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Sickle Cell Disease Patients (sickle + cell_disease_patient)

Distribution by Scientific Domains
Medical Sciences66%

Selected Abstracts

Subarachnoid Hemorrhage as Complication of Phenylephrine Injection for the Treatment of Ischemic Priapism in a Sickle Cell Disease Patient

THE JOURNAL OF SEXUAL MEDICINE, Issue 4 2008
Hugo H. Davila MD
ABSTRACT Introduction., Ischemic priapism (IP) is a urologic condition, which necessitates prompt management. Intracavernosal injection of phenylephrine is a usual treatment modality utilized for the management of these patients. Aim., We present a case of subarachnoid hemorrhage following intracavernosal injection of phenylephrine for IP in a patient with sickle cell disease. Methods., We analyzed the degree of subarachnoid hemorrhage in our patient after intracavernosal injection of phenylephrine. The patient had an acute rise in blood pressure during corporal irrigation. This was followed by the onset of severe headache. Computed tomography (CT) scan confirmed the diagnosis of a subarachnoid hemorrhage. Main Outcome Measure., Subarachnoid hemorrhage associated with intracavernosal injection of phenylephrine. Result., A 23-year-old African American male with a history of sickle cell disease presented with a painful penile erection. The patient was started on intravenous fluids, oxygen by nasal canula, and analgesic medication. After this, a blood gas was obtained from his left corpora cavernosa. This was followed by normal saline irrigation and injection of phenylephrine. The patient complained of a sudden, severe "terrible headache" immediately following the last injection, and noncontrast CT scan of the head was obtained and a subarachnoid hemorrhage was noted. The patient was admitted for observation and no significant changes were noted. Conclusions., Intracavernosal injection of phenylephrine for the management of IP can be associated with several possible complications. We present our single case complicated with the formation of a subarachnoid hemorrhage. The patient was treated conservatively and had no long-term neurologic sequelae. Davila HH, Parker J, Webster JC, Lockhart JL, and Carrion RE. Subarachnoid hemorrhage as complication of phenylephrine injection for the treatment of ischemic priapism in a sickle cell disease patient. J Sex Med 2008;5:1025,1028. [source]

Vascular at-risk genotypes and disease severity in Lebanese sickle cell disease patients,

AMERICAN JOURNAL OF HEMATOLOGY, Issue 5 2010
Chantal Farra
No abstract is available for this article. [source]

,-Globin gene cluster haplotypes and ,-thalassemia in sickle cell disease patients from Trinidad

AMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 3 2008
Altheia Jones-Lecointe
In this study, we have determined the frequency of ,S haplotypes in 163 sickle cell disease patients from Trinidad. The ,3.7 globin gene deletion status was also studied with an observed gene frequency of 0.17. Among the 283 ,S chromosomes analyzed, the Benin haplotype was the most prevalent (61.8%) followed by Bantu (17.3%), Senegal (8.5%), Cameroon (3.5%), and Arab-Indian (3.2%), while 5.7% of them were atypical. This ,S haplotypes distribution differed from those previously described in other Caribbean islands (Jamaica, Guadeloupe, and Cuba), in agreement with the known involvement of the major colonial powers (Spain, France, and Great Britain) in the slave trade in Trinidad and documented an Indian origin of the ,S gene. Am. J. Hum. Biol., 2008. © 2008 Wiley-Liss, Inc. [source]

Inhibition of caspase-dependent spontaneous apoptosis via a cAMP-protein kinase A dependent pathway in neutrophils from sickle cell disease patients

BRITISH JOURNAL OF HAEMATOLOGY, Issue 1 2007
Nicola Conran
Summary Sickle cell disease (SCD) is a chronic inflammatory condition characterized by high leucocyte counts, altered cytokine levels and endothelial cell injury. As the removal of inflammatory cells by apoptosis is fundamental for the resolution of inflammation, we aimed to determine whether the leucocyte apoptotic process is altered in SCD. Neutrophils from SCD individuals showed an inhibition of spontaneous apoptosis when cultured in vitro, in the presence of autologous serum for 20 h. Intracellular cyclic adenosine monophosphate (cAMP) levels were approximately twofold increased in SCD neutrophils; possible cAMP-upregulating factors present in SCD serum include interleukin-8, granulocyte-macrophage colony-stimulating factor and prostaglandin. Accordingly, co-incubation of SCD neutrophils with KT5720, a cAMP-dependent protein kinase (PKA) inhibitor, abrogated increased SCD neutrophil survival. Caspase-3 activity was also significantly diminished in SCD neutrophils cultured for 16 h and this activity was restored when cells were co-incubated with KT5720. BIRC2 (encoding cellular inhibitor of apoptosis protein 1, cIAP1), MCL1 and BAX expression were unaltered in SCD neutrophils; however, BIRC3 (encoding the caspase inhibitor, cIAP2), was expressed at significantly higher levels. Thus, we report an inhibition of spontaneous SCD neutrophil apoptosis that appears to be mediated by upregulated cAMP-PKA signalling and decreased caspase activity. Increased neutrophil survival may have significant consequences in SCD; contributing to leucocytosis, tissue damage and exacerbation of the chronic inflammatory state. [source]