Production, degradation, and circulating levels of 1,25-dihydroxyvitamin D in health and in chronic glucocorticoid excess.

Seeman, Ego; Kumar, Rajiv; Hunder, Gene G.; Scott, M.; Heath, Hunter; Riggs, B. Lawrence

doi:10.1172/jci109902

Cited by 179 publications

(59 citation statements)

References 28 publications

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“…The mechanism involved in this impairement has been attributed to either the derangement of hepatic production of 250HD (Avioli et al, 1968), the low level of 1,25(OH)2D in plasma (Lindgren et al, 1968) under glucocorticoid excess, or direct inhibition of calcium absorption by glucocorticoid under normal vitamin D metabolism (Kinberg et al, 1971;Seeman et al, 1980). In our patients without marked osteopenia who also showed impaired calcium absorption, the plasma levels of 250HD and 1,25(OH)2D were distributed in the lower range of those for normal subjects.…”

Section: Resultsmentioning

confidence: 99%

“…Most studies have demonstrated an increase in PTH secretion during hypercortisolism (Findlings et al, 1982;Fucik et al, 1975;Hahn et al, 1979;Lukert and Adams. 1976;Suzuki et al, 1983), despite a few reports indicating no change in the plasma iPTH level during hyper-and euglucocorticoid states (Seeman et al, 1980;Slovik et al, 1980). In the present study, plasma iPTH concentrations were measurable only in a few cases with marked osteopenia.…”

Section: Resultsmentioning

confidence: 99%

“…Regarding vitamin D metabolism in the hyperglucocorticoid state, plasma 25OHD or 1,25(OH)2D values have been reported to be decreased (Klein et al, 1977;Lindgren et al, 1982;Suzuki et al, 1983), increased (Findlings et al, 1983, Hahn et al, 1981, or unchanged (Hahn et al, 1977;Seeman et al, 1980;Slovik et al, 1980). In our series, plasma 25OHD and 24,25(OH)2D values were in the lower range of those for normal sujects either in the presence or in the absence of marked osteopenia.…”

Section: Resultsmentioning

confidence: 99%

“…Some studies have demonstrated a secondary increase in parathyroid hormone (PTH) secretion (Findlings et al, 1982;Fucik et al, 1975;Hahn et al, 1979;Lukert and Adams., 1976;Suzuki et al, 1983), while others have shown no difference in PTH secretion during hyper-and euglucocorticoid states (Seeman et al, 1980;Slovik et al, 1980). The previous reports on vitamin D metabolism indicated that glucocorticoids decrease (Klein et al, 1977;Lindgren et al, 1982;Suzuki et al, 1983), increase (Findlings et al, 1983;Hahn et al, 1981), or do not change (Hahn et al, 1977;Seeman et al, 1980;Slovik et al, 1980) plasma 250HD or 1,25(OH)2D. The heterogeneity of the subjects such as the presence or absence and clinical stage of underlying disease, dose and duration of glucocorticoid excess, and the degree of impairment of mineral metabolism might make some differences in these results.…”

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confidence: 99%

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Impaired mineral metabolism in Cushing's syndrome: Parathyroid function, vitamin D metabolites and osteopenia.

et al. 1986

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

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Impaired mineral metabolism in Cushing's syndrome: Parathyroid function, vitamin D metabolites and osteopenia.

et al. 1986

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“…More importantly, it has been reported that the circulating concentration of 1,25-dihydroxyvitamin D (1 ,25[OHI7_D). the physiologically active form of vitamin D, is low (8) or normal (7,(9)(10)(11) in subjects receiving glucocorticoids. These contradictory results are due, in part, to the dosage and length of glucocorticoid administration used in the previous studies.…”

mentioning

confidence: 99%

Low‐dose prednisone therapy in rheumatoid arthritis: effect on vitamin d metabolism

Zerwekh¹,

Emkey²,

Harris³

1984

Arthritis & Rheumatism

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It has long been recognized that treatment with glucocorticoids can produce a significant loss of bone mass (1,2). The mechanism for this steroid-induced bone loss is not fully understood. but is associated with a marked decrease in intestinal calcium absorption and an increased urinary calcium excretion that frequently accompanies administration of supraphysiologic doses of glucocorticoids (3.4).It has been proposed that steroid-induced alterations in vitamin D metabolism are responsible for the decrease in intestinal calcium absorption produced by glucocorticoid therapy. Reports to date have suggested that 25-hydroxyvitamin D (25[OH]D) concentrations are low ( 5 ) or normal in patients treated with corticosteroids (6,7). More importantly, it has been reported that the circulating concentration of 1, 25[OHI7_D). the physiologically active form of vitamin D, is low (8) or normal (7,9-11) in subjects receiving glucocorticoids. These contradictory results are due, in part, to the dosage and length of glucocorticoid administration used in the previous studies. All studies to date have utilired a supraphysiologic dose of glucocorticoid. In order to assess whether long-term administration of low-dose glucocorticoids affects vitamin D metabolism, we measured the circulating concentrations of the vitamin D metabolites, calcium, phosphorus, alkaline phosphatase, and immunorcactive parathyroid hormone (iPTH) in patients with rheumatoid arthritis receiving 5 mg of prednisone per day for up to 6 months (12). Since the study was conducted as a double-blind trial, an age-matched group of patients with rheumatoid arthritis who received placebo served as the control group.Patients and methods. The details of the patient population and study protocol have been previously reported (12). Briefly, 34 patients were initiated into a double-blind trial that lasted 32 weeks. Patients were admitted who were receiving nonsteroidal antiinflammatory drugs including salicylates, or who were receiving a constant dose of gold salts or D-penicillamine for at least I 2 weeks prior to beginning the study. Excluded were patients with active peptic ulcer disease or rectal bleeding, diabetes mellitus, symptomatic idiopathic osteoporosis, or active renal or hepatic disease. Patients who had received intraarticular glucocorticoid injections, vitamin D, or calcium preparations less than 6 weeks prior to entering the study were also excluded. prednisone 24 weeks into the study. The final evaluation of patients in both groups was made at 32 weeks.

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Commentary: Cortisone Acetate Administered Orally in Dermatologic Therapy

Fine¹

1983

Arch Dermatol

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Production, degradation, and circulating levels of 1,25-dihydroxyvitamin D in health and in chronic glucocorticoid excess.

Cited by 179 publications

References 28 publications

Impaired mineral metabolism in Cushing's syndrome: Parathyroid function, vitamin D metabolites and osteopenia.

Impaired mineral metabolism in Cushing's syndrome: Parathyroid function, vitamin D metabolites and osteopenia.

Low‐dose prednisone therapy in rheumatoid arthritis: effect on vitamin d metabolism

Commentary: Cortisone Acetate Administered Orally in Dermatologic Therapy

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