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Kallmann syndrome (KS) is a genetic disorder that prevents a person from starting or fully completing puberty.Kallmann syndrome is a form of a group of conditions termed hypogonadotropic hypogonadism. [1]
Puberty is considered delayed when the child has not begun puberty when two standard deviations or about 95% of children from similar backgrounds have. [7] [8] [9]In North American girls, puberty is considered delayed when breast development has not begun by age 13, when they have not started menstruating by age 15, [2] and when there is no increased growth rate. [8]
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Aromatase deficiency is a rare condition characterized by extremely low levels or complete absence of the enzyme aromatase activity in the body. [2] It is an autosomal recessive disease resulting from various mutations of gene CYP19 (P450arom) which can lead to ambiguous genitalia and delayed puberty in females, continued linear growth into adulthood and osteoporosis in males and virilization ...
Hypergonadotropic hypogonadism (HH), also known as primary or peripheral/gonadal hypogonadism or primary gonadal failure, is a condition which is characterized by hypogonadism which is due to an impaired response of the gonads to the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), and in turn a lack of sex steroid production. [1]
Typically, CHH is diagnosed in adolescence due to a lack of pubertal development, but it can be possible to diagnose in male neonates. Clinical presentations of CHH involve an absence of puberty by 18 years of age, poorly developed secondary sexual characteristics, or infertility. [12]
XX gonadal dysgenesis is a type of female hypogonadism in which the ovaries do not function to induce puberty in a person assigned female at birth, whose karyotype is 46,XX. [1] Individuals with XX gonadal dysgenesis have normal-appearing external genitalia as well as Müllerian structures (e.g., cervix, vagina, uterus).
Glycogenic hepatopathy [1] (also known as Mauriac syndrome [2]) is a rare complication of type 1 diabetes characterized by extreme liver enlargement due to glycogen deposition, along with growth failure and delayed puberty. It occurs in some children and adolescents with type 1 diabetes irrespective of their glycemic control.