Effect of Certain Oral Anti Diabetic Drugs on Coagulation Cascade in Diabetes Mellitus

2017 ◽  
Vol 9 (03) ◽  
Author(s):  
Patil T. R. ◽  
Patil S. T. ◽  
Patil S. ◽  
Patil A.
Keyword(s):  
Diabetes Mellitus ◽  
Membrane Damage ◽  
Blood Glucose Control ◽  
Coagulation Factors ◽  
Lipid Lowering ◽  
Coagulation Cascade ◽  
Factor Vii ◽  
Cardiac Complications ◽  
Ppar Γ ◽  
Tnf Α

Thrombotic events in diabetics contribute for almost 65-80% of cardiovascular events. Diabetes affects the platelet, the coagulation factors and fibrinolytic system leading to a state of hypercoagulation and hypofibrinolysis resulting in to thrombosis. Oral drugs commonly used in management of type II diabetes mellitus are antidiabetics like metformin, PPAR- γ agonist and DPP-4 inhibitor. They rarely produce hypoglycemia. Metformin has been proved to prevent release of mtDNA from arachidonic acid stimulated platelets, reduce membrane damage and mitochondrial ROS production in the platelets. Similarly processes like platelet adhesion, activation and aggregation on collagen coated surfaces which initiate thrombosis are prevented by metformin. PPAR- γ agonists like pioglitazone and rosiglitazone have anti atherogenic effect. They decrease the expression of inflammatory markers and affect the coagulation markers like factor VII: C and inhibit platelet activation. Pioglitazone also reduces the VLDL, triglycerides and increases HDL which further contributes in attenuation of atherosclerosis. DPP-4 inhibitors, which are relatively newer class of antidiabetics, having minimum potential for hypoglycemia induction, due to their novel mechanism of action. Studies have proved that long term use of DPP-4 inhibitors have reduced cardiac mortality by their lipid lowering action, increased release of NO from endothelium and inhibition of TNF- α, PAI-1 and VCAM expression. Increased levels of stromal cell derived factor - 1α helps to maintain endothelial homeostasis and vascular repair. Decreased oxidative stress, inhibition of inflammatory genes like IL- 6, IL-12, TNF- α provide additional benefit. Destabilization of vasculo-atherosclerotic plaque is prevented by DPP-4 inhibitors. Thus these oral antidiabetics drugs offer many benefits beyond blood glucose control which prevent atherosclerosis, inhibits hypercoagulable state and enhances fibrinolysis which translates into decreased cardiac complications in diabetes

scholarly journals Ameliorative Effect of Berberine on Neonatally Induced Type 2 Diabetic Neuropathy via Modulation of BDNF, IGF-1, PPAR-γ, and AMPK Expressions

Dose-Response ◽  
2019 ◽  
Vol 17 (3) ◽  
pp. 155932581986244 ◽  
Author(s):  
Guangju Zhou ◽  
Mingzhu Yan ◽  
Gang Guo ◽  
Nanwei Tong
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Peripheral Neuropathy ◽  
Sciatic Nerve ◽  
Nitrosative Stress ◽  
Ppar Γ ◽  
Tnf Α ◽  
Protein Expressions

Neonatal-streptozotocin (n-STZ)-induced diabetes mimics most of the clinicopathological symptoms of type 2 diabetes mellitus (T2DM) peripheral neuropathy. Berberine, a plant alkaloid, is reported to have antidiabetic, antioxidant, anti-inflammatory, and neuroprotective potential. The aim of the present study was to investigate the potential of berberine against n-STZ-induced painful diabetic peripheral polyneuropathy by assessing various biochemical, electrophysiological, morphological, and ultrastructural studies. Type 2 diabetes mellitus was produced neonatal at the age of 2 days (10-12 g) by STZ (90 mg/kg intraperitoneal). After confirmation of neuropathy at 6 weeks, rats were treated with berberine (10, 20, and 40 mg/kg). Administration of n-STZ resulted in T2DM-induced neuropathic pain reflected by a significant alterations ( P < .05) in hyperalgesia, allodynia, and motor as well as sensory nerve conduction velocities whereas berberine (20 and 40 mg/kg) treatment significantly attenuated ( P < .05) these alterations. Berberine treatment significantly inhibited ( P < .05) STZ-induced alterations in aldose reductase, glycated hemoglobin, serum insulin, hepatic cholesterol, and triglyceride levels. The elevated oxido-nitrosative stress and decreased Na-K-ATPase and pulse Ox levels were significantly attenuated ( P < .05) by berberine. It also significantly downregulated ( P < .05) neural tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 messenger RNA (mRNA), and protein expressions both. Streptozotocin-induced downregulated mRNA expressions of brain-derived neurotrophic factor (BDNF), insulin-like growth factor (IGF-1), and peroxisome proliferator-activated receptors-γ (PPAR-γ) in sciatic nerve were significantly upregulated ( P < .05) by berberine. Western blot analysis revealed that STZ-induced alterations in adenosine monophosphate protein kinase (AMPK; Thr-172) and protein phosphatase 2C-α protein expressions in dorsal root ganglia were inhibited by berberine. It also attenuated histological and ultrastructural alterations induced in sciatic nerve by STZ. In conclusion, berberine exerts its neuroprotective effect against n-STZ-induced diabetic peripheral neuropathy via modulation of pro-inflammatory cytokines (TNF α, IL-1β, and IL-6), oxido-nitrosative stress, BDNF, IGF-1, PPAR-γ, and AMPK expression to ameliorate impaired allodynia, hyperalgesia, and nerve conduction velocity during T2DM.

scholarly journals Phosphatidylserine inside out: a possible underlying mechanism in the inflammation and coagulation abnormalities of COVID-19

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Gustavo A. Argañaraz ◽  
Julys da Fonseca Palmeira ◽  
Enrique R. Argañaraz
Keyword(s):  
Endothelial Cells ◽  
Inflammatory Response ◽  
Viral Infection ◽  
Underlying Mechanism ◽  
Coagulation Cascade ◽  
Factor Vii ◽  
Outer Side ◽  
Extrinsic Pathway ◽  
Coagulation Abnormalities ◽  
Tnf Α

AbstractThe rapid ability of SARS-CoV-2 to spread among humans, along with the clinical complications of coronavirus disease 2019—COVID-19, have represented a significant challenge to the health management systems worldwide. The acute inflammation and coagulation abnormalities appear as the main causes for thousands of deaths worldwide. The intense inflammatory response could be involved with the formation of thrombi. For instance, the presence of uncleaved large multimers of von Willebrand (vWF), due to low ADAMTS13 activity in plasma could be explained by the inhibitory action of pro-inflammatory molecules such as IL-1β and C reactive protein. In addition, the damage to endothelial cells after viral infection and/or activation of endothelium by pro-inflammatory cytokines, such as IL-1β, IL-6, IFN-γ, IL-8, and TNF-α induces platelets and monocyte aggregation in the vascular wall and expression of tissue factor (TF). The TF expression may culminate in the formation of thrombi, and activation of cascade by the extrinsic pathway by association with factor VII. In this scenario, the phosphatidylserine—PtdSer exposure on the outer leaflet of the cell membrane as consequence of viral infection emerges as another possible underlying mechanism to acute immune inflammatory response and activation of coagulation cascade. The PtdSer exposure may be an important mechanism related to ADAM17—mediated ACE2, TNF-α, EGFR and IL-6R shedding, and the activation of TF on the surface of infected endothelial cells. In this review, we address the underlying mechanisms involved in the pathophysiology of inflammation and coagulation abnormalities. Moreover, we introduce key biochemical and pathophysiological concepts that support the possible participation of PtdSer exposure on the outer side of the SARS-CoV-2 infected cells membrane, in the pathophysiology of COVID-19.

scholarly journals Biomarkers of Hemostatic Dysregulation, Inflammation, and Infection in Patients Diagnosed with Sepsis Associated Coagulopathy

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 2281-2281
Author(s):  
Amanda Walborn ◽  
Daniel Kahn ◽  
Debra Hoppensteadt ◽  
Jawed Fareed
Keyword(s):  
Conflicts Of Interest ◽  
Coagulation Factors ◽  
Endothelial Damage ◽  
Factor Ix ◽  
Response To Treatment ◽  
Coagulation Cascade ◽  
Factor Vii ◽  
Molecular Profile ◽  
Healthy Individuals ◽  
Normal Individuals

Abstract Introduction: Sepsis associated coagulopathy (SAC) is one of the major pathophysiological mechanisms of sepsis and has been shown to greatly increase mortality in septic patients. SAC is characterized by the inappropriate activation of the coagulation cascade, leading to the formation of microthrombi and the potential for multiple organ failure. Additionally, the excessive consumption of platelets and coagulation factors can create a risk of excessive bleeding. SAC is a complex syndrome, involving coagulation factors, inflammatory cytokines, and several other notable factors of varied origin. In this study, our aim was to evaluate the levels of endocan, pentraxin, and procalcitonin in individuals with SAC diagnosed according to the ISTH criteria in comparison to healthy individuals. Endocan is a soluble, circulating proteoglycan that normally binds to LFA-1 and inhibits leukocyte diapedesis. It is produced by vascular endothelial cells as well as the lung and kidney and has been proposed as a marker of endothelial dysfunction and disease severity in patients with sepsis. Endocan may be useful in the evaluation and tracking of SAC as a marker of endothelial damage caused by excessive inflammation and coagulation. Pentraxin (PTX3) is a protein structurally similar to CRP that is produced by several cell types in response to inflammatory signals and is known to be a marker of inflammation in a number of disease processes. In addition to being the precursor of the hormone calcitonin, procalcitonin is produced by a variety of tissues and may correlate with degree of infection and response to treatment in individuals with sepsis. Taken together, endocan, pentraxin, and procalcitonin may be useful in the evaluation and monitoring of SAC as they are representative of endothelial damage, inflammation, and systemic infection, respectively. Materials and Methods: Blood from 50 patients with SAC and 33 normal individuals obtained from a commercial source (George King Biomedical, Overland Park, KS) were evaluated. Levels of pentraxin, procalcitonin, endocan, and coagulation factors VII, IX, and X were measured using commercially available ELISA kits from Stago (Parsippany, NJ), Lunginnov (Lillie, France) and R&D Systems (Minneapolis, MN). All results are compiled as group mean and expressed as average mean + SD. These values are compared with normal and results were computed as percent increase or decrease. Results: The levels of coagulation factors VII and X were found to be reduced in patients with SAC compared to normal individuals (p < 0.05); the level of factor IX was statistically unchanged. The reduction in factor X was relatively modest, less than a 20% reduction compared to normal, while the reduction in factor VII was more marked, with a greater than 40% reduction compared to normal. The levels of pentraxin, proxalcitonin, and endocan were all found to be significantly elevated in blood from SAC patients compared to blood from normal healthy individuals (p < 0.05). All three markers exhibited a greater than 100% average increase when compared to normal. Discussion: These results indicate that endocan, pentraxin, procalcitonin, and factor VII are all candidates for further investigation in the identification of a more comprehensive molecular profile of SAC and in the development of diagnostic or prognostic tests. The significant degree of change observed in each marker from normal provides a baseline for future studies of these markers in SAC patients. Although these factors individually are not specific markers of SAC, each is a marker for a specific system that is dysregulated in SAC; endocan for endothelial damage, pentraxin for inflammation, procalcitonin for infection, and factor VII for coagulation. Taken together, these biomarkers may be useful in the diagnosis and monitoring of SAC. Disclosures No relevant conflicts of interest to declare.

scholarly journals Apolipoprotein C-III Strongly Correlates with Activated Factor VII–Anti-Thrombin Complex: An Additional Link between Plasma Lipids and Coagulation

2019 ◽  
Vol 119 (02) ◽  
pp. 192-202 ◽  
Author(s):  
Nicola Martinelli ◽  
Marcello Baroni ◽  
Annalisa Castagna ◽  
Barbara Lunghi ◽  
Filippo Stefanoni ◽  
...  
Keyword(s):  
Plasma Concentration ◽  
Plasma Lipids ◽  
Association Studies ◽  
Plasma Lipoproteins ◽  
Lipid Lowering ◽  
Coagulation Cascade ◽  
Factor Vii ◽  
Genome Wide Association Studies ◽  
Activated Factor Vii ◽  
Potential Biomarker

AbstractActivated factor VII–anti-thrombin (FVIIa-AT) complex is a potential biomarker of pro-thrombotic diathesis reflecting FVIIa–tissue factor (TF) interaction and has been associated with mortality in patients with coronary artery disease (CAD). Previous data indicated plasma lipids as predictors of FVIIa-AT variability, and plasma lipoproteins as potential stimulators of the coagulation cascade. Our aim was to evaluate the relationships between FVIIa-AT plasma concentration and a broad apolipoprotein profile (including ApoA-I, ApoB, ApoC-III and ApoE). Within the framework of the observational Verona Heart Study, we selected 666 subjects (131 CAD-free and 535 CAD, 75.4% males, mean age: 61.1 ± 10.9 years) not taking anticoagulant drugs and for whom plasma samples were available for both FVIIa-AT assay and a complete lipid profile. Plasma concentration of FVIIa-AT levels significantly and directly correlated with total and high-density lipoprotein cholesterol, triglycerides, ApoA-I, ApoC-III and ApoE levels. ApoC-III showed the strongest correlation (R = 0.235, p = 7.7 × 10−10), confirmed in all the sub-group analyses (males/females and CAD/CAD-free). Only ApoC-III remained associated with FVIIa-AT plasma concentration, even after adjustment for sex, age, CAD diagnosis, body mass index, renal function, smoking status, lipid-lowering therapies and FVIIa levels. The APOC3 gene locus-tagging polymorphism rs964184, previously linked with cardiovascular risk and plasma lipids by genome-wide association studies, was associated with both ApoC-III and FVIIa-AT plasma concentration. Our results indicate a strong association between ApoC-III and FVIIa-AT levels, thereby suggesting that an increased ApoC-III concentration may identify subjects with a pro-thrombotic diathesis characterized by an enhanced TF-FVIIa interaction and activity.

scholarly journals Resolvin D1 Decreases Severity of Streptozotocin-Induced Type 1 Diabetes Mellitus by Enhancing BDNF Levels, Reducing Oxidative Stress, and Suppressing Inflammation

2021 ◽  
Vol 22 (4) ◽  
pp. 1516
Author(s):  
Siresha Bathina ◽  
Undurti N. Das
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Lipid Peroxides ◽  
Signaling Proteins ◽  
Ppar Γ ◽  
Tnf Α ◽  
Gsk 3Β ◽  
Type 1 Dm ◽  
Cox 1

Type 1 diabetes mellitus is an autoimmune disease characterized by increased production of pro-inflammatory cytokines secreted by infiltrating macrophages and T cells that destroy pancreatic β cells in a free radical-dependent manner that causes decrease or absence of insulin secretion and consequent hyperglycemia. Hence, suppression of pro-inflammatory cytokines and oxidative stress may ameliorate or decrease the severity of diabetes mellitus. To investigate the effect and mechanism(s) of action of RVD1, an anti-inflammatory metabolite derived from docosahexaenoic acid (DHA), on STZ-induced type 1 DM in male Wistar rats, type 1 diabetes was induced by single intraperitoneal (i.p) streptozotocin (STZ-65 mg/kg) injection. RVD1 (60 ng/mL, given intraperitoneally) was administered from day 1 along with STZ for five consecutive days. Plasma glucose, IL-6, TNF-α, BDNF (brain-derived neurotrophic factor that has anti-diabetic actions), LXA4 (lipoxin A4), and RVD1 levels and BDNF concentrations in the pancreas, liver, and brain tissues were measured. Apoptotic (Bcl2/Bax), inflammatory (COX-1/COX-2/Nf-κb/iNOS/PPAR-γ) genes and downstream insulin signaling proteins (Gsk-3β/Foxo1) were measured in the pancreatic tissue along with concentrations of various antioxidants and lipid peroxides. RVD1 decreased severity of STZ-induced type 1 DM by restoring altered plasma levels of TNF-α, IL-6, and BDNF (p < 0.001); expression of pancreatic COX-1/COX-2/PPAR-γ genes and downstream insulin signaling proteins (Gsk-3β/Foxo1) and the concentrations of antioxidants and lipid peroxides to near normal. RVD1 treatment restored expression of Bcl2/Pdx genes, plasma LXA4 (p < 0.001) and RVD1 levels and increased brain, pancreatic, intestine, and liver BDNF levels to near normal. The results of the present study suggest that RVD1 can prevent STZ-induced type 1 diabetes by its anti-apoptotic, anti-inflammatory, and antioxidant actions and by activating the Pdx gene that is needed for pancreatic β cell proliferation.

Characterization of Monoclonal Anti-human Factor VII Antibody (B101/B1) that Recognized Three-dimensional Structures near Arg at Position 79 in the First EGF-like Domain

1998 ◽  
Vol 79 (01) ◽  
pp. 104-109 ◽  
Author(s):  
Osamu Takamiya
Keyword(s):  
Monoclonal Antibodies ◽  
Tissue Factor ◽  
Human Factor ◽  
Solid Phase ◽  
Three Dimensional ◽  
Coagulation Factors ◽  
Factor Vii ◽  
Dimensional Structure ◽  
Epidermal Growth

SummaryMurine monoclonal antibodies (designated hVII-B101/B1, hVIIDC2/D4 and hVII-DC6/3D8) directed against human factor VII (FVII) were prepared and characterized, with more extensive characterization of hVII-B101/B1 that did not bind reduced FVIIa. The immunoglobulin of the three monoclonal antibodies consisted of IgG1. These antibodies did not inhibit procoagulant activities of other vitamin K-dependent coagulation factors except FVII and did not cross-react with proteins in the immunoblotting test. hVII-DC2/D4 recognized the light chain after reduction of FVIIa with 2-mercaptoethanol, and hVIIDC6/3D8 the heavy chain. hVII-B101/B1 bound FVII without Ca2+, and possessed stronger affinity for FVII in the presence of Ca2+. The Kd for hVII-B101/B1 to FVII was 1.75 x 10–10 M in the presence of 5 mM CaCl2. The antibody inhibited the binding of FVII to tissue factor in the presence of Ca2+. hVII-B101/B1 also inhibited the activation of FX by the complex of FVIIa and tissue factor in the presence of Ca2+. Furthermore, immunoblotting revealed that hVII-B101/B1 reacted with non-reduced γ-carboxyglutaminic acid (Gla)-domainless-FVII and/or FVIIa. hVII-B101/B1 showed a similar pattern to that of non-reduced proteolytic fragments of FVII by trypsin with hVII-DC2/D4 on immunoblotting test. hVII-B101/B1 reacted differently with the FVII from the dysfunctional FVII variant, FVII Shinjo, which has a substitution of Gln for Arg at residue 79 in the first epidermal growth factor (1st EGF)-like domain (Takamiya O, et al. Haemosta 25, 89-97,1995) compared with normal FVII, when used as a solid phase-antibody for ELISA by the sandwich method. hVII-B101/B1 did not react with a series of short peptide sequences near position 79 in the first EGF-like domain on the solid-phase support for epitope scanning. These results suggested that the specific epitope of the antibody, hVII-B101/B1, was located in the three-dimensional structure near position 79 in the first EGF-like domain of human FVII.

The Effects of Therapy with Oestriol Succinate and Ethinyl Oestradiol on the Haemostatic Mechanism in Post-Menopausal Women

1976 ◽  
Vol 35 (02) ◽  
pp. 403-414 ◽  
Author(s):  
Terence Davies ◽  
Gillian Fieldhouse ◽  
George P. McNicol
Keyword(s):  
Coagulation Factors ◽  
Factor Vii ◽  
Oestrogen Therapy ◽  
Qualitative And Quantitative ◽  
Lysis Activity ◽  
Menopausal Women ◽  
Increased Sensitivity ◽  
Post Menopausal ◽  
Incremental Increase ◽  
Ethinyl Oestradiol

SummaryThe effects on the haemostatic mechanism of oestrogen therapy, given to prevent bone loss in post-menopausal women, have been investigated. Oestriol succinate was given orally to 10 women at a level of 2 mg/day for 1 month and for a further 3 months with incremental increase of 2 mg each month. 6 of the 10 women were subsequently treated with 25 μg/day orally of ethinyl oestradiol. Oestriol succinate therapy resulted in a small increase in the level of factor VII, a decrease in factor VIII concentration and increased sensitivity of platelets to aggregating agents. Ethinyl oestradiol treatment resulted in much more widespread changes with marked increases in coagulation factors VII, VIII, IX and X, decreased levels of antithrombin and dramatic increases in circulating plasminogen levels and euglobulin lysis activity. The data suggested that the nature of oestrogens employed therapeutically is important in determining the qualitative and quantitative effect of oestrogen therapy on components of the haemostatic mechanism.

The Effect of Antithrombin III on the Activity of the Coagulation Factors VII, IX and X

1976 ◽  
Vol 35 (02) ◽  
pp. 295-304 ◽  
Author(s):  
B Østerud ◽  
M Miller-Andersson ◽  
U Abildgaard ◽  
H Prydz
Keyword(s):  
Antithrombin Iii ◽  
Factor Xa ◽  
Coagulation Factors ◽  
Disc Electrophoresis ◽  
Polyacrylamide Gel ◽  
Factor Vii ◽  
Native Form ◽  
Factor Ixa ◽  
Plasma Factor

SummaryAntithrombin III, purified to homogeneity according to Polyacrylamide gel disc electrophoresis and immunoelectrophoresis, inhibited the activity of purified factor IXa and Xa, whereas factor VII was not inhibited either in the active or in the native form.Antithrombin III is the single most important inhibitor of factor Xa in plasma. Factor Xa does not, however, reduce the activity of antithrombin III against thrombin.

Cold Promoted Activation of Factor VII

1972 ◽  
Vol 28 (02) ◽  
pp. 155-168 ◽  
Author(s):  
H Gjønnæs
Keyword(s):  
Coagulation Factors ◽  
Oral Contraception ◽  
Factor Vii ◽  
Coagulation System ◽  
Plasma Coagulation ◽  
Main Effect

SummaryThe cold promoted shortening of the thrombotest-times occuring in the plasmas of the majority of women on oral contraception or in the last trimester of pregnancy when incubated overnight at 0°–4° was investigated.The short thrombotest-times were caused by activation of factor VII in a time consuming reaction. Activation was also revealed in the intrinsic coagulation system, but the changes in the activities of coagulation factors other than factor VII were small.Comparison was made between clot promoting effects of cooling and contact, and it was concluded that while contact apparently exerted its main effect in the intrinsic system, cooling predominately activated the extrinsic plasma coagulation system.The cold promoted activation of factor VII seemed to be brought about by an activator.

The Influence of the Thyroid Function on the Metabolic Rate of Prothrombin, Factor VII, and Factor X in the Rat

1976 ◽  
Vol 35 (03) ◽  
pp. 607-619 ◽  
Author(s):  
Allan T. van Oosterom ◽  
Herman Mattie ◽  
Wim Th Hermens ◽  
Jan J. Veltkamp
Keyword(s):  
Metabolic Rate ◽  
Thyroid Function ◽  
Coagulation Factors ◽  
Biologically Active ◽  
Factor Vii ◽  
Synthesis Rate ◽  
Apparent Difference ◽  
Vitamin K1 ◽  
Factor X ◽  
Significant Difference

SummaryThe influence of the thyroid function on the metabolic rate of prothrombin, factor VII, and X was studied in the rat. Disappearance rates of the three coagulation factors were measured after synthesis had been blocked with appropriate doses of warfarin, and reappearance rates were assessed upon induction of synthesis by high doses of vitamin K1 injected into rats displaying coumarin induced hypocoagulability.No statistically significant difference in the disappearance and production rates of any of the factors could be found between normal euthyroid rats and thyroxin-treated hypothyroid rats proven to be euthyroid. The differences between the two euthyroid groups and the hypothyroid group were highly significant, however: hypothyroidism results in an approximately 50% decrease of the metabolic rates of the three coagulation factors under study.The reappearance of the three factors, under euthyroid as well as hypothyroid conditions, showed a biphasic pattern: in the first two hours after vitamin K1 administration to warfarin treated rats, a rapid reappearance was observed, to the same extent for all three factors, in hypo- as well as euthyroid rats. This finding suggests that in vitamin K1 deficiency an intracellular accumulation of precursor proteins (PIVKAs) occurs, which after rapid conversion into biologically active coagulation factors by vitamin K1 are shed into circulation.The subsequent phase of reappearance is much slower and reflects the synthesis rate of coagulation enzymes. It is characteristic for each factor and clearly slower in hypothyroid rats than in euthyroid rats. From this an influence of thyroid function on the synthesis rate of the protein moiety of coagulation factors can be inferred.An apparent difference between disappearance and reappearance rate of the coagulation factors in the plasma, particularly pronounced for factors VII and X in euthyroid rats, could theoretically be explained as the consequence of the model used for derivation of these rates.

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