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At least 145 records · Page 8Linked to original sources
PubMed2001

[Thrombopenia associated to localized scleroderma].

Two patients are reported with localized scleroderma who developed thrombocytopenia. One of these patients had a positive antinuclear antibody (ANA) and Anti-DNA antibodies tests. The occurrence of thrombocytopenia in localized scleroderma suggests an autoimmune mechanism, by the response to steroids and the presence of positive autoantibodies. This possible association emphasizes the need to look for hematologic disorders in patients with systemic, as well as localized scleroderma.

Adolescent↗
PubMed2001

[Thrombopenias induced by heparin: diagnostic and therapeutic innovations].

Heparin-induced thrombocytopenia (HIT) is a difficult immune-mediated phenomenon that physicians have to cope with. It is caused by platelet-activating, heparin-dependent IgG antibody and may be associated with venous and arterial thrombosis, potentially fatal. Simple tests are now available which can detect most antibodies implicated in HIT. The old term "white clot syndrome" suggested that HIT was mostly associated with arterial thromboembolic events, but more recent publications indicate that HIT is also an important risk factor for venous thromboembolism. In case of suspicion of HIT, treatment by heparin should imperatively be stopped and an alternative anticoagulant treatment should be started before any laboratory confirmation.

Anticoagulants↗
PubMed1975

[Critical assessment of cortico-steroid therapy of acute thrombopenia (author's transl)].

Case histories of 75 children aged 6 months to 14 years were analysed, hospitalisation being for purpura due to thrombocytopenia. Sex distribution, age at first manifestation, frequency of infections immediately preceding purpura, frequency of chronic forms and letality coincide with previous literature reports. A favourable influence of corticosteroids on the acute phase of disease e.g. on purpura and disposition to haemorrhage, thrombocyte qualities, spleen- and liver enlargement as well as duration of hospitalisation was not realized.

Acute Disease↗
PubMed1999

[Heparin-induced thrombopenia].

Heparin-induced thrombocytopenia remains a topical subject for at least two reasons. The first reason is the increasing prescription of low molecular weight heparins (LMWH) rather than unfractionated heparins, with limited laboratory surveillance, raising the question concerning the need for twice-weekly platelet counts, according to the recommendations of the Vidal drug directory. The second reason is the recent release onto the market of two products, danaparoid (Orgaran) and lepirudin (Refludin) for this precise indication of heparin-induced thrombocytopenia. These products greatly facilitate the management of this complication. Many basic research teams are trying to optimize the detection of heparin-dependent antibodies and to more clearly elucidate the mechanism of this particular thrombocytopenia, which carries a risk of very severe thrombotic complications when the diagnosis is delayed.

Antibodies↗
PubMedDate not supplied

[Thrombopenia due to pefloxacin (Peflacine): dose-dependent toxicity?].

Pefloxacin (Peflacine) can give rise to thrombocytopenia, although the responsibility of the drug can be difficult to demonstrate in infectious patients and those receiving other drugs simultaneously. We have collated 18 cases in which the responsibility of pefloxacin was suspected. In 13 cases, the patients were also taking other drugs which may have been contributory (heparin, Bactrim, Augmentin, ranitidine,...). The remaining five cases were of particular interest as pefloxacin was the only drug administered. The mean age of the patients was 75 years, and the mean bodyweight 56 kg (range, 47-65 kg). The pefloxacin dosage was 800 to 1,600 mg/day i.v. or p.o., i.e. 13-18 mg/kg/day. Thrombocytopenia occurred from five to 19 days after beginning treatment and resolved between 7 and 12 days after drug withdrawal. A number of factors argue in favor of dose dependency: 1 patient had high plasma concentrations (peak and residual); thrombocytopenia occurred in one patient when the previous, well-tolerated dosage of 800 mg/day (for 15 days) was increased to 1,600 mg/day; thrombocytopenia resolved in one patient when the dosage was reduced to 400 mg/day (1 tablet) and continued for a further 10 days. This toxic reaction may be avoided by reducing the drug dosage to 400 mg/day in elderly patients with a low bodyweight. Differential blood counts appear to be warranted for patients at risk.

Aged↗