[Biguanides and lactic acidosis].
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Biomedical subjects
Publications and source records attributed to A Aro.
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Thyroid function was studied in acromegaly before and after transsphenoidal hypophysectomy followed by cryoapplication. The clinical material comprised 36 euthyroid, 1 hypothyroid and 3 hyperthyroid patients. In addition to the usual thyroid parameters a standard thyrotrophin-releasing hormone (TRH) stimulation test using 200 mug of synthetic TRH given iv was used. In untreated acromegaly with euthyroidism the response of serum TSH to TRH was significantly less than in normal controls, the increment being 7.1 mU/1 vs. 12.5 mU/1. In 23% of the patients the response was subnormal (less than 3.0 mU/1). The total thyroxine was significantly higher than in controls. Goitre occurred in 53% of the patients. After operation 3 patients became hypothyroid. In 30% of the patients remaining euthyroid the response to TRH was subnormal and the mean response in this group was close to the lower normal limit of 3.0 mU/1. In 7 patients who showed a subnormal response to TRH before or shortly after the operation there was a gradual increase and normalization of the response during the next few years. A subnormal, and also a low normal response to TRH before or after hypophysectomy does not necessarily indicate an increased risk for the development of hypothyroidism, and indeed the pituitary remnant seems to have a remarkable capacity for regeneration. In the hypothyroid patient there was a low normal response to TRH, the reason being unknown. In one of the hyperthyroid patients the basal TSH level was 6.5 and 8.9 mU/1 on two occasions in the thyrotoxic phase, showing a small response to TRH. The possibility that hyperthyroidism was due to increased secretion of TSH is discussed but not claimed proven. The incidence of hyperthyroidism in a large material of acromegaly from this department equals 9% which is above the prevalence of hyperthyroidism in the general population in Finland, indicating that acromegaly in one way or another seems to increase the incidence of manifest thyrotoxicosis.
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The association of precipitating anti-adrenal antibodies with different subgroups of idiopathic Addison's disease were studied. We had previously found these antibodies in patients with the moniliasis-polyendocrinopathy syndrome. Sera of 36 adult patients suffering from different froms of Addison's disease were examined for the presence of adrenal antibodies demonstrable either by immunofluorescence (IFL) or by gel diffusion. 3 of the 17 patients with tuberculous and 17 of 19 patients with idiopathic Addison's disease had IFL antibodies but only one had precipitating antibodies. There was one typical case of Schmidt's syndrome, and four additional cases with Addison's disease combined with diabetes or thyroiditis, who may later develop the syndrome. None of htese patients had precipitating anti-adrenal antibodies. The only patients with precipitating adrenal antibodies had the moniliasis-polyendocrinopathy syndrome. He was not typical as Addison' disease appeared unusually late and he did not have hypoparathyroidism. The presence of precipitating anti-adrenal antibodies in this patient, and the absence of these in other groups of Addison's disease, is further evidence for the association of precipitating antibodies with the moniliasis-polyendocrinopathy syndrome.
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A young man, investigated because of tetanic convulsions and arthritic pains, was shown to have hypomagnesemia, hypermagnesuria, hypokalemia, hypercalciuria, progressive nephrocalcinosis and chondrocalcinosis. In this syndrome, renal function was normal except for the abnormal excretion of electrolytes. Renal sodium conservation was normal. Light and electron microscopic studies of renal biopsy specimens showed the presence of several abnormal tubules. Immunofluorescent staining showed deposits of immunoglobulins in the glomeruli and tubules. Magnesium therapy was started under balance study conditions and resulted in decreased calciuria and complete remission of subjective symptoms. The progression of nephrocalcinosis was halted, and there was some decrease in the intra-articular calcium deposits after two years of continuous oral magnesium therapy. The administration of spironolactone decreased urinary magnesium but did not normalize it, whereas triamterene administration was without effect in this respect. The results of the morphologic and electrolyte balance studies are discussed. The patient was found to exhibit several features which have not been described before in connection with hypomagnesemia of unknown origin.
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Glycoproteins that yield non-dialyzable, alkali-labile, N-acetylgalactosamine-containing heteropolysaccharides upon proteolytic digestion show a threefold enrichment in white matter relative to gray matter. Approximately 50% of these glycoproteins appear in soluble extracts prepared from rat brain. This distribution contrasts with that of the predominant alkali-stable sialoglycopeptides, which account for 60% of the total brain glycoprotein-carbohydrate. The latter glycopeptides showed a twofold enrichment in gray matter compared with white, and only about 10% of the glycoproteins that yield these glycopeptides could be solubilized by extraction with aqueous solvents. The concentration of the N-acetylgalactosamine-containing glycoproteins in the 3-year-old cerebral gray matter from human brain was respectively 7-15 and 15-30 times greater than in 8- and 72-year-old tissue. Electrophoretic analysis of the non-dialyzable, alkali-stable, acidic glycopeptides that contain NANA, fucose, mannose, galactose, and N-acetylglucosamine, obtained from the microsomal and synaptosomal fractions, revealed that the composition of these glycopeptides in the two fractions was identical.
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The genetic background of endogenous hypertriglyceridaemia was evaluated in 239 first-degree relatives of 48 probands with serum triglyceride level in excess of 30.0 mM and with either normal (type IV) or elevated (type IIB) serum cholesterol concentration. In one quarter of the families, all examined first-degree relatives of the proband were normolipidaemic and, thus, the disorder was classified as non-genetic. Nine of 26 probands with IV in contrast to only three of 22 probands with type IIB abnormality fell into this category. In 75% of the families the hyperlipoproteinaemia was caused by one or several abnormal genes. A multiple-type (combined) familial hyperlipidaemia could be demonstrated in 30 families and a single-type IIB or IV familial disease was found in 6 instances. Thus, the multiple-type hyperlipoproteinaemia seems to be responsible for the elevated serum triglyceride level in more than one-half of the cases with moderate to severe hyperglyceridaemia while a pure familial endogenous hypertriglyceridaemia is relatively rare. Exactly 50% of the members of families with the multiple-type lipid disorder were affected but the distribution of individual cholesterol and triglycerides values did not show a definite bimodality. It is possible that the abnormality is heterogeneous and includes several disease entities, which are indistinguishable by a conventional lipid or lipoprotein analysis but can be separated by kinetic or enzyme studies.
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