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At least 649 records · Page 36Linked to original sources
PubMed2006

Macroangiopathy in adults and children with diabetes: risk factors (part 2).

Autoimmune or type 1 diabetes mellitus (T1DM), accounts for 90-95% of all cases of diabetes, while type 2 diabetes mellitus (T2DM), characterized by impaired insulin sensitivity and production, accounts for the other 5-10%. Atherosclerotic process starts during childhood and recognize several mechanisms that are activated in response to NOXIUS STIMULI and participate in a complex state which is accepted to be a chronic inflammatory state. T1DM patients, especially those with a non-optimal metabolic control, have a higher risk of developing all macrovascular complications such as myocardial infarction, stroke and silent ischemia. Macrovascular disease is mainly associated with hyperglycemia, dyslipidemia, obesity, hypertension, hypercoagulable state, cigarette smoking, lack of exercise, endothelial dysfunction, hyperhomocysteinemia and vascular wall abnormalities. In this paper we review the importance of traditional and non-traditional risk factors for macrovascular complications in children with T1DM and discuss their role in the pathogenesis of the excess cardiovascular mortality in these patients.

Adult↗
PubMedDate not supplied

Hypertension and the prothrombotic state.

The basic underlying pathophysiological processes underlying the major complications of hypertension (that is, heart attacks and strokes) are thrombogenesis and atherogenesis. Indeed, despite the blood vessels being exposed to high pressures in hypertension, the complications of hypertension are paradoxically thrombotic in nature rather than haemorrhagic. The evidence suggests that hypertension appears to confer a prothrombotic or hypercoagulable state, which can be related to conventional risk factors, target organ damage, complications and long-term prognosis, as well as different antihypertensive treatments. Further work is needed to examine the mechanisms leading to this phenomenon, the potential prognostic and treatment implications, and the possible value of measuring these parameters in routine clinical practice.

Antihypertensive Agents↗
PubMed1992

Hypercoagulability and thrombosis.

This article has summarized known congenital and acquired alterations of hemostasis leading to thrombosis. Decreases in coagulation inhibitors, including antithrombin III, heparin cofactor II, and protein C and protein S, are of major importance in assessing patients with hypercoagulable states or patients with unexplained thrombosis. Newer assays for components of the fibrinolytic system, plasminogen, t-PA and t-PA inhibitor are also now readily available and are important for defining congenital or acquired fibrinolytic defects leading to hypercoagulability and thrombosis. By judicious use of these assays, combined with clinical evaluation, many patients with thrombosis will have an underlying etiologic blood protein defect defined. Delineating reasons for a thrombotic event is of obvious importance for planning long-term prophylactic therapy and for diagnosing and counseling afflicted family members. In this manner, newly found patients can be treated prophylactically before unalterable morbidity or mortality occurs.

Antithrombin III↗
PubMed1993

Thrombogenic mechanisms in the human: fresh insights obtained by immunodiagnostic studies of coagulation markers.

Although in vitro studies have been invaluable in revealing the complex biochemistry of the blood coagulation system, meaningful in vivo studies of thrombogenic mechanisms have previously been hindered by the absence of suitable assays. This article reviews the recent development and/or contemporary clinical application of plasma-based immunoassays for coagulation markers (factor XIIa, factor IX activation peptide, prothrombin fragment F1 + 2, thrombin-antithrombin complex and fibrinopeptide A) and for the fibrinolytic marker, D-dimer, which have enabled a critical re-appraisal of some long-standing hypotheses. In chronic renal disease the intrinsic coagulation pathway was found to be activated before haemodialysis and increased end-stage coagulation activity was detected during dialysis when heparinization was limiting. No evidence was found to support the generally accepted hypothesis that thrombogenesis in dialysis is triggered by stimulation of the contact system following exposure of blood to the dialyser membrane. Instead, it is postulated that it is a failure of regulation of end-stage coagulation proteinases (owing to the absence of endothelium) which is responsible for increased thrombogenesis in the dialyser circuit. Excessive end-stage coagulation activity was observed during cardiopulmonary bypass (CPB) surgery and in patients undergoing general thoracic surgery. The data did not accord with the hypothesis that the contact system provides the major thrombogenic trigger in CPB surgery. It is proposed that, in general thoracic surgery, a powerful procoagulant stimulus is provided via the tissue factor-factor VIIa pathway and that the same mechanism is also primarily responsible for triggering thrombogenesis during CPB surgery. The established hypothesis of a prethrombotic state in hereditary AT III deficiency is challenged by the inability to detect increased coagulation activity in asymptomatic AT III deficient patients. It is concluded that the AT III concentration in deficient members is sufficient to enable regulation of the coagulation system in the basal state, whereas failure to regulate the coagulation system only occurs following a major procoagulant stimulus, which overwhelms the impaired inhibitory capacity and triggers thrombosis. These findings highlight the advantages of using plasma-based immunoassays to investigate thrombogenic mechanisms in hypercoagulable states and have important implications for the further study and treatment of blood-surface interactions and thrombotic disease.

Biomarkers↗
PubMed1999

Procedure-dependence and tissue factor-independence of hypercoagulability during orthopaedic surgery.

The increased risk for deep vein thrombosis (DVT) after orthopaedic surgery has been well documented as well as hypercoagulable state during both total hip arthroplasty (THA) and total knee replacement (TKR). To investigate the influence of the surgical procedure [posterolateral (PL) or lateral (L) approach for THA, use of tourniquet (TQ) or not use of TQ for TKR] on the hypercoagulability and the role of extrinsic pathway activation and endothelial stimulation during orthopaedic surgery we have examined 40 patients (20 patients undergoing primary THA--10 with PL approach and 10 with L approach--and 20 patients undergoing TKR--10 with TQ application and 10 without TQ). Thrombin-antithrombin complexes (TAT), tissue factor (TF), tissue factor pathway inhibitor (TFPI), thrombomodulin (TM) and von Willebrand factor antigen (vWF:Ag) were analyzed before and during the orthopaedic surgery. During THA, TAT plasma levels increased more markedly in patients assigned to the L than PL approach (p <0.05); during TKR an elevation of TAT of higher degree (p <0.05) was observed when TQ was not applicated. Blood clotting activation was significantly (p <0.001) more relevant during THA than TKR. No changes in TF and vWF:Ag plasma levels were observed in all patients undergoing THA and TKR. TFPI plasma levels significantly (p <0.05) decreased 1 h after the end of the THA in group PL and group L, whereas they remained unaffected in the two groups of patients undergoing TKR. Similarly TM plasma levels significantly decreased during THA, but not during TKR. In conclusion, these results show that: 1) the site of surgical procedures and the type of approach affect the degree of hypercoagulability, 2) the blood clotting activation takes place in the early phases of orthopaedic surgery, without signs of extrinsic pathway and endothelial activation.

Aged↗
PubMedDate not supplied

Thrombosis and coagulation abnormalities associated with cancer.

Abnormalities of hemostasis and malignancy have been recognized since the 19th century. Thrombosis and hypercoagulability are reported in as many as 60 percent of patients with malignancies. Decreased levels of protein coagulation factors, circulating anticoagulants and platelet numbers, and function changes are reported. The purpose of this work is to report a case of portal thrombosis in a patient with a myeloproliferative disorder and to review protein coagulation and platelet abnormalities associated with malignancies. The clinical laboratory assessment of these abnormalities is reviewed. The patient was a 59-year-old woman who was referred to the Vanderbilt University Medical Center with a diagnosis of septic portal vein thrombosis. After evaluation, it turned out that she had a myeloproliferative disorder and portal vein thrombosis secondary to that. Hypercoagulative states have been reported with a variety of carcinomas and other neoplasms. They may or may not be associated with acquired or genetic deficiencies of antithrombin III, protein C and/or S. Factors I, V, VIII:C, IX, and XI have all been reported as being elevated and implicated in hypercoagulability in patients with neoplasms. Increased platelet turnover and decreased survival have been noted in patients with disseminated tumors. Thromboses with lysis of the thrombus may be monitored by increased levels of fibrin degradation products, D-dimer, fibrinopeptides A and B, and platelet factor IV among others. There are frequently decreases in coagulation inhibitors including antithrombin III, protein C and protein S. These changes lead to a state of low-grade disseminated intravascular coagulopathy where thrombus formation is a more frequent occurrence than is hemorrhage.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Coagulation Disorders↗
PubMed1982

Detection of hypercoagulability by the measurement of the dynamic loss modulus of clotting blood.

The dynamic loss modulus of clotting whole blood was measured in thrombotic patients to characterize the physical properties of coagulation in the hypercoagulable state. The dynamic loss modulus was measured by a Sonoclot. Thrombotic patients consisted of 30 with deep vein thrombosis and 25 with arterial thrombosis. An accelerated increment rate of the dynamic loss modulus at the beginning of gelling was the characteristic of hypercoagulability. This characteristic occurred more frequently than other abnormalities in other tests for hypercoagulability (beta-thromboglobulin, antithrombin III and TEG). Only in deep vein thrombosis, a moderately positive correlation was noted between the increment rate of the dynamic loss modulus and the plasma fibrinogen level.

Adult↗
PubMed1990

[Hypercoagulability after surgery of esophageal carcinoma].

The purpose of this study was to determine hypercoagulability in patients surgically treated for thoracic esophageal cancer. Twenty-four patients were evaluated; 19 subjected to open chest esophagectomy and 5 closed chest blunt dissection. Six patients subjected to gastrectomy served as controls. In all test patients, preoperative coagulability was within the normal range. Immediately after surgery, however, they were in a hypercoagulable state, showing a marked decrease in platelet count, prothrombin time, antithrombin III level and plasminogen level and an increase in activated partial thromboplastin time and fibrinopeptide B beta 15-42. The controls showed almost no change. There was a close correlation between hypercoagulability on one hand and the time needed for surgery and hemorrhage during 3rd to 7th postoperative day except those with multiple organ failure whose recovery was delayed and those with leakage of anastomosis whose condition did not improve even on the 10th postoperative day.

Adult↗
PubMed2003

The prothrombotic state in hypertension and the effects of antihypertensive treatment.

Hypertension is associated with the flow of blood under high pressures, yet the complications of hypertension, such as myocardial infarction or stroke are paradoxically thrombotic rather than haemorrhagic. This could be explained by increasing evidence which suggests that hypertension fulfils the pre-requisites of the Virchow's triad for thrombogenesis, leading to a prothrombotic or hypercoagulable state. Hypertension leads to changes in the platelets, endothelium and the coagulation and fibrinolytic pathways which help to promote the induction and the maintenance of this prothrombotic state. These changes can to a certain extent be reversed by the treatment of hypertension, although different antihypertensive agents may have variable effects in reversing these changes. Some of the effects may be simply related to normalisation of blood pressure, but certain groups of drugs such as those acting on the renin-angiotensin-aldosterone system appear to have an effect over and above this. Anti-platelet agents have also been shown to confer a degree of benefit to lsqou;high risk' hypertensive patients. The study of the prothrombotic state in hypertension is therefore of paramount importance, as understanding the pathogenic processes underlying it can help prevent many of the complications associated with this condition.

Antihypertensive Agents↗
PubMed1988

Ménétrier's disease. A trivalent gastropathy.

Current conceptions of Ménétrier's disease only obliquely resemble those originally described. Bona-fide cases are so uncommon that, of 125 cases diagnosed as Ménétier's disease, hypertrophic gastritis, or protein-losing gastropathy treated at the Massachusetts General Hospital during the 26-year period of 1962-1987, only six cases merited an unequivocal anatomic diagnosis. Two other cases previously described proved on review to be nondiagnostic in one instance and Campylobacter pylori gastritis in the other. Because abnormalities in the secretion of gastric acid and in the loss of protein from the stomach may coexist, a representation of each case in semiquantitative terms can be described on triaxial coordinates. Three patients had a hypercoagulable state, one in association with gastric carcinoma. One other case of gastric carcinoma and one of esophageal carcinoma coexistant with Ménétrier's disease were identified. Administration of subcutaneous heparin during the perioperative period to patients with Ménétrier's disease is appropriate regardless of whether or not hypercoagulation or carcinoma is manifest. If treatment with anticholinergic drugs and inhibitors of gastric acid secretion fails, total gastrectomy is the best solution, because it stops protein loss, eliminates hyperchlorhydria, prevents development of gastric carcinoma, and permits anastomotic reconstruction between normal esophagus and normal small bowel.

Adult↗
PubMed1992

Cerebral infarction in young men with nephrotic syndrome.

BACKGROUND AND PURPOSE: Thrombosis is one of the main complications of nephrotic syndrome; however, cerebral infarction associated with nephrotic syndrome has been rarely reported. SUMMARY OF REPORT: We describe acute cerebral infarction in two young men with nephrotic syndrome. Both had a hypercoagulable state based on hemostatic studies. By retrospectively reviewing the medical records of the past 10 years at our hospital, we found an additional five cases of cerebral infarction with nephrotic syndrome. Two of the patients were found to have nephrotic syndrome during admission for stroke. CONCLUSIONS: Hypercoagulability may be the major contributing factor of cerebral infarction in patients with nephrotic syndrome.

Acute Disease↗
PubMed2004

Abdominoplasty: thromboembolic risks for both sexes.

During surgical procedures, coagulation complications may occur. Discriminating factors are multiple and may vary because of the anatomical regions involved and because of preexisting diseases. The aim of this study was to analyze changes in such hematological parameters of patients undergoing conventional abdominoplasty with standard surgical procedures under general anaesthesia. For the study, 40 patients (20 men and 20 women) 30 to 60 years with normal coagulation assessments, no previous or current history of hemorrhagic or thrombotic disease, and no primary family history of such problems were selected. All the patients underwent conventional abdominoplasty surgical procedures. Analysis of the results suggests that immediately after surgery, in the absence of any preexisting hypo- or hypercoagulability state, there was no circumstantial modification in coagulation factors considered predictive for thromboembolic risk. However, an interesting difference between male and female patients was noted. In the male group, there was an insignificant uniform downward trend of all values immediately after surgery. In conclusion, women are less hypercoagulative than men in the postoperative period, suggesting that women have limited protection from the development of thromboembolic complications immediately after surgical procedures.

Abdomen↗
PubMed1986

The use of dihydroergotamine and heparin in the prophylaxis of deep venous thrombosis.

Three factors leading to the development of postoperative deep venous thrombosis (DVT) are the hypercoagulable state, stasis, and vein wall injury, which occur in patients undergoing surgical procedures. Vein wall injury is thought to occur as a smooth muscle response to surgical trauma in veins distant from the operative site. Heparin and dihydroergotamine (DHE) were combined in an attempt to decrease the hypercoagulable factor and minimize stasis. We believe that by maintaining venous smooth muscle tone, the degree of endothelial damage is also diminished. Low-dose heparin acts through its effect of factor Xa and activation of antithrombin III; DHE selectively increases venous smooth muscle tone to accelerate venous blood flow velocity and minimize venous pooling. The European experience with combination DHE-heparin prophylaxis shows that this combination is more effective than either agent alone, and studies on orthopedic patients have shown that DHE/5,000 is effective in preventing postoperative DVT in this high-risk group. In the US, the Multicenter Trial evaluated postoperative DVT in general surgical patients. The combination of DHE/5,000 was statistically more effective in the prophylaxis of postoperative DVT than placebo (p = 0.0011). The interim results of an ongoing Multicenter Trial on the prophylaxis of postoperative DVT in patients undergoing total hip replacement indicate that DHE/5000 has significant prophylactic efficacy compared to placebo. It is proposed that the mechanism of action of the DHE-heparin combination is synergistic, since all 3 limbs of Virchow's triad are potentially affected.

Dihydroergotamine↗
PubMed1995

[Activated coagulation factors in various thrombotic diseases].

Various hemostatic abnormalities have been reported and excess activation of coagulation factors, such as prothrombin, factor VII, factor IX, and factor XI, have been detected in thrombotic diseases states by various assay systems. We recently developed the enzyme-linked differential immunoassay for activated factor XI-alpha 1 antitrypsin complex (FXIa-alpha 1 AT) and applied it with other assays for activated factors such as thrombin-antithrombin III complex (TAT) to detect the hypercoagulable state in clinical samples. In patients with DIC, the FXIa-alpha 1 AT level in plasma increased before onset of DIC. In patients with non-insulin-dependent diabetes mellitus, FXIa-alpha 1AT and TAT levels were increased in the patient plasma. FXIa-alpha 1AT was related to the severity of urinary albumin excretion, whereas TAT was not. Plasma FXIa-alpha 1AT levels were significantly increased in patients with angiographically proven coronary artery disease, and showed a positive correlation with TAT, fibrinogen, and Lp(a). Evaluation of activated coagulation factor provides useful information on the diagnosis of thrombotic disease.

Arteriosclerosis↗
PubMed2000

Livedoid vasculopathy associated with heterozygous protein C deficiency.

Livedoid vasculopathy is characterized by recurrent painful ulceration of the feet, ankles and legs that heals with residual white atrophic scars. For many years, livedoid vasculopathy has been considered to be a primary vasculitic process. Recently, however, there has been a trend towards considering livedoid vasculopathy as an occlusive vasculopathy due to a hypercoagulable state. Livedoid vasculopathy (under the designation livedo vasculitis) was first reported to be associated with protein C deficiency in 1992. We describe an additional patient with livedoid vasculopathy associated with heterozygous protein C deficiency. This second reported case suggests that protein C deficiency may be one cause of the hypercoagulable condition in these patients and demonstrates the necessity for further investigation of thrombogenic factors underlying the disease.

Adolescent↗
PubMed2002

Coagulation and fibrinolysis in diabetes.

The accelerated development of atherothrombotic cardiovascular disease in type 2 diabetes mellitus may be enhanced by the presence of a prothrombotic state. This prothrombotic state includes a diminished fibrinolytic capacity and an increased coagulability. Impaired fibrinolytic capacity appears to be a hallmark of the metabolic syndrome of type 2 diabetes and can be a direct consequence of visceral obesity. In addition, a chronic low inflammatory state with hyperinsulinemia and dyslipidemia may further influence the hemostatic balance. The characteristic dyslipidemia of type 2 diabetes, coined the atherogenic lipoprotein profile, with raised plasma levels of fasting and postprandial triglyceride lipoproteins, atherogenic low-density lipoproteins, and low high-density lipoproteins, is involved in promoting a hypercoagulable state. Lifestyle and pharmacologic interventions that reduce cardiovascular risk in the general population and that may improve the metabolic syndrome may also reduce the prothrombotic state.

Arteriosclerosis↗
PubMed2003

The association between blood coagulation markers, atherothrombosis and dementia.

Abnormalities of coagulation and the fibrinolytic system leading to a hypercoagulable state could lead to accelerated atherogenesis. The abnormalities of haemostasis and resulting ischaemic cerebrovascular disease may contribute to cognitive decline in the elderly. There is increasing evidence in the literature of haemostatic abnormalities not only in vascular dementia but also in patients with Alzheimer's dementia. Among the serum markers of hypercoagulability leading to thrombosis and dementia, serum fibrinogen has been one of the factors most commonly studied. Modification and control of these serum markers of hypercoagulability offer an exciting approach to the control of dementia in the community. This article explores the association between serum markers of hypercoagulability, associated atherothrombosis and the risk of dementia.

Arteriosclerosis↗
PubMed1985

Thrombogenic effects of xenobiotics.

The mechanisms by which xenobiotics may cause or promote thrombosis include vascular damage, induction of a hypercoagulable state and disturbances of blood flow. This paper discusses the methods available to detect various types of thrombogenic substances. Pathomorphological techniques are best suited to demonstrate thrombosis caused by localized vascular damage or generalized endothelial lesions. For the assessment of disseminated microcirculatory thrombosis, the consumption of platelets and clotting factors and the appearance of specific platelet proteins and fibrinogen and fibrin split products can be determined in the blood. Hypercoagulability which is defined as a perturbation of the hemostatic equilibrium resulting in a shift in the direction of thrombosis, is of particular importance in toxicology. Many in vitro, ex vivo and in vivo methods have been proposed to detect and to measure the ability of xenobiotics to induce a prethrombotic state. Their usefulness is demonstrated with several examples.

Adrenocorticotropic Hormone↗