Early histological features expected to be seen on examination of gynecomastic tissue attained by fine-needle aspiration biopsy include the following: proliferation and lengthening of the ducts, an increase in connective tissue, an increase in inflammation and swelling surrounding the ducts, and an increase in fibroblasts in the connective tissue. Chronic gynecomastia may show different histological features such as increased connective tissue fibrosis, an increase in the number of ducts, less inflammation than in the acute stage of gynecomastia, increased subareolar fat, and hyalinization of the stroma. When surgery is performed, the gland is routinely sent to the lab to confirm the presence of gynecomastia and to check for tumors under a microscope. The utility of pathologic examination of breast tissue removed from male adolescent gynecomastia patients has recently been questioned due to the rarity of breast cancer in this population.

Mammography is the method of choice for radiologic examination of male breast tissue in the diagnosis of gynecomastia when breast cancer is suspected on physical examination. However, since breast cancer is a rare cause of breast tissue enlargement in men, mammography is rarely needed. If mammography is performed and does not reveal findings suggestive of breast cancer, further imaging is not typically necessary. If a tumor of the adrenal glands or the testes is thought to be responsible for the gynecomastia, ultrasound examination of these structures may be performed.

Female patients may show symptoms of hyperandrogenism in their early life, but physicians become more concerned when the patient is in her late teens or older.

Hyperandrogenism is most often diagnosed by checking for signs of hirsutism according to a standardized method that scores the range of excess hair growth.

Checking medical history and a physical examination of symptoms are used for an initial diagnosis. Patient history assessed includes age at thelarche, adrenarche, and menarche; patterns of menstruation; obesity; reproductive history; and the start and advancement of hyperandrogenism symptoms. Patterns of menstruation are examined since irregular patterns may appear with hirsutism. Family history is also assessed for occurrences of hyperandrogenism symptoms or obesity in other family members.

A laboratory test can also be done on the patient to evaluate levels of FSH, LH, DHEAS, prolactin, 17OHP, and total and free testosterone in the patient's blood. Abnormally high levels of any of these hormones help in diagnosing hyperandrogenism.

A complete physical evaluation should be done prior to initiating more extensive studies, the examiner should differentiate between widespread body hair increase and male pattern virilization. One method of evaluating hirsutism is the Ferriman-Gallwey Score which gives a score based on the amount and location of hair growth on a woman. After the physical examination, laboratory studies and imaging studies can be done to rule out further causes.

Diagnosis of patients with even mild hirsutism should include assessment of ovulation and ovarian ultrasound, due to the high prevalence of polycystic ovary syndrome (PCOS), as well as 17α-hydroxyprogesterone (because of the possibility of finding nonclassic 21-hydroxylase deficiency). Many women present with an elevated serum dehydroepiandrosterone sulfate (DHEA-S) level. Levels greater than 700 μg/dL are indicative of adrenal gland dysfunction, particularly congenital adrenal hyperplasia due to 21-hydroxylase deficiency. However, PCOS and idiopathic hirsutism make up 90% of cases.

Other blood value that may be evaluated in the workup of hirsutism include:

- androgens; androstenedione, testosterone

- thyroid function panel; thyroid-stimulating hormone (TSH), triiodothyronine (T3), thyroxine (T4)

- prolactin

If no underlying cause can be identified, the condition is considered idiopathic.

Since risk factors are not known and vary among individuals with hyperandrogegism, there is no sure method to prevent this medical condition. Therefore, more longterm studies are needed first to find a cause for the condition before being able to find a sufficient method of prevention.

However, there are a few things that can help avoid long-term medical issues related to hyperandrogenism like PCOS. Getting checked by a medical professional for hyperandrogenism; especially if one has a family history of the condition, irregular periods, or diabetes; can be beneficial. Watching your weight and diet is also important in decreasing your chances, especially in obese females, since continued exercise and maintaining a healthy diet leads to an improved menstrual cycle as well as to decreased insulin levels and androgen concentrations.

Like the other forms of CAH, suspicion of severe 3β-HSD CAH is usually raised by the appearance of the genitalia at birth or by development of a salt-wasting crisis in the first month of life. The diagnosis is usually confirmed by the distinctive pattern of adrenal steroids: elevated pregnenolone, 17α-hydroxypregnenolone, DHEA, and renin. In clinical circumstances this form of CAH has sometimes been difficult to distinguish from the more common 21-hydroxylase deficient CAH because of the 17OHP elevation, or from simple premature adrenarche because of the DHEA elevation.

Many women with unwanted hair seek methods of hair removal. However, the causes of the hair growth should be evaluated by a physician, who can conduct blood tests, pinpoint the specific origin of the abnormal hair growth, and advise on the treatment.

The preferable way to diagnose the presence of this syndrome would be to use the help of clinical tests and medical reports after the tests and examinations. Now being aware of the subject that HAIR-AN syndrome is caused by genetic, environmental factors and also the hyperandogenism, insulin resistance and acanthosis nigricans, some of the way we could diagnosis this syndrome is by looking for signs in the body for symptoms leading to relate to those key contributors discussed above.

According to studies HAIR-AN is to be found in 1% to 3% women possessing hyperandrogenism. It is an established concept in physiopathology that the androgen in the female body is produced by the stromal ovarian cells, when stimulated by the LH and HCG. The observed activity of these cells was elevated by insulin, and later was found to be used as a determining element to find how severe the hirsutism was. Physicians must look for obesity, as it is also a diagnostic factor in many possible cases.

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.

Hyperestrogenism can be caused by ovarian tumors, genetic conditions such as aromatase excess syndrome (also known as familial hyperestrogenism), or overconsumption of exogenous sources of estrogen, including medications used in hormone replacement therapy and hormonal contraception. Liver cirrhosis is another cause, though through lowered metabolism of estrogen, not oversecretion or overconsumption like the aforementioned.

Hormone replacement therapy (HRT) with estrogen can be used to treat hypoestrogenism both in premenopausal and postmenopausal women.

Between 5 and 10 percent of women with POF may become pregnant. Currently no fertility treatment has officially been found to effectively increase fertility in women with POF, and the use of donor eggs with in-vitro fertilization (IVF) and adoption are popular as a means of achieving parenthood for women with POF. Some women with POF choose to live child-free. (See impaired ovarian reserve for a summary of recent randomized clinical trials and treatment methods.)

Currently New York fertility researchers are investigating the use of a mild hormone called dehydroepiandrosterone (DHEA) in women with POF to increase spontaneous pregnancy rates. Published results from studies conducted on DHEA have indicated that DHEA may increase spontaneously conceived pregnancies, decrease spontaneous miscarriage rates and improve IVF success rates in women with POF.

Additionally, over the last five years a Greek research team has successfully implemented the use of dehydroepiandrosterone (DHEA) for the fertility treatment of women suffering with POF.The majority of the patients were referred for donor eggs or surrogacy, however after a few months of DHEA administration, some succeeded in getting pregnant through IVF, IUI, IUTPI or natural conception. Many babies have been born after treatment with DHEA.

Ovarian tissue cryopreservation can be performed on prepubertal girls at risk for premature ovarian failure, and this procedure is as feasible and safe as comparable operative procedures in children.

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.

Symptoms-based methods of fertility awareness may be used to detect ovulation or to determine that cycles are anovulatory. Charting of the menstrual cycle may be done by hand, or with the aid of various fertility monitors. Records of one of the primary fertility awareness signs—basal body temperature—can detect ovulation by identifying the shift in temperature which takes place after ovulation. It is said to be the most reliable way of confirming whether ovulation has occurred.

Women may also use ovulation predictor kits (OPKs) which detect the increase in luteinizing hormone (LH) levels that usually indicates imminent ovulation. For some women, these devices do not detect the LH surge, or high levels of LH are a poor predictor of ovulation; this is particularly common in women with PCOS. In such cases, OPKs and those fertility monitors which are based on LH may show false results, with an increased number of false positives or false negatives. Dr Freundl from the University of Heidelberg suggests that tests which use LH as a reference often lack sensitivity and specificity.

The root cause of AES is not entirely clear, but it has been elucidated that inheritable, autosomal dominant genetic mutations affecting "CYP19A1", the gene which encodes aromatase, are involved in its etiology. Different mutations are associated with differential severity of symptoms, such as mild to severe gynecomastia.

A doctor will test for prolactin blood levels in women with unexplained milk secretion (galactorrhea) or irregular menses or infertility, and in men with impaired sexual function and, in rare cases, milk secretion. If prolactin is high, a doctor will test thyroid function and ask first about other conditions and medications known to raise prolactin secretion. The doctor will also request a magnetic resonance imaging (MRI), which is the most sensitive test for detecting pituitary tumors and determining their size. MRI scans may be repeated periodically to assess tumor progression and the effects of therapy. Computed Tomography (CT scan) also gives an image of the pituitary, but it is less sensitive than the MRI.

In addition to assessing the size of the pituitary tumor, doctors also look for damage to surrounding tissues, and perform tests to assess whether production of other pituitary hormones is normal. Depending on the size of the tumor, the doctor may request an eye exam with measurement of visual fields.

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.

It has been estimated that POF affects 1% of the female population.

Hypertension and mineralocorticoid excess is treated with glucocorticoid replacement, as in other forms of CAH.

Most genetic females with both forms of the deficiency will need replacement estrogen to induce puberty. Most will also need periodic progestin to regularize menses. Fertility is usually reduced because egg maturation and ovulation is poorly supported by the reduced intra-ovarian steroid production.

The most difficult management decisions are posed by the more ambiguous genetic (XY) males. Most who are severely undervirilized, looking more female than male, are raised as females with surgical removal of the nonfunctional testes. If raised as males, a brief course of testosterone can be given in infancy to induce growth of the penis. Surgery may be able to repair the hypospadias. The testes should be salvaged by orchiopexy if possible. Testosterone must be replaced in order for puberty to occur and continued throughout adult life.

HAIR-AN syndrome as discussed earlier is caused by both gentic and environmental factors. It is found out that women affected by this syndrome or PCOS (polycystic ovary syndrome) are generally accompanied by obesity. Weight loss is most suggested way to combat this syndrome and is helpful for reducing insulin resistance of the body. It is also a good way to have a control on diet. This might help the body to refunction properly and show some resistance to HAIR-AN syndrome. "Suppression of gonadotropin with estrogen-progesterone oral contraceptives" or can say as reducing hyperandrogenism by the use of estoprogestatif can reduce production of androgen by ovaries by cutting down the LH (leutinizing hormone) level in body. Even their sex hormone binding to globulin increase is also responsible for decreasing body's bio-availability of testosterone. There are also few pills of new progestins, such as desogestrel and norgestimate. This pills appear to have fewer androgenic side effects and may be safer to use in persons with abnormal lipid levels or hirsutism. Some antiandrogenic agents can be also used alone or combining it with other oral pills.

"Spironolactone inhibit the actions of testosterone by binding to its receptors." The standard dose for its use is considered to be 50 to 100 mg twice a day. This might lead to irregular menstrual bleeding, which can be improved by oral contraceptives. Flutamide, an another antiandorgen that is used to treat HAIR-AN syndrome, but it has risk of hepatotoxicity. Finasteride is a 5α-reductase inhibitor which can reduces the conversion of testosterone to dihydrotestosterone. It is useful in the treatment of hirsutism with a dosages as low as 5 mg per day.

Insulin-resistant patients can also be treated with metformin which has shown promising results to reduce the insulin resistivity. Metformin improves peripheral tissue sensitivity to insulin but inhibits hepatic glucose formation. The drug reduces the levels of circulating insulin and androgens. Women have shown improved reproductive functioning after the use of metformin.

Some of the childhood management issues are similar those of 21-hydroxylase deficiency:

- Replacing mineralocorticoid with fludrocortisone

- Suppressing DHEA and replacing cortisol with glucocorticoid

- Providing extra glucocorticoid for stress

- Close monitoring and perhaps other adjunctive measures to optimize growth

- Deciding whether surgical repair of virilized female genitalia is warranted

However, unlike 21-hydroxylase CAH, children with 3β-HSD CAH may be unable to produce adequate amounts of testosterone (boys) or estradiol (girls) to effect normal pubertal changes. Replacement testosterone or estrogen and progesterone can be initiated at adolescence and continued throughout adult life. Fertility may be impaired by the difficulty of providing appropriate sex hormone levels in the gonads even though the basic anatomy is present.

The European Society of Human Reproduction and Embryology (ESHRE) notes that the aim of ovulation induction should be mono-ovulation and not over-stimulation of the ovaries . The risks associated with multiple pregnancy are much higher than singleton pregnancy; incidences of perinatal death are seven times higher in triplet births and five times higher in twin births than the risks associated with a singleton pregnancy. It is therefore important to adapt the treatment to each individual patient.

Women with polycystic ovary syndrome may be particularly at risk. Multiple pregnancy occurs in approximately 15-20% of cases following cycles induced with gonadotrophins such as hMG and FSH induced ovulations.

During ovulation induction, it is recommended to start at a low dose and monitor the ovarian response with vaginal ultrasound, including discernment of the number of developing follicles. A cycle with supernumerary follicles is usually defined as one where there are more than two follicles >16 mm in diameter. It is generally recommended to have such cycles cancelled because of the risk of multiple pregnancy. In cancelled cycles, the woman or couple should be warned of the risks in case of supernumerary follicles, and should avoid sexual intercourse or use contraception until the next menstruation. Induction of final maturation (such as done with hCG) may need to be withheld because of increased risk of ovarian hyperstimulation syndrome(OHSS). The starting dose of the inducing drug should be reduced in the next cycle.

Alternatives to cancelling a cycle are mainly:

- Aspiration of supernumerary follicles until one or two remain.

- Converting the protocol to IVF treatment with embryo transfer of up to two embryos only.

- Selective fetal reduction. This alternative confers a high risk of complications.

- Proceeding with any multiple pregnancy without fetal reduction, with the ensuing risk of complications. This alternative is not recommended.

Hyperprolactinemia can cause reduced estrogen production in women and reduced testosterone production in men. Although estrogen/testosterone production may be restored after treatment for hyperprolactinemia, even a year or two without estrogen/testosterone can compromise bone strength, and patients should protect themselves from osteoporosis by increasing exercise and calcium intake through diet or supplementation, and by avoiding smoking. Patients may want to have bone density measurements to assess the effect of estrogen/testosterone deficiency on bone density. They may also want to discuss testosterone/estrogen replacement therapy with their physician.

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.

Presentations of low estrogen levels include hot flashes, headaches, lowered libido, and breast atrophy. Reduced bone density leading to secondary osteoporosis and atrophic changes such as pH change in the vagina is also linked to hypoestrogenism.

Low levels of estrogen can lead to dyspareunia and limited genital arousal because of changes in the four layers of the vaginal wall.

Hypoestrogenism is also considered one of the major risk factors for developing uncomplicated urinary tract infections (UTIs) in postmenopausal women who do not take hormone replacement therapy.