Use of testosterone in male hypogonadism

The primary clinical use of testosterone is substitution therapy of male hypogo-nadism. Hypogonadism may be caused by hypothalamic, pituitary, testicular or

Table 13.1 Overview of disorders with male hypogonadism classified according to localisation of cause

Hypothalamic-pituitary origin (hypogonadotropic syndromes = secondary hypogonadism) Idiopathic hypogonadotropic hypogonadism (IHH)

including Kallmann syndrome Congenital adrenal hypoplasia Prader-Labhart-WiHi syndrome Laurence-Moon-Biedl syndrome Constitutional delay of puberty Pituitary insufficiency/adenomas Pasqualini syndrome Isolated lack of FSH Biologic inactive LH or FSH Hyperprolactinemia Hemochromatosis

Testicular origin (hypergonadotropic syndromes = primary hypogonadism) Congenital anorchia Acquired anorchia Maldescended testes Klinefelter syndrome XYY syndrome XX male

Noonan syndrome Gonadal dysgenesis Leydig cell tumors Maldescended testes Varicocele

Sertoli-cell-only syndrome

General disease e.g. renal failure, liver cirrhosis, diabetes, myotonia dystrophica Male pseudohermaphroditism due to enzyme defects in testosterone biosynthesis or

LH-receptor defects (Leydig cell aplasia) General diseases Exogenous factors

Mixed primary and secondary hypogonadism

Late-onset hypogonadism

Target organ resistance to sex steroids

Complete androgen insensitivity (Testicular feminization) Reifenstein syndrome

Perineoscrotal hypospadias with pseudovagina Aromatase deficiency Estrogen resistance target organ lesions. An overview of the various disease entities and syndromes is provided in Table 13.1 and for a detailed description the reader is referred to the textbook by Nieschlag and Behre (2000).

The clinical symptoms of all syndromes and disease entities are predominantly due to a lack of testosterone or its action. The most frequent disorders requiring testosterone substitution are Klinefelter syndrome, Kallman syndrome, idiopathic hypogonadotropic hypogonadism (IHH), anorchia and pituitary insufficiency. Some disorders such as varicocele, orchitis, maldescended testes and Sertoli-cell-only syndrome will not, or only eventually require testosterone substitution. Although discrete endocrine alterations may be noted by laboratory tests in these patients, the endocrine capacity of the Leydig cells remains high enough to maintain serum testosterone in the lower physiological range.

In order to achieve fertility in patients with hypothalamic (IHH) or pituitary insufficiency, treatment with gonadotropins (hCG/hMG) or pulsatile GnRH is required temporarily (e.g. Buchter etal. 1998; Depenbusch etal. 2002; Depenbusch and Nieschlag 2004). Once a pregnancy has been induced these patients will go back on testosterone substitution. Cases with hypogonadism of testicular origin in whom infertility cannot be treated require testosterone substitution continuously. In all these patients testosterone substitution is a life-long therapy.

There is general agreement that patients with "classical" disorders of primary or secondary hypogondadism should receive testosterone substitution therapy. However, there is a relatively large group of patients in whom hypogonadism develops as a corollary of other acute or chronic diseases. Although these patients lack testosterone and show symptoms of hypogonadism, testosterone is usually not administered to them. Just why substitution is withheld is not quite clear. Probably in many physicians' minds testosterone is predominantly associated with sexual functions. However, the better the general effects of testosterone on well-being, mood, bones, muscles and red blood are understood, the more frequently testosterone substitution will be considered. Chapter 15 is dedicated to the possible use of testosterone in these non-gonadal diseases. Similarly, late-onset hypogonadism occurring with increasing incidence in ageing men, and representing a combined form of primary and secondary hypogonadism, is associated with symptoms of testosterone deficiency. But there is no general agreement on treatment strategies of this condition and Chapter 16 deals with late-onset hypogonadism and the controversies and unresolved problems surrounding this area. Furthermore, Chapter 3 covers the possible use of testosterone in androgen resistance syndromes.

For the time being the principle may be followed that any type of hypogonadism documented by decreased serum testosterone concentrations deserves testosterone substitution, unless there is a clear contraindication, of which there are only few.

Table 13.2 Symptoms of hypogonadism relative to age of manifestation

Onset of lack of testosterone before after

Affected organ/function completed puberty before after

Affected organ/function completed puberty

Larynx

No voice mutation

No change

Hair

Horizontal pubic hairline,

Diminishing secondary body

straight frontal hairline,

hair, decreased beard

diminished beard growth

growth

Skin

Absent sebum production, lack

Decreased sebum production,

of acne, pallor, skin wrinkling

lack of acne, pallor, skin

wrinkling, hot flashes

Bones

Eunuchoid tall stature, Armspan

Arm span = height,

> height, osteoporosis

osteoporosis

Bone marrow

Low degree anaemia

Low degree anaemia

Muscles

Underdeveloped

Atrophy

Prostate

Underdeveloped

Atrophy

Penis

Infantile

No change of size

Testes

Small volume, often

Decrease of volume and

maldescended testes

consistency

Spermatogenesis

Not initiated

Arrest

Ejaculate

Not produced

Low volume

Libido

Not developed

Loss

Potency

Not developed

Erectile dysfunction

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