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PubMed2001

Effect of sepimostat mesilate on experimental venous thrombosis in rats.

Sepimostat mesilate (FUT-187: 6-amidino-2-naphthyl 4-[(4,5-dihydro-1H-imidazol-2-yl) amino] benzoate dimethane sulfonate) is a newly synthesized serine protease inhibitor. In the present study, the oral administration of FUT-187 inhibited stasis-induced venous thrombosis in rats. We supposed that such effect of this compound was caused by its inhibitory effect on coagulation. However, the dose of FUT-187 that was effective at inhibiting thrombosis (10 and 30 mg/kg, po) had no effect on the plasma recalcification time (PRCT), activated partial thromboplastin time (APTT) and prothrombin time (PT) in rats. Therefore, we investigated the fibrinolytic activity of FUT-187 in rat plasma. The results revealed that rat plasma after FUT-187 administration exhibited increased amidolytic activity for a plasmin-, tissue-type plasminogen activator (t-PA)-, urokinase-type plasminogen activator (u-PA)-, factor Xa-, factor XIa- and factor XIIa-sensitive synthetic peptide substrate. On the other hand, the inhibitory effect of FUT-187 in the thrombosis model was not affected by additional treatment with epsilon-amino-n-caproic acid (EACA), a plasmin-mediated fibrinolysis inhibitor. These results suggest that even if FUT-187 enhanced fibrinolysis, it would be independent of a plasmin-mediated fibrinolytic pathway. To characterize the fibrinolytic activity, which might reduce the thrombus weight in the thrombosis model administered FUT-187, we carried out fibrinogen zymography, and clarified that FUT-187 enhanced the formation of a 20-kDa fibrinolytic fragment. Interestingly, this fragment was not affected by t-PA. Consequently, we consider that the inhibitory effect of FUT-187 on venous thrombosis model is caused by fibrinolysis, which is attributable to the 20-kDa fragment, rather than by inhibition of thrombus formation.

Animals↗
PubMed1998

Search for genetic factors favoring thrombosis in Turkish population.

Common mutations in three genes (MTHFR 677 C-T; MS 2756 A-G; CBS Exon 8,844 ins 68) in homocysteine metabolism have been shown to cause increased plasma homocysteine levels thus causing a predisposition to thrombosis. FV 1691 G-A mutation, which is very common in the Turkish population, was also studied. As there is no existing data in the Turkish population, we aimed to study these mutations in patients with thrombosis and normal controls. The case-control study included 52 patients with the diagnosis of deep vein thrombosis (DVT) and 106 controls, consecutively selected among subjects without personal and family history of atherothrombosis. Patients with DVT were selected if Doppler ultrasonography was positive. The comparison of FV 1691 G-A mutation revealed statistically significant difference in control and DVT group. Risk assessment of double prothrombotic gene alterations indicated only FV 1691 G-A mutation as an independent risk factor for thrombosis, but our data suggested that MTHFR 677 has little effect on its own but may have synergy with FV 1691 G-A. Other possible risk genotypes at the homocysteine pathway did not have a significant effect on thrombosis. Furthermore, being heterozygote at two different loci or homozygosity at least in one locus also did not reveal a significant difference between these two groups in our population.

Case-Control Studies↗
PubMed2000

Effect of methylenetetrahydrofolate reductase 677 C-T, 1298 A-C, and 1317 T-C on factor V 1691 mutation in Turkish deep vein thrombosis patients.

Possible effect of three common mutations in (MTHFR 677 C-T; 1317 T-C; 1298 C-A) and FV 1691 G-A mutation was studied in Turkish patients with thrombosis and compared with normal controls. The case-control study included 68 patients with the diagnosis of deep vein thrombosis and 66 controls, consecutively selected among subjects without personal and familial history of atherothrombosis. Patients with deep vein thrombosis were selected if Doppler ultrasonography was positive. Only, the comparison of factor V 1691 G-A mutation revealed statistically significant difference in control (6.06%) and deep vein thrombosis (23.5%) group. Risk assessment of double prothrombotic gene alterations revealed only FV 1691 G-A mutation as an independent risk factor for thrombosis (odds ratio 4.7 [1.5-15.0]), but our data suggested that MTHFR 677 has effect on its own (odds ratio 1.97 [0.6-2.7]) but may have synergy with FV 1691 G-A (odds ratio 8.12 [2.0-25.3]). However, MTHFR 1298 A-C and 1317 T-C does not have any effect; furthermore, being heterozygote at two different loci or homozygosity at least in a locus for 677 and 1298 revealed a significant increase (odds ratio 9 and 24 [1.3-59.3 and 2.3-240.3]) between these two groups.

Case-Control Studies↗
PubMedDate not supplied

Deep vein thrombosis.

Deep vein thrombosis and its sequelae pulmonary embolism and post-thrombotic syndrome are some of the most common disorders. A thrombus either arises spontaneously or is caused by clinical conditions including surgery, trauma, or prolonged bed rest. In these instances, prophylaxis with low-dose anticoagulation is effective. Diagnosis of deep vein thrombosis relies on imaging techniques such as ultrasonography or venography. Only about 25% of symptomatic patients have a thrombus. Thus, clinical risk assessment and D-dimer measurement are used to rule out deep vein thrombosis. Thrombus progression and embolisation can be prevented by low-molecular-weight heparin followed by vitamin K antagonists. Use of these antagonists for 3-6 months is sufficient for many patients. Those with antithrombin deficiency, the lupus anticoagulant, homozygous or combined defects, or with previous deep vein thrombosis can benefit from indefinite anticoagulation. In cancer patients, low-molecular-weight heparin is more effective than and is at least as safe as vitamin K antagonists. Women seem to have a lower thrombosis risk than men, but pregnancy or use of oral contraceptives or hormone replacement therapy represent important risk factors.

Humans↗
PubMed1997

Platelet glycoprotein IIIa polymorphisms and risk of coronary stent thrombosis.

BACKGROUND: Coronary stents are an effective treatment for selected coronary stenoses. However, thrombosis of the stented segment is a major adverse complication. Platelet aggregation has a key role in stent thrombosis. We investigated whether a polymorphism of platelet glycoprotein IIIa gene (PIA2) is associated with an increased risk of coronary stent thrombosis. METHODS: 318 consecutive patients were followed up for 30 days after coronary stent insertion. The primary endpoints were death, myocardial infarction, stent-vessel occlusion, and coronary artery bypass surgery. Gel electrophoresis of PCR products was used to identify the PIA1 and PIA2 alleles. The relative risk of stent occlusion was calculated from the odds ratio on logistic regression analysis. FINDINGS: 63 (19.8%) of patients had the PIA2 allele and 255 (80.2%) were homozygous for PIA1. Baseline clinical, angiographic, and procedural features did not differ between the groups with and without the PIA2 allele. Occlusion of the stent vessel occurred in five (1.9%) patients homozygous for PIA1 and six (9.5%) patients with PIA2 allele (odds ratio 5.26 [95% CI 1.55-17.85]). On multivariate regression analysis PIA1/A2 genotype was the only significant independent predictor of stent thrombosis. INTERPRETATION: Patients with the pIA2 allele have an increased risk of coronary stent thrombosis, which may warrant antiplatelet therapy with glycoprotein-IIb/IIIa inhibitors, although bleeding complications may also increase.

Alleles↗
PubMedDate not supplied

Ancrod: the use of snake venom in the treatment of patients with heparin-induced thrombocytopenia and thrombosis undergoing coronary artery bypass grafting: nursing management.

Heparin-induced thrombocytopenia and thrombosis, also known as heparin-associated thrombocytopenia and thrombosis, was diagnosed in a 73-year-old man who had sustained a pelvic fracture, which was complicated by a left, deep-vein thrombosis. Heparin was administered and thrombocytopenia and arterial thrombosis of his left foot developed, which required amputation of three lateral toes. Four years later, the patient experienced a heart attack, and subsequently postinfarction angina developed, which was refractory to treatment with aspirin, nitrates, and beta-blockers. He was referred to a large, 750-bed teaching hospital for cardiac catheterization and possible coronary artery bypass grafting. An alternative treatment was needed for rapid anticoagulation. Ancrod, snake venom from the Malayan pit viper, was used to lower plasma fibrinogen levels, which allowed successful cardiac catheterization and coronary artery bypass grafting. We present a case study of the successful treatment of this patient with use of ancrod, and the nursing management for patients with heparin-induced or heparin-associated thrombocytopenia and thrombosis receiving this drug.

Aged↗
PubMed2003

Antibodies to anionic phospholipids and anti-beta2-GPI: association with thrombosis and thrombocytopenia in systemic lupus erythematosus.

In this study, we evaluated the prevalence and association with thrombosis and/or thrombocytopenia of IgG and IgM antibodies to cardiolipin (aCL), phosphatidic acid (aPA), phosphatidylinositol (aPI), phosphatidylserine, and beta(2)-glycoprotein I (abeta(2)-GPI) in systemic lupus erythematosus (SLE). Sera were obtained from 87 patients affected by SLE (77 of the 87 patients were females), 41 of them with a history of arterial and/or venous thrombosis. Antiphospholipid antibodies and abeta(2)-GPI were evaluated by enzyme-linked immunosorbent assay. IgG-aCL, IgG-aPA, IgG-aPI, IgG-aPS, and IgG-abeta(2)-GPI were found in 53%, 37%, 32%, 38%, and 24% of patients, respectively. IgM-aCL, IgM-aPA, IgM-aPI, IgM-aPS, and IgM-abeta(2)-GPI were detected in 15%, 17%, 18%, 14%, and 16%, respectively. With respect to antibody titer, IgG-aCL strongly correlated with all other antiphospholipid antibodies and abeta(2)-GPI of IgG isotype. Thrombosis was significantly associated with IgG-aPA (p = 0.044), IgG-aPI (p = 0.038), IgG-aPS (p = 0.026), IgG-abeta(2)-GPI, IgM-aPA (p = 0.044), IgM-aPI (p = 0.024), and IgM-aPS (p = 0.01), irrespective of antibody titer, whereas IgG-aCL were associated with thrombosis and thrombocytopenia when taken at medium-high titer (p = 0.009 and p = 0.046, respectively). Our results confirm that, besides aCL and abeta(2)-GPI, other antibodies to negatively-charged phospholipids are present in a large percentage of patients with SLE. However, it remains doubtful whether these other antiphospolipid antibodies actually represent an important parameter predictive of thrombosis and thrombocytopenia in SLE.

Adolescent↗
PubMed2003

[Bilateral internal carotid thrombosis: search for strangulation, even very ancient].

INTRODUCTION: We report 2 cases of bilateral carotid thrombosis secondary to repeated attempts of strangulation. EXEGESIS: The first case was discovered in a 31-years-old woman who complained of psychiatric manifestations, memory loss and aphasia. Subsequently she developed hemiplegia which worsened under low dose aspirin. The second case occurred in a 41-years-old woman who presented with sudden hemiplegia and aphasia. Diagnosis of bilateral carotid thrombosis based on angiocomputerized tomography or angioRMI data which suggested dissection. Thrombosis location was similar: bilateral, symmetric, close to the carotid bifurcation. Both women had atherosclerosis risk factors: current smoking, use of estrogen containing pill, dyslipidemia and/or familial cardiovascular history. Search for thrombophilia was negative. Both women had been victims of intimate partner violence with repeated attempts of strangulation, but they were stopped 8 and 6 years before the diagnosis of carotid thrombosis. Several private interviews were necessary before knowing the exact cause. CONCLUSION: Symmetrical bilateral thrombosis of internal carotids near the bifurcation should lead to evoke repeated attempts of strangulation, even if there are arterial risk factors, and especially if the patient is a middle-aged female. The therapy is not codified but prolonged anticoagulation is generally prescribed.

Adult↗
PubMed1998

[Heparin-induced thrombopenia: rapid regression of thrombopenia and thrombosis after plasma exchange. Case report].

INTRODUCTION: Heparin-induced thrombocytopenia with thrombosis is a rare but severe adverse reaction to heparin therapy, whose management is difficult. After heparin withdrawal, the initiation of an alternative anticoagulant therapy, such as recombinant hirudin or danaparoid, is strongly recommended before vitamin K antagonists are effective. Several reports of the efficacity of plasma exchanges in patients with life-threatening thrombosis have been made. EXEGESIS: We report on a patient with severe aortic thrombosis related to heparin therapy in whom a unique plasma exchange resulted in both dramatic improvement in the platelet count and marked reduction of the thrombosis. CONCLUSION: This case provides further evidence that plasma exchanges can be useful in the management of heparin-induced thrombocytopenia with thrombosis. They are rapidly efficient and can be used before heparin alternative treatment is effective.

Anticoagulants↗
PubMed1993

Acute renal allograft dysfunction in the setting of deep venous thrombosis: a case of successful urokinase thrombolysis and a review of the literature.

Acute renal allograft vein thrombosis is a rare but serious complication of renal transplantation. When occurring in the early posttransplant period it is usually associated with surgical complications and often results in the loss of the graft. At later stages, when graft function has stabilized, its development may then be associated with underlying disorders such as glomerulonephritis, immunosuppressive therapy, increased hematocrit, acute rejection, or extension of lower extremity venous thromboses. We report a case of acute allograft dysfunction occurring in the setting of extensive deep vein thrombosis. In our patient, thrombosis in the setting of acute graft tenderness and swelling, anuria, and an increasing creatinine strongly suggest a diagnosis of acute allograft renal vein thrombosis. We describe a successful reversal of acute renal failure through urokinase thrombolysis and review the current literature on the use of thrombolytic agents for the treatment of acute renal allograft vein thrombosis.

Acute Kidney Injury↗
PubMed1983

Mild unilateral proteinuria and renal vein thrombosis associated with oral contraceptive usage.

A previously healthy 15-yr-old female taking oral contraceptives presented with acute, isolated, unilateral renal vein thrombosis as documented by arteriography and venography. Mild proteinuria (760 mg/24 hr) was localized solely to the thrombosed kidney by selective ureteral collections. The case illustrates an oral contraceptive associated renal vein thrombosis in the absence of either inferior vena cava thrombosis, bilateral proteinuria, or the nephrotic syndrome. This patient's proteinuria and clinical course suggest that nephrotic syndrome is a cause of renal vein thrombosis rather than an effect of renal vein thrombosis. The finding of localized, unilateral proteinuria is discussed.

Acute Disease↗
PubMed2002

Chlamydia pneumoniae, systemic inflammation and the risk of venous thrombosis.

Inflammatory mediators are involved in activation of the coagulation system, and elevated plasma concentrations of IL-6 and IL-8 are associated with an increased risk of venous thrombosis. Using serologic and molecular biologic tests, we investigated in a case-control study on patients with recurrent venous thrombosis the association between Chlamydia (C) pneumoniae and venous thrombosis and we evaluated the relation between C. pneumoniae serology and the cytokines IL-6 and IL-8. The presence of C. pneumoniae antibody titers > or = 1:16 was not associated with an increased risk of venous thrombosis (odds ratio 0.8 95% CI, 0.4-1.7). Circulating C. pneumoniae-DNA was detected in only one patient and two control subjects. IgG antibody titers against C. pneumoniae were not correlated with the concentrations of IL-6 and IL-8. These results indicate that the inflammatory process shown in patients with venous thrombosis is not related to C. pneumoniae.

Adult↗
PubMed1997

Arterial thrombosis induces early upregulation of intercellular adhesion molecule in the media.

PURPOSE: Thrombosed peripheral vessels that are pharmacologically or mechanically recanalized have diminished long-term patency rates compared with vessels that are repaired before occlusion. We hypothesized that thrombosis induces proinflammatory changes in the arterial media that may contribute to postthrombotic vascular remodeling. METHODS: We studied expression of intercellular adhesion molecule (ICAM), a mediator of leukocyte recruitment, in the arterial wall after thrombosis. Thrombosis was induced in rabbit superficial femoral arteries by embolizing polystyrene beads (Thr-emb) or by ligation (Thr-lig). Control vessels were dissected but not ligated (C-dis) or were subjected to bead embolization and immediate removal (C-emb). Arterial wall ICAM expression was measured by indirect immunohistochemical analysis at 6 hours, 24 hours, and 1 week. Staining intensity was graded from 0 (none) to 4 (intense) by observers who were blinded to the experimental conditions. RESULTS: No increase in ICAM expression by thrombosed vessels was present at 6 hours. After 24 hours, ICAM expression in the media of thrombosed vessels was increased (Thr-emb, 2.3 +/- 0.5; Thr-lig, 2.0 +/- 0) compared with control vessels (C-dis, 0 +/- 0; C-emb, 0.8 +/- 0.5; p < 0.004). This difference became more marked at 1 week. ICAM staining localized to actin-staining regions of the media. CONCLUSIONS: Arterial thrombosis, but not surgical injury, induces pronounced early and sustained upregulation of ICAM expression in smooth muscle-containing regions of the arterial media. Upregulation of ICAM is likely to promote recruitment of inflammatory cells or mediate vascular remodeling after luminal thrombosis.

Animals↗
PubMed1999

Patterns and distribution of isolated calf deep vein thrombosis.

PURPOSE: In the search for calf deep vein thrombosis (DVT) with color-flow duplex scanning (CFDS), most vascular laboratories investigate only the posterior tibial and peroneal veins. Few laboratories assess the soleal and gastrocnemial veins. This study was designed to determine the patterns and distribution of isolated calf DVT, including the soleal and gastrocnemial veins. METHODS: In the last 3 years, 5250 patients (mean age, 66 +/- 15 years; range, 22 to 93 years) were referred to the vascular laboratory for clinical suspicion of DVT and underwent examination with CFDS. All superficial and deep named veins, excluding the anterior tibial from groin to ankle, were imaged. Of the deep veins in the calf, the peroneal, the posterior tibial, the gastrocnemial, and the soleal veins were examined throughout their length. RESULTS: DVT was detected in 14% of the patients. Isolated calf DVT was detected in 282 limbs of 251 patients (4.8%). No significant difference was noted for the sex (114 men vs 137 women; P =.15) or the limb preference (145 left vs 137 right; P =.5). The peroneal veins were most frequently involved, with 115 limbs (41%) affected. The soleal veins were involved in 109 limbs (39%), followed by the posterior tibial in 105 limbs (37%) and the gastrocnemial in 79 limbs (29%). Thrombus in the soleal vein alone was found in 57 limbs (20%), in the gastrocnemial in 48 limbs (17%), in the peroneal in 41 limbs (15%), and in the posterior tibial vein in 35 limbs (12%). Thrombus confined to a single or paired vein was found in 181 limbs (64%). Thrombus involving two different veins (27%) was the second most frequent pattern, and thrombus in three (7%) or four (1.4%) different veins was less prevalent. Isolated thrombosis in veins not routinely investigated was found in 113 limbs (40%; soleal, n = 57; gastrocnemial, n = 48; soleal + gastrocnemial, n = 8). Multifocal origin of thrombosis, defined as thrombi in two different veins that do not anatomically communicate, was identified in 63 limbs (22%). CONCLUSION: Forty percent of the patients with acute isolated calf DVT would be judged to have normal CFDS examination results if the muscular veins in the calf were not imaged. Multifocal origin of thrombosis was found in 22% of the involved limbs. The prevalence of thrombosis in any calf vein either alone or in combination is comparable. Accordingly, the soleal and gastrocnemial veins should be examined routinely.

Adult↗
PubMed1994

[Mesentric venous thrombosis. Risk factors, treatment and outcome. An analysis of 18 cases].

Eighteen patients with an acute thrombosis of the splanchnic veins were reviewed. Most of apparently idiopathic cases of splanchnic vein thrombosis are related to an increased coagulation related to a congenital or acquired defect of haemostasis. The aim of this study was to assess the effects of a new and effective treatment. Nine male and 9 female patients (range of age: 19 to 81 years) experienced a mesenteric venous thrombosis. There were 14 mesenteric vein thromboses with infarction, two transient mesenteric venous ischaemias without bowel infarction and two acute thromboses of the splanchnic veins without bowel ischaemia. A coagulopathy was detected in seven patients: oral contraception, protein C (PC) or antithrombin III (AT III) congenital deficiencies, acquired deficiency of AT III, PC and protein S (PS), polycythaemia in the post-partum period and primary myeloproliferative disorder. No coagulopathy was associated with thrombosis in eight cases: mesenteric haematoma, splenomegaly, cirrhosis, appendicectomy, cholescytectomy, chronic heart failure, treatment with beta-adrenergic receptor antagonist and digitalis, stenosis of the portal anastomosis after liver transplantation. Twelve patients required surgery: eight intestinal bowel resections with immediate anastomosis, four resections without immediate anastomosis. Only one patient underwent a second look for a repeat bowel resection. No death occurred in the early postoperative period and 17 out of 18 patients were alive after 12 years. An oral anticoagulant therapy was undertaken from two months to seven years. However, three patients suffered a recurrent thrombosis. Two of them required a long-term anticoagulation. Six patients experienced a portal hypertension and oral anticoagulants were discontinued in three of them because of bleeding oesophageal varices. Six patients were treated only by unfractionated heparin (UFH) or low molecular weight heparin (LMWH) followed by oral anticoagulants. After laparotomy, two were only treated with UFH without any bowel resection, as mesenteric venous ischaemia was too extensive. These observations suggest that the choice between an appropriate medical or surgical treatment is important and must be discussed. Since 1989, the therapeutic choice has been modified by ultrasonography and contrast enhanced computed tomographic scan which confirms diagnosis, allows to follow up and check the effects of anticoagulation and to choose the time for surgery. When the diagnosis is established and the patient's risk is low, the IU . kg(-1) . d(-1) to obtain an antifactor Xa activity between 0.3 and 0.6 antiXa IU mL(-1). When the diagnosis is uncertain and the patient's risk if high a laparotomy is required.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1996

Thrombosis and hemorrhage in oncology patients.

As outlined in this review, patients with cancer may harbor many alterations of hemostasis. These are multifaceted and must be considered when trying to control hemorrhage or thrombosis in cancer patients. Also, hemorrhage or thrombosis is often the final fatal event in many patients with metastatic solid tumor or hematologic malignancies. Patients with malignancy present a major clinical challenge in this new era of oncologic awareness and more aggressive care, which has led to prolonged survival for patients and a longer time frame during which these complications may develop. Therefore, these complications are occurring more commonly. It is important to realize that these alterations of hemostasis exist and must be approached in a sequential and logical manner with respect to diagnosis; only in this way can responsible, efficacious, and rational therapy be delivered to patients. By far the most common alteration of hemostasis in malignancy is that of hemorrhage associated with thrombocytopenia, either drug-induced, or radiation-induced, or from bone marrow invasion. Hemorrhage resulting from DIC, however, is also quite common and may present as hemorrhage, thrombosis, thromboembolus, or any combination thereof. Many antineoplastic drugs and radiation therapy may lead to or significantly enhance hemorrhage in patients with malignancy. Thrombosis, also commonly seen in patients with malignancy, is often a manifestation of low-grade DIC. When approaching the patient with malignancy and either hemorrhage or thrombosis, all the potential defects in hemostasis must be considered, defined from the laboratory standpoint, and treated in as precise and logical manner as possible.

Hemorrhage↗
PubMed2006

Effort thrombosis of the upper extremities related to an arm stretching exercise.

"Effort" axillary-subclavian vein thrombosis (Paget-Schroetter syndrome) is an uncommon deep venous thrombosis due to repetitive activity of the upper limbs. Most cases of this condition are related to strenuous or prolonged sport or occupational activities, while others are associated with endogenous or exogenous risk factors. We report the case of a 43-year-old, previously healthy, male who developed right axillary-subclavian venous thrombosis, which was possibly associated with an exercise involving arm extension and shaking in a posture of shoulder abduction and outstretched for 10 minutes on 2 consecutive days. The condition improved but returned with increased severity when he resumed the exercise after a 2-day break, when he presented with a swollen and bluish arm at the emergency department. Sonographic examination showed moderate thrombotic stenosis of the right axillary vein. Effort thrombosis was diagnosed after ruling out associated coagulopathy or concomitant malignancy. External compression of the accessory ribs or lymph nodes were not detected. He was treated with low molecular weight heparin, followed by oral anticoagulant therapy for 6 months. Only partial resolution of thrombosis was achieved after 6 months of anticoagulant therapy, but pulmonary embolism did not occur during 18 months of follow-up. This case illustrates that, although unusual, Paget-Schroetter syndrome can occur in a healthy patient as a result of mild to moderate exercise.

Adult↗
PubMed2001

[Post-varicella thrombosis and factor V Leiden mutation].

BACKGROUND: Varicella is a benign infectious disease that is rarely complicated by thrombosis. Factor V Leiden (FVL) mutation is presently recognized as the most common inherited cause of thrombosis. From a case report the link between varicella associated thrombosis and FVL is discussed. CASE REPORT: An eight year-old boy was admitted on 15th day of a varicella infection for difficulty to walk and painful legs. Doppler ultra sound of the lower limbs venous system showed thrombosis of the left iliac vein and femoral veins. Thrombophilia work-up revealed a FVL heterozygotic status for the patient. Biological screening for molecular abnormalities associated with thrombophilia led to the detection of a heterozygous inherited FVL mutation in the patient. Response to heparine followed by oral anticoagulant treatment was good. CONCLUSION: Thrombosis associated with varicella in child is a rare event. We recommend to realize a thrombophilia screening in such patients. We also support varicella vaccination of children identified as having constitutional prothrombotic disorders like FVL mutation.

Chickenpox↗