Circulating thyroglobulin antibodies (TgAb) and microsomal antibodies (MsAb) and thyroid function (total and free T4 and T3, TSH basal and after TRH) have been evaluated in 92 hyperprolactinaemic patients (82 females and 10 males; 9 with macroprolactinoma, 22 with microprolactinoma, 4 with acromegaly, 5 with organic lesions of the hypothalamus, 2 with empty sella, 2 with idiopathic hypopituitarism, 2 with primary hypothyroidism, and 46 with idiopathic hyperprolactinaemia). Thyroid function was normal in all cases except 3 with hypothalamic disease and central hypothyroidism, the 2 patients with primary hypothyroidism and 2 with thyrotoxicosis (one due to Graves' disease and one to autonomous thyroid adenoma). High titres of TgAb (\m=ge\1/1250) and/or MsAb (\ m=ge\ 1/1600) were found in the subject with Graves' disease, in one acromegalic, in the 2 primary hypothyroids, and in 12 women with either adenomatous or idiopathic hyperprolactinaemia; low titres of one or both antibodies were found in 9 other euthyroid women and in the one with toxic adenoma. In a control population of 185 subjects studied with the same methods, the prevalence of TgAb and/or MsAb positive (low titres) was 3.3% in females and 2.5% in males. Diffuse thyroid hyperplasia was clinically detectable in 12 euthyroid women and in the one with Graves' disease; 3 others had been previously operated for nodular goitre with histological evidence of Hashimoto's thyroiditis (2 cases) or for a cold nodule; a single thyroid nodule was present in the woman with toxic adenoma and in one euthyroid woman. Most of these subjects also had circulating TgAb and/or MsAb, and a few had increased TSH secretion. No significant differences were found in mean thyroid hormone and TSH levels between euthyroid hyperprolactinaemic subjects and healthy controls, but TRH-stimulated TSH levels were significantly higher in thyroid antibodies positive than negative subjects. These data, in agreement with a few previous reports, suggest that autoimmune thyroid disorders (especially asymptomatic autoimmune thyroiditis) occur in hyperprolactinaemic women with a prevalence far exceeding that observed in many surveys in the general population.The association of autoimmune thyroiditis with prolactinoma has been known for some years (Thorner 1977), but thyroid antibodies were found in that study in only 2 of 38 women, corresponding to the general incidence of circulating thyroid antibodies in the population studied (Tunbridge et al. 1977). Recently, Pelkonen et al. (1982) observed autoimmune thyroiditis in combination with pro¬ lactinoma in 3 of 36 women. The diagnosis of autoimmune thyroiditis was based on the criteria of Gordin et al. (1972), i.e. the presence of circulating microsomal and thyroglobulin antibodies in high titres (> 1/100000 and > 1/25000, respectively). Moreover, the same investigators found exagge¬ rated TSH response to TRH in 4 prolactinoma patients without autoimmune thyroiditis (Pelkonen et al. 1982). It seemed therefore of interest to report our data on thyroi...
Abstract. Increased serum growth hormone (GH) and prolactin (Prl) levels and abnormal responses to some stimuli have been reported in patients with chronic liver disease. Serum GH and Prl concentrations were measured in 11 cirrhotic patients and in sex and age matched healthy controls in basal conditions and after administration of L-dopa alone (500 mg), and L-dopa (100 mg) with carbidopa (35 mg) following pre-treatment with carbidopa (50 mg every 6 h for one day), a regimen which results in selective activation of brain dopaminergic pathways. Basal GH and Prl levels were significantly higher in cirrhotics than in controls; serum GH did not increase significantly and serum Prl was subnormally inhibited in patients after both tests. A patient with clearcut hyperprolactinaemia unresponsive to dopaminergic stimulation showed normal basal Prl levels and suppression by L-dopa following clinical improvement, while her elevated GH levels remained unchanged and did not increase after L-dopa. These data confirm the existence of abnormalities in the regulation of GH and Prl release in liver cirrhosis and suggest that dopaminergic dysfunction may be responsible. The subnormal Prl suppression induced by L-dopa, which stimulates both brain and peripheral dopaminergic receptors, suggests that dopaminergic dysfunction is not confined to the central nervous system in liver cirrhosis. It appears that serum Prl concentration may be of value in monitoring decompensated liver disease and that abnormalities of Prl secretion are reversible with clinical improvement.
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