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Background: Hyperkalemia is an electrolyte disorder requiring medical attention because it can cause cardiac arrhythmias. Pseudohyperkalemia is the phenomenon of an elevated potassium concentration that is present in the blood sample but not in the patient. Pseudohyperkalemia can be caused by hemolysis, leukocytosis, thrombocytosis, seasonal pseudohyperkalemia, potassium release from muscle cells due to fist clenching during venipuncture, and contamination due to blood withdrawal from an intravenous line over which potassium was administered. Rarer causes include EDTA contamination and familial pseudohyperkalemia., Case Description: A 23-year old woman was admitted with ascites due to polycythemia vera and essential thrombocytosis for which hydroxycarbamide was started. The reported serum potassium concentrations were 6.1 and 6.8 mmol/l. The use of spironolactone was discontinued and she was treated with sodium polystyrene sulfonate and insulin-glucose infusion. The serum potassium concentration only decreased on the ninth day of admission, when the thrombocyte count was normalizing. A diagnosis of pseudohyperkalemia due to thrombocytosis was established., Conclusion: Knowledge of the causes of pseudohyperkalemia and interaction between the clinician and clinical chemist aids in the differentiation between true hyperkalemia and pseudohyperkalemia and may prevent unnecessary diagnostics and harmful treatment.

Reactive thrombocytosis (RT; thrombocyte count: > 450 x 109/l) is a condition in which an increase in platelet production, stimulated by cytokines in the bone marrow, is secondary to some condition or circumstance. Although RT does often occur in children, the risk of thromboembolic complications is negligible in this group if they have no other risk factors for thrombosis. In the absence of additional risk factors for thrombosis it seems as though RT in adults does not predispose them to thromboembolic complications either. Patients with RT caused by a non-myeloproliferative malignancy do have an increased risk of thromboembolic complications; antithrombotic prophylaxis might be effective in this group, but there is no scientific evidence for this. We advise a watch-and-wait approach in children and adults with RT who have no other risk factors for thromboembolism, even in patients with extreme thrombocytosis (thrombocyte count: > 1000 x 109/l). In patients who do have an increased risk of thromboembolic complications we advise tailoring prescription or non-prescription of antithrombotic prophylaxis to the individual patient.

Objective: To determine if there is a place for radiophosphorus (32P) in the treatment of polycythaemia vera (PV) and essential thrombocytosis (ET)., Design: Retrospective., Setting: Leyenburg Hospital, The Hague, the Netherlands., Method: Data on 144 patients with the diagnoses 'PV' or 'ET' from 1965 to 1994 were collected. Available data were insufficient in 19 of these. Regarding 125 patients, 80 with PV and 45 with ET, the survival and the frequency of acute leukaemia with various forms of treatment (32P, busulfan or combination of several treatment modalities) were studied. Moreover, in the PV group the duration of survival was compared with the expected duration of survival in a comparable group of the population., Results: Of the 80 PV patients, five developed acute leukaemia: two in the 32P group (5%), two in the busulfan group (12%) and one in the group given combination therapy (4%). Of the 26 patients of the ET group treated with busulfan, one developed acute leukaemia (4%). The survival in the PV group was 4 years shorter than the expected duration of survival in a comparable group of the population., Conclusion: Since 32P is efficacious and causes little inconvenience, it should be the drug of first choice in the treatment of PV in the elderly.

Essential thrombocythemia (ET) belongs to the group of clonal myeloproliferative disorders such as polycythemia vera (PV), chronic myelogenous leukemia (CML), and idiopathic myelofibrosis (MF). This rare disorder, characterized by an important thrombocytosis, includes a mucocutaneous hemorrhagic diathesis and thromboembolic events. Neurologic manifestations are frequent in ET and are due to obstruction of the cerebral microvasculature. Both thrombocytosis and platelet dysfunction can be responsible for the thrombo-hemorrhagic phenomena in ET. First symptoms of ET in our patient was thrombosis of the vertebral artery with a secondary embolic event in the thalamus region although the platelet count was below 600.10(9)/l, the classic diagnostic limit for ET. These data strongly suggest that qualitative platelet abnormalities rather than thrombocytosis are the main cause for thrombo-embolic events in ET.