Medizin - Open Access LMU - Teil 05/22 Archiv
250 Episoden
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The prevalence of endemic iodine-deficiency goitre in Europe has been reduced in many areas by the introduction of iodination programmes. Recent reports, however, show that goitre remains a significant problem and that its prevalence has not decreased in a number of European countries. Hetzel1 has pointed out that the high global prevalence of iodine-deficiency disorders could be eradicated within 5-10 years by introduction of an iodised salt programme. The current World Health Organisation recommendations for iodine intake are between 150 and 300 μg/day
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Three uncommon findings were observed in a case of Cushing's disease due to macroadenoma: no suppression of plasma ACTH during an 8-mg dexamethasone test, a negative corticotropin-releasing factor test, and a normal X-ray of the sella turcica. Despite these findings, the diagnosis of pituitary was confirmed Cushing's syndrome by computerized tomography and a transphenoidal operation.
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Thyrotropin releasing hormone is thought to be a tonic stimulator of the pituitary TSH secretion regulating the setpoint of the thyrotrophs to the suppressive effect of thyroid hormones. The peptide stimulates the release of normal and elevated prolactin. ACTH and GH may increase in response to exogenous TRH in pituitary ACTH and GH hypersecretion syndromes and in some extrapituitary diseases. The pathophysiological implications of extrahypothalamic TRH in humans are essentially unknown. The TSH response to TRH is nowadays widely used as a diganostic amplifier in thyroid diseases being suppressed in borderline and overt hyperthyroid states and increased in primary thyroid failure. In hypothyroid states of hypothalamic origin, TSH increases in response to exogenous TRH often with a delayed and/or exaggerated time course. But in patients with pituitary tumors and suprasellar extension TSH may also respond to TRH despite secondary hypothyroidism. This TSH increase may indicate a suprasellar cause for the secondary hypothyroidism, probably due to portal vessel occlusion. The TSH released in these cases is shown to be biologically inactive.
