While hyperandrogenism in women is caused by external factors, it can also appear from natural causes.

Because hyperandrogenism can appear as a symptom of numerous different genetic and medical conditions, it is difficult to make a general statement on whether hyperandrogenic symptoms can be passed from parent to offspring. However, a collection of the conditions with hyperandrogenic symptoms, including polycystic ovary syndrome, have been observed as hereditary in certain cases. One potential cause of polycystic ovary syndrome is maternal hyperandrogenism, where the hormonal irregularities of the mother can affect the development of the child during gestation, resulting in the passing of polycystic ovary syndrome from mother to child.

Hyperprolactinemia occurs more commonly in women. The prevalence of hyperprolactinemia ranges from 0.4% in an unselected normal adult population (10,000 normal Japanese adults working at a single factory) to as high as 9 to 17% in women with reproductive disorders. Its prevalence was found to be 5% in a family planning clinic population, 9% in a population of women with adult-onset amenorrhea, and 17% among women with polycystic ovary syndrome.

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.

Isolated 17,20-lyase deficiency is caused by genetic mutations in the gene "CYP17A1", which encodes for 17,20-lyase, while not affecting 17α-hydroxylase, which is encoded by the same gene.

Observed physiological abnormalities of the condition include markedly elevated serum levels of progestogens such as progesterone and 17α-hydroxyprogesterone (due to upregulation of precursor availability for androgen and estrogen synthesis), very low or fully absent peripheral concentrations of androgens such as dehydroepiandrosterone (DHEA), androstenedione, and testosterone and estrogens such as estradiol (due to the lack of 17,20-lyase activity, which is essential for their production), and high serum concentrations of the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) (due to a lack of negative feedback on account of the lack of sex hormones).

The sex steroid consequences of severe 3β-HSD CAH are unique among the congenital adrenal hyperplasias: it is the only form of CAH that can produce ambiguity in both sexes. As with 21-hydroxylase deficient CAH, the degree of severity can determine the magnitude of over- or undervirilization.

In an XX (genetically female) fetus, elevated amounts of DHEA can produce moderate virilization by conversion in the liver to testosterone. Virilization of genetic females is partial, often mild, and rarely raises assignment questions. The issues surrounding corrective surgery of the virilized female genitalia are the same as for moderate 21-hydroxylase deficiency but surgery is rarely considered desirable.

The extent to which mild 3β-HSD CAH can cause early appearance of pubic hair and other aspects of hyperandrogenism in later childhood or adolescence is unsettled. Early reports about 20 years ago suggesting that mild forms of 3β-HSD CAH comprised significant proportions of girls with premature pubic hair or older women with hirsutism have not been confirmed and it now appears that premature pubarche in childhood and hirsutism after adolescence are not common manifestations of 3β-HSD CAH.

Undervirilization of genetic males with 3β-HSD CAH occurs because synthesis of testosterone is impaired in both adrenals and testes. Although DHEA is elevated, it is a weak androgen and too little testosterone is produced in the liver to offset the deficiency of testicular testosterone. The degree of undervirilization is more variable, from mild to severe. Management issues are those of an undervirilized male with normal sensitivity to testosterone.

If the infant boy is only mildly undervirilized, the hypospadias can be surgically repaired, testes brought into the scrotum, and testosterone supplied at puberty.

Management decisions are more difficult for a moderately or severely undervirilized genetic male whose testes are in the abdomen and whose genitalia look at least as much female as male. Male sex can assigned and major reconstructive surgery done to close the midline of the perineum and move the testes into a constructed scrotum. Female sex can be assigned and the testes removed and vagina enlarged surgically. A recently advocated third choice would be to assign either sex and defer surgery to adolescence. Each approach carries its own disadvantages and risks. Children and their families are different enough that none of the courses is appropriate for all.

The following are some of the possible medical causes of galactorrhea hyperprolactinemia that are listed by the Diseases Database: pregnancy, breastfeeding, sexual intercourse, shingles, prolactin secreting pituitary tumor, along with many others.

3β-HSD II mediates three parallel dehydrogenase/isomerase reactions in the adrenals that convert Δ4 to Δ5 steroids: pregnenolone to progesterone, 17α-hydroxypregnenolone to 17α-hydroxyprogesterone, and DHEA to androstenedione. 3β-HSD II also mediates an alternate route of testosterone synthesis from androstenediol in the testes. 3β-HSD deficiency results in large elevations of pregnenolone, 17α-hydroxypregnenolone, and DHEA.

However, complexity arises from the presence of a second 3β-HSD (3β-HSD I) coded by a different gene, expressed in the liver and placenta, and unaffected in 3β-HSD deficient CAH. The presence of this second enzyme has two clinical consequences. First, 3β-HSD II can convert enough of the excess 17α-hydroxypregnenolone to 17α-hydroxyprogesterone to produce 17α-hydroxyprogesterone levels suggestive of common 21-hydroxylase deficient CAH. Measurement of the other affected steroids distinguishes the two. Second, 3β-HSD I can convert enough DHEA to testosterone to moderately virilize a genetically female fetus.

The prevalence remains sparsely investigated. To date, two population-based nationwide studies have been conducted both estimating a prevalence about 1 in 5000 live female births. According to some reports, Queen Amalia of Greece may have had the syndrome, but a 2011 review of the historical evidence concludes that it is not possible to determine the inability of her and her husband to have a child. Her inability to provide an heir contributed to the overthrow of her husband, King Otto.

WNT4 (found on the short arm (p) of chromosome 1) has been clearly implicated in the atypical version of this disorder. A genetic mutation causes a leucine to proline residue substitution at amino acid position 12. This occurrence reduces the intranuclear levels of β catenin. In addition, it removes the inhibition of steroidogenic enzymes like 3β-hydroxysteriod dehydrogenase and 17α-hydroxylase. Patients therefore have androgen excess. Furthermore, without WNT4, the Müllerian duct is either deformed or absent. Female reproductive organs, such as the cervix, fallopian tubes, ovaries, and much of the vagina, are hence affected.

An association with a deletion mutation in the long arm (q) of chromosome 17 (17q12) has been reported. The gene LHX1 is located in this region and may be the cause of a number of these cases.

Persistent Müllerian duct syndrome (PMDS) is the presence of Müllerian duct derivatives (fallopian tubes, uterus, and/or the upper part of the vagina) in what would be considered a genetically and otherwise physically normal male animal by typical human based standards. In humans, PMDS typically is due to an autosomal recessive congenital disorder and is considered by some to be a form of pseudohermaphroditism due to the presence of Müllerian derivatives.

Typical features include undescended testes (cryptorchidism) and the presence of a small, underdeveloped uterus in an XY infant or adult. This condition is usually caused by deficiency of fetal anti-Müllerian hormone (AMH) effect due to mutations of the gene for AMH or the anti-Müllerian hormone receptor, but may also be as a result of insensitivity to AMH of the target organ.

PMDS type I results from mutations of the gene ("AMH") for AMH on chromosome 19p3.3.

PMDS type II results from mutations of the gene ("AMH-RII") for the AMH receptor on 12q13.

Both types of disorders are inherited as autosomal recessive conditions with expression usually limited to XY offspring.

Most women of reproductive age develop small cysts each month, and large cysts that cause problems occur in about 8% of women before menopause. Ovarian cysts are present in about 16% of women after menopause and if present are more likely to be cancer.

Benign ovarian cysts are common in asymptomatic premenarchal girls and found in approximately 68% of ovaries of girls 2–12 years old and in 84% of ovaries of girls 0–2 years old. Most of them are smaller than 9 mm while about 10-20% are larger macrocysts. While the smaller cysts mostly disappear within 6 months the larger ones appear to be more persistent.

Persistent adrenarche syndrome (also known as "Adrenal SAHA syndrome") is a cutaneous condition seen typically in thin young women who report great psychological and physical stress in their lives.

Although most cases of ovarian cysts involve monitoring, some cases require surgery. This may involve removing the cyst, or one or both ovaries. Technique is typically laparoscopic, unless the cyst is particularly large, or if pre-operative imaging suggests malignancy or complex anatomy. In certain situations, the cyst is entirely removed, while with cysts with low recurrence risk, younger patients, or which are in anatomically eloquent areas of the pelvis, they can be drained. Features that may indicate the need for surgery include:

- Persistent complex ovarian cysts

- Persistent cysts that are causing symptoms

- Complex ovarian cysts larger than 5 cm

- Simple ovarian cysts larger 10 cm or larger than 5 cm in postmenopausal patients

- Women who are menopausal or perimenopausal

PWS affects approximately 1 in 10,000 to 1 in 25,000 newborns. There are more than 400,000 people who live with PWS around the world.

There is not enough known about persistent genital arousal disorder to definitively pinpoint a cause. Medical professionals think it is caused by an irregularity in sensory nerves, and note that the disorder has a tendency to strike post-menopausal women, or those who have undergone hormonal treatment.

Some drugs such as trazodone may cause priapism as a side effect, in which case discontinuing the medication may give relief. Additionally, the condition can sometimes start only after the discontinuation of SSRIs. In some recorded cases, the syndrome was caused by or can cause a pelvic arterial-venous malformation with arterial branches to the penis or clitoris; surgical treatment was effective in this case.

In other situations where the cause is unknown or less easily treatable, the symptoms can sometimes be reduced by the use of antidepressants, antiandrogenic agents, and anaesthetising gels. Psychotherapy with cognitive reframing of the arousal as a healthy response may also be used.

More recently, the symptoms of the condition have also been linked with pudendal nerve entrapment. Regional nerve blocks and less common surgical intervention have demonstrated varying degrees of success in most cases. There is, however, no evidence for the long-term efficacy of surgical intervention.

In one recent case, serendipitous relief of symptoms was noted from treatment with varenicline, a treatment for nicotine addiction.

PWS is commonly associated with development of strabismus. In one study, over 50% of patients had strabismus, mainly esotropia.

The overwhelming majority of reported AIGA patients are Japanese, but whether AIGA is truly rare in whites or has been simply underreported by Western physicians remains unclear.

AIGA is most prevalent among young men. In a 64 case review of the literature 58 reported cases were males and 6 female, with a mean age of onset at 28 ± 11 years. Cholinergic urticaria or sharp pain over the entire body induced by elevated body temperature was reported in 32 cases (50%). Of 28 cases tested, 12 (43%) displayed elevated serum IgE levels. Skin biopsy was performed in 53 cases, with normal findings in 20 cases (38%), and cellular infiltrates in sweat glands or ducts in 23 cases (43%).

The treatment is with a low sodium (low salt) diet and a potassium-sparing diuretic that directly blocks the sodium channel. Potassium-sparing diuretics that are effective for this purpose include amiloride and triamterene; spironolactone is not effective because it acts by regulating aldosterone and Liddle syndrome does not respond to this regulation. Amiloride is the only treatment option that is safe in pregnancy. Medical treatment usually corrects both the hypertension and the hypokalemia, and as a result these patients may not require any potassium replacement therapy.

Intracutaneous injection of pilocarpine (sweat gland stimulant) is known to evoke no sweat response, indicating that lesions are on the post-synaptic side of the nerve-sweat gland junction.

The proposed pathomechanisms of idiopathic pure sudomotor failure include:

- A deficit within muscarinic cholinergic receptors of the eccrine sweat glands.

- Interference in acetylcholine transmission to cholinergic receptors.

- A cross-reactive immune response which interferes with cholinergic transmission in the eccrine glands.

- Components of an immediate-type allergy (based on the dramatic resumption of axon reflex sweating following glucocorticoid treatment).

Liddle's syndrome, also called Liddle syndrome is a genetic disorder inherited in an autosomal dominant manner that is characterized by early, and frequently severe, high blood pressure associated with low plasma renin activity, metabolic alkalosis, low blood potassium, and normal to low levels of aldosterone. Liddle syndrome involves abnormal kidney function, with excess reabsorption of sodium and loss of potassium from the renal tubule, and is treated with a combination of low sodium diet and potassium-sparing diuretic drugs (e.g. amiloride). It is extremely rare, with fewer than 30 pedigrees or isolated cases having been reported worldwide as of 2008.

The cause of congenital hyperinsulinism has been linked to anomalies in nine different genes. The diffuse form of this condition is inherited via the autosomal recessive manner(though sometimes in "autosomal dominant").

Usually observed at birth or shortly thereafter in 94% of patients, in other reports, patients did not develop skin lesions until 3 months or even 2 years after birth. Females are typically affected more often than males (64%).