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Vol. 50. Núm. 7.
Páginas 266-273 (julio 2003)
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Vol. 50. Núm. 7.
Páginas 266-273 (julio 2003)
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Enfermedad aguda crítica e hiperglucemia
Stress-induced hyperglycemia in critically-ill patients
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W. Ricart
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uden.wricart@htrueta.scs.es

Correspondencia: Dr. W. Ricart. Unitat de Diabetes, Endocrinologia i Nutrició. Hospital Universitari de Girona Doctor Josep Trueta. Avda. de França, s/n. 17007 Girona. España.
Unitat de Diabetis, Endocrinologia i Nutrició. Hospital Universitari de Girona Doctor Josep Trueta. Girona. España
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La hiperglucemia que aparece en el contexto de enfermedad crítica de forma transitoria e independientemente de la presencia de diabetes mellitus, conocida como diabetes del estrés, está despertando un progresivo interés clínico. Existen evidencias clinicoepidemiológicas que relacionan la hiperglucemia con el pronóstico de pacientes con diferentes enfermedades agudas y de pacientes ingresados en general. Estos hallazgos están provocando que el facultativo clínico abandone su profunda apatía, no sólo para diferenciar entre la diabetes y la hiperglucemia de estrés, sino incluso para plantearse diferentes cuestiones, como si la hiperglucemia de estrés tiene entidad propia o simplemente es un epifenómeno de la inflamación, o si el hecho de que no sea una diabetes indica un tratamiento hipoglucemiante, o si este tratamiento debe ser conservador o agresivo.

Se revisan los diferentes estudios epidemiológicos y el impacto sobre la supervivencia de los todavía escasos ensayos terapéuticos con insulina. Sobre la base de los conocimientos obtenidos en estos trabajos y en la experimentación básica y clínica, se abre la posibilidad de que el mejor control glucémico puede mejorar la supervivencia. Aunque los beneficios y riesgos de la insulinización intensiva no están de momento suficientemente definidos, todo parece apuntar hacia la obtención de la normoglucemia y de la insulinización. Las intervenciones terapéuticas que mejoran el control metabólico en sujetos con una situación grave son beneficiosas y con una buena relación coste-efectividad. La detección y el tratamiento de los pacientes diabéticos son inexcusables, y la hiperglucemia de estrés en un paciente crítico no debe ser ignorada.

There is growing clinical interest in the short-lived hyperglycemia that occurs in critically-ill nondiabetic patients, known as “stress diabetes”. Evidence from clinical and population-based studies indicates that the presence of this type of hyperglycemia has prognostic value both in acutely ill patients and in hospitalized patients in general. Not only are clinicians abandoning their indifference towards this syndrome and its distinction from diabetes, they are also asking themselves whether stress-induced hyperglycemia is a distinct clinical entity or simply an epiphenomenon of inflammation, whether hypoglycemic therapy is warranted although it is not a bone fide diabetes, and whether treatment of this syndrome should be conservative or aggressive.

Current population-based studies are reviewed, together with the impact on survival of the few clinical trials using insulin to date. Current knowledge from these studies and from available clinical and basic research has created the possibility that improved glycemic control may achieve higher survival rates. Although the benefits and risks of intensive insulin therapy are not clearly established, the available evidence supports attainment of normoglycemia and the use of insulin therapy. Therapeutic interventions aimed at improving metabolic control during acute illness have proven to be beneficial and cost-effective. Detection and treatment of diabetic patients is an unavoidable duty, and stress-induced hyperglycemia in critically-ill patients should not be ignored.

Key words:
Hyperglycemia
Stress diabetes
Critical ill patient
Intensive insulin therapy
Palabras clave:
Hiperglucemia
Diabetes de estrés
Paciente crítico
Insulinización intensiva
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Bibliografía
[1.]
C. Bernard.
Leçons sur le diabète et la glycogenase animale.
[2.]
R.R. Wolfe, M.J. Durkot, J.R. Allsop, J.F. Burke.
Glucose metabolism in severely burned patients.
Metabolism, 28 (1979), pp. 1031-1039
[3.]
D.M. Bhisitkul, A.L. Morrow, A.I. Vinik, J. Shults, J.C. Layland, R. Rohn.
Prevalence of stress hyperglycemia among patients attending a pediatric emergency department.
J Pediatr, 124 (1994), pp. 547-551
[4.]
G. Valerio, A. Franzese, E. Carlin, P. Pecile, R. Perini, A. Tenore.
High prevalence of stress hyperglycaemia in children with febrile seizures and traumatic injuries.
Acta Paediatr, 90 (2001), pp. 618-622
[5.]
D.C. Frankenfield, L.A. Omert, M.M. Badellino, C.E. Wiles 3rd, S.M. Bagley, S. Goodarzi, et al.
Correlation between measured energy expenditure and clinically obtained variables in trauma and sepsis patients.
J Parenter Enteral Nutr, 18 (1994), pp. 398-403
[6.]
S.E. Capes, D. Hunt, K. Malmberg, H.C. Gerstein.
Stress hyperglycaemia and increased risk of death after myocardial infarction in patients with and without diabetes: a systematic overview.
[7.]
S.E. Capes, D. Hunt, K. Malmberg, P. Pathak, H.C. Gerstein.
Stress hyperglycemia and prognosis of stroke in nondiabetic and diabetic patients: a systematic overview.
Stroke, 32 (2001), pp. 2426-2432
[8.]
G.E. Umpierrez, S.D. Isaacs, N. Bazargan, X. You, L.M. Thaler, A.E. Kitabchi.
Hyperglycemia: an independent marker of inhospital mortality in patients with undiagnosed diabetes.
J Clin Endocrinol Metab, 87 (2002), pp. 978-982
[9.]
I.B. Hirsch.
In-patient hyperglycemia—are we ready to treat it yet?.
J Clin Endocrinol Metab, 87 (2002), pp. 975-977
[10.]
J.M. Fernández-Real, W. Ricart.
Insulin resistance and inflammation in an evolutionary perspective: the contribution of cytokine genotype/phenotype to thriftiness.
Diabetologia, 42 (1999), pp. 1367-1374
[11.]
H.B. Stoner, R.A. Little, K.N. Frayn, A.E. Elebute, J. Tresadern, E. Gross.
The effect of sepsis on the oxidation of carbohydrate and fat.
Br J Surg, 70 (1983), pp. 32-35
[12.]
B.A. Mizock.
Alterations in fuel metabolism in critical illness: hyperglycaemia.
Best Pract Res Clin Endocrinol Metab, 15 (2001), pp. 533-551
[13.]
A.A. Rossini.
Why control blood glucose levels?.
Arch Surg, 111 (1976), pp. 229-233
[14.]
E.J. Rayfield, M.J. Ault, G.T. Keusch, M.J. Brothers, C. Nechemias, H. Smith.
Infection and diabetes: the case for glucose control.
Am J Med, 72 (1982), pp. 439-450
[15.]
M.R. Losser, C. Bernard, J.L. Beaudeux, C. Pison, D. Payen.
Glucose modulates hemodynamic, metabolic, and inflammatory responses to lipopolysaccharide in rabbits.
J Appl Physiol, 83 (1997), pp. 1566-1574
[16.]
Y.P. Li, M.B. Reid.
Effect of tumor necrosis factor-alpha on skeletal muscle metabolism.
Curr Opin Rheumatol, 13 (2001), pp. 483-487
[17.]
G.S. Hotamisligil, B.M. Spiegelman.
Tumor necrosis factor alpha: a key component of the obesity-diabetes link.
Diabetes, 43 (1994), pp. 1271-1278
[18.]
J.M. Fernández-Real, M. Vayreda, C. Richart, C. Gutiérrez, M. Broch, J. Vendrell, et al.
Circulating interleukin 6 levels, blood pressure, and insulin sensitivity in apparently healthy men and women.
J Clin Endocrinol Metab, 86 (2001), pp. 1154-1159
[19.]
J.M. Fernández-Real, M. Broch, W. Ricart, R. Casamitjana, C. Gutiérrez, J. Vendrell, et al.
Plasma levels of the soluble fraction of tumor necrosis factor receptor 2 and insulin resistance.
Diabetes, 47 (1998), pp. 1757-1762
[20.]
J.M. Fernández-Real, B. Lainez, J. Vendrell, M. Rigla, A. Castro, G. Penarroja, et al.
Shedding of TNF-alpha receptors, blood pressure, and insulin sensitivity in type 2 diabetes mellitus.
Am J Physiol Endocrinol Metab, 282 (2002), pp. E952-E959
[21.]
G.J. Blake, P.M. Ridker.
Inflammatory bio-markers and cardiovascular risk prediction.
J Intern Med, 252 (2002), pp. 283-294
[22.]
N. Cabioglu, S. Bilgic, G. Deniz, E. Aktas, Y. Seyhun, A. Turna, et al.
Decreased cytokine expression in peripheral blood leukocytes of patients with severe sepsis.
Arch Surg, 137 (2002), pp. 1037-1043
[23.]
S. Gando, J. Nishihira, S. Kobayashi, Y. Morimoto, S. Nanzaki, O. Kemmotsu.
Macrophage migration inhibitory factor is a critical mediator of systemic inflammatory response syndrome.
Intensive Care Med, 27 (2001), pp. 1187-1193
[24.]
A. Beishuizen, L.G. Thijs, C. Haanen, I. Vermes.
Macrophage migration inhibitory factor and hypothalamo-pituitary-adrenal function during critical illness.
J Clin Endocrinol Metab, 86 (2001), pp. 2811-2816
[25.]
U.N. Das.
Critical advances in septicemia and septic shock.
Crit Care, 4 (2000), pp. 290-296
[26.]
G. Mantovani, A. Maccio, C. Madeddu, L. Mura, E. Massa, M.C. Mudu, et al.
Serum values of proinflammatory cytokines are inversely correlated with serum leptin levels in patients with advanced stage cancer at different sites.
J Mol Med, 79 (2001), pp. 406-414
[27.]
F. Arnalich, J. López, R. Codoceo, M. Jiménez, R. Madero, C. Montiel.
Relationship of plasma leptin to plasma cytokines and human survivalin sepsis and septic shock.
J Infect Dis, 180 (1999), pp. 908-911
[28.]
D.J. Torpy, S.R. Bornstein, G.P. Chrousos.
Leptin and interleukin-6 in sepsis.
Horm Metab Res, 30 (1998), pp. 726-729
[29.]
S.R. Bornstein, J. Licinio, R. Tauchnitz, L. Engelmann, A.B. Negrao, P. Gold, et al.
Plasma leptin levels are increased in survivors of acute sepsis: associated loss of diurnal rhythm, in cortisol and leptin secretion.
J Clin Endocrinol Metab, 83 (1998), pp. 280-283
[30.]
A. Blanco-Quiros, J. Casado-Flores, E. Arranz, J.A. Garrote, J. Asensio, A. Pérez.
Influence of leptin levels and body weight in survival of children with sepsis.
Acta Paediatr, 91 (2002), pp. 626-631
[31.]
T. Moulin, L. Tatu, T. Crepin-Leblond, D. Chavot, S. Berges, T. Rumbach.
The Besancon Stroke Registry: an acute stroke registry of 2,500 consecutive patients.
Eur Neurol, 38 (1997), pp. 10-20
[32.]
A. Bruno, J. Biller, H.P. Adams, W.R. Clarke, R.F. Woolson, L.S. Williams, et al.
Acute blood glucose level and outcome from ischemic stroke. Trial of ORG 10172 in Acute Stroke Treatment (TOAST) Investigators.
Neurology, 52 (1999), pp. 280-284
[33.]
A. Davalos, J.M. Fernández-Real, W. Ricart, S. Soler, A. Molins, E. Planas, et al.
Iron-related damage in acute ischemic stroke.
Stroke, 25 (1994), pp. 1543-1546
[34.]
A. Davalos, W. Ricart, F. González-Huix, S. Soler, J. Marrugat, A. Molins, et al.
Effect of malnutrition after acute stroke on clinical outcome.
Stroke, 27 (1996), pp. 1028-1032
[35.]
G. De Courten-Myers, R.E. Myers, L. Schoolfield.
Hyperglycemia enlarges infarct size in cerebrovascular occlusion in cats.
Stroke, 19 (1988), pp. 623-630
[36.]
R. Prado, M.D. Ginsberg, W.D. Dietrich, B.D. Watson, R. Busto.
Hyperglycemia increases infarct size in collaterally perfused but not end-arterial vascular territories.
J Cereb Blood Flow Metab, 8 (1988), pp. 186-192
[37.]
G.M. de Courten-Myers, M. Kleinholz, K.R. Wagner, R.E. Myers.
Normoglycemia (not hypoglycemia) optimizes outcome from middle cerebral artery occlusion.
J Cereb Blood Flow Metab, 14 (1994), pp. 227-236
[38.]
D.J. Combs, R.J. Dempsey, S. Kumar, D. Donaldson.
Focal cerebral infarction in cats in the presence of hyperglycemia and increased insulin.
Metab Brain Dis, 5 (1990), pp. 169-178
[39.]
W. Chew, J. Kucharczyk, M. Moseley, N. Derugin, D. Norman.
Hyperglycemia augments ischemic brain injury: in vivo MR imaging/spectroscopic study with nicardipine in cats with occluded middle cerebral arteries.
Am J Neuroradiol, 12 (1991), pp. 603-609
[40.]
K.R. Wagner, M. Kleinholz, G.M. de Courten-Myers, R.E. Myers.
Hyperglycemic versus normoglycemic stroke: topography of brain metabolites, intracellular pH and infarct size.
J Cereb Blood Flow Metab, 12 (1992), pp. 213-222
[41.]
N.C. Huang, J. Wei, M.J. Quast.
A comparison of the early development of ischemic brain damage in normoglycemic and hyperglycemic rats using magnetic resonance imaging.
Exp Brain Res, 109 (1996), pp. 33-42
[42.]
G.S. Venables, S.A. Miller, G. Gibson, J.A. Hardy, A.J. Strong.
The effects of hyperglycaemia on changes during reperfusion following focal cerebral ischaemia in the cat.
J Neurol Neurosurg Psychiatry, 48 (1985), pp. 663-669
[43.]
G.M. De Courten-Myers, M. Kleinholz, K.R. Wagner, R.E. Myers.
Fatal strokes in hyperglycemic cats.
Stroke, 20 (1989), pp. 1707-1715
[44.]
R.J. Dempsey, M.K. Baskaya, D.J. Combs, D. Donaldson, A.M. Rao, M.R. Prasad.
Delayed hyperglycemia and intracellular acidosis during focal cerebral ischemia in cats.
Acta Neurochir (Wien), 138 (1996), pp. 745-751
[45.]
N. Kawai, R.F. Keep, A.L. Betz.
Effects of hyperglycemia on cerebral blood flow and edema formation after carotid artery occlusion in Fischer 344 rats.
Acta Neurochir Suppl (Wien), 70 (1997), pp. 34-36
[46.]
N. Kawai, R.F. Keep, A.L. Betz, S. Nagao.
Hyperglycemia induces progressive changes in the cerebral microvasculature and blood-brain barrier transport during focal cerebral ischemia.
Acta Neurochir Suppl (Wien), 71 (1998), pp. 219-221
[47.]
C. Wass, B. Scheithauer, J. Bronk, R. Wilson, W. Lanier.
Insulin treatment of corticosteroid-associated hyperglycemia and its effect on outcome after forebrain ischemia in rats.
Anesthesiology, 84 (1996), pp. 644-651
[48.]
R. Tyson, J. Peeling, G. Sutherland.
Metabolic changes associated with altering blood glucose levels in short duration forebrain ischemia.
Brain Res, 608 (1993), pp. 288-298
[49.]
A.R. Laptook, R.J. Corbett, O. Arencibia-Mireles, J. Ruley, D. García.
The effects of systemic glucose concentration on brain metabolism following repeated brain ischemia.
Brain Res, 638 (1994), pp. 78-88
[50.]
M. Ravid, M. Berkowicz, E. Sohar.
Hyperglycemia during acute myocardial infarction. A six-year follow-up study.
JAMA, 233 (1975), pp. 807-809
[51.]
N.G. Soler, S. Frank.
Value of glycosylated hemoglobin measurements after acute myocardial infarction.
JAMA, 246 (1981), pp. 1690-1693
[52.]
J. Leor, U. Goldbourt, H. Reicher-Reiss, E. Kaplinsky, S. Behar.
Cardiogenic shock complicating acute myocardial infarction in patients without heart failure on admission: incidence, risk factors, and outcome. SPRINT Study Group.
Am J Med, 94 (1993), pp. 265-273
[53.]
J. Lewandowicz, J.M. Komorowski, H. Gozlinski.
Metabolic disorders in myocardial infarction. Changes in blood serum zinc, growth hormone, insulin and glucose concentration in patients with acute myocardial infarction.
Cor Vasa, 21 (1979), pp. 305-316
[54.]
G.A. Oswald, C.C. Smith, D.J. Betteridge, J.S. Yudkin.
Determinants and importance of stress hyperglycaemia in non-diabetic patients with myocardial infarction.
BMJ (Clin Res Ed), 293 (1986), pp. 917-922
[55.]
J.J. O'Sullivan, R.M. Conroy, K. Robinson, N. Hickey, R. Mulcahy.
In-hospital prognosis of patients with fasting hyperglycemia after first myocardial infarction.
Diabetes Care, 14 (1991), pp. 758-760
[56.]
G. Bellodi, V. Manicardi, V. Malavasi, L. Veneri, G. Bernini, P. Bossini, et al.
Hyperglycemia and prognosis of acute myocardial infarction in patients without diabetes mellitus.
Am J Cardiol, 64 (1989), pp. 885-888
[57.]
S. Fava, O. Aquilina, J. Azzopardi, H. Agius Muscat, F.F. Fenech.
The prognostic value of blood glucose in diabetic patients with acute myocardial infarction.
[58.]
M. Sewdarsen, S. Vythilingum, I. Jialal, P.J. Becker.
Prognostic importance of admission plasma glucose in diabetic and nondiabetic patients with acute myocardial infarction.
Q J Med, 71 (1989), pp. 461-466
[59.]
A.M. Norhammar, L. Ryden, K. Malmberg.
Admission plasma glucose. Independent risk factor for long-term prognosis after myocardial infarction even in nondiabetic patients.
Diabetes Care, 22 (1999), pp. 1827-1831
[60.]
J. Sala, R. Masia, F.J. González de Molina, J.M. Fernández-Real, M. Gil, D. Bosch, et al.
Short-term mortality of myocardial infarction patients with diabetes or hyperglycaemia during admission.
J Epidemiol Community Health, 56 (2002), pp. 707-712
[61.]
M.J. Tansey, L.H. Opie.
Plasma glucose on admission to hospital as a metabolic index of the severity of acute myocardial infarction.
Can J Cardiol, 2 (1986), pp. 326-331
[62.]
J. Bolk, T. van der Ploeg, J.H. Cornel, A.E. Arnold, J. Sepers, V.A. Umans.
Impaired glucose metabolism predicts mortality after a myocardial infarction.
Int J Cardiol, 79 (2001), pp. 207-214
[63.]
D. Zindrou, K.M. Taylor, J.P. Bagger.
Admission plasma glucose: an independent risk factor in nondiabetic women after coronary artery bypass grafting.
Diabetes Care, 24 (2001), pp. 1634-1639
[64.]
M.F. Oliver, L.H. Opie.
Effects of glucose and fatty acids on myocardial ischaemia and arrhythmias.
Lancet, 343 (1994), pp. 155-158
[65.]
O.D. Mjos.
Effect of free fatty acids on myocardial function and oxygen consumption in intact dogs.
J Clin Invest, 50 (1971), pp. 1386-1389
[66.]
R.A. Kloner, R.B. Jennings.
Consequences of brief ischemia: stunning, preconditioning, and their clinical implications: part 1.
Circulation, 104 (2001), pp. 2981-2989
[67.]
R.A. Kloner, R.B. Jennings.
Consequences of brief ischemia: stunning, preconditioning, and their clinical implications: part 2.
Circulation, 104 (2001), pp. 3158-3167
[68.]
H.T. Sommerschild, K.A. Kirkeboen.
Preconditioning-endogenous defence mechanisms of the heart.
Acta Anaesthesiol Scand, 46 (2002), pp. 123-137
[69.]
P.H. McNulty, A. Darling, J.M. Whiting.
Glycogen depletion contributes to ischemic preconditioning in the rat heart in vivo.
Am J Physiol, 271 (1996), pp. H2283-H2289
[70.]
J.R. Kersten, T.J. Schmeling, K.G. Orth, P.S. Pagel, D.C. Warltier.
Acute hyperglycemia abolishes ischemic preconditioning in vivo.
Am J Physiol, 275 (1998), pp. H721-H725
[71.]
J.R. Kersten, W.G. Toller, E.R. Gross, P.S. Pagel, D.C. Warltier.
Diabetes abolishes ischemic preconditioning: role of glucose, insulin, and osmolality.
Am J Physiol Heart Circ Physiol, 278 (2000), pp. H1218-H1224
[72.]
F. Kehl, J.G. Krolikowski, B. Mraovic, P.S. Pagel, D.C. Warltier, J.R. Kersten.
Hyperglycemia prevents isoflurane-induced preconditioning against myocardial infarction.
Anesthesiology, 96 (2002), pp. 183-188
[73.]
J.L. Hall, J. Henderson, L.A. Hernández, L.A. Kellerman, W.C. Stanley.
Hyperglycemia results in an increase in myocardial interstitial glucose and glucose uptake during ischemia.
Metabolism, 45 (1996), pp. 542-549
[74.]
J.R. Kersten, M.W. Montgomery, T. Ghassemi, E.R. Gross, W.G. Toller, P.S. Pagel, et al.
Diabetes and hyperglycemia impair activation of mitochondrial K(ATP) channels.
Am J Physiol Heart Circ Physiol, 280 (2001), pp. H1744-H1750
[75.]
C.F. Toombs, T.L. Moore, R.J. Shebuski.
Limitation of infarct size in the rabbit by ischaemic preconditioning is reversible with glibenclamide.
Cardiovasc Res, 27 (1993), pp. 617-622
[76.]
J.R. Kersten, W.G. Toller, J.P. Tessmer, P.S. Pagel, D.C. Warltier.
Hyperglycemia reduces coronary collateral blood flow through a nitric oxide-mediated mechanism.
Am J Physiol Heart Circ Physiol, 281 (2001), pp. H2097-H2104
[77.]
R.M. Smith, S. Lecour, M.N. Sack.
Innate immunity and cardiac preconditioning: a putative intrinsic cardioprotective program.
Cardiovasc Res, 55 (2002), pp. 474-482
[78.]
D. Li, L. Zhao, M. Liu, X. Du, W. Ding, J. Zhang, et al.
Kinetics of tumor necrosis factor alpha in plasma and the cardioprotective effect of a monoclonal antibody to tumor necrosis factor alpha in acute myocardial infarction.
Am Heart J, 137 (1999), pp. 1145-1152
[79.]
R. Ferrari.
The role of TNF in cardiovascular disease.
Pharmacol Res, 40 (1999), pp. 97-105
[80.]
H. Fujita, I. Morita, S. Murota.
A possible involvement of ion transporter in tumor necrosis factor alpha and cycloheximideinduced apoptosis of endothelial cells.
Mediators Inflamm, 8 (1999), pp. 211-218
[81.]
D.R. Meldrum, K.K. Donnahoo.
Role of TNF in mediating renal insufficiency following cardiac surgery: evidence of a postbypass cardiorenal syndrome.
J Surg Res, 85 (1999), pp. 185-199
[82.]
K. Malmberg, L. Ryden, S. Efendic, J. Herlitz, P. Nicol, A. Waldenstrom, et al.
Randomized trial of insulin-glucose infusion followed by subcutaneous insulin treatment in diabetic patients with acute myocardial infarction (DIGAMI study): effects on mortality at 1 year.
J Am Coll Cardiol, 26 (1995), pp. 57-65
[83.]
K. Malmberg, L. Ryden, A. Hamsten, J. Herlitz, A. Waldenstrom, H. Wedel.
Effects of insulin treatment on cause-specific one-year mortality and morbidity in diabetic patients with acute myocardial infarction. DIGAMI Study Group. Diabetes Insulin-Glucose in Acute Myocardial Infarction.
Eur Heart J, 17 (1996), pp. 1337-1344
[84.]
K. Malmberg.
Prospective randomised study of intensive insulin treatment on long term survival after acute myocardial infarction in patients with diabetes mellitus. DIGAMI (Diabetes Mellitus, Insulin Glucose Infusion in Acute Myocardial Infarction) Study Group.
BMJ, 314 (1997), pp. 1512-1515
[85.]
K. Malmberg, A. Norhammar, H. Wedel, L. Ryden.
Glycometabolic state at admission: important risk marker of mortality in conventionally treated patients with diabetes mellitus and acute myocardial infarction: long-term results from the Diabetes and Insulin-Glucose Infusion in Acute Myocardial Infarction (DIGAMI) study.
Circulation, 99 (1999), pp. 2626-2632
[86.]
J. Takala, E. Ruokonen, N.R. Webster, M.S. Nielsen, D.F. Zandstra, G. Vundelinckx, et al.
Increased mortality associated with growth hormone treatment in critically ill adults.
N Engl J Med, 341 (1999), pp. 785-792
[87.]
T.A. Raffin.
Intensive care unit survival of patients with systemic illness.
Am Rev Respir Dis, 140 (1989), pp. S28-S35
[88.]
R.R. Wolfe, D.N. Herndon, F. Jahoor, H. Miyoshi, M. Wolfe.
Effect of severe burn injury on substrate cycling by glucose and fatty acids.
N Engl J Med, 317 (1987), pp. 403-408
[89.]
R.E. Shangraw, F. Jahoor, H. Miyoshi, W.A. Neff, C.A. Stuart, D.N. Herndon, et al.
Differentiation between septic and postburn insulin resistance.
Metabolism, 38 (1989), pp. 983-989
[90.]
K.C. McCowen, A. Malhotra, B.R. Bistrian.
Stress-induced hyperglycemia.
Crit Care Clin, 17 (2001), pp. 107-124
[91.]
J.R. Hill, G. Kwon, C.A. Marshall, M.L. McDaniel.
Hyperglycemic levels of glucose inhibit interleukin 1 release from RAW 264 7 murine macrophages by activation of protein kinase C.
J Biol Chem, 273 (1998), pp. 3308-3313
[92.]
F.A. Saeed, G.E. Castle.
Neutrophil chemiluminescence during phagocytosis is inhibited by abnormally elevated levels of acetoacetate: implications for diabetic susceptibility to infections.
Clin Diagn Lab Immunol, 5 (1998), pp. 740-743
[93.]
S.E. Geerlings, A.I. Hoepelman.
Immune dysfunction in patients with diabetes mellitus (DM).
FEMS Immunol Med Microbiol, 26 (1999), pp. 259-265
[94.]
A.J. Rassias, C.A. Marrin, J. Arruda, P.K. Whalen, M. Beach, M.P. Yeager.
Insulin infusion improves neutrophil function in diabetic cardiac surgery patients.
Anesth Analg, 88 (1999), pp. 1011-1016
[95.]
G. Van den Berghe, P. Wouters, F. Weekers, C. Verwaest, F. Bruyninckx, M. Schetz, et al.
Intensive insulin therapy in the critically ill patients.
N Engl J Med, 345 (2001), pp. 1359-1367
[96.]
C.S. Levetan, M. Passaro, K. Jablonski, M. Kass, R.E. Ratner.
Unrecognized diabetes among hospitalized patients.
Diabetes Care, 21 (1998), pp. 246-249
[97.]
T.W. Evans.
Hemodynamic and metabolic therapy in critically ill patients.
N Engl J Med, 345 (2001), pp. 1417-1418
[98.]
N. Satomi, A. Sakurai, K. Haranaka.
Relationship of hypoglycemia to tumor necrosis factor production and antitumor activity: role of glucose, insulin, and macrophages.
J Natl Cancer Inst, 74 (1985), pp. 1255-1260
[99.]
U.N. Das.
Is insulin an anti-inflammatory molecule?.
Nutrition, 17 (2001), pp. 409-413
[100.]
U.N. Das.
Is insulin an endogenous cardioprotector?.
Crit Care, 6 (2002), pp. 389-393
[101.]
H. Orskov.
Somatostatin, growth hormone, insulin-like growth factor-1, and diabetes: friends or foes?.
Metabolism, 45 (1996), pp. 91-95
[102.]
M. Binoux.
The IGF system in metabolism regulation.
Diabetes Metab, 21 (1995), pp. 330-337
[103.]
W. Ricart, J.M. Fernández-Real.
No decrease in free IGF-I with increasing insulin in obesity-related insulin resistance.
Obes Res, 9 (2001), pp. 631-636
[104.]
J.M. Fernández-Real, M. Pugeat, A. Emptoz-Bonneton, W. Ricart.
Study of the effect of changing glucose, insulin, and insulin-like growth factor-I levels on serum corticosteroid binding globulin in lean, obese, and obese subjects with glucose intolerance.
Metabolism, 50 (2001), pp. 1248-1252
[105.]
R.C. Baxter.
Changes in the IGF-IGFBP axis in critical illness.
Best Pract Res Clin Endocrinol Metab, 15 (2001), pp. 421-434
[106.]
G. Van den Berghe.
Dynamic neuroendocrine responses to critical illness.
Front Neuroendocrinol, 23 (2002), pp. 370-391
[107.]
B. Almbrand, M. Johannesson, B. Sjostrand, K. Malmberg, L. Ryden.
Cost-effectiveness of intense insulin treatment after acute myocardial infarction in patients with diabetes mellitus; results from the DIGAMI study.
Eur Heart J, 21 (2000), pp. 733-739
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