Donovanwalther7011

Thoracentesis is one of the most commonly performed procedures in the inpatient setting. Although coagulation profile is usually evaluated prior to thoracentesis, bleeding is a rare complication, occurring in less than 1% of the cases. Several society guidelines recommend holding antiplatelet medications and anticoagulants prior to thoracentesis. Clinical practice guidelines also recommend correcting international normalised ratios of more than two and platelet counts <50 X10

9/L.

This is a retrospective descriptive study that included 292 patients who underwent thoracentesis in the inpatient setting at Ascension St John Hospital in Detroit, Michigan, USA from 2016 to 2018. Carboplatin We identified patients who had uncorrected risk for bleeding and collected data about their demographics, comorbidities, use of antiplatelet or anticoagulants and procedural details including complications. We looked for any postprocedural bleeding events to study their relation to the already established bleeding risk.

Two hundratients in need of thoracentesis.Statins have plausible biological effects against prostate cancer cells and are associated with improved disease-specific mortality. In current randomized placebo-controlled trial, low-dose atorvastatin caused no difference in relapses after radical prostatectomy in Asian men. Future trials should study higher statin doses at later disease stages with survival as the endpoint.See related article by Jeong et al., p. 5004.

In patients with metastatic castration-resistant prostate cancer (mCRPC), resistance to androgen receptor (AR)-targeted therapies, such as enzalutamide, remains an issue. Inactivation of inhibitory PTEN activates PI3K/AKT signaling and contributes to resistance to androgen deprivation therapy and poor outcomes. Therefore, dual targeting of AR and PI3K/AKT pathways may limit tumor growth and reverse resistance.

In this phase I study (NCT02215096), patients with PTEN-deficient mCRPC who progressed on prior enzalutamide received once-daily enzalutamide 160 mg plus PI3Kβ inhibitor GSK2636771 at 300 mg initial dose, with escalation or de-escalation in 100-mg increments, followed by dose expansion. Primary objectives were to evaluate safety/tolerability, determine the recommended phase II dose, and assess the 12-week non-progressive disease (PD) rate.

Overall, 37 patients were enrolled; 36 received ≥1 dose of GSK2636771 (200 mg

= 22; 300 mg

= 12; 400 mg

= 2) plus 160 mg enzalutamide. Dose-limiting toxicities occurred in 5 patients (200 mg

= 1; 300 mg

= 2, 400 mg

= 2). No new or unexpected adverse events or evidence of drug-drug interaction were observed. At the recommended dose of GSK2636771 (200 mg) plus enzalutamide, the 12-week non-PD rate was 50% (95% confidence interval 28.2-71.8,

= 22); 1 (3%) patient achieved a radiographic partial response lasting 36 weeks. Four of 34 (12%) patients had prostate-specific antigen reduction of ≥50%.

Although there was acceptable safety and tolerability with GSK2636771 plus enzalutamide in patients with PTEN-deficient mCRPC after failing enzalutamide, limited antitumor activity was observed.

Although there was acceptable safety and tolerability with GSK2636771 plus enzalutamide in patients with PTEN-deficient mCRPC after failing enzalutamide, limited antitumor activity was observed.Nectin-4 is the target for enfortumab vedotin, a novel antibody-drug conjugate. NECTIN4 gene expression differs considerably across different molecular subtypes and is shown to be important for enfortumab vedotin efficacy.See related article by Chu et al., p. 5123.

Multimodal analgesia pathways have been shown to reduce opioid use and side effects in surgical patients. A quality improvement initiative was implemented to increase the use of multimodal analgesia in adult patients presenting for general anaesthesia at an academic tertiary care centre. The aim of this study was to increase adoption of a perioperative multimodal analgesia protocol across a broad population of surgical patients. The use of multimodal analgesia was tracked as a process metric. Our primary outcome was opioid use normalised to oral morphine equivalents (OME) intraoperatively, in the postanaesthesia care unit (PACU), and 48 hours postoperatively. Pain scores and use of antiemetics were measured as balancing metrics.

We conducted a quality improvement study of a multimodal analgesia protocol implemented for adult (≥18 and≤70) non-transplant patients undergoing general anaesthesia (≥180 min). Components of multimodal analgesia were defined as (1) preoperative analgesic medication (acetaminophenwas associated with reduced OME use in the PACU and 48 hours postoperatively.

A perioperative pragmatic multimodal analgesic intervention was associated with reduced OME use in the PACU and 48 hours postoperatively.

To compare the incidence of psoriatic arthritis (PsA) in patients with psoriasis (PsO) according to different treatments for their skin topics/no treatment, conventional disease-modifying antirheumatic drugs (DMARDs) (cDMARDs) or biological DMARDs (bDMARDs).

Patients with PsO without PsA followed at a university hospital were included in this retrospective cohort study. Patients were classified according to their treatment in topics (topics, phototherapy or no treatment), cDMARDs (methotrexate and cyclosporine) and bDMARDs (tumour necrosis factor inhibitors (TNFi), interleukin 17 inhibitors (IL-17i) and IL-12-23i ((interleukin (IL) 12/IL-23 inhibitor))) groups. Incident cases of PsA were attributed to one treatment if developed during the administration of that treatment. A Cox proportional hazards model was used to evaluate the adjusted risk of PsA development by treatment group.

1719 patients with PsO contributed a total of 14 721 patient/years (py). 1387 (81%) patients were in the topics, 229 (13%) in cDMARDs and 103 (6%) in the bDMARDs group. During follow-up, 239 patients (14%) developed PsA (231 under topics, six under cDMARDs and two under bDMARDs). Global incidence was 1.6 per 100 py. The risk of developing PsA in patients with PsO treated with bDMARDs was significantly lower (incidence rate ratio (IRR)=0.26; 95% CI 0.03 to 0.94; p=0.0111), compared with topics, but not compared with cDMARDs (IRR=0.35; 95% CI 0.035 to 1.96; p=0.1007). Adjusted Cox proportional hazards regression analysis showed that male sex, nail involvement and higher body max index were associated with increased risk of developing PsA, while biologics use was protective (HR 0.19; 95% CI 0.05 to 0.81).

Treatment with biologics in patients with PsO reduced the risk of PsA development.

Treatment with biologics in patients with PsO reduced the risk of PsA development.