Some authors have described that among Hepatitis C Virus (HCV) genotype 1-infected patients treated with dual therapy, anaemia has been associated with higher rates of Sustained Virological Response (SVR) as well as the use of erythropoiesis-stimulating agents.
Purpose
To investigate the relationships between treatment outcomes, anaemia, and their management with ribavirin dose reduction and/or darbepoetin in patients treated with boceprevir (BOC) or telaprevir (TLV) in a tertiary hospital.
Material and methods
Observational study. Data was collected from pharmacotherapeutic records of patients who initiated therapy with TLV or BOC between December'12 and May'13. Anaemia was defined as haemoglobin (Hb) <10.5 mg/dL. Darbepoetin was permitted for anaemic patients after ribavirin dose reduction. The variables were: age, sex, reduction of ribavirin dose and use of darbepoetin.
Results
36 patients were studied (26 men and 10 women). 23 (63.8%) patients were treated with TLV and 13 (36.2%) with BOC. 25 (69.5%) patients reached SVR (16 (69.5%) for TLV and 9 (69.2%) for BOC). 12 of these patients experienced anaemia (48%) (7 (43.8%) for TLV and 5 (55.6%) for BOC). The total number of patients who experienced anaemia was 17 (47.2%) (9 (39.1%) for TLV and 8 (61.5%) for BOC), 16 patients (44.4%) had a reduction in their ribavirin dose (8 (34.8%) for TLV and 8 (61.5%) for BOC) and 12 patients (33.3%) used darbepoetin (6 (26.1%) for TLV and 6 (46.1%) for BOC); 8 of these 12 (66.6%) patients showed SVR, 1 relapsed and 3 abandoned treatment due to adverse events (4 (66.6%) for TLV and 4 (66.6%) for BOC).
Conclusion
Among our genotype 1-infected patients treated with BOC or TLV anaemia was not associated with higher rates of SVR. Patients with darbepoetin did not have higher rates of SVR. Percentages of SVR were similar between TLV and BOC.
Our public healthcare system has developed some quality indicators (QI) based on the selection of drugs that support better evidence of efficiency in areas of prescribing where more deviations were detected in the past.
Purpose
To describe the variability of prescription QI in a public healthcare system, and its evolution per year.
Material and methods
Descriptive retrospective observational study. Variability of QI in hospitals with more than 500 beds from 2012 to 2015 was measured. The unit of measure was defined daily doses (DDD) using QI based on the rational use of medicines criteria. QI included:%omeprazole DDD/DDD proton pump inhibitors (PPIs) (QI1),%DDD gliclazide+glipizide+glimepiride/DDD antidiabetics excluding insulin and metformin (QI2),%DDD intermediate insulins+biphasic/DDD insulins excluding fast (QI3),%DDD simvastatin/DDD lipid lowering drugs (QI4),%DDD ACE inhibitors/DDD renin-angiotensin-aldosterone system inhibitors (QI5),%DDD SSRIs/DDD second generation antidepressants (QI6),%DDD citalopram+fluoxetine+sertraline/DDD SSRIs (QI7) and%DDD alendronic/DDD fracture prevention drugs (QI8). The coefficient of variation allowed us to compare variability in QI between hospitals during the study period.
Results
13 hospitals were studied. Data obtained are reported in table 1. There was a high variability in prescription QI between studied hospitals which increased over the years, especially in diabetes and drugs for hip fracture prevention. In groups of PPIs and antidepressants. variability was smaller.
Conclusion
In therapeutic groups where new drugs have been incorporated (diabetes and fracture prevention), the uncertainty and degree of confusion in the management of these drugs increased. To reduce clinical variability among different hospitals and improve the quality of prescription, it would be necessary to design and implement new strategies. No conflict of interest.
Activation of nuclear hormone receptor peroxisome proliferator-activated receptor β/δ (PPARβ) has been shown to improve insulin resistance and plasma high-density lipoprotein levels, but nothing is known about its effects in genetic hypertension. We studied whether the PPARβ agonist GW0742 might exert antihypertensive effects in spontaneously hypertensive rats (SHRs). The rats were divided into 4 groups, Wistar Kyoto rat-control, Wistar Kyoto rat-treated (GW0742, 5 mg · kg(-1) · day(-1) by oral gavage), SHR-control, and SHR-treated, and followed for 5 weeks. GW0742 induced a progressive reduction in systolic arterial blood pressure and heart rate in SHRs and reduced the mesenteric arterial remodeling, the increased aortic vasoconstriction to angiotensin II, and the endothelial dysfunction characteristic of SHRs. These effects were accompanied by a significant increase in endothelial NO synthase activity attributed to upregulated endothelial NO synthase and downregulated caveolin 1 protein expression. Moreover, GW0742 inhibited vascular superoxide production, downregulated p22(phox) and p47(phox) proteins, decreased both basal and angiotensin II-stimulated NADPH oxidase activity, inhibited extracellular-regulated kinase 1/2 activation, and reduced the expression of the proinflammatory and proatherogenic genes, interleukin 1β, interleukin 6, or intercellular adhesion molecule 1. None of these effects were observed in Wistar Kyoto rats. PPARβ activation, both in vitro and in vivo, increased the expression of the regulators of G protein-coupled signaling proteins RGS4 and RGS5, which negatively modulated the vascular actions of angiotensin II. PPARβ activation exerted antihypertensive effects, restored the vascular structure and function, and reduced the oxidative, proinflammatory, and proatherogenic status of SHRs. We propose PPARβ as a new therapeutic target in hypertension.
We hypothesized that perinatal inhibition of soluble epoxide hydrolase (SEH), which metabolizes epoxyeicosatrienoic acids in the arachidonic acid (AA) cascade, with an orally active SEH inhibitor, 12-(3-adamantan-1-yl-ureido)-dodecanoic acid (AUDA), would persistently reduce blood pressure (BP) in adult SHR despite discontinuation of AUDA at 4 wk of age. Renal cytoplasmic epoxide hydrolase-2 (Ephx2) gene expression was enhanced in SHR vs. WKY from 2 days to 24 wk. Effects of perinatal treatment with AUDA, supplied to SHR dams until 4 wk after birth, on BP in female and male offspring and renal oxylipin metabolome in female offspring were observed and contrasted to female SHR for direct effects of AUDA (8-12 wk). Briefly, inhibition of SEH was effective in persistently reducing BP in female SHR when applied during the perinatal phase. This was accompanied by marked increases in major renal AA epoxides and decreases in renal lipoxygenase products of AA. Early inhibition of SEH induced a delayed increase in renal 5-HETE at 24 wk, in contrast to a decrease at 2 wk. Inhibition of SEH in female SHR from 8 to 12 wk did not reduce BP but caused profound decreases in renal 15(S)-HETrE, LTB4, TBX2, 5-HETE, and 20-HETE and increases in TriHOMEs. In male SHR, BP reduction after perinatal AUDA was transient. Thus, Ephx2 transcription and SEH activity in early life may initiate mechanisms that eventually contribute to high BP in adult female SHR. However, programmed BP-lowering effects of perinatal SEH inhibition in female SHR cannot be simply explained by persistent reduction in renal SEH activity but rather by more complex and temporally dynamic interactions between the renal SEH, lipoxygenase, and cyclooxygenase pathways.
Diabetes mellitus type 2 (DM2) is a chronic disease with major impact on morbidity and mortality and the use of health resources.
Purpose
To analyse the evolution of consumption of antidiabetic drugs from 2001 to 2014. To study the variations in admissions due to lower extremity amputations from 2007 to 2013.
Material and methods
Descriptive study of the use of antidiabetic drugs between 2001 and 2014. Field of study: two tertiary hospitals and their reference areas, the target population consisting of 675 000 people. Prescriptions under the National Health System coverage were studied. The unit of measure was defined daily doses (DDD) per 1000 inhabitants per day (DHD), using the anatomical therapeutic chemical (ATC)/DDD classification (2006). Hospitalisation data were collected from the hospital dat base. For statistical comparisons, the Student's t test was used.
Results
During the study period, consumption of insulins was maintained from 17.9 DHD to 18.3 DHD but oral agents increased from 41.3 DHD to 52.7 DHD. Consumption of sulfonylureas was gradually reduced from 30.1 DHD to 16.4 DHD but metformin (alone) usage increased from 4.3 DHD to 23.7 DHD, being the most consumed agent in 2014 (45% of consumption). Oral combinations were introduced in 2004 (0.1 DHD) and were the third most consumed group in 2014 (6.5 DHD). Consumption of dipeptidyl peptidase-4 inhibitors (since 2008) and 'other hypoglycaemic agents' increased from 0.3 DHD (2008) to 3.8 DHD and from 1.4 DHD to 2 DHD, respectively. On the other hand, the use of thiazolidinediones (since 2004) and alpha-glucosidase inhibitors was reduced from 0.7 DHD (2004) to 0.1 DHD and from 4.5 DHD to 0.2 DHD, respectively. The number of admissions due to lower extremity amputations from 2007 to 2013 was 94, 111, 145, 140, 125, 66 and 72, respectively. The number of amputations decreased significantly from 2008 to 2011 vs. 2013 (p < 0.05).
Conclusion
Metformin (alone) remains the drug of choice in treating DM2. Increased consumption of oral combinations could reflect more patients in more advanced stages of disease who do not respond to monotherapy. To associate the decrease in admissions due to lower extremity amputations with a higher consumption of oral antidiabetic drugs, more studies are needed. No conflict of interest.
Peroxisome proliferator-activated receptor β/δ (PPAR-β) is a ligand-activated transcription factor belonging to the nuclear hormone receptor superfamily that regulates the transcription of many target genes. More recently, acute, nongenomic effects of PPAR-β agonists have also been described. In the present study, we hypothesized that PPAR-β agonists might exert acute nongenomic effects on vascular tone. Here, we report that the structurally unrelated PPAR-β ligands [4-[3-(4-acetyl-3-hydroxy-2-propylphenoxy)propoxy]phenoxy]acetic acid (L-165041) and 4-[[[2-[3-fluoro-4-(trifluoromethyl)phenyl]-4-methyl-5-thiazolyl] methyl]thio]-2-methylphenoxy]acetic acid (GW0742) induced vascular relaxation in phenylephrine-precontracted endothelium-intact rat aortic rings, which was significantly inhibited by endothelial denudation or nitric-oxide synthase (NOS) inhibition with NG-nitro-l-arginine methylester. These relaxant effects reached steady state within 15 min. The relaxation induced by L-165041 and GW0742 in aortic rings precontracted with the thromboxane A2 analog 9,11-dideoxy-11α,9α-epoxymethanoprostaglandin F2α (U-46619) was unaffected either by removal of extracellular calcium or by incubation with calcium-free solution containing the intracellular calcium chelator 1,2-bis-(o-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid tetra(acetoxymethyl) ester. However, the phosphatidylinositol 3-kinase (PI3K) inhibitor 2-(4-morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one hydrochloride (LY-294002) inhibited the endothelium-dependent relaxant responses induced by both PPAR-β agonists. Blockade of PPAR-β with 3-[[[2-methoxy-4-(phenylamino)phenyl]amino]sulfonyl]-2-thiophenecarboxylic acid methyl ester (GSK0660) also partially inhibited these relaxant responses, although PPAR-γ blockade with 2-chloro-5-nitro-N-phenylbenzamide (GW9662) had no effect. In human umbilical vein endothelial cells, L-165041 and GW0742 increased nitric oxide (NO) production and Akt and endothelial NOS (eNOS) phosphorylation, which were sensitive to PI3K inhibition and PPAR-β blockade. In conclusion, the PPAR-β agonists acutely caused vasodilatation, which was partially dependent on endothelial-derived NO. The eNOS activation is calcium-independent and seems to be related to activation of the PI3K-Akt-eNOS pathway.
Liver disease is associated with soybean lipid in Parenteral Nutrition (PN). This led to the development of alternative Intravenous Lipid Emulsions (ILE). Here we compare the effects of Lipoplus® (medium chain triglyceride combined with soybean and fish oil) in treatments of 5-7 days vs. longer treatments.
Retrospective observational study using pharmacotherapeutic records of prematures who initiated PN between December 12 and May 14 in a tertiary care hospital. Infants included had a GA <34 weeks and birth weight between 0.5-2. Data recorded included gender, gestational age, body weight and total (TB), conjugated
(CB) and unconjugated bilirubin (UB) (mg/dL). Comparisons were done with t-tests.
Of the 17 infants selected, 10 (58.8%) (seven male, three female) were treated for five to seven days (Test Group) and seven (41.2%) (five male, two female) were treated for more than a week (Control Group). Mean GA was 29 weeks forboth groups. Average weight at the beginning of PN was 1.37 kg for test Group
and 1.03 kg for control Group.
Differences vs. baseline were observed for either treatment:
— Test Group = CB: 0.35 vs. 0.39; p = n.s. UB: 7.9 vs. 11.25; p = 0.037; TB: 8.25 vs. 11.61; p = 0.028.
— Control Group = CB: 1.71 vs. 1.5; p = n.s. UB: 7.74 vs. 6.15; p = n.s. TB: 9.46 vs. 4.47; p = 0.028.
A significant increase in UB and TB was observed in test group; therefore a significant decrease in TB was detected in the control group.
We found that treatments from eight to 14 days with new ILE significantly lower TB levels in premature infants as described previously. On the other hand,shorter treatments have not shown the same potential. Further trials evaluating the potential hepatoprotective effects of the new ILE over different time periods on a
larger number of patients are needed
To describe and analyse from a clinical and epidemiological point of view, a food borne outbreak in a psychiatric institution in Granada, in 2015, and to examine whether treatment with psychoactive drugs constitutes a risk factor for the development of a food borne disease, analysing the degree of susceptibility according to the therapeutic group consumed.Ambispective cohort study. Residents were the unit of analysis. Our group carried out an active case search and a food survey. A search for other risks was developed as well as a food inspection. Location, time and individual variables were studied. A descriptive analysis was conducted (absolute and relative frequencies). Calculation of attack rates by building and by menu was made. Bi-variant analysis (Chi-square test, t-Student test) and relative risk were used as a measure of strength of association. For risk analysis of medication, a multivariate analysis using logistic regression was carried out.18 cases with diarrhoea without fever were found (incubation period from 6 to 16hours). Cases were mild and self-limiting. The clinical manifestations, the temporal grouping of cases and the characteristics of the ingested foods, focussed suspicion on a bacterial toxin. Being equal in the rest of variables, the N03AF, and N03AG therapeutic groups confer greater risk of disease (odds ratio [OR]: 8.626; 95% confidence interval [95%CI]: 2.050-36.308; p=0.003; and OR: 14.516; 95%CI: 3.155-66.784; p=0.001, respectively).Decreased intestinal transit, caused by the administration of anticonvulsants, may increase exposure time of the intestinal mucosa to the toxin, increasing the risk of disease and suffering from complications. An additional hygienic effort should be made in this type of institution to prevent these pathologies.
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