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Biomedical subjects

V Vicente

Publications and source records attributed to V Vicente.

At least 55 records · Page 3Linked to original sources
PubMed1999

Autoaggression syndrome resembling acute graft-versus-host disease grade IV after autologous peripheral blood stem cell transplantation for breast cancer.

Acute graft-versus-host disease (aGVHD) after autologous progenitor cell transplantation has been associated with blood transfusion or cyclosporine. Mild aGVHD grades I-II, identified as autoaggression or engraftment syndrome, has recently been described in autologous progenitor transplantation. Here, we report the first case of pathologically documented grade IV aGVHD after autologous peripheral blood progenitor cell transplantation in a patient with breast cancer. The allogeneic origin was excluded by molecular techniques, and no cyclosporine or cytokines were administered.

Adult↗
PubMed1999

Quality assessment of platelet concentrates supplemented with second-messenger effectors.

BACKGROUND: While reducing the potential for bacterial contamination, the storage of platelet concentrates (PCs) at refrigerated temperatures is not routine, because of the induction of the so-called platelet storage lesion. As the modulation of second-messenger levels might help to overcome this drawback, a quality assessment of PCs treated with a mixture of second-messengers effectors known as ThromboSol was performed. STUDY DESIGN AND METHODS: The PCs were supplemented with ThromboSol or phosphate-buffered saline, and stored in parallel at 22 degrees C with continuous agitation or at 4 degrees C. At 1, 5, and 9 days, an in vitro quality assessment of the PCs was performed, including measurement of cell number, metabolic and integrity markers, platelet surface expression of glycoproteins, platelet response to ristocetin and thrombin, and levels of cyclic adenosine 3', 5' monophosphate (cAMP) and thromboxane B2 (TxB2). RESULTS: Control PCs stored at 4 degrees C underwent aggregation and displayed a significant decrease in the platelet number (40% on Day 5). By contrast, the ThromboSol-treated PCs maintained 80 percent of their initial platelet concentration after 9 days of storage at 4 degrees C. Compared to PCs stored at 22 degrees C, refrigerated PCs exhibited minor changes in metabolic values throughout storage, but the addition of ThromboSol induced a rise in metabolic rate during storage at 22 degrees C. Platelet responsiveness to both ristocetin and thrombin was maximally preserved in the ThromboSol-treated PCs stored at 4 degrees C. These units also maintained high levels of cAMP and low concentrations of TxB2 during storage. CONCLUSION: The pharmacologic supplementation of PCs with ThromboSol significantly favors the maintenance of in vitro integrity and responsiveness of platelets during extended storage at refrigerated temperature. This protective effect seems to be a consequence of the ability of ThromboSol's components to sustain high levels of cAMP and to inhibit TxB2 production during the entire extended-storage period.

Blood Banks↗
PubMed1999

The number of platelet glycoprotein Ia molecules is associated with the genetically linked 807 C/T and HPA-5 polymorphisms.

BACKGROUND: The neutral 807 C/T (Phe224) polymorphism (807 C/T polymorphism) of the glycoprotein (GP)Ia gene has been recently associated with the number of GPIa molecules on the platelet surface. The association of the number of GPIa molecules with other GPIa polymorphisms, such as HPA-5 (Glu/Lys505) (HPA-5 polymorphism), involved in alloimmune thrombocytopenias is unknown. STUDY DESIGN AND METHODS: The association of the HPA-5 polymorphism with the number of GPIa molecules on the platelet surface in 159 white blood donors was investigated. The genetic linkage between the HPA-5 and the 807 C/T polymorphisms in 316 individuals was also determined. RESULTS: Both the 807 C/T and HPA-5 polymorphisms correlate with the number of GPIa molecules on the platelet surface. The 807 T and HPA-5b alleles are associated with increased numbers of GPIa molecules on the platelet surface. Moreover, the HPA-5b allele is genetically linked to 15.8 percent of the 807 C alleles. Therefore, the number of GPIa molecules on the platelet surface is dependent on both GPIa polymorphisms as follows: 807 T/T, HPA-5 a/a > 807 C/T, HPA-5 a/b > 807 C/T, HPA-5 a/a > 807 C/C, HPA-5 a/b > 807 C/C, HPA-5 a/a. CONCLUSION: Two GPIa polymorphisms (807 C/T and HPA-5) responsible for the variability in the numbers of GPIa/IIa molecules on the platelet surface in whites have been identified. Despite the genetic linkage between the two polymorphisms, their influence on the number of GPIa molecules on the platelet surface may occur through different mechanisms.

Adult↗
PubMed1999

von Willebrand factor contained in a high purity FVIII concentrate (Fanhdi) binds to platelet glycoproteins and supports platelet adhesion to subendothelium under flow conditions.

BACKGROUND AND OBJECTIVE: There is evidence suggesting that von Willebrand factor (VWF) from high purity factor VIII concentrates could be of clinical use in the management of patients suffering from VWD. We analyzed structural and functional characteristics of VWF present in a high purity factor VIII concentrate VWFHPC (Fanhdi). The multimeric structure, the ability to bind to platelet GP Ib/IX or GP IIb/IIIa, and the capacity of VWFHPC to promote platelet adhesion on injured vessels were investigated and compared with that present in standard plasma cryoprecipitates [VWFCRYO]. DESIGN AND METHODS: Binding studies were carried out by incubating radiolabeled VWF and washed platelets, which were activated with either ristocetin (1 mg/mL; for GP Ib/IX), or thrombin (2.5 U/mL; for GP IIb/IIIa). Platelet adhesion was assessed in a perfusion system (shear rate = 800 s-1, 10 min) in which the source of VWF was added (at 0.4 or 0.8 U/mL VWF:Ag) to washed platelets and red cells suspended in a human albumin solution. The deposition of platelets onto the perfused subendothelial surface was morphometrically evaluated and expressed as percentage of surface coverage (%SC). RESULTS: The VWFHPC (152 Units VWF:RCof/mg protein; VWF:RCof/VWF:Ag = 0.97), lacked only a small proportion of high-molecular-weight multimers present in VWFCRYO. Binding affinities (Kd values, nM) of VWFHPC were similar to those of VWFCRYO (5.3 +/- 0.86 vs 5.2 +/- 0.95, for GP Ib/IX; and 11.6 +/- 2.7 vs 15.4 +/- 1.7 for GPIIb-IIIa). A slightly, though not significantly, higher binding capacity for these receptors (Bmax values, molecules/pit) was obtained for VWFHPC. The %SC in perfusions in the presence of albumin was < 10%. Addition of VWFHPC or VWFCRYO significantly increased the %SC, with values of 27.1 +/- 4.9 and 17.5 +/- 2.8%, respectively with 0.4 U/mL (p < 0.004 and p < 0.02 vs albumin); and 30.8 +/- 4.9% and 20.03 +/- 4.1%, respectively, at 0.8 U/mL (p < 0.001 and p < 0.02 vs albumin). INTERPRETATION AND CONCLUSIONS: Our data show that VWF present in the high purity FVIII concentrate Fanhdi retains the functional capacity to bind to GPs Ib/IX and IIb/IIIa and to promote platelet adhesion onto exposed subendothelium.

Albumins↗
PubMed1999

The prothrombin gene variant 20210A in venous and arterial thromboembolism.

Several hereditary disorders affecting coagulation factors have been identified as prothrombotic risk factors. Recently, the prothrombin 20210 A/G mutation has been identified as a second important polymorphism involved in venous thrombosis. This article reviews all published information about this new procoagulant mutation. Our group has been involved in a number of studies about the role and importance of polymorphisms in thromboembolic disease, including the analysis of the prothrombin 20210 A/G mutation. Moreover, an extensive Medline literature search was made to complete the review using the key words: prothrombin mutation, 20210, venous or arterial thrombosis. The combination of environmental and genetic risk factors determines the relative risk that any individual has of suffering a thrombotic episode. Some genetic mutations affecting coagulation factors have been described. Recently, Poort et al. described a new mutation in the 3'-untranslated region of the prothrombin gene. The prothrombin 20210 G/A mutation, associated with elevated levels of factor II in plasma, significantly increases the risk of developing venous thrombosis. In fact, this polymorphism is the second most important genetic risk factor for venous thrombosis in Caucasian populations. Moreover, and supporting the multifactorial feature of thromboembolic diseases, this mutation greatly increases the possibility of developing a thrombotic episode when combined with other environmental or genetic risk factors. The role of this procoagulant mutation in arterial vascular disease is, however, unclear.

Humans↗
PubMed1999

Clinical and analytical relevance of the combination of prothrombin 20210A/A and factor V Leiden: results from a large family.

We analysed the clinical and analytical features of 18 subjects from a Spanish family who bear several combinations of two prothrombotic mutations, factor V Leiden (FVL) and prothrombin 20210A. We identified three subjects homozygous for the 20210A prothrombin mutation which additionally were heterozygous for FVL. The combination of both mutations increases the risk of developing venous thrombotic episodes at the earlier age. However, even in association with FVL, the homozygous condition of the prothrombin 20210A mutation requires additional risk factors to induce a thrombotic event. Finally, the plasma level of factor II showed a significant relationship with the prothrombin genotype.

Adult↗
PubMed1999

Role of the 807 C/T polymorphism of the alpha2 gene in platelet GP Ia collagen receptor expression and function--effect in thromboembolic diseases.

The variability of the platelet GP Ia/IIa density has been associated with the 807 C/T polymorphism (Phe 224) of the GP Ia gene in American Caucasian population. We have investigated the genotype and allelic frequencies of this polymorphism in Spanish Caucasians. The T allele was found in 35% of the 284 blood donors analyzed. We confirmed in 159 healthy subjects a significant association between the 807 C/T polymorphism and the platelet GP Ia density. The T allele correlated with high number of GP Ia molecules on platelet surface. In addition, we observed a similar association of this polymorphism with the expression of this protein in other blood cell types. The platelet responsiveness to collagen was determined by "in vitro" analysis of the platelet activation and aggregation response. We found no significant differences in these functional platelet parameters according to the 807 C/T genotype. Finally, results from 3 case/control studies involving 302 consecutive patients (101 with coronary heart disease, 104 with cerebrovascular disease and 97 with deep venous thrombosis) determined that the 807 C/T polymorphism of the GP Ia gene does not represent a risk factor for arterial or venous thrombosis.

Aged↗
PubMed1999

[Ornidazole in the treatment of liver dysfunction associated to long-term parenteral nutrition].

AIM: to reduction the TPN-related hepatic toxicity with an anaerobicidal therapy (ornidazole in our case). PATIENT: a 24-year-old male surgically treated for intestinal occlusion. He had been treated with abdominal radiotherapy for rabdomyosarcoma of embryonic urogenital sinus when he was five months old. It was found a great abdominal radiotherapy sequelae and occluded and perforated small-bowel loop that was resected. Postoperative time developed pelvic abscess and reoperation was performed. Severe intraabdominal inflammatory-adhesive process was noticed which included all the intestinal loops with multiple perforations. Attempts to release this situation was unsuccessful and several anastomoses, with some loop exclusions and a diverting loop jejunostomy were performed. In postoperative period he developed an enterocutaneous fistula and TPN was initiated. Higher and higher hepatic marker values were detected suggesting a progressive hepatotoxicity. METHODS: anaerobicidal agent (ornidazole) and cyclic total parenteral nutrition as a therapy design were prescribed. RESULTS: there were satisfactory showing a reduction in hepatic marker values (72.5% fall in alanine aminotransferase). CONCLUSIONS: bearing in mind that some theories suggest that total parenteral nutrition may cause atrophic changes in the gut mucosa so giving rise to bacterial translocation, this anaerobicidal treatment designed could be assumed effective for attenuating TPN-related liver damage.

Adult↗
PubMed1998

[Markers of hemostatic activation in the coronary sinus versus peripheral circulation in coronary artery disease. Effects of percutaneous transluminal coronary angioplasty].

BACKGROUND: To evaluate haemostatic changes in coronary sinus (CS) and peripheral circulation (PC) in patients with cardiovascular disease (CAD) following PTCA. PATIENTS AND METHODS: We studied 12 patients scheduled for elective PTCA. Blood samples were obtained from CS and PC before angioplasty and after each balloon dilation. Expression of P selectin and several haemostatic parameters were determined. RESULTS: D-Dimers (DD) plasma levels were significantly increased in samples from CS. No significant differences were found in other haemostatic parameters. A significant decrease of thrombin-antithrombin III levels after PTCA was assessed. CONCLUSIONS: Intracoronary and peripheral hemostatic activation does not occur during and immediately following PTCA. No major differences in hemostatic parameters between CS and PC were observed in patients with CAD.

Adult↗
PubMed1998

Polymorphisms of platelet membrane glycoprotein Ib associated with arterial thrombotic disease.

Platelet membrane glycoprotein Ibalpha (GPIbalpha) is a major receptor for von Willebrand factor and thrombin, which plays a key role in the initial development of thrombi. Two polymorphisms (HPA-2 and VNTR) that affect phenotype have been described in GPIbalpha. The relevance of these polymorphisms to thrombotic disease was investigated by genotypic identification in three case-control studies: 104 case patients with acute cerebrovascular disease (CVD), 101 case patients with acute coronary heart disease (CHD), 95 patients with deep venous thrombosis (DVT), and one control age-, sex-, and race-matched for each case patient. Results show that the C/B genotype of the VNTR and the HPA-2b polymorphisms of GPIbalpha are strongly associated with increased risk of coronary heart disease and cerebral vascular disease but not with deep vein thrombosis. These two polymorphisms of GPIbalpha may represent newly identified risk factors for arterial thrombotic disease, but not for venous thrombosis.

Adult↗
PubMed1998

A radioreceptor assay for mass measurement of inositol (1,4,5)-trisphosphate using saponin-permeabilized outdated human platelets.

The binding of inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] to saponin-permeabilized blood-bank-outdated human platelets, 6 days old, has been characterized (Kd = 3.8 nM; Bmax = 1.7 pmol/mg protein) and used to develop a novel radioreceptor assay which allows the measurement of the Ins(1,4,5)P3 content in resting or agonist-stimulated cells. This assay is as sensitive (0.25 pmol in a 0.25 ml volume), specific, and reproducible as previously proposed methods. In addition, obtaining large batches of the Ins(1,4,5)P3 binding protein by treating outdated platelets with saponin is simple and quick and uses otherwise discarded material. Moreover, the assay is considerably cheaper than commercially available kits. Using this method we confirmed that thrombin evokes a rapid, transient, and dose-dependent increase in the platelet concentration of Ins(1,4,5)P3.

Blood Platelets↗
PubMed1998

Bone marrow steady-state CD34+/CD71- cell content is a predictive value of rG-CSF-mobilized CD34+ cells.

Thirty-four patients diagnosed with breast cancer were included in a prospective study evaluating the bone marrow (BM) CD34+/CD71- cell content, as a predictive parameter of the CD34+ cell mobilization after rG-CSF administration. Analysis of the concentration of medullary CD34+/CD71- cells before priming schedules was significantly related with the collection of CD34+ cells in apheresis day 1 (P = 0.03, r = 0.36), apheresis day 1 + day 2 (P = 0.01, r = 0.42) or the total CD34+ cells collected (P = 0.005, r = 0.47). A BM CD34+/CD71- cell concentration greater than or less than a cut-off value of 30/microl was significantly associated with the yield of CD34+ cells collected by cytapheresis procedures (mean values 3.12 x 10(6)/kg, and 2.19 x 10(6)/kg, respectively, P = 0.013). These results suggest that in breast cancer patients undergoing priming with rG-CSF, steady-state BM CD34+/CD71- measurement is a relevant predictive parameter of CD34+ mobilization.

Adult↗
PubMed1998

New alleles of the platelet glycoprotein Ibalpha gene.

Platelet membrane glycoprotein Ibalpha (GP Ibalpha) bears two molecular polymorphisms which are in linkage disequilibrium: the C/T dimorphism at codon 145 (HPA-2) and the variable number of tandem repeats (VNTR) polymorphism in the macroglycopeptide region. The frequencies of these two polymorphisms, and of another three recently described silent polymorphisms, were investigated by genotypic identification in 729 Caucasian individuals from the south of Spain. Eight different alleles of this gene, including the longest VNTR A allele of the GP Ibalpha gene, were found in this population. Moreover, we detected an unexpected linkage between the B and A variants of the VNTR polymorphism and the HPA-2a allele in 5.9% of this population. These results suggest a new evolutionary model of GP Ibalpha, in which homologous recombination could account for the genetic diversity of the GP Ibalpha.

Adolescent↗
PubMed1998

Migraine and prothrombotic genetic risk factors.

It has been suggested that during attacks of migraine both platelet activation and plasma coagulability are increased. We investigated the prevalence of several prothrombotic genetic risk factors in patients with migraine: factor V R/Q 506, factor II 20210 G/A, decanucleotide insertion/deletion in the factor VII promoter, and the platelet HPA-1 and HPA-2 alloantigenic systems, by genotypic identification in an age- and sex-matched case-control study including 106 patients with migraine (49 with aura, and 57 without aura). The prevalence of all genotypes was similar among case patients and controls. No association in relation to the type of migraine was detected in the factor II, factor VII, HPA-1, or HPA-2 polymorphisms. Our results showed a high prevalence of factor V Leiden in those patients with migraine with aura (6.1%), though that association was not statistically significant. The studied prothrombotic genetic factors do not seem to be associated with the development of migraine and, therefore, are not likely relevant in the previously reported hypercoagulability and platelet hyperaggregability in this disease.

Adult↗
PubMed1998

Genetic polymorphisms of factor VII are not associated with arterial thrombosis.

A high plasma concentration of factor VII procoagulant activity is considered an independent risk factor for coronary heart disease. Recently, two polymorphisms of factor VII gene (insertion of a decanucleotide at -323 [A2], and the variant Q353) have been associated with 20-25% lower levels of this protein in plasma. In this study, the prevalence of these two factor VII polymorphisms were evaluated in relation to the development of acute thromboembolic events. Thus, we conducted three case-control studies of patients diagnosed with acute coronary syndromes, acute cerebrovascular events and deep venous thrombosis (101, 104 and 97 cases, respectively). No significant differences were detected in the prevalence of these polymorphisms between patients and controls, suggesting that the A1/A2 or R/Q alleles do not play an important role in the development of thromboembolic episodes.

Adult↗
PubMed1998

Natural anticoagulant proteins and antiphospholipid antibodies in systemic lupus erythematosus.

OBJECTIVE: Thrombosis is a relatively common complication in patients with systemic lupus erythematosus (SLE) and is strongly associated with the presence of antiphospholipid antibodies (aPL). The mechanism involved in the pathogenesis of this prothrombotic state remains obscure. We studied 4 natural anticoagulant proteins: protein C, protein S, antithrombin III, and plasminogen in 50 patients diagnosed with SLE. METHODS: Protein C, antithrombin III, and plasminogen were measured by chromogenic substrates and total and free protein S by electrophoresis. We also determined the prevalence of different aPL (lupus anticoagulant and antibodies against cardiolipin, phosphatidylserine, and phosphatidylinositol). RESULTS: Ten patients (20%) had a history of thrombosis. Some type of aPL was present in 26 patients (52%). Nine of the 10 patients with history of thrombosis had aPL (p = 0.007). Functional assays for protein C, antithrombin III, and plasminogen were in the normal range in all patients. Low free protein S levels were documented in 19 patients and were associated with the presence of aPL (13/19 were aPL positive) (p < 0.05). Only 4 patients with acquired free protein S deficiency had a history of thrombosis. CONCLUSION: This study shows an association between aPL and reduced free protein S levels in patients with SLE. Further studies are needed to determine the mechanism and role of this acquired deficiency in the pathogenesis of thrombotic episodes in patients with SLE.

Adolescent↗