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Thread: Cytokines and Inflammation

  1. #1
    Senior Member J-Mill's Avatar
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    Default Cytokines and Inflammation

    Just thought I would post some information I received from my doctor who has been treating me for daily persistent headaches. I have been telling him for over a year that I believe there is some common underlying element to both my headaches and Rosacea because when my Rosacea flares so do my headches (or vice versa). I had done some research and found one study that commented on the prevelance of chronic migraine sufferers in Rosacea patients. Now, it appears, for those with Rosacea and chronic headaches, there may be a link, our good friend cytokines:

    Doxycycline for Treatment Resistant New Daily Persistent
    Headache
    Rozen T.D.
    Neurology, MHNI, Ann Arbor, MI, USA
    Objectives:
    •To test the efficacy of doxycycline, a tumor
    necrosis factor (TNF)
    α inhibitor, in patients with treatment
    resistant NDPH with elevated CSF TNF
    α levels.

    Background:
    •NDPH is one of the most treatment resistant
    of all the primary headache disorders. A significant number of
    NDPH patients start having their headaches after an infection, so
    proinflammatory cytokines may play a role in the pathogenesis of
    NDPH. Rozen and Swidan recently demonstrated an elevation of
    CSF TNF
    α levels in 19 of 20 NDPH patients. They hypothesized
    that NDPH was caused by glial cell activation leading to a release
    of TNF
    α into the CSF resulting in CNS inflammation and
    persistent daily headache. Doxycycline is a tetracycline derivative
    that along with its bacteriostatic capabilities has anti-inflammatory
    properties. Doxycycline can suppress TNF
    α production and
    inhibit microglial activation. It has good penetration into the
    brain and CSF. The mechanism of action of doxycycline makes
    it a good preventive candidate for NDPH.

    Methods:
    Four patients with treatment resistant NDPH and

    elevated CSF TNF
    α levels (>8.2pg/ml) were treated with
    doxycycline 100mg PO BID in an open label fashion for 3 months.
    Headache frequency and pain intensity levels were assessed. (Pain
    scale levels were 0-5; 0: no pain, 1-2: mild pain, 3: moderate pain,
    4-5: severe pain). All patients had failed at least five preventive
    agents and thus were deemed treatment refractory. 3 of 4 patients
    failed inpatient headache treatment while another failed outpatient
    infusion therapy. Age of onset of NDPH ranged from 13-39
    years. Duration of NDPH prior to doxycycline therapy ranged
    from 8 months to 3 years. An infection precipitated NDPH in 3
    of 4 patients.
    Results:
    All patients had a positive response to treatment. Two
    patients became pain free. One patient had an 80% improvement
    in daily pain intensity, but did not acheive any pain-free time. One
    patient had a slight improvement in daily pain intensity, but had
    a > 50% reduction in frequency of severe pain episodes. Average
    time to improvement on doxycycline was 2 months, although
    one patient responded within 2 weeks. Doxycycline was welltolerated
    overall, but one patient developed a severe sunburn on

    the medication.
    Conclusions:
    This small open label investigation suggests
    that doxycycline may have efficacy in treatment resistant NDPH
    patients who have elevated CSF TNF
    α levels. Doxycycline
    appears to reduce headache frequency and/or headache intensity.
    Time to onset of action is about 2 months, thus a 3 month treatment
    trial is suggested for all patients. Further study of doxycycline in

    NDPH is suggested.

    I was actually stunned when I read this article because my Rosacea and headaches both started shortly after I finished the worst throat infection I had ever had in my life. It tested negative for strep and was diagnosed as viral. It took 2 months to fight it off completely (and I was in agonizing pain for 3 weeks, lost my voice for 2 of them).

    Could it be that Rosacea, NDPH and other disroders like Rhuematoid are triggered by a breakdown in the immune system response to a virus? Is it as simple in theory as the body simply not knowing to stop producing a certain proinflammatory cytokine originally intended to fight off that virus?

    It bears noting on the treatment front that biologics have been used very successfully in the last few years to suppress cytokines production in other inflammatory diseases, normally resulting in significant improvement if not outright remission.

    Query: Where is our mother#$%#$% biologics for Rosacea
    "Get busy living or get busy dying."

  2. #2
    Moderator Melissa W's Avatar
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    J-Mill,

    Thanks for posting this info. Fascinating and I always felt there was some sort of breakdown in our immune response regarding rosacea. So many questions...so few answers. But every bit of the puzzle helps!

    Melissa

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    Hi J-Mill,

    just incidentally, this article appeared today regarding a portable migraine treatment device.

    http://www.sciencedaily.com/releases...0626075513.htm

    I agree with your suspicions on the immune system as well. i don't like it and i don't trust it. wouldn't take my eyes off it for a second :-)

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    Just gonna throw out what i know on the subject...

    Basically my 'rosacea' is accutane induced, a number of people get this, it can stick with you for life and i for one have terrible bowts of flushign every day, 18 months after finishing accutane.

    I also have several other side effects, all related to the immune system and inflammation.

    Accutane (isotretinoin) in higher doses used for acne (such as in my case). Is known to really mess with the immune function. It causes mast cells to disregulate, pro inflammatory cytokines and numerous other things to increase in numbers. I also have mouth ulcers, Diffuse Alopecia Areata. ocular rosacea, normal rosacea, raynaud's. To name a few, i had none of these before my accutane course.

    Anyway i have numerous studies that explain how accutane alters the immune response, and it would seem like all you guys are on the right track. Maybe some answers can be found by the way in which accutane induces rosacea, which is what Tony Chu tells me accutane induces, it is exactly the same as normal rosacea. Mine is proving very agressive for the short amount of time ive had it.

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    Hi lamarr,

    i'd be interested to read the studies you have on accutane and its effect on the immune system if you have any links available.

    thanks,

    Steve

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    Senior Member Steve95301's Avatar
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    What I find interesting is that LL-37 (cathelicidin) inhibits TNF-a.

    So maybe the abnormal, rosacean form of LL-37 doesn't inhibit TNF-a, and that's why we have too much.

    (LL-37 also promotes angiogenesis; perhaps in the abnormal LL-37, this activity is increased.)
    KNOWLEDGE = POWER

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    cheers lamarr.

    that's a big site, it will keep me reading for a while.

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    heh, no problem. I actually believe studying accutane induced side effects could provide us with some answers as to why things like rosacea develope, same goes for Alopecia Areata, arthritus etc etc.

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    Moderator man_from_mars's Avatar
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    Here's a good story about an itch
    http://www.newyorker.com/reporting/2...a_fact_gawande

    maybe find someway to apply same theory
    to telling the brain to stop trying to fight the virus?

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