Wayne Hale, MD

Evidence summary

Leg cramps (heat cramps) in athletes are defined as painful involuntary muscle contractions, usually in the large muscle groups of the legs, which occur during or in the hours following exercise. Oral quinine is sometimes used to treat nocturnal leg cramps in the general adult and elderly populations. However, its use is controversial secondary to concerns regarding efficacy and safety.

Efficacy of quinine in young athletes has not been well studied. A case series reported on 2 athletes: 1 college basketball player and 1 professional football player.¹ The basketball player experienced heat cramps during games that were resistant to hydration and dietary treatment. A regimen of 60 mg oral quinine sulfate taken 1 hour before game time and again at halftime eliminated cramps during the first game and the subsequent 15 games. The football player’s heat cramps were only partially improved with oral electrolyte repletion and oral hydration. However, he suffered no further cramps after initiating a regimen of 120 mg oral quinine sulfate before games and 60 mg oral quinine during games for an undisclosed period of time. Both players had normal blood chemistries before starting quinine. No side effects were mentioned.

Several trials involving the general adult population exist. A meta-analysis of 4 published and 3 unpublished reports of randomized, double-blind controlled crossover trials (n=409) showed that adult patients had significantly fewer nocturnal cramps when taking quinine compared with placebo.² The absolute reduction in number of leg cramps was 3.6 (95% confidence interval [CI], 2.15–5.05) over a 4-week period, and the relative risk reduction was 0.21 (95% CI, 0.12–0.30).

Two randomized controlled trials were not included in the meta-analysis discussed above. One double-blind, randomized, controlled parallel group trial of 98 adult patients with a mean age of 50 years demonstrated that a regimen of daily quinine sulfate therapy of 200 mg with the evening meal and 200 mg at bedtime significantly reduced the number of nocturnal muscle cramps compared with placebo.³ Over a 2-week treatment period the quinine group experienced a median of 8 fewer cramps (95% CI, 7–10), while the placebo group experienced a median of 6 fewer cramps (95% CI, 3–7). However, patient evaluation of global efficacy of treatment was not statistically significant between the quinine and placebo groups.

A second double-blind, randomized, controlled parallel group trial of 102 adult patients, mean age approximately 50 years, showed that a 2-week treatment period of hydroquinine (not available in the US) also produced a significant reduction in day- and nighttime muscle cramps compared with placebo.⁴ This study used a regimen of two 100-mg hydroquinine or placebo tablets with the evening meal and one 100-mg tablet or placebo at bedtime. The median difference in the number of cramps between the treatment and control groups was 5 (95% CI, 2–8).

It should be noted that during the 2 weeks immediately following the treatment period, numbers of cramps were still low compared with the pretreatment period and no significant difference was seen in number of cramps between groups. This raises suspicion that the improvement in both groups was due to the self-limited nature of cramps and represented the regression-to-the-mean phenomenon rather than a true treatment effect of hydroquinine. In addition, extrapolating results from studies of nocturnal cramps to heat cramps is problematic, as it is unknown whether these differ in physiology or cause.

Use of quinine for common cramps in nonathletes has been controversial. In 1994 the Food and Drug Administration (FDA) issued a statement banning over-the-counter sale of quinine for nocturnal leg cramps, citing lack of adequate data to establish efficacy and concern for potential toxicity.⁵ Between 1969 and 1990 the FDA received 26 adverse reaction reports in which quinine was concluded to be the causative agent. The 3 studies discussed above consistently mention only tinnitus as likely related to quinine use. However, the descriptions and inference testing of side effects were inadequate in each study.

Of note, quinine is a category X drug and should not be used during pregnancy.⁶

Recommendations from others

No specific recommendations exist regarding the use of quinine in athletes. The American Medical Society of Sports Medicine recommends rest, stretching, and oral hydration for simple heat cramps, and intravenous fluids for very severe cases.⁷ Several texts also recommend rehydration with an oral electrolyte solution, as well as rest, stretching, and massage.^8-10

Evidence summary

Leg cramps (heat cramps) in athletes are defined as painful involuntary muscle contractions, usually in the large muscle groups of the legs, which occur during or in the hours following exercise. Oral quinine is sometimes used to treat nocturnal leg cramps in the general adult and elderly populations. However, its use is controversial secondary to concerns regarding efficacy and safety.

Efficacy of quinine in young athletes has not been well studied. A case series reported on 2 athletes: 1 college basketball player and 1 professional football player.¹ The basketball player experienced heat cramps during games that were resistant to hydration and dietary treatment. A regimen of 60 mg oral quinine sulfate taken 1 hour before game time and again at halftime eliminated cramps during the first game and the subsequent 15 games. The football player’s heat cramps were only partially improved with oral electrolyte repletion and oral hydration. However, he suffered no further cramps after initiating a regimen of 120 mg oral quinine sulfate before games and 60 mg oral quinine during games for an undisclosed period of time. Both players had normal blood chemistries before starting quinine. No side effects were mentioned.

Several trials involving the general adult population exist. A meta-analysis of 4 published and 3 unpublished reports of randomized, double-blind controlled crossover trials (n=409) showed that adult patients had significantly fewer nocturnal cramps when taking quinine compared with placebo.² The absolute reduction in number of leg cramps was 3.6 (95% confidence interval [CI], 2.15–5.05) over a 4-week period, and the relative risk reduction was 0.21 (95% CI, 0.12–0.30).

Two randomized controlled trials were not included in the meta-analysis discussed above. One double-blind, randomized, controlled parallel group trial of 98 adult patients with a mean age of 50 years demonstrated that a regimen of daily quinine sulfate therapy of 200 mg with the evening meal and 200 mg at bedtime significantly reduced the number of nocturnal muscle cramps compared with placebo.³ Over a 2-week treatment period the quinine group experienced a median of 8 fewer cramps (95% CI, 7–10), while the placebo group experienced a median of 6 fewer cramps (95% CI, 3–7). However, patient evaluation of global efficacy of treatment was not statistically significant between the quinine and placebo groups.

A second double-blind, randomized, controlled parallel group trial of 102 adult patients, mean age approximately 50 years, showed that a 2-week treatment period of hydroquinine (not available in the US) also produced a significant reduction in day- and nighttime muscle cramps compared with placebo.⁴ This study used a regimen of two 100-mg hydroquinine or placebo tablets with the evening meal and one 100-mg tablet or placebo at bedtime. The median difference in the number of cramps between the treatment and control groups was 5 (95% CI, 2–8).

It should be noted that during the 2 weeks immediately following the treatment period, numbers of cramps were still low compared with the pretreatment period and no significant difference was seen in number of cramps between groups. This raises suspicion that the improvement in both groups was due to the self-limited nature of cramps and represented the regression-to-the-mean phenomenon rather than a true treatment effect of hydroquinine. In addition, extrapolating results from studies of nocturnal cramps to heat cramps is problematic, as it is unknown whether these differ in physiology or cause.

Use of quinine for common cramps in nonathletes has been controversial. In 1994 the Food and Drug Administration (FDA) issued a statement banning over-the-counter sale of quinine for nocturnal leg cramps, citing lack of adequate data to establish efficacy and concern for potential toxicity.⁵ Between 1969 and 1990 the FDA received 26 adverse reaction reports in which quinine was concluded to be the causative agent. The 3 studies discussed above consistently mention only tinnitus as likely related to quinine use. However, the descriptions and inference testing of side effects were inadequate in each study.

Of note, quinine is a category X drug and should not be used during pregnancy.⁶

Recommendations from others

No specific recommendations exist regarding the use of quinine in athletes. The American Medical Society of Sports Medicine recommends rest, stretching, and oral hydration for simple heat cramps, and intravenous fluids for very severe cases.⁷ Several texts also recommend rehydration with an oral electrolyte solution, as well as rest, stretching, and massage.^8-10

Evidence summary

Leg cramps (heat cramps) in athletes are defined as painful involuntary muscle contractions, usually in the large muscle groups of the legs, which occur during or in the hours following exercise. Oral quinine is sometimes used to treat nocturnal leg cramps in the general adult and elderly populations. However, its use is controversial secondary to concerns regarding efficacy and safety.

Efficacy of quinine in young athletes has not been well studied. A case series reported on 2 athletes: 1 college basketball player and 1 professional football player.¹ The basketball player experienced heat cramps during games that were resistant to hydration and dietary treatment. A regimen of 60 mg oral quinine sulfate taken 1 hour before game time and again at halftime eliminated cramps during the first game and the subsequent 15 games. The football player’s heat cramps were only partially improved with oral electrolyte repletion and oral hydration. However, he suffered no further cramps after initiating a regimen of 120 mg oral quinine sulfate before games and 60 mg oral quinine during games for an undisclosed period of time. Both players had normal blood chemistries before starting quinine. No side effects were mentioned.

Several trials involving the general adult population exist. A meta-analysis of 4 published and 3 unpublished reports of randomized, double-blind controlled crossover trials (n=409) showed that adult patients had significantly fewer nocturnal cramps when taking quinine compared with placebo.² The absolute reduction in number of leg cramps was 3.6 (95% confidence interval [CI], 2.15–5.05) over a 4-week period, and the relative risk reduction was 0.21 (95% CI, 0.12–0.30).

Two randomized controlled trials were not included in the meta-analysis discussed above. One double-blind, randomized, controlled parallel group trial of 98 adult patients with a mean age of 50 years demonstrated that a regimen of daily quinine sulfate therapy of 200 mg with the evening meal and 200 mg at bedtime significantly reduced the number of nocturnal muscle cramps compared with placebo.³ Over a 2-week treatment period the quinine group experienced a median of 8 fewer cramps (95% CI, 7–10), while the placebo group experienced a median of 6 fewer cramps (95% CI, 3–7). However, patient evaluation of global efficacy of treatment was not statistically significant between the quinine and placebo groups.

A second double-blind, randomized, controlled parallel group trial of 102 adult patients, mean age approximately 50 years, showed that a 2-week treatment period of hydroquinine (not available in the US) also produced a significant reduction in day- and nighttime muscle cramps compared with placebo.⁴ This study used a regimen of two 100-mg hydroquinine or placebo tablets with the evening meal and one 100-mg tablet or placebo at bedtime. The median difference in the number of cramps between the treatment and control groups was 5 (95% CI, 2–8).

It should be noted that during the 2 weeks immediately following the treatment period, numbers of cramps were still low compared with the pretreatment period and no significant difference was seen in number of cramps between groups. This raises suspicion that the improvement in both groups was due to the self-limited nature of cramps and represented the regression-to-the-mean phenomenon rather than a true treatment effect of hydroquinine. In addition, extrapolating results from studies of nocturnal cramps to heat cramps is problematic, as it is unknown whether these differ in physiology or cause.

Use of quinine for common cramps in nonathletes has been controversial. In 1994 the Food and Drug Administration (FDA) issued a statement banning over-the-counter sale of quinine for nocturnal leg cramps, citing lack of adequate data to establish efficacy and concern for potential toxicity.⁵ Between 1969 and 1990 the FDA received 26 adverse reaction reports in which quinine was concluded to be the causative agent. The 3 studies discussed above consistently mention only tinnitus as likely related to quinine use. However, the descriptions and inference testing of side effects were inadequate in each study.

Of note, quinine is a category X drug and should not be used during pregnancy.⁶

Recommendations from others

No specific recommendations exist regarding the use of quinine in athletes. The American Medical Society of Sports Medicine recommends rest, stretching, and oral hydration for simple heat cramps, and intravenous fluids for very severe cases.⁷ Several texts also recommend rehydration with an oral electrolyte solution, as well as rest, stretching, and massage.^8-10

Evidence summary

Hyperhomocysteinemia is defined as a fasting plasma homocysteine level 15 μmol/L, although levels >10 μmol/L appear to have detrimental effects on risk profiles for CAD and arteriosclerosis.¹ In 22 of 27 retrospective case-control studies, patients with CAD had significantly higher plasma homocysteine levels than control subjects (odds ratio [OR]=1.2–10.9, after adjustment for other CAD risk factors).^2,3 However, only 4 of 7 prospective nested case-control trials showed a correlation between elevated homocysteine and myocardial infarction (MI) and coronary death.²

A meta-analysis of 12 randomized controlled trials found that folate supplementation, with vitamin B₆ and B₁₂, reduces plasma homocysteine levels.⁴ However, the long-term clinical cons quences of these interventions are unknown. At doses of 1 gm/d folate has no known side-effects.⁵

Two randomized, placebo-controlled trials of folate reporting clinical endpoints have been completed. One study analyzed folate supplementation in a patient population with known, stable CAD and found no difference in clinical endpoints at 24 months.⁶ In this study, 593 patients were randomized to receive either 0.5 mg/d of folic acid or placebo. The primary study endpoint was a composite of events including: overall mortality, sudden death, MI, stroke, and major vascular surgery. The study was powered to detect a 50% reduction in clinical events based on existing observational data in populations with CAD. An event rate of 15% for the 2-year interval was assumed.⁶ All patients in this study were on statin therapy prior to initiation of folate supplementation.

The second study analyzed folate supplementation in 553 post-PCI patients. Patients were treated with 1 mg of folate plus 10 mg of vitamin B₆ and 400 μg of vitamin B₁₂ for 6 months after the PCI. After a mean follow-up of 11 months, the rate of restenosis requiring revascularization was lower in the vitamin-treated study arm (9.9% vs 16% restenosis rate; relative risk [RR]=0.62; 95% confidence interval [CI], 0.40–0.97; number needed to treat=16).⁷ There was also a nonsignificant trend toward fewer deaths and MIs in the treated arm at both 6 and 12 months after intervention (death: 1.5% vs 2.8%; RR=0.54; 95% CI, 0.016–1.7; MI: 2.6% vs 4.3%; RR=0.60; 95% CI, 0.24–1.51). Statin use was similar in both control (71%) and treatment groups (69%).

Recommendations from others

The American Heart Association and American College of Cardiology do not recommend the routine use of high-dose folic acid or B-vitamin supplements for the primary or secondary prevention of cardiovascular events. The AHA recommendation is to meet recommended daily allowances of folate (400 μg), B₁₂ (2.4 μg), and B₆ (1.7 mg) primarily through a balanced diet, with use of supplements if diet alone does not meet the above requirements.⁸ Since 1998, wheat flour has been supplemented with folate, adding an estimated 100 μg/day to the average American diet.⁸

The Canadian Task Force on Preventive Health Care (CTFPHC) finds insufficient evidence to advocate screening for hyperhomocysteinemia and rely on expert opinion to advocate treatment in select, high-risk populations.² Currently, the CTFPHC advocates meeting the recommended daily allowance of folate, B₁₂, and B₆.²

Evidence summary

Hyperhomocysteinemia is defined as a fasting plasma homocysteine level 15 μmol/L, although levels >10 μmol/L appear to have detrimental effects on risk profiles for CAD and arteriosclerosis.¹ In 22 of 27 retrospective case-control studies, patients with CAD had significantly higher plasma homocysteine levels than control subjects (odds ratio [OR]=1.2–10.9, after adjustment for other CAD risk factors).^2,3 However, only 4 of 7 prospective nested case-control trials showed a correlation between elevated homocysteine and myocardial infarction (MI) and coronary death.²

A meta-analysis of 12 randomized controlled trials found that folate supplementation, with vitamin B₆ and B₁₂, reduces plasma homocysteine levels.⁴ However, the long-term clinical cons quences of these interventions are unknown. At doses of 1 gm/d folate has no known side-effects.⁵

Two randomized, placebo-controlled trials of folate reporting clinical endpoints have been completed. One study analyzed folate supplementation in a patient population with known, stable CAD and found no difference in clinical endpoints at 24 months.⁶ In this study, 593 patients were randomized to receive either 0.5 mg/d of folic acid or placebo. The primary study endpoint was a composite of events including: overall mortality, sudden death, MI, stroke, and major vascular surgery. The study was powered to detect a 50% reduction in clinical events based on existing observational data in populations with CAD. An event rate of 15% for the 2-year interval was assumed.⁶ All patients in this study were on statin therapy prior to initiation of folate supplementation.

The second study analyzed folate supplementation in 553 post-PCI patients. Patients were treated with 1 mg of folate plus 10 mg of vitamin B₆ and 400 μg of vitamin B₁₂ for 6 months after the PCI. After a mean follow-up of 11 months, the rate of restenosis requiring revascularization was lower in the vitamin-treated study arm (9.9% vs 16% restenosis rate; relative risk [RR]=0.62; 95% confidence interval [CI], 0.40–0.97; number needed to treat=16).⁷ There was also a nonsignificant trend toward fewer deaths and MIs in the treated arm at both 6 and 12 months after intervention (death: 1.5% vs 2.8%; RR=0.54; 95% CI, 0.016–1.7; MI: 2.6% vs 4.3%; RR=0.60; 95% CI, 0.24–1.51). Statin use was similar in both control (71%) and treatment groups (69%).

Recommendations from others

The American Heart Association and American College of Cardiology do not recommend the routine use of high-dose folic acid or B-vitamin supplements for the primary or secondary prevention of cardiovascular events. The AHA recommendation is to meet recommended daily allowances of folate (400 μg), B₁₂ (2.4 μg), and B₆ (1.7 mg) primarily through a balanced diet, with use of supplements if diet alone does not meet the above requirements.⁸ Since 1998, wheat flour has been supplemented with folate, adding an estimated 100 μg/day to the average American diet.⁸

The Canadian Task Force on Preventive Health Care (CTFPHC) finds insufficient evidence to advocate screening for hyperhomocysteinemia and rely on expert opinion to advocate treatment in select, high-risk populations.² Currently, the CTFPHC advocates meeting the recommended daily allowance of folate, B₁₂, and B₆.²

Evidence summary

Hyperhomocysteinemia is defined as a fasting plasma homocysteine level 15 μmol/L, although levels >10 μmol/L appear to have detrimental effects on risk profiles for CAD and arteriosclerosis.¹ In 22 of 27 retrospective case-control studies, patients with CAD had significantly higher plasma homocysteine levels than control subjects (odds ratio [OR]=1.2–10.9, after adjustment for other CAD risk factors).^2,3 However, only 4 of 7 prospective nested case-control trials showed a correlation between elevated homocysteine and myocardial infarction (MI) and coronary death.²

A meta-analysis of 12 randomized controlled trials found that folate supplementation, with vitamin B₆ and B₁₂, reduces plasma homocysteine levels.⁴ However, the long-term clinical cons quences of these interventions are unknown. At doses of 1 gm/d folate has no known side-effects.⁵

Two randomized, placebo-controlled trials of folate reporting clinical endpoints have been completed. One study analyzed folate supplementation in a patient population with known, stable CAD and found no difference in clinical endpoints at 24 months.⁶ In this study, 593 patients were randomized to receive either 0.5 mg/d of folic acid or placebo. The primary study endpoint was a composite of events including: overall mortality, sudden death, MI, stroke, and major vascular surgery. The study was powered to detect a 50% reduction in clinical events based on existing observational data in populations with CAD. An event rate of 15% for the 2-year interval was assumed.⁶ All patients in this study were on statin therapy prior to initiation of folate supplementation.

The second study analyzed folate supplementation in 553 post-PCI patients. Patients were treated with 1 mg of folate plus 10 mg of vitamin B₆ and 400 μg of vitamin B₁₂ for 6 months after the PCI. After a mean follow-up of 11 months, the rate of restenosis requiring revascularization was lower in the vitamin-treated study arm (9.9% vs 16% restenosis rate; relative risk [RR]=0.62; 95% confidence interval [CI], 0.40–0.97; number needed to treat=16).⁷ There was also a nonsignificant trend toward fewer deaths and MIs in the treated arm at both 6 and 12 months after intervention (death: 1.5% vs 2.8%; RR=0.54; 95% CI, 0.016–1.7; MI: 2.6% vs 4.3%; RR=0.60; 95% CI, 0.24–1.51). Statin use was similar in both control (71%) and treatment groups (69%).

Recommendations from others

The American Heart Association and American College of Cardiology do not recommend the routine use of high-dose folic acid or B-vitamin supplements for the primary or secondary prevention of cardiovascular events. The AHA recommendation is to meet recommended daily allowances of folate (400 μg), B₁₂ (2.4 μg), and B₆ (1.7 mg) primarily through a balanced diet, with use of supplements if diet alone does not meet the above requirements.⁸ Since 1998, wheat flour has been supplemented with folate, adding an estimated 100 μg/day to the average American diet.⁸

The Canadian Task Force on Preventive Health Care (CTFPHC) finds insufficient evidence to advocate screening for hyperhomocysteinemia and rely on expert opinion to advocate treatment in select, high-risk populations.² Currently, the CTFPHC advocates meeting the recommended daily allowance of folate, B₁₂, and B₆.²

EVIDENCE-BASED ANSWER

Healthy women who urinate within 15 minutes of sexual intercourse may be slightly less likely to develop a urinary tract infection (UTI) than women who do not urinate afterward (grade of recommendation: D, extrapolation of single case-control study with nonsignificant findings).

Evidence summary

A literature review revealed only 1 small case-control study. The goal of this study was to identify possible risk factors for developing UTIs among young, healthy women who presented to the University of California at Los Angeles student health center.¹ A total of 225 women were enrolled in the study. Exclusion criteria included pregnancy, diabetes, vaginitis, can-didiasis, a history of more than 1 prior UTI, hospitalization, or catheterization 4 weeks before study enrollment. The women were surveyed regarding their dietary habits, clothing, sexual and urinary habits, and birth control methods used. From mid-stream urine samples, the authors identified 44 cases of UTI and 181 controls presenting to the health center without urinary symptoms or a history of UTI. A UTI was defined as the presence of more than 50,000 colony forming units of a single species of bacteria per milliliter of urine and the report of 1 or more of the following symptoms: painful urination, frequent urination, urination at night, and urgent need to urinate, or blood in the urine. A primary UTI case was further defined as a not having had a prior history of UTI; a secondary UTI case was defined as a patient who reported 1 prior UTI.

Women who urinated < 15 minutes after intercourse had an estimated relative risk (RR) of 0.40 (95% confidence interval [CI], 0.09–2.17) for developing a primary case of UTI, and an estimated RR of 0.92 (95% CI, 0.18–4.88) for developing a secondary UTI. These findings were not statistically significant, but the power was too low to rule out a potential effect.

This single small case-control study had several limitations. It was not a randomized controlled trial, which would be required to prove that post-coital voiding is an effective intervention. The study included only young, healthy women and excluded women with recurrent UTIs, a subpopulation of sexually active patients who may particularly benefit from the intervention. Finally, the study lacked adequate sample size to detect a small-to-moderate effect of postcoital voiding.

Recommendations from others

A major urology text does not specifically address the prevention strategy of postcoital voiding.² However, Griffith’s 5 Minute Clinical Consult recommends that women with frequent or intercourse related UTIs should “empty [their] bladder immediately before and following intercourse and consider post-coital antibiotic treatment.”³ Furthermore, the American College of Obstetricians and Gynecologists District II NYS recommends urinating after sexual intercourse to prevent recurrent cystitis.⁴

Read a Clinical Commentary by Jay Moreland, MD, online at http://www.FPIN.org.

EVIDENCE-BASED ANSWER

Healthy women who urinate within 15 minutes of sexual intercourse may be slightly less likely to develop a urinary tract infection (UTI) than women who do not urinate afterward (grade of recommendation: D, extrapolation of single case-control study with nonsignificant findings).

Evidence summary

A literature review revealed only 1 small case-control study. The goal of this study was to identify possible risk factors for developing UTIs among young, healthy women who presented to the University of California at Los Angeles student health center.¹ A total of 225 women were enrolled in the study. Exclusion criteria included pregnancy, diabetes, vaginitis, can-didiasis, a history of more than 1 prior UTI, hospitalization, or catheterization 4 weeks before study enrollment. The women were surveyed regarding their dietary habits, clothing, sexual and urinary habits, and birth control methods used. From mid-stream urine samples, the authors identified 44 cases of UTI and 181 controls presenting to the health center without urinary symptoms or a history of UTI. A UTI was defined as the presence of more than 50,000 colony forming units of a single species of bacteria per milliliter of urine and the report of 1 or more of the following symptoms: painful urination, frequent urination, urination at night, and urgent need to urinate, or blood in the urine. A primary UTI case was further defined as a not having had a prior history of UTI; a secondary UTI case was defined as a patient who reported 1 prior UTI.

Women who urinated < 15 minutes after intercourse had an estimated relative risk (RR) of 0.40 (95% confidence interval [CI], 0.09–2.17) for developing a primary case of UTI, and an estimated RR of 0.92 (95% CI, 0.18–4.88) for developing a secondary UTI. These findings were not statistically significant, but the power was too low to rule out a potential effect.

This single small case-control study had several limitations. It was not a randomized controlled trial, which would be required to prove that post-coital voiding is an effective intervention. The study included only young, healthy women and excluded women with recurrent UTIs, a subpopulation of sexually active patients who may particularly benefit from the intervention. Finally, the study lacked adequate sample size to detect a small-to-moderate effect of postcoital voiding.

Recommendations from others

A major urology text does not specifically address the prevention strategy of postcoital voiding.² However, Griffith’s 5 Minute Clinical Consult recommends that women with frequent or intercourse related UTIs should “empty [their] bladder immediately before and following intercourse and consider post-coital antibiotic treatment.”³ Furthermore, the American College of Obstetricians and Gynecologists District II NYS recommends urinating after sexual intercourse to prevent recurrent cystitis.⁴

Read a Clinical Commentary by Jay Moreland, MD, online at http://www.FPIN.org.

EVIDENCE-BASED ANSWER

Healthy women who urinate within 15 minutes of sexual intercourse may be slightly less likely to develop a urinary tract infection (UTI) than women who do not urinate afterward (grade of recommendation: D, extrapolation of single case-control study with nonsignificant findings).

Evidence summary

A literature review revealed only 1 small case-control study. The goal of this study was to identify possible risk factors for developing UTIs among young, healthy women who presented to the University of California at Los Angeles student health center.¹ A total of 225 women were enrolled in the study. Exclusion criteria included pregnancy, diabetes, vaginitis, can-didiasis, a history of more than 1 prior UTI, hospitalization, or catheterization 4 weeks before study enrollment. The women were surveyed regarding their dietary habits, clothing, sexual and urinary habits, and birth control methods used. From mid-stream urine samples, the authors identified 44 cases of UTI and 181 controls presenting to the health center without urinary symptoms or a history of UTI. A UTI was defined as the presence of more than 50,000 colony forming units of a single species of bacteria per milliliter of urine and the report of 1 or more of the following symptoms: painful urination, frequent urination, urination at night, and urgent need to urinate, or blood in the urine. A primary UTI case was further defined as a not having had a prior history of UTI; a secondary UTI case was defined as a patient who reported 1 prior UTI.

Women who urinated < 15 minutes after intercourse had an estimated relative risk (RR) of 0.40 (95% confidence interval [CI], 0.09–2.17) for developing a primary case of UTI, and an estimated RR of 0.92 (95% CI, 0.18–4.88) for developing a secondary UTI. These findings were not statistically significant, but the power was too low to rule out a potential effect.

This single small case-control study had several limitations. It was not a randomized controlled trial, which would be required to prove that post-coital voiding is an effective intervention. The study included only young, healthy women and excluded women with recurrent UTIs, a subpopulation of sexually active patients who may particularly benefit from the intervention. Finally, the study lacked adequate sample size to detect a small-to-moderate effect of postcoital voiding.

Recommendations from others

A major urology text does not specifically address the prevention strategy of postcoital voiding.² However, Griffith’s 5 Minute Clinical Consult recommends that women with frequent or intercourse related UTIs should “empty [their] bladder immediately before and following intercourse and consider post-coital antibiotic treatment.”³ Furthermore, the American College of Obstetricians and Gynecologists District II NYS recommends urinating after sexual intercourse to prevent recurrent cystitis.⁴

Read a Clinical Commentary by Jay Moreland, MD, online at http://www.FPIN.org.