Male primary or hypergonadogropic hypogonadism is often treated with testosterone replacement therapy if they are not trying to conceive. Adverse effects of testosterone replacement therapy include increased cardiovascular events (including strokes and heart attacks) and death. The Food and Drug Administration (FDA) stated in 2015 that neither the benefits nor the safety of testosterone have been established for low testosterone levels due to aging. The FDA has required that testosterone pharmaceutical labels include warning information about the possibility of an increased risk of heart attacks and stroke.

Commonly used testosterone replacement therapies include transdermal (through the skin) using a patch or gel, injections, or pellets. Oral testosterone is no longer used in the U.S. because it is broken down in the liver and rendered inactive; it also can cause severe liver damage. Like many hormonal therapies, changes take place over time. It may take as long as 2–3 months at optimum level to reduce the symptoms, particularly wordfinding and cognitive dysfunction. Testosterone levels in the blood should be evaluated to ensure the increase is adequate. Levels between 400 and 700 ng/dL are considered appropriate mid-dose levels. Treatment usually starts with 200 mg intramuscular testosterone, repeated every 14 days.

While historically, men with prostate cancer risk were warned against testosterone therapy, that has shown to be a myth.

Other side effects can include an elevation of the hematocrit to levels that require blood withdrawal (phlebotomy) to prevent complications from excessively thick blood. Gynecomastia (growth of breasts in men) sometimes occurs. Finally, some physicians worry that obstructive sleep apnea may worsen with testosterone therapy, and should be monitored.

Another treatment for hypogonadism is human chorionic gonadotropin (hCG). This stimulates the LH receptor, thereby promoting testosterone synthesis. This will not be effective in men who simply cannot make testosterone anymore (primary hypogonadism) and the failure of hCG therapy is further support for the existence of true testicular failure in a patient. It is particularly indicated in men with hypogonadism who wish to retain their fertility, as it does not suppress spermatogenesis like testosterone replacement therapy does.

For both men and women, an alternative to testosterone replacement is low-dose clomifene treatment, which can stimulate the body to naturally increase hormone levels while avoiding infertility and other side effects that can result from direct hormone replacement therapy. This therapy has only been shown helpful for men with secondary hypogonadism. Recent studies have shown it can be safe and effective monotherapy for up to 2 years in patients with intact testicular function and impaired function of the HPTA(http://www.nature.com/ijir/journal/v15/n3/full/3900981a.html). Clomifene blocks estrogen from binding to some estrogen receptors in the hypothalamus, thereby causing an increased release gNRH and subsequently LH from the pituitary. Clomifene is a Selective Estrogen Reuptake Modulator (SERM).

Generally clomifene does not have adverse effects at the doses used for this purpose. Clomifene at much higher doses is used to induce ovulation and has significant adverse effects in such a setting.

For women with hypogonadism, estradiol and progesterone are often replaced. Some types of fertility defects can be treated, others cannot. Some physicians also give testosterone to women, mainly to increase libido.

Treatment of HH may consist of administration of either a GnRH agonist or a gonadotropin formulation in the case of primary HH and treatment of the root cause (e.g., a tumor) of the symptoms in the case of secondary HH. Alternatively, hormone replacement therapy with androgens and estrogens in males and females, respectively, may be employed.

The aim for hormone replacement therapy (HRT) for both men and women is to ensure that the level of circulating hormones (testosterone for men and oestrogen/progesterone for women) is at the normal physiological level for the age of the patient. At first the treatment will produce most of the physical and psychological changes seen at puberty, with the major exception that there will be no testicular development in men and no ovulation in women.

After the optimum physical development has been reached HRT for men will continue to ensure that the normal androgen function is maintained; such as libido, muscle development, energy levels, hair growth, and sexual function. In women, a variety of types of HRT will either give a menstruation cycle or not as preferred by the patient. HRT is very important in both men and women to maintain bone density and to reduce the risk of early onset osteoporosis.

The fertility treatments used for both men and women would still include hormone replacement in their action.

There are a range of different preparations available for HRT for both men and women; a lot of these, especially those for women are the same used for standard HRT protocols used when hormone levels fall in later life or after the menopause.

For males with KS / CHH the types of delivery method available include daily patches, daily gel use, daily capsules, sub cutaneous or intramuscular injections or six monthly implants. Different formulations of testosterone are used to ensure both the anabolic and androgenic effects of testosterone are achieved.

Testosterone undecanoate is commonly used worldwide, though less so in the US, for treating male KS / CHH patients and has proved to be effective in maintaining good testosterone levels with an increased injection period of up to 12 weeks.

The precise treatment method used and interval between injections will vary from patient to patient and may need to be adjusted to maintain a physiological normal level of testosterone over a longer period of time to prevent the mood swings or adverse effects that can occur if testosterone levels are too high or low. Some treatments may work better with some patients than others so it might be a case of personal choice as which one to use.

As an alternative human chorionic gonadotrophin (hCG) can also be used to stimulate natural testosterone production. It acts in the same way as LH; stimulating the Leydig cells in the testes to produce testosterone. hCG can be used as pre-cursor to male fertility treatments but it can be used in isolation just for testosterone production.

There are no specialist HRT treatments available just for women with KS/HH but there are multitude of different HRT products on the market including oral contraceptives and standard post-menopause products. Pills are popular but patches are also available. It may take some trial and error to find the appropriate HRT for the patient depending on how her body reacts to the particular HRT. Specialist medical advice will be required to ensure the correct levels of oestrogen and progesterone are maintained each month, depending on whether the patient requires continuous HRT (no-bleed) or a withdrawal option to create a "menstrual" type bleed. This withdrawal bleed can be monthly or over longer time periods depending on the type of medication used.

Hormone replacement therapy with estrogen may be used to treat symptoms of hypoestrogenism in females with the condition. There are currently no known treatments for the infertility caused by the condition in either sex.

Fertility treatments for people with KS/HH will require specialist advice from doctors experienced in reproductive endocrinology. There is a good success rate for achieving fertility for patients with KS/HH, with some experts quoting up to a 70% success rate, if IVF techniques are used as well. However, there are factors that can have a negative effect on fertility and specialist advice will be required to determine if these treatments are likely to be successful.

Fertility treatments involve the administration of the gonadotropins LH and FSH in order to stimulate the production and release of eggs and sperm. Women with KS or HH have an advantage over the men as their ovaries normally contain a normal number of eggs and it sometimes only takes a few months of treatment to achieve fertility while it can take males up to two years of treatment to achieve fertility.

A new potential new form of fertility treatment underwent clinical trials in 2013 and 2014 by Merck Sharp & Dohme. The trial evaluated a longer acting form of FSH, in the form of corifollitropin alfa. Injections were taken fortnightly instead of the normal twice weekly it is hoped that this would induce sperm production within months rather than the two years it can take with currently available medications.

Human chorionic gonadotrophin (hCG) is sometimes used to stimulate testosterone production in men and ovulation induction in women. For men it acts in the same way as LH; stimulating the Leydig cells in the testes to produce testosterone. Common trade names for hCG products include Pregnyl, Follutein, Profasi, or Choragon. Some men with KS or HH take hCG solely for testosterone production.

Human menopausal gonadotrophin (hMG) is used to stimulate sperm production in men and for multiple egg production and ovulation induction in women. It contains a mixture of both LH and FSH. In men the FSH acts on the sperm producing Sertoli cells in the testes. This can lead to testicular enlargement but can take anything from 6 months to 2 years for an adequate level of sperm production to be achieved. Common trade names for hMG products include Menopur, Menogon, Repronex, or Pergonal.

Purified forms of FSH are also available and are sometimes used with hCG instead of using hMG.

Females with KS / HH would normally require both hCG and FSH in order to achieve fertility. Other cases of female infertility can be treated with just FSH but females (and most males) with KS / CHH would require the use of both forms of gonadotropin injection.

Injections can be intramuscular but are normally taken just underneath the skin (subcutaneous) and are normally taken two or three times a week.

For both men and women, an alternative method (but not widely available), is the use of an infusion pump to provide GnRH (or LHRH) in pulsatile doses throughout the day. This stimulates the pituitary gland to release natural LH and FSH in order to activate testes or ovaries. The use of Kisspeptin delivered in the same pulsatile manner is also under evaluation as a possible treatment for fertility induction.

Treatment of HH is usually with hormone replacement therapy, consisting of androgen and estrogen administration in males and females, respectively.

Treatment may consist of hormone replacement therapy with androgens in either sex. Alternatively, gonadotropin-releasing hormone (GnRH)/GnRH agonists or gonadotropins may be given (in the case of "hypogonadotropic" hypoandrogenism). The Food and Drug Administration (FDA) stated in 2015 that neither the benefits nor the safety of testosterone have been established for low testosterone levels due to aging. The FDA has required that testosterone pharmaceutical labels include warning information about the possibility of an increased risk of heart attacks and stroke.

Administration of luteinizing hormone (LH) (or human chorionic gonadotropin) and follicle-stimulating hormone (FSH) is very effective in the treatment of male infertility due to hypogonadotropic hypogonadism. Although controversial, off-label clomiphene citrate, an antiestrogen, may also be effective by elevating gonadotropin levels.

Though androgens are absolutely essential for spermatogenesis and therefore male fertility, exogenous testosterone therapy has been found to be ineffective in benefiting men with low sperm count. This is thought to be because very high local levels of testosterone in the testes (concentrations in the seminiferous tubules are 20- to 100-fold greater than circulating levels) are required to mediate spermatogenesis, and exogenous testosterone therapy (which is administered systemically) cannot achieve these required high local concentrations (at least not without extremely supraphysiological dosages). Moreover, exogenous androgen therapy can actually impair or abolish male fertility by suppressing gonadotropin secretion from the pituitary gland, as seen in users of androgens/anabolic steroids (who often have partially or completely suppressed sperm production). This is because suppression of gonadotropin levels results in decreased testicular androgen production (causing diminished local concentrations in the testes) and because FSH is independently critical for spermatogenesis. In contrast to FSH, LH has little role in male fertility outside of inducing gonadal testosterone production.

Estrogen, at some concentration, has been found to be essential for male fertility/spermatogenesis. However, estrogen levels that are too high can impair male fertility by suppressing gonadotropin secretion and thereby diminishing intratesticular androgen levels. As such, clomiphene citrate (an antiestrogen) and aromatase inhibitors such as testolactone or anastrozole have shown effectiveness in benefiting spermatogenesis.

Low-dose estrogen and testosterone combination therapy may improve sperm count and motility in some men, including in men with severe oligospermia.

Males and females may be treated with hormone replacement therapy (i.e., with androgens and estrogens, respectively), which will result in normal sexual development and resolve most symptoms. In the case of 46,XY (genetically male) individuals who are phenotypically female and/or identify as the female gender, they should be treated with estrogens instead. Removal of the undescended testes should be performed in 46,XY females to prevent their malignant degeneration, whereas in 46,XY males surgical correction of the genitals is generally required, and, if necessary, an orchidopexy (relocation of the undescended testes to the scrotum) may be performed as well. Namely in genetic females presenting with ovarian cysts, GnRH analogues may be used to control high FSH and LH levels if they are unresponsive to estrogens.

Patients with Leydig cell hypoplasia may be treated with hormone replacement therapy (i.e., with androgens), which will result in normal sexual development and the resolution of most symptoms. In the case of 46,XY (genetically "male") individuals who are phenotypically female and/or identify as the female gender, estrogens should be given instead. Surgical correction of the genitals in 46,XY males may be required, and, if necessary, an orchidopexy (relocation of the undescended testes to the scrotum) may be performed as well.

Treatments vary according to the underlying disease and the degree of the impairment of the male fertility. Further, in an infertility situation, the fertility of the female needs to be considered.

Pre-testicular conditions can often be addressed by medical means or interventions.

Testicular-based male infertility tends to be resistant to medication. Usual approaches include using the sperm for intrauterine insemination (IUI), in vitro fertilization (IVF), or IVF with intracytoplasmatic sperm injection (ICSI). With IVF-ICSI even with a few sperm pregnancies can be achieved.

Obstructive causes of post-testicular infertility can be overcome with either surgery or IVF-ICSI. Ejaculatory factors may be treatable by medication, or by IUI therapy or IVF.

Vitamin E helps counter oxidative stress, which is associated with sperm DNA damage and reduced sperm motility. A hormone-antioxidant combination may improve sperm count and motility. However there is only some low quality evidence from few small studies that oral antioxidants given to males in couples undergoing in vitro fertilisation for male factor or unexplained subfertility result in higher live birth rate. It is unclear if there are any adverse effects.

Pre- and post-testicular azoospermia are frequently correctible, while testicular azoospermia is usually permanent. In the former the cause of the azoospermia needs to be considered and it opens up possibilities to manage this situation directly. Thus men with azoospermia due to hyperprolactinemia may resume sperm production after treatment of hyperprolactinemia or men whose sperm production is suppressed by exogenous androgens are expected to produce sperm after cessation of androgen intake. In situations where the testes are normal but unstimulated, gonadotropin therapy can be expected to induce sperm production.

A major advancement in recent years has been the introduction of IVF with ICSI which allows successful fertilization even with immature sperm or sperm obtained directly from testicular tissue. IVF-ICSI allows for pregnancy in couples where the man has irreversible testicular azoospermia as long as it is possible to recover sperm material from the testes. Thus men with non-mosaic Klinefelter's syndrome have fathered children using IVF-ICSI. Pregnancies have been achieved in situations where azoospermia was associated with cryptorchism and sperm where obtained by testicular sperm extraction (TESE).

In men with posttesticular azoospermia a number of approaches are available. For obstructive azoospermia IVF-ICSI or surgery can be used and individual factors need to be considered for the choice of treatment. Medication may be helpful for retrograde ejaculation.

Medical treatment of gynecomastia is most effective when done within the first two years after the start of male breast enlargement. Selective estrogen receptor modulators (SERMs) such as tamoxifen, raloxifene, and clomifene may be beneficial in the treatment of gynecomastia but are not approved by the Food and Drug Administration for use in gynecomastia. Clomifene seems to be less effective than tamoxifen or raloxifene. Tamoxifen may be used for painful gynecomastia in adults. Aromatase inhibitors (AIs) such as anastrozole have been used off-label for cases of gynecomastia occurring during puberty but are less effective than SERMs. A few cases of gynecomastia caused by the rare disorders aromatase excess syndrome and Peutz–Jeghers syndrome have responded to treatment with AIs such as anastrozole. Androgens/anabolic steroids may be effective for gynecomastia. Testosterone itself may not be suitable to treat gynecomastia as it can be aromatized into estradiol, but non-aromatizable androgens like topical androstanolone (dihydrotestosterone) can be useful.

Treatment may consist of surgery in the case of tumors, lower doses of estrogen in the case of exogenously-mediated estrogen excess, and estrogen-suppressing medications like gonadotropin-releasing hormone analogues and progestogens. In addition, androgens may be supplemented in the case of males.

If chronic gynecomastia is treated, surgical removal of glandular breast tissue is usually required. Surgical approaches to the treatment of gynecomastia include subcutaneous mastectomy, liposuction-assisted mastectomy, laser-assisted liposuction, and laser-lipolysis without liposuction. Complications of mastectomy may include hematoma, surgical wound infection, breast asymmetry, changes in sensation in the breast, necrosis of the areola or nipple, seroma, noticeable or painful scars, and contour deformities.

Treatment takes place within the context of infertility management and needs also to consider the fecundity of the female partner. Thus the choices can be complex.

In a number of situations direct medical or surgical intervention can improve the sperm concentration, examples are use of FSH in men with pituitary hypogonadism, antibiotics in case of infections, or operative corrections of a hydrocele, varicocele, or vas deferens obstruction.

In most cases of oligospermia including its idiopathic form there is no direct medical or surgical intervention agreed to be effective. Empirically many medical approaches have been tried including clomiphene citrate, tamoxifen, HMG, FSH, HCG, testosterone, Vitamin E, Vitamin C, anti-oxidants, carnitine, acetyl-L-carnitine, zinc, high-protein diets. In a number of pilot studies some positive results have been obtained. Clomiphene citrate has been used with modest success. The combination of tamoxifen plus testosterone was reported to improve the sperm situation.

The use of carnitine showed some promise in a controlled trial in selected cases of male infertility improving sperm quality and further studies are needed.

In many situations, intrauterine inseminations are performed with success. In more severe cases IVF, or IVF - ICSI is done and is often the best option, specifically if time is a factor or fertility problems coexist on the female side.

The Low dose Estrogen Testosterone Combination Therapy may improve sperm count and motility in some men including severe oligospermia.

Several treatments have been found to be effective in managing AES, including aromatase inhibitors and gonadotropin-releasing hormone analogues in both sexes, androgen replacement therapy with non-aromatizable androgens such as DHT in males, and progestogens (which, by virtue of their antigonadotropic properties at high doses, suppress estrogen levels) in females. In addition, male patients often seek bilateral mastectomy, whereas females may opt for breast reduction if warranted.

Medical treatment of AES is not absolutely necessary, but it is recommended as the condition, if left untreated, may lead to excessively large breasts (which may necessitate surgical reduction), problems with fertility, and an increased risk of endometriosis and estrogen-dependent cancers such as breast and endometrial cancers later in life. At least one case of male breast cancer has been reported.

Achieving a pregnancy naturally may be a challenge if the male suffers from a low sperm count. However, chances are good if the female partner is fertile; many couples with this problem have been successful. Prognosis is more limited if there is a combination of factors that include sperm dysfunction and reduced ovarian reserve.

Upon diagnosis, estrogen and progesterone therapy is typically commenced, promoting the development of female characteristics.

The consequences of streak gonads to a person with Swyer syndrome:

1. Gonads cannot make estrogen, so the breasts will not develop and the uterus will not grow and menstruate until estrogen is administered. This is often given transdermally.

2. Gonads cannot make progesterone, so menstrual periods will not be predictable until progestin is administered, usually as a pill.

3. Gonads cannot produce eggs so conceiving children naturally is not possible. A woman with a uterus and ovaries but without female gamete is able to become pregnant by implantation of another woman's fertilized egg (embryo transfer).

4. Streak gonads with Y chromosome-containing cells have a high likelihood of developing cancer, especially gonadoblastoma. Streak gonads are usually removed within a year or so of diagnosis since the cancer can begin during infancy.

Direct treatment is geared toward resolving hyperprolactinemic symptoms or reducing tumor size. Patients on medications that cause hyperprolactinaemia should have them withdrawn if possible. Patients with hypothyroidism should be given thyroid hormone replacement therapy. When symptoms are present, medical therapy is the treatment of choice. Patients with hyperprolactinemia and no symptoms (idiopathic or microprolactinoma) can be monitored without treatment. Consider treatment for women with amenorrhea. In addition, dual energy X-ray absorptiometry scanning should be considered to evaluate bone density. The persistent hypogonadism associated with hyperprolactinemia can lead to osteoporosis. Treatment significantly improves the patient's quality of life. If the goal is to treat hypogonadism only, patients with idiopathic hyperprolactinemia or microadenoma can be treated with estrogen replacement therapy and prolactin levels can be monitored. Radiation treatment is another option. However, the risk of hypopituitarism makes this a poor choice. It may be necessary for rapidly growing tumors, but its benefits in routine treatment have not been shown to outweigh the risks.

Treatment is usually medication with dopamine agonists such as cabergoline, bromocriptine (often preferred when pregnancy is possible), and less frequently lisuride. A new drug in use is norprolac with the active ingredient quinagolide. Terguride is also used.

"Vitex agnus-castus" extract can be tried in cases of mild hyperprolactinaemia.

Because hormone treatment rarely achieves average size, several surgical techniques similar to phalloplasty for penis enlargement have been devised and performed; but they are not generally considered successful enough to be widely adopted and are rarely performed in childhood.

In extreme cases of micropenis, there is barely any shaft, and the glans appears to sit almost on the pubic skin. From the 1960s until the late 1970s, it was common for sex reassignment and surgery to be recommended. This was especially likely if evidence suggested that response to additional testosterone and pubertal testosterone would be poor. With parental acceptance, the boy would be reassigned and renamed as a girl, and surgery performed to remove the testes and construct an artificial vagina. This was based on the now-questioned idea that gender identity was shaped entirely from socialization, and that a man with a small penis can find no acceptable place in society.

Johns Hopkins Hospital, the center most known for this approach, performed twelve such reassignments from 1960 to 1980, most notably that of David Reimer (whose penis was destroyed by a circumcision accident), overseen by John Money. By the mid-1990s, reassignment was less often offered, and all three premises had been challenged. Former subjects of such surgery, vocal about their dissatisfaction with the adult outcome, played a large part in discouraging this practice. Sexual reassignment is rarely performed today for severe micropenis (although the question of raising the boy as a girl is sometimes still discussed.) (See "History of intersex surgery" for a fuller discussion.)

A treatment option for micropenis is the insertion of a subcutaneous soft silicone implant under the penile skin. The procedure was developed by urologist James J. Elist.

General indications for pituitary surgery include patient drug intolerance, tumors resistant to medical therapy, patients who have persistent visual field defects in spite of medical treatment, and patients with large cystic or hemorrhagic tumors.

Growth of the penis both before birth and during childhood and puberty is strongly influenced by testosterone and, to a lesser degree, the growth hormone. However, later endogenous hormones mainly have value in the treatment of micropenis caused by hormone deficiencies, such as hypopituitarism or hypogonadism.

Regardless of the cause of micropenis, if it is recognized in infancy, a brief course of testosterone is often prescribed (usually no more than 3 months). This usually induces a small amount of growth, confirming the likelihood of further growth at puberty, but rarely achieves normal size. No additional testosterone is given during childhood, to avoid unwanted virilization and bone maturation. (There is also some evidence that premature administration of testosterone can lead to reduced penis size in the adult.)

Testosterone treatment is resumed in adolescence only for boys with hypogonadism. Penile growth is completed at the end of puberty, similar to the completion of height growth, and provision of extra testosterone to post-pubertal adults produces little or no further growth.

There is no known cure available for the Wilson-Turner Syndrome. Instead, treatment options are available to fight individual symptoms. For obesity, a nutritional diet manipulation is combined with an exercise regimen that has a greater energy expenditure than intake. For hypogonadism, testosterone replacement is done. Finally, for gynecomastia, weight loss using similar methods for obesity is prescribed. However, if the individual finds his increased breast tissue psychologically distressing and/or is too severe, reduction mammaplasty is done. Currently, researchers are investigating therapy using antiestrogens and aromatase inhibitors to treat persistent pubertal gynecomastia.