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PubMed1996

Use of streptokinase in four dogs with thrombosis.

Four dogs with thrombosis were referred for diagnostic testing and were subsequently treated by the use of streptokinase. The range of duration of clinical signs associated with thrombosis was 6 to 120 days. Causes of thrombosis were heart disease (1 dog), protein-losing nephropathy and hyperadrenocorticism (1), hyperadrenocorticism (1), and idiopathic (1). Possible factors that predisposed dogs to hypercoagulability included hypertension (2 dogs) and diabetes mellitus (1). All dogs were treated for underlying disease by use of supportive care. The first dog was treated with a loading dose of 250,000 U of streptokinase, i.v., with a subsequent maintenance dosage of 100,000 U/h, i.v., and also was treated with anticoagulant. The subsequent 3 dogs were treated with a loading dose of 90,000 U of streptokinase, i.v., and maintenance dosage of 45,000 U/ h, i.v., at various intervals. These dogs also were treated with anticoagulant. Three dogs had minor hemorrhage as an adverse effect to streptokinase infusion, but they did not require treatment for the hemorrhage. Complete resolution of the thrombus was observed in 3 dogs, and partial resolution of the thrombus was observed in the other dog. In all dogs, partial or complete resolution of clinical signs associated with thrombosis was seen. Streptokinase may be an effective treatment for dogs with thrombosis.

Adrenocortical Hyperfunction↗

PubMed1996

Gene mutations in 21 unrelated cases of phenotypic heterozygous protein C deficiency and thrombosis. Protein C Study Group.

Mutations have been identified in the protein C gene in 21 patients with venous thromboembolism and phenotypic heterozygous protein C deficiency. In 20 probands, single mutations were the only abnormalities identified by sequencing all coding regions, intron exon boundaries and the promoter region back to -1540. In one proband 2 mutations were identified and in another family 2 mutations were identified (but not both in the proband). Of the 23 mutations, 18 resulted in predicted amino acid substitutions, 3 were mutations resulting in stop codons, one was a mutation within a consensus splice sequence and another a 9 base pair insertion within exon 5 (this region within exon 5 is proposed as a deletion/insertion hot spot). A novel polymorphism was also, uniquely, identified in the propeptide region of the molecule (Pro-21Pro; CCT to CCC) in a kindred from Hong Kong. Cosegregation of the protein C gene mutation with protein C deficiency could be determined in 13 families. In a further family, phenotypic protein C deficiency and the genetic mutation cosegregated in only 4/5 members. The first thrombotic incident occurred in the probands between the ages of 11 and 59 years and 12 individuals suffered recurrent thrombosis. Thrombosis occurred in at least one other family member in 9/21 families, but in 2 of these it was inconsistently associated with protein C deficiency. An independent genetic risk factor, factor V Arg506Gln (FV Leiden) was identified in 2 probands (and 3 family members) and in 4 protein C deficient members of a third family but not in the proband. The results suggest that in the majority of probands with thrombosis and phenotypic protein C deficiency, a single protein C gene mutation is associated with thrombosis. However, it is also possible that additional unknown genetic risk factors contribute to the thrombotic risk. An added, acquired, risk factor leads to thrombosis at an early age (< 25 years).

Adolescent↗

PubMed1996

[Portal thrombosis disclosing antiphospholipid syndrome. 2 cases].

The presence of serum antiphospholipid antibodies is associated with arterial and venous thrombosis. We report two cases of portal vein thrombosis associated with serum antiphospholipid antibodies. In our two patients, systemic lupus erythematosus, chronic liver disease, hepatocellular carcinoma, myeloproliferative disorders and coagulation inhibitor deficiency were excluded after extensive tests were performed to diagnose portal vein thrombosis and after a follow-up period of 6 and 7 years, respectively. The test for serum antiphospholipid antibodies was positive on two occasions in both patients. Both patients were treated with endoscopic sclerotherapy for bleeding esophageal varices and with long term anticoagulant therapy for the prevention of recurrent thrombosis. These two cases suggest that serum antiphospholipid antibodies should be investigated in patients with portal vein thrombosis of unexplained etiology.

Adult↗

PubMed1997

Thrombosis, leiomyoma and GnRH-a therapy. A case report.

BACKGROUND: Diverse complications have been reported in association with the growth and medical treatment of uterine leiomyomata. Infarction and necrosis may be common and incite complications from parasitic vascular attachment, pain and thrombosis. The rarity of severe complications in this situation warrants presentation of the following unique association. CASE: A 33-year-old female, gravida 1, para 1, was treated with gonadotropin-releasing hormone agonist (GnRH-a) for three months prior to laparotomy and removal of a solitary, 5,190-g, pedunculated myoma. The mass had secured an additional vascular supply from the transverse colon and omentum. Although the immediate postoperative course was uncomplicated, delayed onset of abdominal pain and fever lead to the diagnosis of superior mesenteric and portal vein thrombosis. Portal vein thrombosis responded to thrombolytic infusion into the superior mesenteric artery. Superior mesenteric vein thrombosis persisted, with evidence of early vascular recanalization. After six weeks of additional anticoagulation, assessment by computed tomographic scan showed complete resolution of all thrombi. CONCLUSION: While thrombosis has been reported with GnRH-a therapy in men with prostate cancer, its association with treatment in this benign case may have been a consequence of the massive tumor size. Steroid hormone deprivation potentially contributed to neovascularization and bowel involvement.

Adult↗

PubMed1997

Evaluation of original and modified APC-resistance tests in unselected outpatients with clinically suspected thrombosis and in healthy controls.

APC-resistance is the most common hereditary condition associated with venous thrombosis. It is in a majority of cases due to a single point mutation in the factor V gene (FVR506Q). Currently used functional APC-resistance tests have 85-90% sensitivity and specificity for the FVR506Q mutation. A modified test which includes predilution of patient plasma in factor V depleted plasma has increased the sensitivity and specificity for the factor V mutation. However, neither the original nor the modified APC-resistance test have been evaluated in patients with acute thrombotic events. We have therefore used the original and the modified APC-resistance tests in 220 patients with clinically suspected acute deep venous thrombosis and in 278 healthy controls. The FVR506Q mutation was determined in all patients. The patients were classified as either DVT (deep venous thrombosis)-negative or DVT-positive depending on the outcome of contrast phlebography. In individuals with normal factor V genotype, the original APC-resistance test gave significantly lower APC-ratio values both in DVT-positive and DVT-negative patients than in healthy controls. The specificity of the original APC-resistance test for the FVR506Q mutation in controls and in DVT-negative and DVT-positive patients were 85%, 54% and 28%, respectively, when a cut off APC-ratio of 3.2 which insured 100% sensitivity was used. Using the modified APC-resistance test, essentially no difference in APC-ratios between patients with normal factor V genotype and healthy controls with normal factor V genotype was observed. The modified APC-resistance test had a specificity for the FVR506Q mutation of 98.8% at an APC-ratio cut off of 2.1 which ensured 100% sensitivity. The original APC-resistance test gave lower APC-ratios in women than in men and in patients with acute thrombosis as compared to controls. In conclusion, the modified APC-resistance test is highly sensitive and specific for the FVR506Q mutation. This test can be used in clinical practice as an easy to perform screening test for the FVR506Q allele. Moreover, the test performs equally well in patients with acute suspected venous thrombosis as in healthy controls.

Adult↗

PubMed1997

Resistance to activated protein C as risk factor for thrombosis: molecular mechanisms, laboratory investigation, and clinical management.

Protein C (PC) is the key component of a natural anticoagulant pathway that is activated on the surface of endothelial cells by thrombin bound to thrombomodulin. Activated protein C [APC] cleaves and inhibits membrane bound factor Va and factor VIIIa, which leads to specific and efficient downregulation of the coagulation pathway. In these reactions, protein S (PS) and intact factor V (FV) function as cofactors to APC. Inherited deficiencies of PC, PS, or antithrombin were until recently the major genetic causes of familial venous thrombophilia, but they were found in less than 5% to 10% of patients with thrombosis. The situation changed dramatically with the description in 1993 of resistance to APC as a major risk factor for venous thrombosis. Inherited APC resistance, which is found in 20% to 60% of patients with venous thrombosis, is caused by a single point mutation in the FV gene predicting substitution of arginine [R] at position 506 with a glutamine (Q). The mutation, which is the result of a founder effect, is common in Caucasians with 1% to 15% prevalence in the population, whereas it is not found in other human races. Mutated FV (FVR506Q, FV:Q506 or FV Leiden) has normal procoagulant properties but shows partial resistance to APC, which results in a hypercoagulable state conferring a lifelong increased risk of thrombosis. As a result of its high prevalence, the FV mutation is not uncommon among patients with other inherited defects such as deficiency of PS, PC, or antithrombin. Those having combined defects have a higher incidence of thrombosis, and it is now recognized that severe thrombophilia is a typical multigenetic disease. The high prevalence of the FVR506Q mutation and the availability of easy functional and genetic tests will profoundly influence the development of therapeutic and prophylactic regimens and will probably result in a decreased incidence of thromboembolic events.

Blood Coagulation↗

PubMed1997

Combination of activated protein C resistance and antibodies to phospholipids in the development of thrombosis.

An insufficient response to activated protein C (APC) resistance and antibodies against phospholipids (PLa) are frequent laboratory findings associated with thrombosis. Studies investigating the coexistance of these two factors in thrombophilic patients and in patients with autoimmune disorders are summarized. The investigation of thrombophilic patients has revealed PLa in 35%. About half of these patients had a combination of PLa and APC resistance proved by the Arg506-Gln mutation in factor V (FV). A combination of APC resistance with PLa in this group of patients did not increase the risk of thrombosis recurrence. In the PLa-positive patients with autoimmune disorders having thrombosis in 10% to 56%, the incidence of the Arg506-Gln mutation in FV was significantly lower and varied between 2% and 9%. A known ability of PLa to induce APC resistance experimentally was often a reason to avoid the determination of APC response in PLa-positive patients. We suggest that PLa may play a dual role in the development of thrombosis in the carriers of the Arg506-Gln mutation in FV. On the one hand, PLas favor thrombosis by maintaining the APC response at a constantly low level. On the other hand, preventing the interaction of coagulation proteins on the phospholipid surface PLa may protect them from hypercoagulation.

Antibodies, Antiphospholipid↗

PubMed1997

[Successful direct thrombolysis in a patient with extensive dural sinus thrombosis induced by danazol].

A 43-year-old woman was suffered from an increasing headache with nausea and vomiting for nine days. She had received danazol 400 mg daily for endometriosis last two months. CT scan and neurological examinations revealed no evidence of abnormality. MRI showed isosignal intensity on T1-weighted images and high signal intensity on T2-weighted images in the superior sagittal, right transverse, sigmoid and straight sinuses suggesting thrombosis. With angiography, we confirmed extensive dural sinus thrombosis in the superior sagittal, straight, right transverse and sigmoid sinuses. She, then, developed progressing neurological deterioration with dysarthria and drowsy. Microcatheter was placed directly into the thrombus at dural sinus via transfemoral route. Thrombolytic therapy with urokinase was performed in right transverse, confluens sinuum, superior sagittal and straight sinuses. Successful recanalization with remarkable improvement of symptoms was achieved except right transverse sinus. We believe danazol played a role in the occurrence of dural sinus thrombosis. MRI and MRV were noninvasive and useful for diagnosis and follow-up of dural sinus thrombosis. Direct thrombolysis should be considered for dural sinus thrombosis, especially when clinical symptoms are rapidly deterioration with conventional anticoagulant therapy.

Adult↗

PubMed1997

The value of duplex ultrasound in the follow-up of acute calf vein thrombosis.

Calf veins are one of the most common sites for deep vein thrombosis (DVT) but the management of patients with calf vein thrombosis differs. Many centres consider pharmacological treatment unnecessary and elect not to examine the calf veins with duplex ultrasound. Others advocate monitoring the thrombus with serial venous duplex scanning and commence treatment if there is evidence of propagation. In this laboratory duplex scanning of the calf veins is routinely carried out as part of the diagnostic procedure for DVT. A study was carried out where 50 patients with isolated calf vein thrombosis were followed over a one year period to determine the long term outcome in the calf veins. Note was made of the choice of treatment. A high percentage (85%) were treated with heparin/warfarin and only 15% received no pharmacological treatment. There was a propagation rate of 15%, one of which resulted in a fatal pulmonary embolus (PE). The DVT recurrence rate was 14% within the year. No long term effects such as valvular damage were noted during the follow-up period. The results suggest the need for better guidelines for the diagnosis and treatment of isolated calf vein thrombosis. Future studies with larger groups of patients need to be carried out to determine the significance of the recurrence rate and the long term effects. Duplex scanning enhances the diagnosis of calf vein thrombosis and should be used for closer observation of potential thrombus propagation.

Anticoagulants↗

PubMed1996

[Prevalence of thrombosis in secondary antiphospholipid-protein syndrome].

Antiphospholipid-protein syndrome (APS) comprises venous and arterial thrombosis, spontaneous abortion and thrombocytopenia in patients with antiphospholipid-protein antibodies (APA). Such antibodies are detected by immunoenzymatic (ELISA) methods (e.g. anticardiolipin antibodies-ACL) or coagulation assays (lupus anticoagulant-LA). APS in patients showing other symptoms of autoimmune disease is called secondary antiphospholipid-protein syndrome. The aim of the study was to find relation between history of thrombosis and APA in a group of patients with lupus erythematosus and lupus-like disease. Lupus anticoagulant was detected by a three step procedure using phospholipid dependent clotting assays and anticardiolipin antibodies were measured by ELISA. We studied 95 subjects (91 women, 4 men) suffering from lupus erythematosus (67 patients) and lupus-like-disease (28 patients). Lupus anticoagulant was found in 26, anticardiolipin antibodies IgG in 34 and IgM in 27 subjects. In a retrospective study 40 thrombotic events were detected in 36 patients; deep vein thrombosis in 19, pulmonary embolism in 7, ischaemic CNS events in 13 and myocardial infarction in one. Thrombosis was present more often in subjects with LA (61%) and ACL IgG (52%) than in subjects without these antibodies (24%) (p = 0.004 and 0.015, respectively). ACL IgM antibodies were not related to thrombotic episodes. The ACL IgG antibodies and LA are helpful in identifying subjects at risk factors of venous and arterial thrombosis among patients suffering from lupus erythematosus and lupus-like disease.

Adolescent↗

PubMed1996

[Mesenteric-portal thrombosis after hematologic splenectomy].

Venous thrombosis of the portal system following splenectomy for haematological diseases is uncommon, being reported with an incidence of 0.2 to 6%. Diagnosis may be difficult and the clinical presentation varies greatly. We report 4 cases, included in a consecutive series of 350 splenectomies for hematological diseases. Case 1: a man of 22 years, operated on for autoimmune hemolytic anemia developed severe and generalized abdominal pain 20 days after splenectomy. The coeliac arteriography showed a thrombosis of the portal system. The laparotomy revealed segmentary small bowel necrosis. Outcome after intestinal resection was uneventful. Case 2: a man of 56 years, operated on for essential thrombocythemia had the laboratory findings of acute hepatic failure 28 days after splenectomy. Doppler ultrasonography revealed a portal vein thrombosis. He was treated with heparin. Case 3: a man of 69 years, operated on for acquired idiopathic anemia, developed asthenia and fever 23 days after splenectomy. The ultrasonography showed a portal vein thrombosis. He was successfully treated with heparin. Case 4: a man of 20 years, operated on for Minkowsky-Chauffard hemolytic anemia developed a severe and generalized abdominal pain and fever 13 days after splenectomy. The CT-scan showed a thrombosis of the portal system. Outcome after thrombectomy and regional thrombolysis was uneventful. The aim of this presentation is to review the pathophysiological diagnosis, therapeutic and prophylactic aspects of this serious complication of splenectomy.

Adult↗

PubMedDate not supplied

Lupus anticoagulants and thrombosis: the role of phospholipids.

BACKGROUND AND OBJECTIVE: Lupus anticoagulants (LAs) are loosely defined as immunoglobulins that inhibit phospholipid dependent coagulation assays. Antiphospholipid antibodies (APAs) are those immunoglobulins that are observed to bind to phospholipids, usually cardiolipin, in ELISA type assays. Interest in these antibody populations derives from the observation that rather than being associated with bleeding disorders as would be expected, they correlate with an increased risk of thrombosis. Many mechanisms have been proposed to account for the prothrombotic activity of some LAs and APAs. These mechanisms are as diverse as inhibition of the production of endothelial prostacyclin synthesis or impaired fibrinolysis to interaction with beta 2-glycoprotein 1 or prothrombin bound to phospholipids. For the purposes of this review, we would like to focus on a potential mechanism that has been proposed by several labs in addition to our own, namely inhibition of the protein C anticoagulant pathway. INFORMATION SOURCES: The authors have been working in this field and contributing original papers. In addition, the material examined in the present paper includes articles published in journals covered by the Science Citation Index and Medline. STATE OF ART AND PERSPECTIVES: In general, correlation of phospholipid specificity and thrombosis has not been performed on a large scale. We were therefore led to ask two questions. Are the membrane requirements of the protein C anticoagulant pathway really the same as those for the procoagulant complexes? Secondly, if they are not, do the membrane requirements of the anticoagulant complexes mimic those of the thrombotic LAs? The membrane requirements for the activated protein C anticoagulant complex differ from those of the prothrombinase complex. These requirements, i.e. the need for phosphatidylethanolamine for optimal activity, mimic the lipid requirements for at least a population of lupus anticoagulants associated with thrombosis. These observations may provide both the specificity and the link between the activated protein C pathway, lupus anticoagulants and thrombosis. Of course, no conclusion is ever that black and white. Only future studies into the fine specificity of lupus anticoagulants and anti-phospholipid antibodies associated with thrombosis will bear out the hypothesis that those directed towards the activated protein C pathway will be predictive of thrombotic risk.

Humans↗

PubMedDate not supplied

[Results of surgical treatment of pregnancy-associated pelvic vein thrombosis].

We report the results of surgical treatment of iliofemoral vein thrombosis in 49 pregnant women in a seven years period. The patients mean age was 26.5 years (range 18-41 years). Isolated descending pelvic vein thrombosis (PVT) occurred between the 20th and 36th week of pregnancy and was located predominantly left sided. 89.8% of PVT developed in the late period of gestation, three cases of pelvic vein thrombosis were diagnosed after vaginal delivery. An iliac vein spur in one patient and an AT-III deficiency in two cases were registered as additional risk factors. After venous catheter thrombectomy an arteriovenous fistula between the superficial femoral artery and the femoral vein was performed to increase blood flow and velocity in the pelvic veins. Abdominal delivery was performed simultaneously, if thrombosis occurred after the 34th week of pregnancy. Late re-thrombosis was registered in 4 patients (9.0%) after a mean follow-up of 42 months. We have seen symptoms of mild, not life threatening pulmonary embolism in two patients on the first postoperative day (complication rate 4.0%). Re-occlusion rate was high (3/5) after surgical thrombectomy carried out between the 20th and 26th week of gestation. Risk factors were an AT III deficiency in two cases and the continued compression syndrome of the pelvic veins caused by the enlarging uterus. In the late period of gestation surgical thrombectomy of PVT is the preferential method of treatment in selected patients with good therapeutical results. The operation reduces the risk of future venous insufficiency and post-thrombotic syndrome in the young female patients.

Adolescent↗

PubMedDate not supplied

[Clinical significance and predictive value of laboratory tests in thrombosis associated with antiphospolipid antibodies].

Antiphospholipid antibodies are a wide ranging, heterogeneous family of autoantibodies, formerly believed to be directed to anionic phospholipids. Recent research, however, has confirmed that they are directed to plasma proteins bound to suitable (phospholipid) anionic surfaces. The most well-known and best characterized antigens are beta 2-glycoprotein I, recognized by anticardiolipin antibodies, and prothrombin, recognized by most lupus anticoagulants. Lupus anticoagulants are generally identified on the basis of their capacity to prolong the phospholipid-dependent coagulation tests. Two types of lupus anticoagulants, anticardiolipin-type A, and antiprothrombin antibodies, whose presence is associated with different coagulation profiles, have been identified. Anticardiolipin-type A and antiprothrombin antibodies may be detected also by specific immunoassays. The capacity of several methodologies to detect antiphospholipid antibodies reflects chiefly their immunological and functional heterogeneity. Since most of the laboratory methods have not yet been standardized, the results of studies on the clinical relevance of antiphospholipid antibodies must be analyzed with caution. The association between antiphospholipid antibodies with peculiar clinical manifestations such as venous and arterial thrombosis, recurrent miscarriage, and thrombocytopenia, characterizes the so-called "antiphospholipid syndrome". Retrospective and cross-sectional studies have confirmed the role of anticardiolipin antibodies and lupus anticoagulants as risk factors for both venous and arterial thrombosis, the most common clinical manifestations of the antiphospholipid syndrome. Prospective studies performed in different patient populations have confirmed the association between anticardiolipin antibodies and lupus anticoagulants with venous, and possibly, arterial thrombosis, although information on the predictive value of the various laboratory tests with respect to thrombosis is still limited. It is hoped that the development and standardization of assays that selectively identify antiphospholipid antibodies associated with increased risk of thrombosis will lead to therapeutic strategies able to prevent thromboembolic complications of the antiphospholipid syndrome.

Adult↗

PubMed1997

Resistance to activated protein C caused by the R506Q mutation in the gene for factor V is a common risk factor for venous thrombosis.

The protein C system is an important natural anticoagulant pathway. Protein C is the key component of the system and it is activated by thrombin bound to thrombomodulin on the surface of endothelial cells. Activated protein C (APC) inhibits coagulation by cleaving and inactivating coagulation factors factor Va and factor VIIIa. Until recently, the major genetic causes of familial venous thrombophilia were inherited deficiencies of protein C, protein S or antithrombin, but together they were found in less than 5-10% of patients with thrombosis. In 1993, the situation changed drastically with the description of inherited APC-resistance as a novel risk factor for venous thrombosis. APC-resistance is characterized by a poor anticoagulant response to APC. Inherited APC-resistance is the most common genetic risk factor for this disease and it is found in 20-60% of patients. The condition is caused by a single point mutation in the gene for factor V which predicts substitution of arginine (R) at position 506 with a glutamine (Q). Mutated factor V (FVR506Q, FV:Q506 or FV Leiden) expresses normal procoagulant properties but is partially resistant to APC. The resulting hypercoagulable state confers a life long increased risk of venous but not arterial thrombosis. The FVR 506Q mutation is common in Caucasians with a prevalence of 1-15%, whereas it is not found in other human races. The FVR 506Q mutation may, due to its high prevalence, be an additional risk factor in individuals carrying other inherited defects such as deficiency of protein S, protein C or antithrombin. Such individuals have a high incidence of thrombosis and severe thrombophilia is a multigenetic disease. The high prevalence of inherited APC-resistance and the availability of easy functional and genetic tests will stimulate the development of prophylactic regimens and hopefully result in a decreased incidence of thrombosis.

Disease-Free Survival↗

PubMed1997

[Prosthetic heart valve thrombosis: a 3-year experience].

A series of 12 patients with 16 episodes of prosthetic heart-valve thrombosis over 3 years is presented. Most episodes affected mitral or tricuspid bileaflet prostheses. All patients were inadequately anticoagulated at the time of thrombosis. The clinical presentation was acute and severe in 6 patients, and subacute or chronic in the rest. Physical examination was suggestive of stuck valves in most cases. Transthoracic echocardiography revealed increased transvalvular gradients in most. However, clearer evidence of valve thrombosis was obtained from transesophageal echocardiography or fluoroscopy. 9 patients eventually had their valves re-replaced successfully, and the preoperative diagnosis was confirmed in all. 5 patients were operated as soon as the diagnosis was established. and an additional 4 were operated after failure of anticoagulation. In 4 patients the valve leaflets became completely mobile after a course of thrombolysis. Prosthetic valve thrombosis is a severe and potentially fatal complication in patients with mechanical heart valves. Alertness of physicians at all levels- the general practitioner, the internist and the cardiologist- to the possibility of valve thrombosis and to its clinical presentation may lead to prompt and earlier diagnosis and to comprehensive therapy.

Adolescent↗

PubMedDate not supplied

Middle cerebral artery thrombosis following blunt head trauma.

Stroke caused by occlusion of an intracranial artery following blunt head trauma is a rare event. Traumatic dissections of the middle cerebral artery have been reported while thrombosis is very rare. We describe a case of fatal thrombosis of the left middle cerebral artery that occurred in the time interval between 2 and 6 hours after an apparently minor head trauma in a motor vehicle accident. The 25-year-old woman was in normal health on admission to the hospital. Two hours later the patient manifested nystagmus and vomiting. Six hours later she was aphasic with right hemiparesis. Twenty-four hours later the patient was comatose. A third CT scan performed at that time showed a wide infarct of the left cerebral hemisphere and a hyperdense left middle cerebral artery. The patient died 5 days after the collision. The autopsy confirmed the presence of the cerebral infarct and revealed thrombosis of the left middle cerebral artery. Microscopically, the transverse rupture of the intima and of the elastic lamina along the whole circumference of the vessel was found at the beginning of the thrombosed tract. We conclude that the blunt head trauma caused a partial rupture of the wall of the left middle cerebral artery with consequent thrombosis of the vessel and cerebral infarct. Based on the anatomy of the middle cerebral artery and on the review of the morphological literature we propose that the 2 types of lesion, the dissection and the thrombosis, that may follow closed head trauma, might depend on a common denominator that is the primitive rupture of the intima and elastic lamina.

Adult↗

PubMed1997

[Splenic vein thrombosis with pancytopenia and fever: antiphospholipid antibody syndrome].

Antiphospholipid antibody syndrome (APS) is now recognized as one of the most important causes of hypercoagulability. The most common site for venous thrombosis in APS is deep venous thrombosis of the lower extremities. Other sites of venous thrombosis include retinal veins, renal veins, and hepatic veins. The authors report a case of splenic vein thrombosis disclosing antiphospholipid syndrome in which also the cytolytic effect of aPL may play a role of "cofactor" in the genesis of thrombosis through the release of thromboplastin from the lysis of red cells, granulocytes and platelets, making them vulnerable to clearance by splenic macrophages. Important considerations are stressed about differential diagnosis, etiopathogenetic factors, therapy and follow-up of the patient.

Adult↗