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Cited by 118Hormonal and reproductive studiesHypothalamic control of reproductive hormonesAdrenal Hormones and Disorders

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.

Spratt, D I, Bigos, S T, Beitins, I, Cox, P, Longcope, C, Orav, J·1992·The Journal of Clinical Endocrinology & Metabolism
DOI 10.1210/jcem.75.6.1464665
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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.

Overview

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Crossref · 10.1210/jcem.75.6.1464665

Cites

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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
DOI
10.1210/jcem.75.6.1464665
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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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.