Critical illness and sex hormones: response and impact of the hypothalamic-pituitary-gonadal axis.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing physiological mechanisms and observational findings without systematic review methodology.
PubMed 40183031 · doi:10.1177/20420188251328192
What was done
This review examined hypothalamic-pituitary-gonadal (HPG) axis function and sex hormone modifications during critical illness. The authors synthesized mechanisms of endocrine disruption, interactions with cytokines and gastrointestinal microorganisms, and sex-specific hormonal alterations during acute disease states.
What was found
No numerical values or effect sizes were reported in the abstract. Directionally, females in critical illness show decreased follicle-stimulating hormone (FSH) and luteinizing hormone (LH) alongside increased testosterone, estradiol, and progesterone driven by adrenal activation and peripheral aromatization. Males demonstrate decreased FSH, LH, and testosterone (due to inflammation, endotoxin exposure, and aromatization) and increased estradiol and progesterone from stress-induced adrenal activity. Hormone levels generally normalize as clinical status improves.
Why it matters
This paper outlines the divergent male and female endocrine responses to severe physiological stress, providing a mechanistic framework for understanding acute gonadal axis dysfunction in intensive care settings.
Limits
As a narrative review, the abstract provides no primary human trial data, sample sizes, quantitative effect estimates, or systematic search methodology.
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