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▲ 5 r/Autoinflammatory

Symptoms aligning with menstrual cycle - advice?

Hello! 👋🏼

Prior to genetic testing and diagnosis, I had worked out for years that my main symptoms align with ovulation and luteal phase of my menstrual cycle. It means I have 2+ weeks of a flare, beginning with fever, rashes, joint and full body connective tissue pain, insomnia, and some other symptoms. When the fever goes, it rumbles on as general debilitating fatigue, brain fog and worsened reactions until menstruation, when I get relief (despite the other symptoms it brings…😅)! This is not uncommon in autoinflammatory diseases and I’m aware many women experience this.

Does anyone have any advice on how to alleviate symptoms in luteal, excluding birth control?

My GP (not specialist) would like me to go on birth control as a band aid, and though I’m considering it, I have had a terrible time with birth control in the past that has gone unacknowledged, and is now part of a class action lawsuit globally, and I personally would prefer to avoid it.

I am open to any other accessible medical aids, natural aids within reason (I am a physiologist and nutrition scientist so will never go in blindly) or non-medical aids as there may well be things that have never crossed my mind!

I am also open to hearing about successes with birth control if you also have my conditions I listed at the end.

Thank you 🙏

For more info:

I have one pathogenic MEFV variant and two very rare pathogenic variants of two other genes which I cannot recall but are not any of the ones that cause the main, known, conditions. I have numerous VUS for the other known conditions but they are unaware if these are disease-causing variants. My sibling is also affected.

I was tested by the NAC in London and diagnosed by NHS Rheumatology consultant in collab with them. I am yet to receive my letter following the appointment and have not commenced any meds. My CRP has not been raised when tested, though has only been tested at random times. ESR and PV have been raised during random testing, as well as thrombocytopenia, no sign of autoimmunity in bloods.

I have a number of conditions which all overlap/are related in some way, including. Pots, mast cell disease, hEDS, PMOS and insulin resistance (lean), early stage HS (part of overall autoinflammatory picture, also flares in luteal). I believe these all connect to the luteal symptom picture. I take sodium cromoglicate, metformin and fexofenadine.

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u/Finding_Tee — 11 hours ago
▲ 5 r/Autoinflammatory

Kineret “Reimbursement Program”

Located in the US

TLDR: I’m looking for anyone with experience with a Kineret “reimbursement program” for cash payment for Kineret.

I am newly on Kineret through the bridge program and at the end of my 28 days. Insurance has denied (of course). I have also been denied for the OnTrack financial assistance program due to my husband’s income. I am apparently the first person in my rheumatologist office’s history to be denied for OnTrack, so we are all lost!

They believe there is a reimbursement program if I pay cash for the medication, but I can’t find anything about it online. McKesson told me the cash price for 28 days is $7574, and if I can manage to scrape that together, I would absolutely have to get it back. Does anyone know anything about this program or have experience with it?

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u/BitsyMidge — 1 day ago
▲ 4 r/Autoinflammatory+2 crossposts

Could This be Autoinflammatory?

This is a repeat post. But I have more thorough information update. But still no answers.

Who You Are
31. Male. Swiss/Armenian/American. Non smoker. 88kg. 198cm. MSc Nutrition Science. Works in rheumatology NGO. Lifelong systemic illness since childhood. Hospitalised at age 1 with systemic bacterial infection.

What A Flare Looks Like
Flares are triggered by foods, such as peanut butter, walnuts, sauerkraut, yoghurt, UHT milk, and other proteins, with severity proportional to the amount consumed. Onset begins within a few hours of exposure, peaking over several days. Symptoms include chills, fatigue, feverish feeling, sore throat, burning ears, runny nose, red eyes, stomach irritation, nausea, irritability, and stiff internal neck with lymph node pain. There is no fever. 

Most symptoms present at baseline to some capacity, with great QOL impact

Without rescue treatment, flares persist for weeks. The only reliable rescue is ⭐️azithromycin (2 x 250mg spaced over a few days). Azithromycin works every time without exception. Prednisone definitely provides relief (3 days to work). But relief is incomplete. Doxycycline does nothing.

Even after exposure stops, the flare continues, and it is unclear whether it ever fully resolves on its own anymore.​​​​​​​​​​​​​​​​ Quercetin also provided notable relief (3 days to work). Felt like healing even compared to azith which just stops flares. But then tacphylaxis.

Symptom Clusters During Flare
Flu / Infection Feeling: Chills, hot flu-like sensation, sore throat, runny nose, red eyes, skin itching

Headache/Burning: Temporal headache and pressure, burning hands/abdomen (worsened by omega-3s, relieved by Advil and quercetin)

Lymph / Neck: Previous periods of very swollen neck and face lymph nodes (particularly 2013). Regular left cervical lymph node and groin lymph pain, stiff neck, with internal blocked sensation

GI: lower abdominal pain, gas, intermittent diarrhoea, nausea, occasional rectal bleeding, urethral burning, rectal ache, back of throat ache, rectal itching

Continued…
Fatigue — exercise improves, or neutral. Bad sleep severely effects

Erectile dysfunction — absent on waking, non-responsive to PDE5 inhibitors

Difficulty concentrating, cognitive slowing

Vibration/frog noise/sensation rising through the throat

*Bug-bite-like rashes — erythematous, raised, non-pruritic, lasting hours, concurrent with flares

Knee pain during flare 

Notes (I have lab documents for these)
Antihistamines failed (ketotifen/cetirizine/monteluklast, famotidine, loratadine, fexofenadine) — rules out primary MCAS?

CRP 0.5 mg/l is normal between flares 

Normal CBC, metabolic panel, TSH, HbA1c, testosterone, LH, cortisol/Synacthen

Colonoscopy and endoscopy with biopsies: normal (2019 and 2025). Normal calprotectin. 

Probiotics provide some relief, but then heavy symptoms

OJ helps burning feeling, headaches and sleeplessness caused by alcohol and nitrite

Tried multiple elimination diets

Lymphopenia (.75g/l) but maybe irrelevant

Immunomodulator response, food response and flare-associated rash, lifelong history since infancy, are inconsistent with functional illness

Ideas
Incomplete/atypical Autoinflammatory (lack of fevers, which seems exclusionary)

Secondary MCAS

Ask for:
⭐️Rheumatology referral

Immunological panel: ANA, ANCA, complement C3/C4, SAA, SPEP. 

Baseline serum tryptase

24-hour urine: histamine, N-methylhistamine, prostaglandin D2

Periodic fever panel (TNFRSF1A, NLRP3, MVK, CECR1, NOD2, all FMF/MEFV variants including E148Q, Yao)

Colchicine 0.6mg BID prescription

Anakinra

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u/Steph_Arabian — 1 day ago
▲ 9 r/Autoinflammatory

Behçet's and Organ Involvement Predictions

AB0404 (2026)

BASELINE CLINICAL AND LABORATORY PREDICTORS OF NEW MAJOR ORGAN INVOLVEMENT IN BEHÇET’S DISEASE: RESULTS FROM AN INCEPTION COHORT

Keywords: Prognostic factors, Biomarkers, Uveitis, Descriptive Studies, Rare/orphan diseases

R. Deniz1, O. Altun1, A. Gül2, C. Bes1

1University of Health Sciences Başakşehir Çam ve Sakura City Hospital, Rheumatology, Istanbul, Türkiye

2İstanbul University Faculty of Medicine, Department of Internal Medicine Division of Rheumatology, İstanbul, Türkiye

Background: Behçet’s disease (BD) is a chronic, relapsing, multisystem inflammatory disorder characterized by a wide clinical spectrum ranging from mucocutaneous manifestations to severe, life-threatening major organ involvement (MOI), including ocular, vascular, neurological, and gastrointestinal disease. Early identification of patients at risk for progression to MOI is a major unmet need in routine clinical practice, as delayed recognition is associated with irreversible organ damage, disability, increased morbidity, and mortality. Although several clinical features have been associated with MOI in cross-sectional studies, there is limited prospective inception-cohort evidence evaluating which baseline clinical or laboratory characteristics may predict the development of new major organ involvement (NMOI) during follow-up. Understanding these predictors may support risk stratification and guide early intensified monitoring or tailored immunosuppressive strategies.

Objectives: This study aims to address this gap by investigating the prognostic value of baseline demographic, clinical, and routine laboratory parameters for predicting incident NMOI in a well-defined cohort of newly diagnosed BD patients whether a MOI is present or not at diagnosis.

Methods: This study was designed as a prospective inception cohort including patients newly diagnosed with BD according to the International Study Group (ISG) criteria. Demographic features, clinical manifestations, and routine laboratory parameters were systematically recorded at diagnosis and at scheduled follow-up visits. Major organ involvement (MOI) was defined as ocular, vascular, neurological, or gastrointestinal involvement meeting accepted clinical and radiological criteria. Patients were classified into two groups: those who developed new MOI (NMOI) during follow-up in addition to MOI at diagnosis and those who did not. Follow-up outcomes included type and timing of new MOI, relapse frequency, treatment response, and cumulative organ involvement.

Results: A total of 117 patients were included in the inception cohort, of whom 16 developed at least one new major organ involvement (NMOI) during follow-up. Sex distribution was similar between groups, whereas patients who developed NMOI were older at baseline (32 vs 39.5 years, p=0.087). Although MOI at diagnosis appeared more frequent in the group without NMOI, none of the phenotypes differed significantly. Detailed characteristics are presented in Table 1. Among the 16 NMOI cases, the distribution was as follows: 5 ocular, 9 vascular, 1 neurological, and 2 gastrointestinal events; 1 patient developed both ocular and vascular involvement.

Baseline clinical manifestations were generally comparable between the two groups, with the exception of folliculitis, which was significantly more common in patients who did not develop NMOI (64.4% vs 37.5%, p=0.040). Genital ulcers also tended to be less frequent among patients who later developed NMOI, although this difference did not reach statistical significance (66.3% vs 56.3%, p=0.302).

During follow-up, thrombotic vascular events, specifically uveitis, superficial thrombophlebitis, deep venous thrombosis, arterial, and gastrointestinal involvement, were more frequent in the NMOI group (Table 2). Presentation with MOI at diagnosis did not differ between groups; however, baseline CRP and ESR levels were tended to be higher in patients who subsequently developed NMOI (CRP 6 vs 22.7 mg/L, p=0.034; ESR 11.5 vs 25 mm/h, p=0.005). HLA-B51 positivity was not associated with NMOI development (p>0.05). By the last visit, the NMOI group had significantly higher frequencies of ocular, vascular, and gastrointestinal involvement. Cumulative follow-up duration was longer in NMOI group (24 vs 28.5 months, p=0.06). Relapse rate was similar during follow up and patients with NMOI has more active status at last visit (10.9 vs 31.1%, p=0.025).

Conclusions: In this inception cohort, some certain baseline clinical and laboratory features were associated with the development of NMOI in Behçet’s disease. While recurrent oral ulcers appeared to be a universal and phenotype-independent manifestation, folliculitis and genital ulcers were more characteristic of a stable phenotypic course and seemed to be associated with a lower likelihood of progression to NMOI.

Conversely, elevated acute phase reactants (CRP, ESR) at diagnosis emerged as potential predictors of NMOI, likely reflecting subclinical inflammatory and ischemic pathways that predispose to vascular and ocular complications. Importantly, HLA-B51 positivity did not differentiate patients who developed NMOI from those who did not, indicating limited prognostic value in this context.

These findings highlights the importance of a comprehensive baseline clinical and laboratory assessment in newly diagnosed BD patients. Identifying high-risk individuals early may allow clinicians to personalize follow-up intensity, implement more vigilant monitoring strategies, and potentially initiate timely therapeutic interventions to prevent irreversible organ damage.

Table 1. Clinical characteristics of Behçet’s disease patients with and without major organ involvement (MOI) at diagnosis

u/Alice-The-Chemist — 2 days ago
▲ 4 r/Autoinflammatory

Cold urticaria, Hypo, and hEDS

Since I've been around 10 I started getting random allergic reactions that would only be controlled by benedryl. It would knock me out as a kid for a few hours then happen again. After numerous stabby allergy panels on my back most were negative alise from regular things such as dander or pollen. Thyroid tests and other blood tests came back normal. The allergist was puzzled so he decided to place an ice cube on my arm then bam hives spreading, swelling, itchy reaction. It made sense since my throat almost closed up from swimming for 10ish minutes. Originally we assumed face paint, sunny d, etc, etc. Caused a lot of issues with teachers in school or the nurses believing me because my hives were internal more than visible aggressive hive welts now.

Anyways... They did an antihistamine treatment of some sort where I would rotate taking different medications and also get a shot at a doc office every so frequently. Allergy goes away for two years. Comes back just slightly less severe. Great! I started the drug trial for xyzal and the results are amazing for me (no drowsiness and long lasting). After it was released to stores over the counter, I continued to take It every other day to avoid an unavoidable reaction for 18 years.

My health has never been "normal". I've always been covered in bruises excessively from head to toe. Was tested for blood clotting due to how long scratches would take to heal and stop bleeding. Cold intolerance, weak immune system, extreme fatigue, weight gain

Fast forward to the last two years of an insane amount of blood testing my doctors are still extremely stumped as to what the hell is going on. My thyroid is swollen, I have fluid behind my ears they can't explain, constant pain. The ultrasound showed no abnormal growths or nodules. TSH finally after multiple tests showed hypo. After begging my doctor after the 4th irregular test that it wasn't a fluke she put me onto a name brand thyroid medication since some fillers cause inflammation.

I have no understanding or explanation but my rare ass cold allergy I've had for 18 YEARS decided to almost entirely go away 3 weeks into taking the medicine. After the initial 10 weeks the bruises disappeared, more energy, and metabolism got faster. All the classic hypo issues. My allergy still has flares but only my palms now. This also leaves me stumped because despite cryo coagulation, hashimoto's , autoimmune, or lupus blood tests all come back as normal or negative. So many women in my family have hypo, thyroid cancer, hashi, or lupus. Due to the hEDS I'm in constant pain but that isn't really my concern.

I wanted to post here so I made an account to see if anyone has gone through something similar. I feel like I'm going crazy lol. I even had a second opinion with a Harvard doc who told me my unexplainable bruising and pain was because I needed therapy??? Oh my bad I didn't realize depression caused sciatica, allergies, or joint dislocation of my hip 4 times this week sleeping pfft...

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u/UnluckyPart1146 — 3 days ago
▲ 6 r/Autoinflammatory+1 crossposts

Behcet's Diagnosis

Hello all!
I’m trying to get a Behcet's diagnosis and am having the hardest time. My PCP and dermatologist both believe that I have Behcet's based on my symptoms, but they are waiting for me to have an outbreak so they can take a biopsy. Unfortunately, I don’t get sores that often anymore and when I do, there’s never an appointment available.

So, how else can I get a diagnosis?
I’ve been to the rheumatologist and she was awful. She literally said "You don’t have a sore, so I can’t do anything for you".

This can’t be right because logically, every single person with Behcet's wasn’t diagnosed from a biopsy. There has to be another way.
I left that rheumatologist and have an appointment with a new one in 5 weeks.

This illness has destroyed my life. Some days I can’t walk, most days I can’t breathe, I can’t exercise, my body is weak, my heart is in bad shape, etc …

Everything else has already been ruled out and I’ve had tests done that show I have inflammation…

Does anyone have any advice on how to get this diagnosis so I can FINALLY get treated?

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u/MissZadejah — 3 days ago
▲ 8 r/Autoinflammatory+2 crossposts

Need your help in a Bechet Disease-related research!

My name is Youssef, an intern at Mansoura University Hospitals, Egypt. We made this survey targeted to rheumatologists worldwide to see ( Real-world Biologic use in Behcet's disease ) :

https://docs.google.com/forms/d/e/1FAIpQLSf3SZJHGNcoo0Aks5Jbyhb-975RaxAuUU0pPSzPB4nqXznyKg/viewform?usp=publish-edito

It won't take much time & would help Behcet patients, so we would be so grateful if you could fill it out . Thank you in advance!

u/Usef106 — 3 days ago
▲ 14 r/Autoinflammatory

NOD2 Variants & Symptoms Research

NOD2

OP0325 (2026)

ASSOCIATION OF NOD2 VARIANTS WITH CLINICAL PHENOTYPES IN AUTOINFLAMMATORY DISEASE: INSIGHTS FROM A COHORT THROUGH A VALIDATED NEXT-GENERATION SEQUENCING PANEL

Keywords: Rare/orphan diseases, Innate immunity, Epitranscriptomics, Epigenetics, And genetics

M. Schermi1, M. T. Perez-Cartier Beingolea2, S. Rizzo1, A. Fu1, S. Moz2, P. Galozzi2, R. Ramonda1, P. Sfriso1, S. Bindoli1

1University of Padova, Rheumatology Unit, Department of Medicine (DIMED), Padova, Italy

2University of Padova, Laboratory Medicine Unit, Department of Medicine (DIMED), Padova, Italy

Background: Variants in the NOD2 gene are associated with increased susceptibility to a broad spectrum of diseases, ranging from granulomatous conditions (e.g. Crohn’s disease, Blau syndrome) to autoinflammatory disorders, such as Yao syndrome. These variants may variably affect NOD2 protein function, depending on the specific mutation, resulting in altered innate immune signaling and dysregulated inflammatory responses upon microbial stimulation. In recent years, targeted next-Generation Sequencing (NGS) gene panels have become a cornerstone of molecular diagnostic, enabling confirmation or diagnostic support for genetically heterogeneous disorders, including adult-onset conditions associated with NOD2 variants.

Objectives: This study aimed to identify amongst adult patients with autoinflammatory manifestation, such as recurrent fever, skin rashes, and gastrointestinal symptoms, those who present NOD2 variants. Additionally, we sought to explore whether specific NOD2 variants correlate with distinct clinical phenotypes, potentially allowing the reclassification of adult patients from the nonspecific “undifferentiated autoinflammatory disease” (uSAID) into potential emerging subgroups of NOD2-related disorders. These conditions span a phenotypic continuum encompassing granulomatous diseases, intestinal pathologies, and autoinflammatory disorders.

Methods: Patients with clinical and biochemical features suggestive of autoinflammatory disease and referred to the outpatient clinic for between February 2023 to December 2025. NGS sequencing was performed using Custom “Fever & Autoinflammatory Disease” panel (SOPHIA Genetics) on an Illumina MiSeq platform. The panel covers the coding regions of 17 genes ( ADA2, CARD14, ELANE, IL10RB, IL10RB, IL1RN, LPIN2, MEFV, MKV, NLRP12, NLRP3, NLRP7, NOD2, PSMB8, PSTPIP1, TNFRSF11A, TNFRSF1A ). Variant calling and data analysis were performed by the Sophia-DDM-V6.5 pipeline. Variant interpretation followed the 2015 ACMG standards and guidelines.

Results: A total of 135 patients (80 females; mean age 37.08 ± 14 years) were enrolled. Of these, 115 patients (85.1%) carried at least one retained non-synonymous variant with a minor allele frequency (MAF) ≤ 0.05. Among them, 25 patients (18%) harbored at least one NOD2 variant classified as pathogenic or as a variant of uncertain significance (VUS). The identified NOD2 variants included heterozygous p.G908R (8 patients), p.R702W (7 patients), p.Leu1007Profs*2 (7 patients), p.A885P (1 patient), p.R1019L (1 patient), and p.S402F (1 patient). The clinical features associated with each variant are detailed in Figure 1 .

Eight of the 25 patients (32%) presented with recurrent fever and skin rashes, along with at least one additional symptom (such as abdominal pain, serositis, arthritis/arthralgia, or sicca manifestation), which may be compatible with a Yao syndrome–like clinical phenotype [1]. The remaining patients did not fully meet the established diagnostic criteria. Two main clinically defined patient groups were identified: one characterised by the p.G908R variant and the other by the p.R702W variant. Almost all patients in both clusters experienced recurrent fever and musculoskeletal symptoms, including arthritis, arthralgia, and myalgia. Abdominal pain was observed in 50% of patients carrying the p.G908R variant, whereas skin rashes were more prevalent among those with the p.R702W variant (71%). Additionally, 57% of patients with the p.Leu1007Profs*2 variant reported headache. About additional genetic findings, among the p.G908R carriers, 5 out of 8 patients also harbored VUS in MEFV gene (3 patients), one had a pathogenic variant in ADA2 , and one had a variant in LPIN2 . Among p.R702W carriers, one patient presented a heterozygous MEFV variant. For those with the p.Leu1007Profs*2 variant, one patient had a co-variation in NOD2 (p.R439C) and another had a pathogenic variation in ADA2 . Additionally, one patient with the p.A885P variant also harbored a VUS in ELANE . The two patients with pathogenic variations in ADA2 did not exhibit typical features of DADA2 and responded adequately to colchicine. All patients with additional VUS in MEFV showed a favourable response to colchicine. Granulomatous skin lesions developed in only one patient with the p.S402F variant, while ascertained inflammatory bowel disease was observed in a patient with the p.Leu1007Profs*2. The coexistence of additional variants in autoinflammatory genes supports a potential oligogenic or modifier-gene contribution to disease expression. Regarding treatment, patients with two VUS across the same or different genes (13 out of 25, or 52%) generally experienced a higher burden of inflammatory symptoms. Eight of these patients had a satisfactory response to colchicine, and in three cases, a combination of colchicine and IL-1 inhibitors resulted in a better clinical outcome.

Conclusions: The use of validated targeted NGS panel is essential for identifying variants that can support or refine clinical diagnosis in autoinflammatory disorders. NOD2-related diseases encompass a wide range of conditions that may not always align with established diagnostic categories such as Yao syndrome, Blau syndrome, or Crohn’s disease. Although patients carrying VUS are typically classified as having uSAID due to uncertain variant pathogenicity, the identification of patient clusters sharing the same NOD2 variants and exhibiting overlapping clinical profiles suggests the existence of previously unrecognized gene-related entities. Further investigations, including whole-exome sequencing and functional studies, are warranted to refine diagnostic frameworks and improved genotype-phenotype interpretation in individuals withNOD2 variants.

Figure 1.

Heatmap illustrating the prevalence of the main clinical features associated with each NOD2 variant detected after NGSseq

u/Alice-The-Chemist — 4 days ago
▲ 7 r/Autoinflammatory

Rescue meds?

Hi everyone!

I’m in the midst of a horrible YAOS flare. I’m still new to the diagnosis and I’m waiting to see a new rheumatologist, so I’m curious, what does everyone do to squash flares when they happen?

Steroids? Something else?

I’m so miserable, but I don’t know what to do or what to ask for. Any advice would be wonderful! Thank you!

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u/Individual-Yam7050 — 7 days ago
▲ 5 r/Autoinflammatory

Vitamin D and prednisone

I've been on prednisone since late January. Started at 25 mg with a quick taper and had to quickly go up to 30 mg with a much longer taper. The good news is that with the tyenne infusion I have been able to go down to 7.5 mg without symptoms which is great because symptoms and the plan is to continue tapering down over the next few months. However my vitamin d level went down from 29.5 to 27.5 in 2 months despite daily supplementation of 5,000 iu. I always take my vit d with a fatty meal as its a fat soluble vitamin. I have also been trying to focus on eating eggs, fatty fish, and food fortified with vit d. I do have rapid gastric emptying which causes absorption issues and prednisone is known to cause issues absorbing vit d, calcium, potassium and a few other nutrients. My doctor said to increase the dose to 6,000 iu. I'm wondering if thats enough or if theres something else I can do? My calcium and potassium are thankfully normal though trending downwards. Does anyone have any advice for this?

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u/No_Satisfaction_7431 — 7 days ago
▲ 5 r/Autoinflammatory+1 crossposts

Myriad of symptoms

Hello I have a chronic disease for which I get the fibromyalgia diagnose in my country
I have extensive blood work and nothing remarkable shows up the only one astronomical height was
CALPROTECTIN in serum (lab normal value , below 3000 ) and mine was 24000
Th/to, nxp2, pm scl 100- INCONCLUSIVE from the autoimmune panels
WHOLE genome sequencing -negative
EMG-negative
The usual blood work -negative

Some of my symptoms:

Body wide twitching
Innapropiate laughting
Exaggerated gag reflex
Severe scalp hair falling and fragile (also thinning eyebrows )
My body is becoming thinner; both muscle mass and fatty tissue appear to be wasting away (atrophying), which is especially noticeable in my face.
I feel facial tightness, and the contour of my face has changed.
I experience a sensation of pressure/tightness around my eyes and pain when moving my eyes.
I have almost continuous pain in the tissues of my face.
My face appears unhealthy or sickly, and my facial expression seems more fixed and less expressive than before.
My facial features have become more drawn and my face looks noticeably different I have adipose atrophy on my entire face and I think the muscle too although the emg on my face it s normal .
Muscle pain throughout my body, as if I had run a marathon.
My fingernails are brittle, break easily, and no longer grow long.
I feel inflammation throughout my body, with a general feeling of being unwell that fluctuates in intensity.
I have a sensation of acid in my body, as if I had been poisoned.
My ears pop and become blocked everyday it s happening.
The sensation of inflammation can occur anywhere in my body.
I also feel inflammation in my head, with difficulty concentrating, poor memory, and almost continuous headaches,difficulty finding my words
I have eczema on my scalp, around my ears, and on my trunk (torso).
I am still able to do all my usual activities, but with difficulty. I feel as though my entire body has become weaker and is wasting away.
I get tired very quickly and start sweating almost immediately with exertion.
Small granules or bumps appear all over my scalp, similar to the material that comes out of blackheads.
My teeth have become sensitive to cold foods and cold water.
Sometimes I experience abdominal pain, and at the same time I feel warmth/heat and a throbbing or pulsating sensation in my face.
I have difficulty swallowing, with the sensation that food has trouble passing all the way down the esophagus to the stomach, as if the esophagus has narrowed. Also I experience frecquent regurgitation
All my joints and cartilage make sounds, cracking,poping , even my throat and eyes make some trance sounds at movement
I frequently experience abdominal cramps and pain.
I have intermittent constipation.
I really don’t know what it s going on and what and where to go anymore

The only thing that was extremely out of place was calprotectin and I read that it means that the neutrophil or macrophages are activated in some way and it means inflammation in the body , anyone have any idea ?

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u/No_Cheesecake5861 — 8 days ago
▲ 14 r/Autoinflammatory

A few papers published in May 2026 referencing Neurological Manifestations and Autoinflammatory Disease

Was looking into some information regarding Neurological Manifestations of Autoinflammatory Diseases. Here are some new publications I came across published May 2026.

Some New Research to Peruse:

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u/AdventurousMorningLo — 7 days ago
▲ 9 r/Autoinflammatory

Widespread Muscle Pain

u/Northbreak has asked in a few comment sections about this and I wanted to get more eyes on it as a post. For me yes, sometimes my muscle pain is one of my worst symptoms? Do you get weakness also? I ask because of something called myositis. There are multiple forms of it. I dont know why my muscles hurt: sometimes culprits include low potassium or magnesium, needing to stretch and do light movement more. It feels so deep someday I use heating pad/ice and it just doesnt feel deep enough. I hope others have answers.

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u/Alice-The-Chemist — 10 days ago
▲ 8 r/Autoinflammatory

Vent Because When Do We Get Breaks From Our Bodies?

First I need to add a tag or flair for venting.

Anyways thats all this is feel free to skip.

I had surgery to replace wires on my pacemaker that were malfunctioning on May 1st. Felt great to be not feeling like heart failure because not one but two leads were malfunctioning. So no wonder I was out of breathe talking and couldnt keep fluid off.

Anyways I woke up May 25 to my left side of shirt soaked in fluid from my incision opening up. My surgeron was like can you fit a finger it, but don't do that. Cephalexin, antibitoics started as precaution due to my history. Dermabond OTC and 5 days later I am more hives than I am my normal skin. I had the though of I Now Im on prednisone because allergy medicine didnt cut it.

95% chance of surgery on Friday at 745 be there at 545 (Im narcoleptic I dont see those times). To laser lead extract out the leads they had to leave in on May 1 due to not being able to secure a cardio thoracic surgeron require to be avaliable. Most likely issue is those extra two wires plus caps my body has decided it doesn't want them hence the pushing on my incision.

But at least I got my Actemra this past Wednesday, Arcalyst Friday. Surviving. But I need a break. A vacation. There should be retreats for chronic illness people. Rant over.

If you ever see my replies and they say Ill be back its because the narcolepsy is taking over but I want everyone to know their posts are being read. Sometimes I just cant stop the sleep and then start typing like Im drunk.

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u/Alice-The-Chemist — 10 days ago