A Study On Hypogonadotropic Hypogonadism And Hypergonadotropic Hypogonadism

Me: When I was doing research on the effects of  combining Gonadotropin releasing hormone analogues (GnRH-A) with human growth hormones (hGH) as a way to treat the many diverse forms of short stature, this very interesting disorder really caught my attention and I wanted to devote some time to learn more about this disorder since it might help us remove some confusion over certain issues. We know that the control and flow of the sex hormones is what can ultimately determine out final height since we have already seen how certain people without the right types of hormones or hormone receptors never even reach puberty or don’t have closed growth plates resulting in continued growth even into their 30s.

Analysis & Interpretation:

There is two main conditions we are finding with very similar names, except that one process is the opposite of the other. One is called Hypogonadotropic Hypogonadism and the other is called Hypergonadotropic Hypogonadism. The prefix “hyper” has always meant “excessive” in common english terms while the prefix “hypo” means “not enough” in common english terms. From the two Wikipedia articles I have posted below, the summarize idea is that HH and HH, the hyper and the hypo, both results in hypogonadism, which is where the body doesn’t get enough hormones from the gonads, the reproductive organs. The hypogonadotropic hypogonadism sees an impaired secretion of the gonadotropins like the FSH and LH by the pituitary gland and the hypothalamus of the brain. Since the endocrine system works from a top–>down approach, this will eventually lead to less sex hormones produced in the gonads of the person. The is why the 2nd term is hypogonadism.

The hypergonadotropic hypogonadism in comparison has the pituitary gland and the hypothalamus being just fine in function and releasing the neccessary amount of gonadotropins like the FSH and the LH but the problem is that the gonads can’t seem to be able to receive the gonadotropins or can’t process them correctly to release the high enough levels of gonad hormones, like the androgen and estrogen. The symptoms of hypogonadism in general is low sex drive, infertility, and not puberty signs like hair growth, etc. To treat the first type, where the brain areas don’t release enough, physicians can directly add the needed hormones using a GnRH agonist or a gonadotropin formulation. To treat the 2nd type, the physician can just add synthetic androgens as a hormone therapy to get the level of sex hormones in the body correct.

The connection with height increase with the two conditions is that from many genetic disorders and cases, we find that people who have no sensitivity to the sex hormones like the androgens or estrogen have often led to delayed puberty, and thus resulted in a later age for growth plate cartilage closure. There are at least 3 cases of males who had no receptors for the estrogen in their growth plates and they resulted in being very tall with the cartilage still existing in late adulthood.

From my personal analysis, it would seem that the case for tall stature can only be found with people who suffer from hypergonadotropic hypogonadism, NOT hypogonadotropic hypogonadism.  I would guess that the lack of ability to release the FSH and the LP by the hypothalamic-pituitary connection would also cause insufficient release of the growth hormones too. So it would make logical sense then that the human body which can release growth hormones but stop the process of reeleasing the testosterone and estrogens which will lead to both puberty/increased growth rate but also growth plate closure means that the person who suffers only from hypergonadotropic hypogonadism will note that they never went through the great growth spurt that their peers did in adolescent, noticed that they were more likely on the short side while young, but as they grew older, they did not stop growing completely like their peers but eventually surpasses in height of their peers in their late 20s due to their open growth plate cartilage.


From the Wikipedia article on it HERE

Hypogonadotropic hypogonadism (HH), also known as secondary or central hypogonadism, as well as gonadotropin-releasing hormone deficiency or gonadotropin deficiency (GD), is a condition which is characterized by hypogonadism due to an impaired secretion of gonadotropins, including follicle-stimulating hormone (FSH) and luteinizing hormone (LH), by the pituitary gland in the brain, and in turn decreased gonadotropin levels and a resultant lack of sex steroid production.

Causes

The type of HH, based on its cause, may be classified as either primary or secondaryPrimary HH, also called isolated HH, is responsible for only a small subset of cases of HH, and is characterized by an otherwise normal function and anatomy of the hypothalamus and anterior pituitary. It is caused by congenital syndromes such as Kallmann syndrome and gonadotropin-releasing hormone (GnRH) insensitivity. Secondary HH, also known as acquired or syndromic HH, is far more common than primary HH, and is responsible for most cases of the condition. It has a multitude of different causes, including brain orpituitary tumors, pituitary apoplexy, head trauma, ingestion of certain drugs, and certain systemic diseases and syndromes.

Symptoms

Examples of symptoms of hypogonadism include delayed, reduced, or absent puberty, low libido, and infertility.

Treatment

Treatment of HH may consist of administration of either a GnRH agonist or a gonadotropin formulation in the case of primary HH and treatment of the root cause (e.g., a tumor) of the symptoms in the case of secondary HH. Alternatively, hormone replacement therapy with androgens and estrogens in males and females, respectively, may be employed.


Now let’s look at the opposite of it which is termed Hypergonadotropic Hypogonadism

From the Wikipedia article on it HERE

Hypergonadotropic hypogonadism (HH), also known as primary or peripheral/gonadal hypogonadism, is a condition which is characterized by hypogonadism 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 and elevated gonadotropin levels (as an attempt of compensation by the body). HH may present as either congenital or acquired, but the majority of cases are of the former nature.

Causes

  • Chromosomal abnormalities (resulting in gonadal dysgenesis) – Turner’s syndrome, Klinefelter’s syndrome, Swyer’s syndrome, XX gonadal dysgenesis, and mosaicism.
  • Defects in the enzymes involved in the gonadal biosynthesis of the sex hormones – 17α-hydroxylase deficiency, 17,20-lyase deficiency, 17β-hydroxysteroid dehydrogenase III deficiency, and lipoid congenital adrenal hyperplasia.
  • Gonadotropin resistance (e.g., due to inactivating mutations in the gonadotropin receptors) – Leydig cell hypoplasia (or insensitivity to LH) in males, FSH insensitivity in females, and LH and FSH resistance due to mutations in the GNAS gene (termed pseudohypoparathyroidism type 1A).

Acquired causes (due to damage to or dysfunction of the gonads) include gonadal torsion, vanishing/anorchia, orchitis, premature ovarian failure, ovarian resistance syndrome, trauma, surgery, autoimmunity,chemotherapy, radiation, infections (e.g., sexually-transmitted diseases), toxins (e.g., endocrine disruptors), and drugs (e.g., antiandrogens, opioids, alcohol).

Symptoms

Examples of symptoms of hypogonadism include delayed, reduced, or absent puberty, low libido, and infertility.

Treatment

Treatment of HH is usually with hormone replacement therapy, consisting of androgen and estrogen administration in males and females, respectively.

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