TH. OLBRICHT, H.-G. HOFF and D. REINWEIN
TH. OLBRICHT, ST. BIENIEK, H.G. HOFF and H. SCHULTE
G. Benker, C. Splittstößer, H. Meinhold, Th. Olbricht and D. Reinwein
Abstract. Bovine TSH was administered iv to 10 normal volunteers in doses of 2.5, 7.5, 15 and 30 mU/kg. Brisk elevations of serum diiodotyrosine occurred already after the smallest dose (mean, + 183%) while larger doses had only slight additional effects. T3 rose much higher than T4 (+71% compared to +23% after 15 mU bTSH/kg), and free thyroid hormones exhibited changes similar to total T3 and total T4. The mean absolute increase in serum fT3 ranged from 2.03 to 9.04 pmol/l and proved to be an easily measurable parameter for the TSH effect. Dose-response effects were seen for the increases of fT4, fT3 and T3. TBG and rT3 did not change but the degradation product 3,3'-T2 showed large increments of serum levels. There was no correlation between the response of T3 and T4, fT3 and fT4, or diiodotyrosine and any of the other parameters of thyroid function. The interindividual differences in the magnitude of thyroid hormone response to TSH were considerable, and there was no relationship between this response and thyroid volume by ultrasound. We conclude that direct stimulation of the thyroid gland with bTSH in small doses leads to consistent increases of thyroid hormones, especially T3 and fT3, that the response varies between individuals, and that the precursor diiodotyrosine is released together with thyroid hormones.
G. BENKER, C. SPLITTSTÖSSER, H. MEINHOLD, TH. OLBRICHT, D. REINWEIN and H. G. HOPF
G. BENKER, H. RASCHE, TH. OLBRICHT, J. TEUBER, R. WINDECK, H. SCHULTE and D. REINWEIN
G. Benker, H. Rasche, Th. Olbricht, H. Meinhold, J. Teuber and D. Reinwein
Abstract. Thirty-three patients with Addison's disease were studied. Twenty-two had idiopathic Addison's disease; within this group, 14 patients had clinical or subclinical hypothyroidism, and 16 had increased titres of thyroid autoantibodies. Five patients had tuberculous, and eight had unclassifiable Addison's disease; only one patient in the latter group had evidence of thyroid autoimmunity. A stimulation test with 15 mU bTSH/kg was performed in three patients with Schmidt's syndrome (coexisting Addison's disease and manifest primary hypothyroidism), 15 patients with either subclinical hypothyroidism or increased titres of thyroid autoantibodies, 10 patients without thyroid involvement, and 10 normal controls. There was no detectable increase of 'free' and total thyroid hormones in Schmidt's syndrome. The mean increases after 3–4 h of T4, fT4, T3 and fT3 were 22, 35, 63 and 66%, respectively, in patients without thyroid involvement, and 13, 24, 46 and 45% in patients with subclinical hypothyroidism. 'Free' but not total thyroid hormones rose significantly (P <0.01) higher in patients without signs of thyroid involvement than in patients with subclinical hypothyroidism and/or thyroid autoantibodies. Thyroid hormone response to bTSH in Addison's disease with apparently healthy thyroid glands was not different from normal controls. Serum diiodotyrosine rose in all groups except in hypothyroidism; hypothyroid patients had, however, basal levels well within the normal range. Thus, thyroid hormone synthesis appears to be blocked at a point distal to diiodotyrosine formation in this particular situation. These results support the assumption that TSH elevation in idiopathic Addison's disease is due to coexisting thyroid autoimmunity and that it reflects incipient thyroid failure. This can be demonstrated by a diminished response of 'free' T4 and 'free' T3 to exogenous stimulation with bTSH.
TH. OLBRICHT, S. RIEDERER, G. BENKER, R. WINDECK, H. G. HOFF and D. REINWEIN
G. BENKER, H. ALBERS, TH. OLBRICHT, S. LEDERBOGEN, H.G. HOFF, N. SCHEIERMANN and D. REINWEIN
G. Benker, U. Schäfer, U. Hermanns, M. K. Mahmoud, Th. Olbricht, H. M. Schulte, R. Windeck and D. Reinwein
Abstract. Twenty-three patients (13 females, 10 males) with panmyelopathy (N = 9), chronic leukemia (N = 5), and acute leukemias (N = 9) were studied 1 to 6 years following allogenic bone marrow transplantation. All patients had received conditioning treatment with cyclophosphamide prior to aBMT, and 2 of the patients with bone marrow aplasia and all of the leukemia patients had been given radiotherapy. An endocrine assessment was performed by means of TRH, GnRH, oCRF and GHRH tests and estimation of thyroid and gonadal hormones. Whereas pituitary-adrenal function appeared to remain stable, there was a 17.4% incidence of subclinical hypothyroidism (25% of the irradiated patients). Growth hormone reserve was diminished, and ovarian failure occurred in all female patients after radiotherapy, whereas in the men, only a moderate elevation of gonadotropins was observed. Our results warrant observation of thyroid and gonadal function, and in children of growth hormone secretion, after allogenic bone marrow transplantation. They also show that replacement therapy may be needed in some patients.
G. Benker, Th. Olbricht, R. Windeck, R. Wagner, H. Albers, S. Lederbogen, H. G. Hoff and D. Reinwein
Abstract. Fifty-three patients with subacute thyroiditis (SAT) were seen during the acute stage of the disease. HLA-Bw 35 was positive in 33 out of 39 tested patients. At first presentation, all examined patients (N = 23) had ultrasound abnormalities (generalized hypodensity, single or multiple hypodense areas). Serum T4 and/or T3 were increased in 24/52, free T4 in 11/23, and the TSH response to TRH was flat in 8/11 patients. Six of 12 in whom volumetry was performed had goitres. Thirty-seven patients were re-examined after a mean follow-up interval of 46.5 months. At this follow-up, serum T4, free T4 and T3 levels as well as the sonographically determined thyroid volume had decreased, but there was still abnormalities by ultrasound detected in 14/36 patients; 19.4% had focal sonolucent lesions, whereas the prevalence of such lesions was only 3.1% in asymptomatic controls. Three patients were subclinically hypothyroid at the follow-up, whereas all others were euthyroid. Patients with abnormal ultrasound findings were of the same age and had a similar thyroid size, but a slightly higher TSH and a significantly (P<0.02) lower free T4 than those with normal ultrasound findings. They also had a higher prevalence of thyroid autoantibodies in low titres. Serum thyroglobulin was elevated in more than half of the patients during the acute phase, but only in 1 out of 11 patients during follow-up. Thyroglobulin at the follow-up was not related to TSH, but there was a correlation with thyroid volume (r = 0.57). In conclusion, thyroid abnormalities regarding both function and ultrasound findings are sufficiently frequent after SAT to warrant close observation of the patient. Conversely, abnormal ultrasound findings and diminished thyroid function, when not explained by other factors, should suggest the possibility of past SAT.