[Quality assurance and reference programs].
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Biomedical subjects
Publications and source records attributed to I Hornum.
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This investigation includes 17,187 patients in 417 hospitals in 16 countries admitted within 24 hours of the commencement of symptoms of acute myocardial infarction (AMI). The patients were allotted at random to the following treatments 1) intravenous infusion of 1.5 million International Units streptokinase (SK) during one hour, 2) 160 mg acetyl salicylic acid (ASA) daily for 30 days, 3) both SK and ASA and 4) placebo treatment only. The five-week cardiovascular mortality was reduced by 25% following infusion of streptokinase from 12.0% to 9.2% and by 23% during ASA treatment from 11.8% to 9.4%. The combination of SK and ASA resulted in 42% reduction in the cardiovascular mortality after five weeks compared with the placebo. The effect of SK was greatest if treatment was instituted within six hours but effects were obtained after all of the first 24 hours. The preliminary results show that the reduction in mortality obtained by both SK and ASA appears to continue during the subsequent one to two years. SK treatment resulted in haemorrhage requiring treatment in 0.5% as compared with 0.2% in the placebo group, more cases of proved cerebral haemorrhage, 0.1% as compared with 0.0%, but fewer cases of cerebral apoplexy, 0.7% as compared with 0.8%. It is concluded that thrombolysis with SK combined with prophylaxis of repeated thrombosis with ASA is the indicated treatment in cases of AMI and less than 6-24 hours duration.
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Simultaneous determinations of serum total calcium(TOCa), protein corrected total calcium (TOCac), ultrafiltrable calcium (UFCa) and ionised calcium (Ca++) were undertaken in 63 controls and in 76 patients with primary hyperparathyroidism. Raised levels of Ca++ were used as one criterion of the diagnosis which was confirmed by operation in all. For the purpose of estimating the relative value of TOCa and TOCac in the detection of mild hyperparathyroidism we selected all patients with TOCa values below 3.00 mmol/l (n = 46). As a group these patients turned out to be mildly hypoproteinaemic (p less than 0.01), probably because of high age and complicating conditions. Further subdivision of this group into frank hypercalcaemia, borderline hypercalcaemia and normocalcaemia was undertaken according to the respective 99% and 95% confidence limits of normal. Twenty-seven patients were classified as frankly hypercalcaemic by TOCa as well as by TOCac. The distribution of the remaining 19 patients within the three categories was 1:6:12 as judged from TOCa while TOCac gave a better distinction from normal, 9:4:6 (p less than 0.01). This compared well with the classification obtained by UFCa, 10:5:4. It is concluded that TOCac is definitely advantageous to TOCa in the detection of hypercalcaemia in mild primary hyperparathyroidism.
Ten psychiatric patients were given a protein-rich meal in periods on and off lithium administration. The concentrations of gastrin in serum were measured radioimmunochemically before and during the meal. The results show that lithium suppresses basal as well as food-stimulated gastrin secretion.
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Combined calcium balance and 47Ca turnover studies in sarcoidosis (4 patients) and vitamin D intoxication (1 patient) disclosed three different patterns of calcium metabolism. On patient with sarcoidosis had a normal metabolism of calcium, and two patients presented the usual pattern of intestinal hyperabsorption, hypercalcemia, and hypercalciuria. The fourth patient with sarcoidosis and the patient with vitamin D intoxication, both studied during spontaneous remissions, presented the third pattern. The main features here were hypercalcemia despite normal intestinal absorption of calcium, enlarged exchangeable calcium pool, accelerated accretion and resorption rates, hypercalciuria, and a distinctly negative calcium balance. This pattern of remission seems to represent a mobilization of extraosseous or metastatic calcifications, rather than a resorption of bone calcium.
The effect of protein-rich food, intravenous calcitonin injections, and intragastric instillation of hydrochloric acid on serum gastrin concentrations and gastrin component pattern was studied in hypergastrinemic patients (pernicious anemia) and matched control subjects. Moreover, plasma secretin concentrations were measured during intragastric acidification. The intragastric acidification resulted in rapid fall in serum gastrin concentrations, although not below the upper limit of normal range. The small components, III (gastrin-17-like) and IV (gastrin-13-like), almost disappeared, whereas the concentrations of component I and component II (gastrin-34-like) were less affected. The increase in secretin concentrations after intragastric acidification was smaller in patients with pernicious anemia than in normal subjects, although the difference was not significant. In contrast to the results in normal control subjects, neither food nor calcitonin produced significant variations in serum gastrin concentrations and gastrin component pattern of pernicious anemia patients. The failure of food to stimulate and of calcitonin to inhibit release of gastrin in the majority of pernicious anemia patients might suggest that gastrin secretion in these patients is autonomous. However, considering the recently recognized slow metabolic clearance rate of big gastrins, the effect of intragastric acidification suggests that the mechanism for acid inhibition of the antral gastrin secretion is intact in patients with achlorhydria.
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Synthetic salmon calcitonin (sCT, doses of 0.7 Medical Research Council U per kg) was injected into nine normal subjects and three patients with hypergastrinemia (pemicious anemia). sCT depressed basal as well as food-stimulated serum gastrin concentrations without concomitant changes in total and ultrafiltrable concentrations of calcium in serum. Gel filtration of sera revealed that sCT reduced mainly the small components, III (gastrin-17 or "little" gastrin) and IV (gastrin-13 or "mini"-gastrin).
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