Medical University of South Carolina

About: Medical University of South Carolina is a education organization based out in Charleston, South Carolina, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 23436 authors who have published 45440 publications receiving 1769397 citations. The organization is also known as: MUSC & Medical College of the State of South Carolina.

Outcomes of patients with multiple myeloma refractory to CD38-targeted monoclonal antibody therapy.

Abstract: The introduction of CD38-targeting monoclonal antibodies (CD38 MoABs), daratumumab and isatuximab, has significantly impacted the management of patients with multiple myeloma (MM). Outcomes of patients with MM refractory to CD38 MoABs have not been described. We analyzed outcomes of 275 MM patients at 14 academic centers with disease refractory to CD38 MoABs. Median interval between MM diagnosis and refractoriness to CD38 MoAB (T0) was 50.1 months. The median overall survival (OS) from T0 for the entire cohort was 8.6 [95% C.I. 7.5–9.9] months, ranging from 11.2 months for patients not simultaneously refractory to an immunomodulatory (IMiD) agent and a proteasome inhibitor (PI) to 5.6 months for “penta-refractory” patients (refractory to CD38 MoAB, 2 PIs and 2 IMiDs). At least one subsequent treatment regimen was employed after T0 in 249 (90%) patients. Overall response rate to first regimen after T0 was 31% with median progression-free survival (PFS) and OS of 3.4 and 9.3 months, respectively. PFS was best achieved with combinations of carfilzomib and alkylator (median 5.7 months), and daratumumab and IMiD (median 4.5 months). Patients with MM refractory to CD38 MoAB have poor prognosis and this study provides benchmark for new therapies to be tested in this population.

The platelet in diabetes: focus on prevention of ischemic events.

Abstract: Accelerated atherosclerosis and the increased risk of thrombotic vascular events in diabetes may result from dyslipidemia, endothelial dysfunction, platelet hyperreactivity, an impaired fibrinolytic balance, and abnormal blood flow. There is also a correlation between hyperglycemia and cardiovascular (CV) events. The importance of platelets in the atherothrombotic process has led to investigation of using antiplatelet agents to reduce CV risk. A meta-analysis conducted by the Antiplatelet Trialists' Collaboration demonstrated that aspirin reduced the risk of ischemic vascular events as a secondary prevention strategy in numerous high-risk groups, including patients with diabetes. Based on results from placebo-controlled randomized trials, the American Diabetes Association recommends low-dose enteric-coated aspirin as a primary prevention strategy for people with diabetes at high risk for CV events. Clopidogrel is recommended if aspirin allergy is present. There is occasionally a need for an alternative to aspirin or for additive antiplatelet therapy. Aspirin in low doses inhibits thromboxane production by platelets but has little to no effect on other sites of platelet reactivity. Agents such as ticlopidine and clopidogrel inhibit ADP-induced platelet activation, whereas the platelet glycoprotein (Gp) IIb/IIIa complex receptor antagonists block activity at the fibrinogen binding site on the platelet. These agents appear to be useful in acute coronary syndromes (ACSs) in diabetic and nondiabetic patients. A combination of clopidogrel plus aspirin was more effective than placebo plus standard therapy (including aspirin) in reducing a composite CV outcome in patients with unstable angina and non-ST segment elevation myocardial infarction. In a meta-analysis of six trials in diabetic patients with ACSs, intravenous GpIIb-IIIa inhibitors reduced 30-day mortality when compared with control subjects. Results from controlled prospective clinical trials justify the use of enteric-coated low-dose aspirin (81-325 mg) as a primary or secondary prevention strategy in adult diabetic individuals (aged >30 years) at high risk for CV events. Recent studies support the use of clopidogrel in addition to standard therapy, as well as the use of GpIIb-IIIa inhibitors in ACS patients.

The sphingosine kinase 1/sphingosine-1-phosphate pathway mediates COX-2 induction and PGE2 production in response to TNF-α

Abstract: In this study we addressed the role of sphingolipid metabolism in the inflammatory response. In a L929 fibroblast model, tumor necrosis factor-α (TNF) induced prostaglandin E2 (PGE2) production by ...

Baclofen decreases acid and non‐acid post‐prandial gastro‐oesophageal reflux measured by combined multichannel intraluminal impedance and pH

Abstract: Summary Background : Omeprazole controls acid but not non-acid reflux. The GABA B agonist baclofen decreases acid reflux through the inhibition of transient lower oesophageal sphincter relaxations (TLESRs) and should similarly decrease non-acid reflux. Using combined multichannel intraluminal impedance and pH (MII/pH), we compared acid and non-acid reflux after placebo and baclofen. Methods : Nine healthy volunteers and nine heartburn patients underwent two 2-h studies of combined MII/pH in right lateral decubitus after a refluxogenic meal in random order: on placebo and after baclofen 40 mg p.o. Tracings were analysed for acid and non-acid reflux episodes, re-reflux and symptoms in the heartburn patients. Results : In normal subjects baclofen significantly reduced the median number of episodes of acid (7 vs. 1, P = 0.02), non-acid (2 vs. 0, P = 0.005), and all reflux combined (10 vs. 2, P = 0.006); re-reflux was not reduced (0 vs. 0, P = N.S.). In heartburn patients, baclofen significantly decreased the median number of episodes of acid (15 vs. 6, P = 0.004), non-acid (4 vs. 2, P = 0.003), re-reflux (2 vs. 0, P = 0.02), and all reflux combined (23 vs. 8, P = 0.004); it also reduced the median number of acid-related (9 vs. 1, P = 0.008) and non-acid-related (1 vs. 0, P = 0.04) symptoms. Conclusions : Baclofen reduces post-prandial acid and non-acid reflux and their associated symptoms. GABA B agonists may have a role in treating GERD.