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Selenium Deficiency, Reversible Cardiomyopathy and Short-Term Intravenous Feeding J.B

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Selenium Deficiency, Reversible Cardiomyopathy and Short-Term Intravenous Feeding J.B Postgrad Med J: first published as 10.1136/pgmj.70.821.235 on 1 March 1994. Downloaded from Postgrad Med J (1994) 70, 235 -236 i) The Fellowship of Postgraduate Medicine, 1994 Selenium deficiency, reversible cardiomyopathy and short-term intravenous feeding J.B. Levy2, H.W. Jones' and A.C. Gordon3 'Department ofGeratology, 2Nuffield Department ofMedicine and 3Surgery, John Radcliffe Hospital, Oxford OX3 9DU, UK Summary: We report the case of a patient with Crohn's disease receiving short-term postoperative parenteral nutrition supplemented with trace elements who nevertheless became selenium deficient with evidence of a cardiomyopathy. This was fully reversible with oral selenium supplementation. Current parenteral feeding regimes may not contain enough selenium for malnourished patients. Introduction Selenium deficiency is well documented to cause ment of systolic function and a mildly dilated left cardiac disease both endemically (Keshan disease),' ventricle. Ejection fraction was calculated at 0.48. and in patients receiving long-term intravenous He had no further episodes of tachyarrhythmia feeding.2`5 There have been no reports of cardiac and was discharged after 3 days. Serum selenium dysfunction after short-term postoperative paren- levels at this time were markedly reduced at teral feeding. 0.3 ILmol/l (normal 0.8-2 jLmol/l) and red cell copyright. glutathione peroxidase activity was also impaired (10 u/g Hb; normal 13-25 u/g Hb). Case report He was treated with oral selenite (100l.g/24 hours). Repeat echocardiogram one month later A 27 year old man presented with symptomatic showed minimal diffuse hypokinesia (ejection frac- tachycardia and chest pain. He had no symptoms tion 0.62) and the ECG remained abnormal. After of cardiac failure. Two months previously he had 3 months treatment his electrocardiogram, serum been diagnosed as having small bowel Crohn's selenium and red cell glutathione peroxidase disease on the basis of a small bowel enema activity had all returned to normal. Echocardio- http://pmj.bmj.com/ demonstrating multiple strictures. One month later gram demonstrated good systolic contraction, with a laparotomy revealed a pre-sacral abscess in ejection fraction 0.70. There was no clinical history addition to active inflammatory bowel disease. An suggestive ofviral infection, and antibody titres for ileostomy was fashioned and parenteral feeding coxsackie, influenza, mumps and cytomegalovirus, was begun postoperatively with Synthamin 14®, mycoplasma and psittacosis showed no evidence 60% glucose and 20% Intralipid, supplemented for recent infection. daily with trace elements (Additrace) and vitamins (Vitilipid®, Multibionta®9 and folicacid). Parenteral on October 2, 2021 by guest. Protected nutrition was continued for 19 days. Discussion Electrocardiogram (ECG) on the current admis- sion confirmed a supraventricular tachycardia rate Selenium is a trace element present as seleno- 180/minute. Serum electrolytes and haemoglobin cysteine residues at four catalytic sites in the were all normal. Adenosine intravenously (21 mg enzyme glutathione peroxidase.6 Whole body sele- total) failed to terminate the tachycardia. Sinus nium has been estimated at approximately 6 mg rhythm was restored by DC cardioversion under with a mean positive selenium balance in normal general anaesthetic. The ECG post-cardioversion individuals of0.3 ,g/day.7 Intestinal absorption of showed global T wave inversion. Echocardiogram food selenium is 80% of intake, and hospital food performed the following day revealed a dysfunc- provides 65-2 10 pg/day.8 Selenium is predomin- tional myocardium with moderate diffuse impair- antly excreted in urine (60-80%). In patients receiving total parenteral nutrition, negative balances have been demonstrated for selenium, with Correspondence: J.B. Levy, M.D., M.R.C.P. mean losses of between 11 and 19 tLg/day.9"'0 Dep- Accepted: 12 August 1993 rivation may compromise intracellular antioxidant Postgrad Med J: first published as 10.1136/pgmj.70.821.235 on 1 March 1994. Downloaded from 236 CLINICAL REPORTS defences and may also increase platelet aggregability and salmonella species as part of the formate by impairing glutathione peroxidase activity in the dehydrogenases,'6 but whether bacterial over- lipoxygenase pathway. In cattle combined vitamin growth could prevent systemic selenium absorp- E and selenium deficiencies can induce preferential tion is not known. degeneration and necrosis within the cardiac con- Finally, the standard trace element supplementa- ducting system." tion (Additrace) contains only 0.4 pmol (32 yg) Selenium deficiency is endemic in regions of selenium. This compares poorly with the absolute China and causes a dilated cardiomyopathy (Kes- minimum requirement to prevent the cardiomyo- han disease) which can be prevented by supplemen- pathy of Keshan disease of 0.24 pmol and tation.' Similarly myocardial impairment and 0.16 gLmol per day (19 and 13 ig) for men and arrhythmias (ventricular tachycardia and fibrilla- women, respectively, and a recommended daily tion) have been associated with selenium deficiency allowance of 0.9 yImol and 0.7 pmol (70 and in the setting of long-term parenteral nutrition.25 55 jLg).17 This is the first report ofcardiac dysfunction and The possibility of selenium deficiency should be documented selenium deficiency occurring after considered in all malnourished patients who just 19 days of intravenous feeding, and despite receive parenteral nutrition, even if for only a daily selenium supplementation (0.4 pmol or limited period and despite supplementation with 32 fig/day). It is likely that our patient was already trace elements. Selenium status should be moni- selenium deficient prior to surgery and parenteral tored in all such patients, with serum selenium feeding. Both whole blood and serum selenium levels and erythrocyte glutathione peroxidase deficits have been noted in patients with Crohn's activity measured at initiation of intravenous disease,'213 and there is evidence for the malabsorp- feeding. Patients with borderline or low selenium tion of other trace elements.14"'5 It is also possible status should receive supra-normal trace element that bacterial overgrowth in the involved and supplementation. Enzyme activity and serum sele- strictured small bowel contributed to selenium nium should be checked after initiation of paren- depletion. The element is utilized by both coliform teral nutrition to ensure adequate replacement. copyright. References 1. Keshan Disease Research Group of the Clinical Academy of 10. Van Rij, A.M., Thomson, C.D., McKenzie, J.M. & Robin- Medical Sciences, Beijing. Epidemiologic studies in the son, M.F. Selenium deficiency in total parenteral nutrition. etiologic relationship of selenium and Keshan's disease. Chin Am J Clin Nuir 1979, 51: 2076-2085. Med J 1979, 92: 472-482. 11. Kennedy, S. & Rice, D.A. Selective morphological alteration 2. Johnson, R.A., Baker, S.S. & Fallon, J.T. An occidental case ofthe cardiac conduction system in calves deficient in vitamin of cardiomyopathy and selenium deficiency. N Engl J Med E and selenium. Am J Pathol 1988, 130: 315-325. http://pmj.bmj.com/ 1981, 304: 1210-1212. 12. Hinks, L.J., Inwards, K.D., Lloyds, B. & Clayton, B. 3. Fleming, C.R., Lie, J.T., McCall, J.T. et al. Selenium Reduced concentration ofselenium in mild Crohn's disease. J deficiency and fatal cardiomyopathy in a patient on home Clin Pathol 1988, 41: 198-201. parenteral nutrition. Gastroenterology 1982, 83: 689-693. 13. Jacobson, S. & Plantin, L.O. Concentration of selenium in 4. Quercia, R.A., Karn, S., O'Neill, D. et al. Selenium deficiency plasma and erythrocytes during total parenteral nutrition in and fatal cardiomyopathy in a patient receiving long-term Crohn's disease. Gut 1985, 26: 50-54. home parenteral nutrition. Clin Pharm 1984, 3: 531-535. 14. Galland, L. Magnesium and inflammatory bowel disease. 5. Lockitch, G., Taylor, G.P., Wong, L.T.K. et al. Cardio- Magnesium 1988, 7: 78-83. myopathy associated with nonendemic selenium deficiency in 15. R., Stoll, Schmidt, H., Stein, H., Ruppin, H. & Domschke, W. on October 2, 2021 by guest. Protected a Caucasian adolescent. Am J Clin Nutr 1980, 52: 572-577. Functional defect of zinc transport in patients with Crohn's 6. Stadtman, T.C. Selenium dependent enzymes. Ann Rev disease. Hepatogastroenterology 1987, 34: 178-181. Biochem 1980, 49: 93-100. 16. Stadtman, T.C. Selenium biochemistry. Ann Rev Biochem 7. Stewart, R.D.H., Griffiths, N.M., Thomson, C.D. & Robin- 1990, 59: 111-157. son, M.F. Quantitative selenium metabolism in normal New 17. Levander, O.A. Scientific rationale for the 1989 recom- Zealand women. Br J Nutr 1980, 40: 45-54. mended dietary allowance for selenium. J Am Diet Assoc 8. Wester, P.O. Trace element balances in two cases of pan- 1991, 91: 1572-1576. creatic insufficiency. Acta Med Scand 1971, 190: 155-161. 9. Jacobson, S. & Wester, P.O. Balance study of twenty trace elements during total parenteral nutrition in man. Br J Nutr 1977, 37: 107- 126..
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