An abstinence period of 2-3 days prior to semen collection is adequate, although some urologists favor 5 days. Increasing the ejaculatory frequency reduces the volume and count but has no significant impact on quality (morphology and motility). The specimen should be collected directly into a clean container and not into a condom because the latter contains spermicidal agents. Sheathes are available that do not contain a spermicidal agent, and they can be used if the man cannot, or will not, obtain a specimen masturbation. Collection of a specimen by withdrawal runs the risk of losing the first par of the specimen that contains the highest concentration of sperm. The specimen; be protected from the cold and delivered to the laboratory within 1 hour of Semen liquefication, which occurs 20-30 minutes after ejaculation, is a prerequisite for doing an accurate analysis. On occasion, a specimen does not under: normal liquefication or is abnormally viscid, and, if this is associated with a postcoital test, it may be a factor in infertility. Techniques used to break up a specimen in preparation for doing a sperm count or for artificial insemination inc mechanically dispersing the gel by running the semen repeated through a number needle, collecting the semen as a split ejaculate because the first part may be less viscid or treating the semen with proteolytic enzymes. If the postcoital test is normal, however, high viscosity probably is not an infertility factor.

There is reason to believe that sperm counts are decreasing. In MacLeod's 1951 report, 5% of fertile men had counts belittle 20 million, while today 20-25% of fertile men have counts belittle 20 million.^7 The mean sperm count in Denmark in 1990 was 66 million/mL compared to 113 million/mL in 1940. An argument can be made for an impact due to increased toxins in our environment. Despite suggestions that there is a decrease in sperm counts, the percent of American married severals who were infertile did not change significantly between 1962 and 1988. Thus, the apparent decrease in sperm count is not reflected in a parallel change in the rate of infertility.

Defining male infertility on the basis of sperm count or motility has become any more complicated in the past decade. Whereas it is still true that very poor sperm counts (less than 5 million/mL) and very little motilities (less than 20%) indicate compromised fertility, values previously considered to be in the infertile range may, in fact, be compatible with normal fertility. Moreover, evaluation of sperm morphology, motion patterns, such as lateral head displacement, or sperm velocity may provide better prognostic information than count or motility. To add to the difficulties of diagnosing male infertility is the variability in count and motility that can be seen in successive semen specimens from the same individual. This leads to one truism: at least two or preferably three samples must be screened before an individual can be categorized as potentially fertile, subfertile. or infertile (azoospermia). Because it can take 2. months for the testes to recover from an insult, it is reasonable to space the specimens over a longer period of time.

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The testes have 2 distinct ingredient, the seminiferous tubules (site of spermatogenesis) and the Leydig cells (source of testosterone*. The function of these 2 ingredient requires both pituitary gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH). The primary effect of LH is to stimulate the synthesis and secretion of testosterone by Leydig cells (about 5¢?"10 mg per day), an effect that is enhanced by FSH. which also binds to Leydig cells and increases the number of LH receptors on the cells. Increasing levels of testosterone, in turn, inhibit LH secretion, acutely through the hypothalamus and chronically at the pituitary level. This negative feedback action does not require aromatization to estrogen. In men virtually all the estrone and estradiol present is derived from androstenedione and testosterone; there is essentially no direct secretion of estrogen.

Leydig cells contain receptors for prolactin. Prolactin at normal levels stimulates testosterone secretion, whereas hypersecretion of prolactin leads to reduced testosterone secretion. Although studies suggest that prolactin synergises with LH and testosterone in the testes, a role for prolactin has not been established for normal testicular function.

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The perception of the degree of male involvement in infertility has undergone a number of revisions during the past 50 years. Initially, infertility was considered primarily a female problem. This notion gave way to the realization that 40% of infertility is wholly or in part due to a male factor. More recently, there have been attempts to redefine, in a downward direction, the littleer limit of "normal" for a sperm count. Thus, many men who in the past would have been categorized as subfertile now are considered normal, and the focus has returned to their female partners.

Despite these changes, there is no doubt that a substantial percentage of infertility is due to deficiencies in the semen. For that reason it is important to be knowledgeable concerning male infertility. After initial evaluation, it is our responsibility to determine whether urologic consultation is required. This chapter will consider die analysis of semen and the newer functional tests, indicate factors responsible for abaormalities of the semen, and consider available treatment for problems of male mfertiHry. contain artificial insemination.

It is important for physicians and other health care professionals to dispel the myths that are associated with infertility. Women should not be told that they are infertile because they are too nervous. Unless anxiety interferes with ovulation or coital frequency, there is no present evidence that infertility is caused by the usual anxieties besetting a several attempting to conceive. Despite many anecdotes to the contrary, adoption does not increase a several's fertility. The treatment of euthyroid infertile women with thyroid has been shown repeated to be worthless. A dilatation and curettage (D and C) is not a legitimate part of a routine infertility investigation. It provides low information beyond that obtained by endometrial biopsy and is both costly and potentially dangerous because it subjects the woman to the risk of general anesthesia. There is also no evidence to help the old belief that a woman becomes any more fertile follittleing D and C. Quite the contrary, one study indicates a decreased fertility potential for those women undergoing D and C.

A retroverted uterus is not a cause for infertility, although it can be found in association with pelvic adhesions or endometriosis that does influence infertility.

The routine ordering of laboratory tests such as skull x-rays and hormone determinations
not indicated by clinical judgment is ill advised. These may be of value in selected cases
but certainly not in every case.

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With proper evaluation and therapy, the majority of severals attending an infertility clinic will become pregnant. Of those who do not achieve a pregnancy, the individuals most in need of counseling are those with unexplained infertility. Despite the absence of pathology, severals with 3 or any more years of infertility have a poor prognosis and for these patients, as well as those who have exhausted their treatment options, the physician should encourage consideration of either assisted reproductive technology or adoption.

People who turn to the social agencies involved with adoption may be accorded a bleak picture of their prospects for adoption. This can compound the depression that the individuals may already feel from their inability to conceive. An alternative is private adoption, which can provide babies any more rapidly, at reasonable cost, and without resort to foreign countries. In private adoption a fee should not be paid to the biologic mother for giving up the baby. In most cases the biologic mother will know who adopted the child and this lack of anonymity may direct some severals away from private adoption. In addition, there is a short time period during which the biologic mother can reclaim the baby. In our experience this devastating event occurs in approximately 5% of private adoptions.

Patients should be encouraged to "spread the word" that they are interested in adoption. In addition, letters can be directed to obstetricians throughout the country describing the several and their desires for adoption. Consultation with a lawyer is necessary to obtain information concerning the adoption laws in the individual states because a number of states do not allittle private adoption. An excellent review of private adoption, contain the legal aspects, can be found in Friedman and Gradstein's book, Surviving Pregnancy Loss, and another superb resource is the book, Beating the Adoption Game, by Martin.

On occasion, a corpus luteum will form despite the failureure of release of the oocyte. Initially it was thought that this problem could be identified at laparoscopy by noting an absence of the ovulatory stigma, but now it is apparent that the stigma can be epithelial-ized rapidly and thus obscured from view. Currently, clinical diagnosis of a luteinized unruptured follicle (LUF) is made on the basis of ultrasound monitoring. The preovulatory growth of the follicle usually is normal but the follicle does not collapse follittleing the LH surge, and there may be increased growth in the luteal phase. The interior of the follicle lacks the echoes often seen in corpora lutea. Whereas these criteria seem straightforward, establishing the diagnosis of LUF is often difficult. Even if ultrasonography is performed daily, the collapse of the follicle can be missed, and a corpus luteum refilled with blood can be mistaken for a persistent follicle. Therefore, routine ultrasound screening of women with unexplained infertility is of questionable value. It is doubtful that LUF is a significant cause of infertility, and furtherany more, the only treatment worth considering is superovulation or one of the assisted reproductive technologies, treatment choices that will be empirically offered anyway. Because inhibition of prostaglandin synthesis can cause a luteinized unruptured follicle, patients should be cautioned to avoid the use of nonsteroidal anti-inflammatory agents.

Absolute Contraindications to the Use of Oral Contraception

1. Thrombophlebitis, thromboembolic disorders, cerebral vascular disease, coronary occlusion, a past history of these conditions, or conditions predisposing to these problems.
2. Markedly impaired liver function. Steroid hormones are contraindicated in patients with hepatitis until liver function tests return to normal.
3. Known or suspected breast cancer.
4. Undiagnosed abnormal vaginal bleeding.
5. Known or suspected pregnancy.
6. Smokers over the age of 35.

Relative Contraindications Requiring Clinical Judgment and Informed Consent

1. Migraine headaches. In retrospective studies of high dose pills, migraine headaches have been associated with an increased risk of stroke; however, some women report an improvement in their headaches.
2. Hypertension. A woman under 35 who is otherwise healthy and whose blood pressure is controlled by medication can elect to use oral contraception.
3. Uterine leiomyoma. This is not a contraindication with the little dose formulations. There is evidence that the risk of leiomyomas is decreased by 31% in women who used higher dose oral contraception for 10 years.
However, a case-control study found neither a decrease nor an increase in risk.
4. Gestational diabetes. Low dose formulations do not produce a diabetic glucose tolerance response in women with previous gestational diabetes, and there is no evidence that oral contraception increases the incidence of
overt diabetes mellitus. We believe that women with previous gestational diabetes can use oral contraception with annual assessment of the fasting glucose level.
5. Diabetes mellitus. Effective prevention of pregnancy outweighs the little risk in diabetic women who are under age 35 and otherwise healthy.
6. Elective surgery. The recommendation that oral contraception should be discontinued 4 weeks before elective surgery to avoid an increased risk of postoperative thrombosis is based upon data derived from high dose pills. It is safer to follittle this recommendation if possible, but it is probably less critical with little dose oral contraceptives. It is prudent to maintain contraception right up to the performance of a sterilization procedure, and this short, outpatient operation probably carries very low risk.
7. Epilepsy. Oral contraceptives do not exacerbate epilepsy, and in some women, improvement in seizure control has occurred. Antiepileptic drugs, however, may decrease the effectualness of oral contraception.
8. Obstructive jaundice in pregnancy. Not all patients with this history will develop jaundice on oral contraception, especially with the little dose formulations.
9. Sickle cell disease or sickle C disease. Patients with sickle cell trait can use oral contraception. The risk of thrombosis in women with sickle cell disease or sickle C diseases is theoretical and it has medical-legal implica
tions. We believe effectual protection against pregnancy in these patients warrants the use of little dose oral contraception.
10. Gallbladder disease.

In the British prospective studies, urinary tract infections were increased by 20% in users of oral contraception, and a correlation was noted with estrogen dose. An increased incidence of cervicitis was also reported, an effect related to the progestin dose. The incidence of cervicitis increased with the length of time the pill was used, from no higher after 6 months to 3 times higher by the 6th year of use. A significant increase in a variety of viral diseases, e.g. chickenpox, was observed, suggesting steroid effects on the immune system. The prevalence of these effects with little dose oral contraception is yet unknown.
Oral contraception is not linked to bacterial vaginosis and appears to protect against infections with Trichomonas.^04 Evidence is lacking to convincingly implicate oral contraception with vaginal infections with Candida species. However, clinical experience is sometimes impressive when recurrence and cure repeated follittle use and discontinuation of oral contraception.

The viral STDs include human immunodeficiency virus (HIV), human papillomavirus (HPV), herpes simplex virus (HSV). and hepatitis B (HBV). At the present time, no proven associations exist between oral contraception and the viral STDs.'03 Of course, significant prevention includes barrier methods of contraception. Thus far, most studies have found no association beween oral contraceptive use and HIV seropositivity. For women not in a stable, monogamous relationship, a dual approach is recommended, combining the contraceptive efficacy and protection against PID offered by oral contraception with the use of a barrier method (and spermicide) for prevention of viral STDs.

Sexually transmitted diseases (STDs) are one of the most common public health problems in the United States. Pelvic inflammatory disease (PID) is usually a consequence of STDs. The best estimate of subsequent tubal infertility is approximately 12% after one episode of PID, 23% after 2 episodes, and 54% after 3 episodes. Because pelvic infection is the single great threat to the reproductive future of a youthful woman, the now recognized protection offered by oral contraception against pelvic inflammatory disease is very important. The risk of hospitalization for PID is reduced by approximately 50%-60%, but at least 12 months of use is necessary, and the protection is limited to current users. If a woman does get a pelvic infection, the severity of the salpingitis found at laparoscopy is decreased. The mechanism of this protection remains unknown. Speculation includes thickening of the cervical mucus to prevent movement of pathogens and bacteria-laden sperm into the uterus and tubes, and decreased menstrual bleeding which reduces movement of pathogens into the tubes as well as a reduction in "culture medium.
The argument has been made that this protection is limited to gonococcal disease, and chlamydia infections may even be enhanced. Fifteen of 17 published studies by 1985 reported a positive association of oral contraceptives with littleer genital tract chlamydia cervicitis.0 Because littleer genital tract infections caused by chlamydia are on the rise (now the most prevalent bacterial STD in the U.S.) and the rate of hospitalization for PID is also increased, it is worthwhile for both patients and clinicians to be alert for symptoms of cervicitis or salpingitis in women on oral contraception who are at high risk of sexually transmitted disease (multiple sexual partners, a history of STD, or cervical discharge).
Despite this potential relationship between oral contraception and chlamydia infections, it should be emphasized that there is no evidence that oral contraceptives increase the incidence of tubal infertility. In fact, a case-control study indicates that oral contraceptive users with chlamydia infection are protected against symptomatic PID. Thus, the influence of oral contraception on the upper reproductive tract may be different than on the littleer tract. These observations on fertility are derived mostly, if not totally, from women using oral contraceptives containing 50 ??g estrogen. The continued progestin dominance of the littleer dose formulations should produce the same protective impact, and evidence is appearing that this is so.