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At least 19 recordsLinked to original sources
PubMed1992

Asymptomatic thrombocytopenia developing during pregnancy (gestational thrombocytopenia)--a clinical study.

During pregnancy some women develop unexplained thrombocytopenia (gestational thrombocytopenia). Previous studies have detected abnormal platelet antibodies, suggesting an autoimmune aetiology. To determine whether gestational thrombocytopenia is associated with increased maternal bleeding or adversely affects the fetus, 31 pregnant women with asymptomatic thrombocytopenia were compared with 12 women with thrombocytopenia associated with pre-eclampsia and 34 normal pregnant controls. There was no increase in maternal bleeding in those with asymptomatic thrombocytopenia compared with the normal controls, but pre-eclamptic women experienced more bleeding (mean difference 181 ml, 95 per cent confidence limits 50-312 ml, p < 0.01). There was no difference in the mean weights of the babies or placenta, nor in the APGAR scores between infants born to controls and those with asymptomatic thrombocytopenia. Cord blood platelet levels were measured in 26 women with asymptomatic thrombocytopenia and were normal in 25 and mildly reduced in one. Thus measures used for the treatment and delivery of pregnancies complicated by autoimmune thrombocytopenia are not indicated in gestational thrombocytopenia. Pregnant women should not be considered thrombocytopenic unless the platelet count has fallen below 120 x 10(9)/l.

Adult↗
PubMed1990

Alloimmune neonatal thrombocytopenia associated with incidental maternal thrombocytopenia.

In this report, we describe a mother with mild incidental thrombocytopenia who delivered a severely thrombocytopenic infant having alloimmune thrombocytopenia. This coincidental association should be considered because the recognition and proper diagnosis of alloimmune neonatal thrombocytopenia is important, not only in the current pregnancy, but also in future pregnancies.

Adult↗
PubMed1991

Recommendations for the evaluation and treatment of neonatal autoimmune and alloimmune thrombocytopenia. The Working Party on Neonatal Immune Thrombocytopenia of the Neonatal Hemostasis Subcommittee of the Scientific and Standardization Committee of the ISTH.

The following recommendations of the Neonatal Hemostasis Subcommittee of the Scientific and Standardization Committee of the ISTH for the management of neonatal immune thrombocytopenia were prepared by the working party on neonatal immune thrombocytopenia. Evaluation, diagnosis, and treatment of the mother and neonate with alloimmune and autoimmune thrombocytopenia are discussed and current recommendations provided. This document is likely to require frequent future revision(s).

Autoimmune Diseases↗
PubMed1978

[Pathogenesis of thrombocytopenia. 2. Distribution disorders, pseudo-thrombocytopenias].

A review of the pathogenesis of thrombocytopenias is given. The various types of thrombocytopenia are classified according to the main pathogenetic mechanisms such as reduced platelet production, increased platelet destruction and disturbed platelet distribution by splenic pooling. Finally thrombocytopenia by artefacts is discussed such as platelet satillitism and spontaneous aggregation. In the second part of the paper the differential diagnosis of several forms of thrombocytopenic purpura is presented.

Adult↗
PubMed1977

Experimental immunologic thrombocytopenia in dogs: a study of thrombocytopenia and megakaryocytopoiesis.

Immunologic thrombocytopenia was induced in dogs by intravenous or intraperitoneal injection of rabbit anti-canine platelet serum (APS) or by intraperitoneal injection of the IgG fraction of the APS. In contrast, dogs injected with normal rabbit serum (NRS) or the IgM fraction of the APS did not develop thrombocytopenia. Marrow samples obtained at 24-96 h after inoculation of the IgG fraction contained megakaryocytes giving a positive reaction with flurescein isothiocyanate or horseradish peroxidase-conjugated anti-rabbit globulin. In contrast, negative results were obtained with megakaryocytes in marrow samples collected before injection of the IgG fraction or after injection of the IgM fraction or NRS. The attachment of anti-platelet antibody to the surface of megakaryocytes was associated with appearance of morphologic abnormalities, particularly in mature megakaryocytes. Simultaneously, the number of immature megakaryocytes and acetylcholine esterase (AChE)-positive small cells (presumably megakaryocyte precursors) increased considerably. These changes coincided with the development of thrombocytopenia, and subsided as recovery ensued.

Acetylcholinesterase↗
PubMed1992

Diagnosis of microthrombocytosis and immune-mediated thrombocytopenia in dogs with thrombocytopenia: 68 cases (1987-1989).

The mean platelet volume (MPV) was evaluated in 68 dogs with thrombocytopenia attributable to various causes. Platelet size was high or low in some dogs. The most clinically useful observation was that low MPV (microthrombocytosis) was a specific indicator of immune-mediated thrombocytopenia (IMT) in these thrombocytopenic dogs. All but one case of microthrombocytosis (MPV less than 5.4 fl) was found in dogs with IMT. Microthrombocytosis was detected in 17 of 31 dogs with IMT and appeared at the onset of the disease. Macrothrombocytosis (MPV greater than 9.4 fl) indicated active thrombopoiesis, but was not unique to any disease category. Macrothrombocytosis was detected in 18 of 31 dogs with IMT, 3 of 17 dogs with disseminated intravascular coagulation, and 3 of 9 dogs with primary bone-marrow disease.

Animals↗
PubMed1988

Immunologic thrombocytopenic purpura in human immunodeficiency virus--seropositive patients with hemophilia. Comparison with patients with classic autoimmune thrombocytopenic purpura, homosexuals with thrombocytopenia, and narcotic addicts with thrombocytopenia.

The immunologic platelet profile of 29 patients with hemophilia who had received multiple transfusions (14 had thrombocytopenia) was compared with profiles of 15 patients with classic autoimmune thrombocytopenia. Thrombocytopenic hemophiliacs who were seropositive for the human immunodeficiency virus (13 out of 14) had platelet-bound immunoglobulin G and C3C4 levels as well as circulating immune complexes that were 15.1-, 4.0-, and 2.4-fold greater, respectively, than normal control subjects' platelets and 3.4-, 2.6-, and 2.4-fold greater, respectively, than autoimmune thrombocytopenic patients' platelets. Hemophiliacs with normal platelet counts (nine out of 13 seropositive) had elevated values that were intermediate in level between those of thrombocytopenic hemophiliacs and those of classic autoimmune thrombocytopenic patients. The four seronegative hemophiliacs had normal values (except for one platelet-bound IgG measurement). An inverse correlation was noted between platelet count and platelet-bound IgG, r = -0.838, P less than 0.001. Serum antiplatelet reactivity (1:256 mean titer compared with control sera) resided predominantly in the 7S IgG fraction, and bound to autologous as well as homologous platelets at concentrations as low as 0.06 to 0.13 mg/ml. F(ab')2 fragments of the 7S IgG fraction inhibited binding of hemophilic IgG to normal platelets and bound to normal platelets at concentrations as low as 0.06 mg/ml. Antiplatelet IgG could be eluted from six of six hemophilic and eight of eight classic autoimmune thrombocytopenic patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Anti-Idiotypic↗
PubMed1990

Continuing controversy in alloimmune thrombocytopenia: fetal hyperimmunoglobulinemia fails to prevent thrombocytopenia.

Two patients with severe alloimmune thrombocytopenia were managed by weekly intrauterine platelet transfusions at 25 to 36 weeks. In one patient high-dose immunoglobulin was also administered weekly to the mother, and high maternal and fetal immunoglobulin levels were achieved. Fetal platelet counts were similar in both patients. The only variable that affected fetal platelet concentration was the posttransfusion platelet count from the previous transfusion.

Blood Transfusion, Intrauterine↗
PubMed1989

Thrombocytopenia following routine blood transfusion: micro-aggregate blood filters prevent worsening thrombocytopenia in patients with low platelet counts.

11 patients with anaemia and thrombocytopenia due to bone marrow failure each received 2 sets of red-cell transfusions. They were randomised to receive 1 blood transfusion through a standard 170-micron giving set filter and another through a 40 micron micro-aggregate filter. After transfusion, the mean fall in platelet count was 15 x 10(9)/l (41.7%) and 1.4 x 10(9)/l (4.6%), respectively (p less than 0.01). The results confirm the findings of a previous study which showed that micro-aggregate filters prevent a post-transfusional decrease in platelet counts. In addition, this new study shows that this is clinically relevant in patients who are thrombocytopenic at the time of their blood transfusion.

Anemia↗
PubMed1987

Measurement of platelet-associated IgG in animal models of immune and nonimmune thrombocytopenia.

Platelet-associated IgG (PAIgG) is elevated in idiopathic thrombocytopenic purpura (ITP), but it also is elevated in other thrombocytopenic disorders traditionally considered to be nonimmune. Consequently it is possible that elevated PAIgG is a nonspecific finding secondary to thrombocytopenia. To study this issue we developed a rabbit model of immune and nonimmune mediated thrombocytopenia. The mechanism of the thrombocytopenia was validated by platelet survival studies. Immune thrombocytopenia was produced by injection of antirabbit platelet serum that was raised in guinea pigs. Nonimmune aregenerative thrombocytopenia was produced by irradiation of the animals; nonimmune consumptive thrombocytopenia was produced by injection of adenosine diphosphate (ADP). PAIgG was measured in a direct binding assay using 125I-labeled staphylococcal protein A (SpA). Washed platelets from normal, nonthrombocytopenic rabbits bound an average of 81 molecules of SpA per platelet (81 +/- 168, mean +/- 2 SD, n = 39). Infusion of the antiplatelet antiserum produced thrombocytopenia with a rise in PAIgG that was closely correlated with the level of PAIgG (r = 0.86, n = 12). The thrombocytopenia was consumptive, as shown by a very short platelet life span using 111In-labeled platelets. In contrast, both nonimmune thrombocytopenic states resulted in an equal or greater drop in the platelet count but no change in the level of PAIgG. The animals with aregenerative thrombocytopenia had normal or only moderately reduced platelet life spans; however, in every animal the level of PAIgG was not different from the nonthrombocytopenic controls, irrespective of the platelet count. Similarly, the level of PAIgG was unchanged in those rabbits with nonimmune consumptive thrombocytopenia following infusion of ADP (82 +/- 55 molecules of SpA per platelet, mean +/- SD, n = 6). These studies indicate that elevated PAIgG is a specific finding of immune thrombocytopenia and is not secondary to thrombocytopenia itself. Indirectly these results support our hypothesis that immune mechanisms contribute to more thrombocytopenic disorders than was once thought likely.

Animals↗
PubMed1987

Regulation of thrombopoiesis: effects of the degree of thrombocytopenia on megakaryocyte ploidy and platelet volume.

We have established a murine model and techniques with which to serially study thrombocytopoiesis after induction of experimental immune thrombocytopenia of variable severity and duration. Bone marrow megakaryocyte ploidy distribution was determined by using unfractionated bone marrow, a polyclonal megakaryocyte-specific probe, and two-color, fluorescence-activated flow cytometry. With these techniques, the modal megakaryocyte ploidy class in normal murine bone marrow was 16N. Serial studies of bone marrow megakaryocyte ploidy after the induction of acute, severe thrombocytopenia (platelet count, less than 0.05 X 10(6) microL) demonstrated no detectable change in the ploidy distribution at 12, 24, and 36 hours after the onset of thrombocytopenia. At 48 hours, the modal ploidy class shifted from 16N to 32N, and the 64N class increased significantly (P less than .001). The ploidy distribution returned to normal 120 hours after the onset of thrombocytopenia. A lesser degree of thrombocytopenia (platelet count reduction to 0.100 to 0.200 X 10(6)/microL) delayed the modal ploidy class shift from 16N to 32N until 72 hours after the onset of thrombocytopenia. Chronic, severe thrombocytopenia (platelet count, less than 0.05 X 10(6)/microL for seven days) resulted in a modal ploidy class shift from 16N to 32N during the thrombocytopenic phase and an enhanced increase in the 64N megakaryocyte class during the recovery phase. Mean platelet volume (MPV) was simultaneously measured on isolated total platelet populations after induction of thrombocytopenia. MPV was significantly increased (P less than .001) as early as eight hours after the onset of acute, severe thrombocytopenia, 40 hours before a shift in the ploidy distribution. Mild thrombocytopenia (platelet count reduction to 0.400 X 10(6)/microL) was not associated with a ploidy shift but did result in a significantly increased MPV (P less than .001). These studies demonstrate that the temporal relationship and magnitude of the effects of thrombocytopenia upon megakaryocyte ploidy distribution are dependent upon the degree and the duration of the thrombocytopenic stimulus and that the effects of experimental thrombocytopenia on platelet volume and megakaryocyte ploidy are dissociated.

Acute Disease↗
PubMed1988

Incidentally detected thrombocytopenia in healthy mothers and their infants.

The unexpected discovery of thrombocytopenia in an asymptomatic pregnant woman--often considered to be equivalent to the diagnosis of idiopathic thrombocytopenic purpura--leads to a variety of interventions, including delivery by cesarean section. However, the actual risk to mothers and their infants posed by incidentally noted thrombocytopenia is not known. To investigate this issue, we performed a prospective study of a group of normal women who delivered at our medical center and their infants during a period of one year. Of the 2263 women who delivered during the year, 1357 were considered to be normal. One hundred twelve of the women (8.3 percent) had mild thrombocytopenia (range of platelet counts, 97 to 150 x 10(9) per liter). The thrombocytopenia had no discernible clinical effect on the women or their infants. The frequency of thrombocytopenia in babies born to this group of women was not appreciably different from that in babies born to the other normal patients who did not have thrombocytopenia, and none of the infants of women with thrombocytopenia had a platelet count of less than 100 x 10(9) per liter. This study demonstrates that the frequency of mild thrombocytopenia is high in normal pregnant women at term and that the thrombocytopenia appears to have no adverse effect on either the mothers or their infants. To perform obstetrical interventions such as cesarean section because of thrombocytopenia in these mothers is not justified.

Cesarean Section↗