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PubMedDate not supplied

[Hereditary deficiency of antithrombin III, protein C, protein S and factor XII in 121 patients with venous or arterial thrombosis].

INTRODUCTION: Hereditary thrombophilia is caused by various inherited disorders which lead to familial tendency to recurrent venous thrombosis usually at an early age and with spontaneous onset. In the studies reported so far, the different prevalence of hereditary thrombophilia among patients with venous thrombosis was found, greatly depending on criteria for selection of patients. Arterial thrombosis is most often the consequence of arteriosclerosis but the prevalence of hereditary thrombophilia among young patients with arterial thrombosis and without recognized risk factors for arteriosclerosis is not known . In this study, the frequency of hereditary deficiencies of antithrombin III (AT III), protein C (PC), protein S (PS), plasminogen (PLMG), factor XII (F XII) and dysfibrinogenaemia was investigated over a 2-year period in 121 patients with venous or arterial thrombosis selected according to the recommendations of the British Committee for Standards in Haematology. PATIENTS AND METHODS: The study included total a of 121 patients (58 males and 63 females) with documented venous or arterial thrombosis. Table 1 shows patient's characteristics regarding gender, age and clinical manifestation of thrombosis. Each patient fulfilled at least one of the following criteria: a) venous thrombosis prior to the age of 45; b) arterial thrombosis prior to the age of 30, without risk factors for arteriosclerosis; c) recurrent thrombosis; d) familial tendency to thrombosis; e) thrombosis of unusual localization. A detailed history was taken from each patient on earlier personal or familial occurrence of thrombosis. For the purpose of this study, thrombophilia was characterized as congenital when the deficient protein was constantly below normal value and when the same deficiency was confirmed in a close family member; acquired when the acquired disorder predisposing to thrombosis was present in absence of constant protein deficiency; and idiopathic when the cause of thrombosis was unknown. All tests were performed in plasma obtained after centrifugation of venous blood anticoagulated with 0.129 mol/1 sodium citrate. Concentrations of fibrinogen, PT, PTT and F XII were measured by standard clotting methods. At III, PC and plasminogen activity were determined by chromogenic methods using commercial reagents (Boehring, Marburg, Germany). AT III, PC and total PS antigen were assayed by Laurell immunoelectrophoresis. The presence of lupus anticoagulant was investigated by recommended tests. RESULTS: A total of 15 patients (12.4%) fulfilled criteria for hereditary thrombophilia. Seven of them (5.8%) had AT III deficiency, five (4.1%) PC deficiency, two (1.6%) PS deficiency, and one patient had F XII deficiency. Secondary thrombophilia was found in 21.5% of patients and the cause of thrombosis in 66.1% of patients was not elucidated. A high frequency of hereditary thrombophilia has been found in patients with arterial thrombosis (40%). Among patients with hereditary thrombophilia thrombosis occurred at significantly younger age (29.9 vs. 42.2 and 40.9 yr.) compared to the patients with secondary and idiopathic thrombophilia, respectively. Patients with hereditary thrombophilia had also a higher occurrence of positive family history related to thrombosis (66.7% vs. 7.7% and 27.5%). DISCUSSION: The prevalence of hereditary thrombophilia in nonselected patients with venous thrombosis is relatively low, and for that reason the selection of patients, according recommended criteria, in whom the screening tests for congenital thrombophilia should be performed, is strongly suggested by many authors. In our study we used the generally accepted recommendations for investigation of patients with venous and arterial thrombosis. The presence of congenital thrombophilia was found in 15 (12.4%) of 121 studied patients, what is in accordance with results of other similarly designed studies. (ABSTRACT TRUNCATED)

Adolescent↗
PubMed2001

Hepatic artery thrombosis after orthotopic liver transplantation.

OBJECTIVE: Hepatic artery thrombosis after liver transplantation is uncommon, but represents an important cause of morbidity and mortality. The aim of this study is to identify the possible risk factors for the development of hepatic artery thrombosis, and the impact of hepatic artery thrombosis on the patients and graft survival. METHODS: Between January 1994 and June 1998, we reviewed retrospectively a series of 86 liver transplant procedures performed on 81 adult patients. Arterial anomalies of the donor graft, rejection episodes, cold ischemia time, ABO matching, the use of blood/fresh frozen plasma during and after surgery, and the use of heparin as prophylactic anticoagulation therapy were examined as a possible contributing risk factors for the development of hepatic artery thrombosis. RESULTS: Hepatic artery thrombosis occurred in 7 procedures out of 86 (9%). Early cases of Hepatic artery thrombosis within 15 days after transplant occurred in 4 patients. Late thrombosis occurred in 3 patients. Analysis of potential risk factors for the development of hepatic artery thrombosis was carried out. Five out of 40 patients who did not received prophylactic heparin had hepatic artery thrombosis (12.5%), while only 2 out of 46 patients who received prophylactic heparin had hepatic artery thrombosis 4%. On the other hand, 6 out of the 7 patients developed hepatic artery thrombosis received more than 5 units of blood transfusion during the transplant procedure (11%) while only one patient developed hepatic artery thrombosis who received less than 5 units intra-operatively (3%). Management of hepatic artery thrombosis cases were carried out in the form of: thrombectomy (n = 1), thrombectomy followed by retransplantation (n = 2), and non-surgical or conservative treatment (n = 4). The overall survival rate was (43%) (3 out of 7). Out of four deaths, 3 were directly related to hepatic artery thrombosis while the cause of death iin the remaining patients was attributed to pulmonary sepsis. CONCLUSION: Early hepatic artery thrombosis leads to death unless quick retransplantation follows. Conservative treatment for the late onset hepatic artery thrombosis on occasion has been useful. The use of postoperative prophylactic anticoagulation therapy might be of benefit in the prevention of hepatic artery thrombosis after liver transplantation. Increased transfusion requirement for red blood cells during transplant procedure was independently associated with increase incidence of hepatic artery thrombosis.

Adult↗
PubMed1994

[Echo-Doppler for early diagnosis of deep venous thrombosis in orthopedic surgery and traumatology. A retrospective study of 1,647 patients].

UNLABELLED: The authors report the results of duplex ultrasound scanning investigation for the detection of deep venous thrombosis after orthopedic surgery and compare asymptomatic and symptomatic populations. PURPOSE OF THE STUDY: To estimate the rate of deep venous thrombosis diagnosed by duplex scanning in those 2 populations and precise their features. MATERIAL: A total of 1,647 in-patients all receiving low-molecular-weight heparin and investigated from 1989 to 1993. either for screening because of high risk of thrombosis (asymptomatic group: 930 patients, mean age +/- SD 63 +/- 17 years) or for clinical suspicion of deep vein thrombosis (symptomatic group; 717 patients, mean age +/- SD: 57 +/- 21 years). Difference between the two groups mean ages were significant (p < 10(-8). METHODS: An Hitachi EUB 450 duplex and an Acuson colour duplex 128 XP, with 3.5 MHz and 7.5 MHz linear probes were used. Veins were tested for compressibility in transverse view from caval site to both ankles. Retrospective analysis of patients database results has been achieved. RESULTS: There was no significant difference in deep vein thrombosis rate between screening asymptomatic group (356/930:38%) and symptomatic group (253/717: 35%). There was a linear relation, in the 2 groups, between age and deep vein thrombosis rate, from 10% before twenty to 45% after eighty years old. For a relative risk to have thrombosis detected before twenty definite at 1, it was 2.1 for 20-29, 4.9 for 40-49, 6.2 for 60-69 and 8.6 later than 80 years old. Proximal deep vein thrombosis was detected in only 5% (87/1,647) of patients. Distal muscular soleal veins were the most usual involved sites of thrombosis. Isolated soleal thrombosis were detected in 16% (270/1,647) of patients. There was non significant difference between the deep vein thrombosis rate after total knee or hip arthroplasty among selected patients for duplex scanning from 1989, and the true prevalence assessed among all the patients who have undergone total hip or knee arthroplaty during the last 6 months. DISCUSSION: Pessimistic results previously reported for duplex screening among asymptomatic patients are not confirmed. Calf vein thrombosis rate assessed by duplex scanning exceeds by 15 a 20% usual rates assessed by contrast venography, among patients receiving low-molecular-weight heparins. That difference could be assigned to the isolated muscular soleal thrombosis usually missed at contrast venography. CONCLUSION: Deep vein thrombosis rate among orthopedic surgical patients, is much higher when detected with Duplex ultrasound scanning than detected with contrast venography, and is related to patient age. Screening for deep venous thrombosis by duplex scanning in orthopedic surgery is as efficient among asymptomatic as among symptomatic patients and could become soon a systematic screening. Soleal vein thrombosis are the most usual. Mechanical calf venous pump stimulation in association with low molecular weight heparin, has to be evaluated in attempting to reduce those muscular soleal veins thrombosis.

Aged↗
PubMed2005

The relationship between inflammation and venous thrombosis. A systematic review of clinical studies.

During the past decade, the role of inflammation in the pathophysiology of arterial thrombosis has been elucidated. However, comparatively little is known about the relationship between inflammation and venous thrombosis. The aim of this study was to perform a systematic review of clinical studies that have examined the association between inflammation and venous thrombosis, specifically: (1) the value of inflammatory markers in predicting the future development of venous thrombosis; (2) test characteristics of markers of inflammation in the diagnosis of acute venous thrombosis; and (3) effect of venous thrombosis on blood levels of inflammatory markers. Using keywords venous thrombosis, venous thromboembolism, inflammation, acute phase markers, C-reactive protein (CRP), interleukin (IL)-6, IL-8, and monocyte chemotactic protein (MCP)-1, PubMed and Medline computerized databases were searched for English language articles published after 1980. Search results were restricted to clinical studies in humans that used study designs that were appropriate to address the above objectives. Results show that plasma CRP levels do not appear to predict risk of future venous thrombosis (two studies; N = 41,308). Four studies (N=562) have examined the utility of plasma CRP in the diagnosis of venous thrombosis; pooled positive and negative predictive values were 53% (95% CI:47%,59%) and 85% (95% CI: 81%, 89%), respectively. A two- to six-fold increase in the risk of deep vein thrombosis (DVT) is associated with elevations in plasma levels of CRP, IL-6, IL-8, MCP-1 or TNF-alpha (three studies). We can conclude that the nature of the relationship between inflammation and clinical venous thrombosis is not yet established. CRP does not appear to be useful in predicting future venous thrombosis or in the diagnosis of acute venous thrombosis. While several markers of inflammation are elevated in acute venous thrombosis, further research is needed to determine the precise relationship between these markers and venous thrombosis. The identification and elucidation of inflammatory markers relevant to venous thrombosis could provide targets for future therapy.

Adult↗
PubMed1994

[Detection of deep vein thrombosis of the limbs by ultrasound in orthopedic and traumatologic surgery. Results of 1647 studied patients].

INTRODUCTION: This study was undertaken to estimate the efficiency of duplex ultrasound scanning and its utility to detect deep vein thrombosis in orthopedic patients and to describe their features. MATERIAL AND METHODS: A total of 1647 in-patients, all receiving low-molecular-weight heparin, were investigated from 1989 to 1993, either for screening because of a high risk of thrombosis (asymptomatic group: 930 patients, mean age + SD: 63 + 17 years) or for clinical suspicion of deep vein thrombosis (symptomatic group: 717 patients, mean age + SD: 57 + 21 years). Difference between the two groups mean ages was significant (p < 10(-8)). An Hitachi EUB 450 duplex and an Acuson colour duplex 128 XP, with 3.5 MHz and 7.5 MHz linear probes were used. Veins were tested for compressibility in the transverse view from caval site to both ankles. Retrospective analysis of patients' database results was done. RESULTS: There was no significant difference in deep vein thrombosis rate between screening asymptomatic group (356/930: 38 per cent) and symptomatic group (2531717: 35 per cent). There was a linear relation, in the 2 groups, between age and deep vein thrombosis rate, from 10 per cent before twenty to 45 per cent after eighty years old. For a relative risk to have thrombosis detected before twenty definite at 1, it was 2.1 for 20-29, 4.9 for 40-49, 6.2 for 60-69 and 8.6 later than 80 years old. Proximal deep vein thrombosis was detected in only 5 per cent (87/1647) of patients. Distal muscular soleal veins were the most usual involved sites of thrombosis. Isolated soleal thrombosis were detected in 16 per cent (270/1647) of patients. There was no significant difference between the deep vein thrombosis rate after total knee or hip arthroplasty among selected patients for duplex scanning from 1989, and the true prevalence assessed among all the patients who have undergone total hip or knee arthroplasty during the last 6 months. DISCUSSION: Pessimistic results previously reported for duplex screening among asymptomatic patients are not confirmed. Calf vein thrombosis rate assessed with duplex exceeds by 15 to 20 per cent the rates assessed by contrast venography, among patients receiving low molecular weight heparins. That difference could be attributed to the isolated muscular soleal thrombosis usually missed at contrast venography. CONCLUSION: Deep vein thrombosis rate among orthopedic surgical patients, is much higher when detected with Duplex ultrasound scanning than detected with contrast venography, and is related to patient age. Soleal vein thrombosis is the most prevalent. Duplex ultrasound scanning is an efficient and useful screening method for deep vein thrombosis in orthopedic surgery. Mechanical calf venous pump stimulation in association with low molecular weight heparin, has to be evaluated in attempting to reduce those muscular soleal veins thrombosis.

Adult↗
PubMed1994

Routine postoperative duplex ultrasonography screening and monitoring for the detection of deep vein thrombosis. A survey of 110 total hip arthroplasties.

The use of duplex ultrasonography for routine noninvasive screening, monitoring, and management of deep venous thrombosis after total hip arthroplasty was evaluated. The reliability of duplex ultrasonography for detection of deep vein thrombosis was confirmed in an initial cohort of 51 total hip arthroplasty patients (102 lower extremities), demonstrating 91% sensitivity, 98% specificity, and 97% accuracy when compared with venography. A second cohort of 110 total hip arthroplasty patients using pneumatic compression stockings and aspirin as deep vein thrombosis prophylaxis underwent screening duplex ultrasonography of both lower extremities on postoperative Day 4. Duplex ultrasonography screening showed 10 (9.1%) patients with proximal deep vein thrombosis and 10 (9.1%) with distal deep vein thrombosis, all of whom were asymptomatic. The 10 patients with proximal deep vein thrombosis on duplex ultrasonography were prescribed therapeutic anticoagulation. Duplex ultrasonography subsequently confirmed resolution of proximal deep vein thrombosis in these patients before discontinuation of anticoagulation; none developed symptomatic pulmonary embolism through 12-month clinical followup. The 10 patients with distal deep vein thrombosis diagnosed by duplex ultrasonography were not treated with anticoagulation, but were monitored by serial duplex ultrasonography through postoperative Day 14 for propagation of distal to proximal deep vein thrombosis; none manifested symptomatic deep vein thrombosis or pulmonary embolism through 12-month clinical followup. The 90 patients with negative duplex ultrasonography results were followed clinically; 3 developed late symptomatic proximal deep vein thrombosis (1 of these later manifested pulmonary embolism). Therefore, duplex ultrasonography was used after total hip arthroplasty for the following: (1) to screen routinely in the hospital for asymptomatic proximal and distal deep vein thrombosis; (2) to monitor for potential propagation of distal to proximal deep vein thrombosis; (3) to minimize exposure to therapeutic anticoagulation by confirming the absence of proximal deep vein thrombosis in 97 of 110 patients; and (4) to demonstrate the effectiveness of mechanical and systemic deep vein thrombosis management by confirming the absence or resolution of deep vein thrombosis in all 110 patients.

Anticoagulants↗
PubMed1994

Mesenteric venous thrombosis: still a lethal disease in the 1990s.

PURPOSE: This study was designed to evaluate progress in diagnosis, management, and clinical outcome of mesenteric venous thrombosis (MVT). METHODS: We retrospectively reviewed the clinical course of 72 patients treated for mesenteric venous thrombosis between 1972 and 1993. RESULTS: Fifty-three patients had acute and 19 had chronic mesenteric venous thrombosis. Fifty-seven patients had secondary mesenteric venous thrombosis; previous abdominal surgical procedure and hypercoagulable states were the most prevalent associated conditions. Computed tomography was abnormal in all patients who underwent this test for acute mesenteric venous thrombosis and in 93% of those who had chronic disease. Angiography diagnosed acute mesenteric venous thrombosis in five (72%) of seven patients. Acute mesenteric venous thrombosis presented most frequently as abdominal pain (83%), anorexia (53%), and diarrhea (43%). Thirty-three (75%) had symptoms longer than 48 hours. Thirty-four (64%) patients with acute mesenteric venous thrombosis underwent a surgical procedure. Bowel resection was necessary in 31 patients. One patient had unsuccessful mesenteric venous thrombectomy. Seven patients with acute mesenteric venous thrombosis underwent anticoagulation without a surgical procedure, and 12 were observed. All patients with chronic mesenteric venous thrombosis were observed; nine of the 19 underwent anticoagulation. The median delay in diagnosis for patients with acute mesenteric venous thrombosis was 48 hours and did not decrease during the last decade. Mesenteric venous thrombosis recurred in 19 (36%) patients. The 30-day mortality was 27%. Long-term survival of patients with acute mesenteric venous thrombosis was significantly worse than that of those with chronic disease (36% vs 83% survival at 3 years). The patients with acute mesenteric venous thrombosis who underwent anticoagulation with and without surgical procedure had improved survival when compared with the observed group. CONCLUSION: Acute mesenteric venous thrombosis remains a lethal disease. Mortality has not improved in the last 22 years. Computed tomography is the most sensitive diagnostic test. Anticoagulation and surgical procedure enhanced survival in the acute subgroup. The underlying disease determined survival in chronic disease.

Acute Disease↗
PubMedDate not supplied

Traumatic intracerebral venous thrombosis associated with an abnormal golf swing.

OBJECTIVES: To describe the occurrence of cerebral venous thrombosis in a 40-year-old man whose cerebral event was induced by a poor golf swing, to review the literature on possible mechanisms producing venous thrombosis, and to compare this case with the literature. BACKGROUND: Headache is the most frequent symptom in patients with cerebral venous thrombosis. However, patients presenting with a headache due to cerebral venous thrombosis are uncommon. The known risk factors for thrombosis include both acquired and genetic factors. When the interaction of these two groups occurs, the magnitude of this interaction is thought to produce a dynamic state that can favor thrombosis. Our case report illustrates that moderate levels of anticardiolipin antibodies together with the mild trauma of a golf swing can induce a cerebral venous thrombosis. This case also suggests that although headache is rarely due to cerebral venous thrombosis, it should be excluded by good medical acumen and testing. RESULTS: Minor trauma induced by a poor golf swing was chronologically related to the development of a progressive cerebral venous thrombosis. The patient had none of the risk factors associated with a predisposition to venous thrombosis: hypercoagulable state, concurrent infection, pregnancy/puerperium, collagen vascular disorder, malignancy, migraine, false-positive VDRL, previous deep vein thrombosis, renal disease, factor V Leiden, or a hematological disorder. There was no anatomical abnormality that would predispose the patient to a cerebral venous thrombosis. The only laboratory abnormality was a moderate anticardiolipin antibody level (25 GPL). The patient was placed on warfarin sodium therapy and is currently without clinical sequela from the venous thrombotic event. CONCLUSIONS: Under certain circumstances, minor trauma can induce cerebral venous thrombosis. A review of the literature indicates that cerebral venous thrombosis in the presence of anticardiolipin antibodies and in the absence of systemic lupus erythematosus is a rare event. Previously, only major traumatic events have been reported to be associated with cerebral venous thromboses. The chronological development of cerebral venous thrombosis after a faulty golf swing strongly indicates that given a background of moderate levels of anticardiolipin antibodies, even minor trauma can induce a venous thrombotic event.

Adult↗
PubMed2000

Genetic susceptibility to thrombosis and its relationship to physiological risk factors: the GAIT study. Genetic Analysis of Idiopathic Thrombophilia.

Although there are a number of well-characterized genetic defects that lead to increased risk of thrombosis, little information is available on the relative importance of genetic factors in thrombosis risk in the general population. We performed a family-based study of the genetics of thrombosis in the Spanish population to assess the heritability of thrombosis and to identify the joint actions of genes on thrombosis risk and related quantitative hemostasis phenotypes. We examined 398 individuals in 21 extended pedigrees. Twelve pedigrees were ascertained through a proband with idiopathic thrombosis, and the remaining pedigrees were randomly ascertained. The heritability of thrombosis liability and the genetic correlations between thrombosis and each of the quantitative risk factors were estimated by means of a novel variance component method that used a multivariate threshold model. More than 60% of the variation in susceptibility to common thrombosis is attributable to genetic factors. Several quantitative risk factors exhibited significant genetic correlations with thrombosis, indicating that some of the genes that influence quantitative variation in these physiological correlates also influence the risk of thrombosis. Traits that exhibited significant genetic correlations with thrombosis included levels of several coagulation factors (factors VII, VIII, IX, XI, XII, and von Willebrand), tissue plasminogen activator, homocysteine, and the activated protein C ratio. This is the first study that quantifies the genetic component of susceptibility to common thrombosis. The high heritability of thrombosis risk and the significant genetic correlations between thrombosis and related risk factors suggest that the exploitation of correlated quantitative phenotypes will aid the search for susceptibility genes.

Adolescent↗