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At least 487 records · Page 27Linked to original sources
PubMedDate not supplied

Modulation of C4b-binding protein isoforms during the acute phase response caused by orthopedic surgery.

Orthopedic surgery is described as an event with a high risk of thromboembolic diseases. This is probably a consequence of a synergistic combination of different risk factors in the patients subjected to this type of surgery, including age, immobilization, anesthesia and different hypercoagulable states. After surgery patients develop an acute-phase response that leads to changes in several plasma proteins. One of these proteins is the complement regulator C4b-binding protein (C4BP). We have recently shown that in some acute-phase patients C4BP is incorrectly controlled (with elevation of the C4BP beta-containing isoforms), leading to a potential hypercoagulable state by decreasing the plasma levels of free (active) protein S. Here we have studied whether patients subjected to orthopedic surgery have an appropriate modulation of the C4BP isoforms during their postoperative acute-phase responses. We have analyzed the evolution of the C4BP isoforms in serial samples from 11 patients who have undergone knee (or hip) prosthesis surgery (mean age 70 years), or scoliosis surgery (mean age 18 years). Our data suggest a similar evolution of C4BP isoforms in all these patients, with an almost exclusive increase of C4BP isoforms lacking C4BP beta polypeptides and steady levels of free protein S.

Acute-Phase Reaction↗
PubMed2004

Hemostasis and thyroid diseases revisited.

Several papers have reported various hemostatic abnormalities in patients with thyroid diseases. In this concise review, the traditional associations between hypercoagulable state and hyperthyroidism and between hypocoagulative state and hypothyroidism are critically revised on the basis of more recent literature data. In particular, we analyze the hemostatic balance (primary hemostasis, coagulation factors and fibrinolytic system) in different thyroid disorders. Although most of the studies published so far include limited numbers of patients and their results are sometimes contradictory, we can conclude that hyperthyroidism is generally accompanied by a hypercoagulable state, whereas the hemostatic profile in hypothyroidism and thyroid cancer depends on the severity of the disease.

Hemostasis↗
PubMedDate not supplied

Acute, complete splenic infarction in cancer patient is associated with a fatal outcome.

Splenic infarction frequently occurs in patients with myeloproliferative diseases, endocarditis, and sickle cell anemia. Various sonographic patterns of splenic infarction do exist. but little is known about tumor associated splenic infarction in cancer patients. Between January 1992 and December 2002, 66 patients were diagnosed with splenic infarction by color Doppler sonography (CDS). Ten patients had an underlying solid cancer. Clinical and sonographic data of cancer patients were evaluated retrospectively with regard to age, sex, frequency of thrombotic episodes, splenic size, echomorphology and vascularity of splenic lesions, and follow-up examination. The median age was 53 years (range, 16-73 years). Nine of 10 patients had abdominal metastases, four had evidence of a hypercoagulable state, five had a small spleen (< 7 x 3 cm), and seven had acute complete infarction of the spleen without hilar and parenchymal vessels on CDS. Survival of six patients with acute complete infarction ranged from 1 to 30 days. In cancer patients with splenic infarction, an acute complete infarction is the most common pattern. It is caused predominantly by a hypercoagulable state and is associated with an extremely short survival.

Acute Disease↗
PubMed1998

Microvascular tissue transfer in a pregnant patient.

Pregnancy is a relative contraindication for elective surgery. The primary concerns are for the safety of the fetus and the mother. However, there are particular problems involving microvascular surgery due to the pregnancy-associated hypercoagulable state. The authors were presented with a 35-year woman, 20 weeks pregnant, with a degloved foot and ankle associated with an open distal tibia/fibula fracture (Gustilo IIIB). Salvage of her leg required a microvascular tissue transfer. Accordingly, a combined latissimus dorsi-serratus anterior free flap was performed with a saphenous vein graft to the popliteal vessels. The patient was hypercoagulable and there were extensive platelet clots. Her consumption of heparin was enormous. Postoperatively, she was treated with intravenous dextran for 5 days and for 17 days with intravenous heparin. After discharge, she was placed on subcutaneous heparin until she delivered a healthy baby. The flap survived and her leg was salvaged. The hypercoagulable state of pregnancy, as well as thromboprophylaxis, are discussed.

Adult↗
PubMed2002

[Superior mesenteric venous thrombosis during treatment of malignant lymphoma and of pure red cell aplasia].

Mesenteric vein thrombosis is an uncommon type of intestinal ischemia that can be associated with significant mortality if its diagnosis is delayed. We experienced two patients with hematological disorders--non-Hodgkin's lymphoma (NHL) and pure red cell aplasia (PRCA)--who developed superior mesenteric vein (SMV) thrombosis during treatment. Neither of the patients had underlying disorders of the anticoagulant system that might have produced a hypercoagulable state. The first patient developed SMV thrombosis immediately after chemotherapy for NHL. This patient also had portal hypertension due to chronic hepatitis B. Direct injury to endothelial cells by the anti-cancer drugs and alteration of blood flow were the probable causes of the SMV thrombosis. The second patient with PRCA had regularly taken prednisolone, and this had induced a hypercoagulable state. The clinical symptoms of SMV thrombosis are usually non-specific, and in our patients vague, crampy abdominal pain without bloody diarrhea was the only complaint. Abdominal CT scan under a clinical suspicion of SMV thrombosis revealed the thrombi in the SMV. Urgent surgical resection of the infarcted bowel and immediate postoperative anticoagulation resulted in a favorable outcome. Clinicians should be aware of the vague symptoms of SMV thrombosis, as early diagnosis and urgent therapy are essential to prevent a fatal outcome.

Antineoplastic Combined Chemotherapy Protocols↗
PubMedDate not supplied

Dural sinus thrombosis and venous infarction associated with antiphospholipid antibodies: MR findings.

OBJECTIVE: Our goal was to describe the neuroradiologic findings in hemorrhagic venous infarction related to a hypercoagulable state caused by antiphospholipid antibodies (aPA). MATERIALS AND METHODS: Magnetic resonance imaging was performed on two patients with superior sagittal thrombosis related to the presence of aPA. RESULTS: A parenchymal region of hyperintense signal due to hemorrhagic venous infarction was demonstrated in both patients, along with abnormal signal within the thrombosed superior sagittal sinus. CONCLUSION: Hemorrhagic venous infarction may result from the hypercoagulable state related to aPA. The presence of these antibodies should be considered in the setting of otherwise unexplained dural sinus thrombosis and/or venous infarction.

Adult↗
PubMed2002

[Regional biochemical and hematologic changes in patients after revascularization of the lower extremities in ischemia of the extremities].

INTRODUCTION: Surgical treatment of PAOD is related to iatrogenic ischaemia caused by arterial clamping and ischaemia which is result of natural development of the disease. The pathway of skeletal muscle reperfusion injury is complex and one of the most important factors related to injury is endothelial damage. The expected reason of endothelial damage is increased production of oxygen free radicals by prematurely activated PMN (polymorphonuclear) leukocytes (direct injury). Non-specific tissue injury is related to releasing of PMN elastase. Endothelial dysfunction, hypercoagulable state and microcirculation stasis are responsible for indirect injury and no-reflow fenomena. STUDY DESIGN: Observational pilot study. METHODS: 10 patients underwent surgery because of PAOD (all suffering from critical limb ischaemia). During reperfusion period in defined intervals following parameters were measured (samples were taken from ipsilateral femoral vein): PMN elastase, lactate, total antioxidant status, malondialdehyd, minerals, acid-base balance, blood count, APTT, prothrombin time, fibrinogen and HTI (heparin tolerance index). RESULTS: Patients with PAOD are threatened by hypercoagulable state with its clinical and surgical consequences. Maximal grade of local acidosis is reached 2 hours from the beginning of reperfusion. Tissue damage is expressed by maximum activity of PMN elastase 18-24 hours during reperfusion and represents non-specific tissue damage. Low total antioxidant status reveals high sensibility to oxygen free radicals. MDA does not achieve the pathological range in observed series. CONCLUSION: Our results confirmed inevitable importance of prevention of hypercoagulability, oxygen free radical tissue damage and PMN elastase activation to avoid of non-specific tissue damage.

Antioxidants↗
PubMed2002

Palmar digital vein thromboses: their different expressions.

There have only been a few reports about thrombotic events in the volar digital veins. The observation of 2 such cases gives reason to discuss this rare symptomatology. Thrombosis of the digital veins can be categorised into three subtypes: the first shows clinical similarity to thrombotic events in veins or varicose veins of the limbs and may be related to a hypercoagulable state; the second group develops in a pre-existing normal vein or an acquired venous cavernoma and does not show clinical or histological signs of inflammation; the third category resembles Mondor's disease and may be named Mondor's phlebitis of the finger; histopathological examination has yet to be done. In any case of thrombosis of the volar digital veins, an inherited or acquired hypercoagulable state must be ruled out.

Adult↗
PubMed2006

Effects of VLDL and remnant particles on platelets.

There is a considerable body of evidence supporting an association between hypertriglyceridaemia, a hypercoagulable state and atherothrombosis. A disorder of triglyceride metabolism is a key feature of the metabolic syndrome that increases risk of both ischaemic heart disease and type 2 diabetes approximately 3-fold. An increasing prevalence of obesity and metabolic syndrome is likely to contribute markedly to the prevalent ischaemic heart in the foreseeable future, and therefore it is crucial to understand mechanisms linking hypertriglyceridaemia and a hypercoagulable state. Activation of platelets and the coagulation cascade are intertwined. VLDL and remnant lipoprotein concentrations are often increased with the metabolic syndrome. These lipoproteins have the capacity to activate platelets and the coagulation pathway, and to support the assembly of the prothrombinase complex. VLDL also upregulates expression of the plasminogen activator inhibitor-1 gene and plasminogen activator inhibitor-1 antigen and activity, a process accompanied by platelet aggregation and clot formation. The surface membrane of activated platelets also supports the assembly and activity of the prothrombinase complex, resulting in further thrombin generation and amplification of the coagulation cascade. Fibrinolysis is also less efficient when thrombin is generated. Thrombin induces thrombin activatable fibrinolysis inhibitor. Thrombin activatable fibrinolysis inhibitor is a carboxypeptidase that cleaves the carboxylic lysine residues on fibrin, thereby abolishing the critical binding site for tPA-plasminogen decreasing plasmin formation. Thus the evidence is supportive of dysregulated coagulation, and impaired fibrinolysis with a predisposition to atherothrombosis, in conditions such as the metabolic syndrome, in which there are increased concentrations of VLDL and remnant lipoproteins. The purpose of this review is to describe the current evidence supporting a procoagulant state induced by VLDL and remnant lipoproteins. The role of these lipoprotein classes in (1) platelet activation; (2) the intrinsic coagulation cascade, and (3) clot formation and fibrinolysis is discussed.

Blood Coagulation↗
PubMed1982

[Correlation between coagulation and fibrinolysis in patient with cerebrovascular accident at acute stage].

Ninety five patients with cerebrovascular accidents were studied on their coagulation and fibrinolysis at acute stage of their onset. From the data collected in the present study, following findings were obtained; 1) Hypercoagulable state, which are responsible for the decreased antithrombin III levels, was observed at acute stage of cerebral infarction. 2) Findings from patients with cerebral hemorrhage were normal antithrombin III levels and slightly decreased alpha 2-plasmin inhibitor. These imply the fact of increased fibrinolytic activities. It is suggested that increased fibrinolysis are secondary reaction of cerebral hemorrhage. 3) Findings from patients with subarachnoid hemorrhage showed hypercoagulable state and increased fibrinolytic activities. It is considered that subarachnoid hemorrhage might have mostly a preparatory condition of disseminated intravascular coagulation among cerebrovascular accidents.

Acute Disease↗
PubMed1998

Relevance of markers of hemostasis activation in obstetrics/gynecology and pediatrics.

Pregnancy and puerperium are considered to be hypercoagulable states with increased incidence of thromboembolic events. During normal pregnancy, changes in the hemostatic mechanism involve increased stasis and increased coagulation factors and/or decreased levels of anticoagulant proteins such as protein C and protein S as well as enhanced thrombin generation and decreased fibrinolytic activity. The physiological or pathophysiological activation of hemostasis during pregnancy results in the generation of the so-called activation markers which increase, reflecting hypercoagulability and therefore representing an imbalance in the hemostatic system. The most interesting markers of hemostasis activation and, thus, of thrombin generation are: thrombin-antithrombin III complex (TAT), antithrombin III itself, prothrombin fragment 1+2 (F 1+2), fibrin monomer (soluble fibrin) and D-Dimer (which indicates also an increased fibrinolytic activity). Together with fibrinogen levels and platelet counts, the activation markers are useful tools in different pathological situations in pregnancy to predict and monitor the severity of the condition. Recently, a higher incidence of factor V Leiden mutation has been demonstrated in selected populations in whom thrombotic events developed during pregnancy and puerperium. Therefore, the combination of APC resistance/FV Leiden mutation and pregnancy may predict a high risk for thromboembolic phenomena. In newborns, the activation markers are elevated immediately after birth and decline to near adult levels during the first 24 h of life. During infections the activation markers are increased showing the same behavior as in the mature adult system. In neonates and children, the same etiologies can be responsible for acquired and inherited pathological hypercoagulable states as in the adult.

Adult↗
PubMed1985

Contact phase of coagulation in diabetes mellitus after aspirin administration.

The purpose of our study was to investigate the connection between platelets and the contact phase of coagulation. In 17 patients affected by diabetes mellitus we studied the behaviour of prekallikrein, factor XII and factor XI before and after aspirin administration. To evaluate the activity of aspirin we measured platelet production of thromboxane B2 using a radioimmunoassay. In our diabetic patients a hypercoagulable state was confirmed: PK, factor XII and XI levels were significantly higher as compared with normal controls. After aspirin administration a significant decrease of PK levels was found. After 7 days of aspirin administration and 7 days after stopping aspirin a modest but not significant improvement of factor XII and factor XI was observed. In conclusion, we believe that the contact phase of coagulation is another index of the hypercoagulable state in diabetes mellitus. In addition, the decrease of PK obtained by aspirin administration could support the possible connection between the contact phase of coagulation and platelets.

Aspirin↗
PubMed2001

Characterization of a mouse model for thrombomodulin deficiency.

Mutations in the gene encoding thrombomodulin (TM), a thrombin regulator, are suspected risk factors for venous and arterial thrombotic disease. We have previously described the generation of TM(Pro/Pro) mice carrying a TM gene mutation that disrupts the TM-dependent activation of protein C. Here, it is shown that inbred C57BL/6J TM(Pro/Pro) mice exhibit a hypercoagulable state and an increased susceptibility to thrombosis and sepsis. Platelet thrombus growth after FeCl(3)-induced acute endothelial injury was accelerated in mutant mice. Vascular stasis after permanent ligation of the carotid artery precipitated thrombosis in mutant but not in normal mice. Mutant mice showed increased mortality after exposure to high doses of endotoxin and demonstrated altered cytokine production in response to low-dose endotoxin. The severity of the hypercoagulable state and chronic microvascular thrombosis caused by the TM(Pro) mutation is profoundly influenced by mouse strain-specific genetic differences between C57BL/6 and 129SvPas mice. These data demonstrate that in mice, TM is a physiologically relevant regulator of platelet- and coagulation-driven large-vessel thrombosis and modifies the response to endotoxin-induced inflammation. The phenotypic penetrance of the TM(Pro) mutation is determined by as-yet-uncharacterized genetic modifiers of thrombosis other than TM.

Animals↗
PubMed1992

Hemostatic abnormalities in total artificial heart patients as detected by specific blood markers.

We retrospectively evaluated the hemostatic system of 13 patients during implantation (2 to 35 days) of the Jarvik 7-70 total artificial heart (TAH). Although all patients were clinically manageable while on the TAH, 5 had excessive generalized bleeding. After the heart transplant procedure, 2 patients had neurological events and 1 patient, thrombosis of the leg. While the patients were supported by the TAH, the routine coagulation assays (prothrombin time, activated partial thromboplastin time, fibrinogen, factor assays, and platelet count) showed slight abnormalities but no correlation to hemorrhagic or thrombotic events. In contrast, plasma and cellular activation markers, which are highly sensitive and specific for hypercoagulability, fibrinolysis, or platelet activation, revealed activation in all patients. Most striking was the marked activation of the fibrinolytic system (p less than 0.05 to 0.001). Correlations of individual patient data compared with the average TAH group response could be made between excessive enhancement of fibrinolysis (increased D-dimer and tissue plasminogen activator and decreased plasminogen activator inhibitor) and bleeding. A hypercoagulable state (increased fibrinogen and thrombin-antithrombin complex and decreased antithrombin III and protein C), decreased fibrinolysis (decreased tissue plasminogen activator and D-dimer), activated platelets (increased thromboxane B2), or combinations of these were associated with thrombosis. The hemostatic activation returned to normal 1 day after removal of the TAH. These data suggest that the patient with a TAH requires more sophisticated laboratory monitoring and individualized treatment for excessive fibrinolysis, hypercoagulable state, or platelet activation to avoid thrombotic and hemorrhagic complications.

6-Ketoprostaglandin F1 alpha↗
PubMed2003

Hypercoagulability, a serious problem in patients with ESRD on maintenance hemodialysis, and its correction after kidney transplantation.

BACKGROUND: Recurrent vascular access thrombosis (VAT) resulting in failure to continue maintenance hemodialysis (HD) therapy is not an uncommon event. The cause of VAT in these circumstances remains uncertain. We describe results of our studies to identify changes in hemostatic balance in patients on maintenance HD therapy that probably contributed to a hypercoagulable state. METHODS: We studied 82 patients with end-stage renal disease on maintenance HD therapy who underwent HD for 11 to 52 months (39.3 +/- 27.4 months). Forty-nine episodes of VAT occurred in 22 patients; a single episode occurred in 12 patients; and 2 or more episodes, in 10 patients. Blood coagulation studies, including assays of inhibitors and activated protein C (PC) resistance (APCR), were performed using standard techniques. RESULTS: Investigations showed the presence of lupus anticoagulant (LA) in 5.6%, anticardiolipin antibody immunoglobulin G (IgG) in 3.9% and IgM in 5.3%, APCR in 20.5%, and deficiencies in protein S (PS), PC, and antithrombin III (ATIII) in 32.1%, 24.4%, and 19.2%, respectively. When parameters were compared between patients with and without VAT episodes, LA, PC, PS, and APCR levels were significantly abnormal in those who experienced VAT. Sixteen subjects with hypercoagulable states on HD therapy underwent renal transplantation and were evaluated 9.3 +/- 4.2 months posttransplantation. Deficiencies in PC (P = 0.014), PS (P = 0.001), ATIII (P = 0.017), and APCR (P = 0.0001) were completely corrected in all subjects. CONCLUSION: Hypercoagulability is a risk factor for recurrent VAT in HD patients, and renal transplantation successfully corrects these abnormalities.

Adolescent↗
PubMed2000

[Aspects of thrombophilia in Buerger's disease].

Buerger's disease or thromboangiitis obliterans is a disorder of unknown etiology which affects young heavy smokers, mainly of male sex; it is not clear why this disease afflicts only a little number of heavy smokers. Studies about genetic predisposition, autoimmune phenomena and platelet function have been performed in order to search additional etiologic factors without finding significant alterations. Recently some cases of Buerger's disease in association with hypercoagulable states have been described. The authors reported ten subjects affected by Buerger's disease, who have undergone to a clotting process evaluation. We have found 3 cases with fasting hyperhomocysteinemia in association with low level of plasma folate, 3 cases with high value of lipoprotein(a) (in 1 subject in association with IgG anticardiolipin antibody positivity), 1 case with IgM anticardiolipin antibody positivity. These findings, along with literature data, induce to hypothesize that hypercoagulable states may favour the clinical expression of Buerger's disease.

Adjuvants, Immunologic↗
PubMed1996

Elevated levels of prothrombin activation fragment 1 + 2 in plasma from patients with heterozygous Arg506 to Gln mutation in the factor V gene (APC-resistance) and/or inherited protein S deficiency.

Inherited resistance to activated protein C (APC-resistance), caused by a point mutation in the factor V gene leading to replacement of Arg(R)506 with a Gln (Q), and inherited protein S deficiency are associated with functional impairment of the protein C anticoagulant system, yielding lifelong hypercoagulability and increased risk of thrombosis. APC-resistance is often an additional genetic risk factor in thrombosis-prone protein S deficient families. The plasma concentration of prothrombin fragment 1 + 2 (F1 + 2), which is a marker of hypercoagulable states, was measured in 205 members of 34 thrombosis-prone families harbouring the Arg506 to Gln mutation (APC-resistance) and/or inherited protein S deficiency. The plasma concentration of F1 + 2 was significantly higher both in 38 individuals carrying the FV:Q506 mutation in heterozygous state (1.7 +/- 0.7 nM; mean +/- SD) and in 48 protein S deficient cases (1.9 +/- 0.9 nm), than in 100 unaffected relatives (1.3 +/- 0.5 nM). Warfarin therapy decreased the F1 + 2 levels, even in those four patients who had combined defects (0.5 +/- 0.3 nM). Our results agree with the hypothesis that individuals with APC-resistance or protein S deficiency have an imbalance between pro- and anti-coagulant forces leading to increased thrombin generation and a hypercoagulable state.

Adolescent↗
PubMed2003

Coagulopathy, marantic endocarditis, and cerebrovascular accidents as paraneoplastic features in medullary thyroid cancer--case report and review of the literature.

Medullary thyroid cancers account for approximately 7% of primary thyroid malignancies and are often associated with paraneoplastic syndromes. We discuss the case of a 59-year-old man who presented with a hypercoagulable state, nonbacterial endocarditis, and recurrent strokes in the setting of widespread medullary thyroid cancer. The patient was anticoagulated and underwent thyroidectomy, modified radical neck dissection, and subsequent axillary lymphadenectomy. Despite no recurrent thromboembolic events, the patient ultimately succumbed to his disease 8 months after diagnosis and 6 months after initial thyroidectomy. This is the first report, to our knowledge, of this unique presentation in a patient with thyroid cancer. The literature pertaining to the diagnosis and management of hypercoagulability states in patients with cancer, in general, and thyroid cancer, in particular, is reviewed.

Blood Coagulation Disorders↗