As you know, I don’t like CRAB drugs becuase I don’t think they are effective enough for most people, Never have never will. but obviously I respect people’s choice for these agents. However if you go down this route , this is yet another example of treat early, wait too long and damage is done, meaning that it is less likely that you can get disease undercontrol.
Early treatment meant that you were up to ten times more likely to be active disease -free than delayed treatment. Time is brain what more evidence do we need,
So I find it rather disturbing that some many neurologists don’t get this and create the environment for accumulation of disability. I would love to see a distribution of CRAB drug sales by neurology region and then we can see who are the neurology ludites. I believe the companies have this information as they do Freedom of Information requests to find out our prescription habits. So send me an anonymous email,
I guess that East London is a relatively CRAB dead zone if I am to believe ProfG&K, but I am sure that is not true for other areas of London and the UK.
No evidence of disease activity status in patients treated with early vs. delayed subcutaneous interferon β-1a. Freedman MS, Comi G, Coyle PK, Aldridge J, Chen L, Marhardt K, Kappos L. Mult Scler Relat Disord. 2019 Dec 9;39:10189.
BACKGROUND:Clinically isolated syndrome (CIS) is defined as a monophasic clinical episode highly suggestive of multiple sclerosis (MS). Regardless, studies have shown that treatment at this early stage of MS can delay a second event and prolong the transition to clinically diagnosed MS. The objective of this post-hoc analysis was to determine the effect of early CIS treatment with once weekly (qw) or three times weekly (tiw) subcutaneous interferon (scIFN) β-1a vs. delayed treatment (DT) on the composite endpoint of no evidence of disease activity (NEDA)-3.
METHODS:In REFLEX, patients with CIS were randomized to double-blind scIFN β-1a 44 µg tiw, qw, or placebo for 24 months. Upon clinically-definite MS, patients switched to open-label scIFN β-1a tiw. Patients who completed REFLEX entered an extension (REFLEXION). Patients initially randomized to placebo switched to tiw (DT); scIFN β-1a patients continued their initial qw/tiw regimen for up to 60-months post-randomization. This post-hoc analysis was conducted in the integrated intent-to-treat REFLEX plus REFLEXION population (tiw, n = =171; qw, n = =175; DT, n = =171). All p values are nominal. CIS was defined using the McDonald 2010 criteria.
RESULTS: Patients receiving early treatment (ET) with scIFN β-1a tiw (twice a week i.e Rebif) and qw (one a week i.e. Avonex) were more likely to achieve NEDA-3 than DT at year 2 (tiw vs. DT: OR 4.26, 95% CI 2.02-8.98, p = =0.0001; qw vs. DT: OR 2.99, 95% CI 1.39-6.43, p = =0.005). Compared with DT, ET with scIFN β-1a tiw was more likely to achieve NEDA-3 at year 3 (OR 3.73, 95% CI 1.63-8.55, p = =0.002) and year 5 (OR 12.96, 95% CI 1.66-101.04, p = =0.015). Between ET regimens, the odds of achieving NEDA-3 were not significantly improved by scIFN β-1a 44 µg tiw at year 2 (OR 1.42, 95% CI 0.81-2.50, p = =0.22) but were at year 3 (OR 2.26, 95% CI 1.11-4.60, p = =0.024) and year 5 (OR 3.22, 95% CI 1.01-10.22, p = =0.048), indicating that the beneficial effects of more frequent scIFN β-1a dosing become more apparent over time in patients with CIS. In the subgroup of patients with Gd+ lesions at baseline the odds for achieving NEDA-3 were higher for ET up to year 2 compared with DT (tiw: OR 10.21, 95% CI 1.23-84.82, p = =0.03; qw: OR 8.97, 95% CI 1.08-74.28, p = =0.04). In patients without Gd+ lesions at baseline, those receiving ET were more likely to achieve NEDA-3 at year 2 (OR 3.56, 95% CI 1.56-8.10, p = =0.003), year 3 (OR 2.54, 95% CI 1.05-6.18, p = =0.04) and year 5 (OR 9.63, 95% CI 1.19-77.79, p = =0.034) than patients who received DT.
CONCLUSIONS:ET with scIFN β-1a tiw was associated with a higher likelihood of achieving NEDA-3 not only at 2 but also at 3 and 5 years.
COI:multiple but none-relevant