Clinical Studies With Acth and Cortisone in Renal Disease

Thorn, George W.; Merrill, John P.; Smith, Stephen V.; Roche, Marcel; Frawley, Thomas F.

doi:10.1001/archinte.1950.00230150002001

Cited by 58 publications

(6 citation statements)

References 27 publications

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“…On the other hand, the patients with Cushing's syndrome showed an increased "diuresis" of the salt load after desoxycorticosterone. This observation has been confirmed by others (18,19).…”

supporting

confidence: 86%

“…On the other hand, the patients with Cushing's syndrome showed an increased "diuresis" of the salt load after desoxycorticosterone. This observation has been confirmed by others (18,19).It is conceivable, then, that should patients with essential hypertension have adrenal cortical hyperfunction with respect to electrolyte metabolism they would exhibit this same abnormal response. …”

supporting

confidence: 55%

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The Soffer Test in Essential Hypertension

London¹,

Terry²

1952

J. Clin. Invest.

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The hypertension occurring in association with adrenal cortical hyperfunction (Cushing's syndrome and congenital adrenal hyperplasia), the difficulty in establishing or maintaining experimental hypertension in the absence of the adrenal gland (1-3), and the amelioration of human "essential" hypertension by adrenalectomy (4) or the development of adrenal insufficiency (5) have led several investigators (6-8) to suggest that adrenal hyperfunction might contribute to the pathogenesis of human "essential" hypertension.Attempts by a number of investigators to demonstrate this hyperfunction have been unsuccessful. Selye (9), Bruger, Rosenkrantz and Lowenstein (10), and Daughaday, Jaffe and Williams (11) have found the analysis of metabolic excretory products of the adrenal cortex (17-ketosteroids and 11-oxysteroids) in the urine of patients with hypertension to yield normal or low values. Careful study of carbohydrate metabolism in patients with hypertension (12) by means of the insulin tolerance test has revealed no abnormalities. Nitrogen balance is easily maintained in hypertensive subjects with a small protein intake (13). We and others (14) have found the blood eosinophil count normal in hypertension.Schroeder, Davies and Clark (15) have shown that the excretion of sodium in the sweat is normal in ordinary essential hypertension.The renaissance of interest in the therapeutic efficacy of a low sodium regime in the treatment of hypertension has focused attention particularly on the electrolyte controlling properties of the adrenal cortex as a possible mechanism for adrenal contribution to the pathogenesis of hypertension. The plasma electrolyte abnormality (hypochloremic alkalosis) frequently seen in Cushing's syndrome is not seen in hypertension. Most observers have found no plasma electrolyte abnormality in hypertension although Selye (9) believes the ratio of sodium to chloride is high.Soffer and his associates (16, 17) have pointed out that patients with Cushing's syndrome have an abnormal response to salt loading and the administration of desoxycorticosterone. His normal individuals, after a given salt load, retained more of the salt after the administration of desoxycorticosterone than they did without this drug. On the other hand, the patients with Cushing's syndrome showed an increased "diuresis" of the salt load after desoxycorticosterone. This observation has been confirmed by others (18,19).It is conceivable, then, that should patients with essential hypertension have adrenal cortical hyperfunction with respect to electrolyte metabolism they would exhibit this same abnormal response. METHODSThe salt loading tests were carried out on a group of patients with hypertension following the exact regime outlined by Soffer. The patients were permitted no food during the morning of the test and no fluid after 7 p.m. the night before. At 6 a.m. on the morning of the studies a urine specimen was collected and discarded. The patient was then given 500 cc. of water to drink at one time, and all the urine voided was ...

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“…On the other hand, the patients with Cushing's syndrome showed an increased "diuresis" of the salt load after desoxycorticosterone. This observation has been confirmed by others (18,19).…”

supporting

confidence: 86%

supporting

confidence: 55%

The Soffer Test in Essential Hypertension

London¹,

Terry²

1952

J. Clin. Invest.

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“…The fall in urinary sodium-retaining activity which accompanies the diuresis during the second week of ACTH administration can not be satisfactorily explained in this way, since studies of other adrenal secretions show a continued or increasing level of adrenal activity at this time. Further studies are necessary to evaluate hypotheses concerning changes in metabolism (15), competitive interactions, and variations in responsiveness of the renal tubules (2).…”

Section: Discussionmentioning

confidence: 99%

“…The administration of pituitary adrenocorticotrophin (ACTH) to patients with nephrosis has been reported to initiate diuresis in a large proportion of cases (1)(2)(3)(4)(5)(6). Since this diuresis may occur either during or after the administration of ACTH, it is not clear how such a diuresis is related to the secretions of the adrenal cortex.…”

Section: Introductionmentioning

confidence: 99%

Treatment of Nephrosis With Pituitary Adrenocorticotrophin 1

Luetscher¹,

Deming²,

Johnson³

et al. 1951

J. Clin. Invest.

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“…Cortisone and corticotrophin have also been used to treat acute and latent nephritis (Thorn et al, 1950;Burnett et al, 1950), but the results have generally been disappointing. Some workers (Michaels and Walters, 1953) found an increase of haematuria during treatment, and Philpott and Briggs (1953) concluded that cortisone and corticotrophin were valueless in the treatment or prevention of subacute nephritis complicating the Schonlein-Henoch syndrome.…”

mentioning

confidence: 99%

Case of Latent Nephritis Treated with Prednisolone

Ree¹

1959

BMJ

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CYANOTIC ATTACK IN FALLOT'S TETRALOGYBRDICTNAL 1325 precipitated in this case by the prolonged presence of a cardiac catheter in the pulmonary outflow tract. The diminution of the intensity of the systolic murmur indicated diminished flow across the pulmonary valve, but that this was not due to decreased systemic arterial resistance is shown by the sustained systemic blood pressure. Tachycardia was not responsible for the changes, as the heart rate remained rapid for some time after the disappearance of cyanosis and the return of a loud systolic murmur.Thus the findings in this case confirm Wood's (1958) hypothesis that the cyanotic attack is precipitated by temporarily increased obstruction at the pulmonary outflow tract, with greatly increased shunting of blood from right ventricle into aorta. Unlike Wood's cases, our patient showed only a slight drop in pulmonary artery pressure during the attack with no change in the pulse pressure, and deep coma was present with an arterial oxygen saturation of 52.5% (Wood states that coma ensues when the arterial oxygen saturation falls to about 20%). It would seem that the level of arterial desaturation at which the patient loses consciousness is, at least partly, dependent on the resting level of saturation, which in this patient was presumably normal or almost normal, in view of the absence of clinical cyanosis. The fact that the pulmonary artery pressure diminished only slightly might suggest that the obstruction to the pulmonary flow in our patient was less marked than in Wood's cases. It is significant, however, that the pulmonary artery pressure did not rise, which one would have expected were the obstruction to pulmonary flow produced by an increased pulmonary arterial resistance.The findings in this case indicate that the dangerous cyanotic attack may occur in those patients with Fallot's tetralogy with no clinical cyanosis, a finding which we have observed in other such cases (to be published).When faced with a cyanotic attack the practitioner may use procaine intravenously as an emergency measure, but for a sustained effect morphine would appear to be more suitable. It must be mentioned, however, that we have had patients in whom morphine has failed to stop the attack. Other narcotics might presumably be efficacious, and Wood has recommended cyclopropane anaesthesia. It must be stressed that oxygen administration is not, by itself, effective therapy. Summary A patient with "acyanotic Fallot's tetralogy developed a cyanotic (syncopal) attack during cardiac catheterization. The attack was probably precipitated by the prolonged presence of the catheter in the pulmonary outflow tract. The condition was studied haemodynamically, and it was believed that the attack was due to increased resistance to the flow of blood through the narrowed infundibulum. The treatment of the attack was difficult, and procaine intravenously was found to be effective, although the effect was not sustained. Morphine proved effective in relieving the attack.We thank Drs. M. J. Meyer, W. S...

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Clinical Studies With Acth and Cortisone in Renal Disease

Cited by 58 publications

References 27 publications

The Soffer Test in Essential Hypertension

The Soffer Test in Essential Hypertension

Treatment of Nephrosis With Pituitary Adrenocorticotrophin 1

Case of Latent Nephritis Treated with Prednisolone

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