Prolactin response to TRH in diabetic ketoacidosis

Abstract

Summary. The prolactin response to 200 gg thyrotropin-releasing hormone (TRH) IV was studied in seven patients with diabetic ketoacidosis, at the start of the treatment, and again, in the same patients, five days after recovery, when the diabetes was well controlled. Normal basal prolactin concentrations and prolactin responses to TRH were found in both situations. There was no correlation between basal prolactin concentrations, or magnitude of prolactin responses to TRH, and any of the metabolic variables measured. These findings do not suggest a role for prolactin in the development of diabetic ketoacidosis.Key words: Prolactin, diabetic ketoacidosis, plasma sodium, plasma osmolality, TRH test.Prolactin is said to have diabetogenic properties [1,2] and, in several animal species, plays a role in sodium and water retention [3]. Elevated prolactin concentrations have been reported in diabetic ketoacidosis and it was suggested that prolactin might participate in sodium retention in this condition [4].We recently showed that patients with diabetic ketoacidosis have an abnormally low thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH), in the face of reduced thyroxine (T4) and triiodothyronine (T3) concentrations [5]. Since TRH is also known to be a potent stimulator of prolactin secretion [6], it was considered of interest to investigate the reactivity of the pituitary prolactin cells to TRH in diabetic ketoacidosis. Material and MethodsSeven patients with severe diabetic ketoacidosis were studied, 5 men and 2 women, age range 20 to 74 years (37 _+ 7, mean _+ SEM), body weight range 82 to 117% of ideal body weight (96 _+ 4.5). The precipitating event was infection in 3 and omission of insulin in the others. None of the patients had clinical evidence of pituitary or thyroid disease. None of them used drugs known to affect prolactin secretion. Tests for glycosuria and ketonuria were strongly positive. Plasma glucose ranged from 400 to 830 mg/dl (615 _+ 60 mg/dl, mean _+ SEM); arterial blood pH from 6.80 to 7.21 (7.06 + 0.05); plasma sodium from 119 to 143 mmol/1 (130 + 3); plasma osmolality from 299 to 320 mOsm/kg (315 _+ 4); and plasma bicarbonate from 2 to 5.5 mmol/1 (3.5 __ 0.5). Five of the patients have been reported elsewhere, in a study on thyroid function in diabetic ketoacidosis [5]. All the patients were treated with a standard regimen as described previously, the insulin dosage being 20 IU/hr [7]. The mean duration of treatment was 6 h. Once the plasma glucose had reached 250 mg/dl, the patients received a 2000-2500 kcal diabetic diet and subcutaneous insulin according to glycosuria. After an average of 24 h, good control of the diabetes was achieved (i. e. no ketonuria and plasma glucose below 300 mg/dl).Synthetic thyrotropin-releasing hormone (TRH, Roche Laboratories) 200 ~tg was injected IV on admission, at the same time as the first insulin bolus, and again after 5 days good control of the diabetes. Blood was drawn at -15, 0, 15, 30, 45, 60, 90, and 120 min for prolactin determinations. ...

Exaggerated Prolactin Response to Metoclopramide in Non-Insulin Dependent Diabetes Mellitus

“…The normal PRL response to TRH corroborates the earlier reports (Froland, Hagen and Lauritzen 1977;Naeije et al 1979). PRL response to TRH is not influenced by the metabolic control of diabetes (Naeije et al 1979).…”

“…Reports on prolactin (PRL) secretion in diabetes mellitus are few and controversial. PRL levels were found normal or elevated in diabetes (Hunter, Anderson, Lunn, Horrobin, Boyns and Cole 1974;Naeije, Badawi, Vanhaelst, Cornil and L'Hermite 1979). In the present study we have compared PRL responses to TRH and metoclopramide (MCP) in non-insulin dependent diabetes mellitus (NIDDM).…”