Disease relevance of Thrombocytopenia

• The Wiskott-Aldrich Syndrome (WAS) is a rare X-linked primary immunodeficiency that is characterized by recurrent infections, hematopoietic malignancies, eczema, and thrombocytopenia [1].
• Heparin-induced thrombocytopenia and thrombosis [2].
• Trimetrexate therapy had minimal toxicity; transient neutropenia or thrombocytopenia occurred in 12 patients and mild elevation of serum aminotransferases in 4 [3].
• Quinidine leukopenia and thrombocytopenia with a drug-dependent leukoagglutinin [4].
• We studied five patients in whom severe thrombocytopenia developed during intermittent intravenous heparin treatment of arterial and venous thrombosis [5].

Psychiatry related information on Thrombocytopenia

• The patients suffer from severe mental retardation and have a bleeding tendency with mild thrombocytopenia, and their fibroblasts show increased PACAP mRNA levels [6].
• Transient global amnesia associated with acute heparin-induced thrombocytopenia [7].
• BACKGROUND: To evaluate whether valproic acid (VPA) can cause thrombocytopenia and impaired platelet function in young patients with new-onset bipolar disorder [8].
• The use of filgrastim with increasing doses of chemotherapy prevents neutropenia, but other toxicities, namely thrombocytopenia and lethargy, then become dose limiting [9].
• MAOI causing thrombocytopenia is reviewed and the prescription of tranylcypromine to patients with previous substance abuse is discussed [10].

High impact information on Thrombocytopenia

• Many WAS mutations impair cytoskeletal control in hematopoietic tissues, resulting in functional and developmental defects that define the X-linked Wiskott-Aldrich syndrome (WAS) and the related X-linked thrombocytopenia (XLT) [11].
• Heparin-induced thrombocytopenia [12].
• There were no significant differences in the rates of major bleeding complications or transfusions, but tirofiban was associated with a lower rate of minor bleeding episodes and thrombocytopenia [13].
• Familial dyserythropoietic anaemia and thrombocytopenia due to an inherited mutation in GATA1 [14].
• Here we describe a family with X-linked dyserythropoietic anaemia and thrombocytopenia due to a substitution of methionine for valine at amino acid 205 of GATA-1 [14].

Chemical compound and disease context of Thrombocytopenia

• In contrast, 5 of the 15 patients given one of the two higher doses of interleukin-1 alpha after carboplatin had minimal thrombocytopenia (nadir, 91,000 to 332,000 platelets per cubic millimeter) [15].
• We related the plasma concentration of glycocalicin, a fragment of the platelet-membrane glycoprotein Ib, to the mechanism of thrombocytopenia by evaluating bone marrow megakaryocyte content and measuring platelet life span [16].
• More on zidovudine and HIV-related thrombocytopenia [17].
• Platelets from these three patients had increased levels of IgG and C3, which correlated with the presence of thrombocytopenia; their plasma caused the release of serotonin from normal platelets at concentrations of heparin within the usual therapeutic range [18].
• High-dose pulsed dexamethasone for immune thrombocytopenia [19].
• Because of its high sensitivity, we believe the PF4 ENHANCED enzyme-linked immunosorbent assay should be used to identify heparin-induced thrombocytopenia in patients with multiple potential causes of thrombocytopenia, although false-positive results will not be uncommon [20].
• Several promising novel agents that stimulate TPO and increase platelet levels, such as the oral platelet growth factor eltrombopag, are currently in development for the prevention and/or treatment of thrombocytopenia [21].

Biological context of Thrombocytopenia

• We conclude that intravenous gamma globulin, with or without dexamethasone, is effective in elevating the fetal platelet count in severe cases of neonatal alloimmune thrombocytopenia and in helping to avoid intracranial hemorrhage [22].
• In striking contrast to normal subjects, at moderately high altitude (3,100 m) the high affinity subjects manifested: (a) lesser increments in resting heart rate; (b) minimal increases in plasma and urinary erythropoietin; (c) no decrement in maximal oxygen consumption; and (d) no thrombocytopenia [23].
• These findings suggest that the mechanism of the severe thrombocytopenia secondary to heparin therapy is immunological and the associated thromboembolic complications may be attributed to in-vivo activation of the platelet prostaglandin pathway and platelet aggregation induced by the heparin-dependent antibody [24].
• We report on a breastfeeding woman with deep venous thrombosis treated with hirudin because of heparin-induced thrombocytopenia, in whom hirudin was not detectable in human breastmilk [25].
• Compared with controls, patients with delayed-onset heparin-induced thrombocytopenia had higher titers of IgG antibodies to platelet factor 4-heparin and greater IgG-induced heparin-dependent and heparin-independent platelet activation [26].

Anatomical context of Thrombocytopenia

• Immune endothelial-cell injury in heparin-associated thrombocytopenia [27].
• Study of the factors that cause specific transformation in cultures of lymphocytes from patients with quinine- and quinidine-induced immune thrombocytopenia [28].
• Diagnosis of this potentially fatal complication may be delayed or missed if renal tissue or the peripheral blood smear is not examined, because renal failure may be ascribed to cisplatin nephrotoxicity and the anemia and thrombocytopenia to drug-induced bone marrow suppression [29].
• After 6 Gy TBI, a dose of 0.3 microgram TPO/mouse (12 microgram/kg) intraperitoneally (IP), 0 to 4 hours after TBI, prevented the severe thrombopenia observed in control mice, and in addition stimulated red and white blood cell regeneration [30].
• In six hepsulfam-only control animals thrombocytopenia (platelet count < 100 x 10(9)/L) was observed between days 12 and 25 (nadir 39 +/- 20 x 10(9)/L on day 17), and neutropenia (absolute neutrophil count < 1 x 10(9)/L) occurred between days 8 and 30 (nadir 0.167 +/- 0.120 x 10(9)/L on day 15) [31].

Gene context of Thrombocytopenia

• Thiamine-responsive megaloblastic anaemia syndrome (TRMA; MIM 249270) is an autosomal recessive disorder with features that include megaloblastic anaemia, mild thrombocytopenia and leucopenia, sensorineural deafness and diabetes mellitus [32].
• Amegakaryocytic thrombocytopenia and radio-ulnar synostosis are associated with HOXA11 mutation [33].
• SDF-1 and FGF-4 diminished thrombocytopenia after myelosuppression [34].
• Thrombocytopenia in c-mpl-deficient mice [35].
• Introduction of the genetic background CASA/Rk (a mouse strain with elevated plasma vWF) resulted in the appearance of spontaneous thrombocytopenia in a subset of ADAMTS13-deficient mice and significantly decreased survival [36].

Analytical, diagnostic and therapeutic context of Thrombocytopenia

• Heparin-induced thrombocytopenia and cardiopulmonary bypass [37].
• Splenectomy in the management of the thrombocytopenia of the Wiskott-Aldrich syndrome [38].
• Aminocaproic acid has proved to be a valuable agent in the management of patients with amegakaryocytic thrombocytopenia, especially in decreasing the need for platelet transfusions [39].
• Unexpectedly, the incidence of grades 3 and 4 thrombocytopenia was much greater in patients who received prechemotherapy G-CSF compared with those who did not (54% versus 6%, respectively, over all chemotherapy cycles; two-sided P, adjusted for dose < .001) [40].
• Prostacyclin, either alone or with heparin, abolished microembolisation from the dialyser (as estimated by whole-blood screen filtration pressure) and prevented thrombocytopenia [41].

References