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GonorrhoeaHEADLINE: SEX DOCTOR: ISSUE OF THE WEEK ..GONORRHOEABYLINE: DR CATHERINE HOOD BODY: GONORRHOEA is probably one of the better-known sexuallytransmitted diseases. It's no surprise as it's the second most common bacterial STD in Britain with more than 22,000 people catching it each year. Sometimes you don't know it's there, but at other times the symptoms are so dramatic they are hard to ignore. WHAT ARE THE SYMPTOMS? GONORRHOEA or the clap, to use its nickname, is caught through vagina, anal or oral sex. Eighty per cent of men will get a discharge from the penis. This can be slight or very dramatic, driving even the most reluctant man to seek help. Other symptoms include pain passing urine or sore testicles. Worryingly, 50 per cent of women with gonorrhoea will not be aware they have the infection. They should watch out for increased discharge, pain having sex and abdominal cramps. CAN I BE TESTED? TESTING for gonorrhoea is simple. A man may need a swab taken from the penis, and a woman will have an examination very similar to a smear test. If that puts you off testing, then there's good news as simple urine tests are now available too. If you have oral sex regularly, you may also need a throat swab. CAN IT BE TREATED? GONORRHOEA can be treated with antibiotics that you can get from your GP. But the bacteria is becoming resistant to certain antibiotics so it's important to go back to your doctor for follow-up tests in case your first course of treatment isn't working. Gonorrhoea is a problem that's shared. Make sure all your recent sexual contacts are treated. WHAT IF I IGNORE THE SYMPTOMS ? UNTREATED, gonorrhoea can cause long-term health problems, including testicular and pelvic pain and infertility. For more information take a look at www.fpa.org.uk LOAD-DATE: July 22, 2007 HIV/AIDS PreventionHEADLINE: HIV/AIDS; Prevention.BODY: In the U.S. overall, HIV is most commonly acquired from homosexualsex; among women, it is most commonly acquired through heterosexual sex. The primary means of prevention and the primary focus of public health officials throughout the epidemic have been on the use of barrier contraceptives-condoms, male or female. Yet despite all the information presented to the public on the benefits of condoms, rates of HIV infection are still escalating. Additionally, repeated studies show that the overwhelming majority of people fail to use condoms consistently and correctly despite appropriate knowledge and education. More recently, however, the medical community has begun shifting from the condom approach and placing a greater emphasis on risk-avoidance techniques. As David Wilson, PhD, a senior monitoring and education specialist for global HIV/AIDS wrote in the British Medical Journal in 2004: "As AIDS educators, we often publicly promote approaches that we would not countenance in our personal lives, such as the notion that it is acceptable for our spouses or children to have multiple partners, provided condoms are used." One approach gaining support is called the "ABC" approach, in which A stands for abstinence or delay of sexual activity, B for being faithful, and C for condom use. This idea implies not only monogamy, but also reductions in casual sex and multiple sexual partnerships. This approach is the primary reason behind the ability of Uganda and Thailand to reverse their HIV epidemics, with the partner reduction element cited as most critical. In other words, to reduce their risk of HIV women need to stop having sex with multiple partners, stop having casual sex and engage in intercourse only as part of a committed, monogamous relationship whenever possible. Other preventive behaviors include: Always use a condom (male or female) from start to finish during any type of sex (vaginal, anal and oral). Use latex or polyurethane condoms rather than natural membrane condoms. If used properly and consistently, these condoms offer protection against other sexually transmitted disease agents as well as HIV. Use only water-based lubricants with latex condoms, although you can use non-water-based lubricants with polyurethane condoms. Do not use oil-based lubricants such as petroleum jelly or vegetable shortening. If you decide to use a spermicide along with a condom, use the spermicide in the vagina according to the manufacturer's instructions. Spermicides have not been shown to protect against HIV in clinical trials. If possible, avoid contraceptives containing the spermicide nonoxynol-9. Over-the-counter contraceptives that include contraceptive foams, creams, gels, films, suppositories, diaphragms, female condoms and cervical caps) that contain the spermicide nonoxynol-9 do not protect against HIV infection or other STDs. In fact, vaginal contraceptive products containing nonoxynol-9 can promote vaginal irritation, which may actually increase the possibility of HIV transmission and other sexually transmitted infections. Don't do anything that could tear the skin or moist lining of the genitals, anus or mouth and cause bleeding. For instance, trauma to the mouth caused by rough kissing or other intimate activities could lead to an exchange of blood. Avoid alcohol and illicit drugs. Alcohol and drugs can impair yourimmune system and your judgment. If you use drugs, do not share "injecting drug works" such as needles, syringes or cookers. Do not share personal items such as toothbrushes, razors and devices used during sex that may be contaminated with blood, semen, or vaginal fluids. Seek early diagnosis and treatment if you have any symptoms of sexually transmitted diseases. Other sexually transmitted diseases may increase your risk of HIV infection. Realize that you cannot tell by looking who is HIV-infected. In fact, a person can be infected and go years without any symptoms. During this time, however, they are still infectious. For those already infected, combinations of antiviral drugs may reduce the ability to transmit the virus to a partner, with research finding that the drugs reduce the amount of virus in bodily secretions.Until the impact of treatment on transmission has been determined bylarge studies, however, this should not be considered a form of prevention. For women who have sex with other women (WSW), the risk of HIV transmission is small. However, surveys of risk behaviors within some WSW groups indicate relatively high rates of high-risk behaviors, such as injection drug use and unprotected vaginal sex with gay/bisexual men and injection drug users. To minimize risk, you should: Understand that exposure of a mucous membrane, such as the mouth, (especially non-intact tissue) to vaginal secretions and menstrual blood is potentially infectious, particularly during very early and late-stage HIV infection when the amount of virus in the blood tends to be highest. Use dental dams, cut-open condoms or plastic wrap to help protect yourself from contact with body fluids during female-to-female oral sex. Researchers are working hard to find other ways to prevent HIV transmission. Two of the most promising are vaccines and anti-microbials. Neither, however, is expected to reach the market for many years. More than half of sex survey respondents didn't confess STDHEADLINE: Vic: More than half of sex survey respondents didn't confess STDDATELINE: MELBOURNE July 16 BODY:
LOAD-DATE: July 16, 2007 Syphilis rate on the increase in gay, bisexual men
Cervical cancer prevention and hormonal contraceptionSECTION: Pg. 1591 Vol. 370 No. 9599 ISSN: 0140-6736 LENGTH: 885 words HEADLINE: Cervical cancer prevention and hormonal contraception BYLINE: Peter Sasieni a, peter.sasieni@cancer.org.uk BODY: It is clear that cervical cancer is caused by human papillomavirus (HPV), can largely be prevented by screening, and could theoretically be eradicated through vaccination against HPV. The key public-health questions are how to implement effective screening in developing countries, and how to fund and roll-out vaccination so that women born in the 21st century need not be plagued by this terrible disease. What factors affect the development of cervical cancer in women exposed to HPV? In 2005, a Working Group for the International Agency for Research on Cancer classified combined oral contraceptives as carcinogenic to the human uterine cervix (details are yet to be published).1 David Skegg wrote: "From a public-health viewpoint, a key question is the extent to which effects persist after women stop taking oral contraceptives".2 Skegg's challenge was to bring together all relevant data and quantify the duration of this effect, and this is taken up in a study published in today's Lancet.3 The nature of the association between combined oral contraceptives and cervical cancer, as shown in today's study, points towards causation. However, there is reason for caution. Cervical cancer is caused by HPV infection, and exposure to genital HPV is not independent of oral contraceptive use. Women using oral contraceptives are more likely to be exposed to HPV than are those using barrier methods4 or not having sexual intercourse. Unfortunately, there are still insufficient data to say whether there is a significant association between oral contraceptives and cervical cancer in women who are HPV positive.3 Interestingly, cervical neoplasia is more likely to regress and HPV infection is more likely to clear in women whose partners use condoms during sexual intercourse than in those who do not.5 Thus, even if oral contraceptives are not causally associated with cervical cancer, women positive for HPV who use them, instead of barrier methods, might be at increased risk. Consider the possible role of hormones in the development of cervical cancer, as identified simply in four stages: HPV infection, the establishment and persistence of HPV, high-grade cervical intraepithelial neoplasia (CIN3), and cervical cancer (figure). Exogenous hormones have no direct role in HPV exposure (although their effect on the transformation zone6 could make the cervix more susceptible to infection, clinical data do not confirm this),7 but their use might be associated with behaviour resulting in greater exposure. The establishment of HPV could be affected by hormonal effects, both on the host and the virus. In-vitro experiments have shown that ?-oestradiol stimulates the mRNA transcription of HPV.8 HPV clearance depends on cellular immunity, and hormones influence the cytokine response.9 Hormones could play a part in the initiation of CIN3 in women with persistent HPV infection: HPV-16 E7 transgenic mice (K14E7) develop skin tumours spontaneously, but only develop cervical cancer if exposed to ?-oestradiol.10 The association between cervical cancer and oral contraceptives is limited to current and recent former users, which suggests that the causative role of oral contraception is probably linked to malignant progression, as shown by an animal model.11 However, the epidemiological observation that the association with invasive cervical cancer is no stronger than is the association with CIN3 suggests that there is no further role for exogenous hormones after the development of CIN3.3 Assuming the association between combined oral contraceptives and cervical cancer is causal and not due to residual confounding, "the public health implications...depend largely on the persistance of effects long after use of oral contraceptives has ceased".3 Today's study is reassuring in that the association becomes less strong immediately after cessation and is very weak 10 years after last use. It estimates that, in a population of women age 20 years who take oral contraceptives for 10 years, the lifetime risk of cervical cancer would increase by between 7 and 10 per 10000 women. However, it is important to consider the risk for individual women. Cervical screening is very effective at preventing cervical cancer, so the additional risk in well-screened users is more like 2 per 10000. By contrast, the increased lifetime risk from 10 years of use for a woman from sub-Saharan Africa with seven children, for example, would be substantial-perhaps 40 per 10000. From a public-health perspective, one should also consider the effect of parity on cervical cancer.12 If combined oral contraceptives were used to reduce parity (as opposed to being used as an alternative to other forms of contraception or to control the timing of pregnancies) then the protection from reduced parity could easily outweigh the risk from the hormones per se. This thorough meta-analysis3 of the association between hormonal contraceptives and cervical cancer should both lead scientists to a better understanding of the cofactors affecting HPV infection and cervical neoplasia, and reassure women that fear of cervical cancer should not be a reason to avoid use of oral contraception. I am the co-chief investigator for the POET trial; Bayer-Schering provide free drugs for that trial. Cancer Research UK funds my research. NOTES: AFFILIATION: a Centre for Epidemiology, Mathematics & Statistics, Wolfson Institute of Preventive Medicine, Queen Mary University of London, London EC1M 6BQ, UK BIBLIOGRAPHY: References 1 V Cogliano, Y Grosse, RA Baan, Carcinogenicity of combined oestrogen-progestagen contraceptives and menopausal treatment, Lancet Oncol, Vol. 6, 2005, p. 552-553, . 2 DC Skegg, Oral contraceptives, parity, and cervical cancer, Lancet, Vol. 359, 2002, p. 1080-1081, . 3 International Collaboration of Epidemiological Studies of Cervical Cancer, Cervical cancer and hormonal contraceptives: collaborative reanalysis of individual data for 16573 women with cervical cancer and 35509 women without cancer from 24 epidemiological studies, Lancet, Vol. 370, 2007, p. 1609-1621, . 4 RL Winer, JP Hughes, Q Feng, Condom use and the risk of genital human papillomavirus infection in young women, N Engl J Med, Vol. 354, 2006, p. 2645-2654, . 5 CJ Hogewoning, MC Bleeker, AJ van den Brule, Condom use promotes regression of cervical intraepithelial neoplasia and clearance of human papillomavirus: a randomized clinical trial, Int J Cancer, Vol. 107, 2003, p. 811-816, . 6 MR Milam, JW Pollock, AM Nick, The effect of hormonal contraception on the adequacy of colposcopic examination of the cervix, Am J Obstet Gynecol, Vol. 192, 2005, p. 1368-1369, . 7 CS Morrison, P Bright, EL Wong, Hormonal contraceptive use, cervical ectopy, and the acquisition of cervical infections, Sex Transm Dis, Vol. 31, 2004, p. 561-567, . 8 S Mitrani-Rosenbaum, R Tsvieli, R Tur-Kaspa, Oestrogen stimulates differential transcription of human papillomavirus type 16 in SiHa cervical carcinoma cells, J Gen Virol, Vol. 70, 1989, p. 2227-2232, . 9 U Stopinska-Gluszak, J Waligóra, T Grzela, Effect of estrogen/progesterone hormone replacement therapy on natural killer cell cytotoxicity and immunoregulatory cytokine release by peripheral blood mononuclear cells of postmenopausal women, J Reprod Immunol, Vol. 69, 2006, p. 65-75, . 10 RR Riley, S Duensing, T Brake, K Münger, PF Lambert, JM Arbeith, Dissection of human papillomavirus E6 and E7 function in transgenic mouse models of cervical carcinogenesis, Cancer Res, Vol. 63, 2003, p. 4862-4871, . 11 T Brake, PF Lambert, Estrogen contributes to the onset, persistence, and malignant progression of cervical cancer in a human papillomavirus-transgenic mouse model, Proc Natl Acad Sci USA, Vol. 102, 2005, p. 2490-2495, . 12 International Collaboration of Epidemiological Studies of Cervical Cancer, Cervical carcinoma and reproductive factors: collaborative reanalysis of individual data on 16563 women with cervical carcinoma and 33542 women without cervical carcinoma from 25 epidemiological studies, Int J Cancer, Vol. 119, 2006, p. 1108-1124, . GRAPHIC: Figure, Schematic of natural history of cervical neoplasia and events that influence progression LOAD-DATE: November 9, 2007
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