Researchers found that patients with a higher amount or higher proportion of an inflammatory protein called type 1 interferon beta compared with another inflammatory protein, type 1 interferon alpha, do not respond as well to tumor
necrosis factor inhibitors as others.
A Mayo Clinic study is shedding light on why some rheumatoid arthritis patients respond poorly when treated with tumor
necrosis factor inhibitors, part of a class of drugs called biologics.
«Using tumor
necrosis factor inhibitors decreases risk of heart attacks in rheumatoid arthritis patients.»
Researchers in Sweden sought to determine if use of tumor
necrosis factor inhibitor drugs to treat RA would result in a reduced risk of acute coronary syndrome (commonly called ACS), defined as a diagnosis of a heart attack or unstable angina (the worsening or increasing cardiac symptoms)
Tumor
necrosis factor inhibitor drugs (commonly called Anti-TNFs) modestly reduce the risk of acute coronary syndrome, such as heart attacks and angina, in rheumatoid arthritis patients whose inflammation places them at higher risk of developing coronary heart disease, according to new research findings presented this week at the American College of Rheumatology Annual Meeting in San Diego.
Not exact matches
An
inhibitor of the inflammatory protein tumor
necrosis factor (TNF), adalimumab is the first such medication approved to treat the painful skin disorder.
On the other hand, there are patients who do not show any significant improvement even after the second or third biologic drug treatment — typically with TNF
inhibitors (which blockade the Tumour
Necrosis Factor TNF, which is involved in systemic inflammation).
Abbreviations: ASC, apoptosis - associated speck - like protein containing a caspase - recruitment domain; ATM, adipose - tissue - resident macrophage; BAT, brown adipose tissue; CCR2, CC chemokine receptor 2; CHOP, C / EBP (CCAAT / enhancer - binding protein)- homologous protein; DHA, docosahexaenoic acid; EPA, eicosapentaenoic acid; ER, endoplasmic reticulum; GPCR, G - protein - coupled receptor; HIF, hypoxia - inducible
factor; IFNγ, interferon γ; IKK,
inhibitor of nuclear
factor κB kinase; IL, interleukin; IRS - 1, insulin receptor substrate - 1; JNK, c - Jun N - terminal kinase; LDL, low - density lipoprotein; Ldlr, LDL receptor; LXR, liver X receptor; MCP - 1, monocyte chemoattractant protein 1; miRNA, microRNA; mTOR, mammalian target of rapamycin; NAFLD, non-alcoholic fatty liver disease; NF - κB, nuclear
factor κB; NLRP3, NLR (nucleotide - binding - domain - and leucine - rich - repeat - containing) family, pyrin - domain - containing 3; oxLDL, oxidized LDL; PKR, double - stranded RNA - dependent protein kinase; PPAR, peroxisome - proliferator - activated receptor; STAT6, signal transducer and activator of transcription 6; SVF, stromal vascular fraction; TLR, Toll - like receptor; TNFα, tumour
necrosis factor α; UPR, unfolded protein response; WAT, white adipose tissue
In recent years, tumor
necrosis factor (TNF) alpha
inhibitors, drugs that fight an inflammatory protein, and DMARDs (disease modifying antirheumatic drugs like methotrexate) have helped slow, reduce, and prevent joint damage.
The research, which was funded by the Food and Drug Administration and other federal health agencies, contradicts numerous earlier studies that did find an increased risk of infection associated with the drugs, known as tumor
necrosis factor (TNF)
inhibitors.
✓ Inhibits tumor
necrosis factor (TNF) alpha
inhibitor, NF - kappaB, epidermal growth
factor receptor, and more