Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “THROMBOSIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 991 records · Page 55Linked to original sources
PubMedDate not supplied

Hyperhomocysteinemia is associated with venous thrombosis in patients with short bowel syndrome.

BACKGROUND: Hyperhomocysteinemia is associated with venous thrombosis and vitamin deficiency. Patients with short bowel syndrome have increased risk of venous thrombosis due to central catheters, and of vitamin deficiency due to malabsorption. The current investigation was designed to evaluate the relationship between history of venous thrombosis and current hyperhomocystinemia and vitamin deficiency in patients with short bowel syndrome. METHODS: Plasma total homocysteine (tHcy), serum vitamin B12, folate, B6, and methylmalonic acid (MMA) were measured. Venous thrombosis was documented by venogram or ultrasound. RESULTS: Ten of 17 patients had venous thromboses, including 17 of 38 observed superior and 12 of 26 inferior veins. Total homocysteine was correlated with number of thromboses. The relative risk of multiple thromboses in the highest tHcy tertile was 3.6-fold that of the lowest tertile. Vitamin B12 and folate levels were within normal limits, but B12 deficiency by MMA or tHcy level was apparent in 7 patients. Vitamin-deficient patients had higher tHcy and MMA than those without deficiency. CONCLUSIONS: Venous thrombosis in patients with short bowel syndrome is related to hyperhomocystinemia, which is also related to vitamin B12 deficiency, not detected by serum vitamin B12 concentration. Whether treatment of vitamin deficiencies and associated reduction in tHcy will reduce recurrent venous thrombosis in these patients is not known.

Absorption↗
PubMedDate not supplied

Experimental approach to prevention of catheter-related central venous thrombosis.

The role of catheter material in the formation of deep venous thrombosis during parenteral nutrition has been widely emphasized. Systematic venograms show central venous thrombosis in 20 to 33% of cases with polyethylene catheters and in 4% of cases with silicone catheters. Heparin infusion through the catheter diminishes but does not totally eliminate the risk of thrombosis. The aim of this study was to define the conditions under which the risk of thrombophlebitis was minimal. Four series of experiments were carried out, each on five rabbits. Catheters were inserted into the vena cava and, after 10 days, venograms were performed. The animals were then sacrificed, and the vena cava was macroscopically and microscopically studied. Plastic catheters were used in the first series, heparin-Benzalkonium-bonded plastic catheters in the second, silicone catheters in the third, and heparin-Benzalkonium-bonded silicone catheters in the fourth. The results revealed thrombosis of the vena cava and a fibrin sleeve around the catheters in series 1; thrombosis of the vena cava in series 2; a fibrin sleeve around the catheters in series 3; and neither thrombosis nor a fibrin sleeve in series 4. In conclusion, heparin-Benzalkonium-bonded silicone catheters appear to provide the best protection against thrombophlebitis by reducing the damage caused to the intima by the catheters and by slowing down platelet-aggregation around them.

Animals↗
PubMed2006

Effect of antimalarials on thrombosis and survival in patients with systemic lupus erythematosus.

Antimalarials have shown beneficial effects on systemic lupus erythematosus (SLE) activity. Our aim was to investigate whether antimalarials protect against thrombosis and influence survival in SLE patients. A prospective cohort including 232 patients with SLE were included in the study at the time of lupus diagnosis. End points were documented thrombosis and death due to any cause. A Cox regression-multiple-failure time survival analysis model was fitted to establish the effect of antimalarials on the development of thrombosis. Kaplan-Meier survival curves and propensity score adjusted-Cox regression analysis were performed to investigate the effect of antimalarials use on survival. Of our subjects, 204 patients (88%) were women. 230 patients (99%) were white. 150 patients (64%) had ever received antimalarials. Median time on antimalarials was 52 months (range three to 228 months). The Cox multiple-failure time survival analysis showed that taking antimalarials was protective against thrombosis (HR 0.28, 95% CI 0.08-0.90), while aPL-positivity (HR 3.16, 95% CI 1.45-6.88) and previous thrombosis (HR 3.85, 95% CI 1.50-9.91) increased the risk of thrombotic events. Twenty-three patients died, 19 of whom (83%) had never received antimalarials. No patient treated with antimalarials died of cardiovascular complications. Cumulative 15-year survival rates were 0.68 for never versus 0.95 for ever treated patients (P < 0.001). Age at diagnosis and propensity score-adjusted HR for antimalarials ever versus never users was 0.14 (95% CI 0.04-0.48). Our study shows a protective effect of antimalarials against thrombosis and an increased survival of SLE patients taking these drugs. These data support the routine use of antimalarials in all patients with SLE.

Adult↗
PubMed1998

Antibody-mediated thrombosis: relation to the antiphospholipid syndrome.

Various forms of antibody-mediated thrombosis are presented and the mechanisms involved in their pathogenesis are discussed. Antibody-mediated thrombosis includes heparin-induced thrombocytopenia and thrombosis, autoantibodies to von Willebrand factor mimicking an antiphospholipid syndrome, thrombosis following injection of the murine monoclonal antibody OKT3, hyperacute and acute xenograft rejection, and varicella-associated antibody against protein S. In several of these entities the pathogenesis of thrombosis is closely related to development of cellular procoagulant activity through tight occupancy of Fc receptors, or through complement activation, or through cell-cell interactions. Integrating the antiphospholipid syndrome into the more general category of antibody-mediated thrombosis may provide some hints as to how we could approach the study of those intriguing patients who have the clinical features of the antiphospholipid syndrome but lack those antibodies that currently characterize it.

Adult↗
PubMed2001

Idiopathic deep vein thrombosis and subsequent cancer: suggestions for a patient-oriented and practical approach.

The relationship between an idiopathic deep vein thrombosis and a cancer is well established. It is not clear yet whether all patients with an idiopathic deep vein thrombosis should be thoroughly investigated for an occult cancer or only some. As a matter of fact, once a physician is faced with a patient who has an idiopathic deep vein thrombosis, three approaches are possible, mainly: 1) a wait and see approach; 2) a limited investigation: and 3) an extensive or invasive investigation. No sure criteria for the selection of the patients who should be extensively investigated are available. Suggestions have been made in this regard. Negative family or personal history for thrombosis, advanced age, deep vein thrombosis of upper limbs, existence of silent deep vein thrombosis in contralateral leg, tendency to relapse and/or to migrate, constitutional symptoms, or smoking may represent important clues that may justify an extensive study. This patient-oriented approach is mainly based on the experience of the caring physician.

Decision Trees↗
PubMedDate not supplied

Comparison of access blood flow and venous pressure measurements as predictors of arteriovenous graft thrombosis.

PURPOSE: The purpose of the present study was to prospectively compare the predictive accuracy of static venous pressure (SVP); dynamic venous pressure (DVP) and access blood flow (ABF) in determining subsequent graft thrombosis and/or failure. METHODS: This study included 43 patients with functional arteriovenous grafts (AVG's) who underwent monthly seri-al measurements of SVP, DVP and ABF for 3 consecutive months. Patients were then followed for an additional 6 months. The primary end point was graft thrombosis. RESULTS: Six patients were excluded from the final analysis. Of the 37 patients completing the study, 7 episodes of graft thrombosis occurred within 6 months of follow up. Neither SVP nor DVP exhibited satisfactory sensitivity or specificity for graft thrombosis. Ten patients either began with or developed an ABF < 600 during the 3 months of measurements, but only 5 clotted. delta ABF of >20% provided the best combination of sensitivity (86%) and specificity (90%) for graft thrombosis. In AVG's that have an ABF<600, it is those grafts with falling ABF that appear most likely to clot in the short term. CONCLUSION: The study supports the concept that it is a falling level of access flow rather than the absolute level that is the most potent predictor of graft thrombosis.

Aged↗
PubMed2005

Superficial vein thrombosis and hypercoagulable states: the evidence.

AIM: To assess the demographic features of superficial vein thrombosis and its relation with the occurrence of hypercoagulable states. METHODS: Data were gathered from pertinent papers using a MEDLINE search and an exhaustive bibliography review. Studies were considered only when they contained material to superficial vein thrombosis and hypercoagulable states. RESULTS: The difference among the patients and the methods used made the comparison difficult and did not allow a pool analysis of the data. Superficial vein thrombosis is a common condition, and its prevalence is underestimated. Several risk factors are associated with superficial vein thrombosis, and a strong relation was seen with certain thrombophilias. CONCLUSIONS: Although superficial vein thrombosis most often is perceived as benign, it can coexist with hypercoagulable states. In patients with spontaneous onset of superficial vein thrombosis, there should be a lower threshold in testing for hypercoagulable states.

Comorbidity↗
PubMedDate not supplied

Primary axillary-subclavian venous thrombosis: is aggressive surgical intervention justified?

Multimodal (thrombolysis, surgical decompression, venous reconstruction, oral anticoagulation) treatment of primary axillary-subclavian venous thrombosis was reviewed to assess the impact of venous patency on functional outcome. Since 1996, 7 patients (6 men, 1 woman) of ages 16-53 years (mean 33 years) presented with symptomatic acute axillosubclavian venous thrombosis as a result of a recent athletic or strenuous arm activity. Five patients had undergone previous (>2 weeks) catheter-directed thrombolysis and venous angioplasty. Diagnostic contrast venography followed by repeat catheter-directed thrombolysis demonstrated abnormal (residual stenosis [n=6] or occlusion [n=1]) axillosubclavian venous segments in all patients. Surgical intervention was performed at a mean interval of 7 days (range 1-19 days) after thrombolysis and consisted of thoracic outlet decompression with scalenectomy and 1st rib resection via a paraclavicular (n=4) or supraclavicular (n=3) approach. Medial claviculectomy or cervical rib resection was performed in 2 patients. Concomitant venous surgery was performed in all patients to restore normal venous patency by circumferential venolysis (n=7) and balloon catheter thrombectomy (n=3), or vein-patch angioplasty (n=2), or endovenectomy (n=5), or internal jugular transposition (n=2). Postoperative venous duplex testing beyond 1 month identified recurrent thrombosis in 4 patients despite therapeutic oral anticoagulation. Subsequent venous recanalization was documented in 3 patients. Poor functional outcome was associated with an occluded venous repair and extensive venous thrombosis on initial presentation. A patent or recanalized venous repair present in 6 of 7 patients was associated with good functional outcome and may justify multimodal intervention in patients with primary axillosubclavian effort thrombosis presenting with recurrent thrombosis and significant residual disease after thrombolysis.

Adolescent↗
PubMedDate not supplied

Lower extremity deep venous thrombosis: vascular laboratory quality assurance without correlation between ultrasound and venography.

Venography is rarely available for comparison with ultrasonography (US) as a means for quality assurance (QA) in the detection of lower extremity venous thrombosis. New QA methods must be implemented. We compared results of multiple serial studies performed in the same extremity as a QA indicator. From a 3-year sample of close to 9,000 venous tests, we obtained a subset of 44 patients who had 331 tests in 71 lower extremities throughout the years. A positive or negative study preceded or followed by another positive or negative study was considered as a confirmed study. A negative or positive study not preceded or followed by a negative or positive study was considered as unconfirmed. Explanations were then sought to explain unconfirmed results. There were 169 (51%) and 124 (37%) confirmed positive and negative studies, respectively, and 13 (4%) and 25 (8%) unconfirmed positive and negative studies, respectively. Of the 13 unconfirmed positive tests, 2 were preceded by negative tests, 3 were preceded and followed by negative tests, and 8 were followed by negative tests. Of these 13 tests, 4 documented extensive venous thrombosis. Of the 25 unconfirmed negative tests, 11 followed treatment for venous thrombosis, 6 had recurrent thrombosis with intermittent lysis, and 8 were followed by positive tests. Considering the low probability of extensive thrombosis being a false-positive test, positive predictive value was 95% (173/182). Excluding 11 negative tests following treatment for venous thrombosis, negative predictive value was 90% (124/138) and accuracy was 93% (297/320). US versus US and literature US versus venography comparisons of these statistics were similar.

Female↗
PubMed2004

Deep vein thrombosis after total hip arthroplasty in Indian patients with and without enoxaparin.

PURPOSE: To study the incidence of deep vein thrombosis in Indian patients undergoing total hip arthroplasty with or without prophylaxis, and the effect of enoxaparin on deep vein thrombosis. METHODS: The study covered a total of 50 hips in 40 patients who underwent total hip arthroplasty. Patients were assessed for deep vein thrombosis using Doppler ultrasonography. The hips were numbered and divided into 2 groups: the odd-numbered hips did not receive any thrombo-prophylaxis, whereas the even-numbered hips received 40 mg of enoxaparin subcutaneously, once a day for 2 weeks, until the time of discharge. RESULTS: Deep vein thrombosis was not found in both groups. We found wound haematomas in 9 patients (all of whom were on enoxaparin) (p<0.05), superficial infection in 2 patients (one on enoxaparin, one not), and local bruising in 4 patients (all of whom were on enoxaparin). Major haemorrhage did not occur in any of the cases. CONCLUSION: The incidence of deep vein thrombosis in Indian patients is very low compared to that in European and American patients. Enoxaparin failed to provide any advantage to the patients. It is therefore not advisable to give prophylaxis/low-molecular-weight heparin for deep vein thrombosis to patients undergoing total hip arthroplasty without any risk factors.

Adult↗
PubMed2006

Bradykinin B2 receptor knockout mice are protected from thrombosis by increased nitric oxide and prostacyclin.

Bradykinin (BK) liberates nitric oxide, prostacyclin, and tissue plasminogen activator from endothelial cells. We hypothesized that BK B2 receptor knockout (KO) mice (BKB2R(-/-)) have increased thrombosis risk. Paradoxically, the BKB2R(-/-) mice have long bleeding times and delayed carotid artery thrombosis, 78 +/- 6.7 minutes, versus 31 +/- 2.7 minutes in controls. The mechanism(s) for thrombosis protection was sought. In BKB2R(-/-) plasma coagulation, fibrinolysis and anticoagulant proteins are normal except for an increased prekallikrein and decreased factor XI. BKB2R(-/-) mice have elevated BK 1-5 (160 +/- 75 fmol/mL, vs 44 +/- 29 fmol/mL in controls) and angiotensin II (182 +/- 41 pg/mL, vs 49 +/- 7 pg/mL in controls). Ramipril treatment shortens vessel occlusion time. BKB2R(-/-) mice have elevated plasma 6-keto-PGF1alpha (666 +/- 232 ng/mL, vs 23 +/- 5.3 ng/mL in controls) and serum nitrate (61 +/- 5.3 microM, vs 24 +/- 1.8 microM in controls). Treatment with L-NAME (NG-mono-methyl-L-arginine ester) or nimesulide shortens the thrombosis time. BKB2R(-/-) mice have increased angiotensin receptor 2 (AT2R) mRNA and protein expression. Treatment with an AT2R antagonist, PD123 319, normalizes the thrombosis time and nitrate and 6-keto-PGF1alpha. The long bleeding times in BKB2R(-/-) mice also correct with L-NAME and nimesulide therapy. In BKB2R(-/-) mice, angiotensin II binding to an overexpressed AT2R promotes thromboprotection by elevating nitric oxide and prostacyclin. These investigations indicate a pathway for thrombosis risk reduction via the plasma kallikrein/kinin and renin angiotensin systems.

Animals↗
PubMed2006

The risk of dialysis access thrombosis is related to the transforming growth factor-beta1 production haplotype and is modified by polymorphisms in the plasminogen activator inhibitor-type 1 gene.

Transforming growth factor-beta1 (TGF-beta1) and plasminogen activator inhibitor-type 1 (PAI-1) might play a role in the development of fibrosis and stenosis of hemodialysis vascular accesses. We studied polymorphisms in the TGFbeta1 (869T>C; 915G>C), and PAI-1 (4G/5G) genes in 416 hemodialysis patients (107 access thrombosis cases, 309 controls), to determine if they are related to vascular access thrombosis. Three TGF-beta1 production haplotypes (low, intermediate, and high) were defined according to the combination of polymorphisms found. The adjusted odds ratio (OR) and 95% confidence interval (CI) for access thrombosis in low TGF-beta1 producers was 7.31 (2.15-24.88; P = .001). The interaction between low TGF-beta1 production haplotype and the 4G/4G PAI-1 genotype was strongly associated with access thrombosis (adjusted OR 19.3; 95% CI 2.82-132.40; P = .003). Mean access thrombosis-free survival times in years (95% CI) were 14.65 (12.05-17.25), 11.96 (8.67-15.25), and 4.94 (3.06-6.83) in high, intermediate, and low TGF-beta1 producers, respectively (P = .044). Analysis of the synergy index and the case-only cross-product supported the presence of an interaction. We concluded that low TGF-beta1 production haplotype is a risk factor for hemodialysis access thrombosis and that in the presence of the 4G/4G PAI-1 genotype there is an additional increase in risk.

Aged↗
PubMed2006

Leukocytosis is a risk factor for thrombosis in essential thrombocythemia: interaction with treatment, standard risk factors, and Jak2 mutation status.

Leukocytes contribute to the pathogenesis of thrombosis in essential thrombocythemia (ET) through recently discovered mechanisms of activation and interaction with platelets and endothelial cells. To evaluate whether an increased leukocyte count was associated with thrombosis and whether this effect can be modulated by therapy, we analyzed the clinical course of 439 patients with ET followed at the Ospedali Riuniti di Bergamo. The strength of the association was measured at diagnosis or before thrombotic events by multivariable analyses carried out using data at baseline as well as time-varying covariates. The results showed that (1) an increased leukocyte count at diagnosis was associated with thrombosis during follow-up ("baseline analysis," relative risk [RR] 2.3, 95% confidence interval [CI] 1.4-3.9, P = .001); (2) hydroxyurea (HU) lowered leukocytosis and reduced the strength of the association between leukocytosis and thrombosis ("time-dependent analysis," RR 1.6, 95% CI 0.9-2.0, not significant [NS]); (3) the association of leukocytosis and thrombosis was more evident in untreated low-risk patients (RR 2.7, 95% CI 1.2-6.4, P = .01) compared with HU-treated high-risk patients (RR 1.6, 95% CI 0.8-3.2, NS); and (4) the presence of JAK2 V617F was not identified as a risk factor for thrombosis during follow-up despite a significant association between the mutation and leukocytosis. We suggest validation of these findings in prospective clinical studies.

Adolescent↗
PubMed2006

Mobilization versus immobilization in the treatment of acute proximal deep venous thrombosis: a prospective, randomized, open, multicentre trial.

OBJECTIVE: The aim of prescribing strict bed rest for acute deep venous thrombosis is to reduce the risk of pulmonary embolism and pain in the legs, as well as swelling. This study was performed in order to compare outcome of mobilization against 5 days of strict bed rest in patients with acute proximal deep venous thrombosis (DVT). METHODS: 103 in-patients with proximal DVT or patients admitted to the hospital because of proximal DVT were recruited to a randomized study. All patients were treated in hospital and given a lower leg and thigh compression bandage as well as therapeutic doses of the low molecular weight heparin, dalteparin-sodium (Fragmin). RESULTS: Seven of 52 patients (13.5%) in the mobile group versus 14 of 50 patients (28.0%) in the immobile group suffered at least one of the outcomes defined under the combined primary endpoint (clinically relevant pulmonary embolisms, pulmonary embolisms detectable by scintigraphy or computer tomography, progression of thrombosis or new thrombosis, nosocomial infections and/or serious adverse events) (p = 0.088), whereby serious adverse events occurred once in the mobile group and three times in the immobile group. New pulmonary embolisms over the course were seen in 10 of 50 patients (20%) with a perfusion disorder at baseline scintigraphy, while such was ascertained only in one of 52 patients (1.9%) without a perfusion disorder at baseline scintigraphy. Leg pain was reduced from 54.1 (+/-30.4) to 20.7 (+/-19.2) in the mobilized group and from 41.0 (+/-26.8) to 14.0 (+/-11.1) in the immobilized patients. Leg pain was assessed using the visual analogue scale (0 = no pain, 100 = maximum pain). More immobilized patients complained of increasing back pain (23% versus 6%) and disturbed micturition (10% versus 2%) as well as defecation (13% versus 6%) on day 5. More patients in the mobile group reported increased stress from the thrombosis and its treatment (15% versus 6%). CONCLUSIONS: No benefit of prescribing bed rest in patients with deep venous thrombosis could be detected in this study. Based on data available, strict bed rest for at least 5 days is not justified if adequate therapy with low molecular weight heparin and adequate compression is assured. It remains open whether patients with initial signs of pulmonary embolism might profit from a brief immobilization.

Anticoagulants↗
PubMed2004

Homocysteine, antiphospholipid antibodies and risk of thrombosis in patients with systemic lupus erythematosus.

Cardiovascular disease is a major cause of morbidity and mortality in patients with systemic lupus erythematosus (SLE). Antiphospholipid syndrome (APS) is one of the most important causes of thrombosis in SLE. In addition, an association between hyperhomocysteinemia and increased cardiovascular risk has also been reported. Our aim is to analyse the association of thrombosis with plasma total homocysteine (ptHcy), antiphospholipid antibodies (aPL) and other vascular risk factors in SLE patients. Fasting plasma levels of ptHcy, vitamin B12, folate, total cholesterol and creatinine were measured in 117 SLE patients. Clinical and immunological data were obtained from our prospective computerized database. aPL-positivity was defined according to Sapporo criteria. There was no association between aPL and ptHcy. ptHcy was higher in patients with arterial (median 13.02 versus 10.16 micromol/L, P = 0.010) but not venous thrombosis. In the subgroup analysis, this association was only seen in aPL-negative patients. In logistic regression, aPL (OR 6.60, 95% CI 1.86-23.34) and ptHcy (OR 1.10, 95% CI 1.01-1.19) were independently associated with arterial thrombosis. However, when hypertension, smoking and plasma total cholesterol were added to the model, only aPL (OR 7.38, 95% CI 2.02-26.91) and hypertension (OR 7.70, 95% CI 2.33-25.39), but not ptHcy, remained independently related to arterial events. aPL was the only variable independently related to venous thrombosis (OR 7.68, 95% CI 1.60-36.86). ptHcy concentrations are higher in SLE patients with arterial thrombosis. No interaction between homocysteine and aPL was found. Raised ptHcy may be a marker of increased vascular risk in aPL-negative SLE patients. The role of homocysteine as a marker of vascular risk may depend on the presence of traditional risk factors, although a modest intrinsic effect cannot be entirely excluded.

Adult↗
PubMed2007

Risk of thrombosis with lenalidomide and its prevention with aspirin.

Lenalidomide, an analog of thalidomide, is an effective new treatment for multiple myeloma. Both compounds are associated with an increased risk of venous thromboembolism, particularly when used in combination with high-dose dexamethasone. As new trials with lenalidomide are being planned and performed, investigators are placing high importance on reducing the risk of thrombosis by incorporating an antithrombotic agent into the therapeutic regimen. Low-molecular-weight heparin, warfarin, and aspirin have all been suggested as candidate drugs for thromboprophylaxis, but none of these agents have been evaluated in randomized clinical trials. A body of opinion has evolved that aspirin is very effective in preventing venous thrombosis in myeloma patients treated with lenalidomide. If correct, this view has important implications, because aspirin is inexpensive and is safer and more convenient than anticoagulants. On the other hand, aspirin is less effective than anticoagulants for preventing venous thrombosis in other high-risk groups, and therefore might not be the most appropriate choice for preventing of venous thrombosis in myeloma patients. This commentary examines the strength of the evidence supporting the effectiveness of aspirin in preventing venous thrombosis in multiple myeloma patients treated with lenalidomide. It is concluded that the evidence that aspirin is efficacious in preventing venous thrombosis in myeloma patients is based on "before/after" and retrospective studies, with potential for bias and confounders. There is, therefore, a critical need to incorporate a randomized comparison of aspirin with an anticoagulant in future trials evaluating lenalidomide in multiple myeloma.

Anticoagulants↗
PubMed2001

Hyperhomocysteinemia as a risk factor for venous thrombosis.

Classical homocystinuria is associated with arterial vascular diseases and venous thrombosis. In the last decade, several studies have been published indicating that even mild hyperhomocysteinemia is a risk factor for venous thrombosis. The 677C-->T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene is an important cause of mild hyperhomocysteinemia, but this polymorphism does not seem to be a risk factor for venous thrombosis. Studies on the interaction between hyperhomocysteinemia and other thrombotic risk factors are conflicting. Little is known about the pathophysiology of venous thrombosis in hyperhomocysteinemia. Several mechanisms proposed for vascular disease may be applied to venous thrombosis as well. However, up to now there is no satisfying model which might explain a thrombophilic state at plasma homocysteine concentrations in the range of mild hyperhomocysteinemia. The results of a first clinical intervention study are expected in 2002. As the results are pending, clinicians could perform homocysteine measurements in patients with venous thrombosis if screening for thrombophilia is indicated. Vitamin supplementation could be prescribed if homocysteine levels are elevated. However, the patient should be informed about the uncertainty of the benefits of vitamin supplementation.

Case-Control Studies↗
PubMed2003

Hyperhomocysteinaemia as a risk factor for venous thrombosis: an update of the current evidence.

Classical homocystinuria is associated with arterial vascular diseases and venous thrombosis. In the last decade, many studies, including some prospective studies, have been published indicating that moderate hyperhomocysteinaemia is also a risk factor for venous thrombosis. The 677C>T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene is an important cause of mild hyperhomocysteinaemia. Recent metaanalyses show an elevated risk of venous thrombosis for subjects with the TT-genotype. Based on the concept of 'Mendelian randomisation', this observation supports the hypothesis that hyperhomocysteinaemia is a causal risk factor for venous thrombosis. The results of one homocysteine-lowering trial regarding venous thrombosis are awaited at the end of 2003. In this paper the current evidence for hyperhomocysteinaemia as a risk factor for venous thrombosis is being discussed.

Humans↗