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PubMed1986

[Post-transfusion thrombopenia treated with gammaglobulins].

Thrombopenia and a haemorrhagic syndrome occurring on the eighth postoperative day were probably related to a post-transfusion purpura, confirmed by the discovery of antiplatelet antibodies not belonging to the PLA1 antigen system. The stabilization of this haemorrhage and a full recovery were obtained by giving high doses of intravenous human gammaglobulins. Blood replacement only rarely induces postoperative immuno-allergologic thrombopenia; heparin is the best known causative agent. It is concluded that platelets should never be given so long as the responsible agent is not formally identified.

Diagnosis, Differential↗
PubMed1998

Coronary artery bypass grafting in a patient with type II heparin associated thrombopenia.

Two types of heparin-associated thrombopenia can be distinguished. Patients with the type II condition present a particularly difficult management problem when they require full anticoagulation. There is no consensus about the proper anticoagulation management for type II patients who have to undergo cardiopulmonary bypass. The case is reported of a type II heparin-associated thrombopenia patient who underwent successful aortocoronary saphenous vein grafting. Sodium-danaparoid was used for anticoagulation. The anti-factor Xa level was kept below the value reported in the literature for patients undergoing cardiopulmonary bypass. No fibrin formation was observed during the time of cardiopulmonary bypass, nor was any severe postoperative haemorrhage seen, as is frequently described in the literature.

Aged↗
PubMed1999

[Thrombopenia and acute renal insufficiency after treatment with streptokinase. Role of steroids].

Proteinuria is common after streptokinase treatment. An immunological mechanism in the renal glomerulus has been suggested to explain this side effect. However, thrombopenia and acute renal failure streptokinase induced are uncommon. We present a case of thrombopenia and acute renal failure after streptokinase administration for myocardial infarction that improved with steroid therapy. We discuss the probable pathophysiology of these adverse effects of streptokinase and the potential usefulness of steroids in its prevention and treatment.

Acute Kidney Injury↗
PubMed1979

[Thrombopenia and radial aplasia: 2 cases with platelet function and ultrastructural studies of megakaryocytes and platelets (author's transl)].

The authors report on two cases of congenital thrombopenia with radial aplasia. Both children display several formative abnormalities and a mild thrombopenia; hemorragic manifestations occurred in the first case only. Megacryoblastic to platelets series, as studied with electronic microscopy, show small-sized, "microcytic" and hypogranular megacaryocytes, displaying a maturative disorder (dysmegacaryocytopoiesis). In functional studies, platelets of the first patient show an imperfect nucleotidic release and do not agregate normally with ristocetin. The second case exhibits mostly a PF3 reduction. The variety of expression of the megacaryocytic-platelets disorders appears likewise in the squelettal and visceral malformations. The whole disorder could be ascribed to a pleiotropic abnormal gene with a variable expressivity.

Blood Platelets↗
PubMedDate not supplied

[Thrombopenia and radial aplasia: 2 cases with platelet function and ultrastructural studies of megakaryocytes and platelets (author's transl)].

The authors report on two cases of congenital thrombopenia with radial aplasia. Both children display several birth defects and a mild thrombopenia; hemorragic manifestations occured in the first case only. Megakaryoblastic to platelets series, as studied with electronic microscopy, show small-sized, "microcytic" and hypogranular megakaryocytes, displaying a maturative disorder (dysmegakaryocytopoiesis). In functional studies, platelets of the first patient show an imperfect nucleotidic release and do not agregate normally with ristocetin. The second case exhibits mostly a PF3 reduction. The variety of expression of the megakaryocytic-platelets disorders appears likewise in the skeletal and visceral malformations. The whole disorder could be ascribed to a pleiotropic abnormal gene with a variable expressivity.

Blood Platelets↗
PubMed1994

[Antiphospholipid antibodies in megakaryocytic thrombopenias].

We investigated the prevalence of antiphospholipid antibodies (APA) in megakaryocytic thrombopenias in order to establish their clinical significance and prognostic value. We studied 82 thrombopenic patients: 38 women and 44 men (age: 17-91 years). We assessed circulating lupus antibody (LA) through thromboplastin inhibition test (TIT), anticardiolipin antibodies (ACL) through ELISA and antiplatelet antibodies through flow cytometer. We conducted a statistical study RSIGMA, comparing patients with ACL + against ACL-. We found ACL positive in 21%, LA in 33% and antiplatelet antibodies in 42%. We observed a direct correlation (p < 0.05) between ACL and LA and between ACL and anticore antibodies, but not between ACL and antiplatelet antibodies. There was also a significant correlation between ACL and abortion, thrombosis and bleeding in thrombopenic patients. We conclude that APAs are present in 39% of the megakaryocytic thrombopenias and that they are not correlated with antiplatelet antibodies. Positivity of APA in thrombopenic patients is associated to poor prognosis and long term follow-up.

Adolescent↗
PubMed1977

[ABO compatibility and isoimmune neonatal thrombopenia].

25 families with serologically documented isoimmune neonatal thrombopenia were investigated for ABO-antigens of mother and child. In all cases mother and child were ABO-compatible. It is concluded that feto-maternal ABO-compatibility is a prerequisite for the development of isoimmune neonatal thrombopenia; hence, platelets must have ABO-antigens or be covered by soluble ABO-antigens.

ABO Blood-Group System↗
PubMed1998

Aortocoronary Vein Bypass in a Patient with Type II Heparin-Associated Thrombopenia: A Case Report

Two types of heparin-associated thrombopenia (HAT) can be distinguished. Patients with type II HAT (HAT II) present a particularly difficult management problem when they require full anticoagulation. There is no consensus about the proper anticoagulation management for patients with HAT II who have to undergo cardiopulmonary bypass (CPB). We present a HAT II patient who underwent successful aortocoronary saphenous vein grafting. Sodium-danaparoid (SD) was used for anticoagulation. The anti-factor Xa level was kept below the values reported in the literature for patients undergoing CPB. We did not observe any fibrin formation during the time of CPB or any severe postoperative hemorrhage, which is frequently described in the literature. We discuss the management of our patient with SD intra- and postoperatively.

Journal Article↗
PubMed2001

[Postoperative heparin-induced thrombopenia with thromboembolism (HITT)--a rare complication of heparin therapy?].

Many surgical patients receive either unfractionated or low-molecular weight heparin in a prophylactic or therapeutic intention. Feared upon the administration of heparin is the heparin-induced thrombopenia (HIT). In HIT type 1, the heparin directly interacts with the platelets. The platelet count rarely falls below 100,000/microliter and normalizes again despite continuous administration of heparin. In HIT type 2 or HIT with thrombosis (HITT) the platelet count usually falls more than 50% and due to an antibody-dependent platelet activation, thromboembolic episodes may occur. Compared to non-surgical patients, the incidence of HITT in the postoperative phase is markedly increased. In suspicion of a HITT, heparins should immediately be stopped and replaced by an alternative coagulant because of a high risk of further thromboembolic complications. Direct thrombin-inhibitors such as the recombinant hirudins are considered to be safe and effective. They have no heparin-like immunological properties and therefore, they seem to become the therapeutic and prophylactic "gold-standard" in patients with HITT.

Heparin↗
PubMed1987

[Heparin-induced thrombopenia].

Cutaneous necroses, acute renal failure and an adrenocortical insufficiency appeared during heparin therapy in a 47 year old patient with myocardial infarction. The thrombocytes fell to 73,000/microliter and displayed intensified spontaneous aggregation. In histological investigation of the cutaneous necroses, intensive thromboses of the cutaneous and subcutaneous blood vessels were found. The findings indicate a thromboembolic etiology of the acute renal failure and the adrenocortical insufficiency. This case involves a complex example of a heparin-induced thrombopenia with thromboembolic complications.

Acute Kidney Injury↗
PubMedDate not supplied

Fusiform coronary aneurysm in the left circumflex artery with recurrent myocardial infarction and idiopathic thrombopenia.

The authors describe the rare case of a patient with fusiform coronary aneurysm with myocardial infarction in the left circumflex artery complicated by idiopathic thrombopenia. Medical treatment with a combination of warfarin and aspirin could not prevent recurrence of angina pectoris and myocardial infarction, but surgical ligation of the proximal site of the fusiform aneurysm and coronary bypass to the distal site of the fusiform aneurysm prevented further myocardial infarction and angina pectoris.

Coronary Aneurysm↗
PubMed2004

A case of refractory bullous pemphigoid with plasmapheresis-associated thrombopenia: efficacy of pulsed intravenous cyclophosphamide therapy.

We present a 69-year-old woman with refractory bullous pemphigoid successfully treated with pulsed intravenous cyclophosphamide therapy. Because various other early treatments including 4,4'-diaminodiphenylsulphone (DDS), minocycline/nicotinamide, cyclosporin, azathioprine, high-dose oral prednisolone, and methylprednisolone pulse therapy were either ineffective or intolerable, she was treated with double filtration plasmapheresis, but she responded poorly with the rare complication of severe transient thrombopenia. Finally, she gradually recovered with pulsed intravenous cyclophosphamide therapy.

Aged↗
PubMed1991

[Therapy of immune thrombopenia].

Idiopathic thrombocytopenic purpura (ITP) belongs to the family of autoimmune diseases. The term "idiopathic", however, is no longer correct as it is in fact an immunologically-related thrombocytopenia. This is why nowadays it is referred to as immune thrombopenia. Clinically the acute and chronic forms of ITP can be distinguished. We discuss the different forms of treatment based upon data provided by various studies of ITP. If treatment with prednisone or with gammaglobulins fails, or after unsuccessful splenectomy, then alternative experimental therapies may have to be used. Some of these treatments are described with reference to their therapeutic benefit and their function.

Acute Disease↗
PubMedDate not supplied

[Upper extremity abnormalities, thrombopenia and thrombopathy. 3 cases].

Three cases of congenital radial aplasia and amegakaryocytic thrombopenia are discussed from clinical, genetic and hematological viewpoints. Electron microscope studies of the megakaryocytes in the first two patients revealed the presence of microcytic, immature and hypogranular cells. Platelet aggregability studies in the first patient demonstrated the presence of pathological intra-platelet nucleotide release as well as membrane abnormalities of the Willebrand factor binding site. The second case presented an isolated deficiency in platelet factor 3.

Abnormalities, Multiple↗