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Hypogonadism

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Hypogonadism
SpecialtyEndocrinology Edit this on Wikidata

Hypogonadism is a medical term for a defect of the reproductive system which results in lack of function of the gonads (ovaries or testes). The gonads have two functions: to produce hormones (testosterone, estradiol, antimullerian hormone, progesterone, inhibin B), activin and to produce gametes (eggs or sperm). Deficiency of sex hormones can result in defective primary or secondary sexual development, or withdrawal effects (e.g., premature menopause) in adults. Defective egg or sperm development results in infertility.

The term hypogonadism is usually applied to permanent rather than transient or reversible defects, and usually implies deficiency of reproductive hormones, with or without fertility defects. The term is less commonly used for infertility without hormone deficiency.

Classification

There are many possible types of hypogonadism and several ways to categorize them.

by Congenital vs. acquired

by Hormones vs. fertility

Hypogonadism can involve just hormone production or just fertility, but most commonly involves both.

  • Examples of hypogonadism that affect hormone production more than fertility are hypopituitarism and Kallmann syndrome; in both cases fertility is reduced until hormones are replaced but can be achieved solely with hormone replacement.
  • Examples of hypogonadism that affect fertility more than hormone production are Klinefelter syndrome and Kartagener syndrome.

by Affected system

Hypogonadism is also categorized by endocrinologists by the level of the reproductive system which is defective.

  • A fourth form of hypogonadism has been detailed by world leading andrologist Dr Eugene Shippen called metabolic hypogonadism. This is a form of secondary hypogondism where no defect exists at the hypothalamic/pituitary level; but where gonadotropins are decreased via excess levels of SHBG (sex hormone binding globulin) and/or estradiol.

Steroid use

Hypogonadism may be induced by chronic use of anabolic/androgenic steroids (AAS). The negative-feedback system of the hypothalamic-pituitary-gonadal axis (HPTA) shuts down pituitary production of gonadotropins after extended exposure to AAS. This has been documented both in patients receiving AAS for legitimate medical reasons such as AIDS or cancer as well as athletes using AAS illicitly.

Hypogonadism may persist for some time after steroid use is discontinued.

Symptoms

Low Testosterone (Low T) symptoms include loss of energy, fatigue, loss of libido, muscle mass decline, decreased positive mood factors and an increased negative mood factors. Low testosterone can increase the statistical chances of developing the following;

Osteoporosis (an associated condition and common in long term untreated hypogonadism).

Type 2 Diabetes (an associated condition, a third of all such men have hypogonadism).

Alzheimer’s Disease (increased risk for the development of AD (Pike et al, 2006, Rosario 2004).

Cardio Vascular Disease (CVD) (recent studies have shown that testosterone is required for adequate vascularisation and function of the heart).

Obesity (low testosterone has been found to increase adipose, visceral fat around the waist).

Depression and anxiety disorders (many men with untreated low testosterone suffer from depression and/or anxiety).

Gynecomastia (male breast development is an associated condition)

Low Libido (adequate androgens/testosterone is required for a normal functioning libido)

Erectile Dysfunction (adequate androgens/testosterone is required in order to achieve and maintain erectile function).

Recent studies have shown a significantly increased mortality rate in men over 50 who have low testosterone/hypogonadism.

Diagnosis

Low Testosterone cannot be identified through a simple blood test, it requires an understanding of the importance of clinical presentation via examination and symptomatology and it also requires a careful view of the individuals medical case history. Normal testosterone levels range from 300 - 1098 ng/dl, but what testosterone level is correct for any indiviudal is more difficult to say as is any abstract cut-off point for low levels of testosterone. The situation is further complicated by the differing ancillary hormones and globulins that effect the crucial level of free circulating testosterone, dihydrotestosterone and estradiol levels. Physicians measure gonadotropins (LH and FSH) to try and distinguish primary from secondary hypogonadism. In primary hypogonadism the LH and/or FSH are usually elevated, while in secondary hypogonadism both are normal or low. Many forward thinking endocrinologists that work in the field of andrology argue that pathology alone should not be considered to be diagnostic alone unless testosterone or dihydrotestosterone levels are unequivically low. They argue that symptoms should be considered first and foremost and that blood level should merely be confirmitory and that a diagnosis of hypogondism should not be excluded on the basis of bloods alone.

Hypogonadism is often discovered during evaluation of delayed puberty, but ordinary delay which eventually results in normal pubertal development and reproductive function is termed constitutional delay.

Treatment

Hypogonadism is most often treated by replacement of the appropriate hormones. For men this is testosterone. Commonly used testosterone formulations include transdermal testosterone, injectable testosterone, and buccal testosterone. Oral testosterone is no longer used in the U.S. because it is broken down in the liver and rendered inactive. Another feasible alternative is hCG. For women estradiol and progesterone are replaced. Some types of fertility defects can be treated; some cannot. It is now quite common in the United States for men to also have estradiol tested and if high treated with an ancillary medicine such as anastrozole (brand name arimidex) to lower this potent estrogen level and maximize well-being.

References


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