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Biomedical subjects

M L Scrobohaci

Publications and source records attributed to M L Scrobohaci.

At least 37 records · Page 2Linked to original sources
PubMed1991

[Antiphospholipid antibodies--antiphospholipid syndrome. Cause or consequence of thrombosis].

Antiphospholipid antibodies (APA) are heterogeneous immunoglobulines of G, M or A classes with specificity directed towards anionic phospholipids. The APA are associated with a wide variety of diseases. They have been found to represent risk factor for development of arterial and/or veinous thrombosis. The APA would perturbed the biological activities of anionic phospholipid surface in a manner that could decrease the natural anti-coagulant pathway in order to lead to thrombosis. In the latter hypothesis APA would appear as a secondary response to the exposure of phospholipid "self antigens" by activated or damaged blood vascular cells by known stimuli able to induce thrombosis. In these cases APA would therefore constitute a marker of risk of thrombosis. The question which remains to be solved is if APA possess their own pathogenic potential or if they appear as the result of an up-stream pathological event known to be favourable to the development of thrombosis or if both mechanism are involved.

Antiphospholipid Syndrome↗
PubMed1990

Use of prostaglandin E1 for prevention of liver veno-occlusive disease in leukaemic patients treated by allogeneic bone marrow transplantation.

Prostaglandin E1 (PGE1) was used to prevent veno-occlusive disease (VOD) of the liver after allogeneic bone marrow transplantation (BMT) for leukaemia. It was given in continuous i.v. infusion from day--8 to day 30 after BMT at a dose of 0.3 micrograms/kg/h. The patients were studied according to the risk factors for VOD: diagnosis, intensification of the conditioning and previous liver abnormalities. The diagnosis of VOD was made on at least two of the following factors: weight gain, hepatomegaly, jaundice, ascitis, pain of the right upper quadrant, increased platelet consumption. 109 patients were studied, 50 were treated by PGE1 and 59 did not receive it. The actuarial incidence of VOD was 12.2% in the PGE1 group and 25.5% in the non PGE1 group (P = 0.05). In acute leukaemia, the incidence was 39.1% in the non-treated group and 12.8% in the PGE1 treated group (P = 0.02). Patients with previous hepatitis had an incidence of 62.5% in the non treated group and 15.5% in the treated group (P = 0.05). A positive cytomegalovirus (CMV) serology seemed to increase the risk of VOD: the incidence of VOD was 31.4% in non-treated patients and 22% in PGE1 treated patients. The multivariate analysis of the risk factors for VOD shows that unfavourable factors were: recipient positive CMV serology (P = 0.06), hepatic disease prior to transplant (P = 0.02) and the absence of PGE1 treatment (P = 0.02). This study suggests that prophylactic PGE1 treatment may decrease the incidence of VOD in patients treated for leukaemia by allogeneic bone marrow transplantation.

Adult↗
PubMed1990

Endothelial cells: target for the HIV1 virus?

Plasmatic levels of endothelial markers [von Willebrand's factor (VWF), fibronectin (FN), and angiotensin converting enzyme (ACE)] were measured in patients at various stages of evolution of HIV1 infection. VWF levels were elevated at all stages, while other markers were significantly altered only for the most advanced stages. These results can be interpreted as indicating an endothelial involvement during HIV infection and VWF being the most sensitive marker. Endothelial markers, mainly VWF, could be used as prognosis marker of the infection. Capillary density was measured in the dermis of uninvolved skin showing a significant angiogenesis associated with the HIV1 infection. These biochemical and histological results however do not indicate whether these changes are directly linked to endothelial infection by the virus or to an indirect effect. The endothelial cell being an immunocompetent cell what is its involvement in the genesis of the immuno deficiency syndrome?

Acquired Immunodeficiency Syndrome↗
PubMed1990

Role of PGE1 to prevent veno-occlusive disease of the liver after bone marrow transplantation.

Prostaglandin E1 was used to prevent veno-occlusive disease of the liver after allogeneic bone marrow transplantation for leukemia. It was given in continuous IV infusion from day -8 to day 30 after BMT at the dose of 0.3 microgram/kg/h. The patients were studied according to the risk factors of VOD: diagnosis, intensification of the conditioning and previous liver abnormalities. The diagnosis of VOD was made on at least two of the following factors: weight gain, hepatomegaly, jaundice, ascitis, pain of the right upper quadrant, increased platelet consumption. One hundred and nine patients were studied, 50 were treated by PGE1 and 59 did not receive it. Univariate analysis shows that the actuarial incidence of VOD was 12.2% in the PGE1 group and 25.5% in the non PGE1 group (P = 0.05). In acute leukemia, it was 39.1% in the non treated group and 12.8% in the PGE1 treated group (P = 0.02). Patients with previous hepatitis had an incidence of 62.5% in the non treated group and 15.5% in the treated group (P = 0.05). A positive CMV serology seemed to increase the risk of VOD: the incidence of VOD was 31.4% in non treated patients and 22% in PGE1 treated patients. The multivariate analysis of the risk factors of VOD show that unfavorable factors were: recipient positive CMV serology (P = 0.06), hepatic disease prior to transplant (P = 0.02) and the absence of PGE1 treatment (P = 0.02). This study suggests that prophylactic PGE1 treatment may decrease the incidence of VOD in patients at risk treated for leukemia by allogeneic bone marrow transplantation.

Alprostadil↗
PubMed1988

Cutaneous and plasma values of von Willebrand factor in AIDS: a marker of endothelial stimulation?

Patients infected by the human immunodeficiency virus (HIV) represent a model in which endothelial proliferation and/or damage are of concern. We studied Von Willebrand factor (VWF) plasma values as a presumed marker of endothelial proliferation in patients with the lymphadenopathy syndrome (LAS) (n = 45), AIDS-related Kaposi's sarcoma (KS) (n = 23), and AIDS opportunistic infections (n = 9), in comparison with normal controls (n = 19) and classical KS (n = 12). VWF was increased in AIDS patients with KS (p less than 10(-6)), in AIDS patients without KS (p less than 10(-7)), and to a lesser extent in classical KS (p less than 10(-3)) and LAS (p less than 10(-2] patients. To evaluate the diffusion of the vascular proliferation in HIV-infected patients, we studied the number of vessels within the superficial dermis of clinically uninvolved skin by an indirect immunoperoxidase method. We used an antibody directed against VWF in skin biopsies from 20 LAS patients and 10 AIDS-related KS patients compared to 11 controls and 10 classical KS patients. An increase in the number of blood vessels in normal skin was found in LAS (p less than 10(-2)), classical KS (p less than 0.05), and AIDS-related KS (p less than 10(-2]. Statistical studies and comparisons between plasma and cutaneous values of VWF indicate that plasma VWF is a good marker of endothelial damage but a poor marker of vascular proliferation in HIV-infected patients.

AIDS-Related Complex↗
PubMed1988

[Hemostasis tests as markers of hepatic and endothelial toxicity in chemotherapy].

Two short-lived vitamin K-dependent factors, factor VII and protein C, were measured by both functional and antigenic techniques in 3 hematological conditions known for their risk of hepatotoxicity: Following use of asparaginase and bisantrene, and patients at high risk of hepatic veno-occlusive disease after allogenic bone marrow transplantation for relapse of acute leukemia of accelerated phase of evoluted chronic myelogenic leukemia. In these 3 conditions functionally measured levels of protein C and factor VII, and antigenically measured levels of both these factors proved to be early markers of incipient hepatic involvement. These tests were easy to use routinely were reproducible, and proved to be predictive of veno-occlusive disease in grafted patients at the preconditioning stage. In the follow-up of bone marrow grafted patients plasma markers of endothelial function (von Willebrand's factor, tissue type plasminogen activator, and plasma activity of angiotensin converting enzyme) were significantly altered at the time of overdose with cyclosporin A, probably due to a drug-induced in vivo lesion of the endothelium. In the search for cytoprotective drugs for the prevention of veno-occlusive disease in bone marrow grafted patients prostaglandin E1 (PGE1) was given prior to and for at least 4 weeks after transplantation and proved to be effective by biological criteria (the level of protein C mainly). This deserves further study in a prospective clinical trial of the potential usefulness of PGE1 in preventing liver veno-occlusive disease in bone marrow grafted patients.

Alprostadil↗