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At least 1,243 records · Page 69Linked to original sources
PubMed2000

Acute arterial thrombosis with antithrombin III deficiency in nephrotic syndrome: report of a case.

Nephrotic syndrome frequently causes venous thromboembolic complications. Arterial thrombosis has rarely been reported and is mainly observed in children. Only six cases of lower extremity arterial thrombosis in adults have been reported in the literature. The outcome in these cases was unsatisfactory because of the high rates of limb loss and recurrence of thrombosis. We report successful treatment of a 39-year-old man who suffered from right lower extremity arterial thrombosis associated with decreased levels of serum antithrombin III. He was admitted to our hospital with severe pain in his right foot. No pulse was palpable in his right dorsalis pedis or posterior tibial arteries. His right foot was cold and mottled, with a reduced sensation and motor activity. The laboratory data revealed a serum total protein concentration of 3.9g/dl and an albumin concentration of 1.5 g/dl. The coagulation profile showed a fibrinogen level of 879 mg/dl and antithrombin III value of 9.5%. Right lower extremity arteriography showed a complete occlusion of the right deep femoral artery and popliteal artery, and a filling defect in the common femoral artery. An emergency thrombectomy was performed under general anesthesia. The patient was treated successfully, and surgical treatment was followed by anticoagulant therapy with 1,000 units of antithrombin III. A renal biopsy revealed histologic evidence of minimal change of glomerulonephritis. He was discharged 3 months later, and no recurrence of thrombosis has yet been observed.

Acute Disease↗
PubMed2001

Primary subclavian venous thrombosis which developed after sleeping with the arm in an outstretched position: report of a case.

Primary subclavian venous thrombosis is more rare than secondary thrombosis. This type of thrombosis is called "effort thrombosis" or Paget-Schroetter syndrome, and develops after a strenuous effort of the superior limb. A day after a 55-year-old man got drunk and slept in the left lateral position in combination with an abducted and elevated position of the left superior limb, he became aware of swelling and an oppressive feeling in his left superior limb and was admitted 9 days later. Thrombus of the left axillary-subclavian vein was confirmed by venography, and thrombolytic therapy with urokinase was performed immediately. The left arm symptoms improved for the most part. Venography after the therapy revealed thrombolysis at the site of the axillary vein, while the subclavian vein enhanced the collateral vessel pathway. The patient was discharged on the seventh hospital day, and anticoagulant therapy with oral warfarin sodium has since been continued. This is considered to be a rare case of subclavian venous thrombosis caused by sleeping in an abnormal position with the arm outstretched.

Alcoholic Intoxication↗
PubMed2004

Acute appendicitis-like symptoms as initial presentation of ovarian vein thrombosis.

Postpartum ovarian vein thrombosis is a rare condition, with an incidence rate being 1/600 deliveries. It most often arises in the right ovarian vein. A 33-year-old patient who had had normal vaginal delivery presented with fever, pain in the right iliac fossa, and leukocytosis on the sixth day after delivery. An antibiotic course was instituted but 3 days later symptoms reappeared. Diagnosis of acute appendicitis was made. At surgery through a McBurney incision, a woody tumoration consistent with ovarian vein thrombosis was found. Anticoagulation therapy with heparin and antibiotics were instituted. Phlebography and color Doppler sonography confirmed the presence of thrombosis of both the common femoral iliac and inferior vena cava. Fribrolysis with urokinase was performed. The patient has remained stable and symptom-free over a 4-year follow-up. Ovarian vein thrombosis typically presents with symptoms suggestive of acute appendicitis, as was the case in our patient. Color Doppler sonography is the favored diagnostic procedure, with CT being a supplementary tool. Surgery is not necessary and treatment consists of anticoagulants and antibiotics. Even though postpartum ovarian vein thrombosis is rare, early recognition of the condition is of paramount importance to institute the adequate treatment and avoid potential serious sequelae.

Adult↗
PubMed2003

Superior mesenteric vein thrombosis after colectomy for inflammatory bowel disease: a not uncommon cause of postoperative acute abdominal pain.

PURPOSE: Thromboembolism is a significant cause of morbidity and mortality in inflammatory bowel disease. Several prothrombotic conditions have been investigated in inflammatory bowel disease. The aim of this study was to evaluate the incidence of symptomatic postoperative superior mesenteric vein thrombosis in inflammatory bowel disease patients undergoing colonic resections and to identify and characterize their clinical presentation. METHODS: Between January 1999 and December 2001, 83 consecutive patients undergoing total colectomy for inflammatory bowel disease were studied retrospectively. Patients who developed new-onset postoperative acute abdominal pain were evaluated by CT scan of the abdomen. A complete coagulation profile, including thrombin time, platelet count, protein C, protein S, antithrombin III, homocysteine level, factor V Leiden mutation, plasminogen, and prothrombin G20210A mutation, was obtained in patients diagnosed with superior mesenteric vein thrombosis. RESULTS: Four patients (4.8 percent; 3 females; 3 patients with ulcerative colitis and 1 with Crohn's colitis) developed symptomatic postoperative superior mesenteric vein thrombosis. Two of these patients had extension of the clot into the portal vein. Their presenting symptom was abdominal pain, with a median interval of ten days from the index surgery. The hematologic workup was negative in three patients, with one heterozygous for prothrombin G20210A mutation. All patients were treated with systemic anticoagulation for at least six months. One ulcerative colitis patient was diagnosed after abdominal colectomy and underwent an uneventful ileal pouch-anal anastomosis after systemic anticoagulation. CONCLUSION: Postoperative superior mesenteric vein thrombosis is a more frequent occurrence than previously reported in patients with inflammatory bowel disease. Direct surgical trauma to the middle colic veins, with resulting thrombosis, is likely to be the precipitating factor in a borderline intrinsically hypercoagulable environment. All patients became asymptomatic after systemic anticoagulation and recovered uneventfully.

Abdomen, Acute↗
PubMed2005

Once-daily enoxaparin in the outpatient setting versus unfractionated heparin in hospital for the treatment of symptomatic deep-vein thrombosis.

BACKGROUND: Once- and twice-daily low-molecular-weight heparin administered in hospital have been shown to be effective and safe for treating deep-vein thrombosis. The aim of this study was to compare the efficacy and safety of deep-vein thrombosis treatment using once-daily subcutaneous enoxaparin in the outpatient setting with intravenous unfractionated heparin in hospital. METHODS: This randomized, parallel-group, open-label study was conducted in 18 centers in 4 countries. In total, 298 patients with symptomatic deep-vein thrombosis who were eligible for home treatment were randomized to treatment with enoxaparin in the outpatient setting (1.5 mg/kg subcutaneously once-daily) or unfractionated heparin in hospital (5000 IU bolus and 1250 IU/hour intravenous infusion) for > or =5 days. Clinical endpoints were assessed during a 6-month follow-up period. RESULTS: Among all patients treated with enoxaparin, there was a trend towards fewer recurrent deep-vein thromboses (1.3% vs. 5.4%; p = 0.060) and pulmonary emboli (1.3% vs. 4.1%; p = 0.17) compared with patients treated with unfractionated heparin. When considering a post-hoc combined endpoint of deep-vein thrombosis and pulmonary embolism, significantly fewer events occurred in the enoxaparin group than in the unfractionated-heparin group (2.7% vs. 8.8%; p = 0.026). The incidences of bleeding events and adverse events in the enoxaparin and unfractionated-heparin groups were similar. CONCLUSIONS: Once-daily subcutaneous enoxaparin in the outpatient setting is at least as effective and as well tolerated as in-hospital intravenous unfractionated heparin for treatment of deep-vein thrombosis.

Adult↗
PubMed2007

Deficiency in thrombin-activatable fibrinolysis inhibitor (TAFI) protected mice from ferric chloride-induced vena cava thrombosis.

Thrombin-activatable fibrinolysis inhibitor (TAFI) is a plasma carboxypeptidase that renders a fibrin-containing thrombus less sensitive to lysis. Since the role of TAFI in thrombus formation is still controversial in mice, our present study was designed to evaluate mice deficient in TAFI (TAFI(-/-)) on FeCl(3)-induced vena cava and carotid artery thrombosis. Parallel studies were carried out in wild-type mice using a potato carboxypeptidase inhibitor (PCI), a selective inhibitor of activated TAFI (TAFIa). Significant reduction in thrombus formation was observed in TAFI(-/-) mice (n = 8, P < 0.05 compared to wild-type littermates) but not in heterozygous (TAFI(+/-)) mice in 3.5% FeCl(3)-induced vena cava thrombosis. A similar effect was observed following treatment with 5 mg/kg bolus plus 5 mg/kg/h PCI in the same venous thrombosis model in C57BL/6 mice (n = 8, P < 0.01 compared to vehicle). No compositional difference was observed for the venous thrombi in TAFI(-/-) and wild-type littermates with or without PCI treatment using histological assessment. In contrast, neither TAFI deficiency nor treatment with PCI showed antithrombotic efficacy in the 3.5% FeCl(3)-induced carotid artery thrombosis model. In a tail transection bleeding time model, both TAFI deficiency and PCI treatment increased bleeding time up to 4.5 and 3.5 times, respectively, over controls (P < 0.05, n = 8). Similar ex vivo fibrinolytic activities were demonstrated for both TAFI deficiency and PCI treatment as enhanced lysis of thrombin-induced plasma clots and lysis of whole blood clot in a thrombelastograph. These data provide direct evidence for the role of TAFIa in vena cava thrombosis without the addition of exogenous thrombolytic in mice. The strong ex vivo fibrinolytic activity of TAFI deficiency or TAFIa inhibition by PCI provides a biomarker of TAFIa inhibition that tracks in vivo antithrombotic efficacy.

Animals↗
PubMed2006

Genetic susceptibility to thrombosis.

Thrombosis is associated with atherosclerosis, sepsis, cancer, and numerous other inflammatory diseases. Complications of thrombosis, such as myocardial infarction, stroke, and venous thromboembolism, contribute significantly to morbidity and mortality. Susceptibility to thrombosis is conferred by both genetic and environmental factors. Tissue factor is the primary cellular initiator of blood coagulation and is a major contributor to thrombosis. In this review, we discuss the association between various polymorphisms and the risk for thrombosis.

Cytokines↗
PubMed1994

Thrombosis and restenosis after stenting in failed angioplasty: comparison with elective stenting.

The results of Palmaz-Schatz stent implantation in failed angioplasty in 60 consecutive patients were compared with those of elective stent implantation in 100 consecutive patients. Stent implantation was successful in all of the failed group and in 99% of the elective. Stent thrombosis occurred in 16.7% of the failed group and 2% of the elective (p = 0.001). In the failed angioplasty group, stent thrombosis was associated with a greater frequency of preprocedure complex morphology (40% vs 12% in the nonthrombosis group, p = 0.05), persistent uncovered dissection after stenting (60% vs 14%, p = 0.004), and greater residual stenosis (39.9% +/- 25.3% vs 24.9% +/- 13.08%, p = 0.008) after stenting. Vessel patency was reestablished by angioplasty in 5 of 10 with stent thrombosis. Of these 5 patients, however, 2 suffered repeat stent thrombosis; 1 died suddenly four months later; and restenosis occurred in the remaining 2. Follow-up angiography was performed in 98% of the elective group at 6.3 +/- 2.6 months and 96% of the failed angioplasty group at 6.4 +/- 2.1 months. Restenosis (> or = 50% stenosis) occurred in 32% of the elective group and 50% of the failed angioplasty group (p = 0.041). Multiple logistic regression analysis identified multiple stent implantation (F = 6.75, p = 0.01) and triple-vessel disease (F = 3.46, p = 0.06) as independent positive predictors of restenosis. In conclusion, stent implantation in cases of failed angioplasty could be performed with a success similar to that of elective stent implantation but was associated with a greater frequency of stent thrombosis and restenosis.

Age Factors↗
PubMed1991

Lupus anticoagulant inhibition of in vitro prostacyclin release is associated with a thrombosis-prone subset of patients.

PURPOSE: The effect of lupus anticoagulant-containing sera on endothelial prostacyclin generation (both basal and after thrombin stimulation) was determined. Subsets of patients who had experienced arterial, venous, or no thrombosis were compared with respect to the quantitation of antiphospholipid antibody and effects on prostacyclin production. PATIENTS AND METHODS: Serum antiphospholipid antibodies were detected in 26 patients by immunologic (enzyme-linked immunosorbent assay) and kinetic (anticoagulant) assays. Cultured human endothelial cells were exposed to patient or normal serum, and the release of prostacyclin was determined by radioimmunoassay of supernatants. Release was determined in the absence and presence of the secretagogue, thrombin (1 U/mL), corrected for interassay variation, and correlated with other clinical and laboratory variables. RESULTS: The normal prostacyclin response was a 2.5-fold increase after thrombin (1 U/mL) compared to basal production. Patients with a history of arterial thrombosis (Group 1, n = 10) had the highest IgG anticardiolipin antibody titers (449 +/- 115 [OD x 1,000]), most prolonged kaolin clotting times (140 +/- 15 seconds), and the least prostacyclin response to thrombin (1.36-fold). Patients with venous thrombosis (Group 2, n = 6) had lower titers (329 +/- 120), intermediate clotting times (125 +/- 19 seconds), and slightly impaired prostacyclin responses (2.18-fold). Patients with no history of thrombosis (Group 3, n = 10) had low antibody titers (220 +/- 20), mildly prolonged clotting times (108 +/- 6 seconds), and normal prostacyclin responses (2.33-fold). Patient serum did not alter basal or arachidonate-induced prostacyclin production. Group 1 had significantly lower platelet counts (99 +/- 19) compared to Group 2 (167 +/- 35) or Group 3 (167 +/- 34), but were similar in age and associated diagnoses. CONCLUSIONS: Inhibition of prostacyclin responses is commonly found in serum from patients with lupus anticoagulants, and is likely to be present in patients with high IgG anticardiolipin antibodies, strong lupus anticoagulants, low platelet counts, and a recent arterial thrombosis.

Adult↗
PubMed1992

Association of anti-beta 2 glycoprotein I antibodies with lupus-type circulating anticoagulant and thrombosis in systemic lupus erythematosus.

PURPOSE: Antiphospholipid antibodies (including anticardiolipin antibodies and circulating anticoagulant) are associated with thrombosis in systemic lupus erythematosus. Since it has been shown that beta 2 glycoprotein I (beta 2 gp I) acts as a cofactor of anticardiolipin antibody binding to cardiolipin, the presence and clinical meaning of anti-beta 2gp I antibodies in sera from patients with lupus were examined. PATIENTS AND METHODS: An enzyme-linked immunosorbent assay technique for the detection of anti-beta 2gp I antibodies was developed, and 47 lupus sera were studied retrospectively, as well as 88 healthy blood donors' sera. RESULTS: It was found that 17 of 47 patients with lupus (36%) had anti-beta 2gp I antibodies. Anti-beta 2gp I antibodies were statistically associated with anticardiolipin antibodies, thrombosis, and lupus anticoagulant. Eight of nine lupus patients with thrombosis had anti-beta 2gp I antibodies and lupus anticoagulant, and seven of them had anticardiolipin antibodies. Of 18 patients with anticardiolipin antibodies without anti-beta 2gp I antibodies or lupus anticoagulant, only one had thrombosis (due to nephrotic syndrome). Among anti-beta 2gp I-positive patients, 14 of 16 had lupus anticoagulant activity, whereas only three patients with lupus anticoagulant were anti-beta 2gp I-negative. CONCLUSIONS: The presence of anti-beta 2gp I antibodies is a new immunologic feature of lupus patients with thrombosis. In addition, since anti-beta 2gp I antibodies are closely associated with lupus anticoagulant activity, they may contribute to explain antiprothrombinase activity.

Autoantibodies↗
PubMed1995

Hepatic arterial resistance in cirrhosis with and without portal vein thrombosis: relationships with portal hemodynamics.

BACKGROUND/AIMS: Little information is available on hepatic arterial hemodynamics in cirrhosis because of the invasiveness of methods. Hepatic arterial resistance indexes were evaluated noninvasively by Doppler ultrasonography and were correlated with portal hemodynamics evaluated both noninvasively and invasively. METHODS: Hepatic arterial resistance indexes, portal blood flow velocity and volume, and portal vein congestion index were evaluated in 31 controls and 171 cirrhotic patients with (n = 13) or without (n = 158) portal vein thrombosis. Resistance to portal blood flow was also calculated in 15 patients from hepatic venous pressure gradient, measured by hepatic vein catheterization, and portal blood flow. RESULTS: Resistance indexes were significantly higher in cirrhotics without portal thrombosis than in controls (pulsatility index, 1.30 +/- 0.29 vs. 0.89 +/- 0.09; P < 0.001; resistive index, 0.71 +/- 0.07 vs. 0.59 +/- 0.04; P < 0.001). In patients with portal thrombosis, the pulsatility index (1.86 +/- 0.39) and resistive index (0.81 +/- 0.06) were significantly higher than in controls (P < 0.001) and in patients without thrombosis (P < 0.001). Resistance indexes directly correlated with portal resistance (P < 0.01), the congestion index (P < 0.01), and the degree of esophageal varices (P < 0.01). CONCLUSIONS: Hepatic arterial resistance indexes increase in cirrhosis, particularly with portal vein thrombosis. The pathophysiology of the increase in hepatic arterial resistance seems to be parallel to that of portal resistance.

Adult↗
PubMed1995

Renal transplant thrombosis in children.

Data concerning 100 consecutive renal transplantations in children were analyzed to determine factors enhancing the risk of renal transplant thrombosis. The incidence of renal transplant thrombosis was high, at 12%. It is concluded that in addition to young age and low body weight of recipient and young age of the donor, also a high preoperative urine production contributes to the occurrence of thrombosis. Children with hypoplastic or dysplastic kidneys are at greater risk for thrombosis. Considering the influence of high urine production of the native kidneys, it may be possible to prevent thrombosis by albumin and ample fluid administration.

Age Factors↗
PubMed1995

Postpartum ovarian vein thrombosis after vaginal delivery: a report of 11 cases.

OBJECTIVE: To review and characterize the presentation of postpartum ovarian vein thrombosis after vaginal delivery. METHODS: We reviewed medical records of patients with the prior diagnosis of septic pelvic thrombophlebitis, deep vein thrombosis, and pulmonary embolism associated with pregnancy. The study covered the 10-year period from July 1984 through August 1994 and included women hospitalized at E.H. Crump Women's Hospital, Regional Medical Center, University of Tennessee, Memphis, Tennessee. RESULTS: During the study period, there were 76,858 deliveries: 13,109 cesareans and 63,749 vaginal deliveries. Eleven patients had documented postpartum ovarian vein thrombosis after vaginal delivery. Ten patients were readmitted an average of 7.6 days after delivery (range 3-17). The diagnosis was documented by computed tomography (CT) scan or ultrasound in ten women and laparotomy in one. Nine patients were readmitted with the presumptive diagnosis of endometritis, the other two with the presumptive diagnosis of pyelonephritis. Nine were treated initially with ampicillin, gentamicin, and clindamycin. Heparin therapy was added when failure of clinical response was noted. No patient defervesced within 24 hours of beginning heparin therapy; only two patients defervesced within 48 hours, and the remaining patients became afebrile at an average of 6.8 days (range 4-18, median 5). CONCLUSION: The diagnosis of ovarian vein thrombosis should be considered early in the care of patients readmitted with a diagnosis of endometritis after vaginal delivery. If prompt defervescence does not occur with aggressive intravenous antibiotic therapy, a CT scan should be obtained in a timely manner for prompt diagnosis and therapy. Our findings do not support the time-honored rule that septic pelvic thrombophlebitis and ovarian vein thrombosis respond within 24-48 hours to therapeutic anticoagulation with heparin.

Adolescent↗
PubMed1987

Antithrombotic activity of a synthetic heparin pentasaccharide in a rabbit stasis thrombosis model using different thrombogenic challenges.

A synthetic pentasaccharide, representing the critical sequence required in heparin for binding to antithrombin III (AT III), produces strong anti-factor Xa activity in vitro in the presence of AT III and is devoid of any activity directed towards thrombin. This pentasaccharide provides a unique tool to study the question of whether an agent capable of inhibiting factor Xa but devoid of anti-factor IIa activity in vitro, has the capacity to produce an antithrombotic effect in vivo. We have previously demonstrated in a rabbit stasis thrombosis model using a human serum challenge, a significant antithrombotic effect of the pentasaccharide. This finding and discrepancies with some earlier reports on the antithrombotic actions of other oligosaccharide fragments, led us to extend these studies. Four modifications of the stasis thrombosis model were developed using the following thrombogenic challenges selected for their specified induction sites of thrombosis, thromboplastin, an activated prothrombin complex concentrate, a non-activated prothrombin complex concentrate administered simultaneously with Russell's viper venom, and factor Xa. Dose-dependent antithrombotic responses were obtained in all four systems with ED50 values between 25-43 ug/kg for pentasaccharide as compared to 16-47 ug/kg for heparin. Complete inhibition of induced thrombosis was obtained in all four systems for pentasaccharide. Ex vivo analysis revealed expected anti-factor Xa levels but no anti-factor IIa activity. It is concluded that an oligosaccharide with high anti-factor Xa activity and devoid of anti-factor IIa activity is capable of inhibiting thrombosis induced in rabbit stasis models, but that higher dosages than heparin are required for this effect.

Animals↗
PubMed1995

Effects of thromboxane A2 synthase inhibitors (CV-4151 and ozagrel), aspirin, and ticlopidine on the thrombosis caused by endothelial cell injury.

The antiplatelet and antithrombotic effects of CV-4151 (isbogrel), a potent selective thromboxane A2 (TXA2) synthase inhibitor, were compared with those of ozagrel (OKY-046), aspirin, and ticlopidine in rats. Two hours after oral administration, CV-4151, ozagrel and aspirin inhibited blood TXA2 generation with ID50 values of 0.04, 0.3 and 6.4 mg/kg, respectively. These values were similar to the oral ID50 values of CV-4151 (0.06 mg/kg), ozagrel (0.92 mg/kg) and aspirin (7.0 mg/kg) for arachidonic acid (AA)-induced platelet aggregation ex vivo. Two hours after p.o. administration, CV-4151 and ozagrel inhibited femoral vein platelet-rich thrombosis caused by endothelial injury with ID50 values of 2.46 and 13.7 mg/kg, respectively. However, aspirin (100 mg/kg, p.o.) only slightly inhibited the thrombosis. Ticlopidine (300 mg/kg, p.o.) slightly but significantly inhibited AA-induced and ADP-induced platelet aggregation, however, it potently inhibited the thrombosis. CV-4151 and ozagrel given by i.v. injection showed therapeutic effects on the thrombosis with ED50 values of 0.026 and 0.066 mg/kg, respectively. These values were similar to the i.v. ED50 values of CV-4151 (0.0056 mg/kg) and ozagrel (0.042 mg/kg) for blood TXA2 generation. However, aspirin (30 mg/kg, i.v.) only moderately reduced the thrombosis. CV-4151 (> 0.3 mg/kg, p.o.), ozagrel (> 3 mg/kg, p.o.) and ticlopidine (300 mg/kg, p.o.) all significantly prolonged tail bleeding time. Aspirin (100 mg/kg, p.o.) tended to prolong the bleeding time. The antiplatelet and antithrombotic effects of CV-4151 are more potent than those of ozagrel, aspirin and ticlopidine in rats. CV-4151 may therefore be a useful drug for the treatment of thrombotic diseases.

Animals↗
PubMed1996

Antithrombotic actions of selective inhibitors of blood coagulation factor Xa in rat models of thrombosis.

The antithrombotic actions of selective factor Xa (FXa) inhibitors, recombinant tick anticoagulant peptide (rTAP) and DX-9065a, were evaluated in experimental thrombosis models in anesthetized rats. In the first model, thrombosis was induced by exposing flowing blood to a silk thread anchored in an arteriovenous (AV) shunt. rTAP, DX-9065a and heparin, given as an iv infusion 1 hr before blood was circulated in the AV shunt, had ID50s of 0.007, 0.6 mumol/kg/hr and 16 U/kg/hr, respectively. In the model of venous thrombosis which was induced by hypotonic saline (0.225%) followed by 15-min stasis of abdominal vena cava, rTAP and heparin had ID50s of 0.007 mumol/kg/hr and 3.5 U/kg/hr, respectively. In both models, full inhibition of thrombus formation was achieved with FXa inhibition at doses which only modestly increased ex vivo plasma clotting time APTT (1.26 to 1.82 over the baseline). By contrast, the maximum antithrombotic effect of heparin was associated with high and significant APTT prolongation (> 5 fold over the baseline). Therefore, our study suggests that FXa inhibitors are effective agents in preventing thrombosis in both rat thrombosis models and may have therapeutic antithrombotic potential.

Animals↗
PubMed1996

[Renal vein thrombosis and constitutional protein S deficiency].

Venous and arterial thrombosis due to a constitutional protein S deficiency is well-known. We report the case of a 36 year-old patient admitted to hospital in 1991 for primary renal vein thrombosis due to a constitutional protein S deficiency of type I. The diagnosis was made by CT scan and angiography. Left nephrectomy, which was made because of doubt with regard to subjacent neoplasm, showed left renal vein thrombosis and multiple renal infarcts. In 1994, after 4 months of discontinuation of oral anticoagulants, the patient presented pulmonary embolism documented by pulmonary scintigraphy and CT scan, partial portal thrombosis and sural thrombophlebitis documented by echography coupled with Doppler. To our knowledge, this is the first reported case of a constitutional protein S deficiency associated with primary renal vein thrombosis.

Adult↗
PubMed1995

Anticardiolipin antibody in patients on maintenance hemodialysis and its association with recurrent arteriovenous graft thrombosis.

To investigate the relationship between dialysis access thrombosis (arteriovenous grafts [AVG] and arteriovenous fistulas [AVF]) and the presence of elevated concentration of immunoglobulin G-anticardiolipin antibody (IgG-ACA), we conducted a cross-sectional study of all patients, in a single dialysis facility, who had a minimum of 6 months of uninterrupted hemodialysis. Episodes of thrombosis of AVGs and AVFs in the preceding 30 months were documented and each patient's IgG-ACA titer was determined. Sixteen of 74 patients with AVGs (22%) had a raised titer of IgG-ACA compared with only one of 17 patients (6%) with AVFs. In the patients with AVGs the odds ratio for patients with raised IgG-ACA titer to have experienced two or more episodes of thrombosis, compared with none or only one episode, was 3.7 (95% confidence interval, 1.2 to 11.8; P < 0.04). No events of AVF thrombosis were encountered during the same period. We conclude that in end-stage renal disease patients undergoing hemodialysis, there is a greater prevalence of elevated IgG-ACA titer in patients with AVGs than in patients with AVFs, and this in turn is associated with increased odds of having had recurrent AVG thrombosis.

Adult↗