Leukocyte migration test (LMT) in patients with thyroid disease: the response to human thyroid subcellular fractions.

The response of circulating leukocytes to thyroid subcellular fractions was investigated in 19 patients with Graves' disease, 15 patients with Hashimoto's thyroiditis, 7 patients with toxic adenoma, 19 patients with nontoxic goiter and in 10 healthy students as control subjects. For this purpose, the leukocyte migration test of Soborg and Bendixen was performed against human crude thyroid extract (CTE), cell plasma membranes, nuclei, ribosomes, mitochondria and microsomes. Our results show positive LMT against: 1) CTE in patients with Graves' disease (61 +/- 13, p less than 0.001) and Hashimoto's thyroiditis (65 +/- 11, p less than 0.001) compared to controls (90 +/- 11); 2) cell plasma membranes in patients with Graves' disease (41 +/- 14, p less than 0.001) and Hashimoto's thyroiditis (64 +/- 21, p less than 0.05) compared to controls (88 +/- 19); 3) nuclei in patients with Graves' disease (53 +/- 25, p less than 0.001) and Hashimoto's thyroiditis (53 +/- 23, p less than 0.001) compared to controls (83 +/- 11). Our findings of circulating leukocytes sensitized to cell plasma membranes and nuclear fraction in patients with Graves' disease and Hashimoto's thyroiditis provide the additional information that these patients have a specific defect in immune-surveillance.

[Interrelation between gastrin and insulin in a group of normal subjects]. / Studio delle interrelazioni tra gastrina ed insulina in un gruppo di soggetti normali.

The insulin secretory action of gastrin during O.G.T.T. has been assessed. The insulinaemic and gastrinaemic curves were evaluated in a group of normal subjects submitted to oral glucose load, using radioimmunological measurement techniques. At a later stage, the insulinaemic values were considered in the same subjects after administration of a gastrin analogue (pentagastrin) by the subcutaneous route in a dose such as to provoke a maximal gastric acid response. The data suggest that any participation of gastrin in the regulation of insulin secretion following a glucose meal can be excluded.