PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 6330714

Steroid use in the elderly. Guidelines for avoiding adverse effects.

F E Kaiser·R P Doe
View original source ↗Export metadata ↓

Abstract

The effects of aging on adrenal function should be considered when prescribing steroid for the elderly. For glucocorticoids, the changes of decreased production and decreased clearance are relatively balanced, resulting in levels that are still within the normal range. Responses of the hypothalamic-pituitary-adrenal axis to stress are not altered. However, androgens appear to be affected by an "adrenopause," the mechanism(s) and the clinical relevance of which remain to be elucidated. The risk/benefit factors in steroid use are always of utmost concern. The physician may consider lowering the steroid dose in elderly patients of asthenic build because of the diminution of muscle mass and plasma volume that occurs with aging. Despite the physiologic changes that accompany aging, steroid used carefully and appropriately can be both safe and effective in the elderly.

Explore related subjects

Adrenal GlandsAdrenocorticotropic HormoneAgedGlucocorticoidsHumansHydrocortisoneHypothalamo-Hypophyseal SystemPituitary-Adrenal SystemRiskJournal ArticleResearch Support, U.S. Gov't, Non-P.H.S.

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

F E Kaiser, R P Doe. 1984. Steroid use in the elderly. Guidelines for avoiding adverse effects.. https://doi.org/10.1080/00325481.1984.11698664

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Molecular aspects of adrenal regulation for circadian glucocorticoid synthesis by chronic voluntary exercise.

Chronic voluntary running of mice is known to increase the circadian peak of plasma corticosterone without change in the level of adrenocorticotropic hormone (ACTH). In order to investigate how chronic exercise modulates the circadian HPA axis, we used two weeks of voluntary wheel running of mice and confirmed the significant increase of the circadian peak of plasma corticosterone without alteration in ACTH level. To elucidate the mechanisms of exercise modulation on corticosterone synthesis, we first examined the levels of transcripts involved in corticosterone synthesis of the adrenal gland. Among them, only steroidogenic acute regulatory protein (StAR), the rate-limiting factor that transfers substrate cholesterol into inner mitochondrial membrane, showed significantly higher expression in the exercise group. Since the splanchnic nerve input to the adrenal gland has been reported as a factor involved in the direct modulation of corticosterone synthesis, we next examined the expression levels of enzymes for the catecholamine synthesis as indices of sympatho-adrenomedullary activity. We found that the only rate-limiting enzyme, tyrosine hydroxylase (TH), was significantly higher in the adrenals of exercise group. In addition to the increment of StAR and TH mRNA in response to the chronic exercise, surprisingly, we found only these factors showed the circadian variation in its expression levels that was correlated to the circadian rhythm of corticosterone. Chronic exercise seems to alter the circadian corticosterone synthesis, at least partially via altering the levels of circadian-regulated transcripts, StAR and TH of the adrenal gland.

Adrenal Glands↗
PubMed2007

Microarray and real-time PCR analysis of adrenal gland gene expression in the 7-day-old rat: effects of hypoxia from birth.

We hypothesize that changes in adrenal gene expression mediate the increased plasma corticosterone and steroidogenesis in rat pups exposed to hypoxia from birth. In the current study, rat pups (with their dams) were exposed to hypoxia from birth and compared with pups from normoxic dams fed ad libitum or pair fed to match the decreased maternal food intake that occurs during hypoxia. Microarray analysis was performed, followed by verification with real-time PCR. Furthermore, the expression of selected genes involved in adrenal function was analyzed by real-time PCR, regardless of microarray results. Hypoxia increased plasma ACTH and corticosterone, while food restriction had no effect. Microarray revealed that many of the genes affected by hypoxia encode proteins that require molecular oxygen (monooxygenases, oxidoreductases, and electron transport), whereas only a few genes known to be involved in adrenal steroidogenesis were affected. Interestingly, the expression of genes involved in mitochondrial function and intermediary metabolism was increased by hypoxia. Real-time PCR detected a small but significant increase in the expression of Cyp21a1 mRNA in the hypoxic adrenal. When decreased maternal food intake was controlled for, the effects of hypoxia were more pronounced, in that real-time PCR detected significant increases in the expression of Star (244%), Cyp21a1 (208%), and Ldlr (233%). The present study revealed that increased plasma corticosterone in rat pups was due to hypoxia per se, and not as a result of decreased food intake by the hypoxic dam. Furthermore, hypoxia induced changes in gene expression that account for more productive and efficient steroidogenesis.

Adrenal Glands↗
PubMed2007

Adrenal cholesterol utilization.

There are multiple systems for cellular cholesterol delivery for steroidogenesis, including uptake of lipoprotein-derived cholesterol via LDL receptor mediated endocytic pathways and SR-BI mediated "selective" pathways, as well as from endogenous cholesterol synthesis and the mobilization of stored cholesteryl esters. The vast majority of lipoprotein-derived cholesterol utilized for murine adrenal steroidogenesis is obtained via SR-BI mediated "selective" uptake of cholesteryl esters. Hormone-sensitive lipase (HSL) is responsible for neutral cholesteryl ester hydrolase activity in the adrenal and is critical for hydrolyzing stored cholesteryl esters, as well as cholesteryl esters that are selectively delivered from lipoproteins via SR-BI. Marked defects in steroid production are observed in adrenal cells from HSL knockout mice, due to an inability to process and utilize cholesteryl esters selectively derived from lipoproteins. Although the LDL receptor is responsible for receptor-mediated endocytic delivery of cholesteryl esters, adrenal steroid hormone production is normal in mice lacking LDL receptors.

Adrenal Glands↗