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1 This article was downloaded by:[heal- Link Consortium] On: 21 November 2007 Access Details: [subscription number ] Publisher: Informa Healthcare Informa Ltd Registered in England and Wales Registered Number: Registered office: Mortimer House, Mortimer Street, London W1T 3JH, UK Platelets Publication details, including instructions for authors and subscription information: Multiple metabolic abnormalities in a patient with essential thrombocytosis M. Elisaf; H. Milionis; P. Tomos; K. C. Siamopoulos Online Publication Date: 01 July 1997 To cite this Article: Elisaf, M., Milionis, H., Tomos, P. and Siamopoulos, K. C. (1997) 'Multiple metabolic abnormalities in a patient with essential thrombocytosis', Platelets, 8:4, To link to this article: DOI: / URL: PLEASE SCROLL DOWN FOR ARTICLE Full terms and conditions of use: This article maybe used for research, teaching and private study purposes. Any substantial or systematic reproduction, re-distribution, re-selling, loan or sub-licensing, systematic supply or distribution in any form to anyone is expressly forbidden. The publisher does not give any warranty express or implied or make any representation that the contents will be complete or accurate or up to date. The accuracy of any instructions, formulae and drug doses should be independently verified with primary sources. The publisher shall not be liable for any loss, actions, claims, proceedings, demand or costs or damages whatsoever or howsoever caused arising directly or indirectly in connection with or arising out of the use of this material.

2 /97/ $ Carfax Publishing Ltd Platelets (1997) 8, 275±277 Case report Multiple metabolic abnormalities in a patient with essential thrombocytosis M. Elisaf, H. Milionis, P. Tomos, K.C. Siamopoulos A patient with extreme essential thrombocytosis who exhibited an array of real or spurious metabolic abnorm alities is described. C areful venipuncture and prompt m easurem ent avoided unnecessary further laboratory investigation and potentially dangerous overtreatm ent. Introduction We describe a patient with severe throm bocytosis who exhibited a cluster of real and spurious metabolic abnorm alities. This case report points out the problems that m ay arise in these patients in relation to the interpretation of several laboratory tests. C ase report Correspondence to: M. Elisaf, Department of Internal Medicine, Medical School, University of Ioannina, Ioannina, Greece. An asymptomatic 62-year-old man with extreme thrombocytosis, that was revealed during a routine laboratory investigation, was adm itted to our out-patient clinic. There was no history of blood loss, splenectomy, or other chronic inflammatory or neoplastic disease. Physical examination was unremarkable except for mild splenomegaly. A laboratory investigation of a non-haemolysed blood sample obtained at admission of the patient is shown in Table 1. The patient denied the use of drugs that interfere with potassium, phosphate or calcium hom eostasis. An electrocardiogram was within normal limits. Because of the profound hyperkalaemia, potassium concentration in the serum was m easured again after careful venipuncture and gentle handling of the blood sample. Levels of potassium in the serum were then 6.6 mmol/l, while at the same time plasma potassium concentration was 5.4 m mol/l. However, levels of potassium in a plasma sample that was carefully obtained and imm ediately sent to the laboratory, was 4.5 mmol/l. Similarly, calcium and phosphate levels were also within norm al limits (2.52 mmol/l and 1.16 mm ol/l, respectively) in the same sample. A normalization of arterial po 2 was also found when the blood sample was carefully obtained and immediately m easured. All the above blood tests were carried out within a few hours. Essential thrombocytosis was eventually confirmed after a careful diagnostic work-up. Discussion Our patient presented with a number of metabolic abnorm alities some of which were directly correlated with the thrombocytosis. Specifically, hyperuricaemia and increased lactate dehydrogenase activity were found due to an increased cellular turnover. However, a number of spurious disturbances were also evident. Pseudohyperkalaem ia was observed and was suspected because of the absence of neuromuscular com plaints, the normal electrocardiogram, and the lack of other apparent causes for the elevation of potassium concentration in the serum (such as acidosis, hyperglycaemia, administration of b -adrenergic blockers, severe exercise, tissue catabolism, renal failure, hypoaldosteronism or drugs that interfere with potassium homeostasis). This increase in serum potassium concentration was possibly due to the

3 276 THROMBOCYTOSIS-INDUCED METABOLIC ABNORMALITIES Table 1. Laboratory investigations on admission Parameters Reference values a Haematocrit ± 0.50 Total leukocyte count /l 3.8± /l Platelet count /l 140± /l Serum glucose (mmol/l) ± 6.87 Serum urea (mmol/l) ± 17.8 Serum creatinine (l mol/l) ± Serum uric acid (l mol/l) ± 386 Serum sodium (mmol/l) ± 145 Serum potassium (1st sample b ) (mmol/l) ± 5.0 Serum potassium (2nd sample b ) (mmol/l) 6.6 Plasma potassium (2nd sample b ) (mmol/l) c 5.4 Plasma potassium (3rd sample b ) (mmol/l) c 4.5 Serum chloride (mmol/l) 99 97± 103 Serum calcium (mmol/l) d ± 2.6 Plasma calcium (mmol/l) c,d 2.52 Serum phosphate (mmol/l) ± 1.45 Plasma phosphate (mmol/l) c 1.16 Serum total proteins (g/l) 80 62± 82 Serum albumin (g/l) 44 36± 50 Serum total iron (l mol/l) 24 9± 31 Serum iron binding capacity (l mol/l) 68 45± 80 Serum ferritin (pmol/l) ± 590 Serum lactate dehydrogenase (IU/l) ± 280 Serum alanine aminotransferase (IU/l) 18 7± 53 Serum aspartate aminotransferase (IU/l) 24 11± 47 Serum creatine kinase (IU/l) ± 220 Arterial ph ± 7.45 po 2 (kpa) ± 14.0 pco 2 (kpa) 5 4.7± 6.0 a Reference values from our laboratory in accordance with those stated by the manufacturers. b See text for explanation. c Under normal circumstances the concentrations of potassium and phosphate in plasma are 0.1± 0.5 mmol/l and 0.06± 0.10 mmol/l lower than that of serum, respectively, while the plasma calcium levels are 0.9% greater than serum values. d The corrected serum and plasma calcium levels were 2.64 and 2.44 mmol/l for the serum and plasma samples, respectively. However, this calculation is only an approximation. Corrected Ca: Ca (40 ± albumin concentration). in vitro release of potassium from platelets during the clotting process. 1 ±3 In fact, plasma potassium concentration was significantly lower (5.4 mmol/l), although still above the upper end of the reference range. However, in view of the severe throm bocytosis, this degree of difference between serum (clotted sample) and plasma (anticoagulated sample) potassium levels is expected according to previously published data. 2,4 Another mechanism for the observed hyperkalaem ia may be the prolonged storage of blood at room temperature before its determination, since this causes potassium release from platelets. 5 For these reasons, it is advised that patients with marked leukocytosis or throm bocytosis should have potassium levels determined without delay by carefully obtaining plasma samples that are separated promptly from the cellular elements. 2,3,5 Accordingly, in our case, plasma potassium levels were within normal limits when the determination was performed using these precautions. Mild hyperphosphataemia was also found, which was similarly `corrected when plasma samples were carefully obtained and prom ptly analysed. It has recently been stated 6 that thrombocytosis is associated with false elevations in measured serum potassium and phosphorus concentrations. The magnitude of elevation of the potassium and phosphorus concentrations appears to be related, implying that phosphates, as anions concentrated in the intracellular fluid, follow the cation potassium out of the cells to preserve electrical neutrality. 6 Interestingly, mild hypercalcaemia was also reported in the serum sample although this was essentially no longer evident when correcting for the albumin concentration (see Table 1). The normal, and considerably lower, plasma calcium levels implicate a similar pathogenetic mechanism, i.e. the in vitro release of calcium anions from platelets during the clotting process. Pseudohypercal caemia, in serum samples, does not appear to have been previously reported in cases of throm bocytosis. Hypoxaemia has been occasionally described in patients with extreme leukocytosis or throm bocytosis and has been ascribed to an increased rate of oxygen consumption, especially if the analysis of blood gas is delayed and the sample is kept at room temperature. 7 The problem can be averted if the arterial blood sam ple is immersed in ice immediately after it is drawn and kept at 2ÊC until the analysis is performed. Alternatively, the sample should be promptly analysed. It is concluded that in patients with extrem e thrombocytosis a number of false metabolic abnorm alities can occur. To avoid further laboratory investigation and

4 PLATELETS 277 potentially dangerous overtreatment, the determinations should be perform ed on plasm a samples soon after careful venipuncture. References 1. Hartmann RC, Auditore JV, Jackson DP, Bingham CP. Studies on thrombocytosis: I. Hyperkalemia due to release of potassium from platelets during coagulation. J Clin Invest 1958; 37: 699± Graber M, Subramani K, Corish D., Schwab A. Thrombocytosis elevates serum potassium. Am J Kidney Dis 1988; 12: 116± Ifudu O, Markell MS, Friedman EA. Unrecognized pseudohyperkalemia as a cause of elevated potassium in patients with renal disease. Am J Nephrol 1992; 12: 102±4. 4. Nijsten MWN, De Smet BJGL, Dofferhoff ASM. Pseudohyperkalemia and platelet counts. N Engl J Med 1991; 325: Colussi G, Cipriani D. Pseudohyperkalemia in extreme leukocytosis. Am J Nephrol 1995; 15: 450±2. 6. Lutomski DM, Bower RH. The effect of thrombocytosis on serum potassium and phosphorus concentrations. Am J Med Sci 1994; 307: 255 ±8. 7. Hess CE, Nichols AB, Hunt WB, Suratt PM. Pseudohypoxemia secondary to leukemia and thrombocytosis. N Engl J Med 1979; 301: 361±3.

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