Diss. (sammanfattning) Stockholm : Karol. inst., 2004. / Härtill 6 uppsatser.

Orientadores: Cristina Laguna Benetti Pinto, Joyce Maria Annichino-Bizzacchi / Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas / Made available in DSpace on 2018-08-21T06:46:28Z (GMT). No. of bitstreams: 1 Mendonca-Louzeiro_MariaRaquelMarquesFurtadode_M.pdf: 1924432 bytes, checksum: 662032611d6d778ba5a4f7f7764ce617 (MD5) Previous issue date: 2012 / Resumo: Introdução: Os distúrbios hemostáticos são pouco estudados na Síndrome dos Ovários Policísticos (SOP). Mulheres com SOP manifestam frequentemente fatores de risco tromboembólico como obesidade, hiperandrogenismo e resistência insulínica, representando evidências indiretas que sugerem maior probabilidade de alterações na coagulação. Objetivo: Avaliar alguns marcadores do sistema hemostático e sua associação com parâmetros clínicos e laboratoriais em mulheres com SOP. Sujeitos e Método: Estudo transversal para avaliação de 45 mulheres com SOP atendidas no Ambulatório de Ginecologia Endócrina do Departamento de Tocoginecologia da Faculdade de Ciências Médicas, UNICAMP, e de 45 mulheres com função gonadal normal, pareadas por idade em anos completos (± 2 anos) e IMC (± 2kg/m2). Foram avaliados parâmetros clínicos [circunferência da cintura (CC), circunferência do quadril (CQ), relação cintura-quadril (C/Q), índice Ferriman-Gallwey (IFG)] e laboratoriais [glicemia de jejum, insulina de jejum, testosterona total (TT) e livre (TL)], e dosados os marcadores de hemostasia: inibidor do ativador do plasminogênio do tipo 1 (PAI-1), inibidor da fibrinólise ativado pela trombina (TAFI), D-dímero e teste de geração de trombina (TGT). Os dados foram comparados entre os grupos através dos testes t Student pareado ou Mann-Whitney. A correlação entre os marcadores de hemostasia e alguns parâmetros clínicos e laboratoriais de mulheres com SOP foi avaliada pelo índice de Pearson. O nível de significância foi de 5%. Resultados: As mulheres do grupo SOP e controles eram jovens (26,13 ± 4,31 e 26,22 ± 4,28 anos, respectivamente) e com sobrepeso (29,32 ± 6,37 e 29,25 ± 6,32kg/m2), tendo sido pareadas para estas variáveis (idade e IMC). Mulheres com SOP apresentaram maior relação C/Q (0,79 ± 0,08 e 0,76 ± 0,05, p=0,03), IFG (9,42 ± 5,32 e 0,62 ± 0,83, p<0,01), TT (0,53 ± 0,30 e 0,30 ± 0,29ng/ml, p<0,01) e TL (1,42 ± 1,00; 0,88 ± 0,32pg/ml, p=0,02) quando comparadas ao grupo-controle. Os grupos não diferiram quanto às dosagens de glicemia, insulina e HOMA-IR. Dentre os marcadores hemostáticos, observou-se que o tempo para o início da geração de trombina (T lag) do TGT apresentou diferença significativa entre os grupos SOP e controle (25,65 ± 2,61 e 26,76 ± 2,11 s, p=0,03, respectivamente) significando que, nas mulheres com SOP, a geração de trombina ocorre mais rapidamente, sugerindo maior risco de hipercoagulabilidade. Nas mulheres com SOP, os níveis séricos dos marcadores fibrinolíticos PAI-1 e D-dímero correlacionaram-se positivamente com os parâmetros clínicos idade, IMC, CC, CQ e relação C/Q, enquanto que o TAFI correlacionou-se positivamente com IMC, CC e relação C/Q, ressaltando o papel da obesidade como fator de risco tromboembólico. Dentre os parâmetros laboratoriais, observou-se correlação direta do PAI-1 com insulina e HOMA-IR, e do TAFI, com glicemia. Nas mulheres com SOP, a idade correlacionou-se diretamente com PAI-1 e D-dímero e inversamente ao T lag e ao tempo para o pico de geração de trombina (Tmáx) do TGT, sugerindo que, com o avançar da idade, ocorra elevação dos níveis de PAI-1 e D-dímero (aumentando o risco de hipofibrinólise), e redução tanto do tempo até a primeira explosão de trombina ocorrer, quanto do tempo para o pico de geração de trombina, levando a um estado de hipercoagulabilidade. Os parâmetros IMC, CC e TL apresentaram correlação positiva direta com a concentração máxima de trombina (Cmáx) e com a área sob a curva (AUC) ou potencial de trombina endógena (ETP) do mesmo teste. Conclusão: Mulheres jovens com SOP geram trombina mais rapidamente que mulheres jovens de mesmo IMC sem a presença de SOP. A distribuição de gordura androide, o avanço da idade, a resistência insulínica e a testosterona livre podem influenciar diretamente alguns marcadores de hemostasia, elevando o risco tromboembólico / Abstract: Introduction: Few studies have been conducted on hemostatic disorders in polycystic ovary syndrome (PCOS). In women with PCOS, thromboembolic risk factors such as obesity, hyperandrogenism and insulin resistance are often present, indirectly suggesting a greater probability of coagulation disorders. Objective: To evaluate some markers of the hemostatic system and their association with the clinical and laboratory parameters of women with PCOS. Subjects and Methods: A cross-sectional study was conducted to evaluate 45 women with PCOS receiving care at the Gynecological Endocrinology Outpatient Clinic of the Department of Obstetrics and Gynecology, School of Medical Sciences, University of Campinas (UNICAMP) and 45 women with normal ovarian function, paired for age (± 2 years) and body mass index (BMI) (± 2kg/m2). The following clinical parameters were evaluated: waist circumference (WC), hip circumference (HC), waist/hip ratio (W/H ratio) and the Ferriman-Gallwey index (FGI), as well as the following laboratory parameters: fasting glucose, fasting insulin, total testosterone (TT) and free testosterone (FT). In addition, the hemostatic markers plasminogen activator inhibitor-1 (PAI-1), thrombin-activatable fibrinolysis inhibitor (TAFI) and D-dimer were measured and the thrombin generation test (TGT) was performed. The groups were compared using Student's paired t-test or the Mann-Whitney test. The correlation between the hemostatic markers and some clinical and laboratory parameters of women with PCOS was evaluated using Pearson's correlation coefficient. Significance level was defined at 5%. Results: Since the women in the PCOS group were paired with those in the control group according to age and BMI, the women in both groups were young (26.13 ± 4.31 and 26.22 ± 4.28 years, respectively) and overweight (29.32 ± 6.37 and 29.25 ± 6.32kg/m2, respectively). However, the women with PCOS had a higher W/H ratio (0.79 ± 0.08 and 0.76 ± 0.05; p = 0.03), FGI (9.42 ± 5.32 and 0.62 ± 0.83; p<0.01), TT (0.53 ± 0.30 and 0.30 ± 0.29ng/ml; p<0.01) and FT levels (1.42 ± 1.00 and 0.88 ± 0.32pg/ml; p = 0.02) compared to those in the control group. There were no statistically significant differences between the two groups with respect to glucose or insulin levels or the homeostasis model of assessment - insulin resistance (HOMA-IR). With respect to the hemostatic markers, the only statistically significant difference between the PCOS and the control group was in the thrombin generation lag-time (25.65 ± 2.61 and 26.76 ± 2.11 s, respectively, p = 0.03), meaning that thrombin generation was faster in the women with PCOS, suggesting a higher risk of hypercoagulability. In the women with PCOS, serum levels of the fibrinolytic markers PAI-1 and D-dimer correlated positively with the following clinical parameters: age, BMI, WC, HC and W/H ratio, whereas TAFI correlated positively with BMI, WC and with the W/H ratio, emphasizing the role of obesity as a risk factor for thromboembolism. Of the laboratory parameters, a direct correlation was found between PAI-1 and insulin and HOMA-IR and between TAFI and glucose. In the women with PCOS, age correlated positively with PAI- 1 and D-dimer and inversely with the lag time and the time to peak thrombin generation (Tmax) of the TGT, suggesting an increase in PAI-1 and D-dimer levels with increasing age (elevating the risk of hypofibrinolysis), as well as a reduction both in the time until the initial thrombin burst and in the time to peak thrombin generation, leading to a state of hypercoagulability. In addition, BMI, WC and FT correlated positively with the maximum concentration of thrombin (Cmax) and with the area under the thrombin generation curve (AUC) or the endogenous thrombin potential (ETP) in the same test. Conclusion: Thrombin generation is faster in young women with PCOS compared to young women with the same BMI but without PCOS. Android fat distribution, increasing age, insulin resistance and free testosterone may directly affect some hemostatic markers, increasing the risk of thromboembolism / Mestrado / Fisiopatologia Ginecológica / Mestra em Ciências da Saúde

Patients with rheumatoid arthritis (RA) have a shorter life span than the general population. An increased death due to cardiovascular disease (CVD) has been reported. RA is characterized by synovitis and joint destruction accompanied by an acute phase reaction and systemic features. The present work investigates the epidemiology of CVD in patients with RA in the county of Västerbotten and the influence of inflammation on lipid metabolism and haemostasis. In a retrospective cohort study on 606 RA patients, the overall mortality was significantly higher than in the general population, with an excess death rate for CVD and for ishemic heart diseae (IHD) in both sexes. Multiple Cox regression, showed that male sex, higher age at disease onset and cardiovascular event increased the risk for death. Male sex, high age at disease onset and hypertension increased the risk for cardiovascular event. Diabetes mellitus, treatment with corticosteroids, disease modifying antirheumatic drugs and postmenopausal estrogen neither influenced survival nor the risk of cardiovascular event. In 93 patients with active RA, the levels of cholesterol, high density- (HDL) and low density (LDL) lipoprotein cholesterol were significantly lower, and Lipoprotein(a) was significantly higher compared to controls. In a follow-up on 53 patients, a relation between the change of Lp(a) and acute phase proteins was found only in patients with high levels of Lp(a). Preheparin lipoprotein lipase (LPL) activity and mass were significantly decreased in 17 postmenopausal women with active RA. Preheparin LPL mass correlated inversely to several acute phase proteins and interleukin-6. Low levels of LPL mass may implicate increased hepatic clearence but also increased macrophage ingestion of lipoproteins via the LDL receptor-related protein (LRP). Haemostasis of the circulation was investigated in 74 of the 93 patients with active RA. In patients with extraarticular disease, the release of tissue plasminogen activator (tPA) was significantly decreased, and its inhibitor (PAI-1) was significantly increased compared to patients with nonsystemic disease, implicating hypofibrinolysis. In a two year follow-up, patients with thromboembolic events had significantly elevated levels of von Willebrand factor, PAI-1, triglycerides and haptoglobin compared to event-free patients. In 29 RA patients and 18 spondylarthropathy patients with gonarthritis, radiological joint destruction correlated to PAI-1 antigen in synovial fluid and, inversely, to plasminogen. A relationship between activation of fibrin degrading proteolytic enzymes and joint destruction was implicated. In conclusion, several processes involved in lipid metabolism and haemostasis are influenced in active RA. In view of the increased death rate due to CVD, an efficient control of inflammation should be important, not only for reducing joint destruction, but also for reducing systemical atherogenic and thrombogenic effects. / <p>s. 1-54: sammanfattning, s. 55-133: 6 uppsatser</p> / digitalisering@umu.se

The impact storage has on function of platelet concentrates is not completely known, although some factors have been discovered and measures have been taken to counteract them, such as adding platelet additive solution. There are several methods for analysing platelet function. In this study, the aim was to analyse change of platelet function in platelet concentrates over time and to see what effect fibrogen has on the coagulation. A technique using free oscillation rheometry (FOR), ReoRox®, was used to analyse function in platelet concentrates, both over time and after addition of fibrinogen. The platelets were analyzed at a concentration of 800 x109 Ptl/L and activated with thrombin receptor antigen peptide (TRAP). For fibrinogen efect analysis, four different concentrations were used, 10 g/L, 2,25 g/L, 1,0 g/L and 0,1 g/L. The results showed no statistically significant change in the function over time. However an increase in elasticity and decrease in the decline of elasticity could be seen. While analysing the platelets with fibrinogen it showed that up to 2,25 g/L the aggregation increased, while it decreased significantly at 10 g/L. In conclusion, the platelet concentrates retained a good clotting function from day one to day seven of storage, while the clot became stronger and fibrinolysis decreased. Fibrinogen proved important for coagulation, however a too high concentration inhibits coagulation.

La grippe est une maladie respiratoire aigüe, due à une infection par des virus influenza et qui représente un problème important de santé publique. Une meilleure compréhension des interactions entre le virus influenza et son hôte nous permettra de mieux comprendre la physiopathologie de l'infection grippale, et donc, à terme, de mieux se protéger contre la maladie. La morbidité et la mortalité, causées par les infections grippales sévères, sont associées à une dérégulation de la réponse immunitaire, au niveau pulmonaire. Cette inflammation délétère serait à l'origine de dommages collatéraux du poumon, entrainant une diminution de la capacité respiratoire du patient. Bien que les mécanismes impliqués ne soient pas totalement élucidés, de récents travaux mettent en évidence un rôle central des cellules endothéliales dans la dérégulation de la réponse de l'hôte face à l'infection grippale. Lors d'une agression de l'endothélium, le processus physiologique de l'hémostase (activation plaquettaire, coagulation et fibrinolyse) s'active afin de permettre la cicatrisation de la plaie et de maintenir l'intégrité des vaisseaux sanguins. Dans de nombreuses maladies inflammatoires, la seule dérégulation de l'hémostase est directement liée à une réponse inflammatoire délétère. Lors de ma thèse, nous avons émis l'hypothèse que l'hémostase pouvait être à l'origine de la dérégulation inflammatoire durant les infections grippales. Nos données montrent le rôle de deux facteurs fortement impliqués dans l'hémostase : le récepteur activé par la thrombine, PAR-1 (Protease Activated Receptor J) ainsi que le plasminogène, dans l'inflammation délétère des poumons et dans la pathogénicité des virus influenza. Outre le rôle de l'hémostase, nous avons également pu mettre en évidence que le virus influenza incorpore des protéines cellulaires dans l'enveloppe virale, lui permettant d'échapper au système immunitaire, ce qui pourrait aussi contribuer à la dérégulation de la réponse de l'hôte. L'ensemble des résultats obtenus ont permis de mieux comprendre les mécanismes à l'origine d'une réponse immunitaire dérégulée dans les infections grippales et de proposer de nouvelles cibles thérapeutiques pour lutter contre la maladie / Influenza is an acute respiratory disease caused by infection with influenza virus and is a major public health problem. A better understanding of the interaction between influenza virus and host allow us to better understand the pathophysiology of influenza infection, and thus, ultimately, to better protect themselves against the disease. Morbidity and mortality caused by severe influenza infections are associated with dysregulation of the immune response in the lung. This deleterious inflammation is the cause of lung collateral damage, causing a decrease in the patient's breathing capacity. Although the mechanisms involved are not fully understood, recent studies point to a central role of endothelial cells in the deregulation of the host response to influenza infection. During endothelium aggression, the physiological process of hemostasis (platelet activation, coagulation and fibrinolysis) is activated in order to allow wound healing and to maintain the integrity of blood vessels. In many inflammatory diseases, the only dysregulation of hemostasis is directly linked to a deleterious inflammatory response. During my thesis, we hypothesized that hemostasis could be the cause of the inflammatory dysregulation during influenza infections. Our data show the role of two factors strongly involved in hemostasis: the thrombin activated receptor, PAR-1 (protease activated receptor 1) and plasminogen, in the deleterious lung inflammation and in the pathogenicity of influenza virus. Besides the role of hemostasis, we have also been able to show that the influenza virus incorporates cellular proteins in the viral envelope, allowing it to evade the immune system, which could also contribute to the deregulation of the host response. All the results obtained allowed to better understand the mechanisms involved in immune response dysregulation during influenza infection and suggest new therapeutic targets to fight against the disease

No description available.

A dissertation submitted to the Faculty of Health Sciences, University of the Witwatersrand, in fulfillment of the degree of Master of Science in Medicine, 2014 / The earliest possible initiation of reperfusion therapy is necessary to reduce morbidity and mortality from acute STEMI. Therefore improving the time to thrombolysis where percutaneous coronary interventional facilities are limited or do not exist is critical. The most effective system would integrate three key components to deliver continuous patient care, including: 1) from time of call for help through to emergency response; 2) transportation to and admission to hospital; 3) assessment and initiation of thrombolytic therapy. The purpose of this prospective study is: to develop a chest pain awareness education programme appropriate for the South African context; to assess safe initiation of thrombolytic therapy by emergency care practitioners for STEMI; and to compare the performance of emergency care practitioner thrombolysis with historical control data.

Hintergrund: Abdominale Adhäsionen entstehen vor allem durch Operationen. Sie können ernste Beschwerden auslösen, wie Dünndarmileus, Infertilität und chronische Schmerzen. Eine allgemein anerkannte Prophylaxe und/oder Therapie existiert trotz intensiver Forschung nicht. Steigende Lebenserwartung und erweiterte Operationsindikationen verschärfen das Problem. Ziel: Diese Studie soll zeigen, dass der Angiogeneseinhibitor Thalidomid postoperative Verwachsungen im Tiermodell hemmt ohne die Wundheilung zu gefährden. Methoden: 40 New Zealand White Kaninchen wurden bei einem operativen Eingriff einmalig intraperitoneal mit Thalidomid oder einem Placebo behandelt. Nach drei oder sieben Tagen wurden die Tiere erneut operiert. Danach wurden Adhäsionsbildung und Angiogenese beurteilt. Von TNF-alpha, einem wichtigen Mediator für Adhäsionen, wurden die Serumspiegel ermittelt. Die Wundheilung wurde durch visuelle Inspektion sowie durch Bestimmung von Berstungsdruck und –stelle kontrolliert. Ergebnisse: Thalidomid hemmt postoperative Adhäsionen. In der Therapiegruppe hatten 75 Prozent der Tiere keine und 25 Prozent minimale Adhäsionen. In der Kontrollgruppe dagegen traten bei knapp 50 Prozent der Tiere mäßige oder dichte Adhäsionen auf. Drei Mechanismen scheinen für die adhäsionsinhibierende Wirkung von Thalidomid verantwortlich zu sein: Hemmung der Angiogenese, Modulation der Fibrinolyse und Reduzierung der Entzündungsreaktion. Das Operationsergebnis gefährdet Thalidomid nicht. Bei der Inspektion wiesen alle Kaninchen regelgerechte Wundverhältnisse auf. Die ermittelten Berstungsdrücke und -stellen zeigten keine signifikanten Unterschiede zwischen Therapie- und Kontrollgruppe. Schlussfolgerungen: Wegen der entscheidenden Rolle der Angiogenese für die Wundheilung, aber auch wegen der teratogenen Effekte von Thalidomid, muss die adhäsionsinhibierende Wirkung von Thalidomid vor einem klinischen Einsatz in weiteren Tierversuchen verifiziert werden. Überprüft werden sollte dabei, ob neben den drei diskutierten Mechanismen, weitere vor allem immunmodulatorische Prozesse die Adhäsionshemmung bewirken. / Background: Abdominal adhesions mainly result from surgery. They can cause severe trouble like small bowel obstruction, female infertility and chronic pain. A generally recognised prevention and/or therapy does not exist despite intensive research. Increasing life expectancy and a wider range of indications for operations make matters worse. Objective: The purpose of the study is to demonstrate that the angiogenesis inhibitor thalidomide inhibits postsurgical adhesions in an animal model without impacting wound healing. Methods: 40 New Zealand White rabbits were treated once in an operation intraperitoneal with either thalidomide or with a placebo. After three or seven days the animals again underwent an operation. Thereafter the adhesions formation and angiogenesis was assessed. The level of TNF-alpha, an important mediator for adhesions, in blood was measured. The wound healing was controlled by visual inspection and the determination of the bursting pressure und location. Resuts: Thalidomid inhibits postsurgical adhesions. In the therapy sample 75 per cent of the animals had no and 25 per cent had minimal adhesions. In the control sample almost 50 per cent of the animals had moderate or dense adhesions. Three mechamisms appear to be responsible for thalidomide to inhibit adhesions: the inhibition of the angiogenesis, the modulation of the fibrinolysis and the reduction of the inflammation. The result of the operation was not impacted by thalidomide. All rabbits showed normal wound healing. The bursting pressure and location did not differ significantly between the therapy and the control sample. Conclusions: Because of the importance of the angiogenesis for wound healing as well as the teratogenic effects of thalidomide, thalidomide must be further analysed in animal tests before being applied in clinical practice. As part of this it should be examined whether in addition to the three mechansims discussed, other proceeses, in particular immune modulating processes contribute to inhibit adhesions.

Despite major advances in the treatment and prevention of atherosclerosis the last several decades, cardiovascular disease still accounts for the majority of deaths in Sweden. With the population getting older, more obese and with rising numbers of diabetics, the cardiovascular disease burden may increase further in the future. The focus in cardiovascular disease has shifted with time from calcification and narrowing of arteries to the biological processes within the atherosclerotic plaque. C-reactive protein (CRP) has emerged as one of many proteins that reflect a low grade systemic inflammation and is suitable for analysis as it is more stable and easily measured than most other inflammatory markers. Several large prospective studies have shown that CRP is not only an inflammatory marker, but even a predictive marker for cardiovascular disease. C-reactive protein is associated with several other risk factors for cardiovascular disease including obesity and the metabolic syndrome. Our study of twenty healthy men during a two week endurance cross country skiing tour demonstrated a decline in already low baseline CRP levels immediately after the tour and six weeks later. In a study of 200 obese individuals with impaired glucose tolerance randomised to a counselling session at their health care centre or a one month stay at a wellness centre, we found decreased levels of CRP in subjects admitted to the wellness centre. The effect remained at one, but not after three years of follow-up. In a prospective, nested, case-referent study with 308 ischemic strokes, 61 intracerebral haemorrhages and 735 matched referents, CRP was associated with ischemic stroke in both uni- and multivariate analyses. No association was found with intracerebral haemorrhages. When classifying ischemic stroke according to TOAST criteria, CRP was associated with small vessel disease. The CRP 1444 (CC/CT vs. TT) polymorphism was associated with plasma levels of CRP, but neither with ischemic stroke nor with intracerebral haemorrhage. A study on 129 patients with atrial fibrillation was used to evaluate whether inflammation sensitive fibrinolytic variables adjusted for CRP could predict recurrence of atrial fibrillation after electrical cardioversion. In multivariate iv models, lower PAI-1 mass was associated with sinus rhythm even after adjusting for CRP and markers of the metabolic syndrome. In conclusion, lifestyle intervention can be used to reduce CRP levels, but it remains a challenge to maintain this effect. CRP is a marker of ischemic stroke, but there are no significant associations between the CRP1444 polymorphism and any stroke subtype, suggesting that the CRP relationship with ischemic stroke is not causal. The fibrinolytic variable, PAI-1, is associated with the risk of recurrence of atrial fibrillation after electrical cardioversion after adjustment for CRP. Our findings suggest a pathophysiological link between atrial fibrillation and PAI-1, but the relation to inflammation remains unclear.

Le rôle physiologique du caillot est d’éviter un épanchement excessif de sang en présence d’une brèche vasculaire. Une fois cette fonction remplie, il doit pouvoir être facilement détruit, afin qu’il ne passe pas dans le système veineux et ne gêne la circulation sanguine. La formation d’un caillot de fibrine et sa lyse, processus clés de l’hémostase, impliquent à la fois la polymérisation des monomères de fibrinogène en un réseau de fibres de fibrine, et la résorption du réseau de fibres de fibrine constitué. Bien que ce réseau contrôle l’ensemble des propriétés physiques et mécaniques du caillot, sa structure aux échelles inférieures au micron est très mal caractérisée. Le principal verrou à la caractérisation physique du caillot en environnement clinique est l’absence de méthode de mesure quantitative, fiable, sensible et reproductible. Il est donc nécessaire de produire une méthode de mesure adéquate, couplée à un système de mesure sensible. Nous avons démontré dans ce travail, grâce à notre méthode utilisant plusieurs longueurs d’onde, que l’analyse du spectre de lumière visible transmis à travers un caillot permet de déterminer simultanément, quantitativement et en conditions quasi-physiologiques, plusieurs paramètres essentiels de structure du caillot de fibrine, à savoir le nombre de protofibrilles par fibre de fibrine, le rayon et la densité de ces fibres, ainsi que les temps de formation et de lyse du caillot. Cette technique a été validée via les résultats avec des CV inférieurs dans l’ensemble à 6% sous plusieurs conditions de tests et différents profils plasmatiques : normaux, hypo/hyper coagulants et hypo/hyper fibrinolytiques, attestant de la robustesse et de la fiabilité de la technique de mesure aussi bien pour le suivi de la coagulation que de la lyse. Cette méthode de spectrophotométrie a pu être implantée sur un automate modifié à des fins de diagnostic et à vocation hospitalière pour des plasmas de patients présentant des troubles de l’hémostase. Les informations cliniques et intérêts attendus de ce nouveau test, concernent à la fois la qualité du réseau de fibrine, sa lyse accélérée ou sa résistance à la fibrinolyse ainsi que la résultante de la balance coagulo-lytique. / The physiological role of the clot is to avoid excessive bleeding in the presence of a vascular breach. Once this function is filled, the clot must be able to be easily destroyed, so that it is not transported in the venous system and does not hamper blood circulation. The formation of a fibrin clot and its lysis are key processes of hemostasis, implying simultaneously the polymerization of the fibrinogen monomers in a fibrin fibers network, and the destruction of this constituted network.Although this network controls the physical and mechanical properties of the clot, its structure at scales smaller than the micron is poorly characterized. The main problem in the physical characterization of clot in clinical settings is the current absence of a quantitative, sensitive and reproducible measurement method.We demonstrated in this work, thanks to our method using several wavelengths, that the analysis of the visible spectra of light transmitted through a clot allows to determine simultaneously, quantitatively and in quasi-physiological conditions, several essential parameters of structure of the fibrin clot, namely the number of protofibrils per fibrin fibers, the radius and the density of fibers, and various times of clotting and lysis of the clot. This method was validated by the results with CV inferior to 6 % under all test conditions and various plasmatic profiles: normal, hypo / hyper coagulant and hypo / hyper fibrinolytic. This demonstrates the robustness and reliability of the measurement method when measuring both clotting and clot lysis.This spectrophotometric method was implemented on a modified automaton dedicated to diagnosis of patients presenting hemostatic disorders. The clinical information and the interests expected from this new test concern at the same time the quality of the fibrin network, its accelerated lysis or its resistance to fibrinolysis, and the resultant of the coagulo-lytic balance.