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Asymmetric dimethyl-arginine (ADMA) response to inflammation in acute infections.

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Asymmetric dimethyl-arginine (ADMA) response to inflammation in acute infections. / Zoccali, Carmine; Maas, Renke; Cutrupi, Sebastiano; Pizzini, Patrizia; Finocchiaro, Piero; Cambareri, Francesco; Panuccio, Vincenzo; Martorano, Carmela; Schulze, Friedrich; Enia, Giuseppe; Tripepi, Giovanni; Böger, Rainer.

In: NEPHROL DIAL TRANSPL, Vol. 22, No. 3, 3, 2007, p. 801-806.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Zoccali, C, Maas, R, Cutrupi, S, Pizzini, P, Finocchiaro, P, Cambareri, F, Panuccio, V, Martorano, C, Schulze, F, Enia, G, Tripepi, G & Böger, R 2007, 'Asymmetric dimethyl-arginine (ADMA) response to inflammation in acute infections.', NEPHROL DIAL TRANSPL, vol. 22, no. 3, 3, pp. 801-806. <http://www.ncbi.nlm.nih.gov/pubmed/17166859?dopt=Citation>

APA

Zoccali, C., Maas, R., Cutrupi, S., Pizzini, P., Finocchiaro, P., Cambareri, F., Panuccio, V., Martorano, C., Schulze, F., Enia, G., Tripepi, G., & Böger, R. (2007). Asymmetric dimethyl-arginine (ADMA) response to inflammation in acute infections. NEPHROL DIAL TRANSPL, 22(3), 801-806. [3]. http://www.ncbi.nlm.nih.gov/pubmed/17166859?dopt=Citation

Vancouver

Zoccali C, Maas R, Cutrupi S, Pizzini P, Finocchiaro P, Cambareri F et al. Asymmetric dimethyl-arginine (ADMA) response to inflammation in acute infections. NEPHROL DIAL TRANSPL. 2007;22(3):801-806. 3.

Bibtex

@article{9c9ae8d49c4743ea8563c1de365d758b,
title = "Asymmetric dimethyl-arginine (ADMA) response to inflammation in acute infections.",
abstract = "BACKGROUND AND METHODS: The endogenous inhibitor of nitric oxide synthase (NOs) asymmetrical dimethyl-arginine (ADMA) has been implicated as a possible modulator of inducible NOs during acute inflammation. We examined the evolution in the plasma concentration of ADMA measured at the clinical outset of acute inflammation and after its resolution in a series of 17 patients with acute bacterial infections. RESULTS: During the acute phase of inflammation/infection, patients displayed very high levels of C-reactive protein (CRP), interleukin-6 (IL-6), procalcitonin and nitrotyrosine. Simultaneous plasma ADMA concentration was similar to that in healthy subjects while symmetric dimethyl-arginine (SDMA) levels were substantially increased and directly related with creatinine. When infection resolved, ADMA rose from 0.62 +/- 0.23 to 0.80 +/- 0.18 micromol/l (+29%, P = 0.01) while SDMA remained unmodified. ADMA changes were independent on concomitant risk factor changes and inversely related with baseline systolic and diastolic pressure. Changes in the ADMA/SDMA ratio were compatible with the hypothesis that inflammatory cytokines activate ADMA degradation. CONCLUSIONS: Resolution of acute inflammation is characterized by an increase in the plasma concentration of ADMA. The results imply that ADMA suppression may actually serve to stimulate NO synthesis or that in this situation plasma ADMA levels may not reflect the inhibitory potential of this methylarginine at the cellular level.",
author = "Carmine Zoccali and Renke Maas and Sebastiano Cutrupi and Patrizia Pizzini and Piero Finocchiaro and Francesco Cambareri and Vincenzo Panuccio and Carmela Martorano and Friedrich Schulze and Giuseppe Enia and Giovanni Tripepi and Rainer B{\"o}ger",
year = "2007",
language = "Deutsch",
volume = "22",
pages = "801--806",
journal = "NEPHROL DIAL TRANSPL",
issn = "0931-0509",
publisher = "Oxford University Press",
number = "3",

}

RIS

TY - JOUR

T1 - Asymmetric dimethyl-arginine (ADMA) response to inflammation in acute infections.

AU - Zoccali, Carmine

AU - Maas, Renke

AU - Cutrupi, Sebastiano

AU - Pizzini, Patrizia

AU - Finocchiaro, Piero

AU - Cambareri, Francesco

AU - Panuccio, Vincenzo

AU - Martorano, Carmela

AU - Schulze, Friedrich

AU - Enia, Giuseppe

AU - Tripepi, Giovanni

AU - Böger, Rainer

PY - 2007

Y1 - 2007

N2 - BACKGROUND AND METHODS: The endogenous inhibitor of nitric oxide synthase (NOs) asymmetrical dimethyl-arginine (ADMA) has been implicated as a possible modulator of inducible NOs during acute inflammation. We examined the evolution in the plasma concentration of ADMA measured at the clinical outset of acute inflammation and after its resolution in a series of 17 patients with acute bacterial infections. RESULTS: During the acute phase of inflammation/infection, patients displayed very high levels of C-reactive protein (CRP), interleukin-6 (IL-6), procalcitonin and nitrotyrosine. Simultaneous plasma ADMA concentration was similar to that in healthy subjects while symmetric dimethyl-arginine (SDMA) levels were substantially increased and directly related with creatinine. When infection resolved, ADMA rose from 0.62 +/- 0.23 to 0.80 +/- 0.18 micromol/l (+29%, P = 0.01) while SDMA remained unmodified. ADMA changes were independent on concomitant risk factor changes and inversely related with baseline systolic and diastolic pressure. Changes in the ADMA/SDMA ratio were compatible with the hypothesis that inflammatory cytokines activate ADMA degradation. CONCLUSIONS: Resolution of acute inflammation is characterized by an increase in the plasma concentration of ADMA. The results imply that ADMA suppression may actually serve to stimulate NO synthesis or that in this situation plasma ADMA levels may not reflect the inhibitory potential of this methylarginine at the cellular level.

AB - BACKGROUND AND METHODS: The endogenous inhibitor of nitric oxide synthase (NOs) asymmetrical dimethyl-arginine (ADMA) has been implicated as a possible modulator of inducible NOs during acute inflammation. We examined the evolution in the plasma concentration of ADMA measured at the clinical outset of acute inflammation and after its resolution in a series of 17 patients with acute bacterial infections. RESULTS: During the acute phase of inflammation/infection, patients displayed very high levels of C-reactive protein (CRP), interleukin-6 (IL-6), procalcitonin and nitrotyrosine. Simultaneous plasma ADMA concentration was similar to that in healthy subjects while symmetric dimethyl-arginine (SDMA) levels were substantially increased and directly related with creatinine. When infection resolved, ADMA rose from 0.62 +/- 0.23 to 0.80 +/- 0.18 micromol/l (+29%, P = 0.01) while SDMA remained unmodified. ADMA changes were independent on concomitant risk factor changes and inversely related with baseline systolic and diastolic pressure. Changes in the ADMA/SDMA ratio were compatible with the hypothesis that inflammatory cytokines activate ADMA degradation. CONCLUSIONS: Resolution of acute inflammation is characterized by an increase in the plasma concentration of ADMA. The results imply that ADMA suppression may actually serve to stimulate NO synthesis or that in this situation plasma ADMA levels may not reflect the inhibitory potential of this methylarginine at the cellular level.

M3 - SCORING: Zeitschriftenaufsatz

VL - 22

SP - 801

EP - 806

JO - NEPHROL DIAL TRANSPL

JF - NEPHROL DIAL TRANSPL

SN - 0931-0509

IS - 3

M1 - 3

ER -