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Articoli di riviste sul tema "Non-insulin-dependent diabetes"

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Pandya, Maitrey, e Miral Damani. "NEUROPHYSIOLOGICAL CHANGES IN PERSON WITH INSULIN DEPENDENT AND NON INSULIN DEPENDENT DIABETES MELLITUS". International Journal of Physiotherapy and Research 7, n. 2 (11 marzo 2019): 3011–15. http://dx.doi.org/10.16965/ijpr.2019.102.

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Mera, Carlos Andree Cevallos. "Therapeutic Adherence in Patients with Diabetes Mellitus Non-insulin Dependent". International Journal of Psychosocial Rehabilitation 24, n. 5 (31 marzo 2020): 1571–78. http://dx.doi.org/10.37200/ijpr/v24i5/pr201828.

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Grunstein, H. S., G. A. Smythe, L. H. Storlien, Per Westermark e Erik Wilander. "NON-INSULIN-DEPENDENT DIABETES". Lancet 326, n. 8446 (luglio 1985): 104–5. http://dx.doi.org/10.1016/s0140-6736(85)90212-0.

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Pandya, Maitrey, e Miral Damani. "NEUROPHYSIOLOGICAL CHANGES IN CONTEXT TO DURATION OF EXPOSURE IN INSULIN DEPENDENT AND NON INSULIN DEPENDENT DIABETES MELLITUS". International Journal of Physiotherapy and Research 5, n. 2 (11 aprile 2017): 1902–5. http://dx.doi.org/10.16965/ijpr.2016.178.

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Knowler, W. C., K. M. Narayan, R. L. Hanson, R. G. Nelson, P. H. Bennett, J. Tuomilehto, B. Schersten e D. J. Pettitt. "Preventing non-insulin-dependent diabetes". Diabetes 44, n. 5 (1 maggio 1995): 483–88. http://dx.doi.org/10.2337/diabetes.44.5.483.

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Knowler, W. C., K. M. V. Narayan, R. L. Hanson, R. G. Nelson, P. H. Bennett, J. Tuomilehto, B. Schersten e D. J. Pettitt. "Preventing Non-Insulin-Dependent Diabetes". Diabetes 44, n. 5 (1 maggio 1995): 483–88. http://dx.doi.org/10.2337/diab.44.5.483.

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Nelson, Roger L. "Non-insulin-dependent diabetes mellitus". Postgraduate Medicine 81, n. 6 (maggio 1987): 177–86. http://dx.doi.org/10.1080/00325481.1987.11699825.

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Hales, C. N. "Non-insulin-dependent diabetes mellitus". British Medical Bulletin 53, n. 1 (1 gennaio 1997): 109–22. http://dx.doi.org/10.1093/oxfordjournals.bmb.a011594.

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Flick, Mary, e Lorna Schumann. "Non?Insulin-Dependent Diabetes Mellitus". Journal of the American Academy of Nurse Practitioners 9, n. 7 (luglio 1997): 337–44. http://dx.doi.org/10.1111/j.1745-7599.1997.tb01201.x.

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Temple, RosemaryC, StephenD Luzio, AnneroseE Schneider, ChristineA Carrington, DavidR Owens, WendyJ Sobey e C. Nicholas Hales. "INSULIN DEFICIENCY IN NON-INSULIN-DEPENDENT DIABETES". Lancet 333, n. 8633 (febbraio 1989): 293–95. http://dx.doi.org/10.1016/s0140-6736(89)91306-8.

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Tesi sul tema "Non-insulin-dependent diabetes"

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Gormley, M. J. J. "Aspects of insulin treatment of non-insulin-dependent diabetes". Thesis, Queen's University Belfast, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.373006.

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Baynes, Christospher. "Insulin action and dyslipidaemia in non-insulin-dependent diabetes". Thesis, University of Southampton, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316405.

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Dornhorst, Anne. "Gestational diabetes : a model of non-insulin dependent diabetes". Thesis, University of Oxford, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334887.

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Gelding, Susan Valerie. "Metabolic abnormalities preceding non-insulin dependent diabetes". Thesis, University College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283202.

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McGurk, Colm. "Endothelial function in non-insulin dependent diabetes mellitus". Thesis, Queen's University Belfast, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387879.

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Pinkney, Jonathan Henley. "Origins of hypertension in non-insulin dependent diabetes". Thesis, University of London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286682.

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Alcolado, Juan Carlos. "The genetics of non-insulin dependent diabetes mellitus". Thesis, University of Southampton, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.358901.

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Jaap, Alan James. "Microvascular function in non-insulin-dependent diabetes mellitus". Thesis, University of Glasgow, 1994. http://theses.gla.ac.uk/30732/.

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Epidemiological studies suggest differences in the prevalence and natural history of microvascular complications between subjects with insulin dependent (IDDM) and non-insulin dependent (NIDDM) diabetes. The haemodynamic hypothesis proposes that early functional changes in the microcirculation result in the eventual development of diabetic microangiopathy. There is now a large body of experimental evidence in support of this hypothesis in patients with IDDM, with abnormalities in blood flow, capillary pressure and permeability having been demonstrated. In contrast, there have been few studies investigating microvascular function in NIDDM; however, preliminary work has identified a profound limitation in microvascular vasodilation at an early stage, while capillary pressure does not appear to be elevated. The aim of this thesis was to further investigate functional changes in the skin microcirculation in patients with NIDDM and impaired glucose tolerance (IGT). 1. Using a sensitive plethysmographic system, no difference was found in microvascular fluid permeability between patients with NIDDM and control subjects (5.3 (3.2-9.1) x 10-3 ml.min-1.100g tissue-1.mmHg-1 vs 5.4 (3.5-8.0) x 10-3 ml.min-1. 100g tissue-1 .mmHg-1 median and range; p = 0.98, Mann-Whitney). 2. In confirmation of previous studies, reduced microvascular hyperaemia in response to local heating of the skin was found (using laser Doppler fluximetry) in NIDDM patients with large vessel disease excluded (0.82 (0.42-1.41) V vs 1.40 (0.89-2.13) V control subjects; p < 0.005). Limited vasodilation correlated with fasting plasma insulin (Rg =-0.63, p < 0.04) but not glycaemic control. Microvascular hyperaemia increased after one year of improved glycaemic control in recently diagnosed patients (1.20 (0.51-3.93) V vs 0.97 (0.22-2.17) V at baseline; p < 0.05). In hypertensive NIDDM patients, there was no further reduction in microvascular vasodilation (1.05 (0.70-1.42) V vs 1.04 (0.79-1.63) V normotensive NIDDM, p = 0.82), although there was an increase in calculated resistance to blood flow (127.2 (87.5-181.3) mmHg.V-1 vs 84.7 (61.9-123.0) mmHg.V-1 normotensive patients, p < 0.02). 3. Reduced microvascular hyperaemia was found in subjects with IGT (1.01 (0.71-1.57) V vs 1.41 (1.32-2.13) V control subjects, p < 0.001), and also insulin resistant patients with acromegaly (0.96 (0.56-1.70) V vs 1.46 (1.24-2.13) V control subjects, p < 0,05). In subjects with IGT, limited vasodilation was found to correlate with fasting plasma insulin (Rg = -0.7; p < 0.001) and insulin sensitivity (Rs = 0.52; p < 0.02), but not with β-cell function, plasma glucose or serum lipid concentrations. 4. Using iontophoresis and laser Doppler fluximetry, defective endothelium-dependent vasodilation was found in subjects with IGT (518 (410-905) AU-min-l vs 1236 (875-1588) AU.min-1 control subjects, median and range; p < 0.003). In contrast there was no significant difference in myogenic (683 (301-1175) AU.min-1 vs 898 (303-998) AU.min-1 control subjects; p = 0.5) or neurogenic vasodilation ( 61 (31-109) AU vs 46 (37-146) control subjects; p = 0.8). 5. No differences in skin capillary density were found between patients with NIDDM, subjects with IGT and control subjects under basal conditions (112 (71-144) caps.mm-2 vs 107 (76-140) caps.mm-2 vs 112 (76-138) caps.mm-2 respectively; p= 0.9, Kruskal Wallis), or after venous occlusion (122 (87-157) caps.mm-2 vs 121 (90-143) caps.mm-2 IGT vs 123 (81-147) caps.mm-2; p= 0.9). In light of the above results, a unifying hypothesis has been proposed to explain the differences in epidemiology and pathophysiology of microvascular disease between IDDM and NIDDM.
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Al-Hussary, Nabeel A. J. "Insulin receptor binding in hypertension and non-insulin dependent diabetes mellitus". Thesis, Aston University, 1986. http://publications.aston.ac.uk/14510/.

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Tan, Kathryn Choon Beng. "Postprandial lipoprotein metabolism in non-insulin-dependent diabetes mellitus". Thesis, Cardiff University, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.323795.

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Libri sul tema "Non-insulin-dependent diabetes"

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Malcolm, Nattrass, e Hale P. J, a cura di. Non-insulin-dependent diabetes. London: Baillière Tindall, 1988.

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Day, John L. The diabetes handbook: Non-insulin dependent diabetes. Wellingborough: Thornsons in collaboration with the British Diabetic Association, 1986.

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Belfast. Royal Victoria Hospital. Diabetic Clinic., a cura di. Good health and diabetes: Non-insulin dependent diabetes. 4a ed. Belfast: EHSSB, for the Diabetic Clinic, Royal Victoria Hospital, 1985.

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Jovanovic-Peterson, Lois. A touch of diabetes. Minneapolis, MN: Chronimed Pub., 1995.

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Suad, Efendić, e Grill Valdemar, a cura di. Pathogenesis of non-insulin dependent diabetes mellitus. New York: Raven Press, 1988.

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Valdemar, Grill, e Efendić Suad, a cura di. Pathogenesis of non-insulin dependent diabetes mellitus. New York: Raven Press, 1988.

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Jovanovic-Peterson, Lois. A touch of diabetes: A guide for people who have type II, noninsulin-dependent diabetes. Minneapolis, MN: DCI Pub., 1991.

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English, Patrick. Type 2 Diabetes: Pocketbook. London: Informa Healthcare, 2001.

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McCarren, Marie. American Diabetes Association guide to insulin and type 2 diabetes. Alexandria, Va: American Diabetes Association, 2007.

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Farid, Mamdouh Salah. Periodontal disease in non-insulin and insulin dependent diabetes mellitus. Manchester: University of Manchester, 1997.

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Capitoli di libri sul tema "Non-insulin-dependent diabetes"

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Stilwell, Barbara. "Non-Insulin-Dependent Diabetes". In Skills Update, 8–9. London: Macmillan Education UK, 1992. http://dx.doi.org/10.1007/978-1-349-12990-4_4.

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Johansen, Klaus, e Sam Dagogo-Jack. "Non-Insulin-Dependent Diabetes Mellitus". In Diabetes Guide, 79–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76868-2_8.

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Tiro, Jasmin, Simon J. Craddock Lee, Steven E. Lipshultz, Tracie L. Miller, James D. Wilkinson, Miriam A. Mestre, Barbara Resnick et al. "Non-insulin-Dependent Diabetes Mellitus". In Encyclopedia of Behavioral Medicine, 1342. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_101158.

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Gentile, L., S. Turco, E. Rossi e R. Torella. "Non-Insulin-Dependent Diabetes mellitus and Liver Cirrhosis." In Frontiers in Diabetes, 168–71. Basel: KARGER, 1998. http://dx.doi.org/10.1159/000060908.

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Köbberling, J. "Non-Pharmacological Management of Non-Insulin-Dependent Diabetes". In Oral Antidiabetics, 43–62. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-09127-2_3.

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Volk, Bruno W., e Klaus F. Wellmann. "Type II (Idiopathic) Diabetes (Non-Insulin-Dependent)". In The Diabetic Pancreas, 233–63. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4757-0348-1_10.

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Webb, Judith A. W. "Non-Insulin-Dependent Diabetes and Contrast Media". In Medical Radiology, 87–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-72784-2_11.

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Perlmuter, Lawrence C., Steven H. Goldfinger, Anne R. Shore e David M. Nathan. "Cognitive Function in Non-Insulin-Dependent Diabetes". In Contributions to Psychology and Medicine, 222–38. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3290-2_12.

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Kribben, A., U. Heemann e Th Philipp. "Antihypertensive treatment in non-insulin-dependent diabetes mellitus (NIDDM)". In Pharmacology of Diabetes, a cura di C. E. Mogensen e E. Standl, 247–62. Berlin, Boston: De Gruyter, 1990. http://dx.doi.org/10.1515/9783110850321-019.

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Schmitz, Anita. "Microalbuminuria and Mortality in Non-Insulin-Dependent Diabetes". In The Kidney and Hypertension in Diabetes Mellitus, 65–70. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4757-1974-1_9.

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Atti di convegni sul tema "Non-insulin-dependent diabetes"

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HU, HAIYAN, e XIAOMAN LI. "NETWORKING PATHWAYS UNVEILS ASSOCIATION BETWEEN OBESITY AND NON-INSULIN DEPENDENT DIABETES MELLITUS". In Proceedings of the Pacific Symposium. WORLD SCIENTIFIC, 2007. http://dx.doi.org/10.1142/9789812776136_0026.

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Alava, I., L. J. Garcia Frade, H. de la Calle, J. L. Havarro, L. J. Creighton e P. J. Gaffney. "DIABETES MELLITUS: HYPERCOAGULABILITY AID HYPOFIBRIHOLYSIS". In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643108.

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A hypercoagulable state has been related to the presence of microvascular and macrovascular disease in Diabetes Mellitus. The aim of this study was to establish when this hypercoagulable state appears and the response of the fibrinolytic system.43 patients (29 males, 14 females, aged 19-73), 28 insulin-dependent (10 of them with micro and/or macrovascular disease), 15 non insulin- dependent (all of them with vascular disease) were studied.Platelet aggregation and adenine nucleotides, plasma and serum thromboxane B2 (TxB2), Factor VIII Coagulant (VIII-C), Factor VIII Related antigen (VIII-RAg), Factor VIII Ristocetin Cofactor (VIII-RCoF), Fibronectin, Tissue Plasminogen Activator (t-PA) and X-Oligomers fibrin fragments were measured.In the diabetic patients maximal aggregation was induced by a threshold concentration of adenosin diphosphate and arachidonic acid lower than in controls (p<0.01 and p<0.05). Diabetic patients also presented elevated platelet ADP and decreased platelet c-AMP. They had higher plasma TxB* levels than the control group.FVIII-C, FVIII-RAg and Fibronectin were increased (p<0.001) both in patients type I and II, with and without vasculopathy. FVIII-RCoF was highly increased in vasculopathy (p<0.001) while was non significant without it.The patients with vasculopathy presented decreased t-PA plasma levels (p<0.05). lo difference in X-Oligomers was found related to controls.These findings suggest: 1) A hypercoagulable state previously to the development of clinical vasculopathy. 2) A decreased fibrinolytic response associated to vasculopathy.
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Woo, D. G., Q. J. Lee, W. P. Park, C. Y. Ko, D. Lim, H. S. Kim e B. Y. Lee. "Relationship Between Obesity and Osteopenia in Lumbar Spines of Rats Using Mechanical and Morphological Studies". In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192537.

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Obesity (OB) and osteopenia (OP), grave consequences for human health, quality of life, and even the efficiency of the labor force and economy, are two common complex diseases. Two public health problems have exploded in prevalence over the past decade [1]. OB, now a major epidemic in the developed world and frequent among elderly subjects, is a condition of excessive body fat that causes or exacerbates several risk of developing non-insulin dependent diabetes mellitus, cardiovascular disease, cancer and other diseases [2]. OP is defined as a systemic skeletal disease caused by low bone mass and microstructural deterioration of the bone.
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Yulianti, Kartika, Aris Wibudi e Mila Citrawati. "Relation Between Tiroid Status with Glycemic Control of Type 2 DM Patients at RSPAD Gatot Soebroto". In The 7th International Conference on Public Health 2020. Masters Program in Public Health, Universitas Sebelas Maret, 2020. http://dx.doi.org/10.26911/the7thicph.05.12.

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ABSTRACT Background: Diabetes Mellitus (DM) is a group of symptoms that arise due to increased blood sugar levels. Diabetes Mellitus type 2 has a higher risk of developing thyroid dysfunction. Thyroid dysfunction can affect various body metabolism and result in insulin resistance, significantly affecting glycemic control in DM patients. This study aimed to determine the relation between thyroid status as assessed by the level of thyroid-stimulating hormone (TSH), free thyroxine (FT4), and glycemic control (HbA1c). Subjects and Method: A cross-sectional study. A sample of 38 DM patients was selected by purposive sampling. The dependent variable was glycemic control. The independent variables were TSH and FT4. Patients were classified into 4 quartiles (Q) based on their TSH and FT4 levels. Statistic test used was non parametric for category group of variables, which was Chi square test. Results: Mean of fasting blood glucose was 200,56 mg/dL (modus 137 mg/dL), mean of 2 hours post prandial blood glucose was 247 mg/dL (modus 305 mg/dL). Subjetcs with poor glycemic control dominated as much as 76%. Most subjects had TSH level at Q4 (36%), while most of the subjects had FT4 level at Q1 (34%). The results showed that 38 samples with poor glycemic control were 72% in the 4th quartile (Q4) (> 3.1750 mU / L) TSH, and 64.7% were in Q1 (≤ 11.8400) FT4. The analysis showed that there was a significant relation between TSH (p = 0.047) and FT4 (p = 0.041) with glycemic control in type 2 DM patients. Conclusion: FT4 and TSH levels relate to glycemic control in type 2 DM patients Keywords: TSH, FT4, HbA1c, Diabetes Mellitus Correspondence: Mila Citrawati. Department of Faal, Faculty of Medicine, UPN Veteran, Jakarta. Jl. RS Fatmawati, Pondok Labu, South Jakarta 12450, Telp. (021) 7656971. E-mail: milacitrawati@upnvj.ac.id. Mobile: 081282990515 DOI: https://doi.org/10.26911/the7thicph.05.12
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Mombaerta, P., V. Ballegeer, P. Declerck, F. A. Van Assche e D. Collen. "FIBRINOLYTIC RESPONSE TO VENOUS OCCLUSION, AND FIBRIN FRAGMENT D-DIMER AND FIBRONECTIN LEVELS IN NORMAL AND COMPLICATED PREGNANCY". In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643143.

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The fibrinolytic response to venous occlusion was assessed in pregnant women with measurements of total and free t-PA, using specific ELISAs based on monoclonal antibodies.Total t-PA levels increased after venous occlusion with 11±8 ng/ml (mean ± SD) in healthy fertile non-pregnant women (n=6), with 0.8 ± 1.3 ng/ml in 2nd trim. (n=5) and with 3.8 ± 3.9 ng/ml in 3rd trim. (n=4) healthy pregnant women. The increase in free t-PA was 12 ± 11; 1.2 ± 0.9 and 0 ng/ml respectively. The difference in post- and pre-occlusion levels in 3rd trim, pregnant women with insulin dependent diabetes mellitus IDDM (n=4) was 3.2 ± 4.2 ng/ml, with intrauterine growth retardation (IUGR) (n=4) 2.6 ± 3.0 ng/ml and with preeclampsia (n=5) 3.2 ± 3.5 ng/ml for total t-PA and 0, 0 and 0 ng/ml for free t-PA.Fibrin fragment D-dimer levels in plasma measured with a specific ELISA were 130 ± 36 ng/ml in healthy fertile non-pregnant women (n=8). A significant increase was found in 4 out of 5 1st trim., 25 out of 25 2nd trim, and 21 out of 22 3rd trim, normal pregnant women. In these groups, plasma levels were 340 ± 160, 400 ± 170 and 440 ± 220 ng/ml respectively.Fibronectin levels, measured with a Laurell electroimmunoassay and expressed as percentage of pooled human plasma (=330 yg/ml) were 83 ± 26% in 2nd trim, patients (n=24) and 102 ± 35% in 3rd trim, patients (n=17). Normal fibronectin levels were found in 4 patients with IDDM and in 6 with IUGR, whereas in 6 out of 8 preeclamptic patients significantly increased levels were observed.These results confirm, with the use of a newly developed free t-PA assay, that the fibrinolytic response to venous occlusion is completely inhibited in the 3rd trimester of pregnancy. A reduced release of t-PA from the vessel wall during venous occlusion and/or an increased inhibition of released t-PA were observed. No difference was found in the fibrinolytic response between normal and complicated pregnancy. D-dimer levels are significantly elevated during pregnancy. Finally, the usefulness of fibronectin for the diagnosis of preeclampsia is confirmed.
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