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PubMed2006

A comprehensive analysis of 12 thrombophilic mutations and related parameters in patients with inflammatory bowel disease: data from Turkey.

BACKGROUND: Possible association of inflammatory bowel disease (IBD) with the most common inherited prothrombotic conditions has been the focus of many investigations. Advance in modern molecular biology is expanding the thrombophilia evaluation steadily. We tried to put forward a comprehensive thrombophilic profile in IBD and to see the probable role of this profile in pathogenesis. METHODS: A total of 60 adults (33 patients and 27 healthy controls) were included. We used the CVD-StripAssay which is based on the reverse-hybridization principle to identify a total of 12 thrombophilic gene mutations: Factor V R506Q, Factor V H1299R, prothrombin G20210A, Factor XIII V34L, beta-Fibrinogen-455 G-A, PAI-1 4G/5G, platelet GPIIIa L33P, MTHFR C677T, MTHFR A1298C, ACE I/D, Apo B R3500Q and Apo E2/E3/E4, respectively. Besides, we evaluated many related blood parameters such as protein C, protein S, AT-III, IL-6, TNF-alpha, Apo-A1, Apo-B100, homocysteine (tHcy) etc. using commercially available assays. RESULTS: The frequencies of genetic polymorphisms were found to be statistically insignificant among patients and controls, except for three: Beta-Fibrinogen-455G-A, MTHFR A1298C and ACE-I/D. Two patients with a history of deep venous thrombosis had more than one polymorphism. Patients with MTHFR C677T and MTHFR A1298C gene mutations had a similar mean tHcy levels with controls. Patients with Apolipoprotein B R3500Q and Apolipoprotein E4 gene mutations had similar mean LDL-cholesterol levels. Mean total cholesterol and triglyceride levels were similar in patients and controls of Apo E2, E3, E4 alleles. CONCLUSION: Predominantly, the presence of genetic mutations that predispose to hypercoagulable states does not appear to be in correlation with IBD. There was a statistical difference between the proportions of the mutated allele frequencies of Beta-Fibrinogen-455G-A, MTHFR A1298C and ACE-I/D in IBD.

Adolescent↗
PubMed2002

Hypertension, left ventricular hypertrophy, and sudden death.

Left ventricular hypertrophy (LVH), a form of end-organ damage in hypertension, is associated with increased incidence of sudden cardiac death (SCD). This review explores the possible mechanisms behind this phenomenon. SCD in LVH could be thrombotic/ischemic or arrhythmic (eg, myocardial ischemia, even in the absence of significant coronary artery disease, may be one important factor). Abnormalities of flow-mediated dilatation, endothelial function, and a hypercoagulable state are well-observed abnormalities in association with hypertension and LVH, although their precise contributory role is as yet undefined in the pathogenesis of sudden death. Electrophysiologic abnormalities are also well documented in LVH, and such patients are more predisposed to arrhythmias. In the past decade, many studies have investigated the regression of LVH, and recent studies are addressing whether the latter translates into a prognostic benefit.

Arrhythmias, Cardiac↗
PubMed2006

Management of the antiphospholipid syndrome.

Antiphospholipid antibodies are associated with a hypercoagulable state leading to a wide variety of systemic manifestations and obstetric complications. The different pathologic manifestations can be a result of arterial and venous thrombosis, microthrombotic angiopathy, embolization, obstetric disease, and non-thrombotic phenomenon. Presently, the treatment centers on anticoagulation. Two randomized prospective studies in patients with antiphospholipid syndrome with initial thromboembolic event support the target international normalized ratio of 2.0 to 3.0 for the prevention of future thrombotic events. With pregnancy, the combination of aspirin and heparin is still the standard of care. In addition, non-thrombotic features and any associated autoimmune disease may need to be treated. Underlying risk factors precipitating the thromboembolic phenomenon need to be addressed as well.

Anticoagulants↗
PubMed2001

Recurrent Acute Pancreatitis.

Patients with recurrent acute pancreatitis should be treated with the same supportive and symptom-oriented measures as those with acute pancreatitis. The need for specific treatment depends on the cause of the pancreatitis. Patients should discontinue alcohol use, putative causative medications, and exposure to toxins or helminths in endemic areas. Metabolic abnormalities need to be corrected, and appropriate treatment should be initiated for associated infections, autoimmune diseases, vasculitis, and hypercoagulable states. For patients with gallstone pancreatitis, endoscopic retrograde cholangiopancreatography is indicated if biliary obstruction persists or if cholangitis is present. Elective cholecystectomy may be performed in appropriate patients; otherwise, consider biliary sphincterotomy and ursodeoxycholic acid for prevention of recurrent attacks. Transpapillary stenting or sphincterotomy of the minor papilla benefits some patients with pancreas divisum and no other explanation for recurrent pancreatitis. Surgical sphincteroplasty is reserved for those failing endoscopic treatment. Biliary sphincterotomy benefits more than 50% of patients with sphincter of Oddi dysfunction and recurrent acute pancreatitis. Some authors advocate pancreatic sphincter manometry and sphincterotomy for persistent pancreatic segment hypertension in patients who have recurrent pancreatitis after biliary sphincterotomy. In patients with pancreatic duct strictures, transpapillary stent placement serves as a short-term measure; most patients ultimately require surgery.

Journal Article↗
PubMed1975

Nonbacterial thrombotic endocarditis in a Japanese autopsy sample. A review of eighty cases.

A study of nonbacterial thrombotic endocarditis has been carried out in a series of 3,404 autopsies performed upon atomic bomb survivors in Hiroshima in the period 1953-1970. The prevalence of the lesion was 2.4 per cent, with a greater frequency among the elderly and among females, and with a significant relationship to malignant neoplasms. In contrast to other reported series, there was a greater prevalence among cancers of the colon, rectum, and female genitourinary tract. No relationship was noted between the presence of NBTE and exposure to ionizing radiation. Histologic findings in the heart-valve leaflets in close proximity to the verrucae, like experimental studies reported by others, suggest that in association with severe systemic disease there appears a process consisting of degenerative changes in valve collagen and ground substance, with subsequent denudation of endothelium, localized almost entirely to the apposing leaflet surfaces of the left-heart valves. The verrucae of nonbacterial thrombotic endocarditis are then formed upon this abnormal leaflet surface. While the relationship between systemic disease and the pathologic changes observed in cardiac valve tissue is unclear, and although it is not known whether a "hypercoagulable state" may accentuate the tendency for thrombi to form upon these abnormal valves, there is no doubt that this lesion represents a clinically important complication of severe systemic disease. It also seems likely that in some cases NBTE may complicate an illness which may otherwise be curable. Increasing awareness of this pathologic entity among clinicians, coupled with appropriate laboratory techniques, most likely echocardiography, will permit more frequent diagnosis in living patients.

Adenocarcinoma↗
PubMed1981

Hematologic alterations in diabetes mellitus.

Several hematologic abnormalities have been defined in patients with diabetes mellitus, despite the lack of classic hematologic pathologic findings in this condition. Studies of the erythrocyte and the formation of hemoglobin A1c have provided a means of documenting glycemia and a model reaction for diabetic sequelae through postsynthetic protein modification. Oxygen affinity has been noted to be abnormal in the diabetic erythrocyte, concomitant with a decreased concentration of inorganic phosphorus, glycosylation of the 2,3-diphosphoglycerate binding site or preexisting vascular disease. Red cell membrane viscosity has also been documented to be increased in the hyperglycemic subject. Abnormalities in the polymorphonuclear leukocyte have been described, involving the properties of adherence, random migration, chemotaxis, phagocytosis and killing. Certain metabolic abnormalities are also present in this cell type. The lymphocyte has been shown to have abnormal metabolic properties, mitogen responses and cell surface properties in diabetes both in animals and human subjects. Certain subpopulations of lymphocytes appear to be especially vulnerable to changes concomitant with diabetes mellitus. In vitro abnormalities of platelet behavior have been widely studied, although the in vivo significance of these findings remains controversial. Studies of the fluid phase of coagulation have suggested the existence of a hypercoagulable state in hyperglycemic subjects. The clinical significance of most of these findings remains to be defined. Nevertheless, the observation that many of the abnormalities described are reversible when hyperglycemia is corrected has given impetus to the development of improved systems of glucose "control" for diabetic patients.

Animals↗
PubMed1982

Primary cerebral venous thrombosis in patients with cancer--a rarely diagnosed paraneoplastic syndrome. Report of three cases and review of the literature.

Idiopathic thrombosis of the cerebral venous structures is a rare complication of malignancy. The clinical, radiologic, pathologic, and laboratory findings in the 15 previously reported cases are reviewed, and three additional cases are reported. The clinical syndrome that develops in such patients is similar to that seen in other patients with cerebral venous or sinus thrombosis. However, the diagnosis is often not made clinically because cerebral involvement by neoplastic disease provides a more common and readily acceptable explantation of the observed phenomena. If venous thrombosis involving the brain is suspected, angiography provides the only certain method of diagnosis. The relationship of this thrombotic process to a cancer-associated hypercoagulable state is discussed.

Adenocarcinoma↗
PubMed1986

Infection and infarction. Acute viral (and other) infection in the onset, pathogenesis, and mimicry of acute myocardial infarction.

Because a prospective controlled investigation showed a highly significant association of the onset of acute myocardial infarction with signs of preceding respiratory infection, the clinical, laboratory, experimental, and epidemiologic evidence more directly supporting this association was analyzed. Inflammation--specifically of infectious, usually viral, origin--has been shown by several lines of evidence to be capable of precipitating or mimicking clinical myocardial infarction. Myocardial biopsy is producing rapidly increasing confirmation that myocarditis can perfectly mimic clinical acute myocardial infarction. Coronary arteritis, with implications for vasospasm and thrombosis, is being increasingly demonstrated when deliberately sought in necropsy and biopsy material. Effects of blood-borne infectious agents, particularly viremia, on platelets in vivo and in vitro--aggregation and lysis with release of vasoactive substances--have even more serious potential for coronary thrombosis and vasospasm. It is not clear whether such mechanisms operate entirely independently or are more potent in high-risk patients, particularly in view of the demonstrable hypercoagulable state in many patients with coronary disease. Because of the great importance of confirming precipitating mechanisms for acute myocardial infarction (as well as its frequent mimic, myocarditis), intensive investigation of the relation between infection and infarction has important preventive and therapeutic implications.

Aged↗
PubMed1975

Oral contraceptives and thromboembolism: a reassessment.

The relationship between oral contraceptive usage and thromboembolism is controversial. Since thromboembolism is often undiagnosed, both clinically and at routine autopsy, most epidemiologic analyses rest or a very uncertain factual base. There are increases in blood coagulation factors in oral contraceptive users similar to, but less than, those seen in pregnancy, which is not associated with increased thromboembolism. Hematologists emphasize that these changes do not define a "hypercoagulable" state, and they do not define or predict the occurrence of thrombosis. Intrinsic vascular wall changes, unrelated to drug use, may play a role in sporadic cases of thromboembolism. When the incidence of thromboembolism in very large Phase III trials of conventional oral contraceptives is compared to that in other populations (patients admitted to the hospital, women who visit a physician, pregnant women, or users of nonestrogenic oral contraceptives), no difference is seen. Epidemiologic studies by the "case-control" ("trohoc") method consistently show an increase "relative risk" associated with oral contraceptive use in subjects with "idiopathic" thromboembolism but no increased risk in thromboembolism patients as a whole or in those with predisposing factors. This retrospective epidemiologic technique, its particular applications, and the inferences drawn are open to serious criticism, as are studies claiming a relationship between estrogen dose and thromboembolism incidence. An Australian prospective survey found no increased risk among users, and a large British study which initially reported an increased risk is currently undergoing recalculation. The only controlled clinical experiment (with random assignment of subjects to vaginal versus high-estrogen contraceptives) showed no increased incidence in the drug-treated group. Statistical associations derived from "trohoc" studies do not establish causal relationships; moreover, their risk estimates are in conflict with the findings of large Phase III clinical surveys including subjects using estrogen-free contraceptives, with at least one prospective clinical survey, and with a randomized, controlled clinical trial. The data relating estrogen dosage to thromboembolism incidence are ambiguous, at best. Thus, the claim of a causal relationship between oral contraceptive steroids and thromboembolism does not appear to be firmly founded, and the belief that predisposing factors increase the risk to contraceptive users is equally insubstantial.

Adolescent↗
PubMed1977

The association of maternal and neonatal thrombocytopenia in high-risk pregnancies.

In this study of 136 women with pre-eclampsia, eclampsia, placenta previa, or abruptio placentae, 21 mothers were noted to have thrombocytopenia. Seventeen of the 21 were in the pre-eclampsia group. Of the 21 thrombocytopenic mothers, nine were associated with thrombocytopenia in the children, seven children had normal platelet counts, and five had no counts performed. Eight of the nine thrombocytopenic neonates were associated with pre-eclampsia in the mother, and five of these were not believed to have disseminated intravascular coagulation as the etiology of the platelet defect. The results suggest that thrombocytopenia is common in high-risk pregnancies in both the mother and the baby. However, the etiology of the platelet defect cannot be easily explained on the basis of a hypercoagulable state.

Arizona↗
PubMed1979

The effect of chlorotrianisene as postpartum lactation suppression on blood coagulation factors.

Coagulation changes and increased risk of thromboembolic disease may occur in association with estrogen administration. The puerperium is also a high-risk period for thromboembolism, and estrogen administration at this time may increase this risk. Patients with congenital deficiency of antithrombin III have recurrent venous thromboembolic disease, suggesting that low levels of this factor may be associated with "hypercoagulability" states. We studied 50 postpartum patients who received chlorotrianisene (Tace) or placebo for lactation suppression in a prospective, double-blind, randomized fashion. Antithrombin III values were significantly lower on the third day post partum in the treated group compared to the placebo group (p less than 0.05). In addition, our clinical data from a total of 99 patients support the previous evidence that estrogens delay rather than prevent breast engorgement. Thus, with questionable benefit and a possible increased thromboembolic risk, it would appear prudent to discontinue the practice of estrogen administration for lactation suppression.

Adult↗
PubMed1981

Response of blood coagulation parameters to elevated endogenous 17 beta-estradiol levels induced by human menopausal gonadotropins.

To elucidate the relationship between estrogen and thrombosis, we studied blood coagulation parameters in women whose ovaries were stimulated with human menopausal gonadotropins (hMG). Daily hMG administration over 1 to 2 weeks in seven anovulatory women increased plasma 17 beta-estradiol levels fivefold over the pretreatment value. Of the coagulation parameters, the fibrinogen level increased significantly from an initial value of 248 +/- 11.7 mg/dl (mean +/- SEM) to 353 +/- 32.2 mg/dl after hMG treatment (P less than 0.05), with a significant positive correlation between estrogen and fibrinogen levels (r = +0.762). In addition, a thrombokinetics study showed that the maximal rate of change in optical density of the prothrombin time and activated partial thromboplastin time was significantly increased, suggesting that the coagulation factors involved in extrinsic, intrinsic, and common pathways could be increased by estrogen. Antithrombin III levels decreased gradually during hMG administration. Thus, increased endogenous estrogen levels appear to induce the so-called "hypercoagulable state" through both an increase in coagulation factors in the coagulation cascade system and a decrease in antithrombin III, a potent natural inhibitor of activated coagulation factors. Patients on a regimen of hMG treatment for induction of ovulation serve as excellent models for the study of alteration of "natural" estrogen-mediated coagulation parameters.

Adult↗
PubMed1987

Pregnancy-induced changes in the fibrinolytic balance: evidence for defective release of tissue plasminogen activator and increased levels of the fast-acting tissue plasminogen activator inhibitor.

Pregnancy is accompanied by an increased risk of thromboembolic disease. One contributing factor to such disease in the nonpregnant patient is disordered fibrinolysis. It has been suggested that defective fibrinolysis may occur in pregnancy, but this defect has been poorly characterized. In the present study of 52 women with normal pregnancies and 56 nonpregnant control women, we found a marked change in levels of releasable tissue plasminogen activator in pregnant women beginning in the first trimester. Whereas nonpregnant women demonstrated releasable levels of tissue plasminogen activator of 0.74 +/- 0.15 IU/ml of plasma, in the pregnant women the amount released was only 0.06 +/- 0.02 IU/ml of plasma (p less than 0.01). These levels were observed beginning in the first trimester. Levels of the recently described fast-acting tissue plasminogen activator inhibitor increased significantly throughout pregnancy. Values ranged from 8.40 +/- 0.27 IU/ml of plasma in the first trimester to 9.92 +/- 0.09 IU/ml of plasma in the third trimester (p less than 0.05) compared with the level of 8.46 +/- 0.19 IU/ml of plasma in nonpregnant subjects. These data suggest that alterations both in releasable tissue plasminogen activator and in the fast-acting tissue plasminogen activator inhibitor contribute to the physiologic hypercoagulable state of pregnancy.

Adult↗
PubMed1990

Clinical aspects of the relationship between oral contraceptives and abnormalities of the hemostatic system: relation to the development of cardiovascular disease.

Epidemiologic evidence has established that oral contraceptives increase the risk of both arterial and venous thromboembolic disease. This is dose related in the case of the estrogen component for both arterial and venous events and in the case of progestogens for arterial events. It is probable that the increased rate of thromboembolic events caused by estrogen is related to hypercoagulability. Plasma levels of several clotting factors have been shown to be elevated in oral contraceptive users, and this increase is graduated according to the dose of estrogen. In pregnancy, factor VIIc is increased after cold activation of plasma at 4 degrees C overnight. Likewise, in users of oral contraceptives, both factors VIIc and XIIc are increased, which suggests a direct effect of factor XIIc on the extrinsic system. In men, the risk of ischemic heart disease is strongly and independently related to factor VIIc and fibrinogen levels; thus it is possible that in women taking oral contraceptives, the mechanism of risk is similarly mediated. There is a good case for factor VIIc as the index of flux in the coagulation system and hence of a hypercoagulable state, and indeed it may directly contribute to the generation of thrombin. This article examines the available evidence on clotting factor activity in the risk of cardiovascular disease in oral contraceptive users.

Blood Coagulation Factors↗
PubMed1982

Management of deep venous thrombosis and pulmonary embolism during pregnancy.

Despite venous stasis and a hypercoagulable state during pregnancy, the reported incidences of deep venous thrombosis and pulmonary embolism are remarkably low, about 1 in 2,000 and 1 in 10,000 cases, respectively. Mortality from antepartum thromboembolism has been reported in about 15 percent of untreated patients and less than 1 percent of treated patients. Adequate anticoagulant therapy significantly reduces maternal mortality and decreases postpartum morbidity. The proper anticoagulant agent for use during pregnancy has been widely debated. Coumarin compounds pass through the placenta and into the fetus. Hemorrhagic complications in the fetus are uncommon if prothrombin times are carefully controlled and if the drug is discontinued before delivery. However, coumarin during the first trimester has the teratogenic hazard of producing chondrodysplasia punctata. Heparin, in contrast, does not cross the placental barrier and is considered more effective treatment for deep venous thrombosis; however, long-term intravenous administration during pregnancy has been considered both impractical and possibly hazardous due to the risk of osteoporosis after 6 months of therapy. In our study, a combined regimen of intravenous and subcutaneous heparin was used successfully in four women with deep venous thrombosis. One patient who had recurrent embolization while on adequate intravenous heparin underwent vena caval clipping and had an uneventful Cesarian section at term with a normal infant. Another patient also underwent Caesarian section with a normal infant, while the other two women had normal vaginal deliveries at term. Miniheparin therapy was continued for 3 months postpartum, followed by long-term aspirin and Ascriptin therapy. Carefully controlled heparin therapy in a pregnant woman with deep venous thrombosis both safe and beneficial for mother and fetus.

Adolescent↗
PubMed1986

Pathogenesis determines late morbidity of axillosubclavian vein thrombosis.

The late consequences of axillosubclavian vein thrombosis were evaluated through a clinical follow-up of 41 patients (45 limbs) treated from July 1975 to December 1985. The causes of the obstruction were classified into two main groups: Intrinsic damage, consisting of thrombophlebitis due to intravenous drug abuse (11 patients), central venous catheterization (10 patients), and hypercoagulability state (2 patients); and extrinsic obstruction, involving effort-induced or thoracic outlet obstruction (9 patients), underlying neoplastic disease (5 patients), trauma (3 patients), and congenital venous malformation (1 patient). Clinical diagnosis was confirmed by upper arm venography in all 41 patients, and all were initially treated by anticoagulation with heparin for 1 to 2 weeks, usually followed by oral warfarin for a variable period of 1 week to 5 years. Only three patients had an operation (rib resection for thoracic outlet obstruction, thrombectomy and clavicle fixation, and repair of a congenital venous malformation). Major early morbidity consisted of a documented pulmonary embolus in five patients, two in Group I and three in Group II, for an overall incidence of 12 percent. Clinical follow-up of up to 5 years revealed that chronic morbidity was related to our classification. Thrombosis secondary to intrinsic damage rarely caused persistent symptoms and responded well to anticoagulation alone. Conversely, when extrinsic obstruction was the cause, only 50 percent of patients were symptom-free, whereas many had disabling intermittent arm swelling and pain. Repeat venography in severely symptomatic patients revealed persistent obstruction with no recanalization. We conclude that patients with axillosubclavian venous thrombosis due to intrinsic damage do not require treatment other than anticoagulants, whereas patients with extrinsic obstruction often have poor long-term results from conventional therapy and therefore should be considered for adjunctive treatment with thrombolysins or operative intervention.

Adult↗
PubMed1993

Topical use of aprotinin in open heart operations.

Among various pharmacological agents used to reduce bleeding after open-heart operations, high-dose aprotinin therapy seems most promising. However, its long-term effects are still obscure; there is almost always possibility of bypass graft occlusions produced by the hypercoagulable state induced by aprotinin in coronary bypass operations. Topical application of aprotinin into the pericardial cavity could prevent the adverse effects. Fifty patients were prospectively studied to evaluate the effects of topical aprotinin. One million KIU of aprotinin was poured into the pericardial cavity before closure of the sternotomy in group 1 (n = 25). Patients in group 2 (n = 25) served as controls. Total postoperative bleeding was significantly reduced in group 1 when compared with that of group 2 (722.7 +/- 230.8 versus 1,282.6 +/- 225.7 mL; p < 0.01). The use of banked donor blood products was significantly less in group 1 than in group 2 (0.33 +/- 0.67 versus 1.36 +/- 0.86 units; p < 0.01). These results show that topical use of aprotinin reduces post-operative blood loss and need for transfusion. It seems promising and warrants further studies to be done.

Administration, Topical↗
PubMed1996

Interference with anticoagulation monitoring by procainamide-induced lupus anticoagulant.

A patient scheduled for coronary revascularization was discovered to have elevated partial thromboplastin and activated clotting times. Preoperative testing revealed a lupus anticoagulant, probably secondary to long-term procainamide therapy. The resultant inability to use conventional anticoagulation monitoring for cardiopulmonary bypass was solved by direct measurement of heparin concentration. Operation and recovery were uneventful, and the patient was treated with long-term warfarin anticoagulation for this hypercoagulable state.

Aged↗