Cortisone and Other Steroids in Rheumatoid Arthritis

Copeman, W. S. C.; Savage, Oswald; Bishop, P. M. F.; Dodds, E. C.; Gottlieb, Beth S.; Glyn, John; Henly, A. A.; Kellie, A. E.

doi:10.1136/bmj.2.4684.849

Cited by 41 publications

(15 citation statements)

References 12 publications

(4 reference statements)

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“…Copeman et at. (185) intensively studied five patients with rheumatoid arthritis under the influence of large doses of cortisone and reported that four of the five "dramatically" improved and one "markedly" improved. They noted a fall in ESR and decrease of circulating eospinophiles in all patients.…”

Section: Hormones In Rheumatic Diseasementioning

confidence: 98%

Diseases of Bones and Joints

Kuzell¹

1951

Annu. Rev. Med.

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Section: Hormones In Rheumatic Diseasementioning

confidence: 98%

Diseases of Bones and Joints

Kuzell¹

1951

Annu. Rev. Med.

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“…This level of improvement is assessed by the methods already described, which are based on disappearance of pain and tenderness and performance of functional tests (Copeman et al, 1950). If possible, the patients leave the hospital for a day or two to test their functional capacity in their home surroundings.…”

Section: Selection Of Patientsmentioning

confidence: 99%

Cortisone in Rheumatoid Arthritis

Copeman¹,

Savage²,

Bishop³

et al. 1952

BMJ

Self Cite

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“…It is to be recalled that hydrocortisone is the only steroid thus far found that has an action similar to that of cortisone in altering the clinical course of patients with inflammatory lesions (5,6). Corticosterone appears to be relatively ineffective as an antiarthritic agent in man (5,6).…”

Section: (From the Thorndike Memorial Laboratory Second And Fourth Mmentioning

confidence: 99%

The Effect of Adrenal Steroids, Corticotropin, and Growth Hormone on Resistance to Experimental Infections

Kass

Lundgren

Finland

1954

Journal of Experimental Medicine

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Cortisone acetate, hydrocortisone, and hydrocortisone acetate depress the resistance of mice to pneumococcal and influenza viral infections, although hydrocortisone acetate is somewhat less effective than the free alcohol, when given subcutaneously. Pituitary adrenocorticotropin, even in highly purified form and in oil and beeswax, does not significantly alter the resistance of mice to these experimental infections, even when given in doses which may cause profound eosinopenia, lymphopenia, and weight loss, and which are at the limit of tolerance of the animals. Corticosterone depresses resistance to pneumococcal infections significantly, but fails to alter resistance to influenza viral infections. The findings suggest that murine adrenals may produce one of the known adrenal steroids such as corticosterone along with another steroid, or may produce a steroid other than cortisone, hydrocortisone, or corticosterone. When resistance is decreased by adrenal steroids, survival time is invariably shortened, and the effect of the steroid hormones is frequently demonstrable within the 1st day after infection with pneumococci, making it unlikely that the depression of resistance that is seen is primarily due to depression of antibody formation. A single dose of 5 mg. of cortisone may cause depression of resistance and may decrease the survival time for 3 to 6 days afterward. Growth hormone (somatotropic hormone) in highly purified form, and in the doses used, did not overcome the weight loss induced by cortisone, but the animals treated with growth hormone and cortisone regained their lost weight more rapidly than those receiving cortisone alone. Growth hormone alone caused a slight increase in the rate of gain in weight over controls. Growth hormone alone did not increase resistance to infection, and did not increase the survival time, in mice infected with either pneumococci or influenza virus. Growth hormone in various dosages failed to overcome the effect of cortisone in depressing resistance to these infections. Cortisone, hydrocortisone, corticosterone, and corticotropin did not alter significantly the titers of influenza virus attained in the murine lungs during the first 2 days after infection, but cortisone and hydrocortisone markedly delayed the rate at which virus titers declined during the subsequent 6 days. Corticosterone and corticotropin delayed the rate at which the titers declined but slightly, and growth hormone had no apparent effect, as compared with controls. Growth hormone did not overcome the effect of cortisone and hydrocortisone on viral titers. No detectable antibody was found as late as 6 days after infection, in controls or in hormone-treated animals.

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Cortisone and Other Steroids in Rheumatoid Arthritis

Cited by 41 publications

References 12 publications

Diseases of Bones and Joints

Diseases of Bones and Joints

Cortisone in Rheumatoid Arthritis

The Effect of Adrenal Steroids, Corticotropin, and Growth Hormone on Resistance to Experimental Infections

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