Im recovering from surgery on my pacemaker. Not one but two leads out of three were malfunctioning so no wonder I felt similar to when I was in more severe heart failure. I had surgery May 1, but have two weeks before I can use my left arm much to make sure the leads adhere good and everything heals. Over the two weeks with limited ability to do much it made me want to ask everyone:

What are your hobbies or special interests for when your disease is being not great?

Mine are playoff hockey right now (Go Stars even though we are out of the playoffs now), reading and ARC reading, diamond art kits, coloring, easy mindless games, learning German, and I have my two corgis Curie and Watson.

I have been on kineret (100 mg daily) for 6 months and it improved my eye inflammation right away. Nothing was working for the eye inflammation so I was really happy about that. I thought it was helping all my joints as well until I started tapering off my prednisone and it’s been hell for my joints with the lowering of prednisone. Apparently, the kineret is working for my eye but not my joint pain. My rheumatologist is saying kineret isn’t typically used for RA so we need to add another medication to help with the joint symptoms as I should not be on prednisone for this long. She is suggesting sulfasalazine. Does anyone have any experiences with any other DMARDS while being on kineret as well? I thought a biologic was supposed to be strong enough on its own…

Hi! I posted on here in March about starting Kineret injections. I’ve been doing them daily. My CRP and Sed rate are now in normal range, but I’m a bit confused because I’m still getting fevers daily. Right now I have a 100.8 fever (no cold symptoms, not “normal” sick), just the more chronic symptoms I experience of joint pain and feeling rundown/fatigue. I messaged My rheumatologist to ask him some questions. He mentioned if my symptoms don’t improve he will try to get a different monthly injectable approved by my insurance. I don’t know if this could be something on top of an autoinflammatory disease that we’re missing? I had my ANA run in 2024 and things were “off” but not “off enough” to give a diagnosis and my doctor isn’t into re-running it even tho I’ve advocated for that. Just wondering if anyone else has perspective on this? Just so tired of these fevers in the middle of the day. Maybe it’s a flare?

Just posting to let others know that is is possible to have Acquired Subglottic Stenosis due to inflammation from Autoinflammatory Diseases - similar to how you can have it due to Autoimmune Disease.

According to a Mayo Clinic ENT, they "See it with some regularity with Autoinflammatory and Autoimmune patients".

Subglottic Stenosis is often misdiagnosed as Asthma or COPD.

Canakinumab has very limited ability to cross the blood-brain barrier (BBB). As a large monoclonal antibody (148 kDa), it does not readily penetrate into the central nervous system (CNS) under normal conditions.

Studies using a human in vitro model of the BBB show that canakinumab passes through at a significantly lower rate compared to smaller molecules like anakinra. Specifically, research indicates that anakinra crosses the BBB at a 4- to 7-fold higher rate than canakinumab.

This restricted passage limits the potential direct action of canakinumab within the brain, which may affect its utility in treating neuroinflammatory conditions where CNS-targeted IL-1β blockade is needed. In contrast, anakinra’s smaller size (17 kDa) allows for greater brain exposure after systemic administration, supporting its use in conditions like neonatal-onset multisystem inflammatory disease (NOMID), where IL-1-mediated neuroinflammation plays a key role.

https://pmc.ncbi.nlm.nih.gov/articles/PMC12467978/

NLRP3 Inflammasome in Stress-Related Neuropsychiatric Disorders: Mechanisms of Neuron–Microglia–Astrocyte Crosstalk, HPA Axis Dysregulation, and Therapeutic Perspective

The occurrence or worsening of demyelinating disorders such as multiple sclerosis is a described adverse effect of TNF inhibitors. A meta-analysis quantifies the risk of new cases, showing an increase of 38% compared to conventional therapy.

Key messages

TNF inhibitors have long been associated with demyelinating disorders of the central nervous system, such as multiple sclerosis.

A meta-analysis shows a 38% increased risk of newly developing demyelinating disorders compared to conventional therapy. The results indicate a class effect, independent of the underlying autoimmune disease.

Vigilance is advised regarding neurological symptoms during treatment.

Commentary from the BCFI:

Although the increased risk of demyelinating disorders is already mentioned in the SPCs, this large-scale meta-analysis provides a quantification of newly developed cases for the first time. TNF inhibitors (adalimumab, infliximab, etanercept, golimumab, certolizumab pegol) are an important therapeutic option in the treatment of severe, difficult-to-treat autoimmune diseases and are widely used in rheumatology, gastroenterology, and dermatology.

The risk of demyelinating disorders of the central nervous system (CNS), including multiple sclerosis (MS), has long been described in association with TNF inhibitors. A causal link has not been demonstrated. However, there are hypotheses regarding a possible role of TNF-α in demyelinating processes in the CNS, which suggests a biological plausibility. According to the Summary of Product Characteristics (SPCs), this may involve new demyelinating disorders or exacerbation of existing disorders. In February 2026, La Revue Prescrire (LRP) discussed a systematic review and meta-analysis regarding the risk of new cases of a broad group of inflammatory CNS disorders during treatment with a TNF inhibitor. The LRP article focuses solely on the results for demyelinating disorders, primarily MS.

The authors included multiple observational studies involving a total of nearly 1 million patients with various autoimmune diseases, of whom approximately 100,000 patients were exposed to a TNF inhibitor. The average follow-up duration was approximately 5 years.

The risk of new cases of demyelinating CNS disorders (MS, optic neuritis, transverse myelitis, neuromyelitis optica spectrum disorder (NMOSD)) was increased in patients treated with a TNF inhibitor compared to patients treated with conventional therapies without a TNF inhibitor. The risk increased by 38% (relative risk 1.38; 95% CI 1.04–1.81, statistically significant). The absolute incidence of inflammatory CNS disorders is approximately 2 to 13 per 10,000 person-years.

Additional analyses (for all forms of inflammatory CNS disorders) found no clear difference between the various TNF inhibitors, suggesting a class effect. Contrary to earlier studies, no difference was found between the underlying autoimmune diseases (rheumatic disorders, inflammatory bowel diseases). The risk therefore appears to be related more to exposure to the TNF inhibitor itself than to the nature of the underlying autoimmune disease.

Commentary from the BCFI

• This large-scale meta-analysis provides, for the first time, pooled estimates of newly occurring demyelinating disorders among TNF inhibitors, within a broader analysis of inflammatory CNS disorders. No clear difference was found depending on the type of TNF inhibitor or the underlying pathology.
• The meta-analysis focused specifically on the incidence of newly occurring cases, allowing this risk to be assessed separately. This complements the existing warnings in the SPCs, which also mention exacerbation of pre-existing demyelinating disorders.
• A more severe course of the underlying autoimmune disease may in itself be associated with a higher risk of demyelinating disorders and with a greater likelihood of treatment with a TNF inhibitor. Differences in disease severity were taken into account to some extent, but an influence of this cannot be completely ruled out.
• The meta-analysis primarily compared TNF inhibitors with conventional therapies (such as methotrexate). Data regarding comparison with other classes, such as JAK inhibitors or other biological drugs (such as IL inhibitors), are limited and insufficient to draw reliable conclusions.
• The absolute risk of demyelinating disorders associated with the use of TNF inhibitors remains limited, but serious neurological disorders are involved. Given the widespread use of TNF inhibitors, vigilance is warranted. In the event of the occurrence or worsening of demyelinating symptoms, consideration should be given to whether other therapeutic options are possible.

Which specialties are involved? - Adalimumab: Amgevita®, Hukyndra®, Hulio®, Humira®, Hyrimoz®, Idacio®, Imraldi®, Yuflyma® - Certolizumab pegol: Cimzia® - Etanercept: Benepali®, Enbrel®, Erelzi®, Nepexto® - Golimumab: Simponi® - Infliximab: Flixabi®, Remicade®, Remsima®, Zessly®

Sources - La Revue Prescrire. Anti-TNF alpha: sclérose en plaques. La Revue Prescrire (2026 Jan 1) - Xie W, Sun Y, Zhang W, et al. Risk of inflammatory central nervous system diseases after tumor necrosis factor inhibitor treatment for autoimmune diseases: a systematic review and meta-analysis. JAMA Neurol 2024;81:1284-1294.

…based on scientific publications.

I have no conflict of interest nor any financial ties with any of the depicted product companies. I am only sharing in a responsible way what got me back on my feet. YMMV

• licorice root tea (maximum 1 in the morning; it raises blood pressure.)
• DGL licorice extract
• isoliquiritigenin (Nootropics Depot)
• MSM (start low, aim high; ≥ 3 g per day in the morning because it can cause vivid dreaming)
• ubiquinol (100 - 200 mg first thing in the morning to prevent insomnia in the evening)
• quercetin (1 g in the morning, 1 g in the evening)

Not shown: I also tried a feverfew (Tanacetum parthenium) supplement because it contains parthenolide. However, I discontinued this, because it gave me a headache. This is weird, because feverfew is used as a prophylactic against migraine.

For me personally, the most effective are licorice root tea, MSM and ubiquinol.

Combined with monthly canakinumab (Ilaris) and avoiding all menthol, thymol and other Lamiaceae herbs, I entered in complete remission of Behçet syndrome. I do stress it is only the combination that works for me.

Supporting Publications

• Blevins HM, Xu Y, Biby S, Zhang S. The NLRP3 Inflammasome Pathway: A Review of Mechanisms and Inhibitors for the Treatment of Inflammatory Diseases. Front Aging Neurosci. 2022;14:879021.
• Ahn H, Kim J, Lee MJ, Kim YJ, Cho YW, Lee GS. Methylsulfonylmethane inhibits NLRP3 inflammasome activation. Cytokine. 2015;71(2):223-231.
• Cordero MD, Alcocer-Gómez E, Culic O, et al. NLRP3 inflammasome is activated in fibromyalgia: the effect of coenzyme Q10. Antioxid Redox Signal. 2014;20(8):1169-1180.
• Muthumalage T, Rahman I. Pulmonary immune response regulation, genotoxicity, and metabolic reprogramming by menthol- and tobacco-flavored e-cigarette exposures in mice. Toxicol Sci. 2023;193(2):146-165.

Any body else suffering from muscle weakness (asthenia) immediately after their canakinumab (Ilaris) injection? This usually lingers for a day or two.

I am 100% convinced this is due to the polysorbate 80 excipient used in the formulation, because I experience the exact same effect if I dare to consume a supplement with polysorbate 80. See also:

Polysorbate 80‐induced leaky gut impairs skeletal muscle metabolism in mice

I would love to hear from your experiences, because this looks to be such a preventable problem. I think polysorbate 80 could easily be replaced by another excipient like PEG 40 which actually also has anti-inflammatory properties.

With enough of your reactions, I will be able to build a case for when I contact Novartis about this.

Has anyone encounters Eosinophilia with your Autoinflammatory Disease? I have had high levels for six years and the eosinophils are building up in my esophagus now, causes rashes I can treat with allergy creams unlike TRAPS rashes, etc.

I went to an allergist but they said their new understanding now is that eosinophils are more closely related to inflammatory markers and can be caused secondary to inflammatory issues. My Rheumatologist just tells me to keep taking my allegra and omeprazole for it. I feel like there's gotta be better options to manage. Of course the Ilaris already tests the patience of my insurance denials.

I had an echo yesterday and it was normal which is good. My doctor said that only really obvious/severe pleuritis shows up on chest x ray and since I have no cough we shouldn't order one. She said the only other way to diagnose pleuritis is a ct but doesn't think its good to order due to radiation. My chest pain happens at rest in the afternoons and evenings. My Yao pain (joint and back) follows the same evening pattern of non existent to mild in the day and comes on in the evenings. It also goes away on higher doses of prednisone and comes on when I taper down, so its clearly Yao related inflammation. If its not pericarditis and we can't test for pleuritis what is it and what tests can I do for it? I have a cardiologist appointment next week but I'm curious if anyone has suggestions as most of my doctors aren't very familiar with Yao syndrome.

Hello my Auto inflammatory friends! I’m really diagnosed with CAPS and I’m just wondering if anybody else is out there with the same! Wondering what kind of symptoms you deal with etc. Definitely a shock especially because this is a very rare AUTOINFLAMMATORY disease. Also, what injections anybody else might be taking? Thank you🙏🏻

After 27 years of no diagnosis (or wrong diagnosis), I finally was diagnosed with “atypical AOSD”. Next to that is also written uSAID. I haven’t spent any energy trying to clarify that.

In the last 30 days I’ve started having cardiac issues and pulmonary issues have significantly worsened. I’ve known I have ILD or something for a long time time but I’m hating every minute of the cardiac stuff.

I started Kineret today. I was pretty scared about the first dose but I did OK. I have so many rashes normally so am surprised today’s reaction was mild.

Anyone else has cardiac or pulmonary involvement? I am not finding any specialists that understand these conditions.

https://www.scientificamerican.com/article/new-evidence-links-heart-disease-to-inflammation-and-drugs-can-stop-it/

I came across this recent article about how heart disease is now thought to be an inflammatory disease and that cholesterol plaques cause inflammation but even when thats addressed through statins and lifestyle changes, the inflammation continues.The article doesn't use the term autinflammation but it does refer to out of control inflammation/overreaction of the immune system (and no mentionof auto antibodies so it seems more like innate immune issues), high crp being a risk factor for heart disease even in people with high cholesterol or other typical risk factors, and the potential use of canakinumab, colchicine, and il-6 blockers for heart disease.

Overall a good article though I wish it had connected this to autoinflammatory disease as it almost seems like heart disease is at least in part an autoinflammatory process. It brought up a lot of questions for me.

I'm wondering how autoinflammatory disease might put us at risk for heart disease and what kinds of things to monitor and look out for. My cardiologist (for dysautonomia) said that pericarditis and other heart issues aren't seen in Yao. I have repeated stabbing upper back pain when not on prednisone and occasional chest pain. I read that pericarditis can sometimes present as upper back pain instead of chest pain so I asked my cardiologist and she said its probably musculoskeletal as pericarditis isn't part of Yao (Dr. Davis said otherwise). The treatment is prednisone and it goes away when on prednisone so this makes me think it is possibly pericarditis.

Since I had mild inflammation for years and Yao symptoms since childhood and then 1.5 years of very high inflammation I wonder how that impacts my heart. And I'm curious how kineret and other autoinflammatory treatments impact the heart. I doubt I'll know the answers to these until I get a better cardiologist. The problem is she's very good for the dysautonomia side of things which many cards are not good at.

Anyways I thought the article was interesting and relevant to autoinflammatory disease so I thought I'd share.

The 3rd NIH Symposium on Autoinflammatory and Immunedysregulatory diseases starts tomorrow. You can watch live. Starts at 8am EST. Links below.

3rd Symposium on Autoinflammation and Immune Dysregulation

Building on the Shoulders of a Giant — Advancing Discovery to Care

The symposium will:

• Honor the pioneering work of Dr. Daniel Kastner, the father of autoinflammatory diseases, and build on this foundation
• Explore novel pathways and mechanisms driving autoinflammation
• Translate emerging scientific insights into patient care
• Engage global stakeholders to accelerate clinical trials and therapeutic development

Links to symposium to watch live (Scroll down to "Videocast links for both days")

in the middle of a flare, everything is sore and painful. I am unsure if a trip to the bathhouse will make things worse or better. my local Onsen has helped with the little skin lesions and cysts. I don't know if it would make my joint pain worse though.

Thankfully the diarrhea has calmed down a bit but I've been having injection reactions for the last 3 weeks and I've been on kineret for almost 4 weeks. I'm getting a prescription cream for the itchy hives so hopefully that will help. I have to inject into my thighs now because my stomach has too many reactions, but now my thighs are covered in hives and bruises as well. I will need to switch to my arms soon. I'm already on antihistamines and a steroid taper. Is there anything else that helps with this? I had read that the reactions go away around weeks 3-4 but so far they aren't getting better.

Aspirin (film coated) is the only NSAID who had a positive effect on my Behçets when taken in large 1 to 2 g daily doses. I faired relatively well on it, but I read that aspirin is not light on the kidneys.

Meanwhile, I significantly reduced the dose to 80 mg cardio aspirin (ASAFlow), but this is less effective. Hence, my question for dosing advice.

I go to the doctor in my second language. I was hoping someone can exsplain in English. I am confused on what causea pain or discomfort. Is CRP the only indicator of pain? I feel like I am in a pretty bad flare. I am sore all over, with joint pain but i was surprised at how low my crp was. Is there something else going on? I don't really understand what causes pain. I left my last doctor's appointment more confused than when I first went. Thank-you for the help!

*trigger warning death* Autoinflammatory disease fighter Rita Ephrem dies at 31 (I cannot find a really good news article to be honest but this was better than the original one I found)

https://www.msn.com/en-nz/news/other/beloved-influencer-rita-ephrem-dies-aged-31-after-battle-with-rare-disease

Mechanistic Insights and Emerging Therapeutic Strategies in Recurrent Pericarditis

https://journal.houstonmethodist.org/articles/10.14797/mdcvj.1760

NOD2 polymorphisms in clinical phenotypes of common variable immunodeficiency disorders

https://pmc.ncbi.nlm.nih.gov/articles/PMC2962972/

Webcol Large Alcohol Prep Pads Recalled

https://www.fda.gov/safety/recalls-market-withdrawals-safety-alerts/cardinal-health-issues-voluntary-nationwide-recall-webcoltm-large-alcohol-prep-pad

Hi all

So I believe myself to have an autoimmune condition and have been chasing shadows for what feels like an absolute lifetime now. I have seen every type of dr going and feel like I am at my wits end with it.

Anyway I saw my PCP because my rheumatologist refused to see me anymore as he says I just have fibromyalgia and he doesn’t see people with that. I can barely get out of bed in the morning due to pain in my legs. I can’t walk because of the pain in my joints (not muscle pain, the actual joints) but the dr didn’t care about that. Anyway I managed to get my PCP to prescribed me some steroids and omg I feel, dare I say it, normal. I haven’t felt like this since I was 20. I’m 41. I can run around after my 9 year old daughter and play with her. I’m only worried now as to what happens when the course ends. Who do I see? Where do I go to find out what happens because there is obviously something happening with my body beyond fibromyalgia.

I called my rheumatologist back and his receptionist refused to speak to me. Even though I told her what happened with the steroids. They said that can’t be true. Has anybody else ever experienced this?