Growth hormone replacement inhibits renal and hepatic 11 beta-hydroxysteroid dehydrogenases in ACTH-deficient patients

What Was Tested

Researchers studied ACTH (Corticotropin) in this randomized controlled trial publication.

The commonest side-effects of GH replacement therapy relate to sodium retention but its mechanism is unclear.

In rats, GH inhibits renal and hepatic 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) activities.

In man, this action might impair inactivation of cortisol to cortisone in the distal nephron thereby allowing cortisol to activate mineralocorticoid receptors.

Who Took Part

According to the abstract, 6 men were involved.

The age groups tagged for this paper are adults and middle-aged adults, both men and women.

A randomized double-blind study comparing 6 months GH replacement with placebo in adults with GH deficiency due to pituitary or hypothalamic disease.

6 men and 8 women received placebo and 8 men and 9 women received GH.

How the Study Was Run

The design is described as randomized, double-blind and placebo-controlled.

The men were allocated by chance, so the ACTH (Corticotropin) group and the comparison group should start out alike.

Neither the men nor the staff measuring them knew who was on ACTH (Corticotropin), so expectations could not easily colour the readings.

The comparison arm used a placebo, so changes seen with ACTH (Corticotropin) could be set against what happens without it.

Cortisol and its metabolites were measured in overnight urine samples and in a fasting morning plasma sample at baseline and at 6 months.

What Was Measured

PubMed files the paper under topics including 11-beta-Hydroxysteroid Dehydrogenases, Adrenocorticotropic Hormone, Cortisone, Growth Hormone, Hydrocortisone, Hydroxysteroid Dehydrogenases and Hypopituitarism.

What This Means in Plain Language

The paper is a randomized, double-blind and placebo-controlled study of ACTH (Corticotropin) in 6 men.

With fewer than 40 people, it is a small study, so it is better read as an early signal for further research than as a settled answer.

Its findings take up roughly 9 sentences of the abstract and are left out here on purpose; the source paper is the place to read them.

The publication is from 1998 (Clinical endocrinology), a journal based in England.

More context: the ACTH (Corticotropin) compound page, all human trials.