The Winter edition of LEAP, a publication published by the John Hopkin’s School of Medicine’s Division of Rheumatology, has some very important news. Under the article heading “This Changes Everything”:
Two people with Sjögren’s syndrome can have identical symptoms, and one may respond well to a drug and one won’t. The results of a recent study by Livia CasciolaRosen, Ph.D., Alan Baer, M.D., and colleagues tell us why: The Hopkins scientists have discovered that although patients might look similar on the outside, on the inside they don’t have the same disease at all. For the doctors who treat people with Sjögren’s, and the scientists devoted to finding and testing new medications to modify the disease, these findings, published in the journal, Arthritis & Rheumatology, are revolutionary.
This information really does have the potential to be revolutionary. SS has repeatedly failed in clinical trials for several biologics, despite anecdotal evidence that they work for some people. In my last post, I described a failed Rituxan trial that ran counter to an earlier trial’s success. The Hopkin’s research demonstrates that SS might actually be two or more different diseases, with completely different mechanisms of action. As a result, patients with version A may benefit from a drug like Rituxan, while patients with version B of SS would not. It would go a long way to explaining the clinical trial issues.
So how does a SS patient determine which version they have? By analyzing salivary gland cells on the molecular level:
In previous work published in the Proceedings of the National Academy of Sciences (PNAS), Casciola-Rosen and colleagues developed molecular probes that analyzed tiny bits of frozen salivary tissue from individual patients and determined which particular type of interferon pathway was active in each. One probe detects Type I (alpha) interferon, which can be made by many cells; the other detects the presence of Type II (gamma) interferon, which suggests that certain immune cells, particularly T cells, are active. Although both types share the name interferon – as their name suggests, their job is to “interfere” with the life cycle of a virus or other foreign invader – they are distinctly different.
I also have to wonder if this might not be a reason for such a large number of SS patients (myself included) to have repeated negative blood tests for auto-antibodies. Perhaps one version of SS patients do not produce such antibodies. It is clear that significantly more work will need to be done to incorporate these results into future clinical trials and to make a mass-market version of the tests. It is still early, but this may be one of the more important SS research breakthroughs yet.