Pseudohyperkalaemia in conditions with increased platelet counts is caused by an in vitro rise of the serum potassium concentration during whole blood coagulation and the lysis of the platelets and other cellular components, in the presence of normal renal function and normal plasma potassium levels. The association between pseudohyperkalaemia and aetiology of thrombocytosis was studied in a 6-year retrospective audit on 90 patients with thrombocytosis referred to the Haematology Department in Ulster Hospital Dundonald, a large district general hospital. Over two-thirds of this study population had myeloproliferative disorders, and the most common diagnosis was primary thrombocythaemia (41%, n = 37). Reactive thrombocytosis was observed in approximately one-third of the cases (32%, n = 29). Pseudohyperkalaemia with apparent potassium level above the upper limit of the normal range (reference range K 3.5-5.1 mmol/l) was observed in the majority of patients with thrombocytosis from any aetiology (60%, n = 54). The likelihood of finding pseudohyperkalaemia was highest among patients with primary thrombocythaemia (75.7%, n = 28/37) and polythaemia rubra vera (75%, n = 12/16), followed by myelofibrosis (50%, 4/8) and reactive thrombocytosis (34.5%, n = 10/29). A highly significant positive correlation was observed between the platelet counts and the serum potassium level (Spearman's correlation coefficient, R = 0.998, P = 0.01). Awareness of pseudohyperkalemia in disease conditions with increased platelet counts will lead to the withholding of potentially harmful treatment.
A case of signet-ring cell lymphoma affecting the bone marrow and diagnosed by bone marrow trephine biopsy is reported. Normal marrow was replaced totally by cells with large central vacuoles, many of which displaced the nucleus to the periphery of the cell, imparting a signet-ring appearance. Initially, the favoured morphological diagnosis was metastatic signet-ring adenocarcinoma, but on immunocytochemistry the tumour cells were strongly positive for CD45 (leucocyte common antigen) and the B cell marker CD20 (L26). Electron microscopy revealed electron-lucent vacuoles with no discernable internal structure. The tumour was classified as a high grade centroblastic lymphoma using the upgraded Kiel classification. Despite chemotherapeutic treatment, the patient died during an episode of septicaemic shock within two months of presentation.
Two elderly patients with prolymphocytic leukaemia (PLL) of T helper phenotype were treated with the adenosine deaminase inhibitor--deoxycoformycin--and achieved remission. The first patient has remained in an unmaintained remission for over a year. The second patient, treated with a regime which produced less side effects, subsequently relapsed in skin and lymph nodes and died. In view of the rarity of this condition a multi-centre assessment of the effectiveness of deoxycoformycin is indicated. T-lymphocyte colony formation in both cases was found to be reduced. Co-culture of the patients' lymphocytes with nonadherent mononuclear cells from normal individuals also showed inhibition of T-colony formation indicating that lack of nutrients or accessory cells was not responsible for low T-colony forming capacity.
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