Plasma Catecholamines After Insulin Hypoglycemia in Sheehan’s Syndrome*

N, Klioua; Ruget, G; Selz, Françoise; Cuche, Jean-Louis; Benmiloud, M

doi:10.1210/jcem-64-6-1323

Cited by 5 publications

(3 citation statements)

References 25 publications

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“…In fact, in a recent study (Boyle and Cryer 1991), higher baseline plasma NE levels were observed in patients with hypopituitarism despite adequate thyroidal hormone replacement therapy. In patients with Sheehan's syndrome also, Klioua et al (1987) observed increased baseline levels of plasma NE, however, the ratio of NE-to-E was not increased.…”

Section: Discussionmentioning

confidence: 78%

“…This suggestion however was based on an arbitrary cut-off value of plasma E levels. Furthermore, the study did not provide information regarding plasma insulin levels and the recovery of plasma glucose concentrations after reaching the nadir of plasma glucose (Klioua et al 1987). Others (Rudman, Morrit, Fernhoff, Blackston and Faraj 1981) have noted deficient epinephrine response to exercise in hypopituitary children and suggested epinephrine deficiency in hypopituitarism.…”

Section: Discussionmentioning

confidence: 89%

“…The lack of glucagon and E responses to insulininduced acute hypoglycemia impairs recovery from acute hypoglycemia in patients with insulin-dependent diabetes mellitus (Cryer, White and Santiago 1986;Cryer and Gerich 1985). Klioua et al (1987) have suggested that some hypopituitary patients may have deficient plasma E response to acute hypoglycemia. This suggestion however was based on an arbitrary cut-off value of plasma E levels.…”

Section: Discussionmentioning

confidence: 99%

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Counter-Regulatory Hormone Responses to Insulin-Induced Acute Hypoglycemia in Hypopituitary Patients

Garg¹,

Grizzle²,

Kansal³

et al. 1994

Horm Metab Res

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Patients with hypopituitarism are predisposed to fasting hypoglycemia and are considered unusually sensitive to insulin-induced acute hypoglycemia. However, whether impaired response of counter-regulatory hormones, such as glucagon, epinephrine (E), and nor-epinephrine (NE) contribute to the susceptibility to acute hypoglycemia in hypopituitary patients has not been systematically evaluated. Therefore, we compared counter-regulatory hormone responses to insulin-induced acute hypoglycemia in 9 patients with hypopituitarism who were off hormone replacement therapy and 13 normal healthy subjects. All subjects received aa prime-continuous intravenous infusion of insulin (0.1 Unit/kg body weight.h) till plasma glucose declined to less than 2.5 mmol/l or occurrence of hypoglycemic symptoms. All normal subjects and 7 out of 9 hypopituitary patients recovered spontaneously from hypoglycemia. Two hypopituitary patients with hypothalamic pathology however needed intravenous glucose, glucagon and hydrocortisone to assist recovery from hypoglycemia. Overall, patients with hypopituitarism showed a slower rate of recovery of plasma glucose after hypoglycemia than normal subjects (0.78 +/- 0.33 mmol/l.h vs. 1.72 +/- 0.15 mmol/l.h, respectively; p = 0.02). The responses of key counter-regulatory hormones, glucagon, E and NE, to hypoglycemia however were essentially similar in both the groups. We conclude that the lack of cortisol (secondary to ACTH deficiency) and GH in hypopituitary patients may be primarily responsible for the slow recovery of plasma glucose after acute hypoglycemia; and plasma glucagon, E, and NE responses are not impaired.

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Section: Discussionmentioning

confidence: 78%

Section: Discussionmentioning

confidence: 89%