Subject(s)
Antigens, Human Platelet/immunology , Fetal Diseases/immunology , Intracranial Hemorrhages/congenital , Intracranial Hemorrhages/diagnosis , Thrombocytopenia/congenital , Thrombocytopenia/immunology , Abortion, Eugenic , Adult , Diagnosis, Differential , Female , Fetal Diseases/diagnosis , Humans , Immunity, Maternally-Acquired , Magnetic Resonance Imaging , Maternal-Fetal Exchange , Pregnancy , Thrombocytopenia/diagnosis , Ultrasonography, PrenatalSubject(s)
Acquired Immunodeficiency Syndrome/virology , Blood Platelets/virology , HIV-1/isolation & purification , Megakaryocytes/virology , Thrombocytopenia/virology , Acquired Immunodeficiency Syndrome/complications , Acquired Immunodeficiency Syndrome/immunology , Antigen-Antibody Complex/immunology , Blood Platelets/cytology , Blood Platelets/immunology , Female , Follow-Up Studies , HIV Antigens/analysis , HIV Envelope Protein gp41/analysis , Humans , Male , Thrombocytopenia/complications , Thrombocytopenia/immunologyABSTRACT
The presence of anti-platelet autoantibodies has been reported in many cases of HIV infection, but there is no accordance about their pathogenic role in the onset of thrombocytopenia in the patients studied. In the present study surface anti-platelet antibodies (PAIgG) and serum anti-platelet antibodies (sPAIgG) were assayed in a group of 135 HIV-infected patients (109 men, 26 women), in different clinical stages by using an immunofluorescence test (PSIFT). In order to investigate the possible correlation of the positivity of these autoantibodies and the onset of thrombocytopenia, some of these patients were controlled in a follow-up study, with two successful controls: 10 months (II control: 89 patients) and 20 months (III control: 59 patients) after the first time. In the I control PAIgG were positive in 68 subjects (50.4%) and sPAIgG in 34 (25.2%); both PAIgG and sPAIgG were present in 23 patients (17%). 56 patients did not present anti-plt antibodies (41.5%). No significantly different distribution of these autoantibodies in each stage of disease was observed. The mean value of platelet count resulted in the normal range both in the anti-plt antibody positive and in the anti-plt antibody negative patients, but the value found in the anti-plt antibody positive patients was significantly lower than the one found in the anti-plt antibody negative group (p < 0.01). This difference was more marked between the group with PAIgG and anti-plt antibody negative patients than between the group with sPAIgG and the anti-plt antibody negative patients (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Subject(s)
Autoantibodies/blood , Blood Platelets/immunology , HIV Infections/complications , Thrombocytopenia/complications , Adolescent , Adult , Antibody Specificity , Autoantibodies/biosynthesis , Autoantibodies/immunology , Child , Female , Follow-Up Studies , HIV Infections/blood , HIV Infections/immunology , Humans , Male , Middle Aged , Thrombocytopenia/immunologyABSTRACT
Pseudothrombocytopenia is a phenomenon in which the electronic count shows spuriously low platelet counts in subjects with normal platelet levels. The mechanism of anticoagulant-dependent pseudothrombocytopenia appears to involve cold reactive agglutinins against platelet antigens. The authors report a case of EDTA-dependent pseudothrombocytopenia with evidence of a cold immunoglobulin M antibody against 78-kD platelet membrane glycoprotein (GP). Cell counts were performed by Coulter Counter S-Plus VI (Coulter, Hialeah, FL) in the following anticoagulants: EDTA, Na-citrate, and citrate-theophylline-adenosine-dipyridamole. Anti-platelet antibodies and platelet membrane GP antigens were assayed by an immunofluorescence technique as described by Van dem Borne in 1978. An immunoglobulin M/lambda anti-platelet antibody was found to react in serum as well as in plasma EDTA at room temperature, but not at 37 degrees C. This antibody appeared to be directed against GP78 membrane antigen because this antigen was not detectable by immunofluorescence in platelets collected in EDTA and Na-citrate anticoagulant, whereas a fluorescence signal was revealed in platelets collected in citrate-theophylline-adenosine-dipyridamole. This evidence was confirmed by platelet clumping inhibition tests in which target platelets were pretreated with anti-GP monoclonal antibodies. Clumping in the presence of pseudothrombocytopenia serum was inhibited by anti-GP78kD and anti-GPIIb/IIIa but not by anti-Ib. In this case, GP78 appears to be involved in platelet clumping, together with IIb/IIIa complex. The partial inhibition of the phenomenon observed in citrate-theophylline-adenosine-dipyridamole is probably related to a lower expression of the membrane antigens in platelets collected in this anticoagulant.
Subject(s)
Agglutinins/immunology , Autoantibodies/immunology , Edetic Acid/adverse effects , Immunoglobulin M/immunology , Platelet Membrane Glycoproteins/immunology , Thrombocytopenia/chemically induced , Anticoagulants/therapeutic use , Blood Coagulation Tests , Blood Platelets/immunology , Cold Temperature , Cryoglobulins , Drug Combinations , Female , Fluorescent Antibody Technique , Humans , Middle Aged , Molecular Weight , Platelet Count/drug effects , Platelet Membrane Glycoproteins/chemistry , Thrombocytopenia/drug therapy , Thrombocytopenia/immunologyABSTRACT
An epidemiological study into the prevalence and incidence of anti-H.I.V. antibody seropositivity in closed communities produced preliminary data on 746 subjects, the majority of whom admitted potentially dangerous behaviour. These results demonstrated that residence in a closed community in which one can limit the use of drugs and sexual contacts reduces the risk of infection.
