I second this utterly @tntlamb. Thank you so much. And thanks too @ktel for asking the question in the first place.
What I don’t understand is why aren’t there biologics that target both (psoriasis and arthritis). Wouldn’t that be the ideal biologic? Or, maybe there are, but not perfect ones. And, why can most of us only expect 75% improvement of our symptoms with a biologic? I guess in rereading your explanation, I got the answer for that…
It’s ok, it’s nice of you to explain it and give people like me a glance at what’s happening in our bodies and why it’s impossible to get a diagnosis from blood tests! So, thanks!
Well there are (keep in mind this is pretty recent stuff):
- SAR (Sanofi/Regeneron)
- SIR (Janssen/GSK)
- Clazikizumab (Alder): anti- IL-6 monoclonal antibody in phase III
- Gerilimzumab (Bird Rock Bio): anti-IL-6 monoclonal antibody in phase II
- Vobarilizumab (Ablynx): anti-IL-6R nanobody in phase IIB
- NI-1201 (Novimmune): human anti-interleukin-6 receptor (IL-6R)
Most are in comparative trials and/or stage 2/3 trials. They are also along side developing testing to determine which biologic would be the most effective. That testing is only a year or so away from what I have heard
Then there is a whole new development where instead of just a single inhibitor they are developing an IL6 - IL21 which literally has eliminated the disease in mice. Of course we aren’t mice.
The problem is the newer biologics are very effective for collagen induced arthritis, until the tests are developed there is no way of knowing whether an individuals arthritis is collagen induced…
The approach NOW is combination therapy which patients are resistant to (read through these boards and you can see it. There is no doubt adding a DMARD to a biologic is better than either one alone. BUT convincing a patient that the med they hated or claim didn’t do anything will when combined with others is just a battle overworked rheumies have in many instance quit fighting.
Interesting…so if they know there’s such a thing as collagen-induced arthritis, why can’t they test for it? To you, that’s probably a stupid question—I’m definitely not a scientist. I suppose just because you know something is, doesn’t mean you know how it occurs.
They sort of can test for it, trouble is moving from animal models to Human models is an issue so the only accurate testing is ANA and response to drug therapy as another term is “Seronegative arthritis” (non rheumatory is actually a better description.) They have been dinking with it since 2007 with this Study The overall result has been better and more biologics.
The problem with “combo therapies” is that its working both ends toward the middle. Imagine if you will a coiled rope. You have two ends to pull to uncoil it. Pick the right one and it uncoils easily, pick the wrong one and its not so easy but it does uncoil eventually. Try pulling both at the same time you ALWAYS end up with a balled up mess in the middle. Then its really a pain to unball.
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Greetings Iam a nurse educator so anyhow below is an up to date explanation it is a bit wordy but basically means it is very common not to have esr/crp even if you are in a flare or acute episode hope this helps
"Laboratory findings — Laboratory findings in PsA are nonspecific, consistent with the acute phase response and the degree and chronicity of inflammation; there are no laboratory findings that are characteristic of PsA and distinguish it from other forms of inflammatory arthritis or systemic autoimmune rheumatic disease. Autoantibodies such as rheumatoid factor (RF), antinuclear antibodies (ANA), and anti-citrullinated peptide antibodies (ACPA) are present in a minority of patients.
Acute phase reactants are elevated in about 40 percent of patients. An elevated sedimentation rate and leukocytosis are seen in about one-third of patients, reflecting a nonspecific inflammatory response.
Hi one of the ways the Rheumatologist may diagnose PsA over other rheumatic diseases is that it is not unusual for the crp or esr to be completely normal this is indeed one of the hallmarks of PsA. However this is not to say you won’t have inflammation as many of us I can assume will attest to e.g. you might be in the middle of having a painful knee etc being aspirated or in a full blown flare up episode
Medications can also mask any rises in esr/crp as most of us have never really been off medications when we have our blood tests done.
What an interesting study. The observation of TNF blockade as an analgesic agent is quite fascinating.
I suppose it makes sense - part of the inflammatory response is to make us feel pain more acutely so we don’t re-injure ourselves. Pretty annoying when it all goes haywire and it’s a chronic state though!
I’ve been wondering for a while if it could be rewired through measured pain desensitization. I suppose nobody is studying that due to ethics…
This is probably right off into the long grass … but I’ve been reading up on HLA B27 (which I know is much more common amongst those with AS than with PsA). Still, there’s the connection and some of us have the gene. What fascinates me are the benefits of the gene (molecule? Is a gene a molecule? Lol!). For example one thing I read, dunno if it’s any good, said that HLA B27 may confer resistance to influenza.
The only relevance, I think, to this discussion is that so many of the processes that make us ill do have a positive side. Though I suppose while HLA B27 can be partly responsible for spondyloarthropathy, sufferers may still ‘enjoy’ the benefits. Whereas in PsA the inflammatory response is just a case of the body / immune system being very confused. (Dear body, I have not, repeat not, injured myself so just shut up, all right?)
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My rheum said they were phasing out ESR and using CRP instead - which annoyed me a bit as I was just getting used to being able to track the ESR and make sense of it!
Hmmmm…that’s interesting! I don’t think I was ever tested for the HLA B27 gene—I’ll ask my rheumy about this. Because if I’m positive for it it makes sense why I rarely get sick (crossing my fingers as usually I have to eat my words when I say things like that) but I think you have mentioned you don’t get sick often. I know I’ve only had the Type A flu once in my adult life and probably never any Type B flus.
Anybody else positive for the gene and noticing they don’t catch the flu?
I’m HLAB27 positive and I’ve never had the flu. This is quite interesting as I’ve been very worried about getting the flu this year. It’s really bad in our area and my wbc has been low my last couple of blood tests.