title: Asymmetric dimethyl-arginine (ADMA) response to inflammation in acute infections.
abstract: 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.
authors.affiliation: CNR-IBIM, Clinical Epidemiology and Physiopathology of Renal Diseases and Hypertension, c/o Ki Point, Gransial SRL, Via Filippini n. 85, 89100 Reggio Calabria, Italy. carmine.zoccali@tin.it
authors.forename: Carmine
authors.initials: C
authors.lastname: Zoccali
authors.forename: Renke
authors.initials: R
authors.lastname: Maas
authors.forename: Sebastiano
authors.initials: S
authors.lastname: Cutrupi
authors.forename: Patrizia
authors.initials: P
authors.lastname: Pizzini
authors.forename: Piero
authors.initials: P
authors.lastname: Finocchiaro
authors.forename: Francesco
authors.initials: F
authors.lastname: Cambareri
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Panuccio
authors.forename: Carmela
authors.initials: C
authors.lastname: Martorano
authors.forename: Friedrich
authors.initials: F
authors.lastname: Schulze
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Enia
authors.forename: Giovanni
authors.initials: G
authors.lastname: Tripepi
authors.forename: Rainer
authors.initials: R
authors.lastname: Boger
mesh_terms: D000208:Acute Disease; D001120:Arginine / Q000031:analogs & derivatives* / Q000097:blood; D001424:Bacterial Infections / Q000097:blood* / Q000503:physiopathology; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure / Q000502:physiology; D002097:C-Reactive Protein / Q000378:metabolism; D002116:Calcitonin / Q000097:blood; D015740:Calcitonin Gene-Related Peptide; D002851:Chromatography, High Pressure Liquid; D003404:Creatinine / Q000097:blood; D018450:Disease Progression; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005500:Follow-Up Studies; D006023:Glycoproteins; D006801:Humans; D007249:Inflammation / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000097:blood; D011498:Protein Precursors / Q000097:blood; D012720:Severity of Illness Index; D014443:Tyrosine / Q000031:analogs & derivatives / Q000097:blood
chemical_list: D015415:Biomarkers; C000606589:CALCA protein, human; D006023:Glycoproteins; D015850:Interleukin-6; D011498:Protein Precursors; C002744:3-nitrotyrosine; D014443:Tyrosine; C018524:N,N-dimethylarginine; D002116:Calcitonin; D002097:C-Reactive Protein; D001120:Arginine; D003404:Creatinine; D019001:Nitric Oxide Synthase; D015740:Calcitonin Gene-Related Peptide