UI  - 87000490
AU  - Kiefel V
AU  - Spaeth P
AU  - Mueller-Eckhardt C
TI  - Immune thrombocytopenic purpura: autoimmune or immune complex disease?
LA  - Eng
MH  - Adolescence
MH  - Adult
MH  - Aged
MH  - Antigen-Antibody Complex/analysis
MH  - Autoimmune Diseases/*immunology
MH  - Blood Platelets/immunology/pathology
MH  - Cell Survival
MH  - Child
MH  - Child, Preschool
MH  - Comparative Study
MH  - Female
MH  - Human
MH  - IgG/analysis
MH  - Immune Complex Diseases/*immunology
MH  - Male
MH  - Middle Age
MH  - Purpura, Thrombocytopenic/*immunology
MH  - Support, Non-U.S. Gov't
MH  - Thrombocytopenia/blood/immunology
RN  - 0 (Antigen-Antibody Complex)
PT  - JOURNAL ARTICLE
DA  - 19861112
DP  - 1986 Sep
IS  - 0007-1048
TA  - Br J Haematol
PG  - 57-68
SB  - M
SB  - X
CY  - ENGLAND
IP  - 1
VI  - 64
JC  - AXC
AA  - Author
EM  - 198701
AB  - To assess the pathogenic role of circulating immune complexes (CIC) in
      idiopathic thrombocytopenic purpura (ITP), 39 patients with ITP were
      compared to 17 patients with other forms of thrombocytopenia
      (hypersplenism (N = 12), impaired thrombopoiesis (3), thrombocytopenia of
      unknown origin (2)) and six nonthrombocytopenic subjects. In all patients,
      platelet mean life span (MLS), platelet associated IgG (PAIgG), as well as
      circulating anti-platelet antibodies and C1q binding activities were
      determined. In most cases, immune complex solubilization capacity (ICSC)
      and immune complex precipitation inhibition capacity (ICPIC) of sera were
      also assessed. All patients with ITP had a reduced platelet MLS, but PAIgG
      was elevated in only 16 out of 24 patients with chronic ITP, in six out of
      10 patients with acute ITP and in four out of five patients with secondary
      ITP. In the group of patients with thrombocytopenia due to splenomegaly,
      seven out of 12 patients had elevated PAIgG while the platelet MLS was
      only slightly reduced. Of the 39 patients with ITP only one with secondary
      ITP had C1q binding material in his serum, as opposed to six out of 12
      thrombocytopenic patients with splenomegaly. Whereas only three patients
      with ITP had abnormal immune-complex modulating capacities, such
      deviations were found in seven out of 12 patients with thrombocytopenia
      due to splenomegaly. We conclude that our data render the role of CIC in
      the pathogenesis of ITP very questionable.
PMID- 0002944539
CU  - 1992
EDAT- 1986/09/01 00:00
MHDA- 1986/09/01 00:00
SO  - Br J Haematol 1986 Sep;64(1):57-68




