These have been ranked by the UK's National Institute for Health and Clinical Excellence:

- First line

- Intrauterine device with progesterone

- Second Line

- Tranexamic acid an antifibrinolytic agent

- Nonsteroidal anti-inflammatory drugs (NSAIDs).

- Combined oral contraceptive pills to prevent proliferation of the endometrium

- Third line

- Oral progestogen (e.g. norethisterone), to prevent proliferation of the endometrium

- Injected progestogen (e.g. Depo provera)

- Other options

- Gonadotropin-releasing hormone agonist

Where an underlying cause can be identified, treatment may be directed at this. Clearly heavy periods at menarche and menopause may settle spontaneously (the menarche being the start and menopause being the cessation of periods).

If the degree of bleeding is mild, all that may be sought by the woman is the reassurance that there is no sinister underlying cause. If anemia occurs due to bleeding then iron tablets may be used to help restore normal hemoglobin levels.

The condition is often treated with hormones, particularly as abnormal uterine bleeding commonly occurs in the early and late menstrual years when contraception is also sought. Usually, oral combined contraceptive or progesterone only pills may be taken for a few months, but for longer-term treatment the alternatives of injected Depo Provera or the more recent progesterone releasing IntraUterine System (IUS) may be used. Fibroids may respond to hormonal treatment, and if they do not, then surgical removal may be required.

Tranexamic acid tablets that may also reduce loss by up to 50%. This may be combined with hormonal medication previously mentioned.

Anti-inflammatory medication like NSAIDs may also be used. NSAIDs are the first-line medications in ovulatory menorrhagia, resulting in an average reduction of 20-46% in menstrual blood flow. For this purpose, NSAIDs are ingested for only 5 days of the menstrual cycle, limiting their most common adverse effect of dyspepsia.

A definitive treatment for menorrhagia is to perform hysterectomy (removal of the uterus). The risks of the procedure have been reduced with measures to reduce the risk of deep vein thrombosis after surgery, and the switch from the front abdominal to vaginal approach greatly minimizing the discomfort and recuperation time for the patient; however extensive fibroids may make the womb too large for removal by the vaginal approach. Small fibroids may be dealt with by local removal (myomectomy). A further surgical technique is endometrial ablation (destruction) by the use of applied heat (thermoablation).

In the UK the use of hysterectomy for menorrhagia has been almost halved between 1989 and 2003. This has a number of causes: better medical management, endometrial ablation and particularly the introduction of IUS which may be inserted in the community and avoid the need for specialist referral; in one study up to 64% of women cancelled surgery.

Drug of choice is progesterone.

Management of dysfunctional uterine bleeding predominantly consists of reassurance, though mid-cycle estrogen and late-cycle progestin can be used for mid- and late-cycle bleeding respectively.

Also, non-specific hormonal therapy such as combined high-dose estrogen and high-dose progestin can be given. Ormeloxifene is a non-hormonal medication that treats DUB but is only legally available in India.

The goal of therapy should be to arrest bleeding, replace lost iron to avoid anemia, and prevent future bleeding.

Excessive movement before any treatments or surgeries will cause excessive bleeding.

A hysterectomy may be performed in some cases.

Excessive menstruation between puberty and 19 years of age is called puberty menorrhagia. Excessive menstruation is defined as bleeding over 80 ml per menstrual period or lasting more than 7 days. The most common cause for puberty menorrhagia is dysfunctional uterine bleeding. The other reasons are idiopathic thrombocytopenic purpura, hypothyroidism, genital tuberculosis, polycystic ovarian disease, leukemia and coagulation disorders. The most common physiological reason for puberty menorrhagia is the immaturity of hypothalamic-pituitary-ovarian axis, leading to inadequate positive feedback and sustained high estrogen levels. Most patients present with anemia due to excessive blood loss.

The patient is assessed with a thorough medical history, physical examination (to look for features of anemia), gynaecological examination (to rule out local causes) and laboratory investigations (to rule out coagulopathies and malignancy). It is mandatory to exclude pregnancy. The treatment is determined based on the cause of menorrhagia. In case of puberty menorrhagia due to immaturity of hypothalamic axis, hormonal therapy is beneficial. Treatment for blood loss should be done simultaneously with iron therapy in mild to moderate blood loss and blood transfusion in severe blood loss.

Treatment depends on the cause. In cases where malignancy is ruled out, hormone supplementation or the therapeutic use of hormonal contraception is usually recommended to induce bleeding on a regular schedule. Selective progesterone receptor modulators (SPRMs) are sometimes used to stop uterine bleeding.

A menstrual disorder is an abnormal condition in a woman's menstrual cycle.

One possible treatment is with anastrozole. Histrelin acetate (Supprelin LA), triptorelin or leuprolide, any GnRH agonists, may be used. Non-continuous usage of GnRH agonists stimulates the pituitary gland to release follicle stimulating hormone (FSH) and luteinizing hormone (LH). However, when used regularly, GnRH agonists cause a decreased release of FSH and LH. Prolonged use has a risk of causing osteoporosis. After stopping GnRH agonists, pubertal changes resume within 3 to 12 months.

Dysmenorrhea (or dysmenorrhoea), cramps or painful menstruation, involves menstrual periods that are accompanied by either sharp, intermittent pain or dull, aching pain, usually in the pelvis or lower abdomen.

10% of cases occur in women who are ovulating, but progesterone secretion is prolonged because estrogen levels are low. This causes irregular shedding of the uterine lining and break-through bleeding. Some evidence has associated Ovulatory DUB with more fragile blood vessels in the uterus.

It may represent a possible endocrine dysfunction, resulting in menorrhagia or metrorrhagia.

Mid-cycle bleeding may indicate a transient estrogen decline, while late-cycle bleeding may indicate progesterone deficiency.

Early puberty is believed to put girls at higher risk of sexual abuse, unrelated to pedophilia because the child has developed secondary sex characteristics; however, a causal relationship is, as yet, inconclusive. Early puberty also puts girls at a higher risk for teasing or bullying, mental health disorders and short stature as adults. Helping children control their weight is suggested to help delay puberty. Early puberty additionally puts girls at a "far greater" risk for breast cancer later in life. Girls as young as 8 are increasingly starting to menstruate, develop breasts and grow pubic and underarm hair; these "biological milestones" typically occurred only at 13 or older in the past. African-American girls are especially prone to early puberty. There are theories debating the trend of early puberty, but the exact causes are not known.

Though boys face fewer problems upon early puberty than girls, early puberty is not always positive for boys; early sexual maturation in boys can be accompanied by increased aggressiveness due to the surge of hormones that affect them. Because they appear older than their peers, pubescent boys may face increased social pressure to conform to adult norms; society may view them as more emotionally advanced, although their cognitive and social development may lag behind their appearance. Studies have shown that early maturing boys are more likely to be sexually active and are more likely to participate in risky behaviours.

Severe acute bleeding, such as caused by ectopic pregnancy and post-partum hemorrhage, leads to hypovolemia (the depletion of blood from the circulation), progressing to shock. This is a medical emergency and requires hospital attendance and intravenous fluids, usually followed by blood transfusion. Once the circulating volume has been restored, investigations are performed to identify the source of bleeding and address it. Uncontrolled life-threatening bleeding may require uterine artery embolization (occlusion of the blood vessels supplying the uterus), laparotomy (surgical opening of the abdomen), occasionally leading to hysterectomy (removal of the uterus) as a last resort.

A possible complication from protracted vaginal blood loss is iron deficiency anemia, which can develop insidiously. Eliminating the cause will resolve the anemia, although some women require iron supplements or blood transfusions to improve the anemia.

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.

In 2011, the International Federation of Gynaecology and Obstetrics (FIGO) recognized two systems designed to aid research, education, and clinical care of women with abnormal uterine bleeding (AUB) in the reproductive years.

Menometrorrhagia is a condition in which prolonged or excessive uterine bleeding occurs irregularly and more frequently than normal. It is thus a combination of metrorrhagia and menorrhagia.

If a child is healthy but simply late, reassurance and prediction based on the bone age can be provided. No other intervention is usually necessary. In more extreme cases of delay, or cases where the delay is more extremely distressing to the child, a low dose of testosterone or estrogen for a few months may bring the first reassuring changes of normal puberty.

If the delay is due to systemic disease or undernutrition, the therapeutic intervention is likely to focus mainly on those conditions. In patients with coeliac disease, an early diagnosis and the establishment of a gluten-free diet prevents long-term complications and allows restore normal maturation.

If it becomes clear that there is a permanent defect of the reproductive system, treatment usually involves replacement of the appropriate hormones (testosterone/dihydrotestosterone for boys, estradiol and progesterone for girls).

Pubertal delay due to gonadotropin deficiency is treated with testosterone replacement or with HCG.

Growth hormone is another option that has been described.

Subnormal vitamin A intake is one of the aetiological factors in delayed pubertal maturation. Supplementation of both vitamin A and iron to normal constitutionally delayed children with subnormal vitamin A intake is as efficacious as hormonal therapy in the induction of growth and puberty.

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.

Aromatase deficiency is a condition resulting from insufficient production of the enzyme aromatase, which can result in inappropriate virilization of female fetuses and delayed puberty, as well as inappropriate virilization of the mother during pregnancy.

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.

Aromatase deficiency in the baby can also affect the mother during gestation, with cystic acne, hirsutism, deepening of the voice, and clitoromegaly. Increased circulating testosterone levels are the cause. The mother's symptoms resolve after she gives birth.

Danazol, an estrogen biosynthesis inhibitor, tamoxifen, an antagonistic modulator of the estrogen receptor, and bromocriptine, a prolactin-lowering D receptor agonist, are the main drugs used in the treatment of mastodynia and are effective.

Other medications and supplements have been found to be of benefit. Spironolactone (Aldactone), low dose oral contraceptives, low-dose estrogen have helped to relieve pain. Topical anti-inflammatory medications can be used for localized pain. For anti hormonal treatment, danazol (Danocrine) can be helpful. Tamoxifen citrate is used in some cases of severe breast pain. Vitamin E is not effective in relieving pain nor is Evening primrose oil. Vitamin B and Vitamin A have not been consistently found to be beneficial. Flaxseed has shown some activity in the treatment of cyclic mastalgia.

Pain may be relieved by the use of nonsteroidal anti-inflammatory drugs or, for more severe localized pain, by local anaesthetic. Pain may be relieved psychologically by reassurance that it does not signal a serious underlying problem, and an active life style can also effect an improvement.

Information regarding how the pain is real but not necessarily caused by disease can help to understand the problem. Learning breast self-examination helps to orient the woman to normal and expected texture and structure of the breast and nipple. Yearly breast exams may be suggested. Counseling can also be to describe changes that vary during the monthly cycle. Women on hormone replacement therapy may benefit from a dose adjustment. Another non-pharmacological measure to help relieve symptoms of pain may be to use good bra support. Breasts change during adolescence and menopause and refitting may be beneficial. Applying heat and/or ice can bring relief. Dietary changes may also help with the pain. Methylxanthines can be eliminated from the diet to see if a sensitivity is present. Some clinicians recommending a reduction in salt, though no evidence supports this practice.

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.

It is generally treated surgically, with a hymenotomy or other surgery to remove any tissue that blocks the menstrual flow.

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.

Familial male-limited precocious puberty, often abbreviated as FMPP, also known as familial sexual precocity or gonadotropin-independent testotoxicosis, is a form of gonadotropin-independent precocious puberty in which boys experience early onset and progression of puberty. Signs of puberty can develop as early as an age of 1 year.

The spinal length in boys may be short due to a rapid advance in epiphyseal maturation. It is an autosomal dominant condition with a mutation of the luteinizing hormone (LH) receptor. Treatment is with drugs that suppress gonadal steroidogenesis, such as cyproterone acetate, ketoconazole, spironolactone, and testolactone. Alternatively, the combination of the androgen receptor antagonist bicalutamide and the aromatase inhibitor anastrozole may be used.

Deficiency of sex hormones can result in defective primary or secondary sexual development, or withdrawal effects (e.g., premature menopause) in adults. Defective egg or sperm development results in infertility. The term hypogonadism usually means permanent rather than transient or reversible defects, and usually implies deficiency of reproductive hormones, with or without fertility defects. The term is less commonly used for infertility without hormone deficiency. There are many possible types of hypogonadism and several ways to categorize them. Hypogonadism is also categorized by endocrinologists by the level of the reproductive system that is defective. Physicians measure gonadotropins (LH and FSH) to distinguish primary from secondary hypogonadism. In primary hypogonadism the LH and/or FSH are usually elevated, meaning the problem is in the testicles, whereas in secondary hypogonadism, both are normal or low, suggesting the problem is in the brain.