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At least 19 recordsLinked to original sources
PubMed1998

[Heparin-induced thrombopenia: rapid regression of thrombopenia and thrombosis after plasma exchange. Case report].

INTRODUCTION: Heparin-induced thrombocytopenia with thrombosis is a rare but severe adverse reaction to heparin therapy, whose management is difficult. After heparin withdrawal, the initiation of an alternative anticoagulant therapy, such as recombinant hirudin or danaparoid, is strongly recommended before vitamin K antagonists are effective. Several reports of the efficacity of plasma exchanges in patients with life-threatening thrombosis have been made. EXEGESIS: We report on a patient with severe aortic thrombosis related to heparin therapy in whom a unique plasma exchange resulted in both dramatic improvement in the platelet count and marked reduction of the thrombosis. CONCLUSION: This case provides further evidence that plasma exchanges can be useful in the management of heparin-induced thrombocytopenia with thrombosis. They are rapidly efficient and can be used before heparin alternative treatment is effective.

Anticoagulants↗
PubMed1985

[Biological diagnosis of postoperative thrombopenia].

The recognition of the postoperative thrombopenia is important because thrombopenia give an hemorrhage risk and modify the tolerance to preventive anticoagulant treatments. Some thrombopenias can be iatrogenic: thrombopenias by transfusion of a large volume of preserved blood, or by hemodilution, but require a substitution, therapy are easily diagnosed. Post-transfusional thrombopenias require an antibody analysis (especially for antiPLA1). The search for drugs interactions is often complex; heparin induced thrombopenia constitutes a severe but fortunately a rare complication of the heparin therapy. Other thrombopenias are related to operative complications this is the case of consumption-coagulopathies due to infections, the release of thromboplastin from tissues, hepatic cirrhosis, pancreatitis, etc. The evaluation of hemostasis verifies clinical hypotheses and guides the treatment. Thrombopenias can be due to various disorders revealed or occurring during an operation. Although the concurrences are rare, they do not always preclude the possibility of finding a collagen disease (connectivitis), a thrombocytogenetic thrombotic purpura, and especially an idiopathic thrombopenic purpura. In any case, diagnosis is easier if the preoperative platelet levels are known. Thus, platelet counts should be included in pre and postoperative evaluations.

Antigen-Antibody Complex↗
PubMed1982

[Thrombopenia caused by heparin. Review of the literature apropos of a personal case].

Following operation for bladder papilloma and subcutaneous heparin therapy, a patient developed severe thrombopenia with biological signs of disseminated intravascular coagulation (D. I. C.). Heparin therapy was discontinued and the platelet count became normal, no further signs of (D. I. C.) being apparent. Histological examination of the excised tumor showed that it was non-malignant, the thrombopenia being directly related to the heparin treatment. A review of the published literature demonstrated variations in the frequency of this complication reported, with an apparently higher incidence in the USA than in France. This could possibly depend upon whether the heparin was prepared from pulmonary or intestinal tissue. The thrombopenia may be severe (platelet count less than 100,000/mm3) with resulting hemorrhages or more commonly thromboses, or moderate without clinical expression. The dose or mode of administration of the heparin does not appear to be a factor in the development of the thrombopenia, its mechanism not being clearly elucidated. From the practical point of view, a platelet count should be performed before heparin treatment, and this should be repeated if the treatment is continued for more than four days.

Aged↗
PubMed1987

FcR-mediated clearance in thrombopenic and non-thrombopenic patients with hemophilia A and possible relation of thrombopenia to HIV seropositivity.

As morbidity of thrombopenia in hemophilia A patients is increasing, the pathogenetic influence of the reticuloendothelial system (RES) was measured using autologous anti-Rh0(D)-coated erythrocytes (EA) in 17 patients with or without thrombopenia. Mean survival of EA in patients was reduced to 53% of healthy controls (53.2 +/- 46.1 min vs 100.5 +/- 12.2 min; patients vs controls, mean +/- S.D.). Survival of EA was not significantly different either in thrombopenic vs non-thrombopenic nor anti-HIV (human immunodeficiency virus) positive vs negative patients. Thrombopenia, elevated serum IgG and circulating immune complexes were related to the presence of anti-HIV antibodies. EA survival was also decreased in the absence of anti-HIV antibodies. This indicates activation of RES by a mechanism different from retroviral infection by HIV (1).

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

[Acute adrenal insufficiency due to bilateral adrenal hematoma following severe thrombopenia induced by low-molecular-weight heparin].

BACKGROUND: Bilateral adrenal hematoma is an uncommon cause of acute adrenal insufficiency. An association with thrombopenia induced by low-molecular-weight heparin even more so. Diagnosis is difficult as the clinical manifestations mimic septic shock. CASE REPORT: A 63-year-old woman developed acute adrenal insufficiency due to bilateral adrenal hematoma following severe thrombopenia induced by low-molecular-weight heparin prescribed after an orthopedic operation. Outcome was favorable. CONCLUSION: Acute adrenal insufficiency must be entertained as a possible diagnosis in patients with heparin-induced thrombopenia.

Acute Disease↗
PubMed1987

[Thrombopenia caused by pentosan polysulfate].

Two case-reports of thrombopenias induced by pentosane polysulfate (PSP) are reported. PSP may play a direct role in the genesis of the thrombopenia appearing between the 5th and 15th day of treatment, or a sensitizing role where the thrombopenia occurs quite rapidly following heparin treatment. The clinical complications are haematomas, arterial or venous thromboses and haemorrhages. The platelet aggregation test is always positive in the presence of PSP. The immunological origin is probable. Monitoring of the platelet count is recommanded with this treatment.

Aged↗
PubMed1988

[Myocardial infarct complicating thrombopenia induced by pentosan polysulfate].

The authors report a case of thrombopenia induced by pentosane polysulfate (PSP), complicated by a myocardial infarction. Biological tests showed a platelet pro-aggregating effect of PSP and an IgG immunoglobulin fixed to the platelets. A review of the literature shows that PSP-induced thrombopenias must be known as well as those induced by heparins and that they have similar complications. The thrombopenia may persist with an inappropriate substitution with heparin and the clinical picture may be aggravated. It is desirable to carry out systematic screening for a cross-allergy and prevent it by using anti-vitamin K.

Female↗
PubMed1988

[Thrombopenia induced by heparin in orthopedic surgery. Apropos of 12 cases].

Treatment with heparin for the prevention of thrombosis in orthopaedic surgery may sometimes be responsible for thrombopenia. This can be associated with arterial or venous thrombotic complications. Twelve cases of heparin-induced thrombopenia are reported here. Three cases were demonstrated by a diminution of the platelet count which reversed when heparin treatment was discontinued. Nine patients presented with arterial and/or venous thromboses whose progress was favourable in the long term. The replacement of heparin treatment by anti-vitamin K from the 5th or 6th day can avoid the thrombotic complications of heparin-induced thrombopenia.

Adult↗
PubMed1985

[Digitoxin-induced thrombopenia with recurrence after accidental reexposure].

One case of digitoxin-induced thrombopenia with relapse upon reexposure is reported. Cytopenia was each time rapidly reversible upon withdrawal of the medication. During the two episodes, blood digitoxin was superior to the generally accepted value. No thrombopenia was caused by administration of digoxin. The criteria for diagnosis and the difficulty of causal demonstration are discussed. Up to the present the literature has reported 11 cases of cardiotonic-induced thrombopenia. The features of these observations are reviewed.

Digitoxin↗
PubMed1978

[Platelet volume in essential thrombopenia].

The electronic method for measuring platelet volume using the Coulter Z BI Counter coupled with a Channelyser C 1000 has been standardized. The distribution of platelet volumes was studied in 28 cases of idiopathic thrombocytopenic purpura (ITP) and in 59 cases of thrombocytopenia attributed to a failure of platelet production. Results showed that the volumetric distribution curve of platelet rich plasma (PRP) was altered in 40 cases, by the presence of small particles interfering with platelets of small volume and/or by residual red cells modifying its terminal segment. These abnormalities seem linked to the degree of thrombopenia, but independent of its central or peripheral origin. A method of isolation and concentration of platelets in an albumin gradient allowed the restoration of the classical volume distribution in 24 cases out of 40. Simulated thrombopenias obtained by dilution of platelets in their own platelet poor plasma (PPP) showed that the abnormalities in the small volume range could be reproduced in vitro by modifying the proportion of platelets and of small residual elements in the PRP. When the albumin gradient method was used, the classical distribution of platelet volumes was found. Preliminary electron-microscopy studies show that the small elements in the PRP of thrombopenic subjects could be formed by red cell fragments. Cytoenzymologic studies should be able to confirm this. Volumetric parameters were determined from the asymmetric and unimodual distribution of platelets, either directly on PRP or after concentration and separation of platelets in an albumin gradient. They showed that platelet volumes were very often increased in ITP but also occasionnally in thrombopenia of attributed to a failure of production.

Blood Platelets↗
PubMed1980

[Heparin-induced thrombopenia. Vascular complications in six cases (author's transl)].

The most frequent complication during heparin treatment is hemorrhage from overdosage. Heparin-induced thrombopenia is more rarely observed but is a more serious disorder. Six such cases are reported, of which three were complicated by gangrene of the limbs. Clinical findings are described, together with the methods of detecting the presence of heparin-induced antiplatelet antibodies. The affection becomes evident on the 9th day of treatment by the presence of a thrombopenia and accompanying clinical signs. These may be those of a hemorrhagic syndrome directly related to the thrombopenia, or manifestations of thrombotic lesions. The latter can cause worsening of the condition for which heparin was prescribed, arterial thrombosis of a large vessel, venous thromboses disappearing after interruption of heparin treatment, of distal thrombosis of the microcirculation with a rapidly irreversible onset of gangrene requiring amputation. The lesions are provoked by an immune mechanism and heparin has to be discontinued.

Adult↗
PubMed1997

Clozapine-induced agranulocytosis and thrombopenia in a patient with dopaminergic psychosis.

In patients with Parkinson' disease and dopaminergic psychosis, clozapine treatment is recommended as the drug is free from extrapyramidal side effects and does not worsen motor symptoms of the underlying disease. The use of clozapine, however, is limited due to its hematotoxic side effects. For treatment of clozapine-induced agranulocytosis, granulocyte colony-stimulating factors (G-CSF) are recommended. We report the case of a 72-years-old male patient with clozapine-induced agranulocytosis and thrombopenia. Neutropenia was successfully treated with G-CSF, but thrombopenia persisted and resolved spontaneously after 14 days. Bone marrow toxicity of clozapine is not restricted to white cell maturation, but may also impair thrombocytopoesis.

Aged↗