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[Success of treatment with a low-molecular-weight heparin fraction in a case of pulmonary embolism complicated by heparin-induced thrombopenia].

A 40-year-old woman was admitted to Ambroise-Paré Hospital with a mitral stenosis and right ventricular failure. On the admission, heparino-therapy was started (Heparine Calcique Leo 30,000 IU/24 h); 11 days after, a thrombocytopenia (platelet count 60 . 10(9)/l) was observed and a few days later a pulmonary embolus was diagnosed. "In vitro", a heparin dependent plasma platelet aggregating factor was found (with Heparine Leo and all other standard ones tested) leading to the diagnosis of heparin associated thrombocytopenia; on the other this aggregating factor was not found with a low molecular weight (LMW) heparin fraction (Choay laboratory, Paris, batch CY216). We decided to stop standard heparin and to treat this patient with the LMW fraction (7,500 IU every 8 h SC) associated with oral antivitamin K. A rapid clinical improvement was observed and the platelet count rose progressively reaching 300 . 10(9)/l and has subsequently always been greater than 200 . 10(9)/l. The occurrence of heparin induced thrombocytopenia associated with thrombosis leads to heparin cessation; the treatment of the thrombotic episode seems to be improved by the use of LMW heparin associated with vitamin K antagonists.

Adult↗

[Major thrombopenia induced by heparin treatment. Apropos of 8 cases].

Major thrombocytopenia occupies a special place among the complications of anticoagulant therapy. Based on a series of 8 personal cases, the authors describe the clinical, biological and physiopathological features of this thrombocytopenia. It occurs in 0.5 to 1 p. 100 of patients on heparin. This figure may not be accurate and thrombocytopenia during heparin therapy occurs almost exclusively in venous thromboembolic disease which it complicated in 4 p. 100 of treated cases. It is detected around the 8th day (between the 4th and 10th day) of treatment and is characterised by thromboembolic events (2 arterial embolisms, 2 pulmonary embolisms, 1 cutaneous necrosis, 1 disseminated intravascular coagulation). Cutaneo-mucous purpura was observed in 1 case. The last two cases in this series were asymptomatic. The thrombocytopenia is peripheral (on average 36,000/mm3) and isolated without any deficiency of the factors of coagulation, except in the case of disseminated intravascular coagulation. A platelet aggregant factor was demonstrated in the plasma of these patients by a thrombo-agglutination technique. This disappeared two months after stopping the heparin. The withdrawal of heparin and relay with oral anticoagulant drugs was associated with a normalisation of the platelet count within 1 to 5 days. Physiopathologically, the high molecular weight fractions of heparin are responsible for this immuno-allergic reaction which leads to the fabrication of a heparin-dependent anti-platelet antibody.

Aged↗

[Robinow's syndrome. Apropos of a case with thrombopenia].

We report on a 17 month-old boy with Robinow' syndrome characterized by mild dwarfism, brachymelia, frontal bossing, hypertelorism, upturned nose, gingivodental, vertebral and bone age abnormalities, hypoplastic genitalia with normal gestation, birth weight and length and intelligence. There was an unusual association with idiopathic thrombocytopenic purpura and splenomegaly.

Abnormalities, Multiple↗

[Severe neonatal thrombopenia. Analysis of the etiologic data on 64 cases].

In many cases of neonatal thrombocytopenia, etiology does not fit with usually known causes. Analyzing, in an intensive care unit, 64 cases of severe neonatal thrombocytopenia (platelets less than 50 x 10(9)/l before hour 72), the authors attempted to determine other possible causes of the disorder. In this study, classical etiologies were present in 33% of cases. In the other 67%, hypotrophy and/or hypoxia were significantly more frequent (p less than 0.01) than in the first group. With reference to clinical and experimental data in the literature, the possible role of acute or chronic hypoxia as a cause of thrombocytopenia is discussed.

Acute Disease↗