I am male. At 27 years of age, the first symptoms of AA appeared within 3 months after a severe infection, probably swine influenza. This infection completely destroyed myself; fever over 40 degrees Celsius, I could not sit, I could do not lie in bed, I had delirium. I recovered after 2 weeks and everything seemed to be fine. After 3 months the first sign of AA appeared. The disease evolved towards AU within 1.5 years. I lost all my hair and became a mannequin. No autoimmune diseases in whole family.
* Forgive the casual language and lack of citation. I could write it as a study paper, but this is not the point.
First signs of alopecia areata on the head I treated with acetonide triamcinolone injection 10mg/ml intralesional. I had a positive response. Nonetheless, disease still developed. I decided not to do anything.
Since I lost all of my hair, I decided to start treatment on my own due to complete disappointment after contact with the physicians (medice cura te ipsum). I did QuantiFERON that resulted positive.
Then I did an X-ray. Results: no tuberculosis, clear,sexy lungs. I prescribed myself medicine and started curation to eradicate potential mycobacteria with rifampicin and isoniazid in a 3-month regime in accordance with appropriate guidelines (God bless USA). I vaccinated myself against pneumococcus, shingles (BAYER, one dose vaccination that was withdrawn from USA) and SARS-CoV-2.
After antibiotic treatment and vaccinations I started with ruxolitnib phosphate at a dose 20mg each 12 h. First signs of regrowth I observed after 4.5 months. To accelerate the treatment process, I decided to take 8 mg of dexamethasone biweekly (oral systemic administration) since 4 month of treatment with ruxolitnib. Thereafter, I also decided to increase the dose up to 25mg of ruxolitnib each 12 h (maximal daily dose of ruxolitnib according to the EMA characteristic). Please note that dexamethasone is an unpredictable CYP inducer while the metabolism of ruxolitnib undergoes transformation through CYP. Since I had 75% regrowth on hair, I did intralesional injection with triamcinolone in 1; it worked immediately.
The steroid was planned to be taken 8 mg biweekly within 4 months and then monthly gradually diluted [8,4 ],[ 4,4] , [2,2] , [1,1], [0.5,0.5] and maintain low dose of dexamethasone 0.5 biweekly or discontinue. There are some premises to maintain the lowest dose of steroid (modulation of the nuclear receptors) .
Other adjuvants I used: minoxidil in propylene glycol 5 mg each 12 h (orally). While taking steroids, I did vit D 2000 UI (OCT) and calcium gluconate 800 mg(OCT).
Side effects and infections:
Side effects were associated with the ingestion of 8 mg of dexamethasone; insomnia, depression mood, anxiety for 2 days after the second dose, and water retention. However, no Cushing syndrome appeared. I also noticed increased blood pressure and blurred vision. While I started taking 4mg, water gone, I sleep well, mood gradually is restoring, no problem with eyes. I also took benzodiazepines sometimes (diazepam) to relief side effects of dexamethasone.
I was sick due to infections. 2 usual-winter viral infections and once covid. In every case I get infected from non-immunocompromised individuals that had severe symptoms of infections. All infections I passed mildly. Please note, that for instance ruxolitnib was considered as nice agent against SARS-CoV-2 virus, as well as that dexamethasone dimmish inflammation.
I did diagnostic on cholesterol and triglycerides; elevated but not exceed. I did once diagnostic on cortisol day before taking steroid (morning ofc) after 4 months of taking steroid: level in referential compartment. Sometimes I work to sunset and morning, and I feel cortisol excretion, therefore it appears it is fine with adrenal cortex. I did and still do diet; no weight increased. I try to do sport. I noticed constipation (JAKi side effect). I avoid sun – it is necessary while you do immunosuppressants.
I read some threads over here as well as ten/hundreds of papers with cases and reviews and experiments. It appears, that AA, AT, AU psychophysiology process is not the same for everyone. I am awareness as immunology is complicated. Therefore, treatment must be suitable. I hope I did sniper shoot with JAK1 inhibitor in my situation. To be honest JAKi are shitty drugs but nowadays unfortunately golden standard. There is necessity to discover another approach. There is still necessity to create procedures for screening susceptible units and unravel a lot of things that are unclear.
As medical representant I have to aware you if you do immunosuppressants: be afraid of sun and infections; bacterial as well as virus. It is difficult to figure out when taking medicines such as ruxolinib or dexamethasone help and when it can be life-threatening. In some situations, such as COVID It appears to help, however in case of bacterial infections such as lung tuberculosis taking immunosuppressants can be very dangerous.
I have a lot ideas how to fight with this terrible disease but it take a time until I will able to introduce and throw them due to many aspects of my life. Yes, I am man of science. I wish myself I will have chance to chase the rabbit. Why? Not me. I saw agony in eyes in patients with AU and this triggered my efforts.
Just to be clear. I do not practice, and I do not offer health care as professional. I do science which actually is not inline with immunology. However, if someone need help in Europe, I consider helping.
May God help me and you.
thank you for your post
we are in Europe, do you have an email? thank you again
hello it's incredible I'm French and I feel like I'm reading myself I've also been taking tofacitinib for 4 years and baricitinib for 8 months I took cortisone too and I can't stand cortisone anymore like you I had adverse effects on the neurological system blurred vision, tight head dizziness sweating horrible feeling that lasted 1 month after stopping cortisone like you I took diazepam which lessens the effect but came back 1 hour later doctor did not understand. I have the impression of reading myself I was also self-medicating why cortisone has neurological side effects this is due to what because the first 3 months I did not have this side effects.
the side effects with the jaks for 4 years cholesterol, otitis, shingles, but at the beginning of the treatment otherwise I never got sick no infections.
tofacitinib 11mg and baricitinib 4mg.
baricitinib didn't make me gain more hair.
at the end of October I will ask my dermatologist to switch to upadacitinib which seems more powerful according to my research, what do you think?
I did cortisone injections on the skull,
I also did high dose intravenous cortisone at the hospital 1 week a month for 3 months in 2019 associated with tofacitinib it did not help my hair grow.
I pushed back the beard 90% body hair 40%, eyelashes 50% fallout after stopping cortisone, eyebrows 50%.
I am 34 years old alopecia for 25 years.
treatment in 2008 which worked methotrexate combination with cortisone.
discontinuation of treatment complete relapse.
jaks have been maintaining body hair and hair for 4 years now.
I contacted a private laboratory of FMT IN SLOVAKIA for an intestinal microbiota transplant they were clear and transparent if you want information I can give you the contact details send you their answer
Hello, I don’t know if upadacitinib will improve the results, this chemical appears to the be interesting due to lack of some side effect that occurs during ruxolitinib treatment, also high selectively against isoform 1 is very tempting. Reports from studies on different JAKi aswell as anecdotally found herein are strongly divergent, and answer is does not simple. Nonetheless, there is light in tunnel that jugglery with JAKi brings desired outcome while you find this working one. I think dose also plays the role. Since you have been after persistent treatment with JAKi, did you subcutaneously inject steroid in patches? If so, what was the result? According to cortisone; please note that steroids have two components: anti-inflammatory and mineralocorticoid. Dexamethasone has the highest ratio in favor of anti-inflammatory while cortisone is more balanced in this aspect. I did pulse therapy starting from dose 0.1mg/kg body weight, which differ from sustained administration of cortisone.
According to fecal transplant. For me, the physiology of the gut microbiota is complicated and undeciphered. The relevance of this approach if you do not suffer from some GI inflammatory diseases can be misleading, however I wish I’m wrong. This is very interesting, i will be grateful for some information on private message, especially me how they justify it, and the question is who is the donor?
Hi Maria, text to me on private message herein.
Well, that's interesting. I've heard that it doesn't work. I guess, I've heard lies. Thanks, OP.