The DOI matches its Crossref record; 48 of the 48 references it cites were found in a registry or an index.
Both hyper- and hypogonadotropic hypogonadism occur transiently in acute illness: bio- and immunoactive gonadotropins.
Abstract
Previous reports of hypogonadotropic hypogonadism in critically ill men may not reflect the complexity of changes in the hypothalamic-pituitary-gonadal (HPG) axis during acute illness. We sampled blood throughout hospitalization in 55 men admitted to acute care units to delineate the spectrum of changes in circulating gonadotropin and sex steroid levels at the onset and during recovery from acute illness. Bioactive LH and FSH were measured in a subset of patients. Percent free testosterone was measured to assess changes in binding to sex hormone binding globulin. Medications and serum estrogen and prolactin levels were monitored as potential causes of hypogonadotropism. Sustained suppression of serum testosterone levels below the normal range occurred in 62% of men with varying diagnoses and disease severity. Percent free testosterone remained constant. Hypogonadotropism was observed in most men (60%) and occurred independently from head injury, surgery, medications, or hyperprolactinemia. In a subset of men (n = 16), LH and/or FSH rose transiently above the normal range. Bioactivity of both LH and FSH remained constant while serum testosterone levels decreased. In contrast to serum testosterone levels, mean serum levels of E1, E2 and androstenedione were not less than control values. We conclude that both primary and secondary hypogonadism occur transiently in acutely ill men and cannot be explained solely by medications, hyperprolactinemia, or hyperestrogenemia. Neither biopotency of gonadotropins nor binding of testosterone to SHBG change across the course of acute illness. The hypogonadism, often severe and prolonged, may contribute to the persistent catabolic state observed in many critically ill patients.
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In the citing paper
“Hypogonadotropism in men is also known to occur in the context of acute starvation (19,50) and critical illness (51).”
From Functional Hypogonadotropic Hypogonadism in Men: Underlying Neuroendocrine Mechanisms and Natural History (2019) · cites this paper as [50]
In the citing paper
“Systemic diseases, eating disorders, extensive exercise, and a number of medications or recreational drugs (e.g., GCs, opiates, ketoconazole, barbiturates, cocaine) affect T levels (92,93).”
From Hormonal Replacement in Hypopituitarism in Adults: An Endocrine Society Clinical Practice Guideline (2016) · cites this paper as [92]
Citations
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Corticotropin-Releasing Hormone Inhibits Gonadotropin Secretion in the Ovariectomized Rhesus Monkey*
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Self-citation
Cited by
The Decline of Androgen Levels in Elderly Men and Its Clinical and Therapeutic Implications
Kaufman, J. M., & Vermeulen, A. (2005) · Endocrine Reviews · doi:10.1210/er.2004-0013 · Cited by 1,079
Hormonal Replacement in Hypopituitarism in Adults: An Endocrine Society Clinical Practice Guideline
Fleseriu, M., Hashim, I. A., Karavitaki, N., Melmed, S., Murad, M. H., Salvatori, R., & Samuels, M. H. (2016) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2016-2118 · Cited by 945
Dangerous dogmas in medicine: the nonthyroidal illness syndrome
De Groot, L. J. (1999) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.84.1.5364 · Cited by 505
Corona, G., Goulis, D. G., Huhtaniemi, I., Zitzmann, M., Toppari, J., Forti, G., Vanderschueren, D., & Wu, F. C. (2020) · Andrology · doi:10.1111/andr.12770 · Cited by 431
Neuroendocrine dysfunction in the acute phase of traumatic brain injury
Agha, A., Rogers, B., Mylotte, D., Taleb, F., Tormey, W., Phillips, J., & Thompson, C. J. (2004) · Clinical Endocrinology · doi:10.1111/j.1365-2265.2004.02023.x · Cited by 313
“Suppression of the hypothalamic–pituitary–gonadal axis has been reported in other acute illnesses (Levitan et al., 1984; Spratt et al., 1992) and following head injury (Hackl et al.”
Background
Metadata
- Authors
- Spratt, D. I., Bigos, S. T., Beitins, I., Cox, P., Longcope, C., & Orav, J.
- Affiliations
- Maine Medical Center (US)
- ORCID
- Spratt, D I
- Venue
- The Journal of Clinical Endocrinology & Metabolism
- Publisher
- The Endocrine Society
- Published
- 1992-12
- Volume
- 75
- Issue
- 6
- Pages
- 1562-1570
- ISSN
- 0021-972X (ISSN-L)
- 1945-7197
- OpenAlex
- W2039730717
- Cited by
- 118
- References
- 48
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 3 · 2023: 1 · 2022: 9 · 2021: 1 · 2020: 6 · 2019: 2 · 2018: 2 · 2017: 3 · 2016: 1 · 2015: 3 · 2014: 2 · 2013: 7 · 2012: 3
- FWCI
- 1.69
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal and reproductive studies
- Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Keywords
- hypogonadotropic hypogonadism, hypergonadotropic hypogonadism, acute illness, hypothalamic-pituitary-gonadal axis, gonadotropins, luteinizing hormone, follicle-stimulating hormone, testosterone, sex hormone-binding globulin, free testosterone, estrogen, androstenedione, hyperprolactinemia, catabolic state
- MeSH terms
- Acute Disease, Adult, Aged, Biological Assay, Follow-Up Studies, Follicle Stimulating Hormone, Gonadotropins, Humans, Hypogonadism, Immunologic Techniques, Luteinizing Hormone, Male, Middle Aged, Prolactin, Gonadal Steroid Hormones
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