People with Laron syndrome have strikingly low rates of cancer and diabetes, although they appear to be at increased risk of accidental death due to their stature.

Administration of GH has no effect on IGF-1 production, therefore treatment is mainly by biosynthetic IGF-1. IGF-1 must be taken before puberty to be effective.

The drug product Increlex (mecasermin), developed by the company Tercica, now Genentech, was approved by the US Food and Drug Administration in August 2005 for replacing IGF-1 in patients who are deficient.

IPLEX (Mecasermin rinfabate) is composed of recombinant human IGF-1 (rhIGF-1) and its binding protein IGFBP-3. It was approved by the U.S. Food and Drug Administration (FDA) in 2005 for treatment of primary IGF-1 deficiency or GH gene deletion. Side effects from IPLEX are hypoglycemia. IPLEX's manufacturing company, Insmed, after selling its protein production facility, can no longer develop proteins, thus can no longer manufacture IPLEX as of a statement released in July 2009.

Some people may have some mental slowness, but children with this condition often have good social skills. Some males may have problems with fertility.

Allen Avinoam Kowarski et al. described the first two cases of the Kowarski syndrome in 1978. The group speculated that their patients' growth impairment was caused by a mutation in the growth hormone gene, which altered the structure of their secreted growth hormone, reducing its biological activity while retaining its ability to bind the antibodies used in the RIA-GH. Their RIA-GH measured growth hormone of reduced bioactivity. The children retained the ability to respond to treatment with active growth hormone.

The speculation of Kowarski et al. was confirmed by Valenta et al in 1985, Takahshi et al in 1996 and 1997 and Besson et al in 2005. Valenta et al studied a case of Kowarski syndrome where they confirmed a structural abnormality of the growth hormone molecule. 60 to 90% of circulating growth hormone of the patient was in the form of tetramers and dimers (normal, 14% to 39% in plasma) and the patients' growth hormone polymers were abnormally resistant to conversion into monomers by urea.

Takahashi et al. reported a case of a boy with short stature who was heterozygous for a mutation in the GH1 gene. In this child, growth hormone not only could not activate the GH receptor (GHR) but also inhibited the action of wild type GH because of its greater affinity for GHR and GH-binding protein (GHBP) that is derived from the extracellular domain of the GHR. Thus, a dominant-negative effect was observed.

Takahashi et al. demonstrated in a girl with short stature, a biologically inactive growth hormone resulting from a heterozygous mutation in the GH1 gene. At age 3 years, the girl's height was 3.6 standard deviations below the mean for age and sex. Bone age was delayed by 1.5 years. She had a prominent forehead and a hypoplastic nasal bridge with normal body proportions. She showed lack of growth hormone action despite high immunoassayable GH levels in serum and marked catch-up growth to exogenous GH administration. Results of other studies were compatible with the production of a bioinactive GH, which prevented dimerization of the growth hormone receptor, a crucial step in GH signal transduction.

Besson et al described in 1955 a Serbian patient with Kowarski syndrome who was homozygous for a mutation in the GH1 gene that disrupted the first disulfide bridge in growth hormone. The parents were each heterozygous for the mutation and were of normal stature.

Kowarski syndrome describes cases of growth failure (height and bone age two standard deviations below the mean for age), despite the presence of normal or slightly high blood growth hormone by radioimmunoassay (RIA-GH) and low serum IGF1 (formerly called somatomedin), and who exhibit a significant increase in growth rate following recombinant GH therapy.

The decision to treat is based on a belief that the child will be disabled by being extremely short as an adult, so that the risks of treatment (including sudden death) will outweigh the risks of not treating the symptom of short stature. Although short children commonly report being teased about their height, most adults who are very short are not physically or psychologically disabled by their height. However, there is some evidence to suggest that there is an inverse linear relationship with height and with risk of suicide.

Treatment is expensive and requires many years of injections with human growth hormones. The result depends on the cause, but is typically an increase in final height of about taller than predicted. Thus, treatment takes a child who is expected to be much shorter than a typical adult and produces an adult who is still obviously shorter than average. For example, several years of successful treatment in a girl who is predicted to be as an adult may result in her being instead.

Increasing final height in children with short stature may be beneficial and could enhance health-related quality of life outcomes, barring troublesome side effects and excessive cost of treatments.

The cost of treatment depends on the amount of growth hormone given, which in turn depends on the child's weight and age. One year's worth of drugs normally costs about US $20,000 for a small child and over $50,000 for a teenager. These drugs are normally taken for five or more years.

Children with PSS have extremely low levels of growth hormone. These children possibly have a problem with growth hormone inhibiting hormone (GHIH) or growth hormone releasing hormone (GHRH). The children could either be unresponsive to GHRH, or too sensitive to GHIH.

Children who have PSS exhibit signs of failure to thrive. Even though they appear to be receiving adequate nutrition, they do not grow and develop normally compared to other children of their age.

An environment of constant and extreme stress causes PSS. Stress releases hormones in the body such as epinephrine and norepinephrine engage what is known as the 'fight or flight' response. The heart speeds up and the body diverts resources away from processes that are not immediately important; in PSS, the production of growth hormone (GH) is thus affected. As well as lacking growth hormone, children with PSS exhibit gastrointestinal problems due to the large amounts of epinephrine and norepinephrine, resulting in their bodies lacking proper digestion of nutrients and further affecting development.

While the cure for PSS is questionable, some studies show that placing the child affected with the disease in a foster or group home increases growth rate and socialization skills.

Similar to all genetic diseases Aarskog–Scott syndrome cannot be cured, although numerous treatments exist to increase the quality of life.

Surgery may be required to correct some of the anomalies, and orthodontic treatment may be used to correct some of the facial abnormalities. Trials of growth hormone have been effective to treat short stature in this disorder.

Genetically, there is a postzygotic mutation (spontaneous mutation) of the gene GNAS, on the long (q) arm of chromosome 20 at position 13.3, which is involved in G-protein signaling. This mutation, which occurs only in the mosaic state, leads to constitutive receptor signaling and inappropriate production of excess cAMP.

The mutation that causes McCune–Albright syndrome arises very early during embryogenesis. It is not passed down from parent to child. There are no known risk factors for acquiring McCune–Albright syndrome, and no exposures during pregnancy that are known to either cause or prevent the mutation from occurring.

McCune–Albright syndrome is a complex genetic disorder affecting the bone, skin, and endocrine systems. It is a mosaic disease arising from somatic activating mutations in "GNAS", which encodes the alpha-subunit of the Gs G-coupled protein receptor. These mutations lead to constitutive receptor activation.

It was first described in 1937 by Donovan James McCune and Fuller Albright.

Although the exact pathology of Dubowitz syndrome is not known yet, it is heritable and classified as an autosomal recessive disease. Furthermore, there is an occasional parental consanguinity. Several cases point to Dubowitz syndrome occurring in monozygotic twins, siblings, and cousins. There is considerable phenotypic variability between cases, especially in regards to intelligence. Although substantial evidence points to the genetic basis of this disorder, the phenotypic similarity is found in fetal alcohol syndrome. Further studies need to be done to determine whether this environmental agent effects the expression of the genotype. Breakdown of chromosomes is known to occur.

Dubowitz syndrome is a rare genetic disorder characterized by microcephaly, stunted growth, and a receding chin. Symptoms vary among patients, but other characteristics include a soft, high-pitched voice; partial webbing of the fingers and toes; palate deformations; genital abnormalities; language difficulties; and an aversion to crowds. The pathogenesis of the disease is yet to be identified, and no medical tests can definitively diagnose the disease. The primary method of diagnosis is to identify facial phenotypes. Since it was first described in 1965 by English physician Victor Dubowitz, over 140 cases have been reported worldwide. Although the majority of cases have been reported from the United States, Germany, and Russia, the disorder appears to affect both genders and all ethnicities equally.

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.

Treatment consists of maintaining normal levels of calcium, phosphorus, and Vitamin D. Phosphate binders, supplementary Calcium and Vitamin D will be used as required.

Affected individuals have a somewhat shortened lifespan. The maximum described lifespan is 67 years. Adults with 13q deletion syndrome often need support services to maintain their activities of daily living, including adult day care services or housing services.

Most XY children are so undervirilized that they are raised as girls. The testes are uniformly nonfunctional and undescended; they are removed when the diagnosis is made due to the risk of cancer development in these tissues.

Gonadotropin-releasing hormone (GnRH) insensitivity is a rare autosomal recessive genetic and endocrine syndrome which is characterized by inactivating mutations of the gonadotropin-releasing hormone receptor (GnRHR) and thus an insensitivity of the receptor to gonadotropin-releasing hormone (GnRH), resulting in a partial or complete loss of the ability of the gonads to synthesize the sex hormones. The condition manifests itself as isolated hypogonadotropic hypogonadism (IHH), presenting with symptoms such as delayed, reduced, or absent puberty, low or complete lack of libido, and infertility, and is the predominant cause of IHH when it does not present alongside anosmia.

As a chromosomal condition, there is no cure for Turner syndrome. However, much can be done to minimize the symptoms. For example:

- Growth hormone, either alone or with a low dose of androgen, will increase growth and probably final adult height. Growth hormone is approved by the U.S. Food and Drug Administration for treatment of Turner syndrome and is covered by many insurance plans. There is evidence that this is effective, even in toddlers.

- Estrogen replacement therapy such as the birth control pill, has been used since the condition was described in 1938 to promote development of secondary sexual characteristics. Estrogens are crucial for maintaining good bone integrity, cardiovascular health and tissue health. Women with Turner Syndrome who do not have spontaneous puberty and who are not treated with estrogen are at high risk for osteoporosis and heart conditions.

- Modern reproductive technologies have also been used to help women with Turner syndrome become pregnant if they desire. For example, a donor egg can be used to create an embryo, which is carried by the Turner syndrome woman.

- Uterine maturity is positively associated with years of estrogen use, history of spontaneous menarche, and negatively associated with the lack of current hormone replacement therapy.

Although there is no cure for 13q deletion syndrome, symptoms can be managed, usually with the involvement of a neurologist, rehabilitation physician, occupational therapist, physiotherapist, psychotherapist, nutritionist, special education professional, and/or speech therapist. If the affected child's growth is particularly slow, growth hormone treatment can be used to augment growth. Plastic surgeries can repair cleft palates, and surgical repair or monitoring by a pediatric cardiologist can manage cardiac defects. Some skeletal, neurological, genitourinary, gastrointestinal, and ophthalmic abnormalities can be definitively treated with surgery. Endocrine abnormalities can often be managed medically. Special educators, speech and occupational therapists, and physiotherapists can help a child develop skills in and out of school.

Albright's hereditary osteodystrophy is a form of osteodystrophy, and is classified as the phenotype of pseudohypoparathyroidism type 1A; this is a condition in which the body does not respond to parathyroid hormone.

GH deficiency is treated by replacing GH with daily injections under the skin or into muscle. Until 1985, growth hormone for treatment was obtained by extraction from human pituitary glands collected at autopsy. Since 1985, recombinant human growth hormone (rHGH) is a recombinant form of human GH produced by genetically engineered bacteria, manufactured by recombinant DNA technology. In both children and adults, costs of treatment in terms of money, effort, and the impact on day-to-day life, are substantial.

There are as yet no effective treatments for primordial dwarfism. It is known that PD is caused by inheriting a mutant gene from each parent. The lack of normal growth in the disorder is not due to a deficiency of growth hormone, as in hypopituitary dwarfism. Administering growth hormone, therefore, has little or no effect on the growth of the individual with primordial dwarfism, except in the case of Russell Silver Syndrome. Individuals with RSS respond favorably to growth hormone treatment, this fact is supported by The Magic Foundation. Children with RSS that are treated with growth hormone before puberty may achieve several inches of additional height. In January 2008, it was published that mutations in the pericentrin gene (PCNT) were found to cause primordial dwarfism. Pericentrin has a role in cell division, proper chromosome segregation, and cytokinesis.

GH treatment is not recommended for children who are not growing despite having normal levels of growth hormone, and in the UK it is not licensed for this use. Children requiring treatment usually receive daily injections of growth hormone. Most pediatric endocrinologists monitor growth and adjust dose every 3–6 months and many of these visits involve blood tests and x-rays. Treatment is usually extended as long as the child is growing, and lifelong continuation may be recommended for those most severely deficient. Nearly painless insulin syringes, pen injectors, or a needle-free delivery system reduce the discomfort. Injection sites include the biceps, thigh, buttocks, and stomach. Injection sites should be rotated daily to avoid lipoatrophy. Treatment is expensive, costing as much as US $10,000 to $40,000 a year in the USA.

Due to its mild presentation, MAIS often goes unnoticed and untreated. Management of MAIS is currently limited to symptomatic management; methods to correct a malfunctioning androgen receptor protein that result from an AR gene mutation are not currently available. Treatment includes surgical correction of mild gynecomastia, minor hypospadias repair, and testosterone supplementation. Supraphysiological doses of testosterone have been shown to correct diminished secondary sexual characteristics in men with MAIS, as well as to reverse infertility due to low sperm count. As is the case with PAIS, men with MAIS will experience side effects from androgen therapy (such as the suppression of the hypothalamic-pituitary-gonadal axis) at a higher dosage than unaffected men. Careful monitoring is required to ensure the safety and efficacy of treatment. Regular breast and prostate examinations may be necessary due to comorbid association with breast and prostate cancers.