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Severe hyponatremia caused by secondary adrenal insufficiency in a patient with
giant pituitary prolactinoma
#MMPMID28509288
Kobayashi A
; Otsuka Y
; Yoshizawa T
; Tomita M
; Asada H
; Ikeda J
; Saito M
; Tojo K
; Kuriyama S
; Hosoya T
CEN Case Rep
2013[Nov]; 2
(2
): 184-189
PMID28509288
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A 55-year-old-man was admitted to Saiseikai Central Hospital, Tokyo, Japan,
complaining of nausea and appetite loss, and was found to have severe
hyponatremia. Despite severe hyponatremia and plasma hypo-osmolarity, urinary
sodium excretion was not reduced. A brain magnetic resonance imaging (MRI) scan
revealed a giant pituitary prolactinoma, and endocrinological tests showed a
markedly increased prolactin level. Despite the observation that the basal plasma
ACTH level was normal, serum cortisol and urinary cortisol excretion levels were
low. Rapid ACTH loading sufficiently stimulated an increase in serum cortisol
levels, suggesting secondary adrenal insufficiency. Notably, loading of CRH
induced a good ACTH response; however, the serum cortisol response remained low.
In contrast, the continuous daily administration of exogenous ACTH dramatically
increased serum cortisol levels. These discrepant responses may have been caused
by the low biological activity of innate ACTH. Following partial resection of the
prolactinoma, postoperative adjuvant therapy with cabergoline effectively reduced
prolactin levels, but did not improve the hyponatremia. In contrast,
hydrocortisone replacement therapy recovered the serum sodium level to the normal
range. The present case is the first report describing a link between severe
hyponatremia and biologically inactive circulating ACTH as a likely result of
giant prolactinoma.
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