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Biomedical subjects

M H Aurousseau

Publications and source records attributed to M H Aurousseau.

At least 19 recordsLinked to original sources
PubMed2004

European register of babies born to mothers with antiphospholipid syndrome.

This prospective multicentric register was initiated by the European Forum of Antiphospholipid Antibodies (APL) in 2003 after approval by local ethic committees. This register allows the investigation of infants after written informed parental consent. It collects mothers' clinical pattern of antiphospholipid syndrome (APS), course and outcome of pregnancy, treatment and immunological status. For the babies, clinical and immunological examinations are performed at birth; neurodevelopmental conditions followed up to five years. A re-evaluation of lupus anticoagulant (LA), anticardiolipin (ACL) or other antibodies will be done if they are positive at birth to follow their kinetics. A descriptive and a case control study of babies with versus without APL at birth will be possible after the inclusion of 300 cases.

Antiphospholipid Syndrome↗
PubMed2002

[Neonatal cutaneous lupus. Necessary interdisciplinary collaboration].

INTRODUCTION: Neonatal lupus erythematosus is a rare syndrome (affecting 5% of the children born of mothers with lupus), characterized essentially by cutaneous lesions and/or congenital auricular-ventricular heart block. It is due to the transplacental passage of maternal antibodies (anti-SSA or anti-SSB, or occasionally anti-U1RNP antibodies) into the fetal circulation. OBSERVATION: We report a case of neonatal lupus erythematosus, having appeared 4 weeks after birth. The 26 years old mother exhibited systemic lupus erythematosus concomitant to Gougerot-Sjögren's syndrome, with positive antinuclear factors (1/2560), native anti-DNA, anti-SSA and anti-SSB antibodies and anticardiolipin antibodies. During pregnancy, the mother had been treated with aspirin at the dose of 100 mg/day, followed by subcutaneous enoxaparin 0.4 ml/day, and combined with prednisone 10 mg/d and hydroxychloroquine 400 mg/day. Early and regular cardiac monitoring of the foetus was performed. The clinical examination and the electrocardiogram at birth were normal. Four weeks later, the infant presented with erythematous cutaneous lesions with atrophic center. No systemic treatment was initiated and the lesions partially regressed. CONCLUSION: Cutaneous lesions can also appear after the 4th week of life. It is important that the pediatricians clinically monitor all the children born to mothers exhibiting anti-SSA or anti-SSB antibodies, at least during the first 7 months of life.

Adult↗
PubMed1999

High levels of circulating thrombomodulin in human foetuses and children.

Thrombomodulin (TM) is an endothelial cell surface proteoglycan with anticoagulant functions, also implicated in cell proliferation, cell-cell adhesion and differentiation. In this study we determined circulating plasma TM (pTM) levels in human foetuses at different stages of pregnancy, at birth and in childhood. TM levels increased with gestational age, the median level reaching a peak of approximately 165 ng/ml between the 23rd and 26th week, thereafter decreasing gradually, reaching a value of 108 ng/ml at birth. pTM continues to decrease progressively during childhood, reaching in the 5-15 years group a median of 56 ng/ml which approaches the adult value. The pTM peak was statistically significant and represents a specific foetal phenomenon as it was independent of the corresponding maternal values. As a whole, the pTM pattern during foetal maturation appears totally different from that of protein C, prothrombin and other coagulation activators and inhibitors and thus, TM may play in the foetus another role in addition to its well-known anticoagulant function.

Adolescent↗
PubMed1998

Elevated concentrations of soluble E-selectin and vascular cell adhesion molecule-1 in NIDDM. Effect of intensive insulin treatment.

OBJECTIVE: To evaluate the effects of a 14-day intensive insulin therapy and short-term improvement of glycemic control on serum levels of soluble forms of adhesion molecules, i.e., intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1), and E-selectin (sE-selectin) in NIDDM patients with poor glycemic control. RESEARCH DESIGN AND METHODS: A total of 16 NIDDM patients were compared with 23 healthy subjects (control group) and investigated before and after intensive insulin treatment. RESULTS: On day 0, sE-selectin and sVCAM-1 levels were significantly higher in NIDDM patients than in nondiabetic control subjects (median 87, range 63-115; median 544, range 408-797 vs. 58, 43-80; 443, 395-573 ng/ml, respectively) (P < 0.008 in both cases). On day 15, the fall in sE-selectin levels was significant (P < 0.0001) and at a lesser extent in sVCAM-1 levels (64, 48-85; 506, 417-678 ng/ml, respectively); these levels reached values that no longer differed from those of control subjects (P = 0.23 and 0.15, respectively). Moreover, the fall in sE-selectin was positively associated with the change in LDL cholesterol and the improvement of glycemia. CONCLUSIONS: In poorly controlled NIDDM patients, sE-selectin levels are increased and significantly fall to normal after short-term improvement of glycemic control. This suggests that assaying sE-selectin makes it possible to detect endothelium activation and to follow its reversal with euglycemia.

Apolipoproteins↗
PubMed1997

A three amino acid deletion in glycoprotein IIIa is responsible for type I Glanzmann's thrombasthenia: importance of residues Ile325Pro326Gly327 for beta3 integrin subunit association.

Glanzmann's thrombasthenia (GT) is a recessive autosomal bleeding disorder characterized by abnormal platelet aggregation due to a qualitative or quantitative defect of the glycoprotein (GP) IIb-IIIa complex (integrin alphaIIb beta3). We describe a new mutation in the GPIIIa gene responsible for type I GT in a consanguineous Algerian family. A discordance between phenotyping and genotyping of the GPIIIa-related HPA-1 platelet alloantigen system in three family members heterozygous for the disease suggested a genetic defect in the GPIIIa gene and a normal GPIIb gene. Sequence analysis of amplified genomic DNA fragments showed a 6-bp deletion in exon 7 of the GPIIIa gene resulting in the amino acid deletion/substitution (Ile325pro326Gly327 --> Met) and creating a new BspHI restriction site. Expression of the mutated integrin beta3 subunit cDNA in Chinese hamster ovary cells showed that the cDNA gene was transcribed into a full-length beta3 protein with an apparent molecular weight identical to wild-type beta3 and accumulated as a single-chain molecule in the cell cytoplasm. The absence of heterodimeric complex formation of the mutant beta3 protein with endogenous alpha v was shown by immunoprecipitation experiments, intracellular immunofluorescent labeling, and a semiquantitative enzyme-linked immunosorbent assay using the alpha vbeta3 complex-specific monoclonal antibodies LM609 and 23C6. Substitution of the methionine residue by a proline, present at position 326 of wild-type beta3, did not restore the ability of the recombinant mutant beta3 protein to associate with alpha v , suggesting that the Ile-Pro-Gly motif is located in a beta3 domain important for integrin subunit interaction. The association of a BspHI restriction site with this newly identified mutation has allowed allele-specific restriction analysis of Algerian GT individuals and the identification of two new unrelated type I patients exhibiting the same mutation, suggesting that the described mutation might be significant in this population and that BspHI restriction analysis will provide a useful screening assay for antenatal diagnosis and genetic counselling.

Algeria↗
PubMed1997

Hyperinsulinemia and hypofibrinolysis: effects of short-term optimized glycemic control with continuous insulin infusion in type II diabetic patients.

A defect in the fibrinolytic system results from an increase in type 1 plasminogen activator inhibitor (PAI-1) in diabetes. It can be considered an independent risk factor for the development of cardiovascular disease. In obese and type II diabetic patients, plasma PAI-1 level correlates with fasting insulinemia. However, during the euglycemic clamp, acute hyperinsulinemia does not increase PAI-1 production. The present study was undertaken to investigate the effect of optimized glycemic control by continuous subcutaneous insulin infusion (CSII) on the hypofibrinolytic state for 14 days in 16 type II diabetic patients with poor metabolic control despite maximal oral antidiabetic treatment. Plasma PAI-1 activity levels decreased from 13.38 +/- 2.85 IU/mL to 6.77 +/- 1.81 IU/mL (P = .002) during CSII, along with a concurrent improvement in insulin sensitivity (index obtained by basal glycemia-nadir glycemia/basal glycemia) during the insulin sensitivity test (0.121 +/- 0.03 v 0.057 +/- 0.02, P = .02). These results suggest that insulin resistance rather than hyperinsulinism may be involved in the hypofibrinolytic state in type II diabetic patients. The positive correlation between the changes in triglycerides and in PAI-1 activity (r = .589, P = .026) strongly suggests a role for triglycerides in the impairment of fibrinolysis, which could be a link between insulin resistance and hypofibrinolysis.

Blood Glucose↗
PubMed1995

[Transient dysfibrinogenemia and thrombocytopenia associated with recurrent acute pancreatitis in the course of isotretinoin therapy].

A 17 year-old young man developed two episodes of acute pancreatitis, separated by a 2 year interval and associated with isotretinoin therapy. In 1989, vesicular sludge without lithiasis was evidenced and in 1991, gall bladder stones were found by cholecystectomy. Concomitantly, transient dysfibrinogenemia and thrombopenia were present. It is interesting to note that far away from the use of isotretinoin, the patient suffered from another episode of acute pancreatitis without any coagulation disorder. The involvement of Roaccutane in cellular differentiation is discussed as well as its causal association with acquired dysfibrinogenemia and transient thrombocytopenia.

Acute Disease↗
PubMed1995

Risk of thromboembolism in relation to an in-vitro fertilization programme: three case reports.

Severe thrombotic events following ovarian stimulation for in-vitro fertilization (IVF) procedures in three women are reported. None of these patients presented any concomitant clinical sign of ovarian hyperstimulation syndrome. Coagulation inhibitors were in the normal range but cardiovascular risk factors were present. It is postulated that early thrombosis could be favoured by high endogenous plasma oestrogen concentrations subsequent to ovarian stimulation when associated with another risk factor. Our data are discussed in relation to previous publications. It is suggested that risk factors must be considered individually before each IVF attempt. In patients at high risk, clinical management of the post-transfer period is recommended.

Adult↗
PubMed1995

Platelet phenotyping in carriers for Glanzmann's thrombasthenia: a simple screening test for assessment of the molecular defect.

Glanzmann's thrombasthenia (GT) is a recessive autosomal bleeding disorder characterized by the abnormality of aggregation due to a platelet glycoprotein (GP) IIb-IIIa deficiency or a dysfunctional complex. Molecular abnormalities have been localized on the gene coding for GP IIb or IIIa. The aim of our work was an attempt to obtain indirectly information on the putative localization of the molecular defect in patients with GT type I or II by the determination of the HPA-1 (GP IIIa) and HPA-3 (GP IIb) alloantigenic systems' expression in GT carriers. If GT results from a defective GP IIb gene, a GT carrier would appear homozygous for HPA-3 by serology, because the normal gene product will be expressed while the abnormal GP IIb gene product will not be present. Conversely, if the abnormality is in the GP IIIa gene, such an individual would appear homozygous for HPA-1. Therefore, the heterozygous status for HPA would result from the normal expression of the two genes for the considered alloantigenic system. Among the four families studied with informative members, our presumptions were strengthened by the preliminary genetic results in one family showing a mutation in the GP IIb gene. Thus, serology could be a simple screening test for the possible defective gene responsible for GT allowing molecular investigation focusing only on GP IIb or IIIa gene.

Antigens, Human Platelet↗
PubMed1994

Prospective study of screening for hepatocellular carcinoma in Caucasian patients with cirrhosis.

Screening is widely used to detect early hepatocellular carcinoma in Asian patients with cirrhosis. Its effectiveness in Caucasian patients has been suggested, but remains to be proven. Therefore we prospectively studied 118 French patients (68 males, 50 females, age 55 +/- 12) with Child-Pugh A or B cirrhosis (alcoholic in 82) and without detectable hepatocellular carcinoma. The screening program consisted of ultrasound examination of the liver and determination of blood alpha-fetoprotein and des-gamma-carboxyprothrombin levels every 6 months. The median follow up was 36 months (range 4-48). Only four patients were lost to follow up. Fourteen hepatocellular carcinomas were detected, in six cases by ultrasonography alone, in four by alpha-fetoprotein alone, in three by ultrasonography and alpha-fetoprotein and in one case by ultrasonography and des-gamma-carboxyprothrombin, but never by des-gamma-carboxyprothrombin alone. The tumor presented as a unique nodule in nine patients. The tumor was less than 3 cm in diameter without portal thrombosis or metastasis in three cases. Surgery was performed in only one case. In this study, the annual incidence of hepatocellular carcinoma was high (5.8%), but the screening methods used did not effectively identify potentially resectable tumors in Caucasian patients with cirrhosis.

Biomarkers↗
PubMed1994

[Portal vein thrombosis: a rare complication of Crohn disease].

Among usual extra digestive manifestations of inflammatory bowel diseases, vascular injuries are rare, but often of excessive gravity. The emergence of a portal thrombosis, often accelerated by infection or traumatism, particularly surgical, remains exceptional. We report the case of a young patient who is followed for a severe crohn's disease and affected with a brutal portal vein thrombosis. Although initial prognosis was bad, the patient now lead a normal life ten months after this episode. It's the third described case of portal thrombosis in crohn's disease. We discuss the predisposing role of an acquired protein S deficiency during a estroprogestative treatment.

Adult↗
PubMed1994

Human platelet alloantigen typing: PCR analysis is not a substitute for serological methods.

Currently, five platelet alloantigen (alloAg) systems have been established (HPA-1, -2, -3, -4, -5). Three of these are expressed on the glycoprotein (GP) IIb-IIIa complex, HPA-1, HPA-3 and HPA-4, inherited in an autosomal codominant mode. Recent investigations of the molecular basis of these platelet alloantigen systems have shown that only one nucleic acid base substitution in the genes encoding for GP IIb and GP IIIa is responsible for the polymorphism. This substitution is reflected in a difference in restriction enzyme recognition allowing platelet alloantigen typing by restriction fragment length polymorphism (RFLP) analysis of DNA amplified by the polymerase chain reaction (PCR). To validate the PCR technology for platelet typing, we have compared PCR-RFLP with monoclonal-antibody-specific immobilization of platelet antigens (MAIPA). For this purpose, we have studied different Glanzmann thrombasthenic families and particularly heterozygous individuals, who are not lacking GP IIb-IIIa, as a model to detect the occurrence of discrepancies between these two technologies. In two families, we have found differences between molecular biology and serological methods with the lack of expression of one antigen on the platelet membrane surface. In the first family, the abnormality is related to the HPA-1 alloantigen system with three informative members; in the second, the HPA-3 alloantigen system is concerned with two informative members. Considering these results, there may not always be a perfect correlation between molecular biology and serological methods, as an unknown molecular defect could interfere with the PCR results and lead to false platelet typing.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Monoclonal↗
PubMed1989

Activated partial thromboplastin time performed on capillary blood.

Activated partial thromboplastin time is one of the most frequently used assay in haemostasis investigation, but sampling of venous blood is often difficult in newborns (as well as some adult patients). We analysed a method described by Zondag et al [9] performed on capillary blood samples. We studied normal adults and newborns, patients with liver diseases, and those receiving therapy with vitamin K antagonists and heparin. Capillary assay was correlated with venous blood in normal subjects, in patients with liver diseases and during therapy by vitamin K antagonists. However results both in newborns and adults during heparin therapy were not accurate.

Adolescent↗
PubMed1989

[Mitral valve prolapse and Willebrand disease. Study of 16 cases of Willebrand disease].

We studied mitral valve morphology and kinetics in 16 children aged 3 to 15 years with documented von Willebrand disease. Mitral valve prolapse was demonstrated in four cases (25%); this result is consistent with findings of similar studies in adults. This non-random association between mitral valve prolapse and von Willebrand disease, as well as embryologic evidence and reports of other conditions found in patients with von Willebrand disease, suggest that mesenchymal dysplasia is the underlying anomaly. Patients with von Willebrand disease and mitral valve prolapse may be at increased risk for cerebrovascular events.

Adolescent↗