Sunday, July 6, 2008

Pathogens Other Than Chlamydia Linked to Postgonococcal Urethritis

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Pathogens Other Than Chlamydia Linked to Postgonococcal Urethritis


By Megan Rauscher

NEW YORK (Reuters Health) Oct 11 - Urethritis that persists after successful eradication of laboratory-confirmed gonococcal infection (i.e., postgonococcal urethritis) is significantly associated with Mycoplasma genitalium or Ureaplasma urealyticum biovar 2 coinfection, independent of Chlamydia trachomatis infection, Japanese researchers report.

These observations have implications for presumptive therapy, they note in a report in the October 1 issue of Clinical Infectious Diseases.

Among a cohort of 390 men with documented gonorrhea, the researchers found that 33.8% were coinfected with C. trachomatis, M. genitalium, and/or U. urealyticum biovar 2, based on PCR testing of first-voided urine at the initial visit.

Among men who returned for a follow up exam 7 to 10 days after treatment with either a cephalosporin or spectinomycin, gonorrhea was eradicated in 291. However, of these, 104 (35.7%) were found to have postgonococcal urethritis, based on the presence of polymorphonuclear leukocytes in the urethral smear.

In men with Chlamydia-negative gonococcal urethritis, coinfection with M. genitalium was associated with a greater than 14-fold increased risk of postgonococcal urethritis and coinfection with U. urealyticum biovar 2 was associated with about a 3.6-fold greater risk of postgonococcal urethritis.

"In this study, we provide additional data suggesting that M. genitalium and U. urealyticum (biovar 2) may be pathogens of non-gonococcal urethritis, including post-gonococcal urethritis," senior author Dr. Takashi Deguchi, of the Graduate School of Medicine, Gifu University, told Reuters Health.

"In clinical settings, no sensitive and rapid tests for detection of these pathogens are commercially available," Dr. Deguchi pointed out. Therefore, "Patients with gonococcal urethritis should be treated presumptively with antimicrobial agents that are active against C. trachomatis and these pathogens."

The authors of a related commentary point out that the United States and many other countries (excluding Japan) currently recommend presumptive therapy for chlamydial infection for men with gonorrhea.

However, mounting evidence that doxycycline may not be "sufficiently effective" against M. genitalium and U. urealyticum biovar 2 has raised the question of whether azithromycin should be substituted as presumptive therapy for urethritis, Dr. Lisa E. Manhart and colleagues from the University of Washington, Seattle note.

Double-blind, randomized studies are underway to determine which of these drugs is optimal for M. genitalium, U. urealyticum biovar 2, U. parvum, and idiopathic urethritis. Results are expected in 2010.

In the meantime, Dr. Manhart and colleagues say, "the choice of therapy for urethritis must still be individualized, based primarily on considerations of cost to patients and programs, patient preference, and efforts to optimize compliance."

Clin Infect Dis 2007;45:866-874.
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Screening for Chlamydia expanded

bacterial infections There are plans to introduce a screening programme for the sexually transmitted infection Chlamydia to Jersey next year.

The bacterial infection can affect a woman's fertility if untreated.

About 40% of the young people in Jersey have been tested for the infection and the screening service is only available to a limited number of people.

But Dr Ivan Muscat from the Health Department hopes it will be available on a widespread basis next year.

"We are going to encourage both men and women to come forward for testing," he said.

Chlamydia affects about 9% of screened people under 25 in Jersey.


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Mass Treatment With Azithromycin Reduces Prevalence of Trachoma

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Mass Treatment With Azithromycin Reduces Prevalence of Trachoma


Laurie Barclay, MD

Nov. 3, 2004 — Mass treatment with azithromycin is effective for reducing the prevalence of trachoma, according to the results of a study published in the Nov. 4 issue of the New England Journal of Medicine.

"Trachoma, caused by repeated ocular infection with Chlamydia trachomatis, is an important cause of blindness," write Anthony W. Solomon, MB, BS, PhD, from the London School of Hygiene and Tropical Medicine, U.K., and colleagues. "Current recommended dosing intervals for mass azithromycin treatment for trachoma are based on a mathematical model."

In a Tanzanian community in which trachoma was endemic, the investigators collected conjunctival swabs for quantitative polymerase-chain-reaction assay of C trachomatis before and at two, six, 12, 18, and 24 months after mass treatment with azithromycin. Residents who had clinically active trachoma at six, 12, and 18 months received tetracycline eye ointment.

At baseline, 956 (97.8%) of 978 residents received either one oral dose of azithromycin or a course of tetracycline eye ointment if azithromycin was contraindicated. Infection prevalence was 9.5% before mass treatment, 2.1% at two months, and 0.1% at 24 months.

Compared with the pretreatment level, the quantitative burden of ocular C trachomatis infection in the community was 13.9% at two months and 0.8% at 24 months. At each time point after baseline, subjects who had been positive at their previous test constituted more than 90% of the total community burden of C trachomatis infection.

"The prevalence and intensity of infection fell dramatically and remained low for two years after treatment," the authors write. "One round of very-high-coverage mass treatment with azithromycin, perhaps aided by subsequent periodic use of tetracycline eye ointment for persons with active disease, can interrupt the transmission of ocular C. trachomatis infection."

Study limitations include lack of placebo control and inability to rule out alternative explanations for decreased incidence of infection, such as enhanced personal hygiene among study participants, a reduction in the density of eye-seeking flies in the village, a small contribution from a regional secular trend, or tetracycline treatment in residents with active cases at six, 12, and 18 months.

The Wellcome Trust/Burroughs Wellcome Fund, the Edna McConnell Clark Foundation, the International Trachoma Initiative, and the Medical Research Council supported this study.

In an accompanying editorial, Silvio P. Mariotti, MD, from the World Health Organization in Geneva, Switzerland, urges caution in analyzing the results of this study, but he calls the unusually high coverage achieved "an outstanding and encouraging result."

"Although the social-development components of the SAFE strategy [surgery, antibiotics, facial cleanliness, and environmental improvement] must still be implemented in communities in which trachoma is endemic to ensure the continued elimination of blinding trachoma, the findings of Solomon et al. provide useful, new information on what antibiotic treatment can achieve," Dr. Mariotti writes. "Increased knowledge of the effect of different components of the SAFE strategy can be of great help to poor communities that have already paid too high a toll in the form of preventable blindness."

N Engl J Med. 2004;351:1962-1971, 2004-2007

Reviewed by Gary D. Vogin, MD
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Saturday, July 5, 2008

Doxazosin With Finasteride Effective Against BPH.

Doxazosin With Finasteride Effective Against BPH. By NATURAL EVENT OFpainter Douglas NEW YORK (Reuters Health) Jan 11 - Unit therapy with doxazosin and finasteride is more effective against benign prostatic hyperplasia (BPH) in men with moderate size or enlarged prostates than is either functionary alone, researchers figuring in the January thinking of the Book of Urology. In fact, lead investigator Dr. Kaplan told Reuters Welfare that "essentially, this work demonstrated that we can consider redefining what a large prostate is. Sum as defined by changes in disease patterned move versus therapy with gathering therapy was noted at prostate sizes of 25 to 40 mL." Dr. Kaplan, who is currently at Ezra Cornell Cogent evidence, New York, and colleagues came to this close mass enquiry of data from a assiduousness involving more than 3000 men who had lower urinary methodicalness symptoms secondary winding coil to BPH. They were randomized to 4 to 8 mg of doxazosin, 5 mg of finasteride, a connexion of both agents, or medicament. The norm tending time was 4.5 life. In patients with a size prostate (total intersection of less than 25 mL) union therapy was no combatant than doxazosin alone. However, in patients with moderate intensity level (less than 40 mL) or a large prostate (more than 40 mL) the mathematical cognition was more effective than either adjudicator alone. The improvements included a decreased risk of clinical proffer, a reduced need for invasive therapy, an improved English language West Germanic Urinary Administration cause damage and an increased edge urinary flow rate.
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Thursday, July 3, 2008

Tobacco Education: Emphasizing Impotence as a Consequence of Smoking

impotence

Tobacco use is well-known to be a significant health concern. Nevertheless, millions of men and women around the world continue to use tobacco products. Most antitobacco education and advertising efforts have focused on the traditional warnings of lung cancer, heart disease, and pregnancy complications. However, in the last two decades, the link between smoking and impotence has been described by various authors.[1-12] Despite this, impotence is not well recognized by the general public or even by general practice medical providers as a potential consequence of smoking. Pharmacists and other health professions are missing an opportunity to teach smokers about another good reason to kick the habit.

Literature regarding smoking and impotence describes various mechanisms for the link. McVary et al.[1] published a comprehensive review in 2001 that examined clinical and scientific studies. The investigators found evidence that impotence can be caused directly by smoking-induced reductions in nitric oxide concentrations, which impair endothelium-dependent relaxation of arteries, and indirectly by smoking-induced atherosclerosis.

The likelihood of impotence or erectile dysfunction (ED) in men who smoke has also been described by various authors. The review by McVary et al.[1] indicated that smoking may increase the risk of moderate or complete impotence by two times that of nonsmokers and that smoking cessation may decrease impotence risk. Austoni et al.[9] found that after adjustment for confounding variables, Italian men who smoked more than 10 cigarettes per day and former smokers had significantly higher risks (odds ratio [OR] 1.4 and 1.3, respectively; both p < 0.0001) for ED. Shiri et al.[11] demonstrated similar but nonsignificant findings in Finnish men: OR 1.4 for smokers (95% CI, 0.9–2.3) and 1.3 for former smokers (95% CI, 0.9–1.9). Polsky et al.[12] found that Canadian men with ED were twice as likely to be former smokers (OR 2.2; 95% CI, 1.2–3.9) but that current smoking did not significantly increase ED risk.

Recently, a U.S. epidemiologic study of 1329 white men (smokers and nonsmokers) showed that 15% reported suffering from impotence.[7] The authors concluded that the relative OR of impotence in smokers or past smokers compared with nonsmokers was significant at 1.46 (95% CI, 1.05–2.02). When adjustments were made for age and for age and comorbidity, the relative OR became nonsignificant at 1.42 (95% CI, 1.00–2.02) and 1.38 (95% CI, 0.97–1.97), respectively. A dose–response relationship suggesting that men with a longer smoking history had a higher likelihood of impotence was also seen. In men with greater than a 29-pack-year history, the relative ORs of impotence were significant at 2.08 (95% CI, 1.41–3.08) compared with 1.34 (95% CI, 0.88–2.07) in those with a 12.6–29.0-pack-year history and 0.92 (95% CI, 0.58–1.46) in those with a 1–12.5-pack-year history. When adjustments were made for age and for age and comorbidity, the relative OR for the greater than 29-pack-year group was reduced but still significant at 1.69 (95% CI, 1.10– 2.58) and 1.60 (95% CI, 1.04–2.46), respectively. Interestingly, when the authors stratified the data by age from current smokers and from men who formerly or never smoked, smokers in their 40s had the greatest relative OR of having impotence (2.74; 95% CI, 0.44–16.89).

Unfortunately, not only does smoking tobacco appear to increase impotence risk, data suggest it also predicts a poor response to popular pharmacologic treatment for impotence. Park et al.[13] found that current smoking was significantly associated with sildenafil failure in men over the age of 60 years suffering from impotence (OR 1.34; 95% CI, 1.04–3.52; p = 0.015). The lack of effect was likely due to the failure of sildenafil to potentiate endogenous nitric oxide-mediated vascular responses—responses that are reduced in smokers.[14] Since all phosphodiesterase inhibitors, such as sildenafil, exert their effect through nitric oxide modulation, this therapeutic failure may be a class effect.Effect of Smoking Cessation on Impotence

Data are mixed regarding the usefulness of smoking cessation in smokers to improve erectile function or reverse ED. Some studies have indicated that men who are former smokers are still more likely to have ED than nonsmokers.[9,11,12] Shiri et al.[11] indicated that recovery from ED is reduced in those currently smoking (adjusted OR 0.6; 95% CI, 0.2–1.4) and in former smokers (adjusted OR 0.7; 95% CI, 0.3–1.3) compared with nonsmokers, but the results were not statistically significant and the overall number of patients in this analysis was low. However, results from a study by Derby et al.[15] suggested that smoking cessation in young adulthood (versus later in life) may be necessary to reduce the risk of ED.

A small, prospective study by Guay et al.[16] indicated that smoking cessation significantly decreases the risk of ED. This study evaluated acute changes in smoking status in 10 smokers (ages 32–62 years) using the RigiScan portable home monitor (Dacomed/Urohealth, Minneapolis, MN), which measures penile tumescence and rigidity. At the time of the study, all patients were smoking at least one pack of cigarettes per day and had smoked for at least 30 pack-years. Men were monitored for two nights: one when they smoked and one when they did not smoke for 24 hours. In addition, four men were monitored after smoking cessation (using nicotine patches) for one month. Results of the study showed that after not smoking for 24 hours, the men had a statistically significant improvement in penile tumescence and rigidity (p < 0.05 for all measures). In addition, sustained improvement in ED was found in the four men who were monitored after one month of nicotine replacement and smoking cessation, indicating that nicotine may not be the only mediator of ED from smoking.

A long-term prospective study evaluating whether smoking cessation can improve ED in smokers was recently published. Pourmand et al.[17] evaluated smokers ages 30–60 years who requested nicotine replacement therapy (NRT) for smoking cessation and who also complained of ED starting at least five years after starting to smoke. Of the 2837 smokers, 22.5% (n = 637) reported having ED and 54.3% (n = 346) of those with ED had no other risk factors for ED besides smoking. Those patients without other ED risk factors were followed for one year after stopping NRT. They were then classified as current smokers (those who continued to smoke) or as former smokers (those who stopped smoking with NRT). Results indicated there was a relatively significant correlation between pack-years of smoking and ED status in all patients (Spearman's correlation coefficient, 0.533). At follow-up, there were 118 former smokers and 163 current smokers. The ED status improved by at least one grade in 30 (25%) of the former smokers but in none of the current smokers. Moreover, more current smokers had deterioration in their erectile function: 3 (2.5%) former smokers versus 11 (7%) current smokers. Overall, former smokers tended to have a significantly better ED status after follow-up compared with current smokers (p = 0.09).

In addition to potentially benefiting the health and erectile status of men with ED, smoking cessation may also affect their treatment for ED. Park et al.[13] suggested that stopping or reducing the consumption of cigarettes may ensure better efficacy with sildenafil for the treatment of ED.Tobacco Education and Advertising Regarding Impotence

Two U.S. states and some countries have strived to increase the public's knowledge of the detrimental effects of tobacco on erectile function in an attempt to reduce smoking. In the late 1990s, the California Department of Health Services introduced a one-year marketing campaign targeting the link between smoking and impotence.[18] Newspaper headlines read "The Marlboro Man needs Viagra" and "What Viagra may give, tobacco taketh away." Hawaii followed suit with the "limp" television campaign geared toward 18–24-yearold men.[19] These campaigns were not the first to target impotence as a reason to stop smoking, but they were the most impressive. Unfortunately, published data describing the effects of these advertising campaigns are not available (Stevens CM, personal communication, 2005 Aug 29). However, a 2006 news release from the California Department of Health Services indicates that smoking rates in California have continued to decline since 1996 and are currently at an all-time low of 14%, 25% less than the rest of the nation.[20]

In 2000, Thailand became the first country to go beyond advertising by placing impotence warnings and pictures on cigarette labeling.[21] Subsequently, Canada and Brazil implemented similar warnings on their cigarette packages.[22,23] Currently, the United Kingdom is considering adding various picture warnings to cigarette packages, some of which say that "smoking may reduce the blood flow and causes impotence."[24] Data regarding the results of cigarette labeling indicate that graphic cigarette warning labels reach their intended audience and serve as an effective population-based smoking-cessation intervention.[22] Unfortunately, U.S. requirements are lagging behind other countries, as cigarette manufacturers are only required to include traditional warnings from the U.S. Surgeon General regarding heart disease, lung cancer, emphysema, and complications with pregnancy.Threat of impotence as a Motivator for Smoking Cessation.

On the basis of the association between smoking and impotence and data supporting the benefits of smoking cessation on impotence, it seems logical that this topic be included in smoking-cessation programs. Moreover, data support that there is a need for this information to be communicated to smokers, as a majority of men appear to be unaware that smoking increases ED risk. In a survey of Hong Kong men,[25] only 13.9% were aware of the link between impotence and smoking, and only 12% of British smokers were aware in a 1999 survey.[26] Results of a study conducted by Shiri et al.[11] indicated that smokers with ED were more likely to stop smoking than smokers without ED (23% versus 12.6% stopped, respectively), but the results were not statistically significant likely because of the low numbers of patients in the analysis.

Recently, a small survey in the United States investigated the issue of using impotence as a motivator for smoking cessation.[27] Male smokers ages 18 years and older were surveyed at a local health fair in Denver, Colorado, in April 2004. Surveys were voluntary and anonymous. Participants were surveyed to determine if they knew that smoking increases impotence risk and that regular smoking may reduce impotence drug-treatment response and to assess what effect the risk of impotence would have on their decision to continue smoking.

Sixty-two surveys were completed. Most of the men surveyed were middle age (65% ages 41–60 years) and white (76%). Smoking habits were evenly distributed among 6–10, 11–20, and 21–30 cigarettes smoked per day. The majority of men had attempted to quit smoking at least once, with over one quarter attempting six or more times.

Thirty-four men (55%) stated they were aware that smoking tobacco increases impotence risk, and 56% of the surveyed men maintained that they would be "somewhat more likely" or "much more likely" to stop smoking because of the link between smoking and impotence. Of the men who stated they were unaware of the increased risk of impotence due to smoking, 57% stated they would be somewhat more likely or much more likely to stop smoking. Overall, 39%, 37%, and 19% stated the relationship between smoking and impotence had no effect on their decision to continue smoking, made them somewhat more likely to stop smoking, and made them much more likely to stop smoking, respectively. Three men did not respond to this question.

In total, six men (10%) stated they suffered from impotence; of these, one smoked 6–10 cigarettes per day, two smoked 11–20 cigarettes per day, and three smoked 21–30 cigarettes per day. Three of the impotent men stated they were unaware of the link between impotence and smoking, and five stated that the link made them somewhat more likely or much more likely to stop smoking. Only one impotent man stated that impotence would not affect his decision to continue smoking. Thus, 96% of the men (23 of 24) who planned to continue smoking were not impotent. Overall, 23 men (37%) stated they were aware that smoking could potentially reduce the effects of pharmacologic agents (i.e., sildenafil, vardenafil, and tadalafil) used to treat impotence.Implications for Pharmacists

Pharmacists and other health care providers involved in smoking-cessation programs are ideally situated to educate patients about the association between smoking and impotence. A majority of men will likely respond to smoking-cessation education that is focused on impotence risk, especially if they are already impotent. Younger smokers may be more likely to alter their smoking habits on the basis of potential impotence risk rather than remote threats of heart and lung disease. Moreover, health education programs in schools could incorporate impotence into their discussions of tobacco risks to encourage youths to avoid tobacco altogether.Conclusion

The link between smoking and impotence should be used by pharmacists and other health providers to help motivate men to quit smoking.  Printer- Friendly Email This

References

Am J Health-Syst Pharm.  2006;63(24):2509-2512.  ©2006 American Society of Health-System Pharmacists
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Tuesday, July 1, 2008

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Thursday, June 26, 2008

Dermatology, March 2007.

Graeme Lipper, MD
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