PMID- 14984503
OWN - NLM
STAT- MEDLINE
DCOM- 20040504
LR  - 20190705
IS  - 0007-1048 (Print)
IS  - 0007-1048 (Linking)
VI  - 124
IP  - 4
DP  - 2004 Feb
TI  - Intravenous (IV) anti-D and IV immunoglobulin achieve acute platelet increases by 
      different mechanisms: modulation of cytokine and platelet responses to IV anti-D 
      by FcgammaRIIa and FcgammaRIIIa polymorphisms.
PG  - 511-8
AB  - Intravenous (IV) anti-D and IV immunoglobulin (IVIG) slow the Fcgamma receptor 
      (FcgammaR)-mediated destruction of antibody-coated platelets in patients with 
      immune thrombocytopenic purpura (ITP). This pilot study explored the mechanism of 
      these immunoglobulin preparations by measuring interleukin-10 (IL-10), monocyte 
      chemoattractant protein-1 (MCP-1), IL-6 and tumour necrosis factor alpha 
      (TNFalpha), before and after infusion and by assessing the effect of FcgammaRIIa 
      and FcgammaRIIIa polymorphisms on both cytokine and haematologic responses to 
      anti-D. Following IVIG, only IL-10 was increased at 2 h and MCP-1 on day 7 (P < 
      0.05). In contrast, 2 h after anti-D infusion, plasma levels of all four 
      cytokines were increased (P < 0.01); five of six patients with the highest MCP-1, 
      IL-6 and TNFalpha levels had chills. Higher IL-10 levels correlated with platelet 
      increases at 24 h and haemoglobin decreases at day 7 (P < 0.025). Patients with 
      the FcgammaRIIa-131HH genotype had significantly higher MCP-1, IL-6 and TNFalpha 
      levels. Patients with the FcgammaRIIIa-158VF genotype had higher platelet 
      increments at day 7 (P < 0.05). Soluble CD16 (sCD16) was increased 2 h after IV 
      anti-D; day 7 levels correlated with day 7 haemoglobin decreases (P < 0.01). In 
      conclusion, the relationship of FcgammaRIIa and FcgammaRIIIa polymorphisms with 
      both cytokine levels and platelet increments implicated these receptors in 
      responses to anti-D and supported different mechanisms of FcgammaR interaction to 
      those seen with IVIG.
FAU - Cooper, Nichola
AU  - Cooper N
AD  - Division of Hematology/Oncology, Department of Pediatrics, New York Presbyterian 
      Hospital - Weill Medical College of Cornell University, New York, NY 10021, USA. 
      nicholacooper@yahoo.com
FAU - Heddle, Nancy M
AU  - Heddle NM
FAU - Haas, Masja
AU  - Haas M
FAU - Reid, Marion E
AU  - Reid ME
FAU - Lesser, Martin L
AU  - Lesser ML
FAU - Fleit, Howard B
AU  - Fleit HB
FAU - Woloski, B M R
AU  - Woloski BM
FAU - Bussel, James B
AU  - Bussel JB
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Br J Haematol
JT  - British journal of haematology
JID - 0372544
RN  - 0 (Antigens, CD)
RN  - 0 (Cytokines)
RN  - 0 (Fc gamma receptor IIA)
RN  - 0 (Glucocorticoids)
RN  - 0 (Immunoglobulins, Intravenous)
RN  - 0 (Isoantibodies)
RN  - 0 (RHO(D) antibody)
RN  - 0 (Receptors, IgG)
RN  - 0 (Rh-Hr Blood-Group System)
RN  - 0 (Rho(D) Immune Globulin)
RN  - VB0R961HZT (Prednisone)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Antigens, CD/genetics
MH  - Blood Platelets/*immunology
MH  - Cytokines/*biosynthesis
MH  - Female
MH  - Glucocorticoids/therapeutic use
MH  - Humans
MH  - Immunoglobulins, Intravenous/*therapeutic use
MH  - Isoantibodies/adverse effects/*therapeutic use
MH  - Male
MH  - Middle Aged
MH  - Phenotype
MH  - Pilot Projects
MH  - Platelet Count
MH  - Polymorphism, Genetic
MH  - Prednisone/therapeutic use
MH  - Purpura, Thrombocytopenic, Idiopathic/blood/immunology/*therapy
MH  - Receptors, IgG/genetics
MH  - Rh-Hr Blood-Group System/blood
MH  - Rho(D) Immune Globulin
EDAT- 2004/02/27 05:00
MHDA- 2004/05/05 05:00
CRDT- 2004/02/27 05:00
PHST- 2004/02/27 05:00 [pubmed]
PHST- 2004/05/05 05:00 [medline]
PHST- 2004/02/27 05:00 [entrez]
AID - 4804 [pii]
AID - 10.1111/j.1365-2141.2004.04804.x [doi]
PST - ppublish
SO  - Br J Haematol. 2004 Feb;124(4):511-8. doi: 10.1111/j.1365-2141.2004.04804.x.