Haematology Laboratory

Monastir, Tunisia

Haematology Laboratory

Monastir, Tunisia
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Giannaki K.,Haematology Laboratory | Politou M.,Haematology Laboratory | Rouvas A.,National and Kapodistrian University of Athens | Merkouri E.,Haematology Laboratory | And 3 more authors.
Blood Coagulation and Fibrinolysis | Year: 2013

The role of systemic risk factors (age, smoking, diabetes, arterial hypertension) in the development of retinal vein occlusion (RVO) is well established. However, the association of RVO with genetic predisposition to thrombosis remains poorly understood. The aim of the study was to assess any possible additional effect of genetic predisposition to the already well known 'classical' risk factors of RVO in a cohort of elderly Greek patients. Fifty-one elderly patients with RVO and 51 healthy individuals matched for age and sex were evaluated for systemic risk factors (smoking, diabetes, dyslipidemia, arterial hypertension) and coagulation defects (lupus anticoagulant, natural inhibitors of coagulation). Additionally, genotyping was performed for mutations/polymorphisms involved in haemostasis such as: FV G1691A, FV G4070A, FIIG 20210A, MTHFR C677T and A1298C, PAI-1-675 4G/5G, F XIII exon 2G/T, EPCR A4600G and G4678C. We identified systemic risk factors in the majority of the patients Hypertension (P = 0.001), dyslipidemia (P = 0.029) and diabetes (P = 0.01) are associated with RVO in the majority of the patients. The prevalence of prothrombotic risk factors was not significantly different in the patients with RVO compared to controls. Apart from systemic risk factors, genetic predisposition to thrombosis does not seem to have an important association with RVO in this group of elderly patients. © 2013 Wolters Kluwer Health.

Depince-Berger A.-E.,Jean Monnet University | Aanei C.,Haematology Laboratory | Iobagiu C.,General hospital | Jeraiby M.,Jean Monnet University | Lambert C.,Jean Monnet University
Morphologie | Year: 2016

Cytometry aims to analyze cells, of any type, using dedicated instruments. The quantitative aspect makes flow cytometry (FCM) a good complementary tool for morphology. Most of the identification tools are based on immunostaining of cell structure details and more and more tools are available in terms of specificities and labels. FCM is under exponential development thanks to technical, immunological and data analysis progresses. Actual generations are now routinely using 6 to 10 simultaneous immuno-labeling on 20 to 100,000 cells, at high speed and short sample preparation and can easily detect rare events at frequency below 10-4 cells. Data interpretation is complex and requires expertise. Mathematical tools are available to support analysis and classification of cells based. Cells from tissues can also be analyzed by FCM after mechanical and or enzymatic separation, but in situ cells can also be analyzed with the help of cytometry. Very new instruments bring spectral analysis, image in flow and mass spectrometry. Medical applications are very broad, notably in hemopathies, immunology, solid tumors, but also microbiology, toxicology, drug discovery, food and environmental industry. But, the limit of FCM is its dependence on operator from sample preparation, instrument settings up to data analysis and a strong effort is now under progress for standardization and constitution of international data bank for references and education. La cytométrie vise à analyser les cellules de tout type, en utilisant des instruments dédiés. L'aspect quantitatif fait de la cytométrie de flux (FCM) un bon outil complémentaire à la morphologie. La plupart des outils d'identification sont basés sur une détection immunocytochimique des détails de la structure cellulaire et de plus en plus d'outils sont disponibles en termes de spécificité et de marquages. La FCM est en développement exponentiel grâce aux progrès techniques, immunologiques et en analyse des données. Les générations actuelles d'appareils utilisent maintenant couramment 6 à 10 immuno-marquages simultanés sur 20 à 100 000 cellules, à grande vitesse avec des étapes courtes de préparation des échantillons et peuvent facilement détecter des événements rares à une fréquence inférieure à 10-4 cellules. L'interprétation des données est complexe et nécessite de l'expérience. Des outils mathématiques sont disponibles pour permettre l'analyse et la classification des cellules. Les cellules provenant de tissus peuvent également être analysées par FCM après séparation mécanique ou enzymatique, mais les cellules in situ peuvent également être analysées à l'aide de la cytométrie. Les instruments les plus récents permettent une analyse spectrale, l'image du débit et la spectrométrie de masse. Les applications médicales sont très larges, notamment dans les hémopathies, en immunologie, pour les tumeurs solides, mais aussi la microbiologie, la toxicologie, la découverte de médicaments, l'alimentation et l'industrie de l'environnement. Mais la limite de la FCM est sa dépendance à l'opérateur de la préparation de l'échantillon, les paramètres de l'appareil jusqu'à l'analyse des données et un effort important est actuellement en cours pour la normalisation et de la constitution d'une banque de données internationale pour servir de références et pour l'enseignement. © 2016 Elsevier Masson SAS.

Villa E.,University of Modena and Reggio Emilia | Camma C.,University of Palermo | Marietta M.,Azienda Ospedaliero Universitaria | Luongo M.,University of Modena and Reggio Emilia | And 23 more authors.
Gastroenterology | Year: 2012

Background & Aims: We performed a randomized controlled trial to evaluate the safety and efficacy of enoxaparin, a low-molecular-weight heparin, in preventing portal vein thrombosis (PVT) in patients with advanced cirrhosis. Methods: In a nonblinded, single-center study, 70 outpatients with cirrhosis (Child-Pugh classes B7-C10) with demonstrated patent portal veins and without hepatocellular carcinoma were assigned randomly to groups that were given enoxaparin (4000 IU/day, subcutaneously for 48 weeks; n = 34) or no treatment (controls, n = 36). Ultrasonography (every 3 months) and computed tomography (every 6 months) were performed to check the portal vein axis. The primary outcome was prevention of PVT. Radiologists and hepatologists that assessed outcomes were blinded to group assignments. Analysis was by intention to treat. Results: At 48 weeks, none of the patients in the enoxaparin group had developed PVT, compared with 6 of 36 (16.6%) controls (P =.025). At 96 weeks, no patient developed PVT in the enoxaparin group, compared with 10 of 36 (27.7%) controls (P =.001). At the end of the follow-up period, 8.8% of patients in the enoxaparin group and 27.7% of controls developed PVT (P =.048). The actuarial probability of PVT was lower in the enoxaparin group (P =.006). Liver decompensation was less frequent among patients given enoxaparin (11.7%) than controls (59.4%) (P <.0001); overall values were 38.2% vs 83.0%, respectively (P <.0001). The actuarial probability of liver decompensation was lower in the enoxaparin group (P <.0001). Eight patients in the enoxaparin group and 13 controls died. The actuarial probability of survival was higher in the enoxaparin group (P =.020). No relevant side effects or hemorrhagic events were reported. Conclusions: In a small randomized controlled trial, a 12-month course of enoxaparin was safe and effective in preventing PVT in patients with cirrhosis and a Child-Pugh score of 7-10. Enoxaparin appeared to delay the occurrence of hepatic decompensation and to improve survival. www.isrctn.>org: ISRCTN32383354; www.clinicaltrialsregister.eu: EudraCT2007-007890-22. © 2012 AGA Institute.

Bal Dit Sollier C.,IVS | Berge N.,IVS | Boval B.,Haematology Laboratory | Dubar M.,Sanofi S.A. | Drouet L.,Haematology Laboratory
Thrombosis and Haemostasis | Year: 2010

We previously showed that variability of response to clopidogrel is linked to occupancy of the P2Y 12 receptor by clopidogrel active-metabolite, and that maximal platelet aggregation intensity (MAI) measured by light transmission aggregometry (LTA) correlates with occupancy. The present study compared a range of ex vivo platelet tests at various levels of P2Y 12 occupancy. After screening with clopidogrel 75 mg/day for seven days, subjects were selected to obtain 'low', 'average' and 'high' responders and randomised to clopidogrel (75 mg/day days 1-10; 300 mg day 11), or placebo. Assays were LTA in platelet-rich plasma using 2, 5 and 20 μM ADP, VerifyNow® P2Y 12, flow cytometric analysis of platelet activation markers and vasodilator-stimulated phosphoprotein (VASP) index, and a thromboelastographic test that is sensitive to clopidogrel. The reference test was P2Y 12 receptor occupancy, measured by binding of 33P-2MeS-ADP to platelets. MAI showed the best correlation with P2Y 12 occupancy. Similar results were seen with different ADP concentrations and when LTA data were expressed as inhibition of platelet aggregation. A plot of free receptors/cell versus VASP index was biphasic, with poor correlation for low-level P2Y 12 occupancy. Sensitivity of the VerifyNow P2Y 12 assay decreased at higher clopidogrel responses. Thromboelastography and P-selectin expression had poor correlation with receptor occupancy. In conclusion, LTA data correlate best with P2Y 12 occupancy, the gold standard for detecting clopidogrel's effect at the receptor level. Our results highlight a limitation of the VASP index, which appears unable to distinguish low, average and high responders early after clopidogrel initiation when P2Y 12 occupancy is still low. © Schattauer 2010.

PubMed | Avicenne Hospital, Limoges University Hospital Center, Angers University Hospital Center, Caen University Hospital Center and 6 more.
Type: | Journal: Journal of clinical pathology | Year: 2016

To propose recommendations related to the presentation, content and formulation of full blood count analysis reports.Strong professional agreement among a group of experts from the French-Speaking Cellular Haematology Group (GFHC) was obtained.The following two proposals emerged from the consensus: (1) stratification of comments into three parts upon the discovery of an anomaly in blood cell analysis and (2) selection and/or redefinition of the terms recommended for designating the cell types found in normal and pathological peripheral blood.The recommendations can help biologists who are currently undergoing the process of accreditation.

Wahl D.,French Institute of Health and Medical Research | Wahl D.,University of Lorraine | Wahl D.,Nancy University Hospital Center | Devignes J.,Haematology Laboratory | And 9 more authors.
Lupus | Year: 2012

We conducted a prospective study of anticardiolipin antibody (aCL) testing, performed in our university hospital. Among 6321 consecutive patients tested for both IgG and IgM aCL, 91 patients with medium or high positivity (>99th percentile) had a subsequent confirmatory test. Among them, 53 had a persistent positivity at 12 weeks. In this real world setting, patients with transient positivity had lower values than patients with persistent positivity. © The Author(s), 2012. Reprints and permissions: http://www.sagepub.co.uk/ journalsPermissions.nav.

Lakhdar R.,Biochemistry and Molecular Biology Laboratory | Denden S.,Biochemistry and Molecular Biology Laboratory | Knani J.,CHU Tahar Sfar | Leban N.,Biochemistry and Molecular Biology Laboratory | And 5 more authors.
Genetics and Molecular Research | Year: 2010

Chronic obstructive pulmonary disease (COPD) is a multifactorial disease with possible genetic predisposition and involve-ment of various environmental factors. Several candidate genes have been reported as potentially associated with this lung disease. The glu-tathione S-transferase P1 gene (GSTP1) was proposed to be involved in susceptibility to develop COPD. It belongs to the GST family, which is a group of phase II enzymes that catalyze the glutathione conjugation of many endogenous and exogenous electrophilic compounds, such as car-cinogens, therapeutic drugs, environmental toxins, and oxidative stress products. We conducted a case-control study to investigate genetic poly-morphisms of this enzyme [exon 5 (Ile105Val) and exon 6 (Ala114Val)] in 234 unrelated COPD cases and 182 healthy controls from a Tunisian population. Genotyping was carried out using polymerase chain reaction and restriction fragment length polymorphism methods. GSTP1 Ala114/Val114 and Val114/Val114 genotypes were not found in either patients or healthy controls. However, there were differences in the distribution of various exon 5 GSTP1 genotypes between COPD patients and healthy controls. GSTP1 Val105/Val105 was significantly more com-mon in patients compared to controls (OR = 2.67; 95%CI = 1.45-4.92; P = 0.0013). Multivariate logistic regression analysis confirmed a signifi-cant relationship between the mutant genotype and COPD (OR = 2.58; 95%CI = 1.31-5.09; P = 0.026), after adjustment for classic risk factors. Analysis of variance showed no correlation between age, body-mass in-dex, pack-years, percentage of predicted FEV1 values, and any of the GSTP1 genotypes. We conclude that subjects with GSTP1 Val105 allele are at higher risk of COPD.

Lakhdar R.,Biochemistry and Molecular Biology Laboratory | Denden S.,Biochemistry and Molecular Biology Laboratory | Knani J.,CHU Tahar Sfar | Leban N.,Biochemistry and Molecular Biology Laboratory | And 5 more authors.
Disease Markers | Year: 2011

Smoking is considered as the major causal factor of chronic obstructive pulmonary disease (COPD). Nevertheless, a minority of chronic heavy cigarette smokers develops COPD. This suggests important contribution of other factors such as genetic predisposing. Our objective was to investigate combined role of EPHX1, GSTP1, M1 and T1 gene polymorphisms in COPD risk, its phenotypes and lung function impairment. Prevalence of EPHX1, GSTP1, M1 and T1 gene polymorphisms were assessed in 234 COPD patients and 182 healthy controls from Tunisia. Genotypes of EPHX1 (Tyr113His; His139Arg) and GSTP1 (Ile105Val; Ala114Val) polymorphisms were performed by PCR-RFLP, while the deletion in GSTM1 and GSTT1 genes was determined using multiplex PCR. Analysis of combinations showed a significant association of 113His/His EPHX1/null-GSTM1 (OR=4.07) and null-GSTM1/105Val/Val GSTP1 (OR =3.56) genotypes with increased risk of COPD (respectively P=0.0094 and P=0.0153). The null-GSTM1/ null-GSTT1, 105Val/Val GSTP1/null GSTT1, 113His/His EPHX1/null-GSTM1 and null-GSTM1/105Val/Val GSTP1 genotypes were related to emphysema (respectively P=0.01; P=0.009; P=0.008 and P=0.001). Combination of 113His/His EPHX1/null-GSTM1 genotypes showed a significant association with the decrease of Δ FEV1 in patients (P =0.028). In conclusion, our results suggest combined EPHX1, GSTP1, GSTM1 and GSTT1 genetic polymorphisms may play a significant role in the development of COPD, emphysema and decline of the lung function. © 2011 - IOS Press and the authors. All rights reserved.

Lakhdar R.,Biochemistry and Molecular Biology Laboratory | Denden S.,Biochemistry and Molecular Biology Laboratory | Knani J.,CHU Tahar Sfar | Leban N.,Biochemistry and Molecular Biology Laboratory | And 5 more authors.
Genetic Testing and Molecular Biomarkers | Year: 2010

It is well known that cigarette smoking is the major risk factor for chronic obstructive pulmonary disease (COPD). However, only 10%-20% of chronic heavy cigarette smokers develop symptomatic disease, which suggests the presence of genetic susceptibility. Microsomal epoxide hydrolase (EPHX1) is an enzyme involved in the protective mechanism against oxidative stress. It has been reported that gene polymorphisms of this enzyme may be associated with variations in EPHX1 activity. In this study, we aimed at investigating the relationship between EPHX1 polymorphisms and susceptibility to COPD in the Tunisian population. EPHX1 exon 3 (rs1051740, Tyr113His) and exon 4 (rs2234922, His139Arg) polymorphisms were genotyped by polymerase chain reaction followed by restriction fragment length polymorphism analysis. These techniques were used to examine a total of 416 Tunisian individuals, including 182 blood donors and a group of 234 COPD patients. All subjects were not related. An increased risk for COPD was observed in subjects with EPHX1 His113-His113 genotype (odds ratio=2.168; confidence interval 1.098-4.283; p=0.02386). However, multivariate logistic regression analysis showed no significant relationship between the mutant genotype and the disease after adjustment for sex, age, body mass index, smoking status, and pack-year smoking (odds ratio=1.524; confidence interval, 0.991-6.058; p=0.06137). Regarding the two subtypes of COPD, our investigations demonstrated that there is no significant correlation between exon 3 polymorphism and the chronic bronchitis subgroup (p=0.09034). The relation between exon 3 polymorphism and emphysema was significant in the univariate analysis (p=0.02257), but no association was found after controlling for classic risk factors (p=0.06273). In conclusion, our results showed that there is a weak relation between 113His genotype and COPD, and no apparent relation between 139Arg and COPD in the studied Tunisian population. © 2010, Mary Ann Liebert, Inc.

Ronayne C.,University of Otago | Ronayne C.,Haematology Laboratory
New Zealand Journal of Medical Laboratory Science | Year: 2013

A young woman with a history of Plasmodium falciparum and schistosomiasis presented with anaemia and thrombocytopenia. A diagnosis of Plasmodium ovale malaria was made. Shortly after initiating treatment her anaemia worsened and she developed a circulating lupus anticoagulant, but had no clinical features of antiphospholipid syndrome. Potential mechanisms and interactions relating to her symptoms and laboratory results are explored. © 2013 The author.

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