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PubMed1991

Haemostatic factors associated with vascular thrombosis in patients with systemic lupus erythematosus and the lupus anticoagulant.

To elucidate the mechanism of vascular thrombosis in patients with systemic lupus erythematosus and the lupus anticoagulant changes in factors associated with haemostasis were investigated. The lupus anticoagulant was associated with an increased incidence of thrombosis, particularly cerebral thrombosis. Concentrations of fibrinopeptide A and fibrinopeptide B beta 15-42 were significantly raised in the plasma of patients with systemic lupus erythematosus and the anticoagulant compared with concentrations in patients without the lupus anticoagulant. The tendency towards formation of thrombosis was not found in all lupus patients with the anticoagulant, however. Concentrations of thromboxane B2 were remarkably raised in the plasma of the two patients with the lupus anticoagulant who had recently had thrombosis. Concentrations of 6-keto-prostaglandin F1 alpha, protein C, antithrombin III, and plasminogen were similar in both groups. No significant decrease in serum stimulatory activity on prostacyclin production by cultured aortic endothelial cells was noted in lupus patients with the anticoagulant, but inhibition was present in the two patients with recent thrombosis. These results indicate that although patients with the lupus anticoagulant are not always in a hypercoagulable state, haemostatic abnormalities found in some patients with the anticoagulant may be predictive of thrombotic events.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

Tissue plasminogen activator inhibitor in patients with systemic lupus erythematosus and thrombosis.

OBJECTIVE: To examine the relations among tissue plasminogen activator antigen, plasminogen activator inhibitor, the lupus anticoagulant, and anticardiolipin antibodies in patients with systemic lupus erythematosus. DESIGN: Prospective study of blood samples (a) from selected patients with systemic lupus erythematosus whose disease was and was not complicated by a history of thrombosis or recurrent abortions, or both, and (b) from a series of healthy controls with a similar age and sex distribution. SETTING: University based medical clinic. SUBJECTS: 23 Patients with definite systemic lupus erythematosus (American Rheumatism Association criteria), of whom 11 (eight women) aged 26-51 had a history of thrombosis or recurrent abortions, or both, and 12 (10 women) aged 23-53 had no such history. 15 Healthy subjects (10 women) aged 25-58 served as controls. MAIN OUTCOME MEASURES: Tissue plasminogen activator concentrations, plasminogen activator inhibitor activities, detection of the lupus anticoagulant, and values of anticardiolipin antibodies in the two groups of patients and in the patients with a history of thrombosis or abortions compared with controls. Other measurements included concentrations of proteins that are known to change during the acute phase of systemic lupus erythematosus--namely, fibrinogen, C3 and C4, and C reactive protein. RESULTS: Patients with a history of thrombosis or abortions, or both, had significantly higher values of tissue plasminogen activator and plasminogen activator inhibitor than patients with no such history. A significant correlation between tissue plasminogen activator and plasminogen activator inhibitor (r = 0.80) was found only in the patients with a history of complications of their disease. The lupus anticoagulant was detected in six of the 11 patients with a history of thrombosis or abortions when tested by measuring the activated partial thromboplastin time but was found in all 11 patients when tested by measuring the diluted activated partial thromboplastin time. Nine of these 11 patients had raised values of anticardiolipin antibodies. The findings showed no relation to the activity of the disease. CONCLUSIONS: A significant correlation between tissue plasminogen activator concentrations and plasminogen activator inhibitor activities was found only in patients whose systemic lupus erythematosus was complicated by a history of thrombosis or recurrent abortions. The findings show that these patients have raised plasminogen activator inhibitor activities, and the frequent association between these raised activities and the presence of the lupus anticoagulant suggests that the two may be linked.

Abortion, Habitual↗
PubMed1983

Plain radiographic diagnosis of thrombosis of left atrial appendage in mitral valve disease.

Conventional posteroanterior chest radiographs of 42 patients with mitral valve disease who had had surgery were analyzed, and particular attention was directed to the presence or absence of the convexity of the left lower midcardiac border (left atrial segment). The flatness or concavity of this segment, despite other evidence of left atrial enlargement, was observed in six (60%) of 10 patients who had left atrial thrombosis, and in three (9%) of 32 patients who did not have thrombosis (false positive diagnosis). Four of the 10 patients who had left atrial thrombosis did not show this finding on the radiographs (false negative diagnosis). One of these four had a thrombus only against the posterior wall of the body of the left atrium. Therefore, the accuracy in the diagnosis of thrombosis of the left atrial appendage was 66.7% (six of nine) for patients who had thrombosis of the appendage. Standard chest radiographs are important in the evaluation of the patient with thrombosis of the left atrial appendage.

Adult↗
PubMed1999

Portal vein thrombosis in paroxysmal nocturnal haemoglobinuria.

A 28-year-old man was hospitalized with nausea, vomiting, abdominal pain and low-grade fever. He had a 6-month history of paroxysmal nocturnal haemoglobinuria (PNH), and laboratory data showed anaemia and liver dysfunction. An abdominal ultrasonography showed ascites and portal vein thrombosis. After receiving antithrombotic treatment, the portal vein thrombosis did not extend. Portal vein thrombosis is very rare but should be considered when we encounter liver dysfunction associated with PNH as well as hepatic vein thrombosis. Ultrasonography is very useful in detecting portal vein thrombosis and facilitating early diagnosis. Warfarin is very effective in preventing exacerbation of portal vein thrombosis in PNH.

Adult↗
PubMedDate not supplied

Thrombosis during pregnancy: risk factors, diagnosis and treatment.

Venous thromboembolism occurs infrequently but is a leading cause of illness and death during pregnancy and the puerperium and remains a diagnostic and therapeutic challenge. In the general population the incidence of pregnancy associated VTE has been estimated to vary from 1 in 1000 to 1 in 2000 deliveries. The risk of VTE is five times higher in a pregnant woman than in a nonpregnant woman of similar age. Postpartum VTE is more common than antepartum VTE. Women with congenital abnormalities or persistent presence of antiphospholipid antibodies have an increased risk of VTE during pregnancy and the puerperium. In individuals with well defined hereditary thrombosis risk factors, such as the factor V:R506Q mutation, the factor II:G20210A variation, antithrombin-deficiency or protein C-deficiency, a relative risk of pregnancy associated VTE between 3.4 and 15.2 has been found. Women with previous VTE have an approximately 3.5 fold increased risk of recurrent VTE during pregnancy compared to non-pregnant periods. Our ability to diagnose deep-vein thrombosis clinically is generally poor and is further hampered during pregnancy since dyspnea, tachypnea, swelling and discomfort in the legs are common. Objective diagnosis is essential for treatment decisions. Exposure to radiation of less than 50,000 microGy (5 rad) has not been associated with a significant risk of fetal injury. Therefore, besides sonography, routine diagnostic procedures should be performed, if clinically necessary. Heparin does not cross the placenta and is therefore the anticoagulant treatment of choice during pregnancy. In case of acute new onset of thrombosis during pregnancy, treatment is performed like in non-pregnant patients with acute deep vein thrombosis or pulmonary embolism. There is ongoing debate, whether or not pregnant women with previous venous thrombosis should routinely receive prophylactic anticoagulation. In patients who have hereditary antithrombin deficiency, antiphospholipid antibodies, a combined abnormality or a history of a severe thrombotic event (pulmonary embolism, extended deep vein thrombosis) should be advised to use prophylactic heparin during pregnancy, starting during the first trimester. Post partum prophylaxis should be given in all women with an increased risk for VTE.

Female↗
PubMed2006

Effects of external electrical stimulation on laser-beam-induced experimental thrombosis.

External electrical stimulation (EES) has demonstrated venous antithrombotic properties. The aim of this investigation was to study its antithrombotic properties using unfractionated heparin (UFH) as a reference in arterial and venous mesenteric microvessels. For this purpose a rat model of laser-beam-induced thrombosis was used. Four groups of rats were investigated (n = 7): control, UFH (5 mg /kg), UFH (2.5 mg/kg) and electrical stimulation [e-vascular, E = 10, alternate polarity, in two protocols: (i) 30 min before and during thrombosis induction and (ii) only 30 min before thrombosis induction as preventive stimulation]. This effect was tested in arterial and venous microvessels in the four groups using the continuous protocol and only in arterial microvessels using the preventive protocol. Three parameters were studied: the number of laser beams needed to induce platelet thrombus formation, the number of emboli and the duration of embolization. Induced hemorrhagic time (IHT), platelet aggregation induced by ADP and coagulation tests (activated partial thromboplastin time, aPTT, prothrombin time, pTT, and fibrinogen level) were also determined. Continuous electrical stimulation decreased the number of emboli and the duration of embolization both in arterioles and in venules. It also significantly reduced the amplitude and velocity of the ex vivo platelet aggregation induced by ADP. Contrary to UFH, neither aPTT nor pTT were affected in platelet-poor plasma collected after the induction of thrombosis by laser beam, nor did it modify IHT. Preventive electrical stimulation produced similar results with fewer effects on induced venous thrombosis. These data suggest that EES has a potent antithrombotic effect on arterial and venous thrombosis without any hemorrhagic adverse effects, making it a very promising tool in the prevention and treatment of venous and arterial thromboembolic complications.

Animals↗
PubMed2005

Reduced immunoregulatory CD31+ T cells in the blood of atherosclerotic mice with plaque thrombosis.

OBJECTIVE: Lymphocyte activation is thought to play a major role in the pathogenesis of atherosclerotic complications such as plaque thrombosis. Circulating CD31+ T cells have been shown to regulate human T cell activation. Aim of this study was to evaluate whether the proportion of circulating immunoregulatory CD31+ T cells is correlated to the occurrence of plaque thrombosis in aged apolipoprotein (apo) E knockout (KO) mice. METHODS AND RESULTS: CD31+ T cell depletion of spleen T cells enhanced proliferation (P<0.05) and interferon-gamma production (P<0.01) while reducing interleukin (IL)-4 (P<0.001) and IL-10 (P=0.001) secretion in response to minimally modified low-density lipoprotein. CD31+ T cells were counted in 65 apoE KO mice (46-week-old) by flow cytometry. Organizing thrombi could be documented in 28 of 195 (14%) lesions and in at least one of the aorta root lesions in 23 of 65 mice (35%). CD31+ T cell count was significantly reduced in mice showing plaque thrombosis (72.3+/-1.5% versus 84.1+/-1.2%; P<0.0001), but such reduction did not follow induced plaque rupture or experimentally controlled thrombosis. CONCLUSIONS: Reduced CD31+ T cells in circulating blood is a hallmark of atherosclerotic plaque thrombosis. Our data suggest that CD31+ T cells may play an important regulatory role in the development of plaque thrombosis.

Animals↗
PubMed1995

Venous thrombosis-associated inflammation and attenuation with neutralizing antibodies to cytokines and adhesion molecules.

Thrombosis and inflammation are closely related. However, the response of the vein wall to venous thrombosis has been poorly documented. This study examines the hypothesis that venous thrombosis is associated with an inflammatory response in the vein wall. In a rat model of inferior vena caval thrombosis, vein wall was temporally examined for inflammation by assessment of histopathology, leukocyte morphometrics, and cytokine levels. Animals were killed 1 hour and 1, 3, and 6 days after thrombus induction. Our findings demonstrated an early (day 1) neutrophil infiltration into the vein wall followed by a later (days 3 and 6) monocyte/macrophage and lymphocyte response. Cytokines were elevated only under conditions of venous thrombosis. Levels of epithelial neutrophil activating protein-78 (ENA-78), tumor necrosis factor-alpha (TNF), interleukin-6, and JE/monocyte chemoattractant protein-1 (JE/MCP-1) increased over the 6-day period, while macrophage inflammatory protein-1 alpha (MIP-1 alpha) peaked at day 3 after thrombus induction. Additionally, rats were passively immunized with neutralizing antibodies to TNF, ENA-78, MIP-1 alpha, JE/MCP-1, intercellular adhesion molecule-1 (ICAM-1), and CD18 compared with control antibodies. The most effective antibody early after thrombus induction for attenuating vein wall neutrophil extravasation was anti-TNF (P < .01). The monocyte/macrophage extravasation was inhibited most by anti-ICAM-1 followed by anti-TNF (P < .01). These findings demonstrate that venous thrombosis is associated with significant vein wall inflammation that is partially inhibited by neutralizing antibodies to cytokines and adhesion molecules.

Animals↗
PubMed2000

Factor V antigen levels and venous thrombosis: risk profile, interaction with factor V leiden, and relation with factor VIII antigen levels.

Clotting factor V has a dual function in coagulation: after activation, procoagulant factor V stimulates the formation of thrombin, whereas anticoagulant factor V acts as a cofactor for activated protein C (APC) in the degradation of factor VIII/VIIIa, thereby reducing thrombin formation. In the present study, we evaluated whether plasma factor V levels, either decreased or increased, are associated with venous thrombosis. High procoagulant factor V levels may enhance prothrombinase activity and increase the thrombosis risk. Low anticoagulant factor V levels could reduce APC-cofactor activity in the factor VIII inactivation (APC-resistant phenotype), which might also promote thrombosis. Low factor V levels in combination with factor V Leiden could lead to a more severe APC-resistant phenotype (pseudohomozygous APC resistance). To address these issues, we have measured factor V antigen (factor V:Ag) levels in 474 patients with thrombosis and 474 control subjects that were part of the Leiden Thrombophilia Study (LETS). Factor V:Ag levels increased by 7.6 U/dL for every successive 10 years of age. Mean factor V:Ag levels were 134 (range 41 to 305) U/dL in patients and 132 (range 47 to 302) U/dL in controls. Neither high nor low factor V:Ag levels were associated with venous thrombosis. We found that factor V:Ag and factor VIII antigen levels in plasma were correlated, but factor V did not modify the thrombotic risk of high factor VIII levels. The normalized APC ratio was not influenced by the factor V:Ag level in subjects with or without factor V Leiden. We conclude that neither low nor high factor V:Ag levels are associated with venous thrombosis and that factor V:Ag levels do not mediate the thrombotic risk associated with high factor VIII levels.

Adolescent↗
PubMed2004

In vivo magnetic resonance imaging of coronary thrombosis using a fibrin-binding molecular magnetic resonance contrast agent.

BACKGROUND: The advent of fibrin-binding molecular magnetic resonance (MR) contrast agents and advances in coronary MRI techniques offers the potential for direct imaging of coronary thrombosis. We tested the feasibility of this approach using a gadolinium (Gd)-based fibrin-binding contrast agent, EP-2104R (EPIX Medical Inc), in a swine model of coronary thrombus and in-stent thrombosis. METHODS AND RESULTS: Ex vivo and in vivo sensitivity of coronary MR thrombus imaging was tested by use of intracoronarily delivered Gd-DTPA-labeled fibrinogen thrombi (n=6). After successful demonstration, in-stent coronary thrombosis was induced by x-ray-guided placement of thrombogenic-coated, MR-lucent stents (n=5). After stent placement, 60 micromol of EP-2104R was injected via the left main coronary artery. Free-breathing, navigator-gated 3D coronary MR angiography and thrombus imaging were performed (1) before and after stent placement and (2) before and after EP-2104R. Thrombi were confirmed by x-ray angiography and autopsy. Fibrinogen thrombi: 5 of 6 intracoronarily delivered Gd-labeled fibrinogen clots (approximately 250 micromol/L Gd) were visible on MRI and subsequently confirmed by x-ray angiography. In-stent thrombi: in-stent thrombosis was observed in all stents after EP-2104R. Four of 5 thrombi were confirmed by x-ray angiography. Chemical analysis of 2 thrombi demonstrated 99 to 147 micromol/L Gd. CONCLUSIONS: We demonstrate the feasibility of MRI of coronary thrombus and in-stent thrombosis using a novel fibrin-binding molecular MR contrast agent. Potential applications include detection of coronary in-stent thrombosis or thrombus burden in patients with acute coronary syndromes.

Animals↗
PubMed1994

Arrhythmogenic influence of intracoronary thrombosis during acute myocardial ischemia.

BACKGROUND: Patients with acute coronary artery thrombosis often develop primary malignant ventricular arrhythmias (MVA) early after coronary occlusion. In contrast, acute ischemia induced by nonthrombotic balloon occlusion during routine coronary angioplasty rarely elicits such arrhythmias. This study was designed to assess the role of intracoronary thrombosis in arrhythmogenesis during acute ischemia. METHODS AND RESULTS: We compared the incidence of MVA associated with acute left anterior descending coronary artery (LAD) thrombosis elicited in open-chest anesthetized dogs by electrical injury (n = 10) or intracoronary stent (n = 9) versus LAD balloon occlusion (n = 15). Compared with animals subjected to balloon occlusion, those with thrombotic occlusion had a significantly greater incidence of MVA, defined as nonsustained ventricular tachycardia (total duration > 10 seconds), sustained ventricular tachycardia, or ventricular fibrillation developing within the first 30 minutes of occlusion. In the combined thrombosis groups, MVA developed in 11 of 19 animals (58%) (6 of 10 dogs with electrical injury and 5 of 9 stent animals). In contrast, MVA occurred in only 1 of 15 animals (7%) subjected to balloon occlusion. This striking and significant difference in arrhythmias occurred despite the fact that radioactive microsphere perfusion analysis documented that the extent of left ventricular myocardium rendered ischemic was equal in all groups (percent of left ventricular myocardium with occlusion flow < or = 50% of baseline: electrical injury, 25.2 +/- 5.3%; stent, 27.1 +/- 3.6%; balloon, 34.3 +/- 11.6%; P = NS). Furthermore, there were no differences between the animals with thrombosis or balloon occlusion with respect to changes in echocardiographic parameters of left ventricular function, aortic pressure, or heart rate after occlusion. CONCLUSIONS: These data provide evidence that despite equal magnitudes of jeopardized myocardial mass, acute ischemia induced by thrombotic coronary occlusion results in a greater incidence of MVA than does nonthrombotic balloon occlusion. These findings suggest that the process of intracoronary thrombosis itself exerts arrhythmogenic effects above and beyond the impact of ischemia on myocardium induced by coronary occlusion.

Acute Disease↗
PubMed1996

Coronary plaque erosion without rupture into a lipid core. A frequent cause of coronary thrombosis in sudden coronary death.

BACKGROUND: Coronary thrombosis has been reported to occur most frequently in lipid-rich plaques with rupture of a thin fibrous cap and contact of the thrombus with a pool of extracellular lipid. However, the frequency of coronary artery thrombosis with or without fibrous cap rupture in sudden coronary death is unknown. In this study, we compared the incidence and morphological characteristics of coronary thrombosis associated with plaque rupture versus thrombosis in eroded plaques without rupture. METHODS AND RESULTS: Fifty consecutive cases of sudden death due to coronary artery thrombosis were studied by histology and immunohistochemistry. Plaque rupture of a fibrous cap with communication of the thrombus with a lipid pool was identified in 28 cases. Thrombi without rupture were present in 22 cases, all of which had superficial erosion of a proteoglycan-rich plaque. The mean age at death was 53 +/- 10 years in plaque rupture cases versus 44 +/- 7 years in eroded plaques without rupture (P < .02). In the plaque-rupture group, 5 of 28 (18%) were women versus 11 of 22 (50%) with eroded plaques (P = .03). The mean percent luminal area stenosis was 78 +/- 12% in plaque rupture and 70 +/- 11% in superficial erosion (P < .03). Plaque calcification was present in 69% of ruptures versus 23% of erosions (P < .002). In plaque ruptures, the fibrous cap was infiltrated by macrophages in 100% and T cells in 75% of cases compared with 50% (P < .0001) and 32% (P < .004), respectively, in superficial erosions. Clusters of smooth muscle cells adjacent to the thrombi were present in 95% of erosions versus 33% of ruptures (P < .0001). HLA-DR expression was more often seen in macrophages and T cells in ruptures (25 of 28 cases) compared with expression in macrophages in superficial erosion arteries (8 of 22 cases, P = .0002). CONCLUSIONS: Erosion of proteoglycan-rich and smooth muscle cell-rich plaques lacking a superficial lipid core or plaque rupture is a frequent finding in sudden death due to coronary thrombosis, comprising 44% of cases in the present study. These lesions are more often seen in younger individuals and women, have less luminal narrowing and less calcification, and less often have foci of macrophages and T cells compared with plaque ruptures.

Adult↗
PubMedDate not supplied

Prevention of early restenosis and thrombosis-occlusion after carotid endarterectomy by saphenous vein patch angioplasty.

The hypothesis that saphenous vein patch angioplasty protects against early postoperative restenosis and thrombosis-occlusion was tested by comparing the clinical outcome and carotid artery status of 100 carotid endarterectomies with and 100 without saphenous vein patch angioplasty performed by a single surgeon over a 30-month period. The patient population, selection, perioperative management, and the technical aspects of the operation, except for the vein patch, were essentially identical in both groups. Carotid artery status was assessed by direct continuous wave Doppler and Gee OPG at three to six months and again at one year postoperatively. There were two hospital deaths, both in the nonpatched group, one cardiac and the other neurologic due to internal carotid thrombosis. Two reversible neurological deficits due to thrombosis and one due to restenosis occurred in the non-patched group. Asymptomatic greater than 50% diameter restenosis occurred in four and asymptomatic occlusion in one non-patched carotids. There were no restenosis, no occlusions and no neurologic symptoms in the patched group. Morbidity, mortality, restenosis or thrombosis-occlusion occurred in 10/100 (10%) non-patched and 0/100 (0%) patched arteries (p less than 0.01 by Chi Square). Restenosis or thrombosis-occlusion occurred in 9/100 (9%) of non-patched and 0/100 (0%) patched arteries (p less than 0.01). These results support the use of saphenous vein patch angioplasty reconstruction of carotid endarterectomy to protect against early restenosis and thrombosis-occlusion.

Aged↗
PubMed1990

Cerebral venous thrombosis in systemic lupus erythematosus.

We describe six cases of cerebral venous thrombosis in patients with systemic lupus erythematosus. In one patient, cerebral venous thrombosis was the initial manifestation of lupus; in the five others, it occurred 1-33 years after the diagnosis of lupus. The main clinical features of cerebral venous thrombosis were persistent headache in all six patients, focal symptoms in four, and seizures in three; papilledema was present in only one patient. Cerebral venous thrombosis was diagnosed based on angiography or magnetic resonance imaging. Both the transverse (in five patients) and the superior sagittal (in three) sinuses were involved. Extracranial arterial and/or venous thrombosis were present in three patients, abortion in two, thrombocytopenia in four, and lupus anticoagulant in three. The neurologic symptoms resolved rapidly in five patients treated with steroids and heparin. Cerebral venous thrombosis should be suspected in patients with lupus who complain of persistent headache, especially in the presence of neurologic symptoms.

Adult↗
PubMed1994

Venous sinus thrombosis associated with androgens in a healthy young man.

BACKGROUND: Cerebral venous sinus thrombosis is rare and can be promoted by various conditions. We report the case of cerebral venous thrombosis in a patient using androgens. CASE DESCRIPTION: A 31-year-old man using androgens for bodybuilding was admitted for headache and vomiting. He had cerebral venous sinus thrombosis, but extensive examinations did not reveal any known cause. CONCLUSIONS: We suggest that androgens may promote cerebral venous thrombosis. The mechanisms of venous thrombosis related to androgens may be platelet activation or an increase in coagulation factors. Because androgen use may be frequent and hidden in athletes, it may be an underestimated cause of cerebral venous sinus thrombosis in the young.

Adult↗
PubMed2000

Risk factors for peripartum and postpartum stroke and intracranial venous thrombosis.

BACKGROUND AND PURPOSE: The study goal was to identify potential risk factors for peripartum or postpartum stroke and intracranial venous thrombosis. METHODS: Data from the Healthcare Cost and Utilization Project were analyzed for the years 1993 and 1994. Observed values were weighted with poststratification discharge weights to project to the universe of all discharges from community hospitals located in the United States. Nationally representative estimates of risk were calculated on the basis of age, race, mode of delivery, income, third-party payer, hospital size, hospital ownership, hospital location (rural versus urban), hospital teaching status, census region, and presence of specific complications. Multivariate models were developed with the use of logistic regression. RESULTS: Among 1 408 015 sampled deliveries, there were 183 observed cases of peripartum stroke and 170 cases of peripartum intracranial venous thrombosis in 17 states in the United States in 1993 and 1994. There were an estimated 975 cases of stroke and 864 cases of intracranial venous thrombosis during pregnancy and the puerperium in the United States among 7 463 712 deliveries during 1993 and 1994, for estimated risks of 13.1 cases of peripartum stroke and 11.6 cases of peripartum intracranial venous thrombosis per 100 000 deliveries. Multivariate analysis showed that the following were strongly and significantly associated with both peripartum and postpartum stroke: cesarean delivery; fluid, electrolyte, and acid-base disorders; and hypertension. Covariates that were strongly and significantly associated with both peripartum and postpartum intracranial venous thrombosis included cesarean delivery, hypertension, and infections other than pneumonia and influenza. CONCLUSIONS: Pregnancy-related hypertension and cesarean delivery are important risk factors for both stroke or intracranial venous thrombosis.

Acid-Base Imbalance↗
PubMed1998

Homocysteine associated hypercoagulability and disseminated thrombosis--a case report.

The authors report the occurrence of vascular occlusion due to hyperhomocysteinemia without significant underlying atherosclerotic disease. This unique observation supports the potential of hyperhomocysteinemia to induce thrombosis and the independence of the thrombosis from hyperhomocysteinemia's associated atherosclerosis. The case demonstrates the clinical relevance of the effects of hyperhomocysteinemia on the coagulation cascade. A 42-year-old woman who lacked signs of classic homocystinuria developed disseminated thrombosis with a 24-hour urine homocysteine concentration of 384 mg, twelve times the upper limit of normal. Thrombosis was present in the aortic arch and its major branches and in the mesenteric arteries and veins. A fatal stroke resulted from the thrombosis. Autopsy revealed minimal atherosclerotic disease and no complicated plaques. This case demonstrates an expanded role of hyperhomocysteinemia in clinically significant vascular occlusion. Serum homocysteine concentration determination may be a factor in the evaluation of a hypercoagulable state. Hyperhomocysteinemia should be considered when evaluating arterial or venous thrombosis in a young person regardless of whether atherosclerosis or other signs of abnormal homocysteine metabolism are present.

Adult↗
PubMed1998

Patients with a malignant tumor have more extended thrombosis than patients without.

Changes in the coagulability or rheology of the blood are supposed to cause an increased frequency of thrombosis in patients with a malignant tumor. These procoagulopathic disorders may not only increase the frequency of thrombosis but may also enlarge the extent of the thrombosis. The authors retrospectively analyzed, therefore, the extension of thrombosis in patients with and without a malignant tumor. From 1991 to 1995 in the University Hospital Essen 489 consecutive cases of thrombosis were diagnosed. The diagnosis was made by color Doppler sonography or phlebography; 230 patients (47%) suffered from a malignant tumor (110 men, 120 women). To exclude the influence of the patient's age on the extension of the thrombosis the authors distinguished three different age groups. In the tumor group aged from 21 to 40 years they found 10 large (iliacal, femoral, and crural veins), six medium (femoral and crural veins), and four small thromboses (crural veins). In the tumor group aged from 41 to 60 years they found 38 large, 24 medium, and 27 small thromboses. In the group without a tumor aged from 21 to 40 years they found seven large, 13 medium, and 28 small thromboses, and in the group aged from 41 to 60 years, 12 large, 29 medium, and 41 small thromboses. The difference between the two groups supports the assumption that in patients suffering from a malignant tumor, thromboses tend to be more extended than in patients without a malignant tumor.

Adult↗