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At least 109 records · Page 6Linked to original sources
PubMed2006

[Disseminated tuberculosis and profound thrombopenia].

Thrombocytopenia within the context of disseminated tuberculosis can lead to complications requiring rapid treatment. Although the origin is generally central, thrombocytopenia can arise from an immune disorder. We hereby report a case of disseminated tuberculosis associated with thrombocytopenia, which required, in addition to antituberculosis therapy initiated before bacteriological proof, corticosteroid treatment and multiple platelet transfusions. The discovery of anti-platelet antibodies along with the success of immunomodulator therapy confirmed the auto-immune origin of this thrombocytopenia.

Adrenal Cortex Hormones↗
PubMed2001

[Thrombopenia increased by heparin and danaparoid].

Pathogenesis, frequency, and management of heparin-induced thrombocytopaenia are well-known. They may be related with both unfractioned heparin and low-molecular weight heparin. Suspected heparin must be discontinued as soon as the diagnosis is established. Orgaran (danaparoid sodium) may be used for management of patients with heparin-associated thrombocytopaenia but can itself be associated with a thrombocytopaenia. Our case report allows us to catch in mind such a crossed complication.

Aged↗
PubMed1995

[Heparin-induced thrombopenia during hemodialysis in intensive care: use of a low molecular weight heparinoid, ORG 10172 (Orgaran)].

A 48-yr-old patient was admitted to the ICU for cardiogenic shock and acute renal failure after coronary artery bypass graft surgery. A heparin-induced thrombocytopenia (HIT) occurred during haemodialysis with unfractioned heparin (UFH) as the anticoagulant. The dialysers, the circuits and the catheters were recurrently thrombosing and the platelet count decreased to 9 G.L-1 on postoperative day 7. UFH was discontinued. Attempts to substitute UFH with a low molecular weight heparin (LMWH) failed, due to the presence of a high cross-reactivity rate of LMWH with the heparin-dependent antibody. Intermittent haemodialysis without anticoagulation using a predilution of the dialysers failed also and resulted in recurrent clotting. After informed consent of the patient, a new natural heparinoid Orgaran (Org 10172, Organon, Oss Holland) was administered. This agent is a mixture of several non heparin low molecular weight glycosaminoglycans, with proven anticoagulant efficacy, low cross-reactivity with the HIT antibody, and a half-time prolonged over 18-25 hours. The treatment regimen consisted in a i.v. bolus of 40-45 IU.kg-1 prior to each dialysis procedure, performed every two days. The platelet count increased to 200 G.L-1, seven days after discontinuing heparin injection, and remained stable during the administration of Orgaran. No other thrombosis occurred again. Each procedure of four hours duration was monitored with the plasma anti-Xa activity and APTT test. The mean anti-Xa plasma concentrations (0.44 +/- 0.55 IU.mL-1, 30 min after injection of Orgaran) were well correlated with APTT test (r = 0.73, p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Anticoagulants↗
PubMed1984

[Thrombogenic thrombopenia induced by heparin].

Three cases of heparin induced thrombotic thrombocytopenia are reported. Pathogenesis, clinical and biological manifestations as well as treatment are reviewed. Treatment consisted in replacing the heparin by a vitamin K antagonist or a low molecular weight heparin. During heparin treatment, the risk of thrombotic thrombocytopenia should be kept in mind and the platelet count monitored from time to time.

Aged↗
PubMed1985

[Persistence of thrombopenia induced by heparin despite replacement with low molecular weight heparin].

A 42 year old man, treated for phlebitis with subcutaneous heparin, developed vascular occlusion in both legs with thrombocytopaenia. After surgery, heparin was discontinued and replaced by low molecular weight heparin (CY 216 Choay) without any success. Both commercial heparin and CY 216 Choay produced platelet aggregation in vitro. Heparin was stopped and replaced by dextran 40,000 with anti-aggregating drugs (flurbiprofen) followed by antivitamin K drugs. Thrombocytopaenia resolved three days later and the patient was discharged without sequelae. It therefore appeared necessary to carry out aggregation tests both with heparin and low molecular weight heparin if thrombocytopaenia occurs whilst heparin is being used.

Adult↗
PubMed1986

[Severe thrombopenia associated with treatment with pentosan polysulfate].

Two cases of severe thrombocytopaenia associated with acute thrombo-embolic manifestations during treatment by pentosan polysulphate, a low molecular weight heparinoid, are reported. Plasma samples from both patients caused in vitro aggregation in the presence of pentosan polysulphate. Interruption of the drug led to the recovery of the platelet count. The hypothesis of an immunoallergic mechanism similar to heparin associated thrombocytopaenia is supported. Furthermore, it seemed likely to be found with all the polysulphated X glycosaminoglycans. During treatment by pentosan polysulphate, platelet count should be monitored to avoid this potentially life-threatening syndrome.

Drug Hypersensitivity↗
PubMed1998

[Post-transfusion purpura: and cause of severe postoperative thrombopenia].

A 59-year-old woman developed an acute and severe thrombocytopenia (platelet count below 10.10(9).L-1) with active bleeding, 6 days after a massive transfusion for intraoperative haemorrhagic shock. The diagnosis of post-transfusion purpura (PTP) was confirmed by the presence of an allo-antibody directed against HPA-1a platelet antigen. The patient and her daughter had a rare HPA-1b platelet phenotype, but also belonged to the HLA DR3 phenotype, frequently associated with PTP. This case shows the therapeutic difficulties of postoperative PTP. Despite active bleeding, this syndrome requires the discontinuation of transfusions of incompatible platelets. Transfusion of phenotyped platelets is often inefficient. Red cell concentrates must be platelet and plasma free. Immunomodulating therapy can shorten the time course. Preventive measures, particularly autologous transfusions, are necessary for subsequent haemorrhagic surgery or parturition.

Female↗
PubMed1997

[Neonatal alloimmune thrombopenia in anti-HPA-3a (Baka) immunization].

BACKGROUND: Neonatal alloimmune thrombocytopenia (NAIT) in the HPA-3a system is responsible for less than 5% of all cases of NAIT. CASE REPORT: Thomas, a male infant, was born at 39 weeks of gestation after an uncomplicated pregnancy. Delivery was normal. The Apgar score was 9 at 1 minute, and 10 at 5 and 10 minutes. At 1 hour of age, he displayed extensive petechiae and purpura over the back. The platelet count was 8,000/mm3. Hematesis and extensive petechiae were noted, leading to an exchange transfusion followed by a transfusion of 0.5 U/kg of random donor platelets, 0.4 g/kg/d of intravenous immunoglobulin (IVIg) and 10 mg/kg/d of corticosteroids. IVIg were discontinued on d5 and corticosteroids on d10. There was no relapse of thrombocytopenia. A neonatal alloimmune thrombocytopenia with an HPA-3a (Baka) incompatibility was confirmed. CONCLUSION: HPA-3a incompatibility is certainly more frequent than the rare cases reported and must be searched for in all cases of neonatal thrombocytopenia.

Antigens, Human Platelet↗
PubMed1998

[Jacobsen's syndrome, thrombopenia and humoral immunodeficiency].

BACKGROUND: Clinical features of Jacobsen syndrome include facial dysmorphism, congenital heart defects, digit anomalies and mild to moderate psychomotor retardation. Thrombocytopenia or pancytopenia is observed in one half of patients. PATIENTS: Two unrelated children, a 6-month- and a 12-year-old, presented with a moderate thrombocytopenia associated with the clinical features of Jacobsen syndrome. Bone marrow aspirates showed, in both patients, normal cellularity with an increased number of micromegacaryocytes. Chromosome analysis showed a partial deletion of the long arm of chromosome 11. The 12-year-old patient had a history of upper respiratory airways infections with immune humoral deficiency (decreased level of IgA and IgM) which, to our knowledge, has never been reported. CONCLUSION: Jacobsen syndrome is a cause of inherited thrombocytopenia in children. Humoral immune functions must be explored in patients with a history of repeated infections.

Child↗
PubMed1989

[Immuno-allergic thrombopenias and leukopenias induced by drugs].

Certain types of cytopenia are due to the destruction of blood cells by an antibody, active only in conjunction with a drug which has previously provoked sensitivity in patients when administered in standard doses. Drug-induced thrombocytopenia and leucopenia of allergic origin are relatively rare. They produce characteristic symptoms, i.e. brutal onset and acute development of the disease; healing takes place when the drug in question is withdrawn. Haematological diseases of drug-related aetiology are being brought to light by serological methods which detect the specific antibody for the drug responsible for the accident. The physiopathological mechanism is still not clearly elucidated.

Drug Hypersensitivity↗
PubMed1988

[Disorders of liver function, thrombopenia and hemolysis in a special clinical form of hypertension in pregnancy (the so-called HELLP syndrome)].

The so called HELLP syndrome is a severe complication of pregnancy-induced hypertension, characterized by haemolysis (H), elevated liver enzymes (EL) and low platelet counts (LP). The data of 37 patients with a HELLP syndrome are presented. In addition to the clinical symptoms of pregnancy-induced hypertension, 21 patients suffered from abdominal pain and 5 patients from icterus. Thrombocytopenia, haemolysis and elevated liver enzymes were observed in every case. In 28 of the patients a Caesarean section was performed to prevent further deterioration of the disease. Three patients died post partum as a consequence of severe complications. In five pregnancies intrauterine deaths were observed. The results of this retrospective study confirm the great risk for both the mother and the foetus, if pregnancy-induced hypertension is complicated by a so called HELLP syndrome.

Adult↗