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Thank you Lynnie!
I didn't realize green tea could interfere with so many medications. I'll stick to water as you suggest.
By the way, I should add that I was on Enbrel for about 7 months, but weaned off prior to starting AP. Enbrel did help some, but not enough to warrant the risk for me.
Lori
Lori,
Glad to see you on the Roadback website. You didn't elaborate how your pain level is, and do you maintain normal physical activity. I contiunue to do well on AP and LDN with some occasional Diclofenac. I don't have any pain that limits any activity in my daily life. I have been pretty stable since adding the LDN in Feb, 2009.
vinnylid
Psoriatic Arthritis: 100mg Minoz Minocycline TABLET daily; twice daily 400mg Pentoxifylline;125mcg Levotyroxine: Have been using some level of Minocycline since 2008
Hi Vinny,
You are actually one of the people I need to thank for turning me in the direction of AP. I started LDN (2/2009); and on the LDN website you encouraged me to consider AP (as well as my doctor). My thinking at the time was that all antibiotics were 'bad' – which of course is not the case. The LDN has helped so much in some ways, but not for the PsA pain. So, I thank you very much for taking the time to tell me about AP. I just wish I had taken your advice sooner.:?
My pain is bad enough in the pelvis area to keep me from working a part time job for more than a year now. It is difficult to sit/stand/walk for more than a few minutes at a time. I was injured in a severe sledding accident as a teenager. I was often extremely sick as a child with measles/mumps/chicken pox. I was a Girl Scout, and was covered in ticks at times, so does Lyme play a part in all this?
I gave Enbrel a try, but that didn't do too much for me. Besides, I was told LDN and Enbrel work against each other, and that turned out to be true. Wanting to give AP a true shot, I weaned off Enbrel about two months ago.
I hope you continue to be well! Thanks for the encouragement.
Lori
[user=1858]vera[/user] wrote:
I was a Girl Scout, and was covered in ticks at times, so does Lyme play a part in all this?
Hi Lori and just adding a warm welcome to the RBF forum! 🙂
As to your question above…yes, Lyme can remain latent for decades and emerge later in life as an opportunistic infection triggering all kinds of immune-dysfunction, if it was not caught early enough after an initial innoculation from a tick. This seems to be particularly so in folk with certain genetic predispositions (HLA genetic haplotypes).
Lyme, or borreliosis, or Bb, for short, is a clever organism that has multiple cloaking mechanisms. It has outer surface proteins (OSPs) that enable it to mimic our own cell's proteins (molecular mimickry) and can hang out for years in either an active or dormant form (possibly relative to strength of immune function). But, in its active forms it also has the ability to evade immune detection altogether by changing shape (spirochete, to L-form, to dormant cystic form, etc) and each of these forms produce different outer surface proteins (antigens), which trick our normal immune surveillance. The cystic forms are probably what cause chronicity, because these forms have reduced outer surface proteins that manage to evade immune detection to a greater degree and protect the organism from antibiotic onslaught, but still produce these “blebs” or fragments that they emit like decoys to divert the attention of immune surveillance away from them. It's such a complicated organism, that much is known.
Minnesota is emerging as a veritable hotbed of Lyme disease, unfortunately. It's been around for centuries, this organism, and there's all kinds of theories as to why it's becoming so prevalent today….possibly one of those reasons being that people are just now becoming more aware of this serious set of tickborne infections and it just wasn't diagnosed prior to the mid-1980s (when Willy Burdorfer first identified the organism here in the US)….but likely also the emergence of strains that weren't here in the US previously and also environmental changes (people encroaching on animal habitats and driving deer and other tick carriers into our living areas).
If you suspect, at all, that Lyme and its hitch-hiking coinfection 'friends' may be a part of your pathogen load, it's just prudent from the get-go to have Lyme testing done. If you haven't had standard tests run (ELISA and Western Blot), then this could be a first step and you may be one of the fortunate ones to test CDC positive. If negative or equivocal, though, it's worth looking further and having the more sensitive IGeneX labs run for Lyme disease. It's not difficult having these labs run, but you would need an open physician willing to sign off on the labs. IGeneX labs sends the kit to your door and the kit includes everything needed for the tests. Most folk here just start with the basic IGeneX western blot test, as this is often enough to see if Lyme may be a player in one's rheumatic disease. Getting this labwork done early also helps with treatment direction, because Lyme antibiotic treatments vary significantly from low dose AP in both combinations used and doses and it would need a Lyme Literate MD (LLMD) to manage treatment.
If you need any further insight as to how to go about all this, then there are many of us here who have been through this process who can share our experiences with you. Just ask away! 🙂
Peace, Maz
Hi Maz,
Thank you so much for the wealth of information here. I think you're absolutely right about getting tested for lyme – especially considering how prevalent lyme is in our area.
I DID test positive by my rheumy for HLA-B27. Sounds like I may be even more susceptible to lyme from what you wrote because of that – if I understood it right. If not, please correct me.
Would you (or someone else) be able to PM me a list of LLMD's in my area? I live in the St. Paul/Minneapolis area of Minnesota.
Many thanks for letting me know about this! I appreciate your help!:)
Lori
[user=1858]vera[/user] wrote:
Would you (or someone else) be able to PM me a list of LLMD's in my area? I live in the St. Paul/Minneapolis area of Minnesota.
Hi Lori,
Will send you the MN LLMD list in a PM (private message). Just look top right of this page and click where it will say, “You have 1 new message.”
All the best in finding the best doc for you!
Peace, Maz
Hello Psaoff,
I've read through your post & wanted to let you know that my husband has psoriatic arthritis also.
When his first flare hit a few years ago his psoriasis had flared a bit, then his knee got swollen, red & hot. He had to walk on crutches. He was rxd mtx. The mtx cleared his skin and made his knee 100% better within a few months. He wasn't sure the diagnoses was correct (more likely wishful thinking) & so he went off the mtx because he didn't relish the idea of having to take such a potent med.
He was fine for about 6 mos or so, then it hit again in his knee. He immediately went back on mtx, but he had to more than double his original dosage because he'd been on it previously & the body tends to need more if you've taken mtx then stopped. He ended up needing to take a dosage that was so large it made him extremely ill. He had to split the dosage into 2 days because he couldn't tolerate one dose that high. Even that high dosage did not give him 100% relief like it had before. He dealt with the mtx for as long as he could…I think it was about a year or so. Then he quit taking it because he was out of commission for 3-4 days out of every week because of the med.
He didn't have a backup plan…just hoped that he could manage somehow on his own. He did ok for about 6 months again (like the first time discontinuing it). The last flare he had in Nov 09 was horrible. Instead of just hitting his knee, he experienced pain in multiple joints from his jaw (making it difficult to eat) to his toes & nearly everything in between. Both of his ankles swelled up like they were broken making it near to impossible to walk. He was desperate for help. At the time, I was just researching AP for him. His rheumy prescribed prednisone to take his inflammation down quickly & it did, but not completely. But, my husband knew that he didn't want to rely on pred, so eventually he got his dr. to rx minocycline. Once he'd experienced some relief from the pred & had been on the mino for a spell, he began to wean off the pred. This caused a huge flare in his psoriasis. He was practically covered from head to toe.
The topical steroids prescribed to help him hardly worked & started making his hair fall out rapidly. He started eating coconut oil every day & the psoriasis is now minimal…maybe a couple of spots on his legs. But, during this whole psoriasis flare, his joint pain was continuing to get better even though he was off the pred. We attribute it to the mino working. He's had a great summer working in the garden…unthinkable just 8 months ago!I asked him the question you posed about whether methotrexate or AP works better & he said that he wished he'd known about AP before going through everything with the mtx. We have been thinking that the courses of mtx may have just masked what was really going on with him & that's why his last flare was more widespread than the first two. Just a theory. Anyhow, he feels like the AP is working (although right now he's having some pain in his fingers & back…we're hoping this is just a flare/herx that will not get as serious as his other flares & that it will pass soon – it seems like that's been happening). He has been off the mtx for over a year now & hopefully won't have to ever go back on it because of how bad it made him feel. Now, that being said, we've known people who take it & don't have any bad reactions like he did…everybody's different.
Well, that's his story in a nutshell. If you have any questions, let me know & I'll try to answer. Sounds like you're going through something very similar to my husband. You should check out the threads that I've posted about my hubby's experiences…there may be stuff that I wrote while he was going through all this that I haven't covered here.
Sorry for the long post, but your story spoke to me & I wanted to give you some encouragement. Perhaps had he stayed on the mtx at the initial dose (which didn't cause any ill effects), he would still be on it & doing fine. I guess we'll never know, but he's happy that he's on the mino & not taking the toxic med.
Good luck to you!! Hope you find relief soon. I'm sure that you will.
~mj[user=27]Maz[/user] wrote (in her first post):
Before considering a biologic drug, such as Enbrel, you may want to ensure whether or not your palmar and plantar psoriasiform-like eruptions rashes are Keratoderma blenorrhagicum. This type of rash is a result of chlamydia trachomatis (infection that causes reactive arthritis), which your dermatologist may be able to diagnose for you with a skin biopsy.
http://ard.bmj.com/content/67/8/1181.abstract
Another type of rash that can occur on palms and soles due to infection (borreliosis) is ACA (acrodermatitis chronica atrophicans). If you scroll down this link a ways, you will see pics of this pustular, psoriasis-like rash. Lyme may also caused a condition, called Bell's Palsy, which usually affects one side of the face – was your facial swelling ever diagnosed?:
Both rashes are psoriasis-like, both are of infectious cause. Looking at different pictures of the two, it becomes obvious that both can wary a lot, and that they can look very similar. How are they differentiated? Is there a clear way to do it? Carter mentions that Keratoderma blenorrhagicum is even histologically indistinguishible from Psoriasis.
I was recently diagnosed with ACA, but the doctor the nail changes (hardening, brittle and weak spots, full pits earlier) as irrelevant. In ReA, nail pitting is mentioned as a symptom (at least Carter mentions it in his may 2009 paper “Reactive arthritis”). Does anyone know how sensitive PCR is for those skin changes (All three patients in the paper “Psoriasis lesions ? a skin deep conundrum” were positive for Ctr by PCR of skin biopsies).
Thank you for input.
Maz, Thank you for very good points!
[user=2031]nord[/user] wrote:
Both rashes are psoriasis-like, both are of infectious cause. Looking at different pictures of the two, it becomes obvious that both can wary a lot, and that they can look very similar. How are they differentiated? Is there a clear way to do it? Carter mentions that Keratoderma blenorrhagicum is even histologically indistinguishible from Psoriasis.
I was recently diagnosed with ACA, but the doctor the nail changes (hardening, brittle and weak spots, full pits earlier) as irrelevant. In ReA, nail pitting is mentioned as a symptom (at least Carter mentions it in his may 2009 paper “Reactive arthritis”). Does anyone know how sensitive PCR is for those skin changes (All three patients in the paper “Psoriasis lesions ? a skin deep conundrum” were positive for Ctr by PCR of skin biopsies).
Hi Nord,
Very good question and I don't know the answer. 😕 I would think that differentiating between psoriasiform-like eruptions caused by either Borreliosis or Chlamydia trachomatis would require a physician who was a skilled diagnostician in both types of infection and who would take skin biopsies of the lesions to look for the offending organisms. Whether PCR is the best type of test to use or not, I don't know. The article above mentioning Keratoderma blenorrhagicum doesn't elaborate on the type of testing used in that instance. The following article cites an 80% accuracy rate of detecting borreliosis by taking a 2mm skin biopsy from an EM rash and using quantitative PCR.
http://jcm.asm.org/cgi/content/abstract/40/4/1249
A further conundrum may arise if one considers that the rashes may not be caused by just one of the infections, but both. Borreliosis seems to have innate capacity to re-activate latent infections by seriously compromising immune function.
With my untrained eye, just looking at the following pics of Keratoderma blenorrhagicum (KB), although there seems to be variation in presentation depending on severity or duration of diease state, my best patient guess is that there is a degree of visual difference. That is, in the case of KB, a thickening of skin on palms and soles is evident that in advanced stages appears cracked and crusty.
http://www.lexic.us/definition-of/keratoderma
Acrodermatitis chronica atrophicans ACA, on the other hand, has a more reddened, swollen, vascular, bruised, inflammed appearance and I've often wondered if ACA may often be confused in a diagnostic work-up for dermatomyositis:
http://emedicine.medscape.com/article/1051695-overview
Perhaps there is overlap with pustular eruptions and skin peeling in some cases. My best suggestion, though, is that a skilled diagnostician would probably be best qualified to differentiate, based on observation of clinical presentation of symptoms?
Peace, Maz
Hello Maz,
and thank you for your input!
[user=27]Maz[/user] wrote:Whether PCR is the best type of test to use or not, I don't know. The article above mentioning Keratoderma blenorrhagicum doesn't elaborate on the type of testing used in that instance. The following article cites an 80% accuracy rate of detecting borreliosis by taking a 2mm skin biopsy from an EM rash and using quantitative PCR.
Interesting! The German LLMD that diagnosed me and his colleauge has done a study where they looked at all clinical cases of Lyme where Borrelia could be confirmed with PCR, culture or histology. Of those, 97% were PCR positive. He wanted to do all three tests for Lyme, but only serology for chlamydias (which is a similar miss-hit-miss as it is in Lyme). I declined, as he considered the diagnosis certain without (I hadn't seen the the PCR sensitivity at the time, PCR being the least expensive test). From what I see now PCR for both kinds of microbes would be the most sensible testing.
A further conundrum may arise if one considers that the rashes may not be caused by just one of the infections, but both. Borreliosis seems to have innate capacity to re-activate latent infections by seriously compromising immune function.
Exactly my thought :), and I'd add a question about the inverse situation (Cpn doing severe harm to the immune system), part of the problem of both being so difficult to diagnose and treat.
With my untrained eye, just looking at the following pics of Keratoderma blenorrhagicum (KB), although there seems to be variation in presentation depending on severity or duration of diease state, my best patient guess is that there is a degree of visual difference. That is, in the case of KB, a thickening of skin on palms and soles is evident that in advanced stages appears cracked and crusty.
http://www.lexic.us/definition-of/keratoderma
Acrodermatitis chronica atrophicans ACA, on the other hand, has a more reddened, swollen, vascular, bruised, inflammed appearance and I've often wondered if ACA may often be confused in a diagnostic work-up for dermatomyositis:
I agree, although my own symptoms wary a lot over time, too, and actually look more like KB. The Dr that looked at me was particularly interested in the thickening and cracking at the outside of the soles “a clear case of ACA”. 😕
Perhaps there is overlap with pustular eruptions and skin peeling in some cases. My best suggestion, though, is that a skilled diagnostician would probably be best qualified to differentiate, based on observation of clinical presentation of symptoms?
Peace, Maz
I agree, but then many clinicians that are aware of the conditions at all, are only very knowledgeable of one of the infections chronic presentation (e.g. with the general understanding of Lyme, how likely is the average dermatologist to diagnose Lyme ACA: “Former borreliosis, and you were treated with a three-week course of abx? That's not ACA, then.” *looks for other dx* :headbang:). Many of the symptoms for chronic Lyme and chronic chlamydiales are very similar, and where they wary, are the symptoms lists complete? Are simultaneous infections so common as to make some of the symptoms that actually belong to “the other infection” attributed to the one that the clinician is knowledgeable about (and now how difficult it can be to confirm via labs)?
I suspect that there is a lot of bias of observation in the clinical experience. This is not as bad as it may sound (as both infections seem to respond to similar treatment etc), but there would probably be a lot more to learn by combining knowledge from the two areas (as well as from the knowledge of the different areas where the symptoms arise).
Thank you again Maz for interesting discussion and input!
[user=30]lynnie_sydney[/user] wrote:
<span style="color: "blue"]Welcome to the Road Back Forum Lori! Here is a link to some info about medications that probably should not be taken with green tea. [/color]http://www.umm.edu/altmed/articles/green-tea-000910.htm%5B/color%5DThey include beta lactam antibiotics (which include the penicillin derivatives). It doesnt say anything about the tetracyclines. If it was me, however, I'd take stick to water with the mino and have my green tea at another time. You could also check with your doctor about this.
Hello Lynnie,
and thank you for the link!
I note that they mention that green tea can enhance the effect of beta-lactam abx. Is there a specific problem with this? Many natural antimicrobals do enhance the effect of (pharmaceutical) antibiotics, and not rarely in a synergistic way (thus multiplying the effect rather than adding) as well as reducing the risk of developing abx resistance, and even breaking such if present. It seems to be from several mechanisms, and some anti-inflammatories do enhance the effect of abx as well (and most ofthe antimicrobals are anti-inflam too, a bit of a mess :))
Of course there could be a specific interaction of uptake and similar, and that would be something to be more careful about.
My thought has been the opposite, to add some things along those lines (eg grape seed extract against Lyme; green tea, garlic, bilberry, ginger etc for general effect, and some very tasty side-effects :)). Of course, one has to take care not overdoing things (reactions etc), but are there more specific drawbacks?
Interestingly, many of the interactions for other medicines they mention on the site are speculative, and the message seem to be like avoid the natural foodstuffs that are potentially active for the effect of the medication and stick to the latter. I'd personally prefer to choose the other way: prioritise the natural substances and lifestyle changes, and resort to the pharmaceutical things if the initial approach is insufficient. 🙂
Nord – in principle I absolutely agree with you. However, I think it's is always better to be fore-armed so that we can inform oursleves with various points o view before making decisions. I am increasingly in awe of the amazingly complex system that is the human body. Lynnie
Be well! Lynnie
Palindromic RA 30 yrs (Chronic Lyme?)
Mino 2003-2008 100mg MWF - can no longer tolerate any tetracyclines
rotating abx protocol now. From Sep 2018 MWF - a.m. Augmentin Duo 440mg + 150mg Biaxsig (roxithromycin). p.m. Cefaclor (375mg) + Klacid 125mg + LDN 3mg + Annual Clindy IV's
Diet: no gluten, dairy, sulphites, low salicylates
Supps: 600mg N-AC BID, 1000mg Vit C, P5P 40mg, zinc picolinate 60mg, Lithium orotate 20mg, Magnesium Oil, Bio-identical hormones (DHEA + Prog + Estrog)Hi Victor,
I'm based in the UK and have had PSA for a little over 5 years. Funnily enough, it started in my feet as well though it was the soles of my feet more than the toes. For 4 years I managed my PSA with the occasional painkiller and regular visits to the gym just to keep the joints moving. Sept 09 I had quite a severe flare (affecting multiple joints) and went onto anti-inflammatories (1000mg per day). Whilst they helped for a few months, around Christmas 09 things were deterioriating fast. At this same time my c-reactive protein blood test (which tests the level of inflammation in your system) had climbed alarmingly (almost doubled in 3 months) and my doctor urged me to go and see a rheumatologist before the damage done by the escalating inflammation was irreperable. It was then I started to search for alternatives….
I found the roadback web-site and took the plunge on 21st Jan 2010. The first 3-4 months were particularly tough as I herxed quite badly, my hands swelled dramatically, the pain worsened in all of my affected joints and I came close to packing the AP in. However, the always constructive and thoughtful advice from the likes of Maz and Lynnie convinced me to take a washout period (i.e. stop taking the AP for a few weeks to let my system deal with the antigens produced as the bacteria is killed off by the AP) and after 2 weeks things really started to improve. Since then my c-reactive protein blood markers have more than halved and I have also halved the anti-inflamms I need to take as well. I have since found that 4 weeks on AP followed by 1 week off works best for me. It is now 7+ months since I started AP and the difference in both my physical and mental wellbeing has been dramatic.
It is also worth noting that during my time on the AP, I have not changed anything; not my diet, not my drinking habits, not my exercise routines and no supplements either. So, AP has to take all of the credit for the marked improvement I have made during this period.
Best of luck with your treatment and keep the faith.
Frank 🙂
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