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Which technique for removing nevi is least scarring?
A shave biopsy with a razor blade or #15 scalpel is the best approach for a facial nevus, assuming malignancy is not suspected. the resulting scar is usually flat, smaller than the lesion, has no suture lines, and—if shaved in mid or upper dermis—has a low risk of producing a hypertrophic or hypotrophic scar (strength of recommendation: C, expert opinion, committee guidelines).
Shave biopsies are quick and well-tolerated
Parul Harsora, MD
University of Texas Southwestern, Dallas
If you suspect malignancy in a nevus, obtain an excisional or incisional biopsy. Shave biopsies are best suited for raised, flesh-colored nevi and are generally quick, well-tolerated, and cost-effective. tissue from a shave biopsy can be submitted for histological evaluation.
Shave biopsies are preferred by patients because there are no sutures and scarring is minimized. the site may be pink and may take several months to develop a normal appearance. the final result may be unnoticeable, or leave an indentation or be hypo- or hyperpigmented.
Hairy, pigmented, and compound nevi are likely to do better with a punch biopsy. to prevent recurrence, seek histologic confirmation that the entire nevus has been removed.
Evidence summary
Numerous reports and guidelines indicate that if a nevus is even slightly suspicious for malignancy, it should be removed by excisional biopsy or sampled for diagnosis by punch or incisional biopsy. There are no randomized controlled trials or cohort studies comparing techniques for removing raised nevi from the face.
Shave biopsy has good outcomes
Expert opinion and individual prospective case series show acceptable outcomes for shave biopsy. One prospective study followed 55 patients after removal of nevi from the head and neck. These nevi were removed using a shave procedure with a#15 scalpel and hot cautery for bleeding. Of the 55 sites, 4 retained pigment and 30 had a visible scar with a mean diameter of 5 mm at 6- to 8-month follow-up.1 The mean diameter of the original lesions was 6 mm. There was no difference between the size of those lesions that scarred and those that didn’t.
Researchers conducting a second retrospective study, done at least 1 year after the procedure, used a questionnaire to ask 76 patients (with a total of 83 nevi removed from the face by shave excision) about their perceptions of the scar.2 Patients described their lesions as: no scar (33%), white and flat (25%), depressed (19%), raised (15%), and pigmented (7%). Eighty-six percent thought their scars looked better than the nevus and 79% were “happy with the way the scar looks now.” Two additional studies, based on both patient and provider perceptions, with similar conclusions, are presented in the (TABLE).3,4
TABLE
Favorable cosmetic results following shave biopsy of facial nevi
| STUDY | NO. PTS/NEVI | % WITH RET AINED PIGMENT OR RECURRENCE | % WITH VISIBLE SCARRING | FOLLOW-UP INTERVAL | EVALUATION/DONE BY |
|---|---|---|---|---|---|
| Hudson-Peacock1 | 55/55 | 13 | 55 | 6-8 mo | Cosmetically acceptable/patients |
| Bong2 | 76/83 | 28 | 67 | ≥1 yr | 86%: better than nevus/patients |
| Zanardini3 | 206/ 215 | 4 | 9 | 3 mo | 90%: excellent* 9%: good/surgeons |
| Ferrandiz4 | Not known/59 | 20† | 67 | 3 mo | 98%: better than nevus/pts; 92%: excellent or acceptable‡/surgeons |
| Excellent=no noticeable scar, good=slightly noticeable scar with normochromia or hypochromia, poor=depressed scar or intense dyschromia. | |||||
| † Some lesions not papular. | |||||
| ‡ Excellent cosmetic result=imperceptible scar without erythema, hyper- or hypo-pigmentation, hypertrophy or atrophy. Acceptable=scar better than original mole. poor=left scar worse than original mole. | |||||
Atypical lesions should be excised
Atypical lesions require excisional biopsy. The depth and architecture of the lesion, if melanoma, cannot be determined by shave biopsy, and both treatment and prognosis depend on those characteristics.
These guidelines derive from well-designed, nonexperimental descriptive studies.5 However, a recent retrospective study compared the Breslow depth determination of 4 different biopsy techniques, performed by experienced dermatologists, with the subsequent depth on definitive surgery for melanoma. This study found that superficial shave, deep shave, and punch biopsy predicted the Breslow depth 88% (95/108) of the time.6 As expected, excisional biopsy predicted the depth 100% (30/30) of the time. The location of the biopsy sites were not reported. The choice of biopsy was influenced by the suspicion of melanoma; thin (< 1 mm) melanomas were more likely to be superficially shaved than deep-shaved or punched.
Recommendations from others
Guidelines on nevocellular nevi from the American Academy of Dermatology recommend a simple excisional or incisional biopsy; they do not discuss the method of removal for benign appearing facial lesions.7
The UK Guidelines for the Management of Cutaneous Melanoma recommend that suspicious lesions be excised completely (excisional biopsy) and sent for confirmatory histopathological examination.5 A biopsy that transects the depth of the lesion (for example, superficial shave biopsy) should be avoided because histological depth of invasion is the basic criterion for staging and shave biopsy makes the staging impossible in some cases.
1. Hudson-Peacock MJ, Bishop J, Lawrence CM. Shave excision of benign papular naevocytic nevi. Br J Plast Surg 1995;48:318-322.
2. Bong JL, Perkins W. Shave excision of benign facial melanocytic naevi: a patient’s satisfaction survey. Dermatol Surg 2003;29:227-229.
3. Zanardini Pereira CA, Alchorne AOA. angential excision of nevocellular nevus on the face. Int J Dermatol 2004;43:533-537.
4. Ferrandiz L, Moreno-Ramirez D, Camacho FM. Shave excision of common acquired melanocytic nevi: cosmetic outcome, recurrences, and complications. Dermatol Surg 2005;3(Pt 1)1:1112-1115.
5. Roberts DLL, Anstey AV, Barlow RJ, et al. U.K.Guidelines for the management of cutaneous melanoma. Br J Dermatol 2002;146:7-17.
6. Ng PC, Barzilai DA, Ismail SA, Averitte RL Jr, Gilliam AC. valuating invasive cutaneous melanoma: Is the initial biopsy representative of the final depth? J Am Acad Dermatol 2005;48:420-424.
7. Drake L A, Ceilley R I, Cornelison RL , et al Drake LA, Ceilley RI, Cornelison RL, et al. Guidelines of care for nevi I (nevocellular nevi and seborrheic keratoses). J Am Acad Dermatol 1992;26:629-631.
A shave biopsy with a razor blade or #15 scalpel is the best approach for a facial nevus, assuming malignancy is not suspected. the resulting scar is usually flat, smaller than the lesion, has no suture lines, and—if shaved in mid or upper dermis—has a low risk of producing a hypertrophic or hypotrophic scar (strength of recommendation: C, expert opinion, committee guidelines).
Shave biopsies are quick and well-tolerated
Parul Harsora, MD
University of Texas Southwestern, Dallas
If you suspect malignancy in a nevus, obtain an excisional or incisional biopsy. Shave biopsies are best suited for raised, flesh-colored nevi and are generally quick, well-tolerated, and cost-effective. tissue from a shave biopsy can be submitted for histological evaluation.
Shave biopsies are preferred by patients because there are no sutures and scarring is minimized. the site may be pink and may take several months to develop a normal appearance. the final result may be unnoticeable, or leave an indentation or be hypo- or hyperpigmented.
Hairy, pigmented, and compound nevi are likely to do better with a punch biopsy. to prevent recurrence, seek histologic confirmation that the entire nevus has been removed.
Evidence summary
Numerous reports and guidelines indicate that if a nevus is even slightly suspicious for malignancy, it should be removed by excisional biopsy or sampled for diagnosis by punch or incisional biopsy. There are no randomized controlled trials or cohort studies comparing techniques for removing raised nevi from the face.
Shave biopsy has good outcomes
Expert opinion and individual prospective case series show acceptable outcomes for shave biopsy. One prospective study followed 55 patients after removal of nevi from the head and neck. These nevi were removed using a shave procedure with a#15 scalpel and hot cautery for bleeding. Of the 55 sites, 4 retained pigment and 30 had a visible scar with a mean diameter of 5 mm at 6- to 8-month follow-up.1 The mean diameter of the original lesions was 6 mm. There was no difference between the size of those lesions that scarred and those that didn’t.
Researchers conducting a second retrospective study, done at least 1 year after the procedure, used a questionnaire to ask 76 patients (with a total of 83 nevi removed from the face by shave excision) about their perceptions of the scar.2 Patients described their lesions as: no scar (33%), white and flat (25%), depressed (19%), raised (15%), and pigmented (7%). Eighty-six percent thought their scars looked better than the nevus and 79% were “happy with the way the scar looks now.” Two additional studies, based on both patient and provider perceptions, with similar conclusions, are presented in the (TABLE).3,4
TABLE
Favorable cosmetic results following shave biopsy of facial nevi
| STUDY | NO. PTS/NEVI | % WITH RET AINED PIGMENT OR RECURRENCE | % WITH VISIBLE SCARRING | FOLLOW-UP INTERVAL | EVALUATION/DONE BY |
|---|---|---|---|---|---|
| Hudson-Peacock1 | 55/55 | 13 | 55 | 6-8 mo | Cosmetically acceptable/patients |
| Bong2 | 76/83 | 28 | 67 | ≥1 yr | 86%: better than nevus/patients |
| Zanardini3 | 206/ 215 | 4 | 9 | 3 mo | 90%: excellent* 9%: good/surgeons |
| Ferrandiz4 | Not known/59 | 20† | 67 | 3 mo | 98%: better than nevus/pts; 92%: excellent or acceptable‡/surgeons |
| Excellent=no noticeable scar, good=slightly noticeable scar with normochromia or hypochromia, poor=depressed scar or intense dyschromia. | |||||
| † Some lesions not papular. | |||||
| ‡ Excellent cosmetic result=imperceptible scar without erythema, hyper- or hypo-pigmentation, hypertrophy or atrophy. Acceptable=scar better than original mole. poor=left scar worse than original mole. | |||||
Atypical lesions should be excised
Atypical lesions require excisional biopsy. The depth and architecture of the lesion, if melanoma, cannot be determined by shave biopsy, and both treatment and prognosis depend on those characteristics.
These guidelines derive from well-designed, nonexperimental descriptive studies.5 However, a recent retrospective study compared the Breslow depth determination of 4 different biopsy techniques, performed by experienced dermatologists, with the subsequent depth on definitive surgery for melanoma. This study found that superficial shave, deep shave, and punch biopsy predicted the Breslow depth 88% (95/108) of the time.6 As expected, excisional biopsy predicted the depth 100% (30/30) of the time. The location of the biopsy sites were not reported. The choice of biopsy was influenced by the suspicion of melanoma; thin (< 1 mm) melanomas were more likely to be superficially shaved than deep-shaved or punched.
Recommendations from others
Guidelines on nevocellular nevi from the American Academy of Dermatology recommend a simple excisional or incisional biopsy; they do not discuss the method of removal for benign appearing facial lesions.7
The UK Guidelines for the Management of Cutaneous Melanoma recommend that suspicious lesions be excised completely (excisional biopsy) and sent for confirmatory histopathological examination.5 A biopsy that transects the depth of the lesion (for example, superficial shave biopsy) should be avoided because histological depth of invasion is the basic criterion for staging and shave biopsy makes the staging impossible in some cases.
A shave biopsy with a razor blade or #15 scalpel is the best approach for a facial nevus, assuming malignancy is not suspected. the resulting scar is usually flat, smaller than the lesion, has no suture lines, and—if shaved in mid or upper dermis—has a low risk of producing a hypertrophic or hypotrophic scar (strength of recommendation: C, expert opinion, committee guidelines).
Shave biopsies are quick and well-tolerated
Parul Harsora, MD
University of Texas Southwestern, Dallas
If you suspect malignancy in a nevus, obtain an excisional or incisional biopsy. Shave biopsies are best suited for raised, flesh-colored nevi and are generally quick, well-tolerated, and cost-effective. tissue from a shave biopsy can be submitted for histological evaluation.
Shave biopsies are preferred by patients because there are no sutures and scarring is minimized. the site may be pink and may take several months to develop a normal appearance. the final result may be unnoticeable, or leave an indentation or be hypo- or hyperpigmented.
Hairy, pigmented, and compound nevi are likely to do better with a punch biopsy. to prevent recurrence, seek histologic confirmation that the entire nevus has been removed.
Evidence summary
Numerous reports and guidelines indicate that if a nevus is even slightly suspicious for malignancy, it should be removed by excisional biopsy or sampled for diagnosis by punch or incisional biopsy. There are no randomized controlled trials or cohort studies comparing techniques for removing raised nevi from the face.
Shave biopsy has good outcomes
Expert opinion and individual prospective case series show acceptable outcomes for shave biopsy. One prospective study followed 55 patients after removal of nevi from the head and neck. These nevi were removed using a shave procedure with a#15 scalpel and hot cautery for bleeding. Of the 55 sites, 4 retained pigment and 30 had a visible scar with a mean diameter of 5 mm at 6- to 8-month follow-up.1 The mean diameter of the original lesions was 6 mm. There was no difference between the size of those lesions that scarred and those that didn’t.
Researchers conducting a second retrospective study, done at least 1 year after the procedure, used a questionnaire to ask 76 patients (with a total of 83 nevi removed from the face by shave excision) about their perceptions of the scar.2 Patients described their lesions as: no scar (33%), white and flat (25%), depressed (19%), raised (15%), and pigmented (7%). Eighty-six percent thought their scars looked better than the nevus and 79% were “happy with the way the scar looks now.” Two additional studies, based on both patient and provider perceptions, with similar conclusions, are presented in the (TABLE).3,4
TABLE
Favorable cosmetic results following shave biopsy of facial nevi
| STUDY | NO. PTS/NEVI | % WITH RET AINED PIGMENT OR RECURRENCE | % WITH VISIBLE SCARRING | FOLLOW-UP INTERVAL | EVALUATION/DONE BY |
|---|---|---|---|---|---|
| Hudson-Peacock1 | 55/55 | 13 | 55 | 6-8 mo | Cosmetically acceptable/patients |
| Bong2 | 76/83 | 28 | 67 | ≥1 yr | 86%: better than nevus/patients |
| Zanardini3 | 206/ 215 | 4 | 9 | 3 mo | 90%: excellent* 9%: good/surgeons |
| Ferrandiz4 | Not known/59 | 20† | 67 | 3 mo | 98%: better than nevus/pts; 92%: excellent or acceptable‡/surgeons |
| Excellent=no noticeable scar, good=slightly noticeable scar with normochromia or hypochromia, poor=depressed scar or intense dyschromia. | |||||
| † Some lesions not papular. | |||||
| ‡ Excellent cosmetic result=imperceptible scar without erythema, hyper- or hypo-pigmentation, hypertrophy or atrophy. Acceptable=scar better than original mole. poor=left scar worse than original mole. | |||||
Atypical lesions should be excised
Atypical lesions require excisional biopsy. The depth and architecture of the lesion, if melanoma, cannot be determined by shave biopsy, and both treatment and prognosis depend on those characteristics.
These guidelines derive from well-designed, nonexperimental descriptive studies.5 However, a recent retrospective study compared the Breslow depth determination of 4 different biopsy techniques, performed by experienced dermatologists, with the subsequent depth on definitive surgery for melanoma. This study found that superficial shave, deep shave, and punch biopsy predicted the Breslow depth 88% (95/108) of the time.6 As expected, excisional biopsy predicted the depth 100% (30/30) of the time. The location of the biopsy sites were not reported. The choice of biopsy was influenced by the suspicion of melanoma; thin (< 1 mm) melanomas were more likely to be superficially shaved than deep-shaved or punched.
Recommendations from others
Guidelines on nevocellular nevi from the American Academy of Dermatology recommend a simple excisional or incisional biopsy; they do not discuss the method of removal for benign appearing facial lesions.7
The UK Guidelines for the Management of Cutaneous Melanoma recommend that suspicious lesions be excised completely (excisional biopsy) and sent for confirmatory histopathological examination.5 A biopsy that transects the depth of the lesion (for example, superficial shave biopsy) should be avoided because histological depth of invasion is the basic criterion for staging and shave biopsy makes the staging impossible in some cases.
1. Hudson-Peacock MJ, Bishop J, Lawrence CM. Shave excision of benign papular naevocytic nevi. Br J Plast Surg 1995;48:318-322.
2. Bong JL, Perkins W. Shave excision of benign facial melanocytic naevi: a patient’s satisfaction survey. Dermatol Surg 2003;29:227-229.
3. Zanardini Pereira CA, Alchorne AOA. angential excision of nevocellular nevus on the face. Int J Dermatol 2004;43:533-537.
4. Ferrandiz L, Moreno-Ramirez D, Camacho FM. Shave excision of common acquired melanocytic nevi: cosmetic outcome, recurrences, and complications. Dermatol Surg 2005;3(Pt 1)1:1112-1115.
5. Roberts DLL, Anstey AV, Barlow RJ, et al. U.K.Guidelines for the management of cutaneous melanoma. Br J Dermatol 2002;146:7-17.
6. Ng PC, Barzilai DA, Ismail SA, Averitte RL Jr, Gilliam AC. valuating invasive cutaneous melanoma: Is the initial biopsy representative of the final depth? J Am Acad Dermatol 2005;48:420-424.
7. Drake L A, Ceilley R I, Cornelison RL , et al Drake LA, Ceilley RI, Cornelison RL, et al. Guidelines of care for nevi I (nevocellular nevi and seborrheic keratoses). J Am Acad Dermatol 1992;26:629-631.
1. Hudson-Peacock MJ, Bishop J, Lawrence CM. Shave excision of benign papular naevocytic nevi. Br J Plast Surg 1995;48:318-322.
2. Bong JL, Perkins W. Shave excision of benign facial melanocytic naevi: a patient’s satisfaction survey. Dermatol Surg 2003;29:227-229.
3. Zanardini Pereira CA, Alchorne AOA. angential excision of nevocellular nevus on the face. Int J Dermatol 2004;43:533-537.
4. Ferrandiz L, Moreno-Ramirez D, Camacho FM. Shave excision of common acquired melanocytic nevi: cosmetic outcome, recurrences, and complications. Dermatol Surg 2005;3(Pt 1)1:1112-1115.
5. Roberts DLL, Anstey AV, Barlow RJ, et al. U.K.Guidelines for the management of cutaneous melanoma. Br J Dermatol 2002;146:7-17.
6. Ng PC, Barzilai DA, Ismail SA, Averitte RL Jr, Gilliam AC. valuating invasive cutaneous melanoma: Is the initial biopsy representative of the final depth? J Am Acad Dermatol 2005;48:420-424.
7. Drake L A, Ceilley R I, Cornelison RL , et al Drake LA, Ceilley RI, Cornelison RL, et al. Guidelines of care for nevi I (nevocellular nevi and seborrheic keratoses). J Am Acad Dermatol 1992;26:629-631.
Evidence-based answers from the Family Physicians Inquiries Network
What is the best way to identify patients with white-coat hypertension?
Ambulatory blood pressure monitoring is currently the gold standard for detecting patients with white-coat hypertension. Women and all patients with lower office systolic blood pressures, stage I hypertension, and no target organ damage are more likely to have white-coat hypertension (strength of recommendation [SOR]: B, based on prospective cohort studies) ( TABLE ).
Self or home blood pressure monitoring has also been used to detect patients with white-coat hypertension. However, it has a low sensitivity (61%–68%) and low positive predictive value (PV+) (33%–48%) (SOR: B, short-term prospective cohort studies).
Evidence summary
White coat hypertension, also known as isolated office hypertension, refers to elevated blood pressures in a medical setting and normal blood pressures during regular daily life. Patients with white-coat hypertension are defined as patients 1) with an office blood pressure of >140 mm Hg systolic or >90 mm Hg diastolic on at least 3 separate office visits with 2 measurements each visit and 2) mean daytime blood pressure of <135 mm Hg systolic and <85 mm Hg diastolic on ambulatory blood pressure monitoring.1 Other measures of normal blood pressure on ambulatory blood pressure monitoring are <130/80 mm Hg for full 24-hour blood pressure and <120/70 mm Hg for night-time blood pressure.2 A recent Clinical Inquiry summarized 3 cohort trials—2 showed white-coat hypertension patients had lower risk of cardiovascular events and 1 showed no difference between patients with white-coat hypertension and patients with sustained hypertension.3 Identifying patients with white-coat hypertension is important to avoid overtreating individuals at lower risk of cardiovascular events.
Which patients with elevated blood pressure on repeated visits have white-coat hypertension? In studies of patients, most of whom have Stage I hypertension (140–159/90–99 mm Hg), anywhere from 10% to 50% have white-coat hypertension ( TABLE ). In a joint multivariate analysis of 2 cohort studies, which enrolled 1564 subjects with uncomplicated stage I hypertension, white-coat hypertension was associated with lower office systolic blood pressure, female gender, and nonsmoking.2 Similarly, a large international database of 2492 subjects found that women, older subjects, and those with lower and fewer office systolic blood pressure measurements were more likely to have white-coat hypertension.4 In another analysis of 1333 Italian subjects, the prevalence of white-coat hypertension was 33.3% in those with stage I hypertension, 11% with stage II, and 3 % with stage III.5 A study of more than 600 men over 20 years in Finland compared those who developed white-coat hypertension and those with sustained hypertension. The hypertensive patients had more microalbuminuria, a greater left ventricular mass on echo, increased cholesterol esters, and a greater body-mass index (all P.05) than patients with white-coat hypertension. Smoking status was similar in both groups, in contrast to other studies.6 A recent study did not find body-mass index distinguished white-coat hyperten-sion from sustained hypertension.7
TABLE
Patient attributes and white-coat hypertension
| ATTRIBUTE | SUBJECTS | COMPARISON | P VALUE |
|---|---|---|---|
| Gender, % with WCH | 5716* | 17% of females 14% of males | <.001 |
| % female WCH v SH group | 1564† | 45% v 33% | .002 |
| Ratio female: male with WCH | 2634§ | Odds ratio=1.92 (95% CI, 1.45–2.54) | <.001 |
| Mean age, WCH vs SH | 1564† | 40 vs 39 years | .52 |
| % with WCH in 4 age groups | 5716* | <35 y=12%, | <.001 |
| 35–50 y=14%, | |||
| 50–65 y=16%, | |||
| >65 y=17% | |||
| Currently smoking, % with WCH | 5716* | No=16.7%, Yes=11.3% | <.001 |
| Currently smoking % WCH v SH | 1564† | 7% v 24% | .04 |
| BMI, % WCH in 3 groups | 5716* | < 25=16% | NS |
| 25–30=15% | |||
| >30=15% | |||
| BMI, WCH group vs SH group | 1564† | 25.4 vs 25.9 | NS |
| 414‡ | 23.9 vs 24.7 | <.05 | |
| Original clinic SBP, % with WCH | 5716* | 140–159=31.2% | <.001 |
| 160–170=18.7% | |||
| 171–180=11.8% | |||
| 2492§ | 140–150=65% | .004 | |
| 151–160=53% | |||
| 161–170=33% | |||
| LV Mass (g), WCH v SH | 1564† | 160 vs 180 | .001 |
| LV Mass Index (g/m2) WCH v SH | 414‡ | 126 vs 136 | <.01 |
| WCH, white coat hypertension; SBP, systolic blood pressure; SH, sustained hypertension; CI, confidence interval; BMI, body-mass index; NS, not significant; LV, left ventricular. | |||
| *Patients referred to a blood pressure unit over 22-year period.7 | |||
| † A combination of 2 studies of clinic patients with stage I hypertension (140–159/90–99 mm Hg).2 | |||
| ‡ 50-year-old men in a community in Finland invited to a health survey with a 20-year follow-up.6 | |||
| § Data from 24 pooled studies of ambulatory blood pressure monitoring.4 | |||
Using home blood pressure as a screening tool is a problem because of the low sensitivity and poor PV+. In the THOP study (247 subjects), which used ambulatory blood pressure monitoring as the reference method, home blood pressure had a high specificity (89%) and high negative predictive value (PV–) (97%) but a lower sensitivity (68%) and low PPV (33%).8 In other words, if home blood pressure shows hypertension, there is a 97% chance the patient has sustained hypertension, but if home blood pressure returns to normal in patients with office hypertension, two thirds of patients will still have sustained hypertension. In another study that enrolled patients from a hypertension clinic, 133 untreated patients with dias-tolic blood pressure 90 to 115 mm Hg underwent ambulatory blood pressure monitoring for a reference standard. The sensitivity of home blood pressure monitoring in identifying white-coat hypertension was 61% and the PV+ was 48%.9
Recommendations from others
The European Society of Hypertension Working Group on Blood Pressure Monitoring recommends that subjects with blood pressure 140–159/90–99 mm Hg at several visits should have ambulatory blood pressure monitoring because 33% of those people will have white-coat hypertension. Women, nonsmokers, those with recent hypertension, a limited number of blood pressure determinations and small left ventricular mass on echo should also have ambulatory blood pressure monitoring. There should be a search for metabolic risk factors and target organ damage. Those patients aware that their blood pressures are lower outside the office should be considered for ambulatory blood pressure monitoring.10
The latest Joint National Committee report (JNC VII) indicates that ambulatory blood pressure monitoring may be useful to detect white-coat hypertension among patients with hypertension and no target organ damage, and those with episodic hypertension.11
Ambulatory BP monitoring better than home monitoring for ruling out white-coat hypertension
Joseph Saseen, PharmD, FCCP, BCPS
University of Colorado Health Sciences Center, Denver
Landmark placebo-controlled outcome-based trials demonstrating reduced morbidity and mortality with hypertension treatment did not differentiate essential from white-coat hypertension. Patients were included based on elevated office-based blood pressure measurements. Since we now know that the prevalence of white-coat hypertension is high, it should be ruled out before implementing antihypertensive therapy.
Ambulatory blood pressure monitoring is more accurate than home monitoring for ruling out white-coat hypertension. However, ease, simplicity, and availability makes home monitoring a more realistic option for routine clinical practice. When home blood pressure monitoring is used, reliable measurement devices (eg, newer automatic or manual home devices) should be used and patients should be instructed regarding proper use and documentation of blood pressure values to facilitate an appropriate clinical assessment.
1. O’Brien E, Asmar R, Beilin L, et al. on behalf of the European Society of Hypertension Working Group on Blood Pressure Monitoring. European Society of Hypertension recommendations for conventional, ambulatory and home blood pressure measurement. J Hypertens 2003;21:821-848.
2. Verdecchia P, Palatini P, Schillaci G, Mormino P, Porcellati C, Pessina AC. Independent predictors of isolated clinic (‘white-coat’) hypertension. J Hypertens 2001;19:1015-1020.
3. Rao S, Liu C-T, Wilder L. What is the best way to treat patients with white-coat hypertension?. J Fam Pract 2004;53:408-412.
4. Staessen JA, O’Brien ET, Atkins N, Anery AK. on behalf of the Ad-Hoc Working Group: Short report: Ambulatory blood pressure in normotensive compared with hypertensive subjects. J Hypertens 1993;11:1289-1297.
5. Verdecchia P, Schillaci G, Borgioni C, et al. White-coat hypertension and white-coat effect: Similarities and differences. Am J Hypertens 1995;8:790-798.
6. Bjorklund K, Lind L, Vessby B, Andren B, Lithell H. Different metabolic predictors of white-coat and sustained hypertension over a 20-year follow-up period. Circulation 2002;106:63-68.
7. Dolan E, Stanton A, Atkins N, et al. Determinants of white-coat hypertension. Blood Pressure Monit 2004;9:307-309.
8. Den Hond E, Celis H, Fagard R, et al. Self-measured versus ambulatory blood pressure in the diagnosis of hypertension. J Hypertens 2003;21:717-722.
9. Stergiou GS, Skeva II, Baibas NM, Kalkana CB, Roussias LG, Mountokalakis TD. Diagnosis of hyper-tension using home or ambulatory blood pressure monitoring: comparison with the conventional strategy based on repeated clinic blood pressure measurements. J Hypertens 2000;18:1745-1751.
10. Verdecchia P, O’Brien E, Pickering T, et al. When can the practicing physician suspect white coat hyperten-sion? Statement from the Working Group on Blood Pressure Monitoring of the European Society of Hypertension. Am J Hypertens 2003;16:87-91.
11. Chobanian AV, Bakris GL, Black HR, et al. Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003;42:1206-1252.
Ambulatory blood pressure monitoring is currently the gold standard for detecting patients with white-coat hypertension. Women and all patients with lower office systolic blood pressures, stage I hypertension, and no target organ damage are more likely to have white-coat hypertension (strength of recommendation [SOR]: B, based on prospective cohort studies) ( TABLE ).
Self or home blood pressure monitoring has also been used to detect patients with white-coat hypertension. However, it has a low sensitivity (61%–68%) and low positive predictive value (PV+) (33%–48%) (SOR: B, short-term prospective cohort studies).
Evidence summary
White coat hypertension, also known as isolated office hypertension, refers to elevated blood pressures in a medical setting and normal blood pressures during regular daily life. Patients with white-coat hypertension are defined as patients 1) with an office blood pressure of >140 mm Hg systolic or >90 mm Hg diastolic on at least 3 separate office visits with 2 measurements each visit and 2) mean daytime blood pressure of <135 mm Hg systolic and <85 mm Hg diastolic on ambulatory blood pressure monitoring.1 Other measures of normal blood pressure on ambulatory blood pressure monitoring are <130/80 mm Hg for full 24-hour blood pressure and <120/70 mm Hg for night-time blood pressure.2 A recent Clinical Inquiry summarized 3 cohort trials—2 showed white-coat hypertension patients had lower risk of cardiovascular events and 1 showed no difference between patients with white-coat hypertension and patients with sustained hypertension.3 Identifying patients with white-coat hypertension is important to avoid overtreating individuals at lower risk of cardiovascular events.
Which patients with elevated blood pressure on repeated visits have white-coat hypertension? In studies of patients, most of whom have Stage I hypertension (140–159/90–99 mm Hg), anywhere from 10% to 50% have white-coat hypertension ( TABLE ). In a joint multivariate analysis of 2 cohort studies, which enrolled 1564 subjects with uncomplicated stage I hypertension, white-coat hypertension was associated with lower office systolic blood pressure, female gender, and nonsmoking.2 Similarly, a large international database of 2492 subjects found that women, older subjects, and those with lower and fewer office systolic blood pressure measurements were more likely to have white-coat hypertension.4 In another analysis of 1333 Italian subjects, the prevalence of white-coat hypertension was 33.3% in those with stage I hypertension, 11% with stage II, and 3 % with stage III.5 A study of more than 600 men over 20 years in Finland compared those who developed white-coat hypertension and those with sustained hypertension. The hypertensive patients had more microalbuminuria, a greater left ventricular mass on echo, increased cholesterol esters, and a greater body-mass index (all P.05) than patients with white-coat hypertension. Smoking status was similar in both groups, in contrast to other studies.6 A recent study did not find body-mass index distinguished white-coat hyperten-sion from sustained hypertension.7
TABLE
Patient attributes and white-coat hypertension
| ATTRIBUTE | SUBJECTS | COMPARISON | P VALUE |
|---|---|---|---|
| Gender, % with WCH | 5716* | 17% of females 14% of males | <.001 |
| % female WCH v SH group | 1564† | 45% v 33% | .002 |
| Ratio female: male with WCH | 2634§ | Odds ratio=1.92 (95% CI, 1.45–2.54) | <.001 |
| Mean age, WCH vs SH | 1564† | 40 vs 39 years | .52 |
| % with WCH in 4 age groups | 5716* | <35 y=12%, | <.001 |
| 35–50 y=14%, | |||
| 50–65 y=16%, | |||
| >65 y=17% | |||
| Currently smoking, % with WCH | 5716* | No=16.7%, Yes=11.3% | <.001 |
| Currently smoking % WCH v SH | 1564† | 7% v 24% | .04 |
| BMI, % WCH in 3 groups | 5716* | < 25=16% | NS |
| 25–30=15% | |||
| >30=15% | |||
| BMI, WCH group vs SH group | 1564† | 25.4 vs 25.9 | NS |
| 414‡ | 23.9 vs 24.7 | <.05 | |
| Original clinic SBP, % with WCH | 5716* | 140–159=31.2% | <.001 |
| 160–170=18.7% | |||
| 171–180=11.8% | |||
| 2492§ | 140–150=65% | .004 | |
| 151–160=53% | |||
| 161–170=33% | |||
| LV Mass (g), WCH v SH | 1564† | 160 vs 180 | .001 |
| LV Mass Index (g/m2) WCH v SH | 414‡ | 126 vs 136 | <.01 |
| WCH, white coat hypertension; SBP, systolic blood pressure; SH, sustained hypertension; CI, confidence interval; BMI, body-mass index; NS, not significant; LV, left ventricular. | |||
| *Patients referred to a blood pressure unit over 22-year period.7 | |||
| † A combination of 2 studies of clinic patients with stage I hypertension (140–159/90–99 mm Hg).2 | |||
| ‡ 50-year-old men in a community in Finland invited to a health survey with a 20-year follow-up.6 | |||
| § Data from 24 pooled studies of ambulatory blood pressure monitoring.4 | |||
Using home blood pressure as a screening tool is a problem because of the low sensitivity and poor PV+. In the THOP study (247 subjects), which used ambulatory blood pressure monitoring as the reference method, home blood pressure had a high specificity (89%) and high negative predictive value (PV–) (97%) but a lower sensitivity (68%) and low PPV (33%).8 In other words, if home blood pressure shows hypertension, there is a 97% chance the patient has sustained hypertension, but if home blood pressure returns to normal in patients with office hypertension, two thirds of patients will still have sustained hypertension. In another study that enrolled patients from a hypertension clinic, 133 untreated patients with dias-tolic blood pressure 90 to 115 mm Hg underwent ambulatory blood pressure monitoring for a reference standard. The sensitivity of home blood pressure monitoring in identifying white-coat hypertension was 61% and the PV+ was 48%.9
Recommendations from others
The European Society of Hypertension Working Group on Blood Pressure Monitoring recommends that subjects with blood pressure 140–159/90–99 mm Hg at several visits should have ambulatory blood pressure monitoring because 33% of those people will have white-coat hypertension. Women, nonsmokers, those with recent hypertension, a limited number of blood pressure determinations and small left ventricular mass on echo should also have ambulatory blood pressure monitoring. There should be a search for metabolic risk factors and target organ damage. Those patients aware that their blood pressures are lower outside the office should be considered for ambulatory blood pressure monitoring.10
The latest Joint National Committee report (JNC VII) indicates that ambulatory blood pressure monitoring may be useful to detect white-coat hypertension among patients with hypertension and no target organ damage, and those with episodic hypertension.11
Ambulatory BP monitoring better than home monitoring for ruling out white-coat hypertension
Joseph Saseen, PharmD, FCCP, BCPS
University of Colorado Health Sciences Center, Denver
Landmark placebo-controlled outcome-based trials demonstrating reduced morbidity and mortality with hypertension treatment did not differentiate essential from white-coat hypertension. Patients were included based on elevated office-based blood pressure measurements. Since we now know that the prevalence of white-coat hypertension is high, it should be ruled out before implementing antihypertensive therapy.
Ambulatory blood pressure monitoring is more accurate than home monitoring for ruling out white-coat hypertension. However, ease, simplicity, and availability makes home monitoring a more realistic option for routine clinical practice. When home blood pressure monitoring is used, reliable measurement devices (eg, newer automatic or manual home devices) should be used and patients should be instructed regarding proper use and documentation of blood pressure values to facilitate an appropriate clinical assessment.
Ambulatory blood pressure monitoring is currently the gold standard for detecting patients with white-coat hypertension. Women and all patients with lower office systolic blood pressures, stage I hypertension, and no target organ damage are more likely to have white-coat hypertension (strength of recommendation [SOR]: B, based on prospective cohort studies) ( TABLE ).
Self or home blood pressure monitoring has also been used to detect patients with white-coat hypertension. However, it has a low sensitivity (61%–68%) and low positive predictive value (PV+) (33%–48%) (SOR: B, short-term prospective cohort studies).
Evidence summary
White coat hypertension, also known as isolated office hypertension, refers to elevated blood pressures in a medical setting and normal blood pressures during regular daily life. Patients with white-coat hypertension are defined as patients 1) with an office blood pressure of >140 mm Hg systolic or >90 mm Hg diastolic on at least 3 separate office visits with 2 measurements each visit and 2) mean daytime blood pressure of <135 mm Hg systolic and <85 mm Hg diastolic on ambulatory blood pressure monitoring.1 Other measures of normal blood pressure on ambulatory blood pressure monitoring are <130/80 mm Hg for full 24-hour blood pressure and <120/70 mm Hg for night-time blood pressure.2 A recent Clinical Inquiry summarized 3 cohort trials—2 showed white-coat hypertension patients had lower risk of cardiovascular events and 1 showed no difference between patients with white-coat hypertension and patients with sustained hypertension.3 Identifying patients with white-coat hypertension is important to avoid overtreating individuals at lower risk of cardiovascular events.
Which patients with elevated blood pressure on repeated visits have white-coat hypertension? In studies of patients, most of whom have Stage I hypertension (140–159/90–99 mm Hg), anywhere from 10% to 50% have white-coat hypertension ( TABLE ). In a joint multivariate analysis of 2 cohort studies, which enrolled 1564 subjects with uncomplicated stage I hypertension, white-coat hypertension was associated with lower office systolic blood pressure, female gender, and nonsmoking.2 Similarly, a large international database of 2492 subjects found that women, older subjects, and those with lower and fewer office systolic blood pressure measurements were more likely to have white-coat hypertension.4 In another analysis of 1333 Italian subjects, the prevalence of white-coat hypertension was 33.3% in those with stage I hypertension, 11% with stage II, and 3 % with stage III.5 A study of more than 600 men over 20 years in Finland compared those who developed white-coat hypertension and those with sustained hypertension. The hypertensive patients had more microalbuminuria, a greater left ventricular mass on echo, increased cholesterol esters, and a greater body-mass index (all P.05) than patients with white-coat hypertension. Smoking status was similar in both groups, in contrast to other studies.6 A recent study did not find body-mass index distinguished white-coat hyperten-sion from sustained hypertension.7
TABLE
Patient attributes and white-coat hypertension
| ATTRIBUTE | SUBJECTS | COMPARISON | P VALUE |
|---|---|---|---|
| Gender, % with WCH | 5716* | 17% of females 14% of males | <.001 |
| % female WCH v SH group | 1564† | 45% v 33% | .002 |
| Ratio female: male with WCH | 2634§ | Odds ratio=1.92 (95% CI, 1.45–2.54) | <.001 |
| Mean age, WCH vs SH | 1564† | 40 vs 39 years | .52 |
| % with WCH in 4 age groups | 5716* | <35 y=12%, | <.001 |
| 35–50 y=14%, | |||
| 50–65 y=16%, | |||
| >65 y=17% | |||
| Currently smoking, % with WCH | 5716* | No=16.7%, Yes=11.3% | <.001 |
| Currently smoking % WCH v SH | 1564† | 7% v 24% | .04 |
| BMI, % WCH in 3 groups | 5716* | < 25=16% | NS |
| 25–30=15% | |||
| >30=15% | |||
| BMI, WCH group vs SH group | 1564† | 25.4 vs 25.9 | NS |
| 414‡ | 23.9 vs 24.7 | <.05 | |
| Original clinic SBP, % with WCH | 5716* | 140–159=31.2% | <.001 |
| 160–170=18.7% | |||
| 171–180=11.8% | |||
| 2492§ | 140–150=65% | .004 | |
| 151–160=53% | |||
| 161–170=33% | |||
| LV Mass (g), WCH v SH | 1564† | 160 vs 180 | .001 |
| LV Mass Index (g/m2) WCH v SH | 414‡ | 126 vs 136 | <.01 |
| WCH, white coat hypertension; SBP, systolic blood pressure; SH, sustained hypertension; CI, confidence interval; BMI, body-mass index; NS, not significant; LV, left ventricular. | |||
| *Patients referred to a blood pressure unit over 22-year period.7 | |||
| † A combination of 2 studies of clinic patients with stage I hypertension (140–159/90–99 mm Hg).2 | |||
| ‡ 50-year-old men in a community in Finland invited to a health survey with a 20-year follow-up.6 | |||
| § Data from 24 pooled studies of ambulatory blood pressure monitoring.4 | |||
Using home blood pressure as a screening tool is a problem because of the low sensitivity and poor PV+. In the THOP study (247 subjects), which used ambulatory blood pressure monitoring as the reference method, home blood pressure had a high specificity (89%) and high negative predictive value (PV–) (97%) but a lower sensitivity (68%) and low PPV (33%).8 In other words, if home blood pressure shows hypertension, there is a 97% chance the patient has sustained hypertension, but if home blood pressure returns to normal in patients with office hypertension, two thirds of patients will still have sustained hypertension. In another study that enrolled patients from a hypertension clinic, 133 untreated patients with dias-tolic blood pressure 90 to 115 mm Hg underwent ambulatory blood pressure monitoring for a reference standard. The sensitivity of home blood pressure monitoring in identifying white-coat hypertension was 61% and the PV+ was 48%.9
Recommendations from others
The European Society of Hypertension Working Group on Blood Pressure Monitoring recommends that subjects with blood pressure 140–159/90–99 mm Hg at several visits should have ambulatory blood pressure monitoring because 33% of those people will have white-coat hypertension. Women, nonsmokers, those with recent hypertension, a limited number of blood pressure determinations and small left ventricular mass on echo should also have ambulatory blood pressure monitoring. There should be a search for metabolic risk factors and target organ damage. Those patients aware that their blood pressures are lower outside the office should be considered for ambulatory blood pressure monitoring.10
The latest Joint National Committee report (JNC VII) indicates that ambulatory blood pressure monitoring may be useful to detect white-coat hypertension among patients with hypertension and no target organ damage, and those with episodic hypertension.11
Ambulatory BP monitoring better than home monitoring for ruling out white-coat hypertension
Joseph Saseen, PharmD, FCCP, BCPS
University of Colorado Health Sciences Center, Denver
Landmark placebo-controlled outcome-based trials demonstrating reduced morbidity and mortality with hypertension treatment did not differentiate essential from white-coat hypertension. Patients were included based on elevated office-based blood pressure measurements. Since we now know that the prevalence of white-coat hypertension is high, it should be ruled out before implementing antihypertensive therapy.
Ambulatory blood pressure monitoring is more accurate than home monitoring for ruling out white-coat hypertension. However, ease, simplicity, and availability makes home monitoring a more realistic option for routine clinical practice. When home blood pressure monitoring is used, reliable measurement devices (eg, newer automatic or manual home devices) should be used and patients should be instructed regarding proper use and documentation of blood pressure values to facilitate an appropriate clinical assessment.
1. O’Brien E, Asmar R, Beilin L, et al. on behalf of the European Society of Hypertension Working Group on Blood Pressure Monitoring. European Society of Hypertension recommendations for conventional, ambulatory and home blood pressure measurement. J Hypertens 2003;21:821-848.
2. Verdecchia P, Palatini P, Schillaci G, Mormino P, Porcellati C, Pessina AC. Independent predictors of isolated clinic (‘white-coat’) hypertension. J Hypertens 2001;19:1015-1020.
3. Rao S, Liu C-T, Wilder L. What is the best way to treat patients with white-coat hypertension?. J Fam Pract 2004;53:408-412.
4. Staessen JA, O’Brien ET, Atkins N, Anery AK. on behalf of the Ad-Hoc Working Group: Short report: Ambulatory blood pressure in normotensive compared with hypertensive subjects. J Hypertens 1993;11:1289-1297.
5. Verdecchia P, Schillaci G, Borgioni C, et al. White-coat hypertension and white-coat effect: Similarities and differences. Am J Hypertens 1995;8:790-798.
6. Bjorklund K, Lind L, Vessby B, Andren B, Lithell H. Different metabolic predictors of white-coat and sustained hypertension over a 20-year follow-up period. Circulation 2002;106:63-68.
7. Dolan E, Stanton A, Atkins N, et al. Determinants of white-coat hypertension. Blood Pressure Monit 2004;9:307-309.
8. Den Hond E, Celis H, Fagard R, et al. Self-measured versus ambulatory blood pressure in the diagnosis of hypertension. J Hypertens 2003;21:717-722.
9. Stergiou GS, Skeva II, Baibas NM, Kalkana CB, Roussias LG, Mountokalakis TD. Diagnosis of hyper-tension using home or ambulatory blood pressure monitoring: comparison with the conventional strategy based on repeated clinic blood pressure measurements. J Hypertens 2000;18:1745-1751.
10. Verdecchia P, O’Brien E, Pickering T, et al. When can the practicing physician suspect white coat hyperten-sion? Statement from the Working Group on Blood Pressure Monitoring of the European Society of Hypertension. Am J Hypertens 2003;16:87-91.
11. Chobanian AV, Bakris GL, Black HR, et al. Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003;42:1206-1252.
1. O’Brien E, Asmar R, Beilin L, et al. on behalf of the European Society of Hypertension Working Group on Blood Pressure Monitoring. European Society of Hypertension recommendations for conventional, ambulatory and home blood pressure measurement. J Hypertens 2003;21:821-848.
2. Verdecchia P, Palatini P, Schillaci G, Mormino P, Porcellati C, Pessina AC. Independent predictors of isolated clinic (‘white-coat’) hypertension. J Hypertens 2001;19:1015-1020.
3. Rao S, Liu C-T, Wilder L. What is the best way to treat patients with white-coat hypertension?. J Fam Pract 2004;53:408-412.
4. Staessen JA, O’Brien ET, Atkins N, Anery AK. on behalf of the Ad-Hoc Working Group: Short report: Ambulatory blood pressure in normotensive compared with hypertensive subjects. J Hypertens 1993;11:1289-1297.
5. Verdecchia P, Schillaci G, Borgioni C, et al. White-coat hypertension and white-coat effect: Similarities and differences. Am J Hypertens 1995;8:790-798.
6. Bjorklund K, Lind L, Vessby B, Andren B, Lithell H. Different metabolic predictors of white-coat and sustained hypertension over a 20-year follow-up period. Circulation 2002;106:63-68.
7. Dolan E, Stanton A, Atkins N, et al. Determinants of white-coat hypertension. Blood Pressure Monit 2004;9:307-309.
8. Den Hond E, Celis H, Fagard R, et al. Self-measured versus ambulatory blood pressure in the diagnosis of hypertension. J Hypertens 2003;21:717-722.
9. Stergiou GS, Skeva II, Baibas NM, Kalkana CB, Roussias LG, Mountokalakis TD. Diagnosis of hyper-tension using home or ambulatory blood pressure monitoring: comparison with the conventional strategy based on repeated clinic blood pressure measurements. J Hypertens 2000;18:1745-1751.
10. Verdecchia P, O’Brien E, Pickering T, et al. When can the practicing physician suspect white coat hyperten-sion? Statement from the Working Group on Blood Pressure Monitoring of the European Society of Hypertension. Am J Hypertens 2003;16:87-91.
11. Chobanian AV, Bakris GL, Black HR, et al. Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003;42:1206-1252.
Evidence-based answers from the Family Physicians Inquiries Network
Is prostate-specific antigen (PSA) screening indicated for any subgroup of men?
Although African American men, men with a first-degree relative with prostate cancer (CaP), and older men constitute higher-risk subgroups, no well-designed randomized controlled trials are available that show PSA testing to improve mortality or quality of life for these or any other groups of men.1 A trend toward detecting more localized cancers and a possible decreasing mortality rate from CaP in all men may be related to PSA testing, lead-time bias, or both. (Grade of recommendation: C, based on inadequate reference standards and an unclear clinical decision rule.)
Evidence summary
The value of screening with PSA in any population is uncertain. This issue will remain controversial at least until the first of 2 well-designed randomized controlled trials reports results in 2004.2,3 However, higher-risk subgroups merit special attention. Screening the 3 groups mentioned above would improve the positive predictive value of PSA, but crucial data to determine whether this will improve outcomes are lacking. Using average estimates, if 3300 African American men (aged 50 to 65 years) were screened, 100 would have cancer. After subsequent radical prostatectomy, 1 screened man would die from the procedure, 60 would become impotent, and 20 would be incontinent.4
If current therapies for localized therapy do not decrease morbidity or mortality, screening higher-risk groups merely puts them at increased risk for potentially harmful interventions. Biopsies cannot reliably predict which cancers will progress and which will lie indolent. The 30% incidence of CaP on autopsy means that more people die with CaP than from it. Using estimates of the prevalence and natural history of the disease, decision analyses report varying years saved by screening compared with watchful waiting (ranging from a gain of 2.5 quality-adjusted life years (QALYs) to an actual decrease in QALYs, depending primarily on the rate of progression to metastatic disease and efficacy of treatment.5,6 Another decision analysis, using quality-of-life measures, concluded that men would favor screening only if the prevalence of CaP were greater than any current estimate.7 Since the mean expected survival at age 70 is slightly more than 10 years, PSA screening for men 70 years or older to detect cancers with a 10-year survival rate of approximately 90% makes little sense.
Recommendations from others
The US Preventive Services Task Force in 1996 recommended against performing routine screening, stating that there was fair evidence to exclude the test. The American Cancer Society (ACS) and the American Urological Association (AUA) recommend that PSA be offered annually, beginning at patient age 50, to men with a life expectancy of more than 10 years. The same recommendation extends to younger African American men (age 40 years [AUA] or 45 years [ACS]) and men with 1 (AUA) or 2 (ACS) affected first-degree relatives. The American College of Physicians and the American Academy of Family Physicians (AAFP) recommend a discussion of the benefits and harms of screening, diagnosis and treatment, and individualizing the decision to screen.
Ellen Beck, MD
Department of Family and Preventive Medicine University of California, San Diego
When ordering a PSA test, note the last time the patient ejaculated. Ejaculation within 48 hours may elevate PSA levels, as may prostatitis, urinary retention, and prostatic massage, although a digital examination does not. Finasteride and herbal remedies such as saw palmetto can lower PSA levels.
In practice, it is helpful to follow the guidelines from the AAFP, which advises counseling the patient about the known risks and uncertain benefits of the test (http://www.familydoctor.org/healthfacts/361/).
1. Barry MJ. N Engl J Med 2001;344:1373-7.
2. Gohagan JK, Prorok PC, Kramer BS, et al. Urology 1994;152:1905-9.
3. Shroder FH. Can J Oncol 1994;4(suppl 1):98-9.
4. Lefevre ML. Am Fam Physician 1998;58:432-8.
5. Benoit R, Naslund M. Urol Clin North Am 1997;24:451-8.
6. Fleming C, Wasson J, Albertsen P, et al. JAMA 1993;269:2650-8.
7. Cantor SB, Spann SJ, Volk RJ, et al. J Fam Pract 1995;41:33-41.
8. Crawford ED, Leewansangtong S, Goktas S, et al. Prostate 1999;38:296-302.
Although African American men, men with a first-degree relative with prostate cancer (CaP), and older men constitute higher-risk subgroups, no well-designed randomized controlled trials are available that show PSA testing to improve mortality or quality of life for these or any other groups of men.1 A trend toward detecting more localized cancers and a possible decreasing mortality rate from CaP in all men may be related to PSA testing, lead-time bias, or both. (Grade of recommendation: C, based on inadequate reference standards and an unclear clinical decision rule.)
Evidence summary
The value of screening with PSA in any population is uncertain. This issue will remain controversial at least until the first of 2 well-designed randomized controlled trials reports results in 2004.2,3 However, higher-risk subgroups merit special attention. Screening the 3 groups mentioned above would improve the positive predictive value of PSA, but crucial data to determine whether this will improve outcomes are lacking. Using average estimates, if 3300 African American men (aged 50 to 65 years) were screened, 100 would have cancer. After subsequent radical prostatectomy, 1 screened man would die from the procedure, 60 would become impotent, and 20 would be incontinent.4
If current therapies for localized therapy do not decrease morbidity or mortality, screening higher-risk groups merely puts them at increased risk for potentially harmful interventions. Biopsies cannot reliably predict which cancers will progress and which will lie indolent. The 30% incidence of CaP on autopsy means that more people die with CaP than from it. Using estimates of the prevalence and natural history of the disease, decision analyses report varying years saved by screening compared with watchful waiting (ranging from a gain of 2.5 quality-adjusted life years (QALYs) to an actual decrease in QALYs, depending primarily on the rate of progression to metastatic disease and efficacy of treatment.5,6 Another decision analysis, using quality-of-life measures, concluded that men would favor screening only if the prevalence of CaP were greater than any current estimate.7 Since the mean expected survival at age 70 is slightly more than 10 years, PSA screening for men 70 years or older to detect cancers with a 10-year survival rate of approximately 90% makes little sense.
Recommendations from others
The US Preventive Services Task Force in 1996 recommended against performing routine screening, stating that there was fair evidence to exclude the test. The American Cancer Society (ACS) and the American Urological Association (AUA) recommend that PSA be offered annually, beginning at patient age 50, to men with a life expectancy of more than 10 years. The same recommendation extends to younger African American men (age 40 years [AUA] or 45 years [ACS]) and men with 1 (AUA) or 2 (ACS) affected first-degree relatives. The American College of Physicians and the American Academy of Family Physicians (AAFP) recommend a discussion of the benefits and harms of screening, diagnosis and treatment, and individualizing the decision to screen.
Ellen Beck, MD
Department of Family and Preventive Medicine University of California, San Diego
When ordering a PSA test, note the last time the patient ejaculated. Ejaculation within 48 hours may elevate PSA levels, as may prostatitis, urinary retention, and prostatic massage, although a digital examination does not. Finasteride and herbal remedies such as saw palmetto can lower PSA levels.
In practice, it is helpful to follow the guidelines from the AAFP, which advises counseling the patient about the known risks and uncertain benefits of the test (http://www.familydoctor.org/healthfacts/361/).
Although African American men, men with a first-degree relative with prostate cancer (CaP), and older men constitute higher-risk subgroups, no well-designed randomized controlled trials are available that show PSA testing to improve mortality or quality of life for these or any other groups of men.1 A trend toward detecting more localized cancers and a possible decreasing mortality rate from CaP in all men may be related to PSA testing, lead-time bias, or both. (Grade of recommendation: C, based on inadequate reference standards and an unclear clinical decision rule.)
Evidence summary
The value of screening with PSA in any population is uncertain. This issue will remain controversial at least until the first of 2 well-designed randomized controlled trials reports results in 2004.2,3 However, higher-risk subgroups merit special attention. Screening the 3 groups mentioned above would improve the positive predictive value of PSA, but crucial data to determine whether this will improve outcomes are lacking. Using average estimates, if 3300 African American men (aged 50 to 65 years) were screened, 100 would have cancer. After subsequent radical prostatectomy, 1 screened man would die from the procedure, 60 would become impotent, and 20 would be incontinent.4
If current therapies for localized therapy do not decrease morbidity or mortality, screening higher-risk groups merely puts them at increased risk for potentially harmful interventions. Biopsies cannot reliably predict which cancers will progress and which will lie indolent. The 30% incidence of CaP on autopsy means that more people die with CaP than from it. Using estimates of the prevalence and natural history of the disease, decision analyses report varying years saved by screening compared with watchful waiting (ranging from a gain of 2.5 quality-adjusted life years (QALYs) to an actual decrease in QALYs, depending primarily on the rate of progression to metastatic disease and efficacy of treatment.5,6 Another decision analysis, using quality-of-life measures, concluded that men would favor screening only if the prevalence of CaP were greater than any current estimate.7 Since the mean expected survival at age 70 is slightly more than 10 years, PSA screening for men 70 years or older to detect cancers with a 10-year survival rate of approximately 90% makes little sense.
Recommendations from others
The US Preventive Services Task Force in 1996 recommended against performing routine screening, stating that there was fair evidence to exclude the test. The American Cancer Society (ACS) and the American Urological Association (AUA) recommend that PSA be offered annually, beginning at patient age 50, to men with a life expectancy of more than 10 years. The same recommendation extends to younger African American men (age 40 years [AUA] or 45 years [ACS]) and men with 1 (AUA) or 2 (ACS) affected first-degree relatives. The American College of Physicians and the American Academy of Family Physicians (AAFP) recommend a discussion of the benefits and harms of screening, diagnosis and treatment, and individualizing the decision to screen.
Ellen Beck, MD
Department of Family and Preventive Medicine University of California, San Diego
When ordering a PSA test, note the last time the patient ejaculated. Ejaculation within 48 hours may elevate PSA levels, as may prostatitis, urinary retention, and prostatic massage, although a digital examination does not. Finasteride and herbal remedies such as saw palmetto can lower PSA levels.
In practice, it is helpful to follow the guidelines from the AAFP, which advises counseling the patient about the known risks and uncertain benefits of the test (http://www.familydoctor.org/healthfacts/361/).
1. Barry MJ. N Engl J Med 2001;344:1373-7.
2. Gohagan JK, Prorok PC, Kramer BS, et al. Urology 1994;152:1905-9.
3. Shroder FH. Can J Oncol 1994;4(suppl 1):98-9.
4. Lefevre ML. Am Fam Physician 1998;58:432-8.
5. Benoit R, Naslund M. Urol Clin North Am 1997;24:451-8.
6. Fleming C, Wasson J, Albertsen P, et al. JAMA 1993;269:2650-8.
7. Cantor SB, Spann SJ, Volk RJ, et al. J Fam Pract 1995;41:33-41.
8. Crawford ED, Leewansangtong S, Goktas S, et al. Prostate 1999;38:296-302.
1. Barry MJ. N Engl J Med 2001;344:1373-7.
2. Gohagan JK, Prorok PC, Kramer BS, et al. Urology 1994;152:1905-9.
3. Shroder FH. Can J Oncol 1994;4(suppl 1):98-9.
4. Lefevre ML. Am Fam Physician 1998;58:432-8.
5. Benoit R, Naslund M. Urol Clin North Am 1997;24:451-8.
6. Fleming C, Wasson J, Albertsen P, et al. JAMA 1993;269:2650-8.
7. Cantor SB, Spann SJ, Volk RJ, et al. J Fam Pract 1995;41:33-41.
8. Crawford ED, Leewansangtong S, Goktas S, et al. Prostate 1999;38:296-302.
Evidence-based answers from the Family Physicians Inquiries Network