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The need for performing isotope ratio measurements by MC-ICPMS on samples only available in small sizes and not allowing any dilution requires the development of sample introduction systems that can run below 10 μL min−1 sample flow rate (continuous mode). With a torch integrated sample introduction system (TISIS), optimisation of the running conditions involves the study of the temperature of the spray chamber (TSC). This paper investigates the consequences of changing TSC up to 100 °C and the sample flow rate down to 5 μL min−1 on mass discrimination effects. The validity of the exponential model commonly used to correct for these effects was tested for strontium isotopic measurements. Two categories of processes favouring the heaviest isotopes were envisaged: at plasma stage –“mechanism 1”, and within the ion beam –“mechanism 2”. The extraction potential applied inside the interface (HV1) was progressively increased, and results obtained for a range of approximately ±5 to 6 V around HV1 = 4004 V at 15 μL min−1 and TSC = 40 °C were used as reference. The intensity of mass discrimination effects increased at 15 μL min−1 and TSC = 60 or 100 °C, and decreased at 5 μL min−1 and TSC = 40 °C. At TSC = 100 °C (15 μL min−1) or at 5 μL min−1 (TSC = 40 °C) the stability of mass discrimination effects and the average efficiency of the exponential model were particularly degraded. The contribution of mechanism 1 (and its influence on mechanism 2) seemed to be the determining factor. At TSC = 100 °C the hypothesis made was the acceleration of the solvent evaporation process inside the TISIS, leading to variations in the characteristics of the tertiary aerosols. And the consequence was an increase of the plasma mass discriminative effects (ion diffusion) reinforced by the extra energy made available to the plasma ions. At 5 μL min−1, changes in the plasma composition arising from the reduction of the water load in combination with the ion production at an earlier stage within the plasma followed by the processes of ion diffusion were also hypothesized as possible causes for the inadequacy of the exponential model. [ABSTRACT FROM AUTHOR]

Background: Whether the treatment of venous thromboembolism (VTE) with unfractionated heparin (UFH) confers a higher risk of thrombocytopenia than does treatment with low molecular weight heparin (LMWH) remains controversial, and very few data are available from routine clinical practice., Objectives: We assessed the incidence, risk factors and prognosis of heparin-associated thrombocytopenia (HAT) according to the type of heparin therapy, UFH or LMWH., Patients/methods: Data were obtained from the international prospective Registro Informatizado de la Enfermedad TromboEmbolica venosa (RIETE), which included 25,369 patients with confirmed VTE until February 2009. Among them, 24,401 patients were treated either with UFH or with LMWH, and had available information about the 6-month occurrence of confirmed thrombocytopenia, defined as a platelet count ≤ 150,000 mm(-3) ., Results: One hundred and forty-one patients receiving UFH and/or LMWH developed thrombocytopenia within a 6-month period. The incidence of HAT was significantly higher in the UFH group (1.36%, 95% confidence interval [CI] 0.79-2.17) than in the LMWH group (0.54%, 95% CI 0.44-0.64). As compared with LMWH, UFH significantly increased the risk of HAT in female patients (adjusted hazard ratio [HR] 4.90%, 95% CI 2.58-9.31, P = 0.001) but not in male patients (adjusted HR 1.60%, 95% CI 0.64-3.97, P = 0.31); P = 0.027 for comparison. In each gender, the UFH-associated excess risk was confined to patients with VTE unrelated to cancer. The poor prognosis of patients with thrombocytopenia was not influenced by the type of heparin therapy., Conclusions: In routine clinical practice, treatment of VTE with UFH seems to confer a higher risk of thrombocytopenia than does treatment with LMWH, especially in women and non-cancerous patients., (© 2011 International Society on Thrombosis and Haemostasis.)

There is little information regarding the behaviour of red blood cell deformability in macrocytosis. We have determined in 114 patients with macrocytosis (MCV > 97 fL) and in 115 age and sex-matched subjects with normocytosis (VCM < 97 fL) erythrocyte deformability by means of ektacytometric techniques (Rheodyn SSD) measuring the erythrocyte elongation index (EEI) at 12, 30 and 60 Pa. Patients with macrocytosis showed statistically higher EEI at all the shear stresses tested when compared with controls (p < 0.001). When patients with macrocytosis were classified according to their main diagnosis as hepatic or renal disease, HIV and miscellaneous, 66.7%, 41.7%, 36.7% and 33.3% of patients, respectively, showed a EEI 60 higher than 61.8% (mean value of the control group + 2 SD). Linear regression analysis demonstrates that MCV, bilirubin, triglycerides and alanine aminotransferase were the main variables influencing EEI 60. An increased surface/volume ratio of the red blood cells may be the main cause related with a higher erythrocyte deformability in a relevant percentage of macrocytosis. Further research is required to confirm our findings by designing case-control pathology-specific studies.

Systemic lupus erythematosus (SLE) is characterised by increased venous and arterial thrombotic risk. Although antiphospholipid antibodies (APAs) have been shown to be related with thrombotic tendency in these patients, in more than 40% of them, thrombosis occurs without the presence of such antibodies. We analysed the association of venous and arterial thrombotic events with acquired (anticardiolipin antibodies (ACAs) and lupus anticoagulant (LA)) and inherited (antithrombin (AT), protein C (PC), protein S (PS) deficiencies, factor V Leiden and the prothrombin G20210A mutation), thrombophilic risk factors in 86 SLE patients and 89 healthy controls. Patients showed a higher significant percentage of ACAs titres IgG>41 GPL u/ml and LA than controls (P=0.009; P<0.001, respectively), although no differences in AT, PC, PS deficiencies, factor V Leiden and prothrombin G20210A mutation was observed (P>0.05). When patients with and without thrombosis were compared, those with thrombosis showed a statistically higher percentage of ACAs IgG>41 GPL u/ml and LA (P=0.048; P=0.001, respectively), OR 4.33; 95% CI 1.01-18.50 and OR 11.57; 95% CI 3.28-40.75, respectively. When venous and arterial thrombotic events were considered separately, the presence of LA constituted a risk factor for arterial thrombosis (P=0.010), OR 11.33; 95% CI 1.86-68.89, as well as for venous thrombosis (P=0.005), OR 10.15; 95% CI 2.12-48.64, while ACAs IgG>41 GPL u/ml on their own, were not associated with arterial or venous thrombosis (P=0.142, P=0.233, respectively). In addition inherited thrombophilic risk factors AT, PC, PS deficiencies, factor V Leiden and PT G20210A mutation do not seem to increase thrombotic risk in SLE patients.

Although complications post-URS are scant and can usually be resolved by conservative methods, these however, may be potentially severe as in the present case in whom a ureteroiliac fistula was observed during a URS procedure that had been performed to dilate a post-URS stenosis. Previously, extravasation had also occurred. The post-URS complications are briefly described and discussed.