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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

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.

Sexual pathogens, cell types and morphologic alterations of urethral epithelial cells were investigated by means of the Papanicolaou smear in 110 heterosexual men. Seventy-five patients with urethritis were included: 17 (22.6%) with gonococcal urethritis (GU) and 58 (77.3%) with non-gonococcal urethritis (NGU). Thirty-five males without symptoms or signs of urethritis comprised the control group. An increase in epithelial cell dissociation was observed in patients with urethritis. Non-specific inflammatory changes were statistically more common in patients with urethritis than in controls, and more severe in GU (65%) than in NGU (15.5%). Nuclear atypia was a common finding (43.5%) in infections due to C. trachomatis. Mucus was associated with the presence of urethritis although no differences regarding etiology were found. No polimorphonuclear neutrophils were observed in the exudate of three patients (5%) with NGU. There was a statistically significant presence of lymphocytes in patients with urethritis, particularly in GU (45%), more frequent than in NGU (15.5%). Erythrocytes were also significantly more frequent in urethritis, with a greater proportion in GU (94%) than in NGU (64%). Plasma cells, eosinophils, and histiocytes were only observed in a few patients with urethritis. The Papanicolaou smear had a sensitivity of 47% and a specificity of 90% in Chlamydia trachomatis infections.

To study the influence of finasteride treatment on the molecular forms of prostate-specific antigen (PSA) in patients with benign prostatic hyperplasia (BPH).Total PSA, free PSA and PSA complexed to alpha1-antichymotrypsin (PSA-alpha1ACT) were measured in plasma and serum from 40 men with BPH and a total PSA of20 ng/mL, using in-house and commercial immunoassays, before and during treatment with finasteride (30 men) or placebo (10 men).The baseline values were not significantly different between the groups, with mean (sd) total plasma PSA levels of 3.6 (4.3) and 4.8 (5.9) ng/mL in the finasteride and placebo groups, respectively. Finasteride, but not placebo, induced a significant reduction in total PSA, free PSA and PSA-alpha1ACT levels in plasma and serum (P0.001). However, complexed-to-total (c/t) and free-to-total (f/t) PSA ratios remained constant in both groups, both in plasma and serum, during the follow-up.The decrease in total PSA after finasteride treatment results from a proportional reduction in its two major molecular forms, free PSA and PSA-alpha1ACT, which explains why the c/t and f/tPSA ratios do not change significantly despite treatment. This suggests that routine analysis of molecular forms of PSA could improve the utility of the change in total PSA associated with finasteride for the early diagnosis of prostate cancer. It also suggests that any subsequent change in both ratios, particularly an increase in c/tPSA or a decrease in f/tPSA ratio, could be considered an early sign of neoplastic degeneration rather than a therapeutic consequence.

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.

To evaluate the influence of several factors, including age, prostate volume, total PSA (PSA-T), clinical stage and Gleason on the PSA:alpha 1ACT/PSA-T (C/T) ratio.Using in-house assays, we measured plasma levels of PSA-T and PSA:alpha 1ACT complex in 622 patients with benign prostate hyperplasia (BPH) (455 with hystological confirmation and 167 with clinical evidence of absence of malignance) and in 255 patients with prostate cancer (CaP), and determined the correlation between different parameters.In BPH patients, PSA-T and PSA:alpha 1ACT significantly increased with age. There was a positive correlation between age and PSA-T (r = 0.161, p0.0001) and PSA:alpha 1ACT (r = 0.141, p = 0.001). In contrast, the C/T ratio remained constant and below 70% in all decades. Similar results were obtained in CaP patients. In BPH patients, there was a positive correlation between prostate volume and PSA-T and PSA:alpha 1ACT, but not with the C/T ratio. In CaP patients, however, there was a negative correlation between prostate volume and the C/T ratio. An excellent correlation was found between PSA-T and PSA:alpha 1ACT, and a good correlation between PSA-T and the C/T ratio and between PSA:alpha 1ACT and C/T ratio. A multiple regression analysis showed that, in HBP and CaP patients, PSA-T and PSA:alpha 1ACT complex were the only parameters that significantly and independently influenced the C/T ratio.The C/T ratio is independent of age, prostate volume, Gleason and clinical stage. Therefore, these factors need not to be considered when using the C/T ratio.

To evaluate the usefulness of the ratio PSA:alpha-1-antichymotrypsin/total PSA (C/T) in the diagnosis of prostate cancer in the range of total PSA between 4 and 10 ng/mL.By using home-made ELISAs we have determined plasmatic concentrations of total PSA and complex PSA:alpha-1-ACT in 300 patients with total PSA between 4-10 ng/mL. All samples were obtained before any manipulation that could interfere the PSA levels.By prostatic biopsy 85 patients (28.3%) were diagnosed of prostate cancer (CaP) and 215 (71.6%) of benign prostatic hyperplasia (BPH). The mean values of the complex PSA:alpha-1-ACT (4.2 ng/mL in the BPH patients vs 5.0 ng/mL in the CaP patients) and of the C/T ratio (0.70 vs 0.82, respectively) showed significant differences between both groups (p =0.0001). The total PSA did not show differences (6.1 ng/mL vs 6.0 ng/mL; p = 0.79). From all three parameter evaluated, the ratio C/T had the biggest area under the ROC (0.884) and statistically significant differences in comparison with total PSA (0.490; p =0.001) and the complex PSA:alpha-1-ACT (0.696: p =0.001). Therefore, by using a ratio C/T0.62 to decide the performance of a biopsy, 27% of the patients with BPH could have avoided this procedure with a 100% sensitivity. Increasing the ratio to 0.68 the specificity is 47% and the sensitivity is 95.2%. Rectal examination did not have influence on the cut-off, sensitivity, specificity and area under the ROC of the ratio C/T.Our results confirm that the ratio C/T improve the diagnostic capacity of the total PSA between 4-10 ng/ml. Moreover, the rectal examination does not influence the selection of ratio C/T cut-off suggestives of CaP neither the diagnostic efficacy.

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 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.

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.

Thrombosis occurs in 20 to 30% of patients with Behçet's disease (BD), but the precise pathogenic mechanism underlying the thrombotic tendency in these patients is not well known. Venous thromboses are commonly located in the lower extremities, but right intracardiac thrombi are extremely rare. We report for the first time on a young patient with BD associated the 20210G-A prothrombin gene mutation and right intracardiac thrombosis. We suggest that the association of BD with this newly recognized prothrombotic genetic mutation may have contributed to the development of the thrombotic event in this patient.

To study the usefulness of the complexed-to-total (C:T) prostate-specific antigen (PSA) ratio in the early detection of prostate cancer in patients with a total PSA value4.0 ng/ml.Total PSA and PSA complexed to alpha(1)-antichymotrypsin were measured in plasma from 193 men with benign prostatic hyperplasia (BPH) and 34 with prostate cancer. The diagnosis was confirmed in 28 BPH and 16 prostate cancer patients by biopsy and in 165 BPH and 18 prostate cancer patients by histological study following transurethral prostatectomy or open prostatectomy.The area under the receiver operating characteristic (ROC) curve was significantly greater for the C:T PSA ratio (0.908) than for total PSA (0.692) (p0.001). Using a cut-off point of 0.83 for the C:T PSA ratio and regardless of the digital rectal examination (DRE) finding, 20 of the 34 prostate cancer patients would have been given a correct diagnosis (59% sensitivity) and in only 8 of the 193 BPH patients would a biopsy have been necessary (96% specificity). With a cut-off of 0.79, the sensitivity increased to 85% with a specificity of 92%. When the analysis was restricted to the 44 patients with abnormal DRE, the area under the ROC curve for the C:T PSA ratio was 0.919, and a cut-off point of 0. 78 gave a sensitivity of 87% and a specificity of 93%. Using a cut-off of 0.63, all prostate cancers were detected (100% sensitivity) and 54% of the negative biopsies would have been eliminated. For the 183 patients diagnosed following surgery, a cut-off of 0.82 gave a sensitivity of 72% and a specificity of 94%.Our results show that the C:T PSA ratio significantly improves the clinical utility of the PSA assay for detecting prostate cancer in patients with total PSA4 ng/ml, increasing the sensitivity without significantly increasing the number of biopsies.

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.

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.

Investigation of the urethral flora in men with urethritis, with particular reference to anaerobic bacteria.Multiple cultures were performed on three urethral samples from 110 men attending the STD Clinic of the School of Medicine in Seville: 35 with no evidence of urethritis (control group), and 75 with urethritis (17 gonococcal urethritis (GU) and 58 non-gonococcal urethritis (NGU)). In the 58 men with NGU, Chlamydia trachomatis was isolated in 16 (27.5%), Ureaplasma urealyticum in 18 (31%), Trichomonas vaginalis in two (3.4%) and no pathogens were isolated in the remaining 22 (38%) patients.Aerobic flora, mainly Staphylococcus spp., were isolated less frequently (41%) in patients with GU than in the control group (80%), and those with NGU (72%). Anaerobic flora were isolated in 62% of patients, with similar isolation rates in each group. Gram-negative anaerobes were more frequently isolated in men with urethritis, especially NGU, compared to controls (P0.05). Prevotella spp. and Bacteroides spp. were significantly more frequently isolated in patients with NGU, including Chlamydia-negative NGU. Fusobacterium spp. were more frequent in the Chlamydia-positive NGU than in the controls (P0.05). P. magnus was the most frequent anaerobic species found in the control group, while P. prevotii was most frequently seen in the urethritis group. B. ureolyticus, P. prevotii and P. tetradius were more frequent on the NGU group (P0.05). B. ureolyticus was commoner in patients with Chlamydia-negative NGU, while P. tetradius and P. asaccharolytica was commoner in those where C. trachomatis was isolated than in the control group.Urethral microflora isolated showed ten bacterial genus and 25 different species of anaerobes. The spectrum of these microflora changed with the presence of urethritis and varied with its aetiology.

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.

The authors present a study in two groups of Wistar rats, which were given two different parenteral nutritions with two different amounts of proteins, during different periods of time (4, 7 and 11 days), with the objective of evaluating their influence on the healing of a colonic anastomosis which was performed prior to the initiation of the TPN. To asses the condition of the colonic anastomosis, we studied the rupture pressure of the colon containing the anastomosis, the hydroxyproline concentration of said anastomosis, and the histological study of the same. The results indicate that the group of animals which were fed with a hyperproteinic diet during a longer period of time, showed a better degree of healing than the rest of the study groups.

The ability of unfractionated (UF) heparin and low-molecular-weight heparin (LMWH) to potentiate the inhibition of fibrinolytic and coagulation factors by protein C inhibitor (PCI) was studied. Inhibition of activated protein C (APC), urokinase plasminogen activator (uPA), tissue plasminogen activator (tPA), thrombin, factor Xa (Xa), factor XIa (XIa) and plasma kallikrein (KK) by PCI was found to be dependent on the size of the polysaccharide. In general, maximal stimulation was reached with UF heparin, except in the case of KK. Differences in heparin stimulation were more pronounced for thrombin, APC, uPA, tPA and XIa, whereas inactivation of Xa by PCI was less dependent on the presence of heparin, and kallikrein showed higher potentiation with LMWH than with UF heparin. The second-order rate constants for enzyme inhibition by PCI were strongly dependent on the ionic strength, and, in general, with an ionic strength higher than 0.15 the heparin stimulation of the inhibition reactions was drastically reduced. These results may explain the large discrepancies in the literature on the effect of heparin on the stimulation of enzyme inhibition by PCI. They also show that LMWH is less efficient in stimulating the PCI inhibition of APC, uPA and tPA, which could contribute to the antithrombotic effect of these enzymes.

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.

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.

The effects of continuous intravenous perfusion of somatostatin on the incidence of ulcers and the histamine and serotonin gastric mucosal content in rats subjected to 12 h of restraint were studied. 51 sets of Sprague-Dawley male rats (102 animals) were divided at random into two groups. Those in group I were immobilized and treated with an intravenous infusion of isotonic saline solution. Animals in group II were also immobilized and given intravenous cyclic somatostatin dissolved in isotonic saline solution; the initial dose was 25 microgram and a continuous infusion of 2.5 microgram/kg/h was administered thereafter. A decrease in the ulcer index was observed in the rats perfused with somatostatin (p less than 0.01) as well as a decrease in the histamine (p less than 0.001) and serotonin (p less than 0.01) gastric mucosal contents. These effects of somatostatin on restraint-induced stress ulcer in rats are probably to be explained by microcirculatory changes in the gastric mucosa determined by the vasoactive amines (histamine and serotonin). They constitute an important factor in the pathogenesis of these lesions.

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

We have studied the clinical efficacy and pharmacokinetics of cefuroxime in 3 children aged 5, 7 and 10 months who were suffering from meningitis due to Haemophilus influenzae group b (beta-lactamase producers). The MICs of chloramphenicol against these three beta-lactamase-producing H. influenzae isolates were 8, 3.1 and 16 micrograms/ml, and those of cefuroxime were 0.25, 0.5 and 0.12 microgram/ml, respectively. The dosage of cefuroxime was 100 mg/kg/day divided in four 6-hourly intravenous doses for 15 days, and 10 mg given intrathecally every 48 h. Blood and spinal fluid levels were determined by microbiological assay. All the 3 children had excellent clinical and bacteriological responses with negative spinal fluid cultures after 48 h of treatment.

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.

The in vitro release of B-thromboglobulin (BTG) from platelets after stirring the platelet rich plasma (PRP) 5 min (37 degrees C/1000 rpm) was studied in a group of 13 healthy subjects before and after 'in vivo' aspirin ingestion, 1 g/d for 3 d. A significant reduction in the platelet BTG release (31%) was observed after aspirin ingestion in comparison to the pre-aspirin values, suggesting that the BTG release by stirring is related to a platelet activation process. Small doses of collagen (0.625 microgram/ml) and thrombin (0.1 U/ml) always released platelet BTG, whether or not there was a visible platelet aggregation, suggesting that platelet activation is not necessarily followed by visible platelet aggregation. A significant correlation was found between the BTG released by stimulation with collagen (2.5 microgram/ml) and thrombin (0.2 U/ml) and the maximum velocity and intensity of the aggregation curve parameters.