Hypogonadism can be differentiated between hyper- and hypo-gonadotropic hypogonadism by measuring serum follicle-stimulating hormone (FSH) and luteinizing hormone (LH) (gonadotropins to measure pituitary output), and estradiol in girls (to measure gonadal output). By the age of 10–12, children with failure of the ovaries or testes will have high LH and FSH because the brain is attempting to jump-start puberty, but the gonads are not responsive to these signals.Stimulating the body by administering an artificial version of gonadotropin-releasing hormone (GnRH, the hypothalamic hormone) can differentiate between constitutional delay of puberty and a GnRH deficiency in boys, although no studies have been done in girls to prove this. It is often sufficient to simply measure the baseline gonadotrophin levels to differentiate between the two.In girls with hypogonadotropic hypogonadism, a serum prolactin level is measured to identify if they have the pituitary tumor prolactinoma. High levels of prolactin would warrant further testing with MRI imaging, except if drugs inducing the production of prolactin can be identified. If the child has any neurological symptoms, it is highly recommended that the physician obtains a head MRI to detect possible brain lesions.In girls with hypergonadotropic hypogonadism, a karyotype can identify chromosomal abnormalities, the most common of which is Turner syndrome. In boys, a karyotype is indicated if the child may have a congenital gonadal defect such as Klinefelter syndrome. In children with a normal karyotype, defects in the synthesis of the adrenal steroid sex hormones can be identified by measuring 17-hydroxylase, an important enzyme involved in the production of sex hormones.
Mildly obese to morbidly obese children are also more likely to begin puberty earlier than children of normal weight. Variation in genes related to obesity such as FTO or NEGRI have been associated with earlier onset of puberty. Children whose parents started puberty at an earlier age were also more likely to experience it themselves, especially in women where onset of menstruation correlated well between mothers and daughters and between sisters. Causes
Pubertal delay can be separated into four categories from most to least common:

Constitutional and physiologic delay
Children who are healthy but have a slower rate of physical development than average have a constitutional delay with a subsequent delay in puberty. It is the most common cause of delayed puberty in girls (30%) and even more so in boys (65%). It is commonly inherited with as much as 80% of the variation in the age of onset of puberty due to genetic factors. These children have a history of shorter stature than their age-matched peers throughout childhood, but their height is appropriate for bone age, meaning that they have delayed skeletal maturation with potential for future growth.It is often difficult to establish if it is a true constitutional delay of growth and puberty or if there is an underlying pathology because lab tests are not always discriminatory. In absence of any other symptoms, short stature, delayed growth in height and weight, and/or delayed puberty may be the only clinical manifestations of certain chronic diseases including coeliac disease.