RGD Reference Report - Complement activation during painful crisis in sickle cell anemia. - Rat Genome Database

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Complement activation during painful crisis in sickle cell anemia.

Authors: Mold, C  Tamerius, JD  Phillips G, JR 
Citation: Mold C, etal., Clin Immunol Immunopathol. 1995 Sep;76(3 Pt 1):314-20.
RGD ID: 11040773
Pubmed: PMID:7554454   (View Abstract at PubMed)

Previous studies documented complement activation in sickle cell disease patients and suggested that this contributes to increased risk of infection. We have demonstrated alternative pathway activation initiated by membrane phospholipid changes which occur in sickled erythrocytes. The present studies compared complement activation products in serial samples from sickle cell anemia patients at baseline and during hospitalization for painful crisis to examine the correlation between complement activation and disease activity. Plasma concentrations of Bb, C4d, and C3a were measured as well as C3 bound to erythrocytes. Patients were subdivided into those with continuous pain and those with intermittent painful episodes. In patients with intermittent pain, there was little evidence of complement activation at baseline and increased plasma concentrations of Bb and C3a during painful crisis. Elevated C3a and C4d levels were observed in patients with continuous pain regardless of hospitalization status, suggesting a continuous underlying inflammatory process in these patients.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
C3Ratsickle cell anemia severityISOC3 (Homo sapiens)protein:increased processingRGD 
C3Mousesickle cell anemia severityISOC3 (Homo sapiens)protein:increased processingRGD 
C3Humansickle cell anemia severityIDA protein:increased processingRGD 

Objects Annotated

Genes (Rattus norvegicus)
C3  (complement C3)

Genes (Mus musculus)
C3  (complement component 3)

Genes (Homo sapiens)
C3  (complement C3)


Additional Information