scholarly journals Induction of Tolerance to Non Steroidal Anti Inflammatory Drugs Might Be an Alternative Therapeutic in the Painful Crisis of Sickle Cell Disease

2014 ◽  
Vol 03 (02) ◽  
pp. 11-21
Author(s):  
Dasse Romuald ◽  
Kouacou Amah ◽  
Akré Paul ◽  
Yeboah Richard ◽  
Nguessan Koffi ◽  
...  
Keyword(s):  
Sickle Cell Disease ◽  
Sickle Cell ◽  
Cell Disease ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Painful Crisis ◽  
Induction Of Tolerance

Pulmonary events induced by non-steroidal anti-inflammatory drugs in patients with sickle cell disease

2011 ◽  
Vol 21 (4) ◽  
pp. 187-191
Author(s):  
Romuald Dassé Séry ◽  
Koffi N’guessan ◽  
Paul Akré Dagra ◽  
Rita Yao ◽  
François Sombo Mambo
Keyword(s):  
Sickle Cell Disease ◽  
Sickle Cell ◽  
Cell Disease ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

scholarly journals Use of anti-inflammatory analgesics in sickle-cell disease

2017 ◽  
Vol 42 (5) ◽  
pp. 656-660 ◽  
Author(s):  
J. Han ◽  
S. L. Saraf ◽  
J. P. Lash ◽  
V. R. Gordeuk
Keyword(s):  
Sickle Cell Disease ◽  
Sickle Cell ◽  
Cell Disease ◽  
Anti Inflammatory

Is the painful crisis of sickle-cell disease due to sickling?

The Lancet ◽  
1991 ◽  
Vol 337 (8743) ◽  
pp. 735 ◽  
Author(s):  
Simon Bailey ◽  
DouglasR. Higgs ◽  
Joanne Morris ◽  
GrahamR. Serjeant
Keyword(s):  
Sickle Cell Disease ◽  
Sickle Cell ◽  
Cell Disease ◽  
Painful Crisis

226 Ketamine Use for Acute Painful Crisis of Sickle Cell Disease: A Randomized Controlled Trial

2019 ◽  
Vol 74 (4) ◽  
pp. S89-S90 ◽  
Author(s):  
M.S. Alshahrani ◽  
A.H. Alsulaibikh ◽  
M.M. ElTahan ◽  
S.Z. AlFaraj ◽  
A.A. AlMulhim ◽  
...  
Keyword(s):  
Randomized Controlled Trial ◽  
Sickle Cell Disease ◽  
Sickle Cell ◽  
Controlled Trial ◽  
Cell Disease ◽  
Randomized Controlled ◽  
Painful Crisis

The painful crisis of homozygous sickle cell disease: clinical features

1994 ◽  
Vol 87 (3) ◽  
pp. 586-591 ◽  
Author(s):  
Graham R. Serjeant ◽  
Charles D. E. Ceulaer ◽  
Rosemary Lethbridge ◽  
Joanne Morris ◽  
Atul Singhal and ◽  
...  
Keyword(s):  
Sickle Cell Disease ◽  
Clinical Features ◽  
Sickle Cell ◽  
Cell Disease ◽  
Homozygous Sickle Cell Disease ◽  
Painful Crisis

Nitrated Lipids in a Murine Model of Sickle Cell Disease at Baseline.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 3758-3758
Author(s):  
Jeffrey Schwartz ◽  
Paul R.S. Baker ◽  
Francisco J. Schopfer ◽  
Bruce A. Freeman
Keyword(s):  
Linoleic Acid ◽  
Sickle Cell Disease ◽  
Sickle Cell ◽  
Ion Trap ◽  
Internal Standard ◽  
Wild Type ◽  
Cell Disease ◽  
Inflammatory Signaling ◽  
No Bioavailability ◽  
Anti Inflammatory

Abstract Introduction Sickle cell disease (SCD) is increasingly recognized as a disorder of inflammatory homeostasis. One major focus in recent years has been understanding the role of Nitric Oxide (NO) in the pathophysiology of SCD. NO is a critical mediator of inflammatory pathways and current evidence supports the precept that NO bioavailability is decreased in SCD, resulting in normal concentrations of NO at baseline but an inability to increase NO during stress. Nitrated fatty acids, such as Nitrolinoleate (LNO2), have recently been reported as potent and abundant anti-inflammatory signaling mediators with the ability to cause vasorelaxation and inhibition of platelet and neutrophil activation. Evidence supports their anti-inflammatory signaling is mediated through the release of NO and NO-related products. LNO2 has not previously been described in patients with SCD and our objective was to quantify LNO2 in a murine model of SCD at baseline. Methods Whole blood was obtained from transgenic sickle cell and wild type mice (n = 5 and 6, respectively). Blood was centrifuged and separated into plasma and packed red blood cells (RBCs). These biological samples were prepared for lipid analysis by the method of Bligh and Dyer; care was taken so that the pH of the extraction milieu was consistently maintained at 7 so as to avoid artifactual nitration. Samples were analyzed for free LNO2 content by electrospray ionization tandem mass spectrometry. Using a hybrid triple quadrupole ion trap mass spectrometer, MRM transitions were monitored that specifically identified nitrated linoleic acid species; these species were concomitantly confirmed by the qualitative analytical abilities of the ion trap. The presence of nitrated linoleic acid was confirmed by HPLC chromatographic retention times, MS/MS “fingerprints” and was quantitated by the inclusion of a known quantity of 13C-labeled LNO2. Results LNO2 concentration was calculated as a function of the ratio of analyte to internal standard peak areas by using an internal standard curve linear over five orders of magnitude. Free LNO2 in the RBCs and plasma of 5 transgenic sickle cell mice were 3.97 ± 2.56 nM and 12.37 ± 9.83 nM, respectively. Free LNO2 in the RBCs and plasma of 6 wild type mice were 9.49 ± 8.32 nM and 14.91 ± 10.08 nM, respectively. There were no significant differences in LNO2 concentration between any of the groups. Conclusions LNO2 is present in both transgenic sickle cell mice and wild type mice in comparable concentrations at baseline. As a mediator of NO anti-inflammatory signaling, this is consistent with human studies showing comparable concentrations of NO metabolites at baseline between sickle cell patients and healthy controls. Further study of LNO2 in sickle cell disease is warranted to better understand its role in the inflammatory process associated with acute stress, such as vaso-occlusive pain crisis and acute chest syndrome, when NO bioavailability is decreased.

Measurement of Urine Pyridinoline and Deoxypyridinoline as Markers of Increased Bone Degradation in Sickle Cell Disease.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 2572-2572
Author(s):  
Erfan Nur ◽  
Willem Mairuhu ◽  
Dees P. Brandjes ◽  
Ton van Zanten ◽  
Bart J. Biemond ◽  
...  
Keyword(s):  
Sickle Cell Disease ◽  
Bone Resorption ◽  
Sickle Cell ◽  
Conflicts Of Interest ◽  
Healthy Controls ◽  
Cell Disease ◽  
Skeletal Involvement ◽  
Asymptomatic Patients ◽  
Bone Degradation ◽  
Painful Crisis

Abstract Abstract 2572 Poster Board II-549 Introduction: Sickle cell disease (SCD) is commonly manifested through skeletal involvement. Besides the characteristic acute musculoskeletal pain, SCD is also associated with chronic skeletal complications such as osteopenia and osteoporosis. During bone resorption, the collagen cross-links pyridinoline (PYD) and deoxypyridinoline (DPD) are released into circulation with subsequent urinary excretion. Measurements of urinary PYD and DPD could serve as valuable tools in detecting osteoporosis in the follow-up of SCD patients but perhaps also in determining the severity of bone infarction during painful crises. Therefore we compared urinary concentrations of PYD and DPD of SCD patients during asymptomatic state and painful crisis with those of race- and age-matched healthy controls. Methods: Urinary concentrations of PYD and DPD, adjusted for urine creatinine, were measured in SCD patients both during asymptomatic state (n=38) and painful crisis (n=27) and healthy controls with normal HbA hemoglobin (n=25) using high performance liquid chromatography (HPLC). Results: PYD and DPD concentrations were higher in asymptomatic SCD patients compared to controls ((54.8 (41.5–68.6) vs. 44.1 (37.7–49.9),P=0.005 and 11.6 (9.3–15.2) vs. 8.5 (6.8–10.4),P=0.004 respectively), with further increments during painful crisis (63.3 (51.8–76.0),P=0.041 and 15.3(13.0–21.5),P=0.003 respectively). In the asymptomatic patients levels of PYD and DPD were significantly correlated to the degree of hemolysis. Conclusion: In sickle cell patients bone resorption is increased and significantly correlated to the degree of hemolysis, compatible with their susceptibility to osteopenia and osteoporosis. Measurement of pyridinoline and deoxypyridinoline could have additional value as biomarkers of osteoporosis in SCD. During painful crises a further increment in bone degradation was observed. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Gene-centric association study of acute chest syndrome and painful crisis in sickle cell disease patients

Blood ◽  
2013 ◽  
Vol 122 (3) ◽  
pp. 434-442 ◽  
Author(s):  
Geneviève Galarneau ◽  
Sean Coady ◽  
Melanie E. Garrett ◽  
Neal Jeffries ◽  
Mona Puggal ◽  
...  
Keyword(s):  
Sickle Cell Disease ◽  
Association Study ◽  
Sickle Cell ◽  
Genome Wide Association Study ◽  
Inflammatory Responses ◽  
Acute Chest Syndrome ◽  
Cell Disease ◽  
Genome Wide ◽  
Key Points ◽  
Painful Crisis

Key Points Using genome-wide association study, we found the first replicated genetic association with acute chest syndrome in sickle cell disease patients. The locus identified includes COMMD7, a gene highly expressed in the lung that interacts with NFκB to control inflammatory responses.

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