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Biomedical subjects

D Blockmans

Publications and source records attributed to D Blockmans.

27 records · Page 2Linked to original sources
PubMed1992

HIV-related thrombocytopenia.

HIV-related chronic ITP is caused by an accelerated platelet destruction due to adsorption of circulating immune complexes and to specific anti-platelet antibodies, but perhaps also by a defective thrombopoiesis resulting from invasion of the megakaryocytes by the retrovirus. Treatment is needed when platelet numbers drop beneath 20.10(9)/L or when severe bleeding symptoms occur. Steroids, commercially available immunoglobulins for IV use, AZT and anti-Rh immunoglobulins can be administered, although relapses are frequent after withdrawal of the drugs. Recurrences after splenectomy are far less common, but the progression towards AIDS might be accelerated.

Antigen-Antibody Complex↗
PubMed1988

Congenital macrothrombocytopenia, leucocyte inclusions, deafness and proteinuria: functional and electron microscopic observations on platelets and megakaryocytes.

We report a patient with a variant of Alport's syndrome: macrothrombocytopenia, leucocyte inclusions, deafness and proteinuria. Ultrastructural studies revealed giant spheroid platelets with a high density of organelles and a disorganized microtubular system. In addition, Fechtner inclusions were observed in neutrophils of the patient and her mother. In platelet rich plasma platelets aggregated normally for the low platelet number, although no shape change was visible. Platelet studies in whole blood using impedance aggregometry gave supernormal aggregation curves; this is not in agreement with the abnormally long bleeding time, showing the limited usefulness of this technique in patients with such large platelets. The megakaryocytes (MK) showed two different distribution patterns of the demarcation membrane system (DMS), which may explain the production of few large platelets. The formation of platelets occurred by fragmentation of the granular zone of the MKs, which seemed to be followed by expulsion of platelets through openings of the peripheral zone. The involvement of cytoskeletal structures in the organization of the DMS and the expulsion of platelets is discussed.

Adult↗
PubMed1988

Adenylate cyclase activation determines the effect of thromboxane synthase inhibitors on platelet aggregation in vitro. Comparison of platelets from responders and nonresponders.

The effect of five thromboxane-synthase inhibitors (UK-37248, UK-38485, UK-34787, CGS-13080 and OKY-1581) on arachidonic acid-induced platelet aggregation has been studied in vitro on platelets from 30 different healthy volunteers. The sensitivity of their platelets to adenylate cyclase stimulators or to dibutyryl cyclic AMP has been evaluated contemporarily. In 4 of the 30 volunteers tested no inhibition of platelet aggregation was obtained with any of the five thromboxane synthase inhibitors: these subjects were defined nonresponders; in 13 volunteers inhibition was observed with all the five drugs (responders). Significantly higher amounts of prostaglandin (PG)D2, prostacyclin and adenosine were required to suppress arachidonic acid-induced aggregation of platelets from nonresponders in vitro. No differences were instead observed between responders and nonresponders concerning platelet sensitivity to forskolin or dibutyryl cyclic AMP. The cyclic AMP rise obtained with exogenous prostacyclin was lower in platelets from nonresponders than in those from responders. PGE2 added in vitro to platelets from nonresponders exerted always a proaggregatory effect whereas this PG was antiaggregatory in most of the nonresponders. PGE2 blunted the antiaggregatory activity of PGD2 and limited the cyclic AMP increase induced by PGD2 in all the subjects tested. These data indicate that the unequal functional response of platelets from different subjects to thromboxane synthase inhibition depends essentially on adenylate cyclase function: a relative insensitivity of this enzyme to activating stimuli and the accumulation of substances (PGE2, PG endoperoxides, etc.) reducing the activity of adenylate cyclase may lead to continued platelet activation in some subjects despite the suppression of the synthesis of thromboxane A2.

Adenylyl Cyclases↗
PubMed1986

Heparin-induced thrombocytopenia platelet aggregation studies in the presence of heparin fractions or semi-synthetic analogues of various molecular weights and anticoagulant activities.

One case of heparin-induced thrombocytopenia is reported. Aggregation was observed in the platelet-rich plasma of this patient in the presence of two commercial standard heparin preparations (from a final concentration of 0.025 IU/ml upwards), of two semi-synthetic heparin analogues (0.1 APTT U/ml) and of three low-molecular weight heparin (LMWH) fractions (0.1 anti-Xa U/ml) but not in the presence of five other LMWH fractions. The patient's isolated platelets no longer aggregated in the The patient's isolated platelets no longer aggregated in the presence of heparin but the phenomenon recurred after addition of the patient's platelet poor plasma (PPP). Furthermore, addition of patient's PPP to control platelets led to heparin-induced aggregation. The phenomenon was associated with thromboxane generation and could be blocked by in vitro addition of aspirin, PGI2, and PGD2 whereas the lag phase was dose-dependently prolonged by adenosine. It is concluded that platelet aggregation may be induced in some patients by standard heparin and by certain LMWH fractions or semi-synthetic analogues, independently of their molecular weight and anticoagulant activity.

Adenosine↗
PubMed1986

Thrombosis and immune disorders.

The purpose of this review has been to draw the attention of clinicians towards the possibility that some of the patients they are treating for thrombosis may have an underlying immune disturbance. This could involve functional abnormalities of the complement system (as in acquired angioneurotic oedema or in paroxysmal nocturnal haemoglobinuria), or cell-mediated immunological damage to the vessel wall (as in Behcet's syndrome or Buerger's disease), or the presence of circulating antibodies (the lupus anticoagulant or antibodies to heparin). While obviously our knowledge on most aspects is still very incomplete, the awareness of the association of thrombosis with certain immune disorders should encourage further detailed studies of mechanisms and enhance our understanding of the role of blood constituents and the vessel wall in thrombogenesis.

Angioedema↗
PubMedDate not supplied

Assessment of the patency of deep leg veins with duplex.

To evaluate the accuracy of venous duplex, results obtained in 101 patients are compared with venography. A first group consisted of 48 patients with clinically suspected deep vein thrombosis. In 30 of them a positive duplex scan was obtained and all had subsequently a positive venography. Eighteen patients with a normal duplex scan had a normal venography. Another group of 53 patients were tested preoperatively for varicose vein surgery. No obstruction of the venous system was withheld with duplex but 3 patients had an old thrombosis on venography. Thus duplex is a highly reliable method to detect proximal thrombosis in clinically suspected patients but detection of late sequelae of thrombosis may be more difficult.

Adolescent↗