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Causes of secondary hypogonadism in males

Author
Peter J Snyder, MD
Section Editors
Alvin M Matsumoto, MD
Mitchell E Geffner, MD
Deputy Editor
Kathryn A Martin, MD

INTRODUCTION

Hypogonadism in a male refers to a decrease in either or both of the two major functions of the testes: sperm production and/or testosterone production (see "Male reproductive physiology"). These abnormalities can result from disease of the testes (primary hypogonadism) or disease of the pituitary or hypothalamus (secondary hypogonadism). The distinction between these disorders is made by measurement of the serum concentrations of luteinizing hormone (LH) and follicle-stimulating hormone (FSH):

The patient has primary hypogonadism if his serum testosterone concentration and/or sperm count are low and/or his serum LH and FSH concentrations are high.

The patient has secondary hypogonadism if his serum testosterone concentration and/or the sperm count are low and/or his serum LH and FSH concentrations are inappropriately normal or low, which would be inappropriate if gonadotroph cell function were normal.

Secondary hypogonadism differs from primary hypogonadism in two characteristics:

Secondary hypogonadism is usually associated with similar decreases in sperm and testosterone production. This occurs because the reduction in LH secretion results in a decrease in testicular testosterone production and, therefore, in intratesticular testosterone, which is the principal hormonal stimulus to sperm production. In contrast, there is generally a greater fall in sperm production than in testosterone secretion in primary hypogonadism because the seminiferous tubules are damaged to a greater degree than the Leydig cells. Men with primary hypogonadism, therefore, might have normal serum testosterone and LH concentrations even when the number of ejaculated sperm is very low or zero and the FSH concentration is elevated.

                               

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Literature review current through: Nov 2016. | This topic last updated: Tue Mar 08 00:00:00 GMT+00:00 2016.
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