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Biomedical subjects

P Alexandre

Publications and source records attributed to P Alexandre.

At least 37 records · Page 2Linked to original sources
PubMed1983

[Practical value of the determination of urinary fibrin degradation products in the early management of renal transplants].

We studied daily urinary excretion of fibrin degradation products (UFDP) during the first month following renal transplantation in 31 patients using the Merskey technique. After the 48 first hours a rise of UFDP was observed in 3 circumstances: 1) acute rejection: twenty-four acute rejections were observed in twenty-two patients. The increase of UFDP was constant. It preceeded the clinical diagnosis of rejection in 63 p. 100 of the patients. It has a predictive value in all cases. 2) Severe urinary infection. In 5 patients with urologic complications UFDP rose markedly. 3) Macroscopic hematuria. In 2 patients with gross hematuria very high rates of excretion were observed.

Female↗
PubMed1983

[Practical interest of the determination of urinary fibrin degradation products in the early monitoring of kidney transplants].

We studied daily urinary excretion of fibrin degradation products (UFDP) during the first month following renal transplantation in 31 patients using the Merskey technique. Passed the 48 first hours a rise of UFDP was observed in 3 circumstances: 1) acute rejection: twenty four acute rejections were observed in twenty two patients. The increase of UFDP was constant. It preceded the clinical diagnosis of rejection in 63 p. 100 of the patients. It has a predictive value in all cases. 2) Severe urinary infection. In 5 patients with urologic complications UFDP rose markedly. 3) Macroscopic hematuria. In 2 patients with gross hematuria very high rates of excretion were observed.

Circadian Rhythm↗
PubMed1982

HLA typing in a new family with Fletcher factor deficiency.

In a nonrelated white family, the Fletcher factor level in the father was 0.41 U/ml and in the mother, 0.30 U/ml (controls, 0.75-1.25 U/ml). One sibling with recurrent epistaxis had a level of 0.012 U/ml, whereas the other without tendency to spontaneous bleeding had levels between 0.75 and 0.32 U/ml. This suggests autosomal recessive transmission with clinical symptoms when the defect is homozygous. HLA antigens were studied to determine whether characters of the histocompatibility system and this defect are linked: we determined that the gene(s) of the disease is (are) not shared on the HLA complex.

Adult↗
PubMed1981

Bond strength of three orthodontic adhesives.

A method was devised to study the bond strength of direct-bonding orthodontic adhesives. A shear load was applied parallel to the tooth-adhesive-bracket interface by means of an Instron Universal Testing Machine. The bond strength was found to increase for some products after 27 days. However, no significant differences could be detected 1 day after placement. The interface was studied to determine the mode of failure. In all cases bond failure occurred as mixed adhesive-cohesive phenomena.

Acrylic Resins↗
PubMed1980

[Acquired coagulation inhibitors. 10 cases (author's transl)].

A circulating anticoagulant with antiprothrombinase activity was detected in 10 patients, 4 of whom had systemic lupus erythematosus. Clinically, haemorrhages occurred only in patients with associated thrombopenia; some developed thrombosis. Recalcification time and activated partial thromboplastin time were prolonged in the patients' plasma and in mixed patients' and control plasma. In 5 cases the anticoagulant was isolated by chromatography as IgG or IgM.

Adolescent↗
PubMed1980

Recurring thrombo-embolic accidents caused by family-related deficiency of the fibrinolysis system.

Several members of the same family underwent examinations on the coagulation and fibrinolysis systems after recurring thrombo-embolic disease was observed in one of the members of the family. The results of biological examinations revealed normal coagulation factors, but a high level of plasminogen activation inhibitors accompanied by an increase in platelet aggregation was observed. These results are compared with the few similar cases reported by other authors. The exact part played in this particular case by the platelets and the inhibitor in the patient's predisposition to venous thrombosis and the spread of the disease is discussed. It would seem that the platelet abnormality merely accompanys the increase in inhibitors which is passed on by recessive autosomal transmission. The authors consider that in all cases of thrombosis, particularly recurring thrombosis, an investigation, comprising a study of the fibrinolysis factors and particularly the inhibitors, must be carried out on the patient's close family.

Adult↗
PubMed1978

[Acute renal failure and consumption coagulopathy in the puerperium].

Disseminated intravascular coagulation accompanied 18% of cases of acute renal failure during puerperal disorders. We studied in particular 31 cases of disseminated intravascular coagulation with renal failure due to obstetric disorders : 12 post-abortion infections, 3 retentions of a dead foetus, 5 infections, 6 cases of toxemia, 2 retroplacental hemorrhages, two hemorrhages during the third stage, one uremohemolytic syndrome. For diagnosis one relies on the clinical data (bleeding, purpura, shock, hemolysis, visceral involvement) and laboratory data, (coagulation should be supervised throughout the course). The renal lesions are either cortical necrosis, or interstitial nephritis. The analogies with experimental phenomena suggest a human equivalent of the Schwartzmann-Sanarelli syndrome.

Acute Kidney Injury↗
PubMed1978

[Heat stroke and disseminated intravascular coagulation. Apropos of 2 cases].

Two cases of fatal heat stroke, concerning a 20 year-old soldier and a 44 year-old psychiatric patient, treated with neuroleptics, are reported. The clinical picture, starting suddenly with coma and hyperthermia, was quite identical for both. Secondarily, while hyperthermia decreases and the conscience improved partially, an hemorrhagic syndrome similar to a consumption coagulopathy, acute renal insufficiency and acute hepatic failure appear. Death occurred after aggravated neurological disorders and respiratory distress. The anatomical lesions spread on all the viscera include tubular nephritis, and hepatic centro-lobular necrosis and an interstitial and alveolar oedema with hemorrhages and hyaline membranes in the lungs.

Acute Kidney Injury↗
PubMed1976

[Acute consumption coagulopathies. 120 cases].

Consumption coagulopathy is frequently observed in a resuscitation department. 120 cases of various etiologies are reviewed: complications of pregnancy (61 cases), infections (23 cases) or various stresses: acute hemolysis, shock, severe hepatic failure, intoxications, acidosis, heat-stroke... Consumption coagulopathy is intricated with the general stress which induces it, and with the visceral lesions induced by the stress and which can be aggravated by the consumption coagulopathy. The state of shock is observed in 76% of the cases, the haemorrhagic syndrome in 73%. Acute hemolysis and the clinical signs evocative of disseminated intravascular coagulation (cutaneous signs) are more rare. Following the initial manifestations, visceral complications may develop: renal, hepatic, respiratory, neurological, digestive. The evolution of the biology must be carefully studied. The diagnosis is made on both clinical and biological data. Etiological and pathophysiological treatment should be carried out. In our series, controlled and adapted heparin therapy was given systematically.

Disseminated Intravascular Coagulation↗
PubMed1976

[Consumption coagulopathy and acidosis in the diabetic patient (author's transl)].

Four cases of intravascular coagulation associated with a state of acidosis in diabetics were observed in 57 patients with diabetic acidosis and 19 with lactic acidosis, in a series of 112 cases of consumption coagulopathy admitted to a department of medical resuscitation. In three cases the coagulopathy was found only on investigation; in one there were clinical and anatomic signs. The coagulopathy may be found either during the phase of recovery from ketoacidosis, or during the course of severe lactic acidosis, particularly during a recurrence of this form of acidosis. In spite of the unfavorable outcome in 3 of the 4 cases, the abnormal findings of coagulopathy reverted toward normal along with successful metabolic corrections. The factors responsible for consumption coagulopathy are acidosis, collapse, generalised systemic reactions and alterations of platelet function, of coagulation, of the balance between fibrin deposition and lysis and of lipid levels, all characteristic of diabetes. The clinical effects of this coagulopathy seldom become apparent but provide a possible explanation of some of the complications of diabetic ketoacidosis, particularly certain hemorrhagic or thrombotic events, as well as certain visceral complications, especially those affecting renal, pulmonary and cerebral areas.

Adolescent↗
PubMed1975

[Study of the osmotic behaviour of human platelets].

Observation of the behaviour of platelets in hypotonic media affords an approach to the evaluation of their fragility. It should be possible to apply such a test to various fields such as the study of rheological properties of platelets, the investigation of certain pathological cases and eventual alterations during storage. The curve obtained reflects a continuous distribution of platelet osmotic fragility.

Blood Platelets↗
PubMed1975

[Capillary blood coagulation in the healthy premature newborn].

Blood coagulation of healthy premature newborns, since birth, was studied for 45 days by a method of capillary blood sampling in a plastic tube. The most often measured clotting factors allowed to establish control coagulation times for the tests performed in premature sick infants. In this study, the clotting factors were identical in at-term and premature children. Vitamin-K dependent factors showed the most important deficits; however, at birth their levels seemed higher in at-term newborns. They reached control values after one month, with a progressive evolution. The other blood-clotting factors were normal.

Blood Coagulation Tests↗