Hormones

New guidelines emphasise clinical diagnosis of pathological hypogonadism


New guidelines from the Endocrine Society of Australia emphasise the importance of obtaining a clinical diagnosis of pathological hypogonadism before confirming the diagnosis with biochemical testing.

Presenting part I of the recommendations to the ESASRBANZBMS 2016 congress here on the Gold Coast lead author Bu Yeap from the University of Western Australia in Perth told delegates the recommendations differed from other international societies because the ESA working group had, “Come right out and said men who need treatment with testosterone are those with pathological hypogonadism”.

Professor Yeap explained that the ESA had first published guidelines on androgen prescribing in 2000 but since then a lot of things had happened.

“We’ve had an increase in rates of prescriptions of testosterone in Australia and globally,” he told delegates.

The ESA council reconvened the working group to update the guidelines but during that process the PBS revised the criteria by which men could qualify for testosterone prescriptions.

“That provoked quite a lot of angst, discussion, debate and referrals to endocrinology clinics,” he said.

The updated guidelines placed a clear emphasis on obtaining a clinical diagnosis before confirmatory biochemical testing, and not the other way around, he said.

“We should be giving testosterone replacement treatment to men who have pathological hypergonadism… we do it to relieve the signs and symptoms of androgen deficiency in those men.”

The second part of the recommendations will be published in the MJA on Monday 29th August. 

Part 1: Main recommendations and key points:

  • Pathological hypogonadism arises due to diseases of the hypothalamus or pituitary gland (hypogonadotropic hypogonadism) or testes (hypergonadotropic hypogonadism). It is a clinical diagnosis with a pathological basis, confirmed by hormone assays.
  • Hormonal assessment is based on measurement of circulating testosterone, luteinising hormone (LH) and follicle-stimulating hormone (FSH) concentrations. Measurement of sex hormone-binding globulin levels can be informative, but use of calculated free testosterone is not recommended for clinical decision making.
  • Testosterone replacement therapy is warranted in men with pathological hypogonadism, regardless of age.
  • Currently, there are limited data from high-quality randomised controlled trials with clinically meaningful outcomes to justify testosterone treatment in older men, usually with chronic disease, who have low circulating testosterone levels but without hypothalamic, pituitary or testicular disease.
  • Obesity, metabolic syndrome and type 2 diabetes are associated with lowering of circulating testosterone level, but without elevation of LH and FSH levels. Whether these are non-specific consequences of non-reproductive disorders or a correctable deficiency state is unknown, but clear evidence for efficacy and safety of testosterone therapy in this setting is lacking.
  • Glucocorticoid and opioid use is associated with possibly reversible reductions in circulating testosterone level, without elevation of LH and FSH levels. Where continuation of glucocorticoid or opioid therapy is necessary, review by an endocrinologist may be warranted. 

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