Search

Acetylsalicylic acid (aspirin) induces an irreversible inactivation of cyclo-oxygenase in blood platelets which lasts for the entire period that the platelets remain in the circulatory system, 7 to 10 days. In order to prevent excessive bleeding, patients presenting for surgery are asked to stop using aspirin 10 days before the procedure. Some studies have found that aspirin causes increased peri-operative blood loss, whilst other studies have found that it does not. All effect studies found in Medline (January 1966-May 2002) on surgery and bleeding complications due to aspirin were analysed. The studies available were assessed for methodological quality and the results were summarised in an evidence table. No clinically relevant bleeding complications were reported for cardiovascular, vascular and orthopaedic surgery and epidural anaesthesia. Most studies reported an increase in clinically non-relevant bleeding induced by aspirin. The literature contains too little information on cataract surgery, dermatological surgery, gynaecological and abdominal surgery, ENT and dental surgery, urological surgery, lung biopsy and endoscopic biopsy. In those types of surgery in which even a minor bleeding leads to severe complications, e.g. neurosurgery, aspirin should be withdrawn 5-10 days in advance. Also in patients with coagulation disorders, aspirin should be withdrawn prior to the operation. There is no scientific evidence for the withdrawal of aspirin in all patients, 5-10 days prior to surgery. Indeed for heart patients in particular, the continued use of aspirin is recommended.

Pyruvate kinase (PK) deficiency is a common cause of hereditary non-spherocytic haemolytic anaemia. It is an autosomal recessive disorder caused by mutations in the gene coding for erythrocyte and liver-type pyruvate kinase (PKLR). So far, more than 130 mutations in this gene have been identified. Clinical symptoms, usually restricted to homozygous and compound-heterozygous individuals, are variable, ranging from neonatal jaundice requiring erythrocyte transfusions to a fully compensated haemolytic anaemia. The exact mechanism of erythrocyte destruction is unknown, however adenosine-triphosphate depletion and an increase in 2,3-disphosphoglycerate are thought to be important. The diagnosis of pyruvate kinase deficiency depends upon the demonstration of low PK enzyme activity. Due to the pitfalls in determining true PK activity, DNA testing is a valuable tool in the diagnosis of pyruvate kinase deficiency. By centralizing the molecular diagnostics of pyruvate kinase deficiency in Utrecht, more care can be provided for the diagnosis, treatment and support of patients.