Malnutrition or chronic disease
When underweight or sickly children present with pubertal delay, it is warranted to search for illnesses that cause a temporary and reversible delay in puberty. Chronic conditions such as sickle cell disease and thalassemia, cystic fibrosis, HIV/AIDS, hypothyroidism, chronic kidney disease, and chronic gastroenteric disorders (such as coeliac disease and inflammatory bowel disease) cause a delayed activation of the hypothalamic region of the brain to send signals to start puberty.Childhood cancer survivors can also present with delayed puberty secondary to their cancer treatments, especially males. The type of treatment, amount of exposure/dosage of drugs, and age during treatment determine the level by which the gonads are affected with younger patients at a lower risk of negative reproductive effects.Excessive physical exercise and physical stress, especially in athletes can also delay pubertal onset. Eating disorders such as bulimia nervosa and anorexia nervosa can also impair puberty due to undernutrition.Carbohydrate-restricted diets for weight loss has also been shown to decrease the stimulation of insulin which in turn does not stimulate kisspeptin neurons vital in the release of puberty-starting hormones. This shows that carbohydrate restricted children and children with diabetes mellitus type 1 can have delayed puberty. Primary failure of the ovaries or testes (hypergonadotropic hypogonadism)
Primary failure of the ovaries or testes (gonads) will cause delayed puberty due to the lack of hormonal response by the final receptors of the HPG axis.
Management
The goals of short-term hormone therapy are to induce the beginning of sexual development and induce a growth spurt, but should be limited to children with severe distress or anxiety secondary to their delayed puberty. Bone age must be monitored frequently to prevent precocious closure of the bone plates, thereby stunting growth. Constitutional and physiologic delay
If a child is healthy with a constitutional delay of growth and puberty, reassurance and prediction based on the bone age can be provided. No other intervention is usually necessary, but repeat evaluation by measuring serum testosterone or estrogen is recommended. Furthermore, the diagnosis of hypogonadism can be excluded once the adolescent has started puberty by age 16–18.Boys aged >14 years old whose growth is severely stunted or are experiencing severe distress secondary to their lack of puberty can be started on testosterone to increase their height. Testosterone treatment can also be used to stimulate sexual development, but it can close bone plates prematurely stopping growth altogether if not carefully administered. Another therapeutic option is the use of aromatase inhibitors to inhibit the conversion of androgens to estrogens as estrogens are responsible for stopping bone growth plate development and thus growth. However, due to side effects, therapy with testosterone alone is most often used.