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Biomedical subjects

J Weeke

Publications and source records attributed to J Weeke.

At least 73 records · Page 4Linked to original sources

Very early changes in circulating T3 and rT3 during development of metabolic derangement in diabetic patients.

Alterations in circulating iodothyronines were studied in 15 juvenile type diabetic patients during the development of metabolic derangement after withdrawal of insulin. By means of measurements of circulating C peptide, one group of patients with and one without residual beta-cell function had been selected. In both groups there was a gradual decrease in serum T3 during the 12-hour period studied after withdrawal of insulin, while an increase in serum rT3 was observed after 4-6 hours. The alterations in serum T3 and the metabolic derangement were significantly more pronounced in patients without than with residual beta-cell function.

C-Peptide↗

Dynamics of serum rT3 and 3,3'-T2 during rT3 infusion in patients treated for thyrotoxicosis with propylthiouracil or methimazole.

rT3 metabolism in patients treated for thyrotoxicosis with prophylthiouracil (PTU), or methimazole (MMI) was studied by infusion of rT3 and measurements of the increase in serum rT3 and serum 3,3'-diiodothyronine. The results indicate that the high serum rT3 observed during treatment with PTU is not due to an increase in rT3 production, but to a decrease in the metabolic clearance rate of rT3. rT3 infusion was followed by an increase in serum 3,3'-T2 which was similar whether PTU or MMI was given. However, after stopping rT3 infusion there was a more rapid fall serum 3,3'-T2 during MMI treatment, compatible with an inhibitory effect of PTU on 3,3'-T2 degradation.

Adult↗

The 24-hour pattern of serum TSH in patients with endogenous depression.

The 24-h pattern of serum thyrotropin (TSH) has been studied using hourly blood-sampling in four patients with severe endogenous depression. All patients showed a pattern similar to that of normal subjects, with lowest levels of serum TSH between 0900 and 2000 h and highest levels between 2100 and 0800 h. A phaseshift of the TSH rhythm can therefore not account for our previous finding of a significant negative correlation between severity of endogenous depression and night increase in serum TSH measured as the difference between the values at 2400 and 1400 h.

Adult↗

24-h profile of serum rT3 and serum 3,3'-T2 in normal man.

In a previous study we found a night surge in serum free T3 varying in parallel with that of serum TSH. In order to evaluate whether diurnal alterations in peripheral iodothyronine monodeiodination may be involved we have measured two products of peripheral deiodination, 3,3',5'-T3 (rT3) and 3,3'-T2 in serum samples obtained at short intervals during a 24-h period in 5 normal male subjects. Serum rT3 was rather stable during the period albeit with a trend towards lower levels during the night when the subjects were in bed. In order to obtain a measure of free rT2 a free rT2 index was calculated using the combined variations in per cent free T4 and free T3. Night and day levels of this rT3 index were found identical, suggesting a lack of diurnal variation in serum free rT3. Likewise serum 3,3'-T2 levels were identical during the day and night periods. The results suggest that variations in peripheral iodothyronine deiodinations are not involved in the night increase in serum free T3.

Adult↗

Circulating iodothyronines in juvenile diabetic outpatients.

Serum T3, rT3, T4 and TSH were measured in ten healthy subjects, in nine juvenile diabetic outpatients in fair metabolic control (fasting plasma glucose 6.5 mmol/1, 2.6-9.5 mmol/1 (mean, range), HbA1 10.1%, 8.1-12.2%), and in ten juvenile diabetic outpatients in poor metabolic control but without ketonuria (fasting blood glucose 15.1 mmol/l, 11.1-22.4 mmol/l, HbA1, 13,8% 10.8-16,2%. Serum T3 was identical in normal subjects and in diabetics in fair metabolic control. Diabetics in poor metabolic control had 13.0% lower serum T3 than normal subjects (2 p less than 0.05). No difference between groups was observed in serum rT3, T4 and TSH. These findings indicate that in diabetic patients, metabolic derangement induces alterations in serum T3 more easily than in serum rT3. However, alteration in serum T3 is not a sensitive indicator of moderate metabolic derangement in diabetic patients.

Adult↗

The pathogenesis of propranolol-withdrawal syndrome in essential hypertension.

1. In hypertension, the beta-adrenoreceptor-blocker-withdrawal syndrome comprises tachycardia, sweating, tremor and general malaise, symptoms resembling thyrotoxicosis. 2. The effect of abrupt cessation of propranolol on serum concentrations of thyroxine (T4) and triiodothyronine (T3) was therefore investigated in five patients with uncomplicated essential hypertension, treated with propranolol in doses from 160 to 480 mg/day. 3. Four of the five patients developed one or more of the above-mentioned symptoms within 2-6 days after withdrawal of propranolol. 4. A mean relative increase in serum free T3 of 51% (range 22-74%) was found in these four patients on the day of onset of symptoms. 5. The increase in free T3 in the five patients correlated positively with total serum propranolol on the last day the drug was given (r = 0.91, 2P = 0.03). 6. As an increase in T3 was found only in patients suffering the withdrawal syndrome, and was maximal the day the symptoms appeared, despite a variation in time of onset from 2 to 6 days, it is suggested that the beta-adrenoreceptor-blocker-withdrawal syndrome, at least partially, is caused by rebound increased production of T3, induced by the well-known inhibition of the monodeiodination of T4 to T3 during beta-adrenoreceptor blockade. 7. This assumption may explain the clinical symptoms and the reported transient increased beta-adrenoreceptor sensitivity with unchanged serum concentrations of catecholamines.

Adult↗

rT3 production in normal man, assessed from variations in serum rT3 during short-term rT3 infusion.

The metabolic clearance rate (MCR) of 3,3'5'-triiodothyronine (reverse T3, rT3) was estimated in normal human subjects by a modified noncompartmental method using the integrated increase in serum rT3 following intravenous infusion of 0.10 nmol/min rT3 for 4 hr. The MCR-rT3 was calculated to be 102.8 +/- 17.01/day and the daily rT3 disposal to be 33.0 +/- 9.5 nmol (mean +/- SD, n = 6). The MCR-rT3 compares well to that of previous studies employing tracer kinetic methods. The disposal rate of rT3 estimated in the present study is considerably lower than found in some previous studies. The discrepancy is due to differences in the measured levels of serum rT3 in normal subjects.

Adult↗

Thyrotropin, free and total triiodothyronine, and thyroxine in serum during surgery.

Changes in free and total thyroxine (T4), triiodothyronine (T3) and thyroid stimulating hormone (TSH) in serum were measured before, during, and for nine days after uncomplicated abdominal surgery in eight patients. The results showed a pronounced fall in total as well as in free T3 levels, amounting to 50% in both variables on the first postoperative day, and returning towards preoperative levels on the seventh and ninth day. Apart from an increase during surgery, free T4 levels were constant in the whole period despite a slight postoperative decrease in total T4. The TSH level fell about 80% within the first 24 postoperative h, but returned to the preoperative level thereafter. These results suggest a suppression of both T3 and TSH production during the pre- and early postoperative period.

Female↗

Propranolol withdrawal and thyroid hormones in patients with essential hypertension.

The effect of abrupt withdrawal of propranolol on serum concentrations of triiodothyronine (T3) and thyroxine (T4) was investigated in 5 patients with uncomplicated essential hypertension. The patients had been treated from 2 to 18 mo before the study was begun. Doses varied from 160 to 480 mg propranolol daily. Four of the patients studied developed tachycardia, sweating, or tremor within 2 to 6 days after withdrawal of propranolol. In 1 patient reversible ischemic ECG changes were recorded. The serum concentrations of free T3 increased in the 4 patients suffering from withdrawal symptoms. The mean increase on the day the symptoms started was 51% (range, 22 to 74, 2 p = 0.01). This increase in serum-free T3 correlated positively with the serum propranolol concentration on the last day propranolol was given (r = 0.91, 2 p = 0.03). In the one patient, who did not develop withdrawal symptoms, the serum concentration of propranolol was very low, and the free T3 level remained unchanged. No significant changes in serum concentrations of free T4 or total thyroid hormones were found in any of the patients. We suggest that the propranolol withdrawal symptoms are, at least partially, caused by an increase in the thyroid hormone, T3.

Adult↗

Plasma prolactin in juvenile diabetics. 24-h studies with somatostatin.

In normal subjects during 24-hours saline infusion, plasma prolactin showed a number of small rises during day and night. The mean night-time level was significantly higher than the day-time level (8.2 +/- 0.6 ng/ml as against 4.7 +/- 0.5 ng/ml). In 12 insulin-dependent diabetics the 24 h plasma prolactin pattern was identical to that found in normals. Somatostatin infusion (4 mg/24 h in normals; 2--6 mg/24 h in diabetics) had no effect on the 24 h plasma prolactin pattern in either normals or in diabetics.

Adult↗

Disturbed circadian variation of serum thyrotropin in patients with endogenous depression.

The relationship between the degree of depression and the circadian variation of serum TSH, T3 and T4 was investigated in 19 endogenously depressed patients. The difference between the hormone concentrations at 2 p.m. and at 12 p.m. was taken as an estimate of the magnitude of circadian variation. It was found that the circadian variation in serum TSH was inversely related to the degree of endogenous depression. This was mainly due to a diminution or absence of the night increase of TSH in severely depressed patients. A circadian variation of serum free T3 was found in the less depressed patients whereas no diurnal change was found in serum free T4. In severely depressed patients there were no significant diurnal changes in free thyroid hormone concentrations. The results indicate a hypothalamic dysfunction in manic-depressive psychosis.

Adult↗

Low serum triiodothyronine and high serum reverse triiodothyronine in old age: an effect of disease not age.

Serum concentrations of T4, T3, T3, free T4, free T3, and TSH were determined in four groups of adult subjects: group A, 27 healthy young volunteers (aged 18-29 yr); group B, 24 carefully selected healthy elderly subjects (aged 70-90 yr); group C, 41 subjects living at a municipal nursing home for the elderly (aged 70-90 yr); and group D, 35 hospitalized patients (aged 70-90 yr). Identical levels of iodothyronines in serum were found in the young and in the elderly healthy subjects. Moderate and severe disease induced alterations in iodothyronine concentrations in serum comparable to those reported earlier. Serum T3 and free T3 levels were low and serum rT3 levels were high in groups C and D subjects; serum free T4 was elevated in group D, while serum T4 was low. Serum TSH was lower in the healthy elderly subjects than in the young subjects. Serum TSH was higher in the elderly sick subjects (groups C and D) than in the healthy subjects (group B). We conclude that advanced age per se is not accompanied by alterations in free or total serum iodothyronine levels.

Adolescent↗

Opposite variations in serum T3 and reverse T3 during propylthiouracil treatment of thyrotoxicosis.

Blood samples for determination of serum total and free reverse triiodothyronine (rT3), triiodothyronine (T3) and thyroxine (T4) were obtained daily in 6 previously untreated thyrotoxic patients during periods of propylthiourazil (PTU) (600 mg per day) or methimazol (MMI) (45 mg per day) administration. PTU induced about 60 per cent increase in both total and free serum rT3. This was accompanied by a rapid decrease in serum T3 and a more gradual decline in serum T4. MMI administration to untreated patients was followed by a gradual parallel decrease in rT3, T3 and T4. Turn from PTU to MMI produced a rapid decrease in serum rT3 and increase in serum T3 in all 6 patients. The relative variations in the free and total concentrations of iodothyronines were practically identical. The increase in serum rT3 after PTU is most likely explained either by enhanced deiodination of T4 to rT3 or by an inhibitory effect of PTU on rT3 degradation.

Adult↗