Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Sunday, January 22, 2017

Effects of Baricitinib on Lipid, Apolipoprotein, and Lipoprotein Particle Profiles in a Phase 2b Study in Patients with Active Rheumatoid Arthritis

Someplace in here something might be useful for us. But it will never occur.
https://www.ncbi.nlm.nih.gov/pubmed/28029752

Abstract

Objective To assess the effects of baricitinib on lipid profile in patients with moderate-to-severe rheumatoid arthritis. Methods Once-daily baricitinib (1, 2, 4, or 8-mg) or placebo was studied in 301 randomized patients. Changes in lipid profile, particle size, and number were assessed at weeks 12/24; associations with clinical efficacy were evaluated. Apolipoproteins were assessed at weeks 4/12 for the placebo, and 4- and 8-mg baricitinib groups. Results Baricitinib treatment resulted in dose-dependent increases by week 12 in serum lipids (low-density lipoprotein cholesterol [LDL-C]: 3.4 mg/dL increase from baseline to week 12 (1-mg) to 11.8 mg/dL (8-mg); high-density lipoprotein cholesterol [HDL-C]: 3.3 mg/dL (1-mg) to 8.1 mg/dL (8-mg); triglycerides: 6.4 mg/dL (1-mg) to 15.4 mg/dL (8-mg) baricitinib). Group-wise mean increases in LDL-C were coincident with mean increases in large LDL particles and mean reductions in small dense LDL particles. Increases from baseline to week 12 in apolipoprotein A-I, B, and total CIII were observed with 4-mg (9.5%, 6.8%, and 23.0%, respectively) and 8-mg (12.2%, 7.1%, and 19.7%, respectively) baricitinib with no increase in LDL-associated CIII (4-mg: -4.5%; 8-mg: -9.0). Baricitinib reduced HDL-associated serum amyloid A at 4-mg (-36.0%) and 8-mg (-32.0%); a significant reduction in lipoprotein (a) was observed only with 8-mg (-16.6%). Increased HDL cholesterol at week 12 correlated with improved Disease Activity Scores and Simplified Disease Activity Index; changes in total cholesterol, LDL cholesterol, and triglycerides did not reveal a similar relationship. Conclusion Baricitinib-associated increases in serum lipids were observed. HDL-C increases correlated with improved clinical outcomes. This article is protected by copyright. All rights reserved.

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