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At least 19 recordsLinked to original sources
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↗
PubMed1975

Protective effect of pantethine on experimental thrombocytopenia in the rat.

The effects of pantethine on circulating platelet counts and platelet functions were studied in normal and experimentally produced thrombocytopenic rats. Administration of pantethine to normal animals did not cause any alterations in both platelet count and function except for a slight enhancement of intravascular platelet aggregation induced by collagen or neuramindase. Injection of anti-rat platelet rabbit serum into rats resulted in acute thrombocytopenia. Administration of pantethine prior to the antiserum promoted recovery from the thrombocytopenia in a dose dependent manner, but administration of the drug after development of the thrombocytopenia was not effective. A similar result was obtained with a transietnt thrombocytopenia induced by exchange transfusion with platelet poor blood. Regardless of whether animals were treated with pantethine or not, the platelets newly generated during the course of recovery from thrombocytopenia were essentially normal in the function tested in vitro. A more chronic thrombocytopenia induced by repeated injections of the antiserum was prevented, to some significant degree, by daily administration of pantethine throughout the experimental period. In contrast to these, such effect of pantethine was not observed with the thrombocytopenia models produced bynitrogen mustard N-oxide and neuraminidase. These findings were idscussed in relation to mechanism of the action of pantethine and to possible clinical application to the drug to thrombocytopenia.

Animals↗
PubMed1979

Heparin-associated thrombocytopenia: low frequency in 104 patients treated with heparin of intestinal mucosal origin.

A prospective study of 104 patients receiving heparin obtained from porcine intestinal mucosa for 4 or more days was conducted to determine the frequency of associated significant thrombocytopenia (platelet count less than 100 x 10(9)/I on 2 consecutive days). No episodes of significant thrombocytopenia were identified in the 13 patients receiving heparin by continuous intravenous infusion for a mean of 8.0 days or in the 38 patients receiving heparin subcutaneously for a mean of 9.9 days. In 1 of the 26 patients receiving heparin as intermittent intravenous boluses for a mean of 8.2 days significant thrombocytopenia developed; this patient had laboratory evidence of disseminated intravascular coagulation. In none of the 17 patients receiving uninterrupted heparin therapy for 4 or more days by more than one route of administration but for less than 4 days by any single route did significant heparin-associated thrombocytopenia develop. Of the 104 patients 13 had one or more platelet counts of less than 150 x 10(9)/I, but in most it was not possible to definitely relate the thrombocytopenia to the heparin therapy. Platelets in normal platelet-rich plasma did not aggregate when heparin and serum from patients with thrombocytopenia were added. The frequency of heparin-associated thrombocytopenia noted in this study was considerably lower than that reported previously.

Aged↗
PubMed1979

Elevated platelet-associated IgG in the thrombocytopenia of septicemia.

The mechanism of thrombocytopenia, a frequent complication of septicemia, is obscure, but indirect evidence suggests that the immune system may be involved. To investigate this possibility, we quantitated platelet-associated IgG on platelets obtained from 44 patients during 46 episodes of septicemia. Thrombocytopenia occurred in 21 of 46 episodes (46 per cent). Platelet-associated IgG was elevated in eight of 11 episodes of gram-negative septicemia and thrombocytopenia (47.3 +/- 11.7 fg of IgG per platelet [mean +/- S.E.]) and in one of 20 patients with gram-negative septicemia and normal platelet counts (5.9 +/- 1.1) (P less than 0.001). Elevated levels occurred in eight of 10 patients with gram-positive septicemia and thrombocytopenia (55.3 +/- 14.7 fg of IgG per platelet) and in none of 11 patients with gram-positive septicemia and normal platelet counts (5.6 +/- 1.7) (P less than 0.001). Serial testing during the thrombocytopenia and recovery showed an inverse relation between the platelet count and platelet-associated IgG. Thrombocytopenia in some patients with septicemia may be related to the binding of IgG to platelets.

Adult↗
PubMed1979

Heparin-induced thrombocytopenia: association with a platelet aggregating factor and arterial thromboses.

Eleven patients with heparin-induced thrombocytopenia were studied. Thrombocytopenia appeared 3-16 days following the initiation of prophylactic or therapeutic doses of heparin. The mean lowest platelet count recorded was 48,000/mm3. When heparin was stopped, recovery from thrombocytopenia began within 24 hours and was complete by ten days. Two patients developed fatal thromboses, and two others had myocardial infarctions while thrombo-cytopenic. In the serum of seven patients, including three of the four with arterial thrombosis, a heparin-dependent platelet aggregating factor was present. The factor caused release of platelet 14C serotonin but did not lyse platelets. It was present in the globulin fraction of all positive sera, and in one serum studied it was isolated in the IgG/IgA immunoglobulin fraction. The factor was not present in 16 normal sera or in the sera of 15 nonthrombocytopenic patients receiving heparin. Our observations suggest that heparin-induced thrombocytopenia is common and that, in some patients it may be accompanied by severe arterial thrombosis. In vivo platelet aggregation is a possible explanation for the thrombocytopenia and the thrombosis in this disorder.

Aged↗
PubMed1979

Differential effects of prostacyclin and prostaglandin E1 on bronchoconstriction and thrombocytopenia during collagen and arachidonate infusions and anaphylactic shock in the guinea-pig.

The antagonism by prostacyclin (PG12) and prostaglandin E1 (PGE1) of bronchoconstriction induced by serotonin (5HT), collagen, arachidonic acid (AA) and anaphylaxis, as well as of thrombocytopenia was studied in the guinea-pig. Under conditions where PGE1 prevented bronchoconstriction by 5HT, by collagen or by AA better than the accompanying thrombocytopenia, PG12 was a selective antagonist of bronchoconstriction due to collagen, but failed to interfere with that due to 5HT or to AA. Collagen-induced bronchoconstriction in the guinea-pig is platelet-dependent. PG12 blocks bronchoconstriction by collagen, because it prevents the platelet activation, and fails to interfere with bronchoconstriction by AA, even though it reduces the accompanying thrombocytopenia, because the role of platelets is negligible. PGE1 and PG12 failed to interfere with thrombocytopenia or with bronchoconstriction of anaphylactic shock, and were inactive even when the acute bronchial effect was suppressed by anti-histamine treatment. Anaphylactic thrombocytopenia is beyond the control of agents which stimulate the cyclic AMP system, and involves specific mechanism which are not stimulated in platelet-rich plasma.

Anaphylaxis↗
PubMed1978

Heparin-induced thrombocytopenia.

Two patients with underlying thromboembolic disorders developed severe thrombocytopenia while receiving heparin sodium; one of these patients developed recurrence of the thrombocytopenia and possible heparin-induced pulmonary emboli when heparin was restarted. In a prospective study of patients receiving heparin in a coronary care unit (CCU), nine of 37 patients developed transient mild thrombocytopenia (platelet counts ranging from 88,000 to 150,000/cu mm). Heparin added to citrated platelet-rich plasma caused platelet aggregation in the two original patients. In three of six CCU patients tested, and in 17 of 87 other subjects, with maximum aggregation at concentrations of heparin likely to be present in vivo during therapy. We herein discuss evidence that suggests that heparin may cause or aggravate thrombosis by causing platelet aggregation. The occurrence of severe heparin-induced thrombocytopenia is well documented, and mild transient thrombocytopenia may be more common than has been recognized. Studies of heparin efficacy should take these responses into account.

Dose-Response Relationship, Drug↗
PubMed1977

Induction of thrombocytopenia by thrombopheresis in man: patterns of recovery in normal subjects during ethanol ingestion and abstinence.

Using the technique of thrombophoresis (TP), platelet and megakaryocyte dynamics following acute thrombocytopenia were studied in two normal subjects during periods of ethanol ingestion and abstinence. Thrombocytopenia was induced over a period of 12 hr. A logarithmic decline in platelet count during TP and the serial morphologic changes in megakaryocytes during recovery from thrombocytopenia are described. Although these parameters were not affected by ethanol ingestion, platelet counts after TP did not return to normal until ethanol was discontinued. 51Cr-labeled platelet survival was normal in one subject studied, and no evidence of increased platelet sequestration was found. It is concluded that heavy ethanol ingestion induces, augments, or sustains thrombocytopenia by impairing megakaryocytopoiesis in man. The mechanism by which ethanol induces thrombocytopenia may be due, in part, to "ineffective thrombopoiesis," impairment of the differentiation of precursor cells into the megakaryocytic compartment, or a combination of these factors.

Adult↗
PubMed1978

Thrombocytopenia in polycythemic mice.

Significant and sustained thrombocytopenia in mice maintained in a polycythemic state with weekly injections of washed packed RBCs prompted the examination of the relationship between the observed thrombocytopenia and the polycythemic state. Platelet production was determined by measurement of 75SeM incorporation into platelets. Platelet survival was studied with 51Cr-labeled platelets. Platelet sequestration was assessed by measuring the trapped platelet 51Cr-bound radioactivity in the spleens of these animals. Blood volume was calculated by measuring the dilution of injected 59Fe-tagged RBCs. These studies failed to reveal decreased platelet production, a shortening of the platelet survival, or significant splenic pooling as factors contributing to the observed thrombocytopenia. The blood volumes in the polycythemic group of animals were 8.9% +/- 0.15 (1 S.D.) body weight vs. 6.4% +/- 0.69 in the normals (p less than 0.001). Contrary to what has been reported for hypoxia-induced polycythemia, our results indicate that transfusion-induced polycythemia does not cause thrombocytopenia by decreasing platelet production. We suggest instead that the observed thrombocytopenia is mainly due to dilution of the circulating platelet mass by the expanded blood volume.

Animals↗
PubMed2026

Recombinant Human Thrombopoietin Reduces the Need for Platelet Transfusion in Patients With Chronic Liver Disease and Thrombocytopenia.

Chronic liver disease (CLD)-related thrombocytopenia can limit the feasibility of invasive procedures. Recombinant human thrombopoietin (rhTPO) has demonstrated a favorable safety profile without hepatotoxicity. We evaluated the efficacy and safety of rhTPO in patients with CLD-related thrombocytopenia who were undergoing elective invasive procedures. In this multicenter, randomized (2:1), double-blind, placebo-controlled phase III trial, 120 adult Chinese patients with CLD-related thrombocytopenia (platelet count <&#x2009;50 &#xd7;&#x2009;109/L) received rhTPO (n =&#x2009;80) or placebo (n =&#x2009;40) once daily for up to 5 or 7&#x2009;days. The primary endpoint was the proportion of patients with sustained platelet counts &#x2265;&#x2009;50 &#xd7;&#x2009;109/L from 24 h before invasive procedure to 7&#x2009;days post-procedure, without requiring emergency bleeding management. The primary endpoint was achieved by 85.0% of patients in the rhTPO group versus 12.5% in the placebo group (p&#x2009;<&#x2009;0.0001). Preoperatively, platelet counts &#x2265;&#x2009;50 &#xd7;&#x2009;109/L were achieved in 92.5% and 20.0% of patients in the rhTPO and placebo groups, respectively (p&#x2009;<&#x2009;0.0001). Platelet transfusion was avoided in 92.5% of rhTPO-treated patients versus 25.0% of placebo-treated patients (p&#x2009;<&#x2009;0.0001). The median duration of platelet counts &#x2265;&#x2009;50 &#xd7;&#x2009;109/L was significantly longer with rhTPO than with placebo (21.0 vs. 3.0&#x2009;days, p =&#x2009;0.0007). Treatment-related treatment-emergent adverse events (TEAEs) occurred in 12.5% of patients in both the rhTPO and placebo groups. No treatment-related serious adverse events were reported. Overall, rhTPO was effective and well tolerated in patients with CLD-related thrombocytopenia and may represent a viable therapeutic option for those undergoing elective invasive procedures. Trial Registration: www.chinadrugtrials.org.cn: number CTR20230919.

Humans↗
PubMed2025

Clinical characteristic of isolated thrombocytopenia in patients with bone marrow failure-related germline variants: a retrospective study from a single centre.

BACKGROUND: Immune thrombocytopenia (ITP) comprises the majority of thrombocytopenia. Some patients respond poorly to first-line ITP therapy or develop pancytopenia years later. Recent studies link heterozygous germline variants in acquired aplastic anemia (AA), yet their role in isolated thrombocytopenia carrying bone marrow failure-related germline variants (ITGV-BMFs) remains unclear. While whole-exome sequencing (WES) detects these variants, its cost limits routine use. This study compares prognosis and clinical features of isolated thrombocytopenia in patients with ITGV-BMFsand those with classic ITP. METHODS: The clinical data of patients diagnosed with ITGV-BMFs were retrospectively analyzed and compared with those of patients with classic ITP from August 2018 to February 2024. The baseline characteristics, genomic systematically background, previous treatment response as well as their follow-up outcomes were compared. RESULTS: Patients with ITGV-BMFs demonstrated earlier onset age (p&#x2009;<&#x2009;0.001), lower bleeding scores and CD34%, along with elevated mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), and reticulocyte (RET) counts (p&#x2009;<&#x2009;0.001). Multivariate logistic regression analysis showed that the patients with ITGV-BMFs may possess distinct characteristics, including an earlier age at onset (p&#x2009;=&#x2009;0.014) and lower bleeding score (p&#x2009;=&#x2009;0.048). Notably, MCV and RET showed promising performance in receiver operating characteristic (ROC) curve analysis. During the follow-up period, 57.69% (15/26) ITGV-BMFs patients were further confirmed as aplastic anemia (AA, n&#x2009;=&#x2009;13) or myelodysplastic syndrome (MDS, n&#x2009;=&#x2009;2), with a median progression-free survival (PFS) of 7.25&#x2009;years (p&#x2009;<&#x2009;0.0001). CONCLUSION: ITGV-BMFs may be diagnosed early using elevated MCV and reticulocyte counts, a diagnostic approach that may lead to earlier intervention and improved prognosis.

Humans↗
PubMed1977

Amelioration of endothelial abnormalities by prednisone in experimental thrombocytopenia in the rabbit.

Experimental thrombocytopenia results in endothelial alterations associated with bleeding. In this study prednisone was shown to prevent or reverse these changes, which supports the clinical inference that adrenocorticosteroids decrease capillary fragility in thrombocytopenia. Rabbits (3-4 kg), intraperitoneally injected with busulfan, developed 98-99% reductions in platelet count and hemorrhaged profusely. Orally administered prednisone (0.2 mg/kg or 1.0 mg/kg daily) reduced bleeding despite persistent thrombocytopenia. Tongue biopsies obtained after 3 days of prednisone treatment were examined by electron microscopy. Normal rabbits served as controls. 25 consecutive capillaries or venules from each of four animals in the control group and each of five experimental groups were examined for fenestrations, "thin spots" (<800 A thick), and mean wall thickness as determined by planimetry. Vessels from control animals had no thin spots or fenestrations, and the mean vessel wall thickness was 4,254+/-105 A SEM. The 100 vessels from the thrombocytopenic animals had a mean vessel wall thickness of 2,081+/-218 A (P < 0.001), and 42 had thin spots of fenestrations. After administration of the smaller dosage of prednisone, the mean vessel wall thickness increased to 3,556+/-40 A (P < 0.001), and only nine vessels had thin spots or fenestrations. With the larger dosage, only six vessels had thin spots or fenestrations and the mean vessel wall thickness of this group increased to 3,704+/-206 A (P < 0.005). All preparations demonstrated normal endothelial junctions. The data are consistent with the hypothesis that the bleeding of thrombocytopenia is caused by altered capillary and venule endothelium and that diminished bleeding observed with prednisone administration results from amelioration of these endothelial changes.

Animals↗
PubMed1975

Platelet recovery after induction of acute thrombocytopenia.

After mild thrombocytopenia (about 50-100% of control platelet level), induced by injection of antiplatelet serum (APS), platelets increased at a fairly constant and moderate rate for about 4 days and reached a maximum count, greater than pretreatment levels, on the fifth day. After moderate to severe thrombocytopenia, an early moderate rate of platelet increase was succeeded within 2 days by a second more rapid rate that persisted for about 3 days. The maximum overshoot of the platelet count was usually less than twice the pretreatment level. After the largest doses of APS, the platelet count remained depressed for several days. Platelet response after acute thrombocytopenia induced with antiserum is therefore variable, depending on the level and duration of thrombocytopenia.

Acute Disease↗
PubMed1975

Thrombocytopenia in trypanosomiasis.

In all of four patients with African trypanosomiasis, thrombocytopenia was present on admission to hospital or developed during the course of the illness. One patient with severe thrombocytopenia died following gastrointestinal haemorrhage shortly after admission to hospital. Kinetic studies in the other three patients showed marked pooling of platelets in the spleen in all, but severe shortening of platelet life-span in only one. Evidence of disseminated intravascular coagulation (DIC) was found in 3 patients, 2 of whom received heparin therapy. These findings provide evidence that thrombocytopenia is a feature of African trypanosomiasis and is due mainly to hypertrophy of the reticuloendothelial system which accompanies the infection. In some patients immune damage to platelets or platelet consumption as part of DIC may be an additional factor contributing to the thrombocytopenia.

Adult↗
PubMed1976

The influence of selective thrombocytopenia on nephrotoxic nephritis.

Anticoagulation with agents that interfere with fibrin formation inhibit the development of the autologous phase of nephrotoxic nephritis (NTN). Platelet participation in the nephritic process has been suggested but not proved, therefore, the influence of selective thrombocytopenia on the autologous phase in rabbits was evaluated. NTN was produced with goat antirabbit glomerular basement membrane antiserum. Thrombocytopenia was induced with goat antirabbit platelet antiserum 24 hours prior to the onset of nephritis. Platelet accumulation within the nephritic kidney was quantitated using chromium labeled platelets. Thrombocytopenia has no inhibitory effect on the development of the autologous phase of NTN in rabbits. There was no platelet accumulation within the nephritic kidney in the presence of thrombocytopenia. Pharmacologic inhibition of platelet aggregation may be of no benefit in glomerulonephritis produced by a fixed antigen-antibody reaction within the glomerular capillary wall.

Animals↗