Adrenocorticotropin Deficiency: Correction of Hyponatremia and Hypoaldosteronism with Chronic Glucocorticoid Therapy*

Merriam, George R.; Baer, Leslie

doi:10.1210/jcem-50-1-10

Cited by 24 publications

(10 citation statements)

References 19 publications

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“…This is in agreement with other published reports (Lopez et al 1980;Birkhäuser et al 1981). Low basal levels have also been described (Major et al 1978;Lefebvre et al 1979;Merriam & Baer 1980 Cortisol replacement therapy significantly de¬ creased basal plasma aldosterone levels. Response to stimulation was still blunted and not significantly different from that of the untreated pa¬ tients.…”

Section: Discussionmentioning

confidence: 90%

Aldosterone in panhypopitutarism: dynamic studies and therapeutic effects in Sheehan's syndrome

Bakiri¹,

Riondel

Benmiloud³

et al. 1986

Acta Endocrinologica

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To appreciate the aldosterone secretion status in panhypopituitarism, the steroid response to stimulation was studied in a homogeneous group of 20 female patients presenting with global hypopituitarism. Specific effects of glucocorticoid and thyroid hormone deficiencies were also assessed by studying the same patients before and after cortisol (F) and cortisol plus thyroid hormone (F + T) substitution. The patients were submitted to two stimulation tests before and after each treatment: the orthostasis test (O-T) and the furosemide test (Furo-T). The results obtained in the 3 situations were compared, each patient serving as her own control. Comparison was also established with the results obtained in healthy women serving as control group. Basal plasma aldosterone levels in the untreated patients were not significantly different from those of the control group (5.43 \m=+-\0.51 vs 7.16 \m=+-\0.80 ng/100 ml, mean \m=+-\SEM). They were significantly lower after F (3.91 \ m=+-\ 0.42) and F + T substitution (3.31 \ m=+-\0.23) than those of untreated patients and controls. Response to both stimulations was blunted in the untreated patients (O-T: 14.10 \ m=+-\2.81; Furo-T: 9.78 \m=+-\1.35) as compared to the control group (O-T: 26.46 \m=+-\4.67; Furo-T: 23.96 \m=+-\ 3.30). F treatment did not improve the response to either tests, (O-T: 11.42 \ m=+-\2.55; Furo-T: 10.32 \m=+-\1.23).F + T treatment normalized the orthostasis response (20.83 \ m=+-\3.59) and increased the response to furosemide which remained, however, lower (15.28 \ m=+-\1.83) than in the control group. These results are in favour of a minor role of the pituitary in the regulation of aldosterone secretion. They emphasize the role of thyroid hormones which may act partly directly, partly through their effect on renin secretion.There is no general agreement on the effect of pituitary insufficiency on aldosterone secretion. Most published data indicate a normal basal secre¬ tion but different responses to various stimuli (Williams et al. 1971;Lefebvre et al. 1979; Me Caá et al. 1981; Birkhäuser et al. 1981). These differ¬ ences can be related to the small number of patients investigated in each series, their hetero¬ geneity with respect to sex, age, aetiology of pituitary insufficiency, degree of pituitary failure, extent of hormonal substitution and protocol of study. Therefore it is difficult to draw any firm conclusion from these studies. To circumvent some of these impedimenta, we have studied a homogeneous group of 20 female patients of child-bearing age, affected by post-partum pitui¬ tary necrosis with global hypopituitarism. In a previous paper (Bakiri et al. 1983) we have stud¬ ied their renin-angiotensin system. We report now their aldosterone response, under the same stimulatory conditions i.e. an orthostasis test and an acute sodium depletion. In order to define a specific role, if any, of glucocorticoid and/or thy¬ roid hormone deficiency, the same patients have been assessed before and after substitutive treat¬ ment with cortisol (F) alone an...

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Section: Discussionmentioning

confidence: 90%

Aldosterone in panhypopitutarism: dynamic studies and therapeutic effects in Sheehan's syndrome

Bakiri¹,

Riondel

Benmiloud³

et al. 1986

Acta Endocrinologica

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“…Concerning the function of ACTH and other pituitary factors (Reid and Ganong 1911;Mulrow, North and FernandezCruz 1979;Matsuoka, Mulrow and Li 1980), it is believed that they are not the major regulators of aldosterone production, but that they can have an influence on aldosterone production. However, in some patient with hypopituitarism there may be little or no increase in aldosterone with sodium depletion (Lieberman and Luetscher 1960;Williams, Rose, Dluhy, Dingman and Lauler 1971), and in a patient with isolated ACTH deficiency a low plasma aldosterone level was observed (Merriam and Baer 1980). Furthermore, stressful stimuli which increase ACTH production stimulate aldosterone production as well, and hypophysectomy blocks the effect (Reid and Ganong 1977).…”

Section: Discussionmentioning

confidence: 99%

The Mechanism of Aldosterone Response to Furosemide Test in Patients with Shy-Drager Syndrome

Sasaki¹,

Murabayashi²,

Baba³

et al. 1983

Horm Metab Res

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We examined the renin-angiotensin-aldosterone system in seven patients with Shy-Drager syndrome by studying their response to the stimulation of 1 mg/kg furosemide injection followed by sitting for 1 hour. Six of the seven patients showed a low response of plasma renin activity to the stimulation. However, in five of the low responders, the plasma aldosterone levels after stimulation were observed to be similar to those of the control subjects; in addition, an increment in the plasma cortisol level appeared although no such increment was observed in normal subjects. Next, we studied the aldosterone response to angiotensin II. The five patients who showed a low plasma renin activity response and a normal aldosterone response to furosemide administration also showed low plasma aldosterone response to angiotensin II. Furthermore, in the patients who demonstrated a low plasma renin activity response and a normal aldosterone response to furosemide administration, the pretreatment with 2 mg dexamethasone for 2 days caused a marked inhibition of aldosterone response to the stimulation. These findings suggested that in most patients with Shy-Drager syndrome, the plasma aldosterone response to the stimulation of furosemide injection followed by sitting for 1 hour might be controlled by ACTH but not by plasma renin activity.

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“…GC therapy was discontinued at least 24 h before the study. Since acute GC withdrawal has an influence on the Nephron 1996;73:301-304levels of PRA and Aid in hypopituitarism [12], it is possi ble that some effect of GC on the levels of PRA and Aid existed in their study. Miyabo et al [14] also reported a case of isolated ACTH deficiency with normoreninemic hypoaldosteronism.…”

Section: Fig 2 the Comparison Of Urine Volume (Uv)mentioning

confidence: 97%

“…11]. Since the suppressed level of Aid in hypopituitarism can be increased by the administration of GC [12], its mecha nism may be due to the increase in PRA after administra tion of GC. In the present case, the level of Aid was not elevated by the administration of GC because of the exis tence of hyporeninemic hypoaldosteronism.…”

Section: Fig 2 the Comparison Of Urine Volume (Uv)mentioning

confidence: 99%

A Case of Isolated ACTH Deficiency with Hyporeninemic Hypoaldosteronism

Okada

Takahashi²

1996

Nephron

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A case of isolated ACTH deficiency with hyporeninemic hypoaldosteronism, presenting severe hyponatremia, is described. A 57-year-old man complaining of nausea, vomiting and fatigability was admitted to our hospital because of hyponatremia (114 mEq/l). The low levels of serum cortisol and urinary 17-OHCS suggested glucocorticoid deficiency, and that the glucocorticoid deficiency was due to isolated ACTH deficiency was confirmed by a continuous ACTH loading test and pituitary gland stimulation tests. Although the low level of serum sodium was normalized after the administration of cortisone acetate (50 mg/day) combined with an increase in oral salt intake, urinary sodium loss persisted by the results of hypertonic saline infusion test. Treatment led to improvement of impairment of water diuresis due to hypersecretion of ADH. Hyporeninemic hypoaldosteronism persisted after treatment. We have shown that severe hyponatremia that occurs with combined deficiency of glucocorticoids and mineralocorticoids can be corrected with high salt intake and glucocorticoid replacement without correcting mineralocorticoid deficiency.

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Adrenocorticotropin Deficiency: Correction of Hyponatremia and Hypoaldosteronism with Chronic Glucocorticoid Therapy*

Cited by 24 publications

References 19 publications

Aldosterone in panhypopitutarism: dynamic studies and therapeutic effects in Sheehan's syndrome

Aldosterone in panhypopitutarism: dynamic studies and therapeutic effects in Sheehan's syndrome

The Mechanism of Aldosterone Response to Furosemide Test in Patients with Shy-Drager Syndrome

A Case of Isolated ACTH Deficiency with Hyporeninemic Hypoaldosteronism

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