Acute fluid shifts influence the assessment of serum vitamin D status in critically ill patients

Anand Krishnan, Judith Ochola, Julie Mundy, Mark Jones, Peter Kruger, Emma Duncan, Bala Venkatesh, Anand Krishnan, Judith Ochola, Julie Mundy, Mark Jones, Peter Kruger, Emma Duncan, Bala Venkatesh

Abstract

Introduction: Recent reports have highlighted the prevalence of vitamin D deficiency and suggested an association with excess mortality in critically ill patients. Serum vitamin D concentrations in these studies were measured following resuscitation. It is unclear whether aggressive fluid resuscitation independently influences serum vitamin D.

Methods: Nineteen patients undergoing cardiopulmonary bypass were studied. Serum 25(OH)D(3), 1α,25(OH)(2)D(3), parathyroid hormone, C-reactive protein (CRP), and ionised calcium were measured at five defined timepoints: T1 - baseline, T2 - 5 minutes after onset of cardiopulmonary bypass (CPB) (time of maximal fluid effect), T3 - on return to the intensive care unit, T4 - 24 hrs after surgery and T5 - 5 days after surgery. Linear mixed models were used to compare measures at T2-T5 with baseline measures.

Results: Acute fluid loading resulted in a 35% reduction in 25(OH)D(3) (59 ± 16 to 38 ± 14 nmol/L, P < 0.0001) and a 45% reduction in 1α,25(OH)(2)D(3) (99 ± 40 to 54 ± 22 pmol/L P < 0.0001) and i(Ca) (P < 0.01), with elevation in parathyroid hormone (P < 0.0001). Serum 25(OH)D(3) returned to baseline only at T5 while 1α,25(OH)(2)D(3) demonstrated an overshoot above baseline at T5 (P < 0.0001). There was a delayed rise in CRP at T4 and T5; this was not associated with a reduction in vitamin D levels at these time points.

Conclusions: Hemodilution significantly lowers serum 25(OH)D(3) and 1α,25(OH)(2)D(3), which may take up to 24 hours to resolve. Moreover, delayed overshoot of 1α,25(OH)(2)D(3) needs consideration. We urge caution in interpreting serum vitamin D in critically ill patients in the context of major resuscitation, and would advocate repeating the measurement once the effects of the resuscitation have abated.

Figures

Figure 1
Figure 1
An illustration of the changes in serum 25(OH)D3 (filled diamonds) and 1α,25(OH)2D3 (filled squares) concentrations across the five time points.
Figure 2
Figure 2
An illustration of the changes in serum PTH (filled diamonds) and ionised calcium (filled squares) concentrations across the five time points.

References

    1. Judd SE, Tangpricha V. Vitamin D deficiency and risk for cardiovascular disease. Am J Med Sci. 2009;338:40–44. doi: 10.1097/MAJ.0b013e3181aaee91.
    1. Hamilton B. Vitamin D and human skeletal muscle. Scand J Med Sci Sports. 2010;20:182–190.
    1. Krishnan A, Ochola J, Venkatesh B. In: Yearbook of Intensive Care and Emergency Medicine. Vincent JL, editor. Heidelberg: Springer-Verlag; 2010. Vitamin D in critical illness; pp. 273–81. full_text.
    1. Zittermann A, Schleithoff SS, Götting C, Fuchs U, Kuhn J, Kleesiek K, Tenderich G, Koerfer R. Calcitriol deficiency and 1-year mortality in cardiac transplant recipients. Transplantation. 2009;87:118–124. doi: 10.1097/TP.0b013e31818c2708.
    1. Munger KL, Zhang SM, O'Reilly E, Hernán MA, Olek MJ, Willett WC, Ascherio A. Vitamin D intake and incidence of multiple sclerosis. Neurology. 2004;62:60–65.
    1. Hyppönen E, Läärä E, Reunanen A, Järvelin MR, Virtanen SM. Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study. Lancet. 2001;358:1500–1503.
    1. Melamed ML, Michos ED, Post W, Astor B. 25-hydroxyvitamin D levels and the risk of mortality in the general population. Arch Intern Med. 2008;168:1629–1637. doi: 10.1001/archinte.168.15.1629.
    1. Lee P, Nair P, Eisman JA, Center JR. Vitamin D deficiency in the intensive care unit: an invisible accomplice to morbidity and mortality? Intensive Care Med. 2009;35:2028–2032. doi: 10.1007/s00134-009-1642-x.
    1. Van den Berghe G, Van Roosbroeck D, Vanhove P, Wouthers PJ, De Pourcq L, Bouillon R. Bone turnover in prolonged critical illness: effect of vitamin D. J Clin Endocrinol Metab. 2003;88:4623–4632. doi: 10.1210/jc.2003-030358.
    1. Zella LA, Shevde NK, Hollis BW, Cooke NE, Pike JW. Vitamin D-binding protein influences total circulating levels of 1,25-dihydroxyvitamin D3 but does not directly modulate the bioactive levels of the hormone in vivo. Endocrinology. 2008;149:3656–3667. doi: 10.1210/en.2008-0042.
    1. Nierman DM, Mechanick JI. Bone hyperresorption is prevalent in chronically critically ill patients. Chest. 1998;114:954–955. doi: 10.1378/chest.114.4.1122.
    1. Lee P, Eisman JA, Center JR. Vitamin D deficiency in critically ill patients. N Engl J Med. 2009;360:1912–1914. doi: 10.1056/NEJMc0809996.
    1. Vincent JL, Sakr Y, Sprung CL, Ranieri VM, Reinhart K, Gerlach H, Moreno R, Carlet J, Le Gall JR, Payen D. Sepsis occurrence in Acutely Ill Patients Investigators: sepsis in European intensive care units: results of the SOAP study. Crit Care Med. 2006;34:344–353. doi: 10.1097/01.CCM.0000194725.48928.3A.
    1. Morgan TJ, Venkatesh B, Hall J. Crystalloid strong ion difference determines metabolic acid-base change during acute normovolaemic haemodilution. Intensive Care Med. 2004;30:1432–1437. doi: 10.1007/s00134-004-2176-x.
    1. Jones G. Pharmacokinetics of vitamin D toxicity. Am J Clin Nutr. 2008;88:582S–586S.
    1. Edwards LJ, Muller KE, Wolfinger RD, Qaqish BF, Schabengerger O. An R2 statistic for fixed effects in the linear mixed model. Stat Med. 2008;27:6137–6157. doi: 10.1002/sim.3429.
    1. Reddy GS, Tserng KY. Calcitroic acid, end product of renal metabolism of 1,25-dihydroxyvitamin D3 through C-24 oxidation pathway. Biochemistry. 1989;28:1763–1769. doi: 10.1021/bi00430a051.
    1. Brenza HL, Kimmel-Jehan C, Jehan F, Shinki T, Wakino S, Anazawa H, Suda T, DeLuca HF. Parathyroid hormone activation of the 25-hydroxyvitamin D3-1alpha-hydroxylase gene promoter. Proc Natl Acad Sci USA. 1998;95:1387–1391. doi: 10.1073/pnas.95.4.1387.
    1. Zehnder D, Bland R, Williams MC, McNinch RW, Howie AJ, Stewart PM, Hewison M. Extrarenal expression of 25-hydroxyvitamin d(3)-1 alpha-hydroxylase. J Clin Endocrinol Metab. 2001;86:888–894. doi: 10.1210/jc.86.2.888.
    1. Chun RF, Lauridsen AL, Suon L, Zella LA, Pike JW, Modlin RL, Martineau AR, Wilkinson RJ, Adams J, Hewison M. Vitamin D-binding protein directs monocyte responses to 25-hydroxy- and 1,25-dihydroxyvitamin D. J Clin Endocrinol Metab. 2010;95:3368–3376. doi: 10.1210/jc.2010-0195.
    1. Lucidarme O, Messai E, Mazzoni T, Arcade M, du Cheyron D. Incidence and risk factors of vitamin D deficiency in critically ill patients: results from a prospective observational study. Intensive Care Med. 2010;36:1609–1611. doi: 10.1007/s00134-010-1875-8.
    1. Roth HJ, Schmidt-Gayk H, Weber H, Niederau C. Accuracy and clinical implications of seven 25-hydroxyvitamin D methods compared with liquid chromatography-tandem mass spectrometry as a reference. Ann Clin Biochem. 2008;45:153–159. doi: 10.1258/acb.2007.007091.

Source: PubMed

Sponsorzy i współpracownicy

Warunki medyczne

Interwencje lekowe

3
Subskrybuj