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Does cranberry juice prevent or treat urinary tract infection?
Cranberry juice (200 mL daily to 250 mL 3 times daily) or cranberry concentrate tablets (at least 1:30 parts concentrated juice twice daily) reduce recurrent, symptomatic urinary tract infection (UTI) in women by 12% to 20% (absolute risk reduction [ARR]) compared with placebo (number needed to treat [NNT]=58) (strength of recommendation: A). There is no conclusive evidence that cranberry juice effectively treats UTI (SOR: D).
Evidence summary
A Cochrane review found only a small number of poor-quality trials, providing insufficient support to recommend cranberry juice to prevent UTI.1 However, 2 recent randomized studies, not included in the Cochrane review, found that women taking cranberry juice have fewer symptomatic UTIs.
In women with prior Escherichia coli UTI, 50 mL of cranberry-lingonberry juice concentrate daily for 6 months reduced the recurrence of symptomatic UTI from 36% in the control group to 16% in the treated group (NNT=5).2
In a placebo-controlled randomized trial, women with prior UTI who took 1 tablet of concentrated cranberry juice (at least 1:30 parts concentrated juice) twice daily (n=50) or drank 250 mL of pure unsweetened cranberry juice 3 times a day for 12 months (n=50) reduced their incidence of symptomatic UTI.3 Women who drank the juice had an ARR of 12% (32% symptomatic UTI on placebo group, 20% in cranberry juice group, NNT=8.3) over 1 year. Use of cranberry juice tablets produced an ARR of 14% (32% symptomatic UTI in placebo group; 18% in cranberry tablet group, NNT=7.1). Self-reported compliance was 75% to 90% in the juice group and 90% in the tablet group.
No dose-response studies have been done to determine the optimal volume of juice or number of tablets needed to prevent infection. Studies have used between 200 mL once a day to 250 mL 3 times a day of the juice or 1 cranberry tablet taken twice daily. The subject dropout rate was as high as 34% in one study using juice,4 implying that cranberry juice—which is acidic and astringent at full strength—may not be acceptable to many patients as a prophylactic therapy over a long period. The 1-month compliance rate of patients taking cranberry tablets was between 88% and 100%, suggesting that this form of cranberry may improve compliance.
The cost of cranberry juice and cranberry tablets was estimated at $1400 and $624 per year, respectively.3 This must be balanced against the cost of treating symptomatic UTIs. No randomized trials have tested the more readily available and palatable cranberry juice cocktail—which is mixed with water, a sweetener, and vitamin C—to prevent recurrent UTI.
Cranberry juice does not inhibit bacterial growth and will not sterilize the urinary tract. Also, cranberry juice does not prevent or treat UTI by changing the pH of the urine. Rather, the suspected mechanism of action is that proanthocyanidins contained in cranberry juice prevent bacterial adherence to uroepithelial cells, thus reducing the development of UTI.5 Cranberry juice has been shown to reduce uroepithelial cell adherence by bacteria resistant to trimethoprim-sulfamethoxazole.6
Recommendations from others
No national practice guidelines have recommended cranberry juice as a preventive strategy for recurrent UTI but, anecdotally, patients are often advised to try cranberry juice to prevent UTI.
Brett Robbins, MD
Steven Bondi
Internal Medicine Pediatrics Residency, University of Rochester, NY.
The protective value of cranberry juice against UTI bacteria is supported by a significant body of data from in vitro studies. The published studies examining the clinical use of cranberry juice for UTI prevention suffer from a number of flaws, including small sample size, poor design, lack of randomization, lack of placebo control, heterogeneous endpoints, and a focus on the geriatric population. Even the best of these studies suffers from a major defect: failure to use commonly available cranberry juice cocktail as the experimental intervention.
Despite these flaws, the weight of the clinical evidence suggests that cranberry juice is an effective intervention for the prevention of UTIs—especially in high-risk populations. Unfortunately, cranberry juice is expensive and its taste is displeasing to some, thus limiting its usefulness. Cranberry capsules/ tablets offer a reasonable alternative, but their composition varies greatly by manufacturer, and patient compliance may be poor.
The decision to use cranberry juice should be left to the patient and her clinician.
Given the evidence, cranberry juice is best suited for secondary prevention of recurrent UTI. Patients with recurrent UTI who are being considered for antibiotic prophylaxis and are willing to drink the juice are ideal candidates. Although the studies have yet to establish an ideal dose, 3 glasses a day should be sufficient.
1. Jepson RG, Mihaljevic L, Craig J. Cranberries for preventing urinary tract infections. Cochrane Database Syst Rev 2001:CD001321. (Updated quarterly.)
2. Kontiokari T, Sundqvist K, Nuutinen M, Pokka T, Kaskela M, Uhari M. Randomised trial of cranberry-lingonberry juice and Lactobacillus GG drink for the prevention of urinary tract infections in women. BMJ 2001;322:1571-3.
3. Stothers L. A randomized trial to evaluate effectiveness and cost effectiveness of naturopathic cranberry products as prophylaxis against urinary tract infection in women. Can J Urol 2002;9:1558-62.
4. Foda MM, Middlebrook PF, Gatfield CT, Potvin G, Wells G, Schillinger JF. Efficacy of cranberry in prevention of urinary tract infection in a susceptible pediatric population. Can J Urol 1995;2:98-102.
5. Lowe FC, Fagelman E. Cranberry juice and urinary tract infections: what is the evidence?. Urology 2001;57:407-13.
6. Howell AB, Foxman B. Cranberry juice and adhesion of antibiotic-resistant uropathogens. JAMA 2002;287:3082-3.
Cranberry juice (200 mL daily to 250 mL 3 times daily) or cranberry concentrate tablets (at least 1:30 parts concentrated juice twice daily) reduce recurrent, symptomatic urinary tract infection (UTI) in women by 12% to 20% (absolute risk reduction [ARR]) compared with placebo (number needed to treat [NNT]=58) (strength of recommendation: A). There is no conclusive evidence that cranberry juice effectively treats UTI (SOR: D).
Evidence summary
A Cochrane review found only a small number of poor-quality trials, providing insufficient support to recommend cranberry juice to prevent UTI.1 However, 2 recent randomized studies, not included in the Cochrane review, found that women taking cranberry juice have fewer symptomatic UTIs.
In women with prior Escherichia coli UTI, 50 mL of cranberry-lingonberry juice concentrate daily for 6 months reduced the recurrence of symptomatic UTI from 36% in the control group to 16% in the treated group (NNT=5).2
In a placebo-controlled randomized trial, women with prior UTI who took 1 tablet of concentrated cranberry juice (at least 1:30 parts concentrated juice) twice daily (n=50) or drank 250 mL of pure unsweetened cranberry juice 3 times a day for 12 months (n=50) reduced their incidence of symptomatic UTI.3 Women who drank the juice had an ARR of 12% (32% symptomatic UTI on placebo group, 20% in cranberry juice group, NNT=8.3) over 1 year. Use of cranberry juice tablets produced an ARR of 14% (32% symptomatic UTI in placebo group; 18% in cranberry tablet group, NNT=7.1). Self-reported compliance was 75% to 90% in the juice group and 90% in the tablet group.
No dose-response studies have been done to determine the optimal volume of juice or number of tablets needed to prevent infection. Studies have used between 200 mL once a day to 250 mL 3 times a day of the juice or 1 cranberry tablet taken twice daily. The subject dropout rate was as high as 34% in one study using juice,4 implying that cranberry juice—which is acidic and astringent at full strength—may not be acceptable to many patients as a prophylactic therapy over a long period. The 1-month compliance rate of patients taking cranberry tablets was between 88% and 100%, suggesting that this form of cranberry may improve compliance.
The cost of cranberry juice and cranberry tablets was estimated at $1400 and $624 per year, respectively.3 This must be balanced against the cost of treating symptomatic UTIs. No randomized trials have tested the more readily available and palatable cranberry juice cocktail—which is mixed with water, a sweetener, and vitamin C—to prevent recurrent UTI.
Cranberry juice does not inhibit bacterial growth and will not sterilize the urinary tract. Also, cranberry juice does not prevent or treat UTI by changing the pH of the urine. Rather, the suspected mechanism of action is that proanthocyanidins contained in cranberry juice prevent bacterial adherence to uroepithelial cells, thus reducing the development of UTI.5 Cranberry juice has been shown to reduce uroepithelial cell adherence by bacteria resistant to trimethoprim-sulfamethoxazole.6
Recommendations from others
No national practice guidelines have recommended cranberry juice as a preventive strategy for recurrent UTI but, anecdotally, patients are often advised to try cranberry juice to prevent UTI.
Brett Robbins, MD
Steven Bondi
Internal Medicine Pediatrics Residency, University of Rochester, NY.
The protective value of cranberry juice against UTI bacteria is supported by a significant body of data from in vitro studies. The published studies examining the clinical use of cranberry juice for UTI prevention suffer from a number of flaws, including small sample size, poor design, lack of randomization, lack of placebo control, heterogeneous endpoints, and a focus on the geriatric population. Even the best of these studies suffers from a major defect: failure to use commonly available cranberry juice cocktail as the experimental intervention.
Despite these flaws, the weight of the clinical evidence suggests that cranberry juice is an effective intervention for the prevention of UTIs—especially in high-risk populations. Unfortunately, cranberry juice is expensive and its taste is displeasing to some, thus limiting its usefulness. Cranberry capsules/ tablets offer a reasonable alternative, but their composition varies greatly by manufacturer, and patient compliance may be poor.
The decision to use cranberry juice should be left to the patient and her clinician.
Given the evidence, cranberry juice is best suited for secondary prevention of recurrent UTI. Patients with recurrent UTI who are being considered for antibiotic prophylaxis and are willing to drink the juice are ideal candidates. Although the studies have yet to establish an ideal dose, 3 glasses a day should be sufficient.
Cranberry juice (200 mL daily to 250 mL 3 times daily) or cranberry concentrate tablets (at least 1:30 parts concentrated juice twice daily) reduce recurrent, symptomatic urinary tract infection (UTI) in women by 12% to 20% (absolute risk reduction [ARR]) compared with placebo (number needed to treat [NNT]=58) (strength of recommendation: A). There is no conclusive evidence that cranberry juice effectively treats UTI (SOR: D).
Evidence summary
A Cochrane review found only a small number of poor-quality trials, providing insufficient support to recommend cranberry juice to prevent UTI.1 However, 2 recent randomized studies, not included in the Cochrane review, found that women taking cranberry juice have fewer symptomatic UTIs.
In women with prior Escherichia coli UTI, 50 mL of cranberry-lingonberry juice concentrate daily for 6 months reduced the recurrence of symptomatic UTI from 36% in the control group to 16% in the treated group (NNT=5).2
In a placebo-controlled randomized trial, women with prior UTI who took 1 tablet of concentrated cranberry juice (at least 1:30 parts concentrated juice) twice daily (n=50) or drank 250 mL of pure unsweetened cranberry juice 3 times a day for 12 months (n=50) reduced their incidence of symptomatic UTI.3 Women who drank the juice had an ARR of 12% (32% symptomatic UTI on placebo group, 20% in cranberry juice group, NNT=8.3) over 1 year. Use of cranberry juice tablets produced an ARR of 14% (32% symptomatic UTI in placebo group; 18% in cranberry tablet group, NNT=7.1). Self-reported compliance was 75% to 90% in the juice group and 90% in the tablet group.
No dose-response studies have been done to determine the optimal volume of juice or number of tablets needed to prevent infection. Studies have used between 200 mL once a day to 250 mL 3 times a day of the juice or 1 cranberry tablet taken twice daily. The subject dropout rate was as high as 34% in one study using juice,4 implying that cranberry juice—which is acidic and astringent at full strength—may not be acceptable to many patients as a prophylactic therapy over a long period. The 1-month compliance rate of patients taking cranberry tablets was between 88% and 100%, suggesting that this form of cranberry may improve compliance.
The cost of cranberry juice and cranberry tablets was estimated at $1400 and $624 per year, respectively.3 This must be balanced against the cost of treating symptomatic UTIs. No randomized trials have tested the more readily available and palatable cranberry juice cocktail—which is mixed with water, a sweetener, and vitamin C—to prevent recurrent UTI.
Cranberry juice does not inhibit bacterial growth and will not sterilize the urinary tract. Also, cranberry juice does not prevent or treat UTI by changing the pH of the urine. Rather, the suspected mechanism of action is that proanthocyanidins contained in cranberry juice prevent bacterial adherence to uroepithelial cells, thus reducing the development of UTI.5 Cranberry juice has been shown to reduce uroepithelial cell adherence by bacteria resistant to trimethoprim-sulfamethoxazole.6
Recommendations from others
No national practice guidelines have recommended cranberry juice as a preventive strategy for recurrent UTI but, anecdotally, patients are often advised to try cranberry juice to prevent UTI.
Brett Robbins, MD
Steven Bondi
Internal Medicine Pediatrics Residency, University of Rochester, NY.
The protective value of cranberry juice against UTI bacteria is supported by a significant body of data from in vitro studies. The published studies examining the clinical use of cranberry juice for UTI prevention suffer from a number of flaws, including small sample size, poor design, lack of randomization, lack of placebo control, heterogeneous endpoints, and a focus on the geriatric population. Even the best of these studies suffers from a major defect: failure to use commonly available cranberry juice cocktail as the experimental intervention.
Despite these flaws, the weight of the clinical evidence suggests that cranberry juice is an effective intervention for the prevention of UTIs—especially in high-risk populations. Unfortunately, cranberry juice is expensive and its taste is displeasing to some, thus limiting its usefulness. Cranberry capsules/ tablets offer a reasonable alternative, but their composition varies greatly by manufacturer, and patient compliance may be poor.
The decision to use cranberry juice should be left to the patient and her clinician.
Given the evidence, cranberry juice is best suited for secondary prevention of recurrent UTI. Patients with recurrent UTI who are being considered for antibiotic prophylaxis and are willing to drink the juice are ideal candidates. Although the studies have yet to establish an ideal dose, 3 glasses a day should be sufficient.
1. Jepson RG, Mihaljevic L, Craig J. Cranberries for preventing urinary tract infections. Cochrane Database Syst Rev 2001:CD001321. (Updated quarterly.)
2. Kontiokari T, Sundqvist K, Nuutinen M, Pokka T, Kaskela M, Uhari M. Randomised trial of cranberry-lingonberry juice and Lactobacillus GG drink for the prevention of urinary tract infections in women. BMJ 2001;322:1571-3.
3. Stothers L. A randomized trial to evaluate effectiveness and cost effectiveness of naturopathic cranberry products as prophylaxis against urinary tract infection in women. Can J Urol 2002;9:1558-62.
4. Foda MM, Middlebrook PF, Gatfield CT, Potvin G, Wells G, Schillinger JF. Efficacy of cranberry in prevention of urinary tract infection in a susceptible pediatric population. Can J Urol 1995;2:98-102.
5. Lowe FC, Fagelman E. Cranberry juice and urinary tract infections: what is the evidence?. Urology 2001;57:407-13.
6. Howell AB, Foxman B. Cranberry juice and adhesion of antibiotic-resistant uropathogens. JAMA 2002;287:3082-3.
1. Jepson RG, Mihaljevic L, Craig J. Cranberries for preventing urinary tract infections. Cochrane Database Syst Rev 2001:CD001321. (Updated quarterly.)
2. Kontiokari T, Sundqvist K, Nuutinen M, Pokka T, Kaskela M, Uhari M. Randomised trial of cranberry-lingonberry juice and Lactobacillus GG drink for the prevention of urinary tract infections in women. BMJ 2001;322:1571-3.
3. Stothers L. A randomized trial to evaluate effectiveness and cost effectiveness of naturopathic cranberry products as prophylaxis against urinary tract infection in women. Can J Urol 2002;9:1558-62.
4. Foda MM, Middlebrook PF, Gatfield CT, Potvin G, Wells G, Schillinger JF. Efficacy of cranberry in prevention of urinary tract infection in a susceptible pediatric population. Can J Urol 1995;2:98-102.
5. Lowe FC, Fagelman E. Cranberry juice and urinary tract infections: what is the evidence?. Urology 2001;57:407-13.
6. Howell AB, Foxman B. Cranberry juice and adhesion of antibiotic-resistant uropathogens. JAMA 2002;287:3082-3.
Evidence-based answers from the Family Physicians Inquiries Network
What is the best diagnostic approach to paresthesias of the hand?
There have been no good studies comparing different strategies for the evaluation of the patient with hand paresthesias. A reasonable strategy is to first evaluate for carpal tunnel syndrome (CTS), the most common condition associated with hand paresthesias. If the patient does not have findings consistent with CTS, then consider other diagnoses (Table). (Grade of recommendation: D, based on expert opinion.)
Findings consistent with CTS include a history of repetitive hand work, asymmetric paresthesias in the distribution of the median nerve, hypoalgesia, weak thumb abduction, or latency of nerve conduction studies. Tingling in the median nerve distribution or on the entire palmar surface also supports the diagnosis. Common conditions associated with CTS are pregnancy, obesity, and hypothyroidism. (Grade of recommendation: B, systematic review of case control studies).
TABLE
Markers for diagnoses other than carpal tunnel
| Symptoms or signs | Conditions | Initial tests |
|---|---|---|
| Point tenderness and/or a history of trauma | Fracture | Wrist radiographs |
| Systemic signs, including fever, weight loss, or malaise | Collagen vascular disease, neoplasm, multiple sclerosis, diabetes, hypothyroidism, hypocalcemia, B12 deficiency | CBC, comprehensive metabolic panel, TSH, ESR |
| Claudication, unilateral edema | Vascular disease | Doppler studies |
| Symmetrical paresthesias | Peripheral neuropathy, Raynaud’s disease, and multiple sclerosis | Based on further information from history or physical |
| Radicular pain | Cervical herniation or spondylolithesis, spinal tumor | Cervical spine imaging |
| Exacerbation with neck/shoulder movement | Thoracic outlet syndrome, brachial plexopathy | Adson’s test |
| Ulnar nerve distribution | Ulnar neuropathy | Tinel’s at elbow |
Evidence summary
The only studies of hand paresthesias that we found pertained to of CTS. A consensus statement on CTS listed intermittent numbness, tingling, and pain along the sensory distribution of the median nerve as diagnostic criteria for CTS.1 Patients often report that these symptoms awaken them at night. Shaking the hand may relieve the discomfort. Commonly, the pain is burning in nature and worsens with use during the day. Repetitive trauma or mechanical stress related to workplace tasks is associated with CTS.
A meta-analysis of studies reviewing the precision and accuracy of the history and physical examination in the diagnosis of CTS in adults found that hypoalgesia (LR+, 3.1), classic or probable hand diagram results (LR+ 2.4, LR- 0.2), and weak thumb abduction strength (weakness of resisted movement of the thumb at right angles to the palm; LR+ 1.8, LR- 0.5) best distinguish those with and those without CTS.2 A hand diagram is a graphical depiction of the distribution of tingling created by the patient; a classical distribution is in that of the median nerve, while a probable distribution involves the entire palmar surface. The reference standard for these studies was a nerve conduction study. Nocturnal paresthesias, Phalen and Tinel signs, and thenar atrophy had little or no diagnostic utility.
Recommendations from others
Collins3 recommends the following approach to paresthesias of the upper extremity. If the paresthesias are symmetric, consider peripheral neuropathy, Raynaud’s, or multiple sclerosis. If asymmetric, evaluate for radiculopathy with a neurological examination. If pain is radicular, and neurologic findings are consistent, consider spinal cord or nerve root compression. If the examination is normal, consider a plexopathy or herpes zoster. If there is no radiculopathy, the following maneuvers may suggest a cause. A positive Adson’s maneuver is consistent with thoracic outlet syndrome, a Tinel’s or Phalen’s sign at the wrist suggests carpal tunnel syndrome, or Tinel’s sign at the elbow suggests ulnar neuropathy. Note that the latter signs are not well validated by good quality diagnostic test studies.
Clinical Commentary by Peter Danis, MD, at http://www.fpin.org.
There have been no good studies comparing different strategies for the evaluation of the patient with hand paresthesias. A reasonable strategy is to first evaluate for carpal tunnel syndrome (CTS), the most common condition associated with hand paresthesias. If the patient does not have findings consistent with CTS, then consider other diagnoses (Table). (Grade of recommendation: D, based on expert opinion.)
Findings consistent with CTS include a history of repetitive hand work, asymmetric paresthesias in the distribution of the median nerve, hypoalgesia, weak thumb abduction, or latency of nerve conduction studies. Tingling in the median nerve distribution or on the entire palmar surface also supports the diagnosis. Common conditions associated with CTS are pregnancy, obesity, and hypothyroidism. (Grade of recommendation: B, systematic review of case control studies).
TABLE
Markers for diagnoses other than carpal tunnel
| Symptoms or signs | Conditions | Initial tests |
|---|---|---|
| Point tenderness and/or a history of trauma | Fracture | Wrist radiographs |
| Systemic signs, including fever, weight loss, or malaise | Collagen vascular disease, neoplasm, multiple sclerosis, diabetes, hypothyroidism, hypocalcemia, B12 deficiency | CBC, comprehensive metabolic panel, TSH, ESR |
| Claudication, unilateral edema | Vascular disease | Doppler studies |
| Symmetrical paresthesias | Peripheral neuropathy, Raynaud’s disease, and multiple sclerosis | Based on further information from history or physical |
| Radicular pain | Cervical herniation or spondylolithesis, spinal tumor | Cervical spine imaging |
| Exacerbation with neck/shoulder movement | Thoracic outlet syndrome, brachial plexopathy | Adson’s test |
| Ulnar nerve distribution | Ulnar neuropathy | Tinel’s at elbow |
Evidence summary
The only studies of hand paresthesias that we found pertained to of CTS. A consensus statement on CTS listed intermittent numbness, tingling, and pain along the sensory distribution of the median nerve as diagnostic criteria for CTS.1 Patients often report that these symptoms awaken them at night. Shaking the hand may relieve the discomfort. Commonly, the pain is burning in nature and worsens with use during the day. Repetitive trauma or mechanical stress related to workplace tasks is associated with CTS.
A meta-analysis of studies reviewing the precision and accuracy of the history and physical examination in the diagnosis of CTS in adults found that hypoalgesia (LR+, 3.1), classic or probable hand diagram results (LR+ 2.4, LR- 0.2), and weak thumb abduction strength (weakness of resisted movement of the thumb at right angles to the palm; LR+ 1.8, LR- 0.5) best distinguish those with and those without CTS.2 A hand diagram is a graphical depiction of the distribution of tingling created by the patient; a classical distribution is in that of the median nerve, while a probable distribution involves the entire palmar surface. The reference standard for these studies was a nerve conduction study. Nocturnal paresthesias, Phalen and Tinel signs, and thenar atrophy had little or no diagnostic utility.
Recommendations from others
Collins3 recommends the following approach to paresthesias of the upper extremity. If the paresthesias are symmetric, consider peripheral neuropathy, Raynaud’s, or multiple sclerosis. If asymmetric, evaluate for radiculopathy with a neurological examination. If pain is radicular, and neurologic findings are consistent, consider spinal cord or nerve root compression. If the examination is normal, consider a plexopathy or herpes zoster. If there is no radiculopathy, the following maneuvers may suggest a cause. A positive Adson’s maneuver is consistent with thoracic outlet syndrome, a Tinel’s or Phalen’s sign at the wrist suggests carpal tunnel syndrome, or Tinel’s sign at the elbow suggests ulnar neuropathy. Note that the latter signs are not well validated by good quality diagnostic test studies.
Clinical Commentary by Peter Danis, MD, at http://www.fpin.org.
There have been no good studies comparing different strategies for the evaluation of the patient with hand paresthesias. A reasonable strategy is to first evaluate for carpal tunnel syndrome (CTS), the most common condition associated with hand paresthesias. If the patient does not have findings consistent with CTS, then consider other diagnoses (Table). (Grade of recommendation: D, based on expert opinion.)
Findings consistent with CTS include a history of repetitive hand work, asymmetric paresthesias in the distribution of the median nerve, hypoalgesia, weak thumb abduction, or latency of nerve conduction studies. Tingling in the median nerve distribution or on the entire palmar surface also supports the diagnosis. Common conditions associated with CTS are pregnancy, obesity, and hypothyroidism. (Grade of recommendation: B, systematic review of case control studies).
TABLE
Markers for diagnoses other than carpal tunnel
| Symptoms or signs | Conditions | Initial tests |
|---|---|---|
| Point tenderness and/or a history of trauma | Fracture | Wrist radiographs |
| Systemic signs, including fever, weight loss, or malaise | Collagen vascular disease, neoplasm, multiple sclerosis, diabetes, hypothyroidism, hypocalcemia, B12 deficiency | CBC, comprehensive metabolic panel, TSH, ESR |
| Claudication, unilateral edema | Vascular disease | Doppler studies |
| Symmetrical paresthesias | Peripheral neuropathy, Raynaud’s disease, and multiple sclerosis | Based on further information from history or physical |
| Radicular pain | Cervical herniation or spondylolithesis, spinal tumor | Cervical spine imaging |
| Exacerbation with neck/shoulder movement | Thoracic outlet syndrome, brachial plexopathy | Adson’s test |
| Ulnar nerve distribution | Ulnar neuropathy | Tinel’s at elbow |
Evidence summary
The only studies of hand paresthesias that we found pertained to of CTS. A consensus statement on CTS listed intermittent numbness, tingling, and pain along the sensory distribution of the median nerve as diagnostic criteria for CTS.1 Patients often report that these symptoms awaken them at night. Shaking the hand may relieve the discomfort. Commonly, the pain is burning in nature and worsens with use during the day. Repetitive trauma or mechanical stress related to workplace tasks is associated with CTS.
A meta-analysis of studies reviewing the precision and accuracy of the history and physical examination in the diagnosis of CTS in adults found that hypoalgesia (LR+, 3.1), classic or probable hand diagram results (LR+ 2.4, LR- 0.2), and weak thumb abduction strength (weakness of resisted movement of the thumb at right angles to the palm; LR+ 1.8, LR- 0.5) best distinguish those with and those without CTS.2 A hand diagram is a graphical depiction of the distribution of tingling created by the patient; a classical distribution is in that of the median nerve, while a probable distribution involves the entire palmar surface. The reference standard for these studies was a nerve conduction study. Nocturnal paresthesias, Phalen and Tinel signs, and thenar atrophy had little or no diagnostic utility.
Recommendations from others
Collins3 recommends the following approach to paresthesias of the upper extremity. If the paresthesias are symmetric, consider peripheral neuropathy, Raynaud’s, or multiple sclerosis. If asymmetric, evaluate for radiculopathy with a neurological examination. If pain is radicular, and neurologic findings are consistent, consider spinal cord or nerve root compression. If the examination is normal, consider a plexopathy or herpes zoster. If there is no radiculopathy, the following maneuvers may suggest a cause. A positive Adson’s maneuver is consistent with thoracic outlet syndrome, a Tinel’s or Phalen’s sign at the wrist suggests carpal tunnel syndrome, or Tinel’s sign at the elbow suggests ulnar neuropathy. Note that the latter signs are not well validated by good quality diagnostic test studies.
Clinical Commentary by Peter Danis, MD, at http://www.fpin.org.
Evidence-based answers from the Family Physicians Inquiries Network
What environmental modifications improve pediatric asthma?
Reducing environmental tobacco smoke exposure decreases health care utilization among poor asthmatic children. Dust mite reduction by chemical measures is potentially harmful. (Grade of recommendations: B, based on single randomized controlled trial.) Evidence is insufficient for or against dust mite reduction by physical means, use of synthetic or feather bedding, removal of cats, use of air filters or reducing indoor humidity. (Grade of recommendations: D, inconsistent studies.)
Evidence summary
Although several studies have shown the benefit of placing asthmatic and allergic children in highly sanitized hospital and sanitarium environments,1 benefit has been extremely difficult to prove with measures used in the child’s home. Only reducing tobacco smoke exposure has been shown to be beneficial. In a randomized trial of predominantly poor minority subjects, fewer acute asthma medical visits were needed by children whose household members underwent behavioral education aimed at decreasing smoke exposure.2
Other methods of modifying the environment have not proved beneficial. Although a group of researchers found that home visits by care providers may decrease acute medical visits, specific allergy avoidance steps did not make a difference.3 Two of these authors also reported that the use of chemicals for house dust mite control and the use of synthetic pillows in lieu of feather pillows may actually exacerbate asthma.4 A Cochrane review was inconclusive on the risks or benefits of feather bedding.5 Benefit from removing cats is difficult to prove because of the ubiquitous nature of cat antigen and the difficulty in eradicating it from the home. Using air filters and reducing indoor humidity have likewise failed to show meaningful improvement in peak flow, medication use, or symptom scores.
The effectiveness of physical methods to reduce house dust mites is unclear. The Cochrane Review of 15 trials noted a small, statistically significant improvement in asthma symptom scores, but the results were not clinically important enough to recommend such measures.6 The potential harm of chemical measures was reiterated in this review.
TABLE
Environmental modifications for children with asthma
| Intervention | Effect |
|---|---|
| Tobacco smoke exposure reduction | Beneficial |
| Chemical reduction of dust mites | Harmful |
| Physical reduction of dust mites | Unknown |
| Bedding material (feather vs synthetic) | Unknown |
| Removal of cats | Unknown |
| Air filters or dehumidification | Unknown |
Recommendations from others
The National Heart, Lung, and Blood Institute continues to recommend physical barriers to reduce house dust mite antigen based on 4 small trials in which the major benefit was decreased bronchial hyperresponsiveness.7 Larger trials, now under way, may help resolve the issue.
Clinical Commentary by Nicholas J. Solomos, MD, at http://www.fpin.org.
1. Simon HU, Grotzer M, Nikolaizik WH, et al. Pediatr Pulmonol 1994;17:304-11.
2. Wilson SR, Yamada EG, Sudhakar R, et al. Chest 2001;120:1709-22.
3. Carter MC, Perzanowski MS, Raymond A, et al. J Allergy Clin Immunol 2001;108:732-7.
4. Platts-Mills TA, Vaughan JW, Carter MC, et al. J Allergy Clin Immunol 2000;106:787-804.
5. Campbell F, Jones K, Gibson P. In: The Cochrane Library, Issue 1, 2002. Oxford, England: Update Software.
6. Gotzsche P, Johansen H, Burr M, et al. In: The Cochrane Library, Issue 1, 2002. Oxford, England: Update Software.
7. National Asthma Education and Prevention Program. Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma. Bethesda, MD: National Institutes of Health, National Heart, Lung, and Blood Institute; 1997. NIH publication 97-4051.
Reducing environmental tobacco smoke exposure decreases health care utilization among poor asthmatic children. Dust mite reduction by chemical measures is potentially harmful. (Grade of recommendations: B, based on single randomized controlled trial.) Evidence is insufficient for or against dust mite reduction by physical means, use of synthetic or feather bedding, removal of cats, use of air filters or reducing indoor humidity. (Grade of recommendations: D, inconsistent studies.)
Evidence summary
Although several studies have shown the benefit of placing asthmatic and allergic children in highly sanitized hospital and sanitarium environments,1 benefit has been extremely difficult to prove with measures used in the child’s home. Only reducing tobacco smoke exposure has been shown to be beneficial. In a randomized trial of predominantly poor minority subjects, fewer acute asthma medical visits were needed by children whose household members underwent behavioral education aimed at decreasing smoke exposure.2
Other methods of modifying the environment have not proved beneficial. Although a group of researchers found that home visits by care providers may decrease acute medical visits, specific allergy avoidance steps did not make a difference.3 Two of these authors also reported that the use of chemicals for house dust mite control and the use of synthetic pillows in lieu of feather pillows may actually exacerbate asthma.4 A Cochrane review was inconclusive on the risks or benefits of feather bedding.5 Benefit from removing cats is difficult to prove because of the ubiquitous nature of cat antigen and the difficulty in eradicating it from the home. Using air filters and reducing indoor humidity have likewise failed to show meaningful improvement in peak flow, medication use, or symptom scores.
The effectiveness of physical methods to reduce house dust mites is unclear. The Cochrane Review of 15 trials noted a small, statistically significant improvement in asthma symptom scores, but the results were not clinically important enough to recommend such measures.6 The potential harm of chemical measures was reiterated in this review.
TABLE
Environmental modifications for children with asthma
| Intervention | Effect |
|---|---|
| Tobacco smoke exposure reduction | Beneficial |
| Chemical reduction of dust mites | Harmful |
| Physical reduction of dust mites | Unknown |
| Bedding material (feather vs synthetic) | Unknown |
| Removal of cats | Unknown |
| Air filters or dehumidification | Unknown |
Recommendations from others
The National Heart, Lung, and Blood Institute continues to recommend physical barriers to reduce house dust mite antigen based on 4 small trials in which the major benefit was decreased bronchial hyperresponsiveness.7 Larger trials, now under way, may help resolve the issue.
Clinical Commentary by Nicholas J. Solomos, MD, at http://www.fpin.org.
Reducing environmental tobacco smoke exposure decreases health care utilization among poor asthmatic children. Dust mite reduction by chemical measures is potentially harmful. (Grade of recommendations: B, based on single randomized controlled trial.) Evidence is insufficient for or against dust mite reduction by physical means, use of synthetic or feather bedding, removal of cats, use of air filters or reducing indoor humidity. (Grade of recommendations: D, inconsistent studies.)
Evidence summary
Although several studies have shown the benefit of placing asthmatic and allergic children in highly sanitized hospital and sanitarium environments,1 benefit has been extremely difficult to prove with measures used in the child’s home. Only reducing tobacco smoke exposure has been shown to be beneficial. In a randomized trial of predominantly poor minority subjects, fewer acute asthma medical visits were needed by children whose household members underwent behavioral education aimed at decreasing smoke exposure.2
Other methods of modifying the environment have not proved beneficial. Although a group of researchers found that home visits by care providers may decrease acute medical visits, specific allergy avoidance steps did not make a difference.3 Two of these authors also reported that the use of chemicals for house dust mite control and the use of synthetic pillows in lieu of feather pillows may actually exacerbate asthma.4 A Cochrane review was inconclusive on the risks or benefits of feather bedding.5 Benefit from removing cats is difficult to prove because of the ubiquitous nature of cat antigen and the difficulty in eradicating it from the home. Using air filters and reducing indoor humidity have likewise failed to show meaningful improvement in peak flow, medication use, or symptom scores.
The effectiveness of physical methods to reduce house dust mites is unclear. The Cochrane Review of 15 trials noted a small, statistically significant improvement in asthma symptom scores, but the results were not clinically important enough to recommend such measures.6 The potential harm of chemical measures was reiterated in this review.
TABLE
Environmental modifications for children with asthma
| Intervention | Effect |
|---|---|
| Tobacco smoke exposure reduction | Beneficial |
| Chemical reduction of dust mites | Harmful |
| Physical reduction of dust mites | Unknown |
| Bedding material (feather vs synthetic) | Unknown |
| Removal of cats | Unknown |
| Air filters or dehumidification | Unknown |
Recommendations from others
The National Heart, Lung, and Blood Institute continues to recommend physical barriers to reduce house dust mite antigen based on 4 small trials in which the major benefit was decreased bronchial hyperresponsiveness.7 Larger trials, now under way, may help resolve the issue.
Clinical Commentary by Nicholas J. Solomos, MD, at http://www.fpin.org.
1. Simon HU, Grotzer M, Nikolaizik WH, et al. Pediatr Pulmonol 1994;17:304-11.
2. Wilson SR, Yamada EG, Sudhakar R, et al. Chest 2001;120:1709-22.
3. Carter MC, Perzanowski MS, Raymond A, et al. J Allergy Clin Immunol 2001;108:732-7.
4. Platts-Mills TA, Vaughan JW, Carter MC, et al. J Allergy Clin Immunol 2000;106:787-804.
5. Campbell F, Jones K, Gibson P. In: The Cochrane Library, Issue 1, 2002. Oxford, England: Update Software.
6. Gotzsche P, Johansen H, Burr M, et al. In: The Cochrane Library, Issue 1, 2002. Oxford, England: Update Software.
7. National Asthma Education and Prevention Program. Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma. Bethesda, MD: National Institutes of Health, National Heart, Lung, and Blood Institute; 1997. NIH publication 97-4051.
1. Simon HU, Grotzer M, Nikolaizik WH, et al. Pediatr Pulmonol 1994;17:304-11.
2. Wilson SR, Yamada EG, Sudhakar R, et al. Chest 2001;120:1709-22.
3. Carter MC, Perzanowski MS, Raymond A, et al. J Allergy Clin Immunol 2001;108:732-7.
4. Platts-Mills TA, Vaughan JW, Carter MC, et al. J Allergy Clin Immunol 2000;106:787-804.
5. Campbell F, Jones K, Gibson P. In: The Cochrane Library, Issue 1, 2002. Oxford, England: Update Software.
6. Gotzsche P, Johansen H, Burr M, et al. In: The Cochrane Library, Issue 1, 2002. Oxford, England: Update Software.
7. National Asthma Education and Prevention Program. Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma. Bethesda, MD: National Institutes of Health, National Heart, Lung, and Blood Institute; 1997. NIH publication 97-4051.
Evidence-based answers from the Family Physicians Inquiries Network
What is the prognosis for acute low back pain?
The proportion of patients who are pain free or completely recovered after an acute episode of low back pain within 2 weeks to 6 months ranges from 21% to 90%, depending on the population studied and the method of measuring outcomes. The reported recurrence rates are also variable, from a low of 35% to a high of 75%, again depending on the length of follow-up and the study design. Grade of recommendation: C (on the basis of case-series, poor quality cohort studies, and case-control studies).
Evidence summary
It has been widely stated that 80% to 90% of attacks of acute low back pain resolve within approximately 6 weeks,1 though there is little evidence to support this claim. Although there are many studies and guidelines regarding treatment methods for low back pain, few studies evaluate the natural history of low back pain. One prospective series in a primary care setting found that 90% of patients were without pain 2 weeks after initial evaluation by their physician.2 This study had a 3-month follow-up period for 103 patients presenting with pain of less than 72 hours’ duration.
Another prospective study found that 94% of patients evaluated for a new episode of low back pain were no longer visiting their physician for treatment after 3 months. However, this was not an adequate measure of resolution of pain. Only 21% (39/188) were pain free at 3 months and only 25% (42/170) were pain free at 12 months.3 A larger study involved 1555 patients during a 6-month follow up after an episode of acute low back pain. The article reports a mean of 16 days to functional recovery, although only 69% of the patients considered themselves “completely recovered” at 6 months.4
Recurrences of low back pain are common. In one prospective cohort study of 443 patients with low back pain, 75% had a recurrence with a mean of 2 relapses in 1 year of follow-up, but only 228 patients completed the study.5 Another prospective study of 208 patients found that 35% to 44% of patients had recurrence of pain within 6 months of their first episode, and 50% to 59% had a recurrence in 22 months of follow-up.6 No studies identified findings or risk factors associated with higher recurrence rates.
Recommendations from others
The Agency for Healthcare Research and Quality (www.ahcpr.gov) section on health outcomes (see http://www.ahcpr.gov/research/jan99/ra6.htm) states, “recent studies suggest that once experienced, low back pain becomes a part of life for almost half of those affected, and for many, it is intermittently disabling. Repeated visits and procedures do not appear to improve patients’ long-term well-being, but they clearly account for substantial health care costs. Finally, back pain prognosis does not differ based on the type of provider initially seen or the level of practitioner confidence.” This site offers several nice summaries of studies on low back pain.
Read the clinical commentary by Anne Fitzsimmons, MD, at www.fpin.org.
1. Dixon AJ. Rheumatol Rehabil 1973;12:165-75.
2. Coste J, Delecoeuillerie G, Cohen de Lara A, Le Parc JM, Paolaggi JB. BMJ 1994;308:577-80.
3. Croft PR, Macfarlane GJ, Papageorgiou AC, Thomas E, Silman AJ. BMJ 1998;316:1356-9.
4. Carey TS, Garrett JM, Jackman A, et al. N Engl J Med 1995;333:913.-
5. van den Hoogen HJ, Koes BW, van Eijk JT, Bouter LM, Deville W. Ann Rheum Dis 1998;57:13-9.
6. Carey TS, Garrett JM, Jackman A, Hadler N. Med Care 1999;37:157-64.
The proportion of patients who are pain free or completely recovered after an acute episode of low back pain within 2 weeks to 6 months ranges from 21% to 90%, depending on the population studied and the method of measuring outcomes. The reported recurrence rates are also variable, from a low of 35% to a high of 75%, again depending on the length of follow-up and the study design. Grade of recommendation: C (on the basis of case-series, poor quality cohort studies, and case-control studies).
Evidence summary
It has been widely stated that 80% to 90% of attacks of acute low back pain resolve within approximately 6 weeks,1 though there is little evidence to support this claim. Although there are many studies and guidelines regarding treatment methods for low back pain, few studies evaluate the natural history of low back pain. One prospective series in a primary care setting found that 90% of patients were without pain 2 weeks after initial evaluation by their physician.2 This study had a 3-month follow-up period for 103 patients presenting with pain of less than 72 hours’ duration.
Another prospective study found that 94% of patients evaluated for a new episode of low back pain were no longer visiting their physician for treatment after 3 months. However, this was not an adequate measure of resolution of pain. Only 21% (39/188) were pain free at 3 months and only 25% (42/170) were pain free at 12 months.3 A larger study involved 1555 patients during a 6-month follow up after an episode of acute low back pain. The article reports a mean of 16 days to functional recovery, although only 69% of the patients considered themselves “completely recovered” at 6 months.4
Recurrences of low back pain are common. In one prospective cohort study of 443 patients with low back pain, 75% had a recurrence with a mean of 2 relapses in 1 year of follow-up, but only 228 patients completed the study.5 Another prospective study of 208 patients found that 35% to 44% of patients had recurrence of pain within 6 months of their first episode, and 50% to 59% had a recurrence in 22 months of follow-up.6 No studies identified findings or risk factors associated with higher recurrence rates.
Recommendations from others
The Agency for Healthcare Research and Quality (www.ahcpr.gov) section on health outcomes (see http://www.ahcpr.gov/research/jan99/ra6.htm) states, “recent studies suggest that once experienced, low back pain becomes a part of life for almost half of those affected, and for many, it is intermittently disabling. Repeated visits and procedures do not appear to improve patients’ long-term well-being, but they clearly account for substantial health care costs. Finally, back pain prognosis does not differ based on the type of provider initially seen or the level of practitioner confidence.” This site offers several nice summaries of studies on low back pain.
Read the clinical commentary by Anne Fitzsimmons, MD, at www.fpin.org.
The proportion of patients who are pain free or completely recovered after an acute episode of low back pain within 2 weeks to 6 months ranges from 21% to 90%, depending on the population studied and the method of measuring outcomes. The reported recurrence rates are also variable, from a low of 35% to a high of 75%, again depending on the length of follow-up and the study design. Grade of recommendation: C (on the basis of case-series, poor quality cohort studies, and case-control studies).
Evidence summary
It has been widely stated that 80% to 90% of attacks of acute low back pain resolve within approximately 6 weeks,1 though there is little evidence to support this claim. Although there are many studies and guidelines regarding treatment methods for low back pain, few studies evaluate the natural history of low back pain. One prospective series in a primary care setting found that 90% of patients were without pain 2 weeks after initial evaluation by their physician.2 This study had a 3-month follow-up period for 103 patients presenting with pain of less than 72 hours’ duration.
Another prospective study found that 94% of patients evaluated for a new episode of low back pain were no longer visiting their physician for treatment after 3 months. However, this was not an adequate measure of resolution of pain. Only 21% (39/188) were pain free at 3 months and only 25% (42/170) were pain free at 12 months.3 A larger study involved 1555 patients during a 6-month follow up after an episode of acute low back pain. The article reports a mean of 16 days to functional recovery, although only 69% of the patients considered themselves “completely recovered” at 6 months.4
Recurrences of low back pain are common. In one prospective cohort study of 443 patients with low back pain, 75% had a recurrence with a mean of 2 relapses in 1 year of follow-up, but only 228 patients completed the study.5 Another prospective study of 208 patients found that 35% to 44% of patients had recurrence of pain within 6 months of their first episode, and 50% to 59% had a recurrence in 22 months of follow-up.6 No studies identified findings or risk factors associated with higher recurrence rates.
Recommendations from others
The Agency for Healthcare Research and Quality (www.ahcpr.gov) section on health outcomes (see http://www.ahcpr.gov/research/jan99/ra6.htm) states, “recent studies suggest that once experienced, low back pain becomes a part of life for almost half of those affected, and for many, it is intermittently disabling. Repeated visits and procedures do not appear to improve patients’ long-term well-being, but they clearly account for substantial health care costs. Finally, back pain prognosis does not differ based on the type of provider initially seen or the level of practitioner confidence.” This site offers several nice summaries of studies on low back pain.
Read the clinical commentary by Anne Fitzsimmons, MD, at www.fpin.org.
1. Dixon AJ. Rheumatol Rehabil 1973;12:165-75.
2. Coste J, Delecoeuillerie G, Cohen de Lara A, Le Parc JM, Paolaggi JB. BMJ 1994;308:577-80.
3. Croft PR, Macfarlane GJ, Papageorgiou AC, Thomas E, Silman AJ. BMJ 1998;316:1356-9.
4. Carey TS, Garrett JM, Jackman A, et al. N Engl J Med 1995;333:913.-
5. van den Hoogen HJ, Koes BW, van Eijk JT, Bouter LM, Deville W. Ann Rheum Dis 1998;57:13-9.
6. Carey TS, Garrett JM, Jackman A, Hadler N. Med Care 1999;37:157-64.
1. Dixon AJ. Rheumatol Rehabil 1973;12:165-75.
2. Coste J, Delecoeuillerie G, Cohen de Lara A, Le Parc JM, Paolaggi JB. BMJ 1994;308:577-80.
3. Croft PR, Macfarlane GJ, Papageorgiou AC, Thomas E, Silman AJ. BMJ 1998;316:1356-9.
4. Carey TS, Garrett JM, Jackman A, et al. N Engl J Med 1995;333:913.-
5. van den Hoogen HJ, Koes BW, van Eijk JT, Bouter LM, Deville W. Ann Rheum Dis 1998;57:13-9.
6. Carey TS, Garrett JM, Jackman A, Hadler N. Med Care 1999;37:157-64.
Evidence-based answers from the Family Physicians Inquiries Network
What is the most effective treatment for external genital warts?
Podofilox (Condylox), imiquimod (Aldara), cryotherapy, and surgical options all seem reasonable alternatives that are superior to podophyllin. (Grade of recommendation: B, based on systematic review.) No studies of surgical options versus home use preparations have been reported. Trichloroacetic acid and 5-fluorouracil (5-FU) have not been sufficiently studied.
Evidence summary
Nonsurgical treatments that are beneficial in eradicating genital warts are podofilox (Condylox) (8 randomized controlled trials [RCTs] with 1035 participants), imiquimod (Aldara) (2 RCTs with 968 participants), and intralesional interferon (8 RCTs). Cryotherapy is equivalent to trichloroacetic acid1,2 and electrosurgery.3 Although surgical treatments have not been compared with placebo or no treatment, both electrosurgery and surgical excision are superior to podophyllin in clinical trials.4,5 Laser surgery is as effective as surgical excision.6 Studies of topical interferon show conflicting results.7 Systemic interferon is not beneficial.7 Topical 5-FU has not been studied with RCTs. Wart clearance rates are summarized in the Table. Treatment duration for nonsurgical options is 4 to 8 weeks. Treatment of genital warts has not been shown to reduce transmission to sex partners.7
Two RCTs4,5 showed more frequent recurrence with podophyllin (60% to 65%) than with surgical excision (19% to 20%). Another trial1 showed recurrence in 22% of participants receiving electrosurgery, in 21% of those receiving cryotherapy, and in 44% of those receiving podophyllin treatment. Data are lacking on recurrence rates with imiquimod, podofilox, and intralesional interferon.
Pain occurs in less than 20% of people with imiquimod, cryotherapy, podophyllin, and electrosurgery; 39% with topical interferon; 44% with electrosurgery; 75% with podofilox; and 100% with surgical excision or laser surgery.7 However, pain has been measured using methods that are unlikely to be comparable across studies. Flulike symptoms, leukopenia, thrombocytopenia, and elevated aspartate transaminase levels are associated with intralesional interferon.7 Topical medications have not been studied in pregnant patients. Cryotherapy is safe in pregnancy based on case series, if only 3 or 4 treatments are given.7
Direct comparisons between home therapies (imiquimod, podofilox) and other treatments are needed. Products for home use are relatively expensive: a 1-month supply of imiquimod costs approximately $150; a 1-month supply of podofilox, $110 to $130. These are average wholesale prices, rounded to the nearest $10, as of Feb. 15, 2002.
TABLE
CLEARANCE RATES REPORTED IN CLINICAL TRIALS
| Therapy | Clearance Rate (%) |
|---|---|
| Cryotherapy | 63–88 |
| Electrosurgery | 61–94 |
| Imiquimod | 37–56 |
| Interferon (topical) | 6–90 |
| Interferon (intralesional) | 17–63 |
| Laser surgery | 23–52 |
| Podofilox | 45–77 |
| Podophyllin | 32–79 |
| Surgical excision | 35–72 |
| Trichloroacetic acid | 50–81 |
| Placebo or no treatment | 0–56 |
Recommendations from others
The CDC endorses podophyllin, bi- and trichloroacetic acid, podofilox, imiquimod, cryotherapy, intralesional interferon, electrosurgery, laser surgery, and surgical excision.8 A United Kingdom guideline on anogenital warts recommends physical ablative methods such as cryotherapy and surgical options for keratinized lesions and topical medications for soft lesions. The guideline also recommends ablative therapy for persons with a small number of warts regardless of type. Interferon and 5-FU are not recommended.9
Clinical Commentary by David White, MD, at http://www.fpin.org.
1. Abdullah AN, Walzman M, Wade A. Sex Transm Dis 1993;20:344-5.
2. Godley MJ, Bradbeer CS, Gellan M, Thin RN. Genitourin Med 1987;63:390-2.
3. Stone KM, Becker TM, Hadgu A, Kraus SJ. Genitourin Med 1990;66:16-9.
4. Khawaja HT. J Reprod Med 1990;35:1019-22.
5. Jensen SL. Lancet 1985;2:1146-8.
6. Duus BR, Philipsen T, Christensen JD, et al. Genitourin Med 1985;61:59-61.
7. Wiley DJ. Genital warts. Clin Evidence Issue 4, December 2000;910-8.
8. Centers for Disease Control and Prevention. Morbid Mortal Weekly Rep MMWR 1998;47(RR-1):91-4.
9. Clinical Effectiveness Group (Association of Genitourinary Medicine and the Medical Society for the Study of Venereal Diseases). Sex Transm Infect 1999;75(suppl 1):71-5S.
Podofilox (Condylox), imiquimod (Aldara), cryotherapy, and surgical options all seem reasonable alternatives that are superior to podophyllin. (Grade of recommendation: B, based on systematic review.) No studies of surgical options versus home use preparations have been reported. Trichloroacetic acid and 5-fluorouracil (5-FU) have not been sufficiently studied.
Evidence summary
Nonsurgical treatments that are beneficial in eradicating genital warts are podofilox (Condylox) (8 randomized controlled trials [RCTs] with 1035 participants), imiquimod (Aldara) (2 RCTs with 968 participants), and intralesional interferon (8 RCTs). Cryotherapy is equivalent to trichloroacetic acid1,2 and electrosurgery.3 Although surgical treatments have not been compared with placebo or no treatment, both electrosurgery and surgical excision are superior to podophyllin in clinical trials.4,5 Laser surgery is as effective as surgical excision.6 Studies of topical interferon show conflicting results.7 Systemic interferon is not beneficial.7 Topical 5-FU has not been studied with RCTs. Wart clearance rates are summarized in the Table. Treatment duration for nonsurgical options is 4 to 8 weeks. Treatment of genital warts has not been shown to reduce transmission to sex partners.7
Two RCTs4,5 showed more frequent recurrence with podophyllin (60% to 65%) than with surgical excision (19% to 20%). Another trial1 showed recurrence in 22% of participants receiving electrosurgery, in 21% of those receiving cryotherapy, and in 44% of those receiving podophyllin treatment. Data are lacking on recurrence rates with imiquimod, podofilox, and intralesional interferon.
Pain occurs in less than 20% of people with imiquimod, cryotherapy, podophyllin, and electrosurgery; 39% with topical interferon; 44% with electrosurgery; 75% with podofilox; and 100% with surgical excision or laser surgery.7 However, pain has been measured using methods that are unlikely to be comparable across studies. Flulike symptoms, leukopenia, thrombocytopenia, and elevated aspartate transaminase levels are associated with intralesional interferon.7 Topical medications have not been studied in pregnant patients. Cryotherapy is safe in pregnancy based on case series, if only 3 or 4 treatments are given.7
Direct comparisons between home therapies (imiquimod, podofilox) and other treatments are needed. Products for home use are relatively expensive: a 1-month supply of imiquimod costs approximately $150; a 1-month supply of podofilox, $110 to $130. These are average wholesale prices, rounded to the nearest $10, as of Feb. 15, 2002.
TABLE
CLEARANCE RATES REPORTED IN CLINICAL TRIALS
| Therapy | Clearance Rate (%) |
|---|---|
| Cryotherapy | 63–88 |
| Electrosurgery | 61–94 |
| Imiquimod | 37–56 |
| Interferon (topical) | 6–90 |
| Interferon (intralesional) | 17–63 |
| Laser surgery | 23–52 |
| Podofilox | 45–77 |
| Podophyllin | 32–79 |
| Surgical excision | 35–72 |
| Trichloroacetic acid | 50–81 |
| Placebo or no treatment | 0–56 |
Recommendations from others
The CDC endorses podophyllin, bi- and trichloroacetic acid, podofilox, imiquimod, cryotherapy, intralesional interferon, electrosurgery, laser surgery, and surgical excision.8 A United Kingdom guideline on anogenital warts recommends physical ablative methods such as cryotherapy and surgical options for keratinized lesions and topical medications for soft lesions. The guideline also recommends ablative therapy for persons with a small number of warts regardless of type. Interferon and 5-FU are not recommended.9
Clinical Commentary by David White, MD, at http://www.fpin.org.
Podofilox (Condylox), imiquimod (Aldara), cryotherapy, and surgical options all seem reasonable alternatives that are superior to podophyllin. (Grade of recommendation: B, based on systematic review.) No studies of surgical options versus home use preparations have been reported. Trichloroacetic acid and 5-fluorouracil (5-FU) have not been sufficiently studied.
Evidence summary
Nonsurgical treatments that are beneficial in eradicating genital warts are podofilox (Condylox) (8 randomized controlled trials [RCTs] with 1035 participants), imiquimod (Aldara) (2 RCTs with 968 participants), and intralesional interferon (8 RCTs). Cryotherapy is equivalent to trichloroacetic acid1,2 and electrosurgery.3 Although surgical treatments have not been compared with placebo or no treatment, both electrosurgery and surgical excision are superior to podophyllin in clinical trials.4,5 Laser surgery is as effective as surgical excision.6 Studies of topical interferon show conflicting results.7 Systemic interferon is not beneficial.7 Topical 5-FU has not been studied with RCTs. Wart clearance rates are summarized in the Table. Treatment duration for nonsurgical options is 4 to 8 weeks. Treatment of genital warts has not been shown to reduce transmission to sex partners.7
Two RCTs4,5 showed more frequent recurrence with podophyllin (60% to 65%) than with surgical excision (19% to 20%). Another trial1 showed recurrence in 22% of participants receiving electrosurgery, in 21% of those receiving cryotherapy, and in 44% of those receiving podophyllin treatment. Data are lacking on recurrence rates with imiquimod, podofilox, and intralesional interferon.
Pain occurs in less than 20% of people with imiquimod, cryotherapy, podophyllin, and electrosurgery; 39% with topical interferon; 44% with electrosurgery; 75% with podofilox; and 100% with surgical excision or laser surgery.7 However, pain has been measured using methods that are unlikely to be comparable across studies. Flulike symptoms, leukopenia, thrombocytopenia, and elevated aspartate transaminase levels are associated with intralesional interferon.7 Topical medications have not been studied in pregnant patients. Cryotherapy is safe in pregnancy based on case series, if only 3 or 4 treatments are given.7
Direct comparisons between home therapies (imiquimod, podofilox) and other treatments are needed. Products for home use are relatively expensive: a 1-month supply of imiquimod costs approximately $150; a 1-month supply of podofilox, $110 to $130. These are average wholesale prices, rounded to the nearest $10, as of Feb. 15, 2002.
TABLE
CLEARANCE RATES REPORTED IN CLINICAL TRIALS
| Therapy | Clearance Rate (%) |
|---|---|
| Cryotherapy | 63–88 |
| Electrosurgery | 61–94 |
| Imiquimod | 37–56 |
| Interferon (topical) | 6–90 |
| Interferon (intralesional) | 17–63 |
| Laser surgery | 23–52 |
| Podofilox | 45–77 |
| Podophyllin | 32–79 |
| Surgical excision | 35–72 |
| Trichloroacetic acid | 50–81 |
| Placebo or no treatment | 0–56 |
Recommendations from others
The CDC endorses podophyllin, bi- and trichloroacetic acid, podofilox, imiquimod, cryotherapy, intralesional interferon, electrosurgery, laser surgery, and surgical excision.8 A United Kingdom guideline on anogenital warts recommends physical ablative methods such as cryotherapy and surgical options for keratinized lesions and topical medications for soft lesions. The guideline also recommends ablative therapy for persons with a small number of warts regardless of type. Interferon and 5-FU are not recommended.9
Clinical Commentary by David White, MD, at http://www.fpin.org.
1. Abdullah AN, Walzman M, Wade A. Sex Transm Dis 1993;20:344-5.
2. Godley MJ, Bradbeer CS, Gellan M, Thin RN. Genitourin Med 1987;63:390-2.
3. Stone KM, Becker TM, Hadgu A, Kraus SJ. Genitourin Med 1990;66:16-9.
4. Khawaja HT. J Reprod Med 1990;35:1019-22.
5. Jensen SL. Lancet 1985;2:1146-8.
6. Duus BR, Philipsen T, Christensen JD, et al. Genitourin Med 1985;61:59-61.
7. Wiley DJ. Genital warts. Clin Evidence Issue 4, December 2000;910-8.
8. Centers for Disease Control and Prevention. Morbid Mortal Weekly Rep MMWR 1998;47(RR-1):91-4.
9. Clinical Effectiveness Group (Association of Genitourinary Medicine and the Medical Society for the Study of Venereal Diseases). Sex Transm Infect 1999;75(suppl 1):71-5S.
1. Abdullah AN, Walzman M, Wade A. Sex Transm Dis 1993;20:344-5.
2. Godley MJ, Bradbeer CS, Gellan M, Thin RN. Genitourin Med 1987;63:390-2.
3. Stone KM, Becker TM, Hadgu A, Kraus SJ. Genitourin Med 1990;66:16-9.
4. Khawaja HT. J Reprod Med 1990;35:1019-22.
5. Jensen SL. Lancet 1985;2:1146-8.
6. Duus BR, Philipsen T, Christensen JD, et al. Genitourin Med 1985;61:59-61.
7. Wiley DJ. Genital warts. Clin Evidence Issue 4, December 2000;910-8.
8. Centers for Disease Control and Prevention. Morbid Mortal Weekly Rep MMWR 1998;47(RR-1):91-4.
9. Clinical Effectiveness Group (Association of Genitourinary Medicine and the Medical Society for the Study of Venereal Diseases). Sex Transm Infect 1999;75(suppl 1):71-5S.
Evidence-based answers from the Family Physicians Inquiries Network