A Low T3 Syndrome in Diabetic Ketoacidosis

Naeije, Robert; Golstein, J.; Clumeck, Nathan; Meinhold, H.; Wenzel, Klaus; Vanhaelst, L.

doi:10.1111/j.1365-2265.1978.tb02183.x

Cited by 69 publications

(37 citation statements)

References 15 publications

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“…Patients with diabetic ketoacidosis have lowered T 3 and T 4 concentrations, and a blunted TSH response to TRH [5]. Our patients had normal prolactin responses to TRH, suggesting that the pituitary abnormality of the "low T 3 syndrome" of diabetic ketoacidosis is selectively situated at the TSH secreting pituitary cells.…”

Section: Discussionmentioning

confidence: 71%

“…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].…”

Section: Methodsmentioning

confidence: 99%

“…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.…”

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confidence: 99%

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Prolactin response to TRH in diabetic ketoacidosis

Naeije

Badawi²,

Vanhaelst³

et al. 1979

Diabetologia

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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. ...

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Section: Discussionmentioning

confidence: 71%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Prolactin response to TRH in diabetic ketoacidosis

Naeije

Badawi²,

Vanhaelst³

et al. 1979

Diabetologia

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“…Diminished TSH response to TRH. due to lack of glucose entry into thyrotroph cells, though considered, may not be the only causative factor since previous studies reported that prompt attainment of euglycaemia by insulin therapy did not nor› malise the TSH secretion [17,18].…”

Section: Discussionmentioning

confidence: 99%

Thyroid Hormones in Non-Insulin-Dependent Diabetes Before and After Therapy

Saini

Dutt

1995

Medical Journal Armed Forces India

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Twenty patients of non-insulin-dependent diabetes mellitus (NIDDM) (15 males and 5 females) who developed sec:ondary failure to oral hypoglycaemic chugs, were evaluated for thyroid hormone abnor› malities before and after control ofdiabetic state with insulin. Blood glucose (mean ± SEM mg/dL) fasting and post prandial levels were 260 ±16 and 370 ± 20 respectively before therapy. After 15 days ofintensive insulin therapy these levels fell to 110 ± 14 and 130 ± 12 respectively (p < 0.005). Glycosylated haemoglobin percent (GHb%) (mean ± SEM) was 10 ± 0.4 before therapy and after therapy it fell to 9.2 -0.3 (p < 0.05). Serum tri-iodothyronine levels (mean -SEM ngImL) were 0.55 -0.03 which was significantly lower (p < 0.05) as compared controls. After therapy it significantly (p < 0.05) rose to 1.22 -0.08). Serum thyroxine (T4) (mean -SEM mcg/dL) was 8.5 -0.6 before therapy and it did not change significantly after therapy. Serum reverse tri-iodothyronine (rT3) values of (mean ± SEM ng/dl) 0.24 ± 0.05 were higher before therapy and decreased to 0.20 ± 0.82 after therapy. However thyrotropin (TSH) values before and after therapy remained same. There was no significant change in TSH response to thyrotropin releasing hormone (TRH) before and after control ofdiabetic state.It was concluded that peripheral changes inT3, T4 and rT3 (low T3, high rT3 and low or normal T4) occurred in uncontrolled diabetic state. However, pituitary thyrotroph function in NIDDM with ideal body weight was not significantly affected. MJAFI 1995; 51 : 117-121

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“…Eine erste schockbedingte, innerhalb der ersten 12-24 h einsetzende, im we sentlichen allerdings an schilddrüsengesunden Schwerstkranken, aber auch im protrahierten Schock untersuchte Veränderung ist darin zu sehen, daß T 4 ver mindert in der 5'-Position zu biologisch wirksamem T 3 und vermehrt in der 5-Stellung zu dem stoffwechselinaktiven rT 3 dejodiert wird. Dieses Phänomen ist als low Τ ^syndrome in die Literatur eingegangen (NAEIJE et al 1978;HEINEN et al 1980;TITLBACH et al 1980;LARSEN et al 1981;WIERSINGA et al 1981;REISERT et al 1982).…”

Section: Schilddrüsenhormoneunclassified