showed a 0.5% reduction in CHD mortality (NNT = 200) and a 0.9% reduction in all-cause mortality (NNT = 111). Neither reduction reached statistical significance.
Several reports have demonstrated that statins safely and effectively lower cholesterol levels in patients aged 65 and older.1-3,8,9 Moreover, statins do not decrease health-related quality of life.10 Approximately 1% to 4% of those who take statins experience side effects, including abnormal liver function, arthralgias, myalgias, rash, sinusitis, and diarrhea.
Recommendations from others
The National Cholesterol Education Program published its updated guidelines in 2001, lending support for statin treatment of elevated low-density lipoprotein cholesterol levels in selected men aged 65 or older and women aged 75 or older without CHD.11 The target low-density lipoprotein level varied from 100 to 160 mg/dL depending on presence of other cardiac risk factors. The recommendation emphasized lifestyle changes, noninvasive testing for subclinical atherosclerosis, and consideration of treatment for individuals with extensive subclinical disease or multiple risk factors, rather than focusing merely on chronological age.
Clinical Commentary by Nicholas Solomos, MD, at http://www.fpin.org.
1. Pedersen TR, Wilhelmsen L, Faergeman O, et al. Am J Cardiol 2000;86:257-62.
2. Miettinen TA, Pyorala K, Olsson AG, et al. Circulation 1997;96:4211-8.
3. Hunt D, Young P, Simes J, et al. Ann Intern Med 2001;134:931-40.
4. Kronmal RA, Cain KC, Ye Z, et al. Arch Intern Med 1993;153:1065-73.
5. Rubin SM, Sidney S, Black DM, et al. Ann Intern Med 1990;113:916-20.
6. American College of Physicians. Clinical Guideline: Part 1. Ann Intern Med 1996;124:515-7.
7. Shepherd J, Cobbe SM, Ford I, et al. N Engl J Med 1995;333:1301-7.
8. Chan P, Lee CB, Lin TS, et al. Am J Hypertens 1995;8:1099-104.
9. Chan P, Huang TY, Tomlinson B, et al. J Clin Pharmacol 1997;37:496-501.
10. Santanello NC, Barber BL, Applegate WB, et al. J Am Geriatr Soc 1997;45:8-14.
11. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection. Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Bethesda, MD: National Institutes of Health, National Heart, Lung, and Blood Institute; May 2001. NIH publication 01-3670. Available at: http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3_rpt.htm.
1. Pedersen TR, Wilhelmsen L, Faergeman O, et al. Am J Cardiol 2000;86:257-62.
2. Miettinen TA, Pyorala K, Olsson AG, et al. Circulation 1997;96:4211-8.
3. Hunt D, Young P, Simes J, et al. Ann Intern Med 2001;134:931-40.
4. Kronmal RA, Cain KC, Ye Z, et al. Arch Intern Med 1993;153:1065-73.
5. Rubin SM, Sidney S, Black DM, et al. Ann Intern Med 1990;113:916-20.
6. American College of Physicians. Clinical Guideline: Part 1. Ann Intern Med 1996;124:515-7.
7. Shepherd J, Cobbe SM, Ford I, et al. N Engl J Med 1995;333:1301-7.
8. Chan P, Lee CB, Lin TS, et al. Am J Hypertens 1995;8:1099-104.
9. Chan P, Huang TY, Tomlinson B, et al. J Clin Pharmacol 1997;37:496-501.
10. Santanello NC, Barber BL, Applegate WB, et al. J Am Geriatr Soc 1997;45:8-14.
11. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection. Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Bethesda, MD: National Institutes of Health, National Heart, Lung, and Blood Institute; May 2001. NIH publication 01-3670. Available at: http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3_rpt.htm.
Evidence-based answers from the Family Physicians Inquiries Network
How effective are nasal steroids combined with nonsedating antihistamines for seasonal allergic rhinitis?
For treating seasonal allergic rhinitis, inhaled nasal corticosteroids are superior to nonsedating antihistamines (Grade of recommendation: A, based on a large meta-analysis of randomized controlled trials [RCTs]). Combining nasal steroids and nonsedating antihistamines yields no additional benefits (Grade of recommendation: A, based on several RCTs). Unless patient preference limits their use, nasal steroids should be first-line therapy.
Evidence summary
A meta-analysis of 16 RCTs compared the efficacy of intranasal steroids and oral antihistamines for alleviating nasal, eye, and global allergy symptoms.1 Intranasal steroids were superior to oral antihistamines for all patient-oriented nasal symptom and global symptom ratings. Eye symptom scores and adverse events were similar in each treatment group.
Several large RCTs have addressed whether combining the 2 classes of drugs would achieve greater symptom control. Only 1 study2 found combination therapy to be superior. This RCT compared beclomethasone dipropionate with loratadine or placebo daily in 154 patients.2 Total symptom scores were better for the combination group mainly due to improved relief from ocular symptoms.
Fluticasone propionate aqueous nasal spray (FPANS) was evaluated alone and in combination with cetirizine in a multicenter double-blind study of 454 patients.3 The mean symptom scores for nasal and eye symptoms were not significantly different between the 2 groups. A more recent RCT had similar results when comparing FPANS with loratadine and with combined therapy.4 This double-blinded placebo-controlled trial, which included 600 patients, measured patient- and clinician-rated total symptom scores, individual nasal symptom scores, and overall evaluations after 7 and 14 days of therapy. Although the symptom scores for the FPANS group were significantly lower than those in the loratadine and placebo groups, no significant difference in scores was found between the FPANS and combined groups. The results were the same for the quality-of-life questionnaire scores. In an RCT of 106 patients, budesonide nasal spray’s efficacy was tested against terfenadine alone and in combination; the nasal steroid alone was more effective than the histamine.5 Combining the 2 drugs yielded no significant improvements.
The newer nasal steroids such as fluticasone may be more effective because of their stronger affinities to glucocorticoid receptors, but no clinical evidence confirms this hypothesis.6
TABLE
Intranasal steroids for treating allergic rhinitis
| Drug | Usual adult dosages | Cost per month* |
|---|---|---|
| Beclomethasone dipropionate | ||
| Beconase AQ | 2 sprays/nostril qd | $44 |
| Vancenase AQ | 2 sprays/nostril qd | $40 |
| Budesonide | ||
| Rhinocort AQ | 2 sprays/nostril bid | $48 |
| Flunisolide | ||
| Nasarel | 2 sprays/nostril bid | $44 |
| Nasalide | 2 sprays/nostril bid | $46 |
| Fluticasone propionate | ||
| Flonase | 2 sprays/nostril qd | $53 |
| Mometasone furoate | ||
| Nasonex | 2 sprays/nostril qd | $56 |
| Triamcinolone acetonide | ||
| Nasacort AQ | 2 sprays/nostril qd | $56 |
| bid, twice a day; qd, every day. | ||
| *Red Book. Medical Economics Data, 2001. | ||
Recommendations from others
The Joint Task Force on Practice Parameters in Allergy, Asthma, and Immunology recommends second-generation oral antihistamines for first-line therapy, but notes that nasal steroids are the most effective medication class for controlling allergy symptoms.7 The task force states that combination drug therapy may be tried. A monograph from the American Academy of Family Physicians notes the lack of consensus guidelines for first-line therapy and recommends that treatment be individualized.8 It states that combination therapy may be tried if monotherapy fails.
Clinical Commentaries by Tsveti Markova, MD, and John W. Tipton, MD, at http://www.FPIN.org.
1. Weiner JM, Abramson MJ, Puy RM. Br Med J 1998;317:1624-9.
2. Drouin MA, Yang WH, Horak F, et al. Allergy 1992;12(suppl):173.-
3. Benincasa C, Lloyd RS. Drug Invest 1994;8:225-33.
4. Ratner PH, Van Bavel JH, Martin BG, et al. J Fam Pract 1998;47:118-25.
5. Simpson RJ. Ann Allergy 1994;73:497-502.
6. Lumry J. Allergy Clin Immunol 2000; 105:394. J Allergy Clin Immunol 1999;104(4 Pt 1):S150-8.
7. Dykewicz M, Fineman S. Ann Allergy Asthma Immunol 1998;81:463-518.
8. Diagnosis and Management of Allergic Rhinitis. American Family Physician Monograph no. 3; 2001.
For treating seasonal allergic rhinitis, inhaled nasal corticosteroids are superior to nonsedating antihistamines (Grade of recommendation: A, based on a large meta-analysis of randomized controlled trials [RCTs]). Combining nasal steroids and nonsedating antihistamines yields no additional benefits (Grade of recommendation: A, based on several RCTs). Unless patient preference limits their use, nasal steroids should be first-line therapy.
Evidence summary
A meta-analysis of 16 RCTs compared the efficacy of intranasal steroids and oral antihistamines for alleviating nasal, eye, and global allergy symptoms.1 Intranasal steroids were superior to oral antihistamines for all patient-oriented nasal symptom and global symptom ratings. Eye symptom scores and adverse events were similar in each treatment group.
Several large RCTs have addressed whether combining the 2 classes of drugs would achieve greater symptom control. Only 1 study2 found combination therapy to be superior. This RCT compared beclomethasone dipropionate with loratadine or placebo daily in 154 patients.2 Total symptom scores were better for the combination group mainly due to improved relief from ocular symptoms.
Fluticasone propionate aqueous nasal spray (FPANS) was evaluated alone and in combination with cetirizine in a multicenter double-blind study of 454 patients.3 The mean symptom scores for nasal and eye symptoms were not significantly different between the 2 groups. A more recent RCT had similar results when comparing FPANS with loratadine and with combined therapy.4 This double-blinded placebo-controlled trial, which included 600 patients, measured patient- and clinician-rated total symptom scores, individual nasal symptom scores, and overall evaluations after 7 and 14 days of therapy. Although the symptom scores for the FPANS group were significantly lower than those in the loratadine and placebo groups, no significant difference in scores was found between the FPANS and combined groups. The results were the same for the quality-of-life questionnaire scores. In an RCT of 106 patients, budesonide nasal spray’s efficacy was tested against terfenadine alone and in combination; the nasal steroid alone was more effective than the histamine.5 Combining the 2 drugs yielded no significant improvements.
The newer nasal steroids such as fluticasone may be more effective because of their stronger affinities to glucocorticoid receptors, but no clinical evidence confirms this hypothesis.6
TABLE
Intranasal steroids for treating allergic rhinitis
| Drug | Usual adult dosages | Cost per month* |
|---|---|---|
| Beclomethasone dipropionate | ||
| Beconase AQ | 2 sprays/nostril qd | $44 |
| Vancenase AQ | 2 sprays/nostril qd | $40 |
| Budesonide | ||
| Rhinocort AQ | 2 sprays/nostril bid | $48 |
| Flunisolide | ||
| Nasarel | 2 sprays/nostril bid | $44 |
| Nasalide | 2 sprays/nostril bid | $46 |
| Fluticasone propionate | ||
| Flonase | 2 sprays/nostril qd | $53 |
| Mometasone furoate | ||
| Nasonex | 2 sprays/nostril qd | $56 |
| Triamcinolone acetonide | ||
| Nasacort AQ | 2 sprays/nostril qd | $56 |
| bid, twice a day; qd, every day. | ||
| *Red Book. Medical Economics Data, 2001. | ||
Recommendations from others
The Joint Task Force on Practice Parameters in Allergy, Asthma, and Immunology recommends second-generation oral antihistamines for first-line therapy, but notes that nasal steroids are the most effective medication class for controlling allergy symptoms.7 The task force states that combination drug therapy may be tried. A monograph from the American Academy of Family Physicians notes the lack of consensus guidelines for first-line therapy and recommends that treatment be individualized.8 It states that combination therapy may be tried if monotherapy fails.
Clinical Commentaries by Tsveti Markova, MD, and John W. Tipton, MD, at http://www.FPIN.org.
For treating seasonal allergic rhinitis, inhaled nasal corticosteroids are superior to nonsedating antihistamines (Grade of recommendation: A, based on a large meta-analysis of randomized controlled trials [RCTs]). Combining nasal steroids and nonsedating antihistamines yields no additional benefits (Grade of recommendation: A, based on several RCTs). Unless patient preference limits their use, nasal steroids should be first-line therapy.
Evidence summary
A meta-analysis of 16 RCTs compared the efficacy of intranasal steroids and oral antihistamines for alleviating nasal, eye, and global allergy symptoms.1 Intranasal steroids were superior to oral antihistamines for all patient-oriented nasal symptom and global symptom ratings. Eye symptom scores and adverse events were similar in each treatment group.
Several large RCTs have addressed whether combining the 2 classes of drugs would achieve greater symptom control. Only 1 study2 found combination therapy to be superior. This RCT compared beclomethasone dipropionate with loratadine or placebo daily in 154 patients.2 Total symptom scores were better for the combination group mainly due to improved relief from ocular symptoms.
Fluticasone propionate aqueous nasal spray (FPANS) was evaluated alone and in combination with cetirizine in a multicenter double-blind study of 454 patients.3 The mean symptom scores for nasal and eye symptoms were not significantly different between the 2 groups. A more recent RCT had similar results when comparing FPANS with loratadine and with combined therapy.4 This double-blinded placebo-controlled trial, which included 600 patients, measured patient- and clinician-rated total symptom scores, individual nasal symptom scores, and overall evaluations after 7 and 14 days of therapy. Although the symptom scores for the FPANS group were significantly lower than those in the loratadine and placebo groups, no significant difference in scores was found between the FPANS and combined groups. The results were the same for the quality-of-life questionnaire scores. In an RCT of 106 patients, budesonide nasal spray’s efficacy was tested against terfenadine alone and in combination; the nasal steroid alone was more effective than the histamine.5 Combining the 2 drugs yielded no significant improvements.
The newer nasal steroids such as fluticasone may be more effective because of their stronger affinities to glucocorticoid receptors, but no clinical evidence confirms this hypothesis.6
TABLE
Intranasal steroids for treating allergic rhinitis
| Drug | Usual adult dosages | Cost per month* |
|---|---|---|
| Beclomethasone dipropionate | ||
| Beconase AQ | 2 sprays/nostril qd | $44 |
| Vancenase AQ | 2 sprays/nostril qd | $40 |
| Budesonide | ||
| Rhinocort AQ | 2 sprays/nostril bid | $48 |
| Flunisolide | ||
| Nasarel | 2 sprays/nostril bid | $44 |
| Nasalide | 2 sprays/nostril bid | $46 |
| Fluticasone propionate | ||
| Flonase | 2 sprays/nostril qd | $53 |
| Mometasone furoate | ||
| Nasonex | 2 sprays/nostril qd | $56 |
| Triamcinolone acetonide | ||
| Nasacort AQ | 2 sprays/nostril qd | $56 |
| bid, twice a day; qd, every day. | ||
| *Red Book. Medical Economics Data, 2001. | ||
Recommendations from others
The Joint Task Force on Practice Parameters in Allergy, Asthma, and Immunology recommends second-generation oral antihistamines for first-line therapy, but notes that nasal steroids are the most effective medication class for controlling allergy symptoms.7 The task force states that combination drug therapy may be tried. A monograph from the American Academy of Family Physicians notes the lack of consensus guidelines for first-line therapy and recommends that treatment be individualized.8 It states that combination therapy may be tried if monotherapy fails.
Clinical Commentaries by Tsveti Markova, MD, and John W. Tipton, MD, at http://www.FPIN.org.
1. Weiner JM, Abramson MJ, Puy RM. Br Med J 1998;317:1624-9.
2. Drouin MA, Yang WH, Horak F, et al. Allergy 1992;12(suppl):173.-
3. Benincasa C, Lloyd RS. Drug Invest 1994;8:225-33.
4. Ratner PH, Van Bavel JH, Martin BG, et al. J Fam Pract 1998;47:118-25.
5. Simpson RJ. Ann Allergy 1994;73:497-502.
6. Lumry J. Allergy Clin Immunol 2000; 105:394. J Allergy Clin Immunol 1999;104(4 Pt 1):S150-8.
7. Dykewicz M, Fineman S. Ann Allergy Asthma Immunol 1998;81:463-518.
8. Diagnosis and Management of Allergic Rhinitis. American Family Physician Monograph no. 3; 2001.
1. Weiner JM, Abramson MJ, Puy RM. Br Med J 1998;317:1624-9.
2. Drouin MA, Yang WH, Horak F, et al. Allergy 1992;12(suppl):173.-
3. Benincasa C, Lloyd RS. Drug Invest 1994;8:225-33.
4. Ratner PH, Van Bavel JH, Martin BG, et al. J Fam Pract 1998;47:118-25.
5. Simpson RJ. Ann Allergy 1994;73:497-502.
6. Lumry J. Allergy Clin Immunol 2000; 105:394. J Allergy Clin Immunol 1999;104(4 Pt 1):S150-8.
7. Dykewicz M, Fineman S. Ann Allergy Asthma Immunol 1998;81:463-518.
8. Diagnosis and Management of Allergic Rhinitis. American Family Physician Monograph no. 3; 2001.
Evidence-based answers from the Family Physicians Inquiries Network