Dietary therapy in diabetes mellitus. Description of a recommendation prepared by the Finnish Diabetes Association's Committee on Nutrition Therapy.
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Biomedical subjects
Publications and source records attributed to A Aro.
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The effects of dietary supplementation with granulated guar gum (21 g/day in three divided doses at the main meals), were compared with placebo response during three months in a double-blind, cross-over trial in 11 Type 2 (insulin-independent) diabetes. The nine patients who complete the study (two dropped out because of side-effects) showed a significant reduction in both basal and post-prandial hyperglycaemia as well as of urinary excretion of glucose during guar gum supplementation. No change in mean bodyweight was observed during the study. Mean fasting and post-prandial plasma insulin levels were similar during both study periods, but the two subjects who received no oral hypoglycaemic agents had lower insulin levels during the guar gum period. Mean serum total- and LDL-cholesterol concentrations were significantly lower during the guar gum period, whereas the HDL-cholesterol level remained unchanged. Long-term administration of guar gum induced a sustained improvement in diabetic control in Type 2 diabetes.
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Control of blood-glucose levels was monitored for 12 wk after withdrawal of biguanides in a group of 118 diabetic patients treated with biguanides (alone or in combination with sulphonylurea) from a population of 39,200. The mean fasting blood-glucose level rose during the first 2 wk from 9.2 +/- 0.3 to 11.3 +/- 0.4 mmol/l (p less than 0.001) and the mean urinary-glucose excretion from 11.7 +/- 3.7 g/24 h to 36.5 +/- 5.5 g/24 h (p less than 0.001), respectively. The change in blood-glucose concentration did not depend on age, sex, bodyweight, or duration of diabetes or biguanide treatment. The mean increase in blood-glucose was similar (2.1-3.1 mmol/l) in subjects with their initial blood-glucose level less than or equal to 6.0 mmol/l, 6.1-11.0 mmol/l, and greater than or equal to 11.1 mmol/l. There were no changes in blood-lipids or bodyweight during the observation period. Biguanides reduced blood-glucose levels in most patients with maturity-onset diabetes. The hypoglycaemic effect was similar in subjects with normal and increased bodyweight and did not depend on the duration or severity of diabetes.
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A double-blind comparative study of 1 alpha-OHD3 and placebo was performed on 37 patients with osteoporotic hip fracture without clinical osteomalacia. 1 alpha-OHD3, in a dose of 1 microgram/day together with 2.5 g CaCO3, did not heal osteoporosis as judged from determinations of bone mineral density and histomorphometric analyses during four months of treatment. However, 1 alpha-OHD3 seemed to have an effect on fracture healing as concluded from the posttreatment alkaline phosphatase level. Hypercalcemia was common, occurring in six out of 19 patients treated with 1 alpha-OHD3. It is concluded that treatment of osteoporosis with 1 alpha-OHD3 and calcium is ineffective and potentially dangerous because it frequently causes hypercalcemia.
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A 35-year-old man who was on treatment for mild arterial hypertension with the beta-blocking agent pindolol and who was accustomed to regular physical exercise, developed severe hypoglycaemia and bradycardia during a routine skiing tour. He recovered from the attack, and subsequent studies revealed no abnormalities of glucose metabolism. Apparently the hypoglycaemic attack was due to the combined effects of prolonged physical exercise of moderate degree and beta-blockade on glucose metabolism.
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Twenty-four patients with biguanide-induced lactic acidosis were reported to the Adverse Drug Reaction Register of the Finnish National Board of Health from 1974-1977. Of them, 23 had been treated with phenformin and one with metformin. The mean age of the patients was 71 years, and all but one were more than 65 years of age. The mortality rate was 63%. One patient had cirrhosis of the liver and one was already known tohave had impaired renal function. Fourteen of the patients had a normal serum creatinine concentration either before or after the development of lactic acidosis. Thus, in most patients it had not been possible to prevent development of lactic acidosis by observing the contraindications to biguanide therapy. Most patients had some form of co-existing cardiovascular disease. Tetracycline therapy was a probable precipitating factor in three cases. Based on the statistics of biguanide consumption in Finland, the annual incidence of biguanide-induced lactic acidosis in 1976 and 1977 was between 1/2000 and 1/3000 and that of fatal lactic acidosis was 1/4000.
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Pituitary function was studied in nine patients who had recovered from pituitary apoplexy. All the patients recovered spontaneously; none required immediate surgery. Four of the patients had acromegaly, two had pituitary-dependent Cushing's syndrome, and a "functionless" pituitary adenoma was found in three. Low serum growth hormone concentrations were observed in three patients with acromegaly whereas the concentration remained increased in the fourth one. Of the two patients with Cushing's syndrome, a selective ACTH-deficiency developed in one and Nelson's syndrome appeared with excessive secretion of ACTH in the other. Transient or persistent hypofunction of the anterior pituitary occurred in al patients. Three patients underwent hypophysectomy after respective intervals of three, eight and 12 months after pituitary apoplex. The operation revealed a hemorrhage in one functionless adenoma and a large cyst in another one. In the third patient who had acromegaly, no signs of the pituitary apoplexy were observed at operation.