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Y Gruel

Publications and source records attributed to Y Gruel.

At least 91 records · Page 5Linked to original sources
PubMed1990

[Gastropericardial fistula. Review of the literature apropos of an original case].

The authors present a case of pneumopericarditis consecutive to a perforating gastric ulcer complicating a left, post-traumatic diaphragmatic hernia, evolving favorably after radical surgery. 52 cases of gastro-pericardial fistulas were reported in the literature, 42 of which related to benign pathology. The overall mortality rate for this disease was 85%, although the course was favorable in one patient out of two, whenever radical surgery had been resorted to. In order to ensure these patients the best chances for survival, treatment should combine pericardial drainage and case-adapted gastro-intestinal surgery in an intensive care setting.

Aged↗
PubMed1989

Prenatal diagnosis of platelet disorders.

The antenatal diagnosis of platelet disorders represents real progress in the early detection of haemorrhagic diseases occurring in the fetus. However, the diagnosis is only possible in some cases during the first trimester of gestation, and not in the first weeks as is the case for other hereditary disorders such as abnormal haemoglobins. This delay can be reduced now that the molecular abnormalities responsible for some platelet disorders have been discovered. If the region of chromosome 17 and the DNA sequence coding for the glycoproteins GP IIb-IIIa were known, this would make possible the recognition of the gene defect responsible for Glanzmann's thrombasthenia. This could also permit the diagnosis of Glanzmann's thrombasthenia at the gene level, i.e. during the first weeks of gestation. However, the use of gene markers could be limited by the fact that a monomorphic clinical expression of Glanzmann's thrombasthenia could correspond to different genetic mutations which can all result in a defect in GP IIb-IIIa synthesis and assembly. If such diagnosis could be made very early, it would only represent real progress if a specific treatment could be applied. New therapeutic approaches to immune thrombocytopenia during pregnancy appear to be possible and can be applied when there is a risk to the fetus, they are still either experimental or anecdotal and there is a real need for a well-designed clinical trial. In all fetal platelet disorders, the risk of fetal death following fetal blood sampling must not be underestimated and very careful, intensive care is necessary after such an investigation. In the absence of a specific therapy, this antenatal diagnosis must be restricted to cases in which the risk of severe haemorrhagic complications are anticipated and where there is a well-documented family history. The patients must be properly informed of all the aspects of the investigation, including the possible risks. As has been the case for other haematological disorders, progress will be made, and we can anticipate that eventually in utero bone-marrow transplantation or gene correction be performed to cure the disease before birth.

Autoimmune Diseases↗
PubMed1989

Hemostasis development in the lamb fetus and neonate.

Fetal and neonatal lamb hemostasis were studied from the 60th day of pregnancy to birth. Platelet counts and blood coagulation, as assessed by tests such as recalcification time and thromboelastography, were similar in fetuses, neonates, and adult sheep. The values of coagulation factors were low, ie, vitamin K-dependent Factors II, VII, IX, and X remained unchanged (30 and 40% of adult reference values) until the last 10 days of gestation, and then increased until birth (40 to 60%). Values of fibrinogen and Factor V followed a similar pattern, although their activities became identical to adult values at birth. Also, we measured values of protein C and antithrombin III, which are synthesized by the liver. The importance of hepatic failure and fetal vitamin K deficiency were discussed. Factors VIII and XII activities increased gradually during pregnancy to reach adult values at birth. Fetal fibrinolytic activity increased. This could not be explained by the values of tissue-type plasminogen activator (it was not detectable) or by the presence of its fast-acting inhibitor, whose concentration did not decrease.

Animals↗
PubMed1988

Levels and plasma distribution of free and C4b-BP-bound protein S in human fetuses and full-term newborns.

Levels and plasma distribution of protein S were measured on umbilical cord plasmas from 25 normal full-term newborns and 25 normal fetuses which were between 20 and 31 weeks of gestation. Fetal blood samples were obtained by direct puncture of the umbilical vein under high resolution real-time ultrasound. Total and Free protein S levels were found to be lower in all fetuses and newborns as compared to normal adults. The calculated ratio Total protein S/Free protein S and crossed immunoelectrophoresis patterns indicate that protein S circulates essentially in the free form in fetuses and newborns. These data may be explained by the low levels of C4b-binding protein observed at these stages of development.

Adult↗
PubMed1988

[Treatment of acute pulmonary embolism with a low molecular weight heparin by the intravenous route. Study of the optimal dosage].

Experimental studies on rabbits have shown that CY 222, a low molecular weight heparin (mean: 2.500 daltons), has the anti-thrombosis properties of heparin but reduces the risk of haemorrhage in optimal doses of 1.000 AXa IC (Institut Choay) units/kg/day. The safety and effectiveness of CY 222 were tested in 47 patients presenting with a less than 5 days' old pulmonary embolism. The patients were divided into three groups according to dosage: group I (n = 16) received 500 AXa ICu/kg/day; group II (n = 17), 750 AX ICu/kg/day, and group III (n = 14), 1.000 AXa ICu/kg/day. The drug was administered by continuous intravenous infusion during 10 days. Its effectiveness was assessed from the Miller index calculated on conventional pulmonary angiograms on days 0, 5 and 10. On the 10th day of treatment, the percentage of revascularization was similar in all three groups (group I 65.9 +/- 9.9 p. 100; group II 71 +/- 6.8 p. 100; group III 68 +/- 8.5 p. 100), but the improvement was significantly more rapid in group III patients. Embolism recurred in 5 cases (2 in group I, 1 in group II, 2 in group III) and was fatal in 1 case (group I). Haemorrhagic complications were noted in 3 cases (group III patients). Except for thromboelastography, all coagulation tests were unmodified by CY 222. The anti Xa and the (very low) anti IIa activities of the drug were directly related to the doses administered.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

[Tumors of the liver secondary to androgen therapy. Apropos of 2 cases in children].

The authors report 2 cases of hepatocellular tumour in children treated with anabolic androgens for aplastic anemia. In both cases, the presentation was by a picture of acute abdomen due to hemoperitoneum caused by tumour rupture. In the first case, there was multiple hepatic adenomas necessitating right hepatic lobectomy. The second infant had a single tumour of segment IV treated by simple excision of the tumour. It was a hepatocellular-carcinoma. Follow-up for one year after the initial operation showed no signs of recurrence in both infants. The review of the literature permitted us to find 48 other cases of hepatocellular tumour secondary to androgen therapy. In order of frequency, the hepatocellular-carcinoma is the most frequent and it is usually single; followed by the adenoma which is usually multiple. The other types of tumours are rare: focal nodular hyperplasia, angiosarcoma and cholangiocarcinoma. The hepatocellular-carcinoma and adenoma have some characteristic features: spontaneous regression may occur after withdrawing of androgens; the risk of rupture is important; their evolution is almost always favorable despite of a severe histopathological picture; the alpha-foeto-protein is nearly always negative; and the metastasis are exceptional. The hepatocellular-carcinomas associated with androgen therapy are probably just adenomas with marked dysplasia, but their long term malignant potential remain unknown. Except in case of rupture, surgical intervention should be postponed until the effect of discontinuing the hormonal therapy is assessed, because of the potential for spontaneous regression. The administration of antineoplastic chemotherapeutic agents should be reserved for the tumours showing evidence of malignancy.

Adenoma↗
PubMed1987

[Role of urokinase in the acute phase of myocardial infarction].

The prourokinase-urokinase system physiologically contributes to fibrinolysis activation. It is therefore rational to envisage the use of urokinase in thrombotic diseases, and notably in the acute phase of myocardial infarction (MI) where coronary thrombosis is virtually constant. The main studies on this subject were published in 1975 and in 1985, thus reflecting the changes in therapeutic concepts that have occurred during these 10 years. The older studies concerned patients who were admitted within the first 12 hours of MI and had no early angiographic examination; the results were evaluated indirectly on clinical and enzymatic criteria and on the regression of electrical signs of myocardial suffering. The more recent studies concern patients who are treated at an early stage, often within the first 3 hours of the accident, on the basis of experimental data which favoured early coronary reperfusion as a means of protecting the myocardium; in these studies coronary arteriography is performed immediately after the thrombolytic treatment; computer-assisted studies of the left ventricular function are also carried out, so that the results of thrombolysis are expressed in terms of coronary patency and improvement in segmental kinetics. The results of these different sets of studies have proved to be similar with time. Urokinase, notably when injected intravenously, has a beneficial effect in the acute phase of MI when compared to the conventional treatment. The coronary reperfusion obtained with urokinase is favourable to the myocardium, and the sooner it occurs the better. This benefit is demonstrated by clinical, electrical, enzymatic and angiographic data. Thus, despite its cost, urokinase remains useful in the treatment of MI, notably because it is well tolerated.(ABSTRACT TRUNCATED AT 250 WORDS)

Fibrinolysis↗
PubMed1986

Determination of platelet antigens and glycoproteins in the human fetus.

The autosomal recessive transmission of Glanzmann's thrombasthenia (GT) and Bernard-Soulier syndrome (BSS), together with requests of families who already had children with these diseases, prompted us to investigate the feasibility of their antenatal diagnosis. The preliminary step leading to the early detection of GT or BSS was to characterize, in the normal human fetus, the platelet antigens and glycoproteins (GPs) and to define their normal amounts on the membrane surface. Blood samples from 32 fetuses between 18 to 26 weeks of gestation were collected by direct puncture of the umbilical vein using an ultrasound-guided needle. Polyclonal antibodies from human origin directed against PLA1, Leka antigens, and the GPIIb IIIa complex (IgGL), or murine monoclonal antibodies specific for GPIb (AN51, 6D1), GPIIIa (AP-3), or GPIIb IIIa (AP-2) were studied using platelet suspension immunofluorescence tests. The binding of each antibody was quantified using a cytofluorograph (Ortho 50H). PLA1 and Leka antigens were expressed in normal amounts on fetal platelets as early as 16 weeks of intrauterine life. The GPIIb IIIa complex quantified by polyclonal or monoclonal antibodies was in the same range in fetuses (IgGL = 427 +/- 23 AUF, AP-2 = 459.5 +/- 8.5; AP-3 = 536 +/- 14) and in adults (IgGL = 420 +/- 30; AP-2 = 498 +/- 11; AP-3 = 515 +/- 13). The platelet binding of antibodies that recognized GPIb was higher in fetuses (AN51 = 491.5 +/- 14; 6D1 = 479 +/- 15) than in adults (AN51 = 426.5 +/- 9; 6D1 = 449 +/- 8.7). These results suggest that immunological techniques can be applied as early as 18 weeks of gestation for the antenatal diagnosis of GT and BSS.

Antigens, Human Platelet↗
PubMed1986

[Thrombocytopenia induced by heparin. Diagnosis, treatment, physiopathology: current concepts].

Iatrogenic thrombocytopenia is a rare, but severe complication of treatments with heparin and heparinoids. Mean temporary thrombocytopenia failing to show any complications are usually diagnosed as quite different from acute and delayed thrombocytopenia of which severity depends mainly on thrombotic symptoms demonstrated in 65 p. 100 of cases; the initial evolution of an average thrombocytopenia is not easy to diagnose; it may as well exist a connection between the two diseases, from a physiopathogenic point of view. The diagnosis of severe thrombocytopenia depends:--clinically, on the initial data, delayed as compared with the heparin treatment beginning and existence of arterial and/or venous thrombosis;--biologically, by demonstrating an aggregating activity for platelets in presence of heparin, in the patient plasma. Such an activity requires the suppression of standard heparinotherapy as well as the choice of substitutive anticoagulant treatment in case of evolutive thrombosis. Low molecular weight heparins are prescribed only if in vitro tests of platelet aggregation with the patient's plasma are negative. Antivitamins K are to be used as soon as possible alone or combined with heparin fractions. Antiaggregants are prescribed alone, above all in case of isolated thrombocytopenia and combined with AVK. Treatment of thrombotic complications depends on surgical disobstruction if arterial thrombosis, and use of fibrinolytics if pulmonary embolisms. The acute reaction of some thrombocytopenia to heparin as well as therapeutic difficulties demonstrate the efficiency of an early diagnosis performed thanks to systematic platelet numerations during the first 15 days of a treatment with heparin, as well as to the prevention along with systematic association with aspirin, especially if replaced with AVK.

Heparin↗
PubMed1986

[Preliminary study of the use of low-molecular weight heparin to prevent thrombotic risk].

This study involved two stages: In vitro study. Three LMWHs, CY 216-CY 222 (Choay) and PK 10169 (Pharmuka), were compared to standard heparin, SH (Choay), and to a high-molecular-weight heparin, HAF (Choay), which particularly revealed a dissociation of anti-Xa (++) and anti-IIa (+) activities for the LMWHs: (table: see text) In vivo study. Healthy volunteers. Subcutaneously injections of PK 10169 or CY 222 according to various protocols (rythm of injections, dosage). For both LMWHs, the dissociation of anti-Xa and anti-IIa activities reoccurs in vivo. A peak of anti-Xa effect was observed 3 to 4 hours after the injections. The duration period of this activity is about 12 hours. The importance of the global platelet tests HT and TEG (modified for the highest doses) should be noted. Study of haemorrhagic tendencies in patients with slight thrombotic risk. From this preliminary study, protocols with CY 216, CY 222 and PK 10169 are proposed for the prevention of thrombotic risk in orthopaedic surgery (injections at 12-hour intervals).

Dose-Response Relationship, Drug↗