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We have a LONG long way to go. All these studies, all these medications and yet what is it for? The patient of course! And yet why isn’t the patient’s input taken into consideration when “experts” come up with all these criteria for measurement? In business there is this 80/20 rule. You focus 80 % of your resources on the top 20% of your customers. With ra we have the 20/80 rule also…80% of the resources (our medical professionals) focus their resources on the 20% of what indicates ra….test results. When in the world are we going to start listening. Listening to what the patient is saying rather then focusing solely on test results. I no longer have faith in the test results and with just cause! Numbers can be manipulated to get the results one is looking to obtain. Until the patient input is also included in these studies…I will use them as only one minute factor in my personal arsenal in this fight. And really…isn’t it what we feel every single day that tells us personally how well managed and successful our ra treatment truly is? Great blog post! It gets us thinking and that is for sure.
Great points, Murph. I hope many are reading the comments.
New to the diagnosis of RA, I really appreciate this info about remission, as I keep wondering what that actually is and if I’ll ever be there!
Jan, there is a tag for remission that will show you several articles with more information. Use the Tags list or click here. Good luck w/your treatment.
After 15 years of treatment and several Drs. I know less than I did when my treatment started. My bloodwork is all at “normal” levels and have no inflammation but my pain level ranges between a 5 to 7, way beyond anything I have experienced in the past. As patients how do we get doctors to listen to us? It seems like they are listening but when looking at the treatment they prescribe I am sure they are just following a script with a standard set of responses!
Wow! That sure gives me hope *sarcasm* as newly diagnosed ra patient!
When I was first diagnosed I had a positive anti-ccp, positive ana, normal esr, and normal crp. I had an elevated complement though which I have never seen addressed here. My rheumy told me that was also an indicator of inflammation. I have never had an elevated esr or crp. I’ve had many surgeries on my feet, knees, wrist, neck and elbow. How do they come up with the test guidlines? I have never even been at the normal level for sex, age, and weight? Something needs to change!
I am now on my 5th rheumatologist in 18 months. It took me a lot of courage to keep fighting. I have all negative labs and no swelling. It took MRI’s to see the fluid in my joints. Fighting doctors and insurance companies in this condition is no fun. Thanks Kelly for helping me keep up the good fight. You have been my inspiration for 18+ months. I (and my five children) thank you for keeping me fighting. I have experienced everything (almost) that you write about. I will now begin down the road of biologics. I pray this rheumatologist keeps listening to me. What a story I could tell feom this whole thing though!
Wow, Gwen. First, I’m sorry. I’m sorry you went thru this because I know how hard it can be. Second, you are inspiring. My own 5 children and I often feel alone in this – even with all of the letters I get. It feels good to know you are out there. It just seems so unreasonable that it could be so hard to get good care & answers. Don’t give up. I’d like to hear back from you to see how it goes! If you think you’ve got a great doctor, please do send his/her name to add to the list we are building.
and most of all – I hope the biologic works for you!
Great set of articles. Thanks for sharing. As I was thinking about the NDB article, it reminded me that I hope your readers know that they can be part of this great research program as long as they have had a rheumatologist confirm the diagnosis of RA. Twice a year RA, lupus, and Fibro patients fill out a detailed health survey (takes about 90 minutes). These statistics are made available to researchers who wish to look at what real RA patients are experiencing given a particular set of treatments. If an unusual adverse action is reported sometimes you will get a follow-up call from the NDB to get more information. It’s a great organization to work with. I have been part of their study group for 5 years now and feel like sharing my experience can really make a difference in the life of someone else with RA.
I agree with chel above. I have been part of the National Data Bank of Rheumatic Diseases studies since 2010. I feel good being part of a study that uses the patients voice and is not funded by drug companies! I too have gotten follow up calls about problems I’ve had that they are studying. Like UTI’s in the RA patient. I wanted to make sure people know that they can be part of this study and encourage them to do so. The more unusual your case the better, so that all are represented!
Here is a link that leads you to the rheum md site that explains their research and includes a link on the page to the NDB site where you can join. On the rheum md site you can also ask a rheum a question and read other question and answers.http://rheummd.org/information/about-ndb
I did have elevated crp and esr at diagnosis, but not since I’ve been on RA meds. The pain is the same, but the crp does not correlate. It seems the mtx masks the crp and esr, but not all the pain. I take pain meds every day and they do help, but I still have pain, stiffness and unrelenting low grade fever. I am fortunate in that my doctor does listen and believe. It has also been proven to be inflammation pain by taking prednisone and feeling relief from the pain. Unfortunately the fever stays the same no matter what I take.
It sure does seem to be a rheum full of contradictions! Love the charlie Brown clip, lol, so fitting.
isn’t that weird about the fever? Mega doses of ibuprofen can give me pretty good relief to pain or swelling, but the fever stays steady. I know there’s acetaminphen in the Lortab too & that doesn’t reduce the fever either. The fever is definitely an interesting symptom. Evidence of inflammation & immune / disease activity, but why doesn’t it respond?
Kelly, do your white counts or platletes tend to run high or low all the time? Just curious. My white cell counts run a bit high, but I don’t run fevers. Before I was diagnosed, or even had pain in my hands, I can remember people telling me how hot my hands and fingers always were. They’ve not been hot since starting treatment.
How many reading here think you’ve had some improvement lately with the hot weather? I did have a hard time with our very cold spring and have welcomed the heat this summer. Still can tell a difference when the lows come thru though.
Chelsea, even before I was diagnosed, I just knew the cold weather affected me. With this CRAZY spring we’ve had in Chicago, and with my son playing HS baseball, I’ve been in tears outside because of the pain shooting through my hands and shoulders. Now that the weather has warmed up…a tiny bit…I look forward to being outside and seeing how my joints respond. Interestingly, during this baseball season, I’ve had a change in meds (going from Humira to Enbrel) and although I am responding well to the Enbrel, the cold weather still gets me.
To me, the million dollar question!! Why… cause I’m curious and need answers.
I’ve been doing a little tracking. My fever starts within 30 minutes of rising in the morning. It increases with activity, increases with worsened symptoms. If I’m on prednisone, It can be 99.8 and I’ll feel okay, like the pred is hiding the weariness of the fever. It is still there but lower at bedtime. Sorry I haven’t woke up in the middle of the night to take it, but it sure feels like it’s there with the night sweats. The only thing that lowers the fever so far is rest and I mean rest. A phone conversation can make it go up.
I’ve been on mtx (and prednisone) for years. Yes, the higher prednisone did help the pain a lot. But still had pain. Doc lately had kept saying is probably due to the damage you already have…But we added Plaquenil oh, maybe a year ago. This did have a positive effect, even on some pain in my OA joints. However, still some signs of RA activity. Recently we upped my Methotrexate from 20 mgs to 25 mgs. But this time decided to split the dose, taking half on Mondays and half on Fridays. I CANNOT TELL YOU WHAT A DIFFERENCE THIS HAS MADE!!! I’ve been wearing splints for years to help with pain and instability. I have been able to go for a couple of weeks now without those darn splints! I think most of this improvement is from the meds (plaquenil and methotrexate work synergistically according to my doc). This is the closest to normal I have felt in years and years. So I say just keep trying to work with your rheumy on different regimines.
Now, I do still have some various pain, skin and muscle problems I need to get looked into. Don’t know if these are RA-related, OA-related, or medication side effect-related or combination of all of above. And won’t be easy or quick to figure out probably.
I find this fascinating Chelsea! I have never heard of splitting the dose of mtx! My doc won’t move me up from 15 mg oral. He thinks anything above this does not help. Frustrating.
In the past doc said anything over 20 mg needed to be by injection to be effective. I AM still taking pills. Perhaps some new info is getting out. I know some of the feeling better is due to the weather, but I certainly think the two meds at this dose/regimine must really be synergizing to gether to work on my pain. I can still feel some tenderness with that “burning” in the skin when I touch my worst joints though, but everyday/work activities are not making them hurt the way they always have. I am a bit concerned to see what this is going to do to the liver/kidneys – will have to keep an eye on that. And have a new rash of some sort that isn’t going away. Just cut my dose of prednisone from 2 mgs to 1.5 mgs last night. Have been tapering off that VERY slowly. Will have to see how that goes. Hoping I can stay on this mtx/plq. combo for a long time. It is even helping my other OA joints. Weird.
There are other things to follow up on with this main article cited. Particularly the differences in the remission criteria.
It seems their main conclusion though was that pain was not correlated with inflammation markers, but rather non-inflammatory variables. I don’t know if the genetic crp would make a difference in those findings or not. I suspect the answers lay somewhere between inflammatory and non-inflammatory factors.
Is there any word on that NDB coming up with individual scales for RA? Or was Wolfe suggesting that the fibro scales they came up with be used for RA but Lupus gets its own? Or is there some reason it’s taking longer to come up with ones for RA?
It did sound like they want to rely heavily on crp to decide what is “inflammatory” & you can probably guess my opinion on that. Looking at it in light of the so-called remission images in the other article, and alongside of the low-crp genes discovery, it does seem wrong to assume crp is the only measure of “inflammatory” activity. Or even a very reliable one.
A little off subject, but what you both said made me think of this. I’m curious about platelet count. Looking back at my labs as far back as 2007, I had a high platelet count long before I had elevated crp. It finally went down with mtx on board, but still rises, correlating with the symptoms of increased pain and inflammation.
I just got a terrible craving for cheese puffs, lol, I wonder what that means??
I found this today and thought it was interesting:
“Currently there is no definitive test for inflammation — the best that conventional medicine can do is measure blood levels of C-reactive protein (a pro-inflammatory marker) and the irritating amino acid called homocysteine. I use the high-sensitivity CRP test now available at most labs. Anything above 1 mg/dL with this test is too high in my book. With the older tests a reading of between 2–5 mg/dL was considered normal. (If you’ve been tested, be sure to ask your doctor for the results.) Newer ways to assess risk early on for future inflammatory disease include markers such as the apolipoprotein B to A1 ratio (ApoB/ApoA-1). This and other tests are in experimental use and only available through a few labs.”
I think they are referring to general inflammation, but still found it interesting that they say there is no definitive test for inflammation. I have never heard of the high sensitivity crp.
I’ve heard of the h-crp. In fact I once asked my rheumy for a crp test. She was reluctant to do it, saying roughly (if I recall correctly from years ago) that it would be difficult to know whether the inflammation was from RA or general cardiovascular related inflammation. I believe we discussed the h-crp, as it had just recently started coming about. I ‘think’ that’s the one we did run but not positive. It was a 2.3, which ever one it was. Rheum doc didn’t know what to make of the result. I’m guessing I wasn’t doing too bad rheum-wise at the time in the eyes of my rheumy. I chalk that up to the prednisone. However she did seem to tend towards looking for lots of obvious swelling in many joints, although she usually only checked my fingers and wrists. Endocrinologist wasn’t thrilled about the number though – wasn’t real high but still ‘higher risk’ than normal, but she would be thinking of overall cardiovascular risk. So, if you have other factors for cardiovascular risk, then doing a crp or h-crp may not be that helpful for assessing RA activity I suppose, but I’ve not researched this. I have often wondered if cholesterol testing could be used to track RA activity though, and for s-o-m-e RA patients that might be possible. They have looked a bit at how statins might be beneficial for RA, although it is probably due to it’s other beneficial factors apart from their cholesterol lowering abilities. It would be very muddied though to tease it all out though, since some RA meds actually raise cholesterol levels.
Interesting about your platelets Ronda. I’ve not tracked the ups and downs of mine. Not sure what they were before treatment but always in normal range since then. Cheese puffs is how I figured out I have lactose intolerance though!
Thought it might be useful to post this excerpt from Brown’s 2006 article which you cited in your other post on swelling when there is no swelling:
An explanation for the apparent dissociation between clinical remission and continued structural deterioration in rheumatoid arthritis
“…While plain radiographs remain the conventional measure accepted by regulatory authorities for the assessment of structural outcome in RA, there is increasing evidence to support the validity of modern imaging modalities such as musculoskeletal US and MRI in this role (22, 32–35). Our study demonstrates the enhanced sensitivity of musculoskeletal US and MRI for the detection of structural damage as well as their superior sensitivity to change as compared with radiography. Furthermore, both musculoskeletal US and MRI allow the valid and reliable assessment of both ongoing inflammatory disease activity and structural outcome in RA at the same time. These observations are endorsed by the data from our normal control population, which are consistent with published findings (36), and confirm the specificity of the imaging findings in this RA cohort.
Our results demonstrate that objective imaging techniques definitively identify inflammation and the potential for further joint damage across the boundaries of the current remission classification systems, with no differences in the proportion of patients with subclinical synovitis who were judged by physicians to be in remission, regardless of whether they fulfilled the ACR/DAS28 criteria. This suggests that satisfying the ACR/DAS28 definitions is a no more valid assessment than that made by an experienced physician. In addition, remission classified according to established clinical criteria may not represent an inflammation-free, nondamaging disease state. So, while the current criteria may confer a safer disease activity level than not, they may still allow persistent, active disease and subsequent structural damage to go unnoticed, thus raising legitimate questions regarding their accuracy.
These data have a number of important clinical implications. Our threshold for additional intervention in such patients may need to be lowered, since even in states of low disease activity, patients may benefit from additional therapy. The effects of dosage titration and treatment strategies involving additional or combination therapy with traditional DMARDs or biologic agents merit further investigation in this population. Monitoring treatment-resistant synovial inflammation with imaging studies in such patients may enable the appropriate selection of patients in whom further therapy may result in a more-effective prevention of structural damage.
The present study supports the use of sensitive imaging techniques for the accurate evaluation of disease status and the prediction of outcome in patients with RA, even when the findings of standard clinical measures of inflammatory activity have returned to normal. Furthermore, an objective imaging assessment improves the sensitivity of inflammation detection, enabling more-informed treatment decisions and an accurate definition of the remission state, which is most likely to correlate with optimal long-term structural outcome.”
http://onlinelibrary.wiley.com/doi/10.1002/art.23945/full
Further on the MRI imaging as useful for MONITORING RA:
Arthritis Res Ther. 2009;11(3):R94. Epub 2009 Jun 22.
The utility of MRI in predicting radiographic erosions in the metatarsophalangeal joints of the rheumatoid foot: a prospective longitudinal cohort study.
Mundwiler ML, Maranian P, Brown DH, Silverman JM, Wallace D, Khanna D, Louie J, Furst DE, Weisman MH.
Source
North Suburban Rheumatologists, Des Plaines, IL 60016, USA. mmundwiler@msn.com
Abstract
INTRODUCTION:
Magnetic resonance imaging (MRI) may reveal rheumatoid arthritis (RA) changes in the feet when hands are normal. The purpose of this study was to determine the sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) of a metatarsophalangeal (MTP) erosion on MRI to predict a subsequent radiographic erosion in the same joint. Similar analyses were performed for bone marrow edema, predicting a subsequent MRI erosion. Descriptive results of other lesions are reported.
METHODS:
Fifty patients with RA of less than 5 years’ duration who were rheumatoid factor-positive and/or anti-cyclic citrullinated peptide-positive were recruited. Patients on anti-tumor necrosis factor (TNF) therapy were excluded. Anti-TNF therapy could begin after enrollment. MRI and radiographs of the 3rd, 4th, and 5th MTP joints bilaterally were taken at baseline and at 6, 12, and 24 months. Clinical data were collected.
RESULTS:
Fifty patients were recruited; 46 patients had suitable data. Results for MRI erosions predicting subsequent radiographic erosions for 6, 12, and 24 months, respectively, were as follows: sensitivity 0.75, 0.60, 0.75; specificity 0.93, 0.94, 0.94; PPV 0.086, 0.10, 0.17; NPV 0.998, 0.995, 0.995. Results for MRI bone marrow edema predicting MRI erosions at 6 and 12 months, respectively, revealed sensitivity 0.50, 0.67; specificity 0.97, 0.97; PPV 0.25, 0.50; NPV 0.99, 0.99. Synovitis was the most common finding and, when present in isolation, resolved on 67.3% of subsequent studies. MRI erosions persisted on subsequent studies with one exception. Forty-six percent of the cohort was on anti-TNF therapy after study inception.
CONCLUSIONS:
The PPV of MRI erosions to predict subsequent radiographic erosions was low. Similarly, the PPV of bone marrow edema to predict a later MRI erosion was low. Alternatively, the NPV of the absence of an MRI erosion or bone marrow edema predicts that a later radiographic erosion or MRI erosion will likely not develop. Anti-TNF therapies may have resulted in the lower-than-anticipated PPVs. MRI descriptions of bone edema may represent a more critical time to treat in order to avoid damage, whereas an MRI erosion represents more permanent damage. This study suggests that imaging modalities more sensitive than radiographs are necessary to monitor disease in the biologic era.
http://www.ncbi.nlm.nih.gov/pubmed/19545417
Patients shouldn’t get too excited though. Ins. co’s aren’t going to want to pay for lots of MRI monitoring in RA patients.
my rheumies cannot ‘see’ the swelling in my hands/wrists and ankles because i am a little overweight. however, i have that body type from my father’s side, where my weight goes to my middle, and that’s it. my arms/legs are slim-ish. i didn’t really notice the swelling myself, i just knew i had pain. my md noticed the swelling, and he should know, because he sees me about once a month for the past few years.
before this, i do believe i was in remission. i had back pain and knee pain, which i assume (and hope to get mris to prove, eventually) were because of the damage that was done before the remission.
but, before that, all of the pain was in my ‘big joints,’ not my hands, but the bloodwork showed active disease. i should’ve gone to a rheumy then, but i was really terrified of the meds. it wasn’t until i was almost completely disabled by the pain that i decided to try a rheumy. and that woman didn’t even really look at me, she just got some blood work back and said ‘you don’t have RA, never have.’ at that point, i didn’t realize that rheumies could be clueless, and took her word for it. turns out, i think i had gone into remission at that point, though i had a lot of pain left from a lot of flares and inactivity.
i’m with you, though. Enough!
I start every day with a cold chill and then casually work into a low grade fever of hot flashes. Was negative on every lab till 3 years ago then everything shot off the charts. Been through many rheum docs on the hunt for one that will listen
Thanks for sharing Jon. Too many of us have been down this road. Good luck to you.