Normoreninemic Hypoaldosteronism in a Case of Isolated ACTH Deficiency

Miyabo, Susumu; Minami, Mutsuo; Inazu, Tetsuya; Tamai, Toshitaka; Aoyagi, Naoki; Miyanaga, Ken; Ooya, Eiichi; Kishida, Shigeru; Nakai, Tsuguhiko

doi:10.1159/000181109

Cited by 2 publications

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References 21 publications

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“…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. Although a relation between renin release stimulation test and the replacement therapy was unclear in the case, hypoaldosteronism persisted after GC therapy.…”

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

confidence: 96%

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

confidence: 96%

A Case of Isolated ACTH Deficiency with Hyporeninemic Hypoaldosteronism

Okada

Takahashi²

1996

Nephron

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Isolated Corticotropin Deficiency in Adults

Yamamoto

Fukuyama²,

Hasegawa³

et al. 1992

Arch Intern Med

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The clinical and laboratory findings in 76 patients with isolated corticotropin deficiency (10 of our own and 66 from literature) were analyzed with the following observations. With the exceptions of hyperpigmentation and hyperkalemia, the similarity of symptoms and signs to those of Addison's disease and their reversibility by glucocorticoids indicate that most, but not all, manifestation of isolated corticotropin deficiency is caused by glucocorticoid deficiency. Isolated corticotropin deficiency seems to be of pituitary origin in most patients, as shown by lack of corticotropin response to insulin-induced hypoglycemia, vasopressin, or corticotropin-releasing factor. Secretion of other pituitary hormones is frequently abnormal, which is mostly attributable to glucocorticoid deficiency. Although the pathogenesis of isolated corticotropin deficiency is unknown in most patients, association with other autoimmune endocrinopathies, postpartum onset in women, or serum antipituitary antibodies suggests an autoimmune pathogenesis in some patients. In two of our 10 patients, cancer developed during glucocorticoid treatment. More observations of complications and long-term prognosis following glucocorticoid therapy are needed for optimal clinical decision making.

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Normoreninemic Hypoaldosteronism in a Case of Isolated ACTH Deficiency

Cited by 2 publications

References 21 publications

A Case of Isolated ACTH Deficiency with Hyporeninemic Hypoaldosteronism

A Case of Isolated ACTH Deficiency with Hyporeninemic Hypoaldosteronism

Isolated Corticotropin Deficiency in Adults

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