GnRH includes LH and FSH.

LH stimulates leydeig cells to produce testosterone

FSH stimulates Sertoli cells to produce sperms.

Testosterone inhibits LH and FSH production.

However, the strong inhibitory stimulus for FSH is inhibin that is produced by the Sertoli cells.

Primary hypogonadism is because of defective testicular or ovarian function.

Secondary hypogonadism is because of defective pituitary function.

In primary hypogonadism, testosterone levels are low while the LH and FSH are elevated.

In secondary hypogonadism, all the three hormones are low.

Causes of primary hypogonadism are:

1. Klinefelter syndrome

2. Cryptorchidism

3. Testicular trauma

4. Medications

Clinical features of hypogonadism:

Antenatal presentation: micropenis and ambiguous genitalia

Pre-pubertal: incomplete or delayed puberty

Adults: fatigue, lethargy, low mood, loss of morning erection, loss of libido, depressed mood, loss of muscle mass and increased adiposity, and low BMI

Pre-pubertal males have:

1. Small testes ( less than 20 ml as measured by orchidometer)

2. Small phallus ( less than 8 CMS)

3. Eunuchoid body

4. No secondary sexual characteristics 

What is Eunuchoid body?

How to investigate male hypogonadism?

The first step is to measure serum testosterone levels at 08 - 10 am.

If testosterone levels are low, it is better to recheck especially in patients without clinical features of hypogonadism.

Next, do LH and FSH levels to label the patient as primary or secondary hypogonadism.

It is better to repeat all the three hormones if LH and FSH are either low or high.

Normal or low FSH and LH means the patient has secondary hypogonadism.

In case the patient comes out to have secondary hypogonadism, check other pituitary hormones such as TSH, ACTH, and prolactin levels

After the patient is labeled as hypopituitarism, or secondary hypogonadism, we may need to do pituitary MR.

Very low levels of testosterone, especially in males younger than 40 years of age, or those with neurologic features, raised prolactin, and defective vision should prompt brain imaging.

The treatment of primary hypogonadism is testosterone replacement. These patients can not become parents.

These patients may benefit from assistive reproductive techniques.

Those with secondary hypogonadism should be managed in such a way so as to achieve fertility.

Testosterone replacement is done by using tablets, injections, gels etc.

Pre-pubertal males require low doses of testosterone replacement to minimise growth and height.

Overtreatment may also result in frontal balding, polycythemia, gynecomastia, and aggression.

Rare side effects are associated with hepatocellular carcinoma.

Patients on testosterone replacement should be monitored for repeat levels one week before the next dose.

Patients on gels or tablets can be tested about 12 hours after treatment initiation.

Also, monitor for polycythemia and PSA levels after six months to one year.

For patients who have secondary hypogonadism where we aim to achieve fertility, the following are the treatment options:

1. HCG

2. Recombinant human LH

3. FSH injections

HCG is given as a subcutaneous injection in a dose of 1500 to 2000 units thrice weekly.

Monitor testosterone levels and adjust the dose. Once the testosterone levels are within the normal ranges, check semen analysis.

In patients who have a poor response to HCG, recombinant LH and FSH may be added