SEARCHLIGHT Navigating the Global Medical Network Of Sexual Health Issues for Sexual Health Matters

You are welcome to this column in Sexual Health Matters that will regularly navigate the medical world to flag recent development in Sexual Health issues. There will be opportunity to take part in regular problem based searchlight medical exercises. The columnist welcomes regular feedback from readers through the feed back e-mail. Enjoy your reading.

Antiphospholipid Autoantibodies Syndrome is associated not only with recurrent abortion but also infertility.
Antiphospholipid syndrome is a multisystem disease with the predominant features of arterial and venous thrombosis, recurrent abortion, foetal death and the presence of antiphospholipid antibodies including lupus anticoagulant (LA) and anticardiolipin antibodies (aCL). Many epidemiological studies focus on antiphospholipid autoantibodies syndrome (APS) as a cause of recurrent spontaneous abortion (RSA). It is found that 7–25% of RSA would have APS as the main risk factor but 60% of recurrent spontaneous abortions are unexplained. "Association" not being synonymous with "cause", the proportion of abortions due to the APS is difficult to estimate for several reasons. This is because the definition of recurrent abortion is variable, the assays for antiphospholipid antibodies are not well standardised, and the inclusion of patients in the study group according to the antibody titre is author dependent. 
A very interesting review paper from Jeanne de Flandre Hospital in Lille Cedex, France 1 , examines recent studies on APS suggesting an association with infertility. New mechanisms are described by which antiphospholipid antibodies acting directly on the surface anticoagulant expressed on trophoblastic cells could cause placental thrombosis and infarction. Only lupus anticoagulant (LA) and anticardiolipin antibodies (aCL) assays are sufficiently standardised to be usable in routine practice. Testing for other antiphospholipid antibodies (aPLs) should remain investigational. Several treatments have been proposed. These include low doses of aspirin, low or immunosuppressive doses of corticosteroids, and preventive or effective doses of heparin, and intravenous immunoglobulin.

1. Vinatier D, Dufour P, Cosson M and Houpeau JL. Antiphospholipid syndrome and recurrent miscarriages. European Journal of Obstetrics & Gynecology and Reproductive Biology . Volume 96, Issue 1 , May 2001 , Pages 8-20.

Endometriosis revisited
Endometriosis is often referred to as a subject of theories. The oldest theory that of metaplasia suggests that under diverse influences, coelomic tissue could be transformed into endometrium. The most often cited theory, that of implantation, proposes that the physiological phenomenon of endometrial reflux into the fallopian tubes during menstruation may, in certain conditions, overcome local defence mechanisms, hence implant, and proliferate. The peritoneal fluid in unaffected women possesses the capacity to prevent endometriotic tissue from becoming established. The reasons for the occurrence of endometriosis and its consequences (pain, sterility, adhesions) are probably numerous. They involve the endometrium, the immune system (macrophages, natural killer cells), the peritoneum, and fallopian tubes. Failure to clear the peritoneal cavity of fragments of endometrium could cause a state of local inflammation with hyperactivity of macrophages secreting a variety of different compounds. Some of these compounds may bring about metaplasia of the peritoneum or the development of Mullerian residues. The subject is further discussed in an interesting review paper from France by Vinatier et al 1 .

1. Vinatier D., Orazi G., M. Cosson and Dufour P. Theories of endometriosis. European Journal of Obstetrics & Gynecology and Reproductive Biology. Volume 96, Issue 1 , May 2001, Pages 21-34 

Effectiveness of Metformin in restoring regular menstrual cycles, ovulation and pregnancy in women with polycystic ovarian syndrome (PCOS).
In a systemic review of pertinent studies using bibliographic databases including Medlars-On-Line (MEDLINE) and EMBASE, Costello et al 1 looked at thirty published studies (12 randomized controlled trials, 2 cohort studies, and 16 uncontrolled descriptive studies) on PCOS treated with Metformin with or without ovulation induction / IVF.
The combined data of the observational uncontrolled descriptive studies tentatively indicate that PCOS patients undergoing treatment with metformin for between 3 to 6 months have a 60% chance of restoration of regular menses and ovulation, with no good data available on pregnancy. The addition of Clomiphene Citrate (CC) to metformin for a total duration of 8 to 9 months results approximately in 66% chance of ovulation and 34% chance of pregnancy. For CC-resistant PCOS patients, however, this chance of ovulation and pregnancy are in the order of 40% and 25%, respectively. 
The data from controlled studies, almost all from RCTs, demonstrate that metformin alone is beneficial in restoring regular menses and inducing ovulation. There are no data supporting an improved pregnancy rate in metformin monotherapy. However, the addition of metformin to CC results in an improved ovulation and pregnancy rate in both unselected and CC-resistant PCOS patients. These conclusions are based on limited data from a small number of clinical trials, and included predominately obese PCOS patients. There are at present no data demonstrating an improvement in restoration of menses, ovulation, or pregnancy in non-obese PCOS patients treated with either metformin monotherapy or metformin in combination with CC. 
There is a need for well-designed, prospective, perhaps multicentre, randomized controlled trials with adequate sample size and power to make firm conclusions about the effectiveness and role of metformin with or without CC in restoring fertility in an-ovulatory women with PCOS.

1. Costello MF, and. Eden JA. A systematic review of the reproductive system effects of Metformin in patients with polycystic ovary syndrome. European Journal of Obstetrics & Gyneacology and Reproductive Biology Volume 96, Issue 1 , May 2001 , Pages 37-50.

Female Sexual Dysfunction: Definition and Therapy
There is no consensus about definition and treatment of female sexual dysfunction. This makes it difficult to design studies of specific interventions and guide choices in medical therapy. A recent effort at defining female sexual dysfunction has come from an international multidisciplinary group in an attempt to create a definition that would be more useful in all types of clinical practice and have more relevance to ongoing outcomes research1. They separate sexual dysfunction into four categories, as follows: 
1. Sexual desire disorders Hypoactive sexual desire disorder 
Sexual aversion disorder
2. Sexual arousal disorder 
3. Orgasmic disorder
4. Sexual pain disorders Dyspareunia 
Vaginismus 
Other sexual pain disorders 
The particular category of dysfunction must be persistent or recurrent, and it must cause personal distress to meet the definition of sexual dysfunction.
The National Health and Social Life study looked at 1749 women ages 18–59 years and found that the overall prevalence of female sexual dysfunction was 43% 2. When these complaints were categorized, 22% of women reported low sexual desire, 14% reported arousal difficulties, and 7% reported sexual pain. This study found that women who have an increased risk of sexual dysfunction tend to be younger, unmarried, have lower levels of education and social status, and be African-Americans. Finally, this study found that higher levels of sexual dysfunction among women negatively impact quality of life.
Medical treatment options are discussed in an article published in primary Care Update for Obstetrics and Gynaecology by Mark and Shifren 3.

1. R. Basson, J. Berman, A. Burnett et al., Report of the international consensus development conference on female sexual dysfunction: definitions and classifications. J Urol 163 (2000), pp. 888–893
2. E.O. Laumann, A. Paik and R.C. Rosen, Sexual dysfunction in the United States: prevalence and predictors. JAMA 281 (1999), pp. 537–544.
3. Mark A and Shifren J. Medical Therapy for female sexual dysfunction. Primary Care Update for OB/GYN Vol. 10, (1), Jan-Feb 2003, Pages 40-43.

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