Risk of haemorrhage from transurethral prostatectomy in acetylsalicylic acid and NSAID-treated patients.

Postoperative bleeding in patients who regularly ingest acetylsalicylic acid (ASA) has been reported after several types of surgery. However, data on the influence of ASA on the risk of haemorrhage from transurethral prostatectomy (TUR-P) have been conflicting. We have studied retrospectively the unselected clinical records of all patients undergoing TUR-P in the Department of Urology at Hvidovre Hospital (during 1992-1994) with special focus on the use of ASA and non-steroidal anti-inflammatory drugs (NSAIDs). In total, 457 records were examined: 99 patients on ASA/NSAID received 42 units of blood, while 358 patients free from such medication received 68 units of blood, a significantly smaller amount (p = 0.0390). We conclude that ASA and NSAIDs increase the risk of bleeding during and after TUR-P, and we recommend the withdrawal of these drugs for one week before TUR-P.

Time course of platelet alpha granule release in acute myocardial infarction treated with streptokinase.

OBJECTIVE: To determine the time course of platelet alpha granule release in patients with acute myocardial infarction treated with streptokinase. DESIGN: A prospective study. SETTING: Coronary care unit. PATIENTS: Nine with myocardial infarction treated with both streptokinase and aspirin, and nine with acute chest pain but without myocardial infarction, who were treated with aspirin only. METHODS: All patients received 250 mg aspirin on admission and 150 mg once daily thereafter. All patients who fulfilled the indications for streptokinase received 1.5 megaunits, in a single infusion. After the initial medication, serial measurements of plasma beta thromboglobulin and plasma platelet factor 4 were performed at fixed intervals after the onset of chest pain. The primary endpoint sought was the peak value of beta thromboglobulin and platelet factor 4 in each individual. RESULTS: The median peak plasma beta thromboglobulin in the infarction group was substantially higher than in those without infarction, at 37 (range 12 to 210) v 15 (9 to 36) mg/litre, P < 0.01. The corresponding values for plasma platelet factor 4 were 4.6 (2.4 to 60.0) v 2.2 (< 2 to 8.5) mg/litre, P < 0.01. Increased values were seen only within the first 12 h after onset of chest pain, and after 12 h there was no difference between the patients with myocardial infarction and those without. Aspirin treatment did not abolish alpha granule release. CONCLUSIONS: In patients with acute myocardial infarction treated with streptokinase the content of the alpha granules is released within the first 12 h after the onset of chest pain. Aspirin apparently does not abolish this release.

[Magnesium and ischemic heart disease]. / Magnesium og iskaemisk hjertesygdom.

Our knowledge about magnesium in health and disease has increased during the past ten years. Many authors have demonstrated possible magnesium depletion in the population as a whole and particularly among cardiac patients receiving diuretics. Evidence suggests that this magnesium depletion may play a role in the development of arteriosclerosis. It has been demonstrated that long term supplementation of the diet with magnesium reduces the frequency of heart disease. However, the matter is still not proven. It is postulated further that magnesium depletion aggravates the outcome of acute myocardial infarct and has a tendency to provoke arrhythmia. Finally, it has been shown that the potassium depletion frequently observed among cardiac patients may actually arise from magnesium depletion. On this basis, many authors have employed magnesium therapy in various cardiac diseases. Some authors have demonstrated that magnesium therapy reduces the mortality in AMI patients. These studies are, however, too few and too limited to be conclusive. In order to investigate this question, an international multicentre trial (ISIS-4) will be conducted to investigate the influence of magnesium therapy on the mortality after acute myocardial infarction.

[Basedow's disease and thyroid stimulating hormone producing pituitary adenoma in a patient]. / Mb. Basedowi og thyreoideastimulerende hormonproducerende hypofyseadenom hos samme patient.

TSH-producing adenomas of the pituitary gland are very rare. Synchronous combinations of TSH-producing adenomas with other causes of hyperthyroidism are certainly extremely rare. We present the second known case, reported in the literature, consisting of observations for 12 years in a woman aged 43 years, who presented with active Graves' disease and an apparently inactive pituitary macro-adenoma. However, after normalisation of serum T3 and serum T4 levels by antithyroid medication for one year, the serum TSH rose inappropriately and continued to rise for the following 11 years. Insidious growth of the adenoma also occurred. After one year of medical treatment, a huge goitre was resected (210 g) leaving the patient euthyroid, clinically and biochemically, for four years. Hereafter, hyperthyroidism developed again this time without Graves' disease. We conclude that the patient experienced hyperthyroidism on two occasions, the first caused by Graves' disease and then caused by a TSH-producing pituitary adenoma.

Fast, stable method for harvesting leukocytes for measuring intracellular magnesium.

A new method for isolating blood leukocytes and measuring intracellular leukocyte magnesium is based on three successive centrifugations (1300 x g, 5 min, 22 degrees C), with no use of Ficoll, followed by two washes. We express the leukocyte magnesium concentration in micromoles of magnesium per gram of protein. Magnesium is measured by atomic absorption spectrophotometry, protein by the classic Lowry method. With the method 8% to 28% of the leukocytes are isolated and 0% to 0.025% of the erythrocytes. Of the isolated leukocytes 86% to 93% are viable. The magnesium concentration is constant at centrifugal forces greater than 1000 x g, at a centrifugation time of 5 to 15 min, and with use of two or three washes. However, the cells lose 1% of their magnesium content per hour when samples are left at 22 degrees C. The temperature influences this. In blood samples from 98 volunteer blood donors, mean leukocyte magnesium concentrations were 26.4 (SD 3.9) mumol/g. There was no significant correlation between the magnesium concentration and the relative amount of neutrophils.