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In this study, 542 individual fish from 20 species from the Patagonian continental shelf of Argentina were examined for acanthocephalans. A total of 1,547 acanthocephalans belonging to 5 species were collected from 18 species of fish. Adult forms were represented by 2 species: Aspersentis johni ( Baylis, 1929 ) (Heteracanthocephalidae) from longtail southern cod, Patagonotothen ramsayi (Regan) (new host record), and Breizacanthus aznari Hernández-Orts, Alama-Bermejo, Crespo, García, Raga and Montero, 2012 (Arhythmacanthidae) from raneya, Raneya brasiliensis (Kaup). Immature worms of B. aznari were also collected from the intestine of pink cusk-eel, Genypterus blacodes (Forster) (new host record). Cystacanths of 3 species of Corynosoma Lühe, 1904 (Polymorphidae) were found encapsulated in the mesenteries of fish. Corynosoma australe Johnston, 1937 was the most abundant acanthocephalan in our study, infecting 18 species of fish and accounting for89.9% of all specimens collected. A cystacanth of Corynosoma bullosum (Linstow, 1892) was found in "castañeta", Nemadactylus bergi (Norman) (new host record), and cystacanths of Corynosoma cetaceum Johnston and Best, 1942 were collected from red searobin, Prionotus nudigula Ginsburg, and flounders Paralichthys isosceles Jordan (new host record) and Xystreurys rasile (Jordan). The Patagonian shelf of Argentina represents a new locality record for A. johni and C. bullosum. This survey is a starting point for understanding the diversity of marine acanthocephalans in Patagonian waters.

Introduction The SMART (Study for Monitoring Antimicrobial Resistance Trends) surveillance study monitors antimicrobial susceptibility and extended spectrum β-lactamases (ESBLs) in Gram-negative bacilli recovered from intra-abdominal infections (IAI). Material and methods Antimicrobial susceptibility of 5,343 isolates from IAI recovered in 11 centres during the 2011-2015 SMART-Spain program was analysed by standard microdilution (EUCAST criteria) and compared with that from 2002-2010. ESBLs were phenotypically detected. Results Escherichia coli, the most common isolate, significantly decreased in community acquired IAI (60.9% 2002-2010 vs. 56.1% 2011-2015, P=0.0003). It was followed in prevalence by Klebsiella pneumoniae that increased both in the community (8.9% vs. 10.8%, P=0.016) and nosocomial (9.2% vs. 10.8%, P=0.029) IAI and P. aeruginosa, which significantly increased in community acquired IAI (5.6% vs. 8.0%, P=0.0003). ESBLs were more prevalent in K. pneumoniae (16.3%) than in E. coli (9.5%) of nosocomial origin and were more frequently isolated from elderly patients (>60 years). Considering all Enterobacteriaceae, ertapenem (92.3-100%) and amikacin (95.5%-100%) were the most active antimicrobials. Ertapenem activity, unlike amoxicillin-clavulanate or piperacillin-tazobactam, remained virtually unchanged in ESBL (100%) and non-ESBL (98.8%) E. coli producers. Its activity decreased in ESBL-K. pneumoniae (74.7%) but was higher than that of amoxicillin-clavulanate (14.0%) and piperacillin-tazobactam (24.0%). Interestingly, ertapenem susceptibility was maintained in >60% of ESBL isolates that were resistant to amoxicillin-clavulanate, piperacillin-tazobactam or fluoroquinolones. Conclusions SMART-Spain results support current guidelines which include ertapenem as empiric treatment in mild-moderate community-acquired IAI, particularly with ESBL producers. These recommendations will need to be updated with the recently introduction of new antimicrobials.

Dactylitis is a typical feature of psoriatic arthritis. However, dactylitis was included as a spondyloarthritis (SpA) feature for both (axial and peripheral) of the ASAS classification criteria, but data about its prevalence are scarce, especially in patients with a recent onset of the disease. Our objective was to determine the prevalence and characteristics associated with dactylitis in patients with early SpA.A baseline dataset from the ESPeranza cohort was used. This programme included patients who were suspected of having SpA (age45 years, symptoms duration of 3-24 months and with inflammatory back pain, or asymmetrical arthritis, or spinal/joint pain plus ≥1 of the SpA features). For this study, 609 patients who were diagnosed with SpA by their physician were included. Descriptive, univariable and multivariable logistic regression analyses were employed to investigate the association between the presence of dactylitis and the characteristics associated with SpA.Fifty-eight (9.5%) patients currently or previously had dactylitis. In the multivariable analysis, dactylitis was independently associated with peripheral arthritis (OR= 4.83; p0.001), enthesitis (OR= 2.49; p=0.01), psoriasis (OR= 3.62; p0.01) and the physician's visual analogue scale (OR= 0.82; p=0.01). However, 67% of the patients who had dactylitis did not have peripheral arthritis or psoriasis and 15% had predominantly axial disease.Dactylitis is a frequent manifestation in patients with SpA, even during the early stages of the disease. Its presence is mainly associated with peripheral manifestations and psoriasis. Nevertheless, dactylitis is not exclusive of patients with PsA or peripheral manifestations.

Acute gastroenteritis (AGE) causes significant morbidity, especially in young children, and frequently requires hospitalization even in developed countries. Surveillance studies of AGE are important to determine the prevalence and variety of bacterial and viral pathogens, to initiate targeted preventive measures, such as vaccine programmes, and to monitor its impact. A prospective study was conducted in children

A patient with functionally defective fibrinogen has been studied. Fibrinogen Almeria I was found to have a prolonged of latency time (LT) and a decrease in rate of gelation (RG) when plasma or isolated fibrinogen were activated by thrombin or reptilase. This fibrinogen also has the unusual formation of cross-linked fibrin; the existence of unpolymerized alpha chains was confirmed.

Some 40 million abortions are performed around the world every year. In Spain, this figure reached 112,390 in 2011. Of these, approximately 5% were medical abortions. This percentage varies widely ...

ObjetivoDiseñar y validar un cuestionario autoadministrado evaluador de la función sexual en la mujerDiseñoEstudio transversal y multicéntricoEmplazamientoAtención primaria. Realizado en 9 centros sanitarios de la Comunidad ValencianaParticipantesMujeres sin riesgo de disfunción sexual, seleccionadas por muestreo consecutivo. Muestra inicial: 600; muestra válida: 212IntervencionesDiseño del cuestionario, de 14 preguntas a cumplimentar en 5–10 min, por un comité de expertos. Las participantes lo realizan en 2 ocasiones (test y retest) con un intervalo de 4 semanas. Evaluación diagnóstica por un comité de observadoresMediciones principalesFiabilidad entre preguntas de test y retest: a) una a una, mediante análisis de concordancia con índice kappa. Variaciones significativas mediante la prueba de la χ2 de bondad de ajuste; b) de las sumas de respuestas: comparación de medias (Wilcoxon) y posterior análisis mediante el coeficiente de correlación intraclase (CCI). La consistencia interna se determinó con el α de Cronbach y para la validez de contenidos se consideraron el consenso de expertos, la correlación interobservadores (CCI) y el análisis factorialResultadosFiabilidad entre preguntas una a una: kappa=0,597–0,743; χ2 no significativa. Fiabilidad entre sumas totales (Wilcoxon): no significativa (z=-0,312; p=0,755) (confianza del 95%). CCI: r=0,9587 (intervalo de confianza del 95%, 0,9460–0,9685), correlación significativa (confianza del 99%). Consistencia interna: a de Cronbach en el test de 0,8954 y en el retest de 0,8973. Correlación interobservadores (CCI): r=0,9498 (intervalo de confianza del 95%, 0,9386- 0,9611), significativa (confianza del 99%). Análisis factorial: agrupaciones de los ítems 9, 13 y 14; 1, 2, 3 y 10; 5, 6, 7 y 8ConclusionesEl cuestionario es estable, válido y fiable. Evalúa las fases de la respuesta sexual, la iniciativa y el grado de comunicación sexual. Recoge datos descriptivos acerca del desempeño sexual y resulta útil en la exploración y el diagnóstico de las disfunciones sexualesObjectiveTo design and validate a self-administered questionnaire to evaluate sexual function in womenDesignCross-sectional, multi-centre studySettingPrimary care, in 9 health centres of the Community of ValenciaParticipantsWomen not at risk of sexual dysfunction, selected by consecutive sampling. Initial sample 600, valid sample 212InterventionsQuestionnaire of 14 questions to be filled out in 5–10 minutes, designed by a committee of experts. The participants filled it out on two occasions (test and retest) with an interval of 4 weeks. Diagnostic assessment by a committee of observersMain measurementsReliability between test and retest questions:- One to one: analysis of concordance: kappa index. Significant variations: χ2 goodness of fit- On the sum of replies: comparison of means (Wilcoxon) and subsequent analysis: intra-class correlation coefficient (ICC). Internal consistency: Cronbach's alpha. Validity of contents: consensus of experts. Inter-observer correlation: ICC and factor analysisResultsReliability: one to one: Kappa from 0.597 to 0.743. χ2 not significant (ns). Between total sums (Wilcoxon), ns (z=-0.312, P=.755) (95% confidence). ICC: r=0.9587 (95% CI, 0.9460–0.9685), significant correlation (99% confidence). Internal consistency: Cronbach's alpha test: 0.8954, retest: 0.8973. Inter-observer correlation: ICC: r=0.9498 (CI, 0.9386–0.9611) significant (confidence 99%). Factor analysis: groupings of items 9, 13, 14; 1, 2, 3, 10; 5, 6, 7, 8ConclusionsThe questionnaire is stable, valid and reliable. It evaluates the stages of sexual response, initiative and degree of sexual communication. It collects data on sexualperformance. It is useful for exploring and diagnosing sexual dysfunction

Susceptibility to erythromycin and clindamycin was determined in 860 consecutive clinical isolates of β-haemolytic streptococci belonging to groups A (GAS, n = 134), B (GBS, n = 689), C (GCS, n = 19) and G (GGS, n = 18). Erythromycin resistance was 26.1% in GAS, 15.7% in GBS, 5.3% in GCS and 33.3% in GGS. The highest rate of clindamycin resistance (33.3%) was in GGS, followed by GBS (15.8%), GCS (15.8%) and GAS (5.2%). The M phenotype was predominant in GAS (80%), the constitutive MLSB phenotype was predominant in GBS (75%), and all GGS isolates showed the inducible MLSB phenotype. The uncommon erythromycin-susceptible and clindamycin-resistant phenotype was found in four GBS and two GCS isolates.

There is little information on cardiovascular longitudinal studies. In Spanish patients with hypertension (AHT)) and/or hypercholesterolemia (HC), with poor initial control of blood pressure (BP) and/or total cholesterol (TC), incidence rate (IR), cumulative incidence (CI), relative risks (RR), survival curves (SC), therapeutic compliance (TC) were quantified and the Framingham-Anderson scale (FAS) was adjusted to our patients.A total of 6,893 primary prevention patients with AHT and/or with HC were included in primary prevention, with an average of 1.22 years of follow-up. A total of 480 physicians participated. Incidence rate (IR), cumulative incidence (CIN), relative risks (RR), survival curves (SC) by Kaplan-Meier method, and therapeutic compliance (TCOM) by Haynes-Sackett self-reported questionnaire were calculated. The Framingham-Anderson scale (FAS) was validated with Pearson's correlation coefficient (r) and intraclass correlation index (ICI).CIN was 1.59% (1.31-1.90); the IR 1,321.6 cardiovascular events/ 100,000 patients/year (1,026.6-1,598.8). RRs with statistical significance were: age (p = 0.03). Blood pressure at the end of the study (p = 0.02), coronary background (p = 0.00), left ventricular hypertrophy (LVH) (p = 0.00), microalbuminuria (p = 0.02), CT/= 250 mg/dl (p = 0.01), fasting glycemia (Gb)/= 126 mg/dl (p = 0.00), creatinine/= 1.2 mg/dl at the beginning (p = 0.00) and at the end of the study (p = 0.00), and poor compliance in HC patients (p = 0.00). SC have statistical significance (p0.05) for AHT background, fasting glucose/= 126 mg/dl, target organ damage, and high cardiovascular risk with FAS scale. The adjusted FAS formula for global cardiovascular risk was (0.415 x FAS Risk%) + 0.517%, r = 0.9962 (p = 0.00) and ICI = 0.9969 (p0.0001).The equation for the FAS scale was adjusted for Spanish AHT/HC patients. Prognostic factors and SC were calculated. Benefit between TC and decrease of CVR in HC patients was quantified.

Scarce information is available on the clinical characteristics and risk factors of patients with chronic heart failure (CHF) attended in Primary Care (PC) setting. The aim of this study was to analyze the clinical characteristics of this population in PC.Multicenter, cross-sectional study in patients with CHF, consecutively recruited by 232 physicians in PC. The collected data included sociodemographic, etiologic, clinical and therapeutic variables.Eight hundred forty seven (847) patients were included (age 73.0 +/- 9.6 years; 50.5% men). Of these, 84.3% had arterial hypertension (AHT), 59.2% hypercholesterolemia and 34.9% diabetes mellitus. The most frequent associated clinical disorders were ischemic heart disease (40.1%) and peripheral artery disease (28.6%). In 69.6% of the patients the physicians knew the type of dysfunction (32.4% systolic, 37.2% diastolic). The main etiologies of CHF were the hypertensive cardiomyopathy (75.0%) and ischemic heart disease (40.1%); the most frequent trigger factor was atrial fibrillation (43.9%). Loop diuretics (72.3%) and angiotensin-converting enzyme inhibitors (60.9%) were the treatments used most and 6.7% of the patients were receiving treatment with beta blockers.AHT appears to be primary cause of CHF in PC. Diastolic dysfunction is more frequent than the systolic one, and the PC physicians do not know the cause of the ventricular dysfunction in one third of the cases. Loop diuretics and angiotensin-converting enzyme inhibitors were the most frequently used in these patients; the use of beta blockers in CHF is very scarce in PC.

Erythrocyte aggregability was determined by a laser backscattering light technique in 23 beta minor thalassemia carriers and in 36 age and sex matched controls. The aggregation time (Ta) was statistically higher in cases than in controls (2.8 +/- 1.0 vs 2.3 +/- 0.4, p0.05) and the aggregation index at 10 sec (AI10) was statistically lower (25.1 +/- 5.7 vs 28.2 +/- 3.8, p0.05), suggesting both parameters a statistically lower erythrocyte aggregability tendency. However, the total disaggregation threshold (gammaD) was statistically higher in cases than in controls (134.4 +/- 34.1 vs 105.1 +/- 33.1, p0.05), indicating that once aggregates are formed a higher shear rate is needed to break them up. No differences were observed in plasmatic factors, i.e., fibrinogen, total cholesterol and triglycerides, that could have influenced erythrocyte aggregation. A negative statistically significant correlation was found between erythrocyte indexes and the total disaggregation threshold. The lower erythrocyte aggregation found in minor thalassemia carriers could be attributed in part to the morphological alterations, although others mechanisms such as modifications in the membrane structure of the RBC can not be ruled out.

An association between an increase in plasminogen activator inhibitor type 1 (PAI-1) and obesity, and also between elevated levels of PAI-1 and the presence of PAI-1 promoter 4G allele has been described in adults and can contribute to increased risk of cardiovascular disease. It has also been suggested that in adults a decrease in adiposity has beneficial effects on the haemostatic system. However, less information is available regarding adiposity and fibrinolysis in children. The aim of the present study is to evaluate the effect of weight loss and the influence of the PAI-1 promoter 4G/5G genotype on the fibrinolytic system and lipid parameters in obese children. The clinical groups included 102 obese children and 105 controls of similar age and sex distribution. A significant decrease in fibrinolytic activity due to a significant increase in PAI-1 antigen and activity levels was observed in the obese children in comparison with the control group. In obese children, no significant differences in PAI-1 levels between the PAI-1 4G/5G genotypes were obtained. A significant correlation was observed between PAI-1 antigenic and functional levels and body mass index (BMI), as well as between PAI-1 levels and both triglyceride and insulin levels. No correlation between PAI-1 levels and either cholesterol or glucose levels was observed. After a three-month period of treatment to reduce weight, an increase in fibrinolytic activity due to a decrease in PAI- levels was observed in the obese children who had reduced their BMI in comparison with the group of obese children who did not show a decrease in their BMI. No significant differences between the two groups with respect to the variations in tissue type plasminogen activator and fibrinogen levels were obtained after three months of intervention to reduce weight. A significant correlation was observed between variations in BMI and variations in PAI-1 levels, and a significant inverse correlation was also observed between previous PAI-1 levels and variation in PAI-1 levels. Therefore, the largest decrease in PAI-1 levels was observed in the obese children with the highest previous PAI-1 levels. In conclusion, a decrease in BMI in obese children shows a favourable effect on the fibrinolytic system due to a decrease in PAI-1 levels. However, no influence of 4G/5G genotype on PAI-1 levels was observed.

Unfractionated heparin (UFH) and enoxaparin (low molecular weight heparin) constitute fundamental therapies in the treatment of patients with acute coronary syndrome (ACS). Since enoxaparin appears to offer clinical advantages over UFH in managing ACS, markers of thrombin generation, endothelial function and acute phase response could manifest different responses to UFH or enoxaparin. The purpose of the present study was to investigate the effect that treatment with either UFH or enoxaparin has on plasma hemostatic markers in 24 patients with ACS.The patients were randomized to receive 5,000 IU intravenous bolus and continuous infusion of 18 IU/Kg/h UFH (n=11) or 1 mg/kg/12h subcutaneous enoxaparin (n=13). The plasma levels of fibrinogen (Fg), prothrombin fragment 1+2 (F1+2), thrombin antithrombin complex (TAT), von Willebrand factor (vWF), tissue factor (TF) and tissue factor pathway inhibitor (TFPI) were assayed at admission and 6, 12, 24 and 48 hours after heparin treatment.Upon admission, UFH and enoxaparin patients showed a significant increase in all the hemostatic parameters measured with respect to the levels in the control subjects. In comparison with the baseline levels of the UFH- and enoxaparin-treated patients, Fg showed a significant increase at 48 h and TFPI at 6, 12 and 24 hours. However, at 48 hours TFPI levels were not significantly higher than the basal values. There were no significant changes in F1+2, TAT, vWF or TF.Markers of thrombin generation, endothelial function and acute-phase reactants manifest a similar response to UFH and enoxaparin. An increase in thrombin generation may be a result of persistently activated inflammatory and endothelial processes, despite UFH and enoxaparin treatment.

The effect of acenocoumarol on hemorheological variables was measured in 35 non-valvular chronic atrial fibrillation patients before starting oral anticoagulant therapy (basal) and one and two months after beginning treatment (INR-2,3). Fibrinogen increased significantly from the basal situation: 332+/-99 mg/dl to 386+/-96 mg/dl in the second month (p0.05). However, this small increase in fibrinogen is not large enough to mediate other rheological changes, and whole blood filterability, blood viscosity, plasma viscosity and erythrocyte deformability and aggregability remained unchanged after treatment. These results suggest that acenocoumarol does not affect rheological parameters and can therefore be used as a "neutral drug" for rheological studies in cardiovascular patients under oral anticoagulant therapy.

The incidence of coronary artery disease (CAD) is higher in post-menopausal than in pre-menopausal women. Epidemiological studies suggest that hormone replacement therapy (HRT) decreases the risk of cardiovascular disease in post-menopausal women. HRT could modify the cardiovascular risk via several mechanisms, including modifications in the fibrinolytic system and lipoprotein (a) levels. Our study was aimed at investigating some of these modifications.In the cross-sectional part of the study we evaluated several components of the fibrinolytic system, coagulation inhibitors and lipid profile in premenopausal (n=15) and post-menopausal women (n=64) with CAD and compared these parameters with those of healthy pre-menopausal (n=31) and post-menopausal women (n=88). The prospective part of the study analyzed the effect of HRT with transdermal estrogen with or without progestogen in post-menopausal women with CAD.Pre- and postmenopausal women with CAD showed significant lower fibrinolytic activity and higher plasminogen activator inhibitor type 1 (PAI-1) levels than their control groups. Lp(a) levels were higher in premenopausal women with CAD than in healthy premenopausal women. In post-menopausal women with CAD, HRT induced a significant decrease in PAI-1 and Lp(a) levels. No significant differences were observed in any parameter studied between the groups treated with transdermal estrogen with and without progestogen.CAD is associated with a decrease in fibrinolytic activity, possibly due to an increase in PAI-1 levels. An increase in fibrinolytic activity and a decrease in PAI-1 and Lp(a) levels were observed in CAD women receiving transdermal HRT and these changes may have a favorable impact on the risk of new cardiovascular events in post-menopausal CAD women.

The prothrombin G20210A mutation and factor V Leiden have been found to be associated with an increased risk of venous thrombosis, but the reported prevalences of the prothrombin gene variant both in the normal population and in patients with deep venous thrombosis (DVT) vary greatly in the literature. Moreover, the influence of oral contraceptives (OC) on thrombotic events in patients with the prothrombin G20210A variant has not been well established. In this study we evaluate both circumstances.A case-control study was run on 229 patients with DVT and 246 healthy controls. The patients' history of thrombosis and acquired thrombotic risk factors, especially OC, were recorded. Prothrombin G20210A mutation, factor V Leiden, antithrombin, heparin II cofactor, plasminogen and proteins C and S were evaluated.Seven and a half percent of the patients and 2.9% of the controls were carriers of the prothrombin mutation, while 12.2% of the patients and 1.6% of the controls had factor V Leiden. Among the 229 DVT patients there were 130 patients with clinically suspected thrombophilia (first thrombotic event occurring before the age of 45 years or positive family history of thrombosis or recurrent venous thrombosis). Ten percent of these 130 patients were carriers of the prothrombin G20210A mutation and 18.5% had the factor V Leiden mutation. The odds ratios (OR) for DVT risk were: 2.4 (95% CI, 1.0-6.3) for the total DVT patients and 5.2 (95% CI, 1.4-19.5) for the patients with clinically suspected thrombophilia with the prothrombin mutation. The risk of thrombosis was 6.9 (95% CI, 2.3-20.6) for the DVT patients and 14.3 (95% CI, 3.3-64.6) for the patients with clinically suspected thrombophilia with factor V Leiden. Fifty-five percent of the patients with combined congenital defects (prothrombin mutation G20210A plus another congenital defect) had recurrent thrombosis. In women receiving OC the risk of DVT was 3.5 (95% CI, 1.5-8.2) that of the patients not receiving OC. When women with combined defects were also taking OC, the risk of thrombosis increased significantly.The prevalence of the prothrombin G20210A mutation in the healthy population in our study is similar to that observed in other southern European countries. The prothrombin G20210A mutation does not by itself seem to be a high thrombotic risk factor. However, when it is present together with other thrombotic risk factors, the predicted risk of thrombotic events increases. The use of OC by women with the prothrombin G20210A variant or FV Leiden, either alone or combined with other thrombotic risk factors, was associated with a significant increase in the risk of venous thrombosis.

We describe the thrombophilic and clinical characteristics of a group of patients who suffered venous thrombosis (VT) (n = 36) and ischemic stroke (n = 8) while taking oral contraceptives (OC). Our purpose is to ascertain whether there are differences between users of second and third generation progestogen and to investigate the influence of concurrent congenital and acquired risk factors (other than OC) on the onset of the thrombosis. The group of patients included 36 women with VT and eight with ischemic stroke. The patients' recognized predisposing factors were recorded. We also considered age, length of time on OC, types of OC, rethrombosis, family history of VT, and the presence of thrombophilic genetic defects. In the group of patients with VT, 54% were treated with second generation OC (n = 23), and 30% (n = 11) were treated with third generation OC. We found no significant statistical differences with respect to age and length of time on OC between the two types of OC. The prevalence of genetic defects in these patients--factor V (FV) Leiden, prothrombin G20210A mutation and protein S deficiency--was 19% (n = 7), 17% (n = 6), and 8% (n = 3) respectively. We observed the shortest time lapse between initiating OC and the first thrombotic event in carriers of FV Leiden and in patients with combined defects, but the differences were not significant. In patients with ischemic stroke, 50% were treated with second generation OC and 50% were treated with third generation OC. Prothrombin G20210A mutation was detected in two patients. In both patients,the stroke occurred earlier than in the rest of the patients, but these differences were not statistically significant. With respect to preventing thrombotic events in these patients, our data suggest that OC therapy should be avoided in patients with a previous history of thrombosis and in patients with an evident thrombotic tendency in the family. In patients in whom the family history of thrombosis is not very evident, it would be recommended to screen for FV Leiden, prothrombin G20210A mutation, and protein S, and to rule out OC if the patient does in fact have one of these risk factors. Moreover, if a patient develops a thrombotic complication while taking OC, an evaluation to search for a thrombophilic defect is warranted, and at the same time, alternative methods of contraception should be considered.

A D-dimer assay can be helpful to rule out thromboembolism provided it is sensitive, reliable, fast and easy to perform. Tests based on the ELISA methodology have a high diagnostic sensitivity, and are therefore adequate for excluding deep venous thrombosis (DVT). The drawbacks are their long assay times, unsuitability to be run on single samples and cost. New methods have been developed, based either on the same principle, by immunofiltration or by microlatex immunoturbidimetric assays which seem to reach the high sensitivity and negative predictive value (NPV) required, but allowing fast and quantitative single sample analysis. The aim of this work was to evaluate one rapid test, a fully automated quantitative assay (IL Test D-dimer, run on an ACL 7000 coagulation analyzer, Instrumentation Laboratory).We compared the diagnostic value of IL Test for DVT with that of an ELISA (Dimertest Gold EIA Agen Biomedical Limited, Acacia Ridge, Australia). Eighty-six patients (43 men, 43 women, mean age: 61 years) showing DVT symptoms formed the population for this non-randomized controlled trial in a referral center. The diagnosis of DVT based on the clinical history, was confirmed by serial compression ultrasonography (CUS) with Doppler flow in 62 patients.The IL Test D-dimer proved to be rapid, automated and well suited for individual tests with a good reproducibility in three control plasmas with different concentrations of D-dimer (coefficient of variation range 0.54-3. 87%). Its performance was comparable to that of the Dimertest Gold EIA, as indicated by the areas under the receiver operating characteristic curves (Dimertest Gold EIA 0.748; IL Test D-dimer 0.70). On the basis of kappa coefficients, there was a good concordance between the Dimertest Gold EIA and IL Test D-dimer when the receiver operating characteristic (ROC) curves suggested cut-offs were used. The sensitivity (98.3%) and NPV (88.9%) shown by IL Test D-dimer are comparable or even better than those obtained for EIA (95%, 80%, respectively).This study shows that the new method can be included in prospective clinical trials to test the utility of D-dimer measurement in combination with other non-invasive diagnostic procedures in the management of DVT diagnosis.

The effect of a binifibrate (Biniwas Retard, Wasserman) on the plasma lipids and hemorheological profile of 30 primary hyperlipemic patients was studied. Our results indicate that the patients under study had evident rheological alterations as well as the expected lipid alterations. Treatment with Biniwas (2 x 550 mg/day) for six months not only substantially improved the alterations in the lipid balance but also tended to normalize the patients' hemorheological alterations, and there was a statistically significant correlation between the two effects. Apart from the decrease in plasma viscosity (1.20 +/- 0.05 vs 1.29 +/- 0.07 mPa.s, p0.001), the most noteworthy effects of Biniwas treatment were the decrease in red blood cell aggregability (8.7 +/- 1.2 vs 9.3 +/- 1.1, p0.05) and increased deformability (55 +/- 3 vs 47 +/- 5%, p0.001). Both changes may be due to modifications in the lipid composition of the erythrocyte membrane due to cell-plasma lipid exchange.

The rheological profile of 45 patients who had kidney failure and were undergoing periodical hemodialysis was studied to ascertain whether they showed rheological alterations and if these alterations improved after hemodialysis. Our results indicate that the patients studied suffer rheological alterations with respect to the control group, specifically increased plasma fibrinogen (436 +/- 119 vs 271 +/- 43 mg/dl, p0.001), increased plasma viscosity (1.30 +/- 0.10 vs 1.22 +/- 0.05 mPa.s, p0.001), higher erythrocyte aggregability (8.3 +/- 1.2 vs 7.4 +/- 1.4, p0.01) and a lower hematocrit (31.2 +/- 5.9 vs 43.4 +/-3.7, p0.001). In contrast, erythrocyte deformability did not seem to be altered with respect to the control group. The analyses carried out immediately after hemodialysis showed that in general the rheological profile worsened during this treatment; there was a significant increase in fibrinogen and in plasma viscosity. The rheological alterations detected may play a role in the development of the atherosclerosis processes often experienced by these patients.

Dead specimens of Corynosoma cetaceum were used to describe the trunk musculature of this species and to infer the use of the trunk as a secondary holdfast. Inferences were based on trunk muscle arrangement, changes in trunk shape, size and distribution of spines, and geometry of tegument thickness. The foretrunk of C. cetaceum is swollen and forms a spiny disk that is bent ventrally. The disk is flattened by several groups of muscles not described previously, which seem able to finely adjust the disk surface over the substratum. Disk attachment appears to be accomplished by two dorsal neck retractor muscles specialized in pulling the anchored proboscis into the foretrunk. This mechanism has been described in other acanthocephalans, becoming surprisingly efficient when used with a flattened, armed foretrunk. The ventrally spined hindtrunk requires force to move downwards in order to attach. A single ventral neck retractor muscle seems specialized in pulling the posterior trunk forward, inducing a downward force due to the muscle's precise points of insertion. This mechanism necessarily generates ventral wrinkling that needs to be eliminated for the spiny surface to be functional. The trunk ventral muscles are apparently arranged so as to concentrate the "excess" of the tegument into a single fold, optimizing the use of the remaining surface for attachment. The size and distribution of spines, as well as the geometry of tegumental thickness, conform to these observations. Morphological changes, seemingly simple, such as structural bending, may have triggered a cascade of subtle modifications and new functions during acanthocephalan evolution, reflecting how morphological integration and novelty interact.

In order to ascertain whether young asymptomatic patients with heterozygous familial hypercholesterolemia (FH) but without clinical signs of atherosclerosis have increased plasma thrombomodulin (TM) levels expressing early endothelial damage, we determined TM in 23 heterozygous FH subjects (aged 28-44 years, x: 32 +/- 6) and in a well matched control group (CG). In addition, carotid Doppler ultrasonography was done in all the patients and controls in order to assess the state of the vascular tree. Results show a tendency for FH subjects to have higher TM values than the CG (37.8 +/- 14.2 ng/ml vs. 30.1 +/- 11.2 ng/ml), although the differences are not statistically significant. When taken together the results of TM and carotid ultrasound, the sensitivity and specificity of the former were only 66% and 80%, respectively. The fact that only 66% of the FH patients with atherosclerotic injury had high TM values eliminates the possibility of using this as an early marker of atherosclerosis in FH individuals.

Epidemiological studies suggest that hormone replacement therapy (HRT) decreases the risk of cardiovascular disease in postmenopausal women via several mechanisms, including modifications in the fibrinolytic system and lipoprotein(a) [Lp(a)] levels. The aim of this study was to examine the influence of the levels and isoforms of Lp(a) on fibrinolytic activity in 91 postmenopausal women in comparison with premenopause and analyze the effect of HRT on those parameters. In postmenopause, an increase in plasma Lp(a) and plasminogen activator inhibitor-1 (PAI-1) levels was found. A significant inverse correlation was observed between Lp(a) or PAI-1 levels and plasmin generation. Plasma samples with low molecular weight (MW) apo(a) isoforms showed higher plasmin inhibition than plasmas with high MW apo(a) isoforms and similar levels of total Lp(a) and PAI-1. HRT induced a significant decrease in Lp(a) and PAI-1 levels and an increase in estradiol levels, as well as an increase in fibrinolytic activity. A significant correlation was found between the percentages of variation in Lp(a) levels and in plasmin generation and between the percentages of variation in PAI-1 levels and in the euglobulin lysis time under HRT. In conclusion, the increase in fibrinolytic activity observed in women under HRT could be explained by two independent mechanisms: (a) the decrease in PAI-1 and (b) the decrease in the inhibition of plasmin generation due to the decrease in Lp(a) levels.

Increased circulating levels of type 1 plasminogen activator inhibitor (PAI-1) have been associated with coronary artery disease (CAD). However, genetic and environmental determinants of PAI-1 expression are only partially understood. The levels of PAI-1 have been found to relate to 4/5 guanosine (4G/5G) polymorphism in the promoter region of the PAI-1 gene. The 4G allele in this polymorphism has been associated with higher levels of plasma PAI-1 activity, but despite the strong correlation between PAI-1 activity and antigen, no association has been found between PAI-1 antigen levels and the PAI-1 promoter 4G/5G genotype. The aim of the present study was to analyze the influence of the PAI-1 promoter 4G/5G genotype on PAI-1 levels in post-menopause women with coronary disease in comparison with healthy women in pre and postmenopausal status, and the influence of this genotype on variations in PAI-1 levels after hormone replacement therapy (HRT). No differences between 4G/5G allele distribution in the groups studied were observed. The group of postmenopausal women with CAD showed significantly increased PAI-1 antigen and activity levels in comparison with the control groups, and the levels of PAI-1 correlated with the 4G/5G genotype. A multivariate analysis revealed that in the CAD group there was a high correlation between 4G allele dosage and PAI-1 antigen levels, which were also influenced by the triglyceride levels but not by estrogen or glucose levels. After hormone replacement therapy the decrease in PAI-1 levels was correlated with the 4G allele dosage. We conclude that in the group of postmenopausal women with CAD the influence of the PAI-1 promoter 4G/5G genotype on PAI-1 levels is more evident than in the control groups, and that the decrease in PAI-1 levels after HRT in CAD women correlates with the 4G allele dosage.

We describe the case of a 39-year-old woman who suffered two iliofemoral venous thromboses, a cerebral ischemic infarct and recurrent fetal loss. Initial studies showed high levels of antiphospholipid antibodies (APAs) and a moderate thrombocytopenia. After her second miscarriage, laboratory diagnosis revealed that the woman was heterozygous for the factor V Leiden mutation and had a functional protein S deficiency as well as anti-protein S and anti-beta 2-glycoprotein I antibodies. The impairment of the protein C pathway at various points could well explain the recurrent thromboses in the patient and supports the role of a disturbed protein C system in the pathophysiology of thrombosis in patients with APAs.

Deep vein thrombosis (DVT) seems to be related to a hypercoagulation and definite hemorheological alterations, but the importance of these alterations in the development of thrombotic events in the deep vein system has not been established. The present study examines both aspects in a group of 55 patients with DVT; the presence of a hypercoagulable state was assessed by quantifying the prothrombin fragment 1+2 (F1+2) and the thrombin-antithrombin III complex (T-AT), and the main hemorheological parameters were evaluated in the acute state and 6 and 12 months later. The results show marked hemorheological, F1+2, and TAT alterations in the acute phase. After 12 months the pattern shows a modest improvement, but erythrocyte aggregation, fibrinogen, F1+2 and T-AT remain increased with respect to the control group (8.51 +/- 1.43; 331 +/- 81 mg/dl; 1.33 +/- 0.60 nmol/l; 3.54 +/- 1.71 ng/ml vs. 8.10 +/- 1.40; 230 +/- 38; 0.94 +/- 0.40; 1.56 +/- 0.59, respectively). These data suggest that the thrombotic event could be influenced by the previous rheological situation and hypercoagulable state.

In order to ascertain whether polygenic hypercholesterolemia (PH), the most common cause of small increases in plasma lipids during childhood, is associated with rheological alterations, we determined the hemorheological and lipid profile of 21 PH children (12 males, 9 females) and a well-matched control group (CG). In addition, a carotid ultrasound was done on all the PH children, but showed no alterations. When compared with the CG, PH children showed increased erythrocyte aggregation both at stasis (EAM0) (4.39+/-1.15 vs. 3.75+/-1.02), p0.05, and at low shear rate (EAM1) (8.22+/-1.42 vs. 7+/-1.39), p0.01, and increased plasma viscosity (PV) (1.19+/-0.04 cP vs. 1.15+/-0.04 cP), p0.01. These results reinforce the hypothesis that lipid metabolic alterations are associated with specific rheological modifications in absence of a demonstrable atherosclerotic lesion.

In order to ascertain whether hemorheological alterations precede the atherosclerotic lesion in familial hypercholesterolemia (FH), we studied the lipid and hemorheological profile of 29 heterozygous FH children (12 males and 17 females), aged 12+/-3 years, and a well-matched control group (CG), and assessed their plasma thrombomodulin level as an early marker of endothelial injury. No differences were found between FH children's plasma thrombomodulin values (31.7+/-11.2 ng/ml) and those of the CG (27.8+/-15 ng/ml). However, the rheological variables of FH children and the CG were statistically different (p0.001) for fibrinogen (Fbg): 266+/-48 mg/dl vs. 205+/-32 mg/dl; erythrocyte aggregation at stasis (EAM0): 4.6+/-1.2 vs. 3.3+/-0.9; erythrocyte aggregation at low shear (EAM1): 7.9+/-1.7 vs. 6.1+/-0.8; and plasma viscosity (PV): 1.18+/-0.03 cP vs. 1.12+/-0.04 cP. Correlations between rheological parameters and lipids were found. The normal values obtained in FH children for plasma thrombomodulin suggest that the hemorheological alterations appear prior to the vascular injury, are in part related to dyslipemia and could contribute to the development of the atherosclerotic process by modifying blood flow conditions.

In order to ascertain whether young familial hypercholesterolemic subjects without atherosclerotic lesions demonstrable on a carotid echo-Doppler show decreased erythrocyte deformability, we determined the erythrocyte elongation index (EEI) by means of a shear stress diffractometer (Rheodyn SSD) in twenty-four children with heterozygous familial hypercholesterolemia (FH), aged 12 +/- 3 years, and their corresponding affected parent. The parents were twenty-three adults with heterozygous FH aged, 32 +/- 6 years. The control group was made up of a similar number of well matched healthy volunteers. The EEI at 6, 12, 30 and 60 Pa showed no statistical differences between FH children and their control group, or between FH parents and their control group. No correlations were found between EEI and plasma lipids or lipoproteins at any of the shear stresses used. These results suggest that the red blood cells of young familial hypercholesterolemic subjects who show no deterioration of the vascular tree are not less deformable than those of healthy normolipemic subjects, and that dyslipemia itself does not produce alterations that damage the rheological properties of the red blood cell.

The cholesterol/phospholipid ratio (C/PL) of the red blood cell membrane, plasma lipids and erythrocyte aggregability were evaluated in 20 children with familial hypercholesterolemia (age: 10.4+/-4.6 years) but without detectable vascular injury. The results indicate that hypercholesterolemic children have a higher erythrocyte membrane C/PL ratio than the control group (0.81+/-0.23 vs. 0.65+/-0.08, p0.01). This membrane lipid alteration correlates inversely with the plasma concentration of HDL-cholesterol (r = -0.558, p0.010). The patients also showed greater erythrocyte aggregability than the control group (8.21+/-1.11 vs. 6.25+/-1.24, p0.001), but this does not seem to correlate with the changes observed in the lipid composition of the cell membrane. These results suggest that from childhood, people with familial hyper-cholesterolemia show alterations in the lipid composition of the red blood cell membrane that are related to the changes observed in plasma lipids and appear prior to atherosclerotic vascular symptoms.

In order to ascertain whether the increased aggregability observed in the red blood cells of diabetic patients is induced exclusively by plasma factors or is also influenced by membrane lipids, we examined the phospholipids of the erythrocyte membrane, the plasma fibrinogen concentration and erythrocyte aggregation in 86 insulin and non insulin-dependent diabetic patients. The data obtained show that the erythrocyte aggregability of the diabetic patients is higher than that of the control group (10.0+/-2.4 vs. 7.8+/-1.6%). This increased aggregability correlates not only with a higher fibrinogen concentration but also with changes observed in the membrane phospholipids. The percentage of sphingomyelin (SP) in the patients is higher than in the controls (22.6+/-6.8 vs. 18.4+/-5.4%) and that of phosphatidylserine (PS) is lower (9.5+/-6.1 vs. 12.1+/-5.1%). No differences in the percentages of the other two phospholipids identified (phosphatidylcholine, PC, and phosphatidylethanolamine, PE) were observed. The increase in the saturated nature of the phospholipids of the erythrocyte membrane, which can be measured by the (SP + PC)/(PE + PS) ratio, is statistically related (r = 0.39; p0.05) to the increased red blood cell aggregability observed in these patients.

This study examined ninety-six patients with essential arterial hypertension (WHO grade I-II) who had been under treatment for a period of at least one year before participating in the study. When the study began the patients received no drug treatment for one month. At the end of this washout period their basal situation was evaluated and drug treatment was begun (26 patients on calcium antagonists, 39 on beta-blockers and 31 on angiotensin converting enzyme inhibitors). The patients were evaluated again after one and two years of uninterrupted treatment with the chosen medication. The results obtained indicate that in a basal situation hypertensive patients have higher blood viscosity and erythrocyte rigidity values than the control group. Regardless of the drug treatment used, the patients experienced during the study a progressive deterioration of their hemorheological situation consisting of an increase in red blood cell rigidity and increased blood viscosity. These results indicate the importance of evaluating the hemorheological parameters of hypertensive patients and suggest that it may be advisable to include in their treatment some kind of medication that prevents progressive rheological deterioration.

We previously reported significantly elevated levels of plasminogen activator inhibitor type 1 (PAI-1) in plasma and placenta from pregnant women with severe pre-eclampsia, and pre-eclampsia is a frequent problem in molar pregnancies. As increases in PAI-1 may contribute to the placental alterations that occur in pre-eclampsia, we have begun to investigate changes in PAI-1 as well as PAI-2 and several other components of the fibrinolytic system in patients with trophoblastic disease. Significant increases in plasma PAI-1 and decreases in plasma PAI-2 levels were observed in molar pregnancies when compared with the levels in normal pregnant women of similar gestational age. PAI-1 antigen levels also were increased, and PAI-2 levels were decreased in placenta from women with molar pregnancies compared with placenta obtained by spontaneous abortion. Immunohistochemical analysis revealed strong positive and specific staining of PAI-1 in trophoblastic epithelium in molar pregnancies and relatively weak staining of PAI-2. No association between the distribution of PAI-1 and vitronectin was found, and no specific signal for tissue type PA, urokinase type PA, tumor necrosis factor-alpha, or interleukin-1 was detected. In situ hybridization revealed an increase in PAI-1 but not PAI-2 mRNAs in placenta from molar pregnancies in comparison with placenta from abortions. These results demonstrate increased PAI-1 protein and mRNA in trophoblastic disease and suggest that localized elevated levels of PAI-1 may contribute to the hemostatic problems associated with this disorder.

Recent studies in adults have shown that hemorrheological alterations are predictive of early cardiovascular disease, but it is unknown if they are related to hyperlipemia or are secondary to an established atherosclerotic process and if they appear during childhood.Several rheological parameters have been studied in 36 patients with familial hypercholesterolemia (FH). These patients were between 2 and 16 years of age and 12 of them were being treated with cholestyramine. Thirty-five controls (CG) were individually matched for age and sex.The FH patients treated with cholestyramine did not show significant differences in any of the six rheological parameters that were studied when compared to the other patients. Therefore, the results of the FH group were analyzed as a whole when they were compared with the CG. The following significant differences were found: Index of erythrocyte aggregation at stasis 5.0 +/- 1.2 vs 3.6 +/- 1.0 (p0.001), index of erythrocyte aggregation at low rate of blood shears 8.1 +/- 1.7 vs 6.9 +/- 1.4 (p0.001) and plasma viscosity 1.19 +/- 0.11 vs 1.16 +/- 0.04 mPA/s (p0.01). There were no significant differences in the plasma fibrinogen nor in the blood viscosity at shear rats of 230/s and 23/s. Carotic echo-doppler was taken in the HF patients which was normal, indicative of the absence of atherosclerosis lesions in the fibrous plaque phase.These results indicate that there are hemorrheological alterations in absences of established atherosclerotic lesions, which are associated with hypercholesterolemia and that emerge in the pediatric population. Therefore, research in FH patients offers new data to evaluate the atherogenic risk and its complications.

The reactivity of subendothelium generated by endothelial cells attained from the umbilical cord of a newborn girl from a patient with type I von Willebrand's disease was evaluated.Platelet adhesiveness was assessed by means of "ex vivo" blood perfusion systems (shearing coefficients from 300 to 1,300 s-1), on umbilical artery subendothelium and over the extracellular matrix (ECM) generated by cultured endothelial cells attained from the umbilical cord of a newborn baby from a type I von Willebrand mother.By means of an ELISA technique, a significant reduction of both the vWF secreted into the culture (p0.05) and of that associated with ECM (p0.05) was noticed. The two subendothelial surfaces examined supported a lesser extent of platelet adhesion than the control surfaces from healthy individuals in the perfusion tests at 1,300 s-1 (p0.05). The experimental results did not agree with the lack of clinical manifestations and laboratory abnormalities in the propositus at age 3.These findings suggest that the endothelial cells cultured from the tissues of a newborn baby from a type I von Willebrand woman expressed less vWF, at the same time confirming the importance of vWF bound to connective tissue in sustaining platelet adhesion. The data attained here illustrate the complex model of inheritance of moderate von Willebrand's disease, along with the technical limitations of cell culture studies. Such observations must be borne in mind whenever any experimental approach is performed with material attained from ill-differentiated tissues such as the umbilical cord vein.

Elevated plasma levels of type 1 plasminogen activator inhibitor (PAI-1) have been implicated in mediating the fibrin deposition and occlusive lesions that occur within the placental vasculature in preeclampsia (PE) and intrauterine growth retardation (IUGR). In this report we identify the cells within the normal-appearing villous tissue that are responsible for the local production of PAI-1 in women with PE and IUGR. Levels for another fibrinolytic inhibitor (ie, type 2 plasminogen activator inhibitor [PAI-2]) were determined for comparative purposes. Elevated levels of PAI-1 were detected in placenta extracts from PE/IUGR patients (121 +/- 38 ng/mg, n = 8) when compared with the levels in placenta extracts from normal women (43 +/- 17 ng/mg, n = 10) or women with IUGR but not PE (51 +/- 22 ng/mg, n = 11). Immunohistochemical analysis of paraffin sections showed an increased immunoreactivity for PAI-1 in the placental villous syncytiotrophoblasts from PE/IUGR women compared with the immunostaining of placental samples from the normal or IUGR group. In contrast, antigen levels and immunostaining for PAI-2 were reduced in the placentas harvested from not only the PE/IUGR women (209 +/- 144 ng/mg) but also the IUGR group (169 +/- 106 ng/mg) in comparison with the PAI-2 levels in normal placentas (535 +/- 98 ng/mg). To document that the increased immunoreactivity for PAI-1 in PE/IUGR syncytiotrophoblasts was mediated by an increased production of PAI-1 within these cells, in situ hybridization analysis was performed. A strong positive signal for PAI-1 mRNA in villous syncytiotrophoblasts from PE patients (n = 5) was obtained after 2 weeks of exposure to the NTB2 emulsion in comparison with the weak signal for PAI-1 mRNA that required a 10-week exposure of the normal placenta sections (n = 10). Northern blotting for PAI-1 mRNA showed that both transcripts (ie, 3.2 and 2.3 kb) were elevated in samples of two PE patients in comparison with the PAI-1 mRNA transcripts present in a normal placenta and an IUGR placental sample. These results show increased PAI-1 and mRNA levels in placentas from PE patients and raise the possibility that localized elevated levels of PAI-1 may play a role in the initiation of placental damage, as well as in the thrombotic complications associated with this disease.

Pyomyositis (PMS) is a primary infection of striated muscle. Recent scanty reports suggest that non-tropical PMS may differ from classical tropical PMS. To address this question, 12 cases of nontropical PMS seen at two hospitals between 1976 and 1992 were reviewed and an English-literature search of similar cases was conducted. Both the series and reported cases are pooled together and herein reported. The age distribution of the 97 patients showed 30-50 and 60-70-year peaks, with a 3:1 (male-female) ratio. Fever, high erythrocyte sedimentation rate, and muscle stiffness or inflammation were present in more than 75% of patients. Muscles of the thigh (54%), back (13%), buttock (11%), arm (9%), or chest wall (4%) were involved. Staphylococci (61%), gram-negative bacilli (16%), streptococci (12%), and fungi (2%) were isolated from muscle specimens. Human immunodeficiency virus infection, diabetes mellitus, hemopoietic disorders, and other conditions with defective neutrophil function were present in 64 patients (66%). Drainage of pus and antibiotic therapy were the standard treatments. The mortality rate reached 10%. Analysis of patients classified by the comorbid condition showed differences in age, causative microorganisms, clinical features, and death rate. It is concluded that several clinical presentations of nontropical PMS are at variance with that of tropical PMS.

The purpose of the study was to test whether APC: alpha 1AT complex is a useful clinical marker of the activation of coagulation. The rationale for this is that activated protein C may appear in circulation at an early stage of blood coagulation, when subcoagulant amounts of thrombin are formed. Given the relatively higher half-life of APC: alpha 1AT as compared to that of thrombin:AT-III (TAT) complexes, we hypothesized that APC:alpha 1AT could represent an amplification of the thrombin generated in the first events of coagulation. Using sandwich ELISA's we measured APC: alpha 1AT and TAT complexes as well as complexes of AT-III with its target proteases in normal subjects and in several clinical groups of patients prone to thrombotic episodes, including pregnancy, preeclampsia, hemodialysis, gynecological tumors, diabetes and oral contraceptives. APC: alpha 1AT complex was significantly increased in all clinical groups as compared to normal subjects and showed relatively higher increases than did TAT and ATM complexes in the majority of the groups studied. There was a significant and positive correlation between APC: alpha 1AT and TAT complex levels in the majority of the groups, as well as between TAT and ATM and between APC: alpha 1AT and ATM complex levels. We conclude that APC: alpha 1AT complex can be used as a sensitive marker of prethrombotic states.

Erythrocytes promoted platelet reactivity in a plasma medium, as demonstrated in an in vitro system that independently evaluated the biochemistry of platelet activation and recruitment. The prothrombotic erythrocyte effects were metabolically regulated, as evidenced by lack of activity of ATP-depleted or glutaraldehyde-fixed erythrocytes. They occurred in the absence of cell lysis as verified by lactate dehydrogenase assays, and had an absolute requirement for platelet activation. The presence of erythrocytes induced a twofold increase in platelet thromboxane B2 (TXB2) synthesis upon collagen stimulation, indicating that erythrocytes modulated platelet eicosanoid formation. Cell-free releasates from stimulated platelet-erythrocyte suspensions, which exhibited increased recruiting capacity, contained 6.9-fold more ADP and 4.9-fold more ATP than releasates from stimulated platelets alone. Following aspirin ingestion, TXB2 formation was blocked, but erythrocyte promotion of platelet reactivity persisted at those doses of collagen that reinduced platelet activation. Moreover, when platelet mixtures consisted of as little as 10% obtained before aspirin plus 90% obtained post-aspirin ingestion, significant erythrocyte enhancement of platelet reactivity occurred, even at low agonist concentrations. These erythrocyte effects would decrease the therapeutic potential of inhibition of platelet cyclooxygenase by aspirin. The erythrocyte-induced modulation of platelet biochemistry and function emphasizes the importance of cell-cell interactions in stimulus-response coupling.

A total of 161 samples from genital sources were evaluated using two different methods for genital Mycoplasma isolation: inoculation to urea broth, arginine broth and A7 solid media (standard method) and a new enzymatic method (Mycoscreen Oxoid). The isolation rates for Ureaplasma urealitycum were 42% (standard method) and 49% (Mycoscreen) (sensitivity: 100%; specificity: 88%). The isolation rates for Mycoplasma hominis were 13% (standard method) and 14% (Mycoscreen) (sensitivity: 80%; specificity: 95%). Using the enzymatic method, manufacturer's positive result is defined as a count greater than 10,000 UCC-ml at 24 hours. When we compare the 24 hours results, the concordance rates was 84% (Ureaplasma urealyticum) and 62% (Mycoplasma hominis). Mycoscreen method is a valid and fast technique for the isolation and identification of genital Mycoplasma. It also allows a fast screening of pathologic counts of Ureaplasma urealyticum in genital exudates.

A report on a new case of Pelger-Huët (PH) leukocyte anomaly in the homozygous form in an 18-month-old girl is presented. Clinically, the proband shows no special symptoms dependent on the leukocyte anomaly, but polydactyly affects both hands (six fingers on one hand) and feet (six toes on both feet). Her pedigree reveals the existence of three couples in which both husband and wife are heterozygous carriers of the PH anomaly. Study of the family lineage suggests that transmission of the leukocyte anomaly is prevailingly dominant in nature with complete penetration and variable expression.

ObjetivoEvaluar la efectividad de lisinoprilhidroclorotiazida a dosis fijas en el control de la presión arterial en hipertensos tratados con monoterapia y mal controlados.DiseñoEstudio observacional, prospectivo.EmplazamientoAtención primaria.ParticipantesCiento noventa y nueve médicos de atención primaria que incluyeron a 931 pacientes (56,7% mujeres), con edad media de 62,0 ± 10,3 años. Finalizaron el estudio 915 pacientes (98%) que se incluyeron en el análisis.Mediciones principalesSe siguieron las recomendaciones de la OMS/SIH en la medición de la presión arterial y el diagnóstico de mal control. Además, se evaluaron presión del pulso, índice de masa corporal y parámetros analíticos básicos. Se realizaron 4 visitas durante 6 meses de seguimiento.ResultadosLisinopril-hidroclorotiazida (20/12,5mg) disminuyó significativamente la PAS (24,6 ± 3,5mmHg) y la PAD (14,3 ± 0,7mmHg) (p < 0,001). El control de la presión arterial aumentó hasta el 52,8% (p < 0,001). La edad fue la única variable que influyó en el control de la presión arterial (OR, 0,81; IC del 95%, 0,71-0,92%; p = 0,001). La presión del pulso disminuyó 10,4 ± 4,3mmHg (p < 0,001). A las 24 semanas de tratamiento, se observó una mejoría en el perfil glucémico y lipídico, y de la HbA1c en los diabéticos.ConclusionesEn atención primaria, lisinopril-hidroclorotiazida (20/12,5mg), controló la presión arterial del 52,8% los de hipertensos mal controlados con monoterapia. Además, disminuyó la presión del pulso y mejoró el perfil lipídico y el glucémico.ObjectiveTo evaluate the effectiveness of the fixed dose of a lisinoprilhydrochlorothiazide combination treatment in the control of blood pressure, in poorly controlled high blood pressure people, treated with monotherapy.DesignProspective observational study.SettingPrimary care frame.Participants931 patients (56.7% women) with an average age of 62.0±10.3 years, were included by 199 primary care physicians. 915 patients (98%) ended the study and finally they were included for the statistical analysis.Main measurementsOMS/SIH recommendations on blood pressure measurement and diagnose of poor control were followed. Pulse pressure, body mass index and basic clinical analyses were assessed. Four continuation visits were made during six months.ResultsLisinopril–hidrochlorothiazide (20/12.5mg) reduced significantly SBP (24.6±3.5mm Hg) and DBP (14,3±0.7mm Hg) (P

Red blood cells (RBC) increase the proaggregatory capacity of a cell-free supernatant obtained by stimulating platelet-rich plasma (PRP) samples with collagen (1 microgram/ml) as measured by the BASIC wave; this effect increases with the number of RBC and is proportionally greater with a lower number of platelets or when lower collagen concentrations are used. Aspirin (ASA) modifies the RBC behaviour in relation to their platelet-collagen interaction. This is demonstrated by the fact that when PRP and RBC obtained from the same subjects before and two hours after the ingestion of ASA (0.5 g) were mixed, it was found that non-ASA-RBC stimulate ASA-PRP, probably through a platelet cyclooxygenase independent pathway; ASA-RBC, however, stimulate non-ASA-PRP, but not ASA-PRP, which suggests that they may need an active platelet cyclooxygenase system for their action. This effect of ASA on RBC is not transient and was also observable 48 h after ASA ingestion. In addition, it was found that ASA-RBC greatly increase the activation of a mixture containing a small proportion of non-ASA-PRP in ASA-PRP, a situation that is expected to be encountered "in vivo" after ASA treatment. This effect of ASA-RBC on platelet activation may help to explain the sometimes contradictory clinical effect of aspirin as an antithrombotic drug.

After the administration of cytostatic drugs, an increase in thromboembolic phenomena has been described in cancer patients. The authors studied the changes in plasmatic coagulation and fibrinolysis in 40 patients with nonoperable Stage III and IV lung cancer after cytostatic chemotherapy. The results show significant postchemotherapy increases in fibrinopeptide A levels, as well as a decrease in fibrinolytic activity reflected by a drop in functional tissue activator. Also the authors studied the potential accumulative effect of three chemotherapy cycles. A significant increase in functional plasminogen activator inhibitor has been noted. Chemotherapy is apparently capable of conditioning a decrease in fibrinolytic activity in these cancer patients that could be related to the enhanced tendency to developing thromboembolic phenomena after cytostatic chemotherapy.

A comparative study of a DNA probe for the detection of Neisseria gonorrhoeae with Gram stain and modified Thayer-Martin medium was performed. The probe was the 2.6 megadaltons (Mda) cryptic plasmid of N. gonorrhoeae, labeled with a nonradioactive system combining sulphonation of DNA with the antibody detection of sulphonated groups (Organics Chemiprobe). Overall 101 samples were evaluated: 39 urethral exudates, 3 rectal exudates, and 59 cervical exudates, from 42 males and 54 females in whom gonococcal infection was suspected. Simultaneously, Gram stain and culture of the several exudates were carried out. The in vitro sensitivity of the method was evaluated with different dilutions of N. gonorrhoeae, from 1 to 1000 cfu/ml, and a minimum of 50 cfu/ml were detected. In the detection of N. gonorrhoeae in clinical samples, there was a 100% sensitivity and a specificity of 83% (males) and 79% (females), with positive predictive value of 97% in males and 53% in females. The negative predictive value was 100% both for males and females.