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Vol. 61. Núm. 4.
Páginas 305-313 (Octubre 2004)
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Vol. 61. Núm. 4.
Páginas 305-313 (Octubre 2004)
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Sepsis meningocócica en pediatría. Parámetros asociados a mala evolución
Meningococcal sepsis in pediatrics. parameters associated with poor outcome
Visitas
10632
A. Blanco Quirósa,
Autor para correspondencia
ablanco@ped.uva.es

Correspondencia: Facultad de Medicina. Pediatría. Ramón y Cajal, 5. 47005 Valladolid. España
, J. Casado Floresb, M. Nieto Morob, J.A. Garrote Adradosa,c, E. Arranz Sanza, J. Asensio Antónb
a Área de Pediatría e Instituto de Biología y Genética Molecular (IBGM). Universidad de Valladolid
b Unidad de Cuidados Intensivos Pediátricos. Hospital Niño Jesús. Madrid
c Hospital Clínico. Valladolid. España
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Estadísticas
Antecedentes

La mortalidad por sepsis meningocócica continúa siendo muy elevada. Los enfermos con mal pronóstico precisan terapias agresivas y deben ser identificados precozmente

Objetivo

Investigar los factores clínicos y biológicos asociados a una mala evolución

Pacientes y métodos

Se estudiaron 71 niños de 2 meses a 13 años de edad con sepsis meningocócica. Los criterios de inclusión fueron aislamiento de meningococo en cultivos o sintomatología característica con exantema purpúrico. Se realizó un estudio descriptivo correlacional. En todos los enfermos se valoró el PRISM (Pediatric Risk of Mortality), la Escala de Glasgow para Sepsis Meningocócicas (EGSM), el recuento de polimorfonucleares y los niveles de procalcitonina, leptina y proteína C reactiva (PCR)

Resultados

Fallecieron 14 enfermos (19,7 %). La muerte se asoció a síndrome de disfunción multiorgánica (SDMO) (p=0,0001), alta puntuación en la EGSM y el PRISM (p=0,0001) y con menor significación a shock (p=0,01). En el grupo de fallecidos, las determinaciones más alteradas al ingreso fueron la procalcitonina (p=0,0009) y los polimorfonucleares (p=0,0005). Los valores de PCR no se asociaron a diferencia de mortalidad pero estaban altos en los casos con shock (p=0,008)

Los niños con percentiles elevados de peso fallecieron con mayor frecuencia y mostraron niveles más altos de procalcitonina (p=0,006) y leptina (p=0,006), pero sin diferencias de valores de EGSM y PRISM. La edad no influyó ni en la mortalidad ni en la procalcitonina, pero sí en el EGSM y PRISM y en los niveles de polimorfonucleares y PCR, desapareciendo estas diferencias antes de los 2-3 años. En los casos con SDMO o shock sólo presentaron diferencias el recuento disminuido de polimorfonucleares (p=0,0001) y la procalcitonina elevada (p=0,0001)

Conclusiones

En la sepsis meningocócica el fallecimiento es más frecuente en niños con altos percentiles de peso. Además presentan elevaciones de procalcitonina y leptina, quedando sin aclarar si actúan de forma independiente

Palabras clave:
Infección meningocócica
Sepsis
Procalcitonina
Leptina
Peso corporal
Mortalidad
Background

Mortality due to meningococcal sepsis continues to be extremely high. Patients with a poor prognosis require aggressive therapy and should be identified early

Objective

To investigate the clinical and biological factors associated with poor outcome

Patients and methods

Seventy-one children aged 2 months to 13 years with meningococcal sepsis were studied. Inclusion criteria were meningococcus isolation in cultures or characteristic clinical features with purpuric exanthema

Methods

A correlational descriptive study was performed. In all patients we evaluated the Pediatric Risk of Mortality (PRISM), the Glasgow Scale for Meningococcal Sepsis (GSMS), polymorphonuclear (PMN) count and prolactin (PRL), leptin (LPT) and C-reactive protein (CRP) levels

Results

Fourteen children (19.7%) died. Death was associated with multiple organ dysfunction syndrome (MODS) (p=0.0001), high GSMS and PRISM scores (p=0.0001) and to a lesser extent with shock (p=0.01). In patients who died, the determinations showing greatest alteration at admission were PRL levels (p=0.0009) and PMN count (p=0.0005). CRP levels were not associated with differences in mortality but were high in patients with shock (p=0.008)

Children with high body weight percentiles were at greater risk of death and showed higher levels of PRL, PCT (p=0.006) and LPT (p=0.006), without differences in GSMS or PRISM scores. Age did not influence mortality or PRL levels but did influence GMSM and PRISM scores and PMN and CRP levels. These differences disappeared after the age of 2-3 years. In patients with MODS or shock, the only differences found were reduced PMN count (p=0.0001) and elevated PRL levels (p=0.0001)

Conclusions

In meningococcal sepsis, death is more frequent in children with high body weight percentiles. Moreover, these children present elevated PRL and LPT levels, although whether these variables act independently remains to be elucidated

Key words:
Meningococcal infection
Sepsis
Procalcitonin
Leptin
Body weight
Mortality
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Bibliografía
[1.]
R. Booy, J.S. Kroll.
Bacterial meningitis and meningococcal infection.
Current Opin Pediatr, 10 (1998), pp. 13-18
[2.]
H. Peltola.
Early meningococcal disease: Advising the public and the profession.
Lancet, 342 (1993), pp. 509-510
[3.]
J.M. Prins, P. Speelman, E.J. Kuijper, J. Dankert, S.J. Deventer.
No increase in endotoxin release during antibiotic killing of meningococci.
J Antimicrob Chemother, 39 (1997), pp. 13-18
[4.]
X. Sáenz-Llorens, G.H. McCraken.
Sepsis syndrome and sepsis shock in pediatric: current concepts of terminology, pathophysiology, and management.
J Pediatr, 123 (1993), pp. 497-508
[5.]
J.F. Sinclair, C.H. Skeoch, D. Hallwort.
Prognosis of meningococcal septicaemia.
Lancet, 2 (1987), pp. 38
[6.]
M.M. Pollack, U.E. Ruttimann, P.R. Getson.
The Pediatric Risk of Mortality (PRISM) score.
Crit Care Med, 16 (1988), pp. 1110-1116
[7.]
M.J.M. Van Brakel, A.J. Van Vught, R.J.B.J Gemke.
Pediatric risk of mortality (PRISM) score in meningococcal disease.
Eur J Pediatr, 159 (2000), pp. 232-236
[8.]
K. Thorburn, P. Baines, A. Thomson, C.A. Hart.
Mortality in severe meningococcal disease.
Arch Dis Child, 85 (2001), pp. 382-385
[9.]
J.D. Wilkinson, M.M. Pollack, U.E. Ruttimann, N.L. Glass, T.S. Yeh.
Outcome of pediatric patients with multiple organ system failure.
Crit Care Med, 14 (1986), pp. 271-274
[10.]
J.T. Algren, S. Lal, S.A. Cutliff, B.J. Richman.
Predictors of outcome in acute meningococcal infection in childhood.
Crit Care Med, 21 (1993), pp. 447-452
[11.]
Q. Mok, W. Butt.
The outcome of children admitted to intensive care with meningococcal septicaemia.
Intensive Care Med, 22 (1996), pp. 259-263
[12.]
M. Hatherill, S.M. Tibby, C. Turner, N. Ratnavel, I.A. Murdoch.
Procalcitonin and cytokine levels: Relationship to organ failure and mortality in pediatric sepsis shock.
Crit Care Med, 28 (2000), pp. 2591-2594
[13.]
R. Booy, P. Habibi, S. Nadel, C. De Munter, J. Britto.
Levin M and the Meningococcal Research Group. Reduction in case fatality rate from meningococcal disease associated with improved healthcare delivery.
Arch Dis Child, 85 (2001), pp. 386-390
[14.]
G. Ceneviva, A. Paschall, F. Maffei, J.A. Carcillo.
Soporte hemodinámico en el shock séptico pediátrico refractario a la fluidoterapia.
Pediatrics (edic esp.), 102 (1998), pp. e19
[15.]
S. Prieto Espuñes, A. Medina Villanueva, A. Concha Torre, C. Rey Galán, S. Menéndez Cuervo, M. Crespo Hernández.
Asistencia a los niños críticamente enfermos en Asturias: características y efectividad.
An Esp Pediatr, 57 (2002), pp. 22-28
[16.]
P. Maruna, K. Nedelnikova, R. Gurlich.
Physiology and genetics of procalcitonin.
Physiol Res, 49 (2000), pp. S57-S61
[17.]
P. Dandona, D. Nix, M.F. Wilson, A. Aljada, J. Love, M. Assicot, et al.
Procalcitonin increase after endotoxin infection in normal subjets.
J Clin Endocrinol Metab, 93 (1994), pp. 54-58
[18.]
W. Karzai, M. Oberhoffer, A. Meier-Hellmann, K. Reinhart.
Procalcitonin - A new indicator of the systemic response to severe infections.
Infection, 25 (1997), pp. 329-334
[19.]
M. Assicot, D. Gendrel, H. Carsin, J. Raymond, J. Guilbaud, C. Bohuon.
High serum procalcitonin concentrations in patients with sepsis and infection.
Lancet, 341 (1993), pp. 515-518
[20.]
M. Lorrot, F. Moulin, J. Coste, S. Ravilly, S. Guerin, P. Lebon, et al.
Procalcitonin in pediatric emergency situations: comparison with C-reactive protein, interleukin-6, and alpha interferon for differentiating bacterial and viral infections.
Presse Medicale, 29 (2000), pp. 128-134
[21.]
D. Gendrel, J. Raymond, M. Assicot, F. Moulin, J.L. Iñíguez, P. Lebon, et al.
Measurement of procalcitonin levels in children with bacterial or viral meningitis.
Clin Infect Dis, 24 (1997), pp. 1240-1242
[22.]
E. García-Zarza Martínez, J.T. Ramos Amador, B. Rubio Gribble, E. Corrales del Río, G. Zeballos Sarrato, J. Herrera Montes.
Utilidad de la procalcitonina en en la orientación etiológica de los niños con neumonía adquirida en la comunidad.
An Pediatr (Barc), 60 (2004), pp. 278-279
[23.]
J. Casado Flores, A. Blanco Quirós, J. Asensio, E. Arranz, J.A. Garrote, M. Nieto.
Serum procalcitonin in children with suspected sepsis: A comparison with C-reactive protein and neutrophil count.
Pediatr Crit Care Med, 4 (2003), pp. 190-195
[24.]
A. Enguix, C. Rey, A. Concha, A. Medina, D. Coto, M.A. Diéguez.
Comparison of procalcitonin with C-reactive protein and serum amyloid for the early diagnosis of bacterial sepsis in critically ill neonates and children.
Intensive Care Med, 27 (2001), pp. 211-215
[25.]
S.S. Braithwaite.
Procalcitonin.
Marker, or mediator? Crit Care Med, 26 (1998), pp. 977-978
[26.]
K. Whang, S. Vath, E. Nylen, B. Muller, Q. Li, L. Tamarkin, et al.
Procalcitonin and inflammatory cytokine interactions in sepsis.
Shock, 12 (1999), pp. 268-273
[27.]
G. Moneret, A. Pachot, B. Laroche, J. Picollet, J. Bienvenu.
Procalcitonin and calcitonin gene-related peptide decrease LPS-induced TNF production by human circulating blood cells.
Cytokine, 12 (2000), pp. 762-764
[28.]
C. Monneret, B. Laroche, J. Bienvenu.
Procalcitonin is not produced by circulating blood cells.
Infection, 27 (1999), pp. 34-35
[29.]
M. Oberhoffer, I. Stonans, S. Russwurm, E. Stonas, H. Vogelsang, U. Junker, et al.
Procalcitonin expression in human peripheral blood mononuclear cells and its modulation by lypopolysacharides and sepsis-related cytokines in vitro.
J Lab Clin Med, 134 (1999), pp. 49-55
[30.]
N.G. Morgenthaler, J. Struck, Y. Chancerelle, W. Weglohner, D. Agay, C. Bohuon, et al.
Production of procalcitonin (PCT) in nonthyroidal tissue after LPS injection.
Horm Metab Res, 35 (2003), pp. 290-295
[31.]
B. Muller, J.C. White, E.S. Nylen, R.H. Zinder, K.L. Becker, J.F. Habener.
Ubiquitous expresión of the Calcitonin-I gene in múltiple tissue in response to sepsis.
J Clin Endocrinol Met, 86 (2001), pp. 396-404
[32.]
A.R. Shuldiner, R. Yang.
Gong D-W. Resistin, obesity and insulin resistance, The emerging role of the adipòcyte as an endocrine organ.
N Engl J Med, 345 (2001), pp. 1345-1346
[33.]
R.S. Ahima, J.S. Flier.
Adipose tissue as an endocrine organ.
Trends Endocrinol Metabol, 11 (2000), pp. 327-332
[34.]
P. Dandona, A. Aljada, A. Bandyopadhyay.
Inflammation: the link between insulin resistance, obesity and diabetes.
Trends Immunol, 25 (2004), pp. 4-7
[35.]
G.S. Hotamisligil, N.S. Shargill, B.M. Spiegelman.
Adipose expression of tumor necrosis factor.alpha: direct role in obesity-linked insulin resistance.
Science, 259 (1993), pp. 87-91
[36.]
V. Mohamed-Ali, S. Goodrick, A. Rawesh, D.R. Katz, J.M. Miles, J.S. Yudkin, et al.
Sucutaneous adipose tissue releases interleukin-6, but not tumor necrosis factor alpha.
J Clin Endocrinol Metab, 82 (1997), pp. 4196-4200
[37.]
V. Mohamed-Ali, S. Goodrick, K. Bulmer, J.M.P. Holly, J.S. Yudkin, S.W. Coppack.
Production of soluble tumor necrosis factor receptors by human subcutaneous adipose tissue in vivo.
Am J Physiol, 277 (1999), pp. E971-E975
[38.]
A. Waage, A. Halstensen, T. Espevik.
Association between tumor necrosis factor in serum and fatal outcome in patients with meningococcal disease.
Lancet, I (1987), pp. 355-357
[39.]
M.M. Mustafa, M.H. Lebel, O. Ramilo, K.D. Olsen, J.S. Reisch, B. Beutler, et al.
Correlation of interleukin-1 beta and cachectin concentrations in cerebroespinal fluid and outcome from bacterial meningitis.
J Pediatr, 115 (1989), pp. 208-213
[40.]
J.S. Sullivan, L. Kilpatrick, A.T. Costarino, S.C. Lee, M.C. Harris.
Correlation of plasma cytokine elevations with mortality rate in children with sepsis.
J Pediatr, 120 (1992), pp. 510-515
[41.]
D.G. Cook, M.A. Mendall, P.H. Whincup, I.M. Carey, L. Ballam, J.E. Morris, et al.
C-reactive protein concentration in children: relationship to adiposity and other cardiovascular risk factors.
Atherosclerosis, 149 (2000), pp. 139-150
[42.]
E.S. Ford, D.A. Galuska, C. Gillespie, J.C. Will, W.H. Giles, W.H. Dietz.
C-reactive protein and body mass index in children: Findings from the Third National Health and Nutrition Examination Survey, 1988-1994.
J Pediatr, 138 (2001), pp. 486-492
[43.]
J. Auwerx, S. Staels.
Leptin.
[44.]
H. Masuzaki, Y. Ogawa, N. Sagawa, K. Hosada, T. Matsumoto, H. Mise, et al.
Nonadipose tissue production of leptin: leptin as a novel placenta-derived hormone in humans.
Nat Med, 3 (1997), pp. 1029-1033
[45.]
S.M. Smith-Kirwin, D.M. O'Connor, J. De Johnston, D.E. Lancey, S.G. Hassink, V.L. Funanage.
Leptin expression in human mammary epithelial cells and breast milk.
J Clin Endocrinol Metab, 83 (1998), pp. 1810-1813
[46.]
F. Arnalich, J. López, R. Codoceo, M. Jiménez, R. Madero, C. Montiel.
Relationship of plasma leptin to plasma cytokines and human survival in sepsis and septic shock.
J Infect Dis, 180 (1999), pp. 908-911
[47.]
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
[48.]
C. Grunfeld, C. Zhao, J. Fuller, A. Pollack, A. Moser, J. Friedman, et al.
Endotoxin and cytokine induce expresion of leptin, the ob gene product, in hamsters. A role for leptin in the anorexia of infection.
J Clin Invest, 97 (1996), pp. 2152-2157
[49.]
A. Blanco Quirós, 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
[50.]
G.L. Carlson, M. Saed, R.A. Little, M.H. Irving.
Serum leptin concentrations and their relation to metabolic abnormalities in human sepsis.
Am J Physiol, 276 (1999), pp. E658-E662
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