L-ARGININE SUPPLEMENTATION DECREASES HEMOLYSIS AND PULMONARY ARTERIAL HYPERTENSION IN SICKLE CELL DISEASE PATIENTS: A RANDOMIZED, DOUBLE-BLINDED, PLACEBO-CONTROLLED TRIAL.
(Abstract release date: 05/19/16)
EHA Library. Friedrisch J. 06/09/16; 135378; LB2267
Dr. Joao Ricardo Friedrisch
Contributions
Contributions
Abstract
Abstract: LB2267
Type: Eposter Presentation
Background
Low nitric oxide (NO) bioavailability contributes to vasculopathy in sickle cell disease (SCD), and is associated with increased morbimortality. Since the obligate substrate for NO production is arginine and enhanced NO bioavailability markedly decreased hemolysis and oxidative stress in SCD, we hypothesized that oral L-arginine (LA) supplementation could be beneficial for SCD outcomes and a reduction the in degree of hemolysis.
Aims
We assessed the impact of 6 months of LA supplementation on SCD clinical outcomes: leg ulcers, priapism, pulmonary arterial hypertension (PAH), and vaso-occlusive pain episodes, and the degree of hemolysis rate.
Methods
Sixty-eight patients with SCD were randomized for this double-blinded placebo-controlled trial. Patients received LA (0.1 g/kg/day) or placebo for 6 months.
Results
The LA group presented more pronounced decrease in lactate dehydrogenase (DHL) (1065 ± 495 U/L to 784 ± 267 U/L vs. 952 ± 383 U/L to 907 ± 395 U/L; p = 0.03) and a tendency of PAH reduction. Ten patients of the study group had PAH (6 in the LA group and 4 in the placebo group). The tricuspid regurgitant jet velocity (TRV) in the 6 patients receiving LA decreased from 2.83 ± 0.36 m/s to 2.46 ± 0.36 m/s, while the TRV in the 4 patients receiving placebo increased from 2.75 ± 0.35 m/s to 2.80 ± 0.18 m/s (p = 0.13), representing a tendency of PAH reduction in the LA group. Non drug-related severe adverse events were perceived.
Conclusion
In conclusion, supplementation of LA was associated with a significant reduction in hemolytic activity with and a tendency towards reduced PAH. Weighing outlays and benefits, these preliminary results provide a strong rationale for therapeutic use of LA in SCD disease and other chronic hemolytic diseases, although an extended multi-center trial with larger number of SCD individuals is warranted to confirm these findings.
Session topic: E-poster
Keyword(s): Arginine, Hemolysis, Pulmonary hypertension, Sickle cell disease
Type: Eposter Presentation
Background
Low nitric oxide (NO) bioavailability contributes to vasculopathy in sickle cell disease (SCD), and is associated with increased morbimortality. Since the obligate substrate for NO production is arginine and enhanced NO bioavailability markedly decreased hemolysis and oxidative stress in SCD, we hypothesized that oral L-arginine (LA) supplementation could be beneficial for SCD outcomes and a reduction the in degree of hemolysis.
Aims
We assessed the impact of 6 months of LA supplementation on SCD clinical outcomes: leg ulcers, priapism, pulmonary arterial hypertension (PAH), and vaso-occlusive pain episodes, and the degree of hemolysis rate.
Methods
Sixty-eight patients with SCD were randomized for this double-blinded placebo-controlled trial. Patients received LA (0.1 g/kg/day) or placebo for 6 months.
Results
The LA group presented more pronounced decrease in lactate dehydrogenase (DHL) (1065 ± 495 U/L to 784 ± 267 U/L vs. 952 ± 383 U/L to 907 ± 395 U/L; p = 0.03) and a tendency of PAH reduction. Ten patients of the study group had PAH (6 in the LA group and 4 in the placebo group). The tricuspid regurgitant jet velocity (TRV) in the 6 patients receiving LA decreased from 2.83 ± 0.36 m/s to 2.46 ± 0.36 m/s, while the TRV in the 4 patients receiving placebo increased from 2.75 ± 0.35 m/s to 2.80 ± 0.18 m/s (p = 0.13), representing a tendency of PAH reduction in the LA group. Non drug-related severe adverse events were perceived.
Conclusion
In conclusion, supplementation of LA was associated with a significant reduction in hemolytic activity with and a tendency towards reduced PAH. Weighing outlays and benefits, these preliminary results provide a strong rationale for therapeutic use of LA in SCD disease and other chronic hemolytic diseases, although an extended multi-center trial with larger number of SCD individuals is warranted to confirm these findings.
Session topic: E-poster
Keyword(s): Arginine, Hemolysis, Pulmonary hypertension, Sickle cell disease
Abstract: LB2267
Type: Eposter Presentation
Background
Low nitric oxide (NO) bioavailability contributes to vasculopathy in sickle cell disease (SCD), and is associated with increased morbimortality. Since the obligate substrate for NO production is arginine and enhanced NO bioavailability markedly decreased hemolysis and oxidative stress in SCD, we hypothesized that oral L-arginine (LA) supplementation could be beneficial for SCD outcomes and a reduction the in degree of hemolysis.
Aims
We assessed the impact of 6 months of LA supplementation on SCD clinical outcomes: leg ulcers, priapism, pulmonary arterial hypertension (PAH), and vaso-occlusive pain episodes, and the degree of hemolysis rate.
Methods
Sixty-eight patients with SCD were randomized for this double-blinded placebo-controlled trial. Patients received LA (0.1 g/kg/day) or placebo for 6 months.
Results
The LA group presented more pronounced decrease in lactate dehydrogenase (DHL) (1065 ± 495 U/L to 784 ± 267 U/L vs. 952 ± 383 U/L to 907 ± 395 U/L; p = 0.03) and a tendency of PAH reduction. Ten patients of the study group had PAH (6 in the LA group and 4 in the placebo group). The tricuspid regurgitant jet velocity (TRV) in the 6 patients receiving LA decreased from 2.83 ± 0.36 m/s to 2.46 ± 0.36 m/s, while the TRV in the 4 patients receiving placebo increased from 2.75 ± 0.35 m/s to 2.80 ± 0.18 m/s (p = 0.13), representing a tendency of PAH reduction in the LA group. Non drug-related severe adverse events were perceived.
Conclusion
In conclusion, supplementation of LA was associated with a significant reduction in hemolytic activity with and a tendency towards reduced PAH. Weighing outlays and benefits, these preliminary results provide a strong rationale for therapeutic use of LA in SCD disease and other chronic hemolytic diseases, although an extended multi-center trial with larger number of SCD individuals is warranted to confirm these findings.
Session topic: E-poster
Keyword(s): Arginine, Hemolysis, Pulmonary hypertension, Sickle cell disease
Type: Eposter Presentation
Background
Low nitric oxide (NO) bioavailability contributes to vasculopathy in sickle cell disease (SCD), and is associated with increased morbimortality. Since the obligate substrate for NO production is arginine and enhanced NO bioavailability markedly decreased hemolysis and oxidative stress in SCD, we hypothesized that oral L-arginine (LA) supplementation could be beneficial for SCD outcomes and a reduction the in degree of hemolysis.
Aims
We assessed the impact of 6 months of LA supplementation on SCD clinical outcomes: leg ulcers, priapism, pulmonary arterial hypertension (PAH), and vaso-occlusive pain episodes, and the degree of hemolysis rate.
Methods
Sixty-eight patients with SCD were randomized for this double-blinded placebo-controlled trial. Patients received LA (0.1 g/kg/day) or placebo for 6 months.
Results
The LA group presented more pronounced decrease in lactate dehydrogenase (DHL) (1065 ± 495 U/L to 784 ± 267 U/L vs. 952 ± 383 U/L to 907 ± 395 U/L; p = 0.03) and a tendency of PAH reduction. Ten patients of the study group had PAH (6 in the LA group and 4 in the placebo group). The tricuspid regurgitant jet velocity (TRV) in the 6 patients receiving LA decreased from 2.83 ± 0.36 m/s to 2.46 ± 0.36 m/s, while the TRV in the 4 patients receiving placebo increased from 2.75 ± 0.35 m/s to 2.80 ± 0.18 m/s (p = 0.13), representing a tendency of PAH reduction in the LA group. Non drug-related severe adverse events were perceived.
Conclusion
In conclusion, supplementation of LA was associated with a significant reduction in hemolytic activity with and a tendency towards reduced PAH. Weighing outlays and benefits, these preliminary results provide a strong rationale for therapeutic use of LA in SCD disease and other chronic hemolytic diseases, although an extended multi-center trial with larger number of SCD individuals is warranted to confirm these findings.
Session topic: E-poster
Keyword(s): Arginine, Hemolysis, Pulmonary hypertension, Sickle cell disease
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