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PubMed2002

Prevention of experimental carotid and coronary artery thrombosis by the glycoprotein IIb/IIIa receptor antagonist CRL42796.

1. The antithrombotic effect of the glycoprotein IIb/IIIa receptor antagonist, CRL42796, was examined in canine models of carotid and coronary artery thrombosis. 2. In the carotid artery thrombosis model, occlusion occurred in all control vessels (time to thrombosis 47.6+/-8.9 min). After treatment with low dose CRL42796 (15 microg kg(-1) loading dose +0.31 microg kg(-1) min(-1) i.v.), two of five vessels occluded. Time to thrombosis increased significantly to 155.2+/-23.1 min. When the drug infusion was increased (0.69 microg kg(-1) min(-1)), each of five vessels remained patent. 3. Ex vivo platelet aggregation in response to arachidonic acid (AA) and ADP was examined in platelet rich plasma (PRP) prepared from citrate or heparin anticoagulated blood. CRL42796 reduced platelet reactivity at low and high doses in PRP from citrate anticoagulated blood. However, in PRP from heparin anticoagulated blood, only the higher infusion dose produced a significant reduction in ex vivo platelet responses. 4. A combination of oral aspirin (4.6 mg kg(-1) -41, -17 h) and the low infusion dose of CRL42796 did not produce an additional benefit beyond that provided by CRL42796 alone. 5. Coronary artery thrombosis was inhibited in four of five vessels treated with the lower infusion dose of CRL42796 and in five of five vessels treated with the higher infusion. Time to thrombosis increased with both doses (Control, 90.8+/-10.4 min; low dose, 165.8+/-14.2 min; high dose, >180.0+/-0 min). 6. The results indicate that CRL42796 is an effective in vivo antithrombotic agent against experimentally-induced carotid and coronary artery thrombosis.

Animals↗

PubMed1998

Oral contraceptives and hormone replacement therapy do not increase the incidence of arterial thrombosis in a nonhuman primate model.

Older oral contraceptive (OC) formulations containing high doses of potent synthetic estrogens and progestins are associated with increased risk of thrombosis. To examine the effects of current low-dose OC and hormone replacement therapy (HRT) regimens on arterial thrombosis, premenopausal and surgically postmenopausal cynomolgus monkeys were divided into four treatment groups. Premenopausal monkeys were given either no OCs or ethinyl estradiol and levonorgestrel as an OC at a dose equivalent to that currently given to women. Postmenopausal monkeys were given either no HRT or conjugated equine estrogens and medroxyprogesterone as an HRT at a dose equivalent to that currently given to women. The monkeys were fed an atherogenic diet containing these treatments for 27 to 30 months. At the end of this time, arterial thrombosis was evaluated with a standardized stenosis/injury procedure in the left carotid artery. Blood flow velocity was monitored for cyclic or permanent occlusive thrombosis. The current OC and HRT regimens did not increase the susceptibility of the artery wall to develop an occlusive thrombus following injury and stenosis. In fact, there was a reduction in the incidence of thrombosis in the OC animals compared with untreated controls. Increased amounts of atherosclerosis were associated with an increased incidence of occlusive arterial thrombosis. Several selected coagulation parameters [von Willebrand factor, protein C, lipoprotein(a), and platelet aggregation] did not appear to be associated with either the amount of atherosclerosis or incidence of arterial thrombosis.

Animals↗

PubMed2001

Variable protection of beta 3-integrin--deficient mice from thrombosis initiated by different mechanisms.

Platelet integrin alpha IIb beta 3 (GPIIb/IIIa) plays a central role in the initiation of arterial thrombosis, but its contribution to disseminated microvascular thrombosis is less well defined. Therefore, wild-type mice (beta 3(+/+)), beta 3-integrin-deficient mice (beta 3(-/-)), and wild-type mice treated with a hamster monoclonal antibody (1B5) that blocks murine alpha IIb beta 3 function were tested in models of large-vessel and microvascular thrombosis. In the large-vessel model, ferric chloride was used to injure the carotid artery, and the time to thrombosis was measured. In beta 3(+/+) mice, the median time to occlusion was 6.7 minutes, whereas occlusion did not occur in any of the beta 3(-/-) mice tested (P <.001). Fab and F(ab')(2) fragments of 1B5 increased the median time to occlusion. To initiate systemic intravascular thrombosis, prothrombotic agents were administered intravenously, and platelet thrombus formation was monitored by the decrease in circulating platelet count. Three minutes after the injection of adenosine diphosphate (ADP), collagen + epinephrine, or tissue factor, the platelet counts in beta 3(+/+) mice decreased by 289, 424, and 429 x 10(3)/microL, respectively. beta 3(-/-) mice and wild-type mice pretreated with 1B5 Fab (1 mg/kg, IP) were nearly completely protected from the effects of ADP. In contrast, beta 3(-/-) mice were only partially protected from the effects of collagen + epinephrine and minimally protected from the effects of tissue factor. In all cases, less fibrin became deposited in the lungs of beta 3(-/-) mice than in wild-type mice. These results suggest that though alpha IIb beta 3 plays a dominant role in large-vessel thrombosis, it plays a variable role in systemic intravascular thrombosis. (Blood. 2001;98:1055-1062)

Animals↗

PubMed2001

Neonatal aortic arch thrombosis as a result of congenital cytomegalovirus infection.

Thrombotic disease is rare in neonates. The main risk factors at this age are perinatal asphyxia, maternal diabetes, sepsis, polycythemia, dehydration, a low cardiac output, and in primis the catheterization of central lines. Another important risk factor is inherited thrombophilia. Arterial thrombosis is even more rare than venous thrombosis and less related to most of the risk factors listed above; it occurs more frequently in the iliac, femoral, and cerebral arteries but very rarely in the aorta. Most of the described cases of aortic thrombosis are associated with the catheterization of an umbilical artery and involve the descending tract and the renal arteries; very few relate to the ascending tract and the aortic arch. The possible role of virus-induced primary vascular endothelium damage in the etiopathogenesis of neonatal arterial thrombosis has been previously hypothesized. Herpesviruses, particularly human cytomegalovirus (HCMV), can infect endothelial cells and directly damage intact vascular endothelium, altering its thromboresistant surface as a result of procoagulant activity mediated by specific viral surface phospholipids, necessary for the coagulation enzyme complex assembly that leads to thrombin generation. We describe a case of congenital aortic arch thrombosis. The clinical, laboratory, and virologic pictures; the anatomopathologic findings (fully compatible with viral infection); the detection of HCMV in various tissues (including the aorta); and the absence of other causes of aortic thrombosis make it possible to attribute the case to a severe congenital HCMV infection with multiple organ involvement, after the primary infection of the mother. The hemostatic system disorders and hemodynamic disturbances related to viral cardiac damage explain the clinical features of the case and indicate that congenital HCMV infection should be included among the causes of neonatal aortic thrombosis.

Aorta, Thoracic↗

PubMed2003

Trend to efficacy and safety using antithrombin concentrate in prevention of thrombosis in children receiving l-asparaginase for acute lymphoblastic leukemia. Results of the PAARKA study.

An association has been reported between thrombotic events and the use of L-asparaginase (ASP) in children with acute lymphoblastic leukaemia (ALL). The mechanism for thrombosis is likely related to an acquired antithrombin deficiency. Since a primary prophylaxis using antithrombin concentrates may prevent thrombosis, the PARKAA (Prophylactic Antithrombin replacement in kids with ALL treated with L-asparaginase) study was performed. The objectives of PARKAA were to determine if there was a trend to efficacy and safety of antithrombin treatment as assessed by 1) incidence of thrombosis 2) incidence of bleeding and 3) plasma markers of endogenous thrombin generation as surrogate outcomes for thrombosis. The study was not powered to answer the question of efficacy and safety, but rather to detect a trend. PARKAA was an open, randomised, controlled study in children with ALL being treated with ASP. Children were randomised to receive antithrombin infusions or no antithrombin treatment. All thrombotic events were confirmed using bilateral venography, ultrasound, echocardiography and MRI. The incidence of thrombosis in patients treated with antithrombin was 28% (95% CI 10-46%), compared to 37% (95% CI 24-49%) in the non treated arm. Two minor bleeds occurred in patients in the treated arm, but were not considered to be related to antithrombin. No significant differences were seen in plasma markers by the treatment group. In conclusion, treatment with antithrombin concentrate shows a trend to efficacy and safety. In contrast, there was no difference in surrogate markers for thrombosis. Carefully designed clinical trials are needed to test the efficacy and safety of antithrombin in this population.

Adolescent↗

PubMed1988

Protein C deficiency. A cause of unusual or unexplained thrombosis.

Familial hypercoagulable states are a collection of syndromes characterized by an inherited deficiency of various proteins involved in the control of coagulation and include antithrombin III, plasminogen, protein C, and protein S. Affected patients usually develop venous thrombosis as adults. During a 15-month interval, we identified five patients with venous thrombosis accompanied by protein C deficiency. Four patients presented with deep venous thrombosis, which was recurrent in two, and one patient developed mesenteric venous thrombosis. The kindred of this last patient suggested an autosomal dominant genetic transmission of protein C deficiency. Patients' ages at the time of diagnosis of disease ranged from 28 to 41 years. All patients had low levels of protein C (range, 34 to 67 U/dL; normal, 70 to 130 U/dL). All patients were treated with heparin sodium immediately and then given long-term oral anticoagulation therapy with warfarin sodium. Protein C deficiency is a predisposing factor to the development of venous thrombosis that has only recently been recognized. Treatment of symptomatic protein C deficiency requires short-term heparin therapy followed by long-term oral anticoagulation therapy with warfarin. Oral anticoagulation treatment must be initiated slowly with no loading dose to avoid warfarin-associated skin necrosis. Patients with unexplained or unusual thrombosis, especially if it occurs at an early age, and patients with recurrent episodes of lower limb venous thrombosis should have their protein C levels measured. If a deficiency is documented, long-term warfarin anticoagulation therapy is recommended.

Adult↗

PubMed1993

Acute thrombosis of the splanchnic veins.

The consequence of an acute thrombosis in the splanchnic veins on the viability of the intestine has not been well defined in the literature. Spontaneous recovery or total necrosis of the bowel have both been described. We treated seven patients with thrombosis of the splanchnic veins and adopted a surgical approach in three patients with extended and complete thrombosis of the superior mesenteric vein, portal vein, and splenic vein, while four patients with partial thrombosis of the superior mesenteric vein or protal vein recovered with conservative treatment. A 22-year literature review has identified 64 cases of acute thrombosis in the splanchnic veins, with complete information regarding the location and extent of the thrombosis, the treatment, and the outcome. Different anatomical patterns of thrombosis with mortality rates varying between 0% and 76% seem to be related to the extent and completeness of venous obstruction.

Acute Disease↗

PubMed1997

Predictors of arterial thrombosis after diagnostic cardiac catheterization in infants and children randomized to two heparin dosages.

Arterial thrombosis is the most frequent major complication of percutaneous arterial catheterization in children. We prospectively studied the effect of randomized dosage of heparin, 50 IU/kg-group I and 100 IU/kg-group II, on the incidence of arterial thrombosis in 366 children and analysed the various factors which may influence the occurrence of this complication. The age of patients ranged from 17 d to 11 yr (mean age 39.5 +/- 40.9 mo) and mean weight was 11.2 +/- 7.8 kg (range 3 to 39 kg). The incidence of arterial thrombosis was 9.8% in group I and 9.3% in group II (P = NS). There was no statistical difference in precatheterization and procedure variables in the two groups and also in the group with absent pulse (n = 35) to the group with pulse present post cath (n = 331). There were 24.9% infants in our study and 14.3% of these had arterial thrombosis. The loss of pulse was more often seen with more number of attempts at arterial puncture (P < 0.001), absence of back bleed at the end of the procedure (P < 0.001), and increased duration of catheterization (P < 0.01). Use of larger sheath size in a given weight and body surface area of children increased incidence of arterial thrombosis. The administration of heparin 50 IU/kg was equally efficacious to heparin 100 IU/kg. Of the patients with arterial thrombosis, 23 responded with intravenous heparin and 12 needed streptokinase. There was no bleeding or haematoma. Thus our study shows that less attempt for arterial puncture, use of smaller sheath size, maintaining shortest procedure time and ensuring back bleed minimises incidence of arterial thrombosis post catheterization.

Anticoagulants↗

PubMed1995

Lupus anticoagulant in children with thrombosis.

Nineteen children who presented with thromboses over a 7-year period were found to have a lupus anticoagulant (LA). The initial thrombosis was proximal deep vein thrombosis (DVT) in six children, central nervous system (CNS) in five, primary pulmonary in four, distal DVT in two, central venous in one, and proximal arterial in one. Five children were diagnosed with systemic lupus erythematosus (SLE), including two children for whom thrombosis was the presenting sign of SLE. The remaining 14 children were diagnosed with the antiphospholipid antibody (APA) syndrome. The APA syndrome was manifest by venous or arterial thrombosis in association with a positive LA; positive anticardiolipin antibodies and a fine, speckled antinuclear antibody (ANA) pattern were additionally found in the majority of children. Approximately one-half of the children with SLE or the APA syndrome had a pulmonary embolus, and one-half developed recurrent thrombosis. Oral anticoagulation with coumadin to achieve an INR of > 2.0 prevented thrombosis recurrence. The recognition of a LA in children with thrombosis necessitates evaluation for SLE, APA, and other autoantibodies.

Adolescent↗

PubMed1998

Donor factor V Leiden mutation and vascular thrombosis following liver transplantation.

The most commonly detected hypercoagulable state involves an abnormal factor V protein synthesized by the liver in which arginine at position 506 is replaced by glutamine as a result of a single-point mutation in the factor V gene (factor V Leiden). Liver transplantation is complicated by hepatic vascular thrombosis in up to 15% of cases, resulting in graft loss in most instances. This retrospective study examined the effect of the factor V Leiden mutation on the risk of hepatic vessel thrombosis after liver transplantation. The mutation was sought by polymerase chain reaction and Mnl I digestion of DNA where available from 214 recipients and 276 donors receiving 319 liver transplants. No donors or patients were homozygous for the factor V Leiden mutation. The prevalence of the heterozygous mutation was 19 of 276 (6.9%) in donors and 19 of 214 (8.9%) in recipients. Forty-one thrombotic episodes occurred after transplantation in the 276 transplants in which donor DNA was available for analysis; 22 involved the hepatic artery, 9 involved the portal vein, and 10 were deep venous thromboses. A donor factor V Leiden mutation was detected in the donor in 6 of 41 (14.6%) with any thrombotic event compared with 13 of 235 (5.5%) without (P = 0.03). The relative risk of any thrombosis with this mutation was therefore 2.32 (95% confidence interval [CI], 1.12-4.81). The factor V Leiden mutation was present in the donor in 4 of 31 (12.9%) cases complicated by hepatic vessel thrombosis (which always led to graft loss or death) and 15 of 245 (6.1%) cases without (P = 0.16). The relative risk of hepatic vessel thrombosis in the presence of this allele was therefore 2.00 (95% CI, 0.78-5.14). As anticipated, the presence of this allele in the recipient was not associated with deep venous or hepatic vessel thrombosis. The factor V Leiden mutation in the donor liver is not a major risk factor for hepatic vessel thrombosis and subsequent graft loss after liver transplantation.

Adolescent↗

PubMed2001

Intracatheter nitroglycerin infusion fails to prevent catheter-related venous thrombosis: a randomized, controlled trial.

OBJECTIVE: Catheter-related thrombosis is a common problem in the pediatric intensive care unit. Strategies that reduce the incidence of thrombosis may have significant clinical advantage. Nitroglycerin (NTG) infusions release nitric oxide (NO). NO is responsible for much of the vasodilating and antithrombotic properties of the vasculature. We hypothesized that an intracatheter NTG infusion would reduce the incidence of catheter-related thrombosis. DESIGN: Prospective, randomized, controlled trial. SETTING: Pediatric intensive care unit. PATIENTS AND PARTICIPANTS: Children of 6 years or less with femoral venous catheters who were not on antithrombotic therapy. INTERVENTIONS: Subjects were randomly assigned to NTG or control groups. NTG group patients received NTG at 0.1 mcg x kg x min in 5 % dextrose; control group patients received only 5 % dextrose. Infusions were delivered continuously through the catheter until the catheter was removed. Demographic data, physical and laboratory findings, catheter insertion attempts and infusate composition were recorded. Clinical evidence of vascular thrombosis or catheter malfunction was noted. Ultrasound examinations were performed within 2 days of catheter insertion and within 2 days after removal. MEASUREMENTS AND RESULTS: Forty-four patients (age 12.0 +/- 2.6 months) completed the study, 21 in the NTG group and 23 in the control group. Duration of catheter placement was 7.5 +/- 0.7 days. Twelve of 44 patients (27 %) had thrombi: 7/21 in the NTG group; 5/23 in the control group (p = NS). There were no significant differences between children with and without thrombi in age, gender, number of insertion attempts, duration of catheter placement, clinical signs of thrombosis or infections. CONCLUSIONS: Catheter-related thrombosis is common after placement of femoral venous catheters in children. Low dose intracatheter NTG infusion does not protect against catheter-related venous thrombosis in children.

Catheterization, Central Venous↗

PubMed2003

Thrombosis in children with cardiac pathology: frequency of factor V Leiden and prothrombin G20210A mutations.

This study analyzed 28 thrombotic children with various cardiac disorders. They comprise 17% of a total of 168 patients with thrombosis from a single center. Among the 28 patients, 21 had congenital heart disease and 7 were diagnosed with cardiomyopathy. The patients with thrombosis were evaluated for congenital and acquired thrombotic risk factors. In addition to cardiac disorders, two, three, or more risk factors were present in 61% of the children with thrombosis. Two common mutations, namely factor V Leiden and prothrombin G20210A mutations, were found in 6 patients (22%). Nine patients (32%) died of infection, congenital heart disease, cardiomyopathy, thrombosis, operation, or a combination of these; two patients required surgical intervention. Following cardiac angiography, due to necrosis, amputation of the right index finger and right lower extremity was performed on 1 patient. The second patient's index fingers had to be amputated and resection of the bowel was performed following the operation on coarctation of the aorta. This study indicates that congenital heart disease and cardiomyopathy are two common cardiac disorders that may lead to the development of thrombosis. The majority of thrombosis develops within the heart and/or its great vessels. The second predominant site for thromboembolic symptoms is in the brain, including sinovenous thrombosis.

Adolescent↗

PubMed2006

Unsuspected lower extremity deep venous thrombosis simulating musculoskeletal pathology.

OBJECTIVE: The purpose of this study was to highlight the critical role that MRI may play in diagnosing unsuspected lower extremity deep venous thrombosis and to stress the importance of scrutinizing MRI studies of the lower extremity showing apparently non-specific muscle edema for any evidence of intramuscular venous thrombosis. DESIGN AND PATIENTS: The imaging studies of four patients in whom deep venous thrombosis was unsuspected on clinical grounds, and first diagnosed on the basis of MRI findings, were reviewed by two musculoskeletal radiologists in consensus. In all four patients the initial clinical suspicion was within the scope of musculoskeletal injuries (gastrocnemius strain, n=3; ruptured Baker cyst, n=1), explaining the choice of MRI over ultrasound as the first diagnostic modality. RESULTS: All patients showed marked reactive edema in the surrounding soft tissues or muscles. Three patients showed MR evidence of branching rim-enhancing structures within intramuscular plexuses characteristic of venous thrombosis (gastrocnemius, n=1; sural, n=2); one patient showed a distended popliteal vein. Ultrasound was able to duplicate the MRI findings in three patients: one patient showed above-the-knee extension on ultrasound; neither of the two patients with intramuscular thrombosis demonstrated on ultrasound showed extension to the deep venous trunks. CONCLUSION: Intramuscular venous thrombosis can present as marked edema-like muscle changes on MRI, simulating primary musculoskeletal conditions. In the absence of clinical suspicion for deep venous thrombosis, only the identification of rim-enhancing branching intramuscular tubular structures will allow the correct diagnosis to be made.

Diagnosis, Differential↗

PubMedDate not supplied

Diagnosis of benign and malignant portal vein thrombosis in cirrhotic patients with hepatocellular carcinoma: color Doppler US, contrast-enhanced US, and fine-needle biopsy.

BACKGROUND: We assessed the role of contrast-enhanced ultrasound (CEUS) in the differential diagnosis between benign and malignant portal vein thrombosis in patients who had cirrhosis with hepatocellular carcinoma (HCC). METHODS: Fifty-four consecutive patients who had cirrhosis, biopsy-proved HCC, and thrombosis of the main portal vein and/or left/right portal vein on US were prospectively studied with color Doppler US (CDUS) and CEUS. CEUS was performed at low mechanical index after intravenous administration of a second-generation contrast agent (SonoVue, Bracco, Milan, Italy). Presence or absence of CDUS signals or thrombus enhancement on CEUS were considered diagnostic for malignant or benign portal vein thrombosis. Twenty-eight patients also underwent percutaneous portal vein fine-needle biopsy (FNB) under US guidance. All patients were followed-up bimonthly by CDUS. Shrinkage of the thrombus and/or recanalization of the vessels on CDUS during follow-up were considered definitive evidence of the benign nature of the thrombosis, whereas enlargement of the thrombus, disruption of the vessel wall, and parenchymal infiltration over follow-up were considered consistent with malignancy. CDUS, CEUS, and FNB results were compared with those at follow-up. RESULTS: Follow-up (4 to 21 months) showed signs of malignant thrombosis in 34 of 54 patients. FNB produced a true-positive result for malignancy in 19 of 25 patients, a false-negative result in six of 25 patients, and a true-negative result in three of three patients. CDUS was positive in seven of 54 patients. CEUS showed enhancement of the thrombus in 30 of 54 patients. No false-positive result was observed at CDUS, CEUS, and FNB. Sensitivities of CDUS, CEUS, and FNB in detecting malignant thrombi were 20%, 88%, and 76% respectively. Three patients showed negative CDUS and CEUS and positive FNB results; follow-up confirmed malignant thrombosis in these patients. One patient showed negative CDUS, CEUS, and FNB findings. However, follow-up of the thrombus showed US signs of malignancy. Another FNB confirmed HCC infiltration of the portal vein. CONCLUSION: CEUS seems to be the most sensitive and specific test for diagnosing malignant portal vein thrombosis in patients with cirrhosis.

Aged↗

PubMed2006

Risk factors contributing to hepatic artery thrombosis following living-donor liver transplantation.

BACKGROUND/PURPOSE: This study was carried out to investigate the risk factors contributing to hepatic artery thrombosis in living-donor liver transplantation. METHODS: Two hundred and twenty-two recipients (113 adults and 109 children) of living-donor liver transplantation were the subjects of this study. The diagnosis of hepatic artery thrombosis was made by color-Doppler ultrasonography and/or hepatic angiography. Parameters for this study were: (1) donor sex, age, and body weight; (2) recipient sex, age, body weight, liver disease, preoperative prothrombin time, and type of arterial reconstruction; and (3) previous liver transplantation. RESULTS: Hepatic artery thrombosis occurred in 12 patients (5.4%) at 3 to 15 days posttransplant. Recipient female sex and metabolic disorder as the original disease were found to be significantly associated with hepatic artery thrombosis. The 5-year patient survival rate in recipients with hepatic artery thrombosis (58.3%) was significantly lower than that in recipients without this complication (84.4%). CONCLUSIONS: Female sex and metabolic disease may be factors contributing to hepatic artery thrombosis after living-donor liver transplantation. More intensive anticoagulation therapy for this patient population might decrease the incidence of hepatic artery thrombosis and, thus, posttransplant recipient mortality.

Adolescent↗

PubMed2026

Association of the PROC rs146922325 variant with venous thrombosis in a Taiwanese population.

BACKGROUND: Hereditary protein C deficiency, caused by pathogenic variants in the PROC gene, is a known risk factor for venous thrombosis. However, data on PROC variants in Asian populations are limited. This study evaluated the clinical relevance of rs146922325 and its association with thrombotic outcomes in Taiwanese patients. METHODS: Using genotyping data from a single-nucleotide polymorphism array as part of the Taiwan Precision Medicine Initiative, we conducted a retrospective case-control study that included 805 carriers of the PROC rs146922325 variant and 8,050 age- and sex-matched non-carriers. The baseline characteristics, coagulation profiles, and thrombotic outcomes were systematically compared. Univariable and multivariable logistic regression analyses were performed to assess the association between rs146922325 and venous thrombosis. Sensitivity analyses were conducted by restricting the cohort to warfarin-naïve participants and incident venous thrombosis events occurring after genotyping. RESULTS: Carriers of the rs146922325 T allele exhibited significantly lower protein C levels than non-carriers (71.28% vs. 114.58%, p < 0.001) and a higher prevalence of venous thrombosis (4.10% vs. 2.48%; p = 0.009). After multivariable adjustment, rs146922325 carrier status remained independently associated with an increased risk of venous thrombosis (adjusted odds ratio [aOR], 1.61; p = 0.015). Allelic analysis further indicated that the T allele was associated with elevated thrombotic risk (aOR, 1.74; p = 0.004). No clear dose-response pattern was observed because of the limited number of homozygous TT individuals. Sex-stratified analyses suggested a similar association across sexes; however, the sex × genotype interaction was not statistically significant. CONCLUSION: The PROC rs146922325 variant was associated with an increased risk of venous thrombosis in the Taiwanese population. These findings expand the current knowledge of PROC-related thrombophilia in East Asians and support the potential value of genetic risk stratification in thrombosis research.

PROC rs146922325↗

PubMed1983

Natural history of ascending thrombosis of the abdominal aorta.

During 1980, 30 patients underwent successful operations for ascending thrombosis of the abdominal aorta in its three forms: low (below the inferior mesenteric artery, 11 patients); middle (above the inferior mesenteric artery, 6 patients); and high (at the level of the renal arteries, 13 patients). An angiogram that reveals high ascending thrombosis of the abdominal aorta is paradoxically more favorable than one that reveals middle or low ascending thrombosis of the abdominal aorta. In fact, the patient with a juxtarenal thrombosis has already overcome two of the three phases that constitute the critical moments of potential failure of the collateral circulation. Progressive ascending thrombosis with a poor prognosis and a rapidly downward course can cause acute ischemia with paraplegia of the legs and intestinal infarction. Most patients die suddenly in the emergency or intensive care unit from paraplegia, acute abdomen, or anuria; the latter is due to further progressive thrombosis with obstruction of the orifice of the renal arteries. On the basis of the angiogram only (apart from subjective symptoms), ascending thrombosis of the abdominal aorta constitutes an absolute indication for surgical treatment.

Adult↗

PubMed1985

Incidence of portal vein thrombosis in liver cirrhosis. An angiographic study in 708 patients.

Portal vein thrombosis was thought to be a common complication of liver cirrhosis in the past. The incidence of angiographically demonstrable portal vein thrombosis was studied in 708 consecutive patients with unequivocal cirrhosis seen in the past 10 yr in whom either transhepatic portography or superior mesenteric arterial portography clearly delineated the major portal vein system. Excluding 2 cases that were thought to be associated with past splenectomy, there were 4 cases of portal vein thrombosis related to cirrhosis, all in a decompensated stage. The calculated incidence of portal vein thrombosis was 0.573% of all cirrhotic patients without splenectomy in the past. They constituted 23.5% of the 17 cases of extrahepatic portal vein obstruction encountered during the same period. There were 78 cases of idiopathic portal hypertension similarly studied angiographically, and the incidence of portal vein thrombosis unrelated to splenectomy was 2.86%. A statistical survey based on 247,728 necropsies recorded in the Japan Autopsy Registries of 1975-1982 showed a 0.05489% incidence of portal vein thrombosis and a 6.58857% incidence of cirrhosis of all types among them, suggesting that portal vein thrombosis is not a common complication of cirrhosis in Japan in recent years.

Adult↗