SYSADOA - Slow-acting symptomatic drugs for OSTEOARTHRITIS
called slow action as opposed to traditional analgesics, whose onset is immediate, because the clinical effect occurs several weeks after starting treatment and are temporarily after removal.
used as symptomatic treatment of osteoarthritis, for reducing pain and improving function, and are postulated as possible disease-modifying or chondroprotective, because delay progression of articular cartilage deterioration.
diacerein is a drug synthesis inhibitory activity of interleukin-1, substance involved in inflammation and cartilage degradation
DMOADs DMOADs What they need to do How they need to do Delay structural progression Prevent the OA Effect on Radiographic Joint Space Narrowing (JSN) Effect on progression to control JSN and pain / function relation Halting progression (improving the x-ray) Reversing progression (normalizing the x-ray)
Diacerein is distinct from all other painkillers & joints treatments due to its ability to reduce joint inflammation and pain, without having negative side effects on the stomach, blood pressure or heart.
Diacerein inhibits the production of ‘Interleukin – 1 beta’, the protein in the human body, which causes osteoarthritis and joint inflammation.
In a study (ECHODIAH) conducted to evaluate the effect of diacerein in a patient of hip Osteoarthritis over a 3 year period using progression of joint space narrowing as assessment criteria, it has been found that mean progression of narrowing was significantly less in patients treated with diacerein from 0.18 per year to 0.13 per year at the end of third year.
For diacerein, this meta-analysis provides evidence for a superiority over placebo and an equality with NSAIDs with respect to improvement in pain and function during the active treatment period in patients with osteoarthritis of the hip and/or knee.
Moreover, diacerein was superior to placebo and NSAIDs during the follow-up period with an NSAID-sparing effect, indicating that the drug has a carryover effect.
Diacerein directly inhibits IL-1 synthesis and release in vitro &down modulate IL-1 induced activities.
IL-1 plays a fundamental role in OA patho-physiology and cartilage destruction & also promotes expression of inducible nitric oxide synthase [iNOS], increases release of prostaglandin E2, IL-6,IL-8 in human OA chondrocytes, which promote joint degradation.