http://www.ncbi.nlm.nih.gov/pubmed/23335582
Hello,
Yes, this is an interesting article - thank you for posting it!
Just to be clear before confusion blooms, the seronegative patients in this study had positive lip biopsies - this is not defined in the Abstract, but is defined in the second paragraph of the full journal article. The full journal article is easily accessed from the abstract by clicking on the link that says "Free PMC Article".
This is another study where all the patients were formally diagnosed with Sjogren's, and then the researchers compared and assessed the symptoms of the group of Primary Sjogren's patients who had "a positive lip biopsy and negative bloodwork", versus those who had "either positive SSA or SSB" in their diagnosis of Sjogren's.
One main difference between these two groups is that the people who had a positive lip biopsy but negative bloodwork, called the "seronegative" patients, reported higher levels of chronic pain than the "seropositive group".
A large percentage of both groups reported a lot of chronic pain on a daily basis though, just the seronegatives reported more pain according to some survey-based measure of reported pain.
Because pain can't be measured, and can only be surveyed, this is pretty qualitative science, or you might call it squishy or survey-science. The authors acknowledge this at the end of the Abstract, saying that mechnisms that produce pain need further study, which is exactly right.
This article is a start at new science though, and like another article recently discussed on this Forum, is more work trying to develop sub-classifications for Primary Sjogren's patients who were correctly diagnosed by symptoms plus either positive SSA or SSB, or else a positive lip biopsy.
I really find this sub-classifications within the Primary Sjogren's diagnosis to be quite interesting. Like the other article on this topic recently discussed said, collectively these types of Sjogren's research studies are going to lead to much tighter and specific types of Primary Sjogren's diagnoses, which in turn may lead to better treatment and earlier recognition of well-defined and scientifically-valid constellations of Sjogren's symptoms. They are trying to develop strictly-defined "types" of Sjogren's, based on the antibodies present, or lack thereof.
For one example, in Lupus a person can have either cutaneous Lupus on discrete areas of their body, or else systemic Lupus. Both are Lupus, but because these variants have well-known differences in prognosis and treatment, doctors immediately make observations to diagnose either one type of Lupus, or the other.
It would be great if we had equally valid and useful sub-classifications for Primary Sjogren's types, however, the Sjogren's research is currently in it's infancy as the topic of this Forum post indicates.
Thanks for this article! If you look on the right side, there are a few other short articles about SJS in people who have chronic fatigue. I definitely think there might be different types of SJS, especially if some are seronegative, as I am. I highly suspect I have CFS as I've had EBV. Gosh, I always thought maybe I had a milder disease since I was seronegative but now I dunno...........
and if u go on reading youll find this
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Abstract
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Scand J Rheumatol. 2014;43(3):234-41. doi: 10.3109/03009742.2013.846409. Epub 2014 Jan 7.
Pain in primary Sj?gren's syndrome: the role of catastrophizing and negative illness perceptions.
Segal BM1, Pogatchnik B, Rhodus N, Sivils KM, McElvain G, Solid CA.
Author information
Abstract
OBJECTIVES:
Pain is a major factor in health quality in Sj?gren's syndrome (SS), but little is known about the factors that contribute to pain severity. Because pain perception has been linked to catastrophizing in other diseases, we assessed subjects with primary SS (pSS) to explore a possible link between pain, illness appraisal, and catastrophizing.
METHOD:
A total of 92 subjects who met American-European consensus criteria for the diagnosis of pSS completed a questionnaire that included health history, medication use, illness perceptions, pain severity, mood, fatigue, pain anxiety, and pain catastrophizing. Linear regression was used to test the effect of each variable on pain severity. Multivariate models were constructed using backwards elimination to assess the significant predictors of pain severity.
RESULTS:
From linear regression analysis, catastrophizing was more strongly predictive of pain severity than age, fatigue, depression, or anxiety in both seropositive and seronegative pSS patients. In the multivariate model identified using backwards selection, four variables (pain catastrophizing, fibromyalgia status, serological status, and the conviction that illness would have severe consequences) predicted 55% of the variance in pain severity.
CONCLUSIONS:
Pain catastrophizing was a significant predictor of pain severity in both seropositive and seronegative pSS patients. This study suggests that behavioural interventions designed to reduce pain catastrophizing and negative appraisal of illness could be of benefit in pSS patients. Research is needed to test the effect of psycho-educational therapies on key patient-reported outcomes, particularly pain, depression, and fatigue, in pSS.
I am seronegative and I found this very interesting. Sometimes I believe a lot of physicians don't believe I'm am sick because I don't have the blood work to back it up. I wish more doctors would become more knowledgeable, educated, and more open minded.
I'm glad they are doing some studies! Thanks for sharing.
Kathy
How do you find a rheumatologist who understands sjogrens? I just wasted an hour of my time and drove 60 miles for nothing. He said I am dry "because I am old"(I am 66 years old). I have all the symptoms---even family dr thinks I have it but rheumatologist says no because the test came back negative. He says all the pain is from Fibromyalgia and "old age". By the way---he is way older than I am! Very discouraging!
Quote from: SjoMan on October 25, 2015, 02:23:02 PM
Hello,
Yes, this is an interesting article - thank you for posting it!
Just to be clear before confusion blooms, the seronegative patients in this study had positive lip biopsies - this is not defined in the Abstract, but is defined in the second paragraph of the full journal article. The full journal article is easily accessed from the abstract by clicking on the link that says "Free PMC Article".
This is another study where all the patients were formally diagnosed with Sjogren's, and then the researchers compared and assessed the symptoms of the group of Primary Sjogren's patients who had "a positive lip biopsy and negative bloodwork", versus those who had "either positive SSA or SSB" in their diagnosis of Sjogren's.
One main difference between these two groups is that the people who had a positive lip biopsy but negative bloodwork, called the "seronegative" patients, reported higher levels of chronic pain than the "seropositive group".
A large percentage of both groups reported a lot of chronic pain on a daily basis though, just the seronegatives reported more pain according to some survey-based measure of reported pain.
Because pain can't be measured, and can only be surveyed, this is pretty qualitative science, or you might call it squishy or survey-science. The authors acknowledge this at the end of the Abstract, saying that mechnisms that produce pain need further study, which is exactly right.
This article is a start at new science though, and like another article recently discussed on this Forum, is more work trying to develop sub-classifications for Primary Sjogren's patients who were correctly diagnosed by symptoms plus either positive SSA or SSB, or else a positive lip biopsy.
I really find this sub-classifications within the Primary Sjogren's diagnosis to be quite interesting. Like the other article on this topic recently discussed said, collectively these types of Sjogren's research studies are going to lead to much tighter and specific types of Primary Sjogren's diagnoses, which in turn may lead to better treatment and earlier recognition of well-defined and scientifically-valid constellations of Sjogren's symptoms. They are trying to develop strictly-defined "types" of Sjogren's, based on the antibodies present, or lack thereof.
For one example, in Lupus a person can have either cutaneous Lupus on discrete areas of their body, or else systemic Lupus. Both are Lupus, but because these variants have well-known differences in prognosis and treatment, doctors immediately make observations to diagnose either one type of Lupus, or the other.
It would be great if we had equally valid and useful sub-classifications for Primary Sjogren's types, however, the Sjogren's research is currently in it's infancy as the topic of this Forum post indicates.
I think your analysis is very interesting SjoMan. I'm seronegative (lip biopsy 100% positive and +ANA) and have been told that not having SSA or B excludes me from trying Rituximab. Fortunately for me the rheumatology registrar hadn't done his homework properly and offered me Mycophenolate/ Cellcept before discussing it with his senior colleagues - so they grudgingly agreed to a four month trial and I'm now two and a half months into it.
I very much agree about the need for clearer and tighter diagnostic criteria in order for more targeted research and trials to get underway. While things continue to be woolly around our disease - we will continue to be offered drugs that will only mask symptoms at best, or Plaquenil. Sjogrens will continue to be viewed as the most benign of the rheumatic diseases and many will continue to feel compelled to self diagnose without real clarification or appropriate treatment.
I was originally diagnosed and treated for RA so have experienced the full gamut of bilateral inflammatory arthritus type pain. I also have very widespread tendinitis and small fibre neuropathy. I did read on the John Hopkins- Birnbaum page on neuro manifestations of Sjogrens - that those with small and large fibre involvement as main symptom of Sjogren's, are significantly more likely to be seronegative. I wonder if this is actually why chronic pain is more prevalent in those who are lip biopsy positive - because these are often the people whose Sjogrens starts with neurological symptoms?
Quote from: SjoGirl on October 25, 2015, 01:17:33 PM
http://www.ncbi.nlm.nih.gov/pubmed/23335582
Very interesting thanks - have saved it in my SS links folder. Where does it say that seronegative is actually those who are lip biopsy positive, as Sjo Man comments, though?
So, I am weird specimen, as I have always known. ;)
I am anti-CCP+ since time of semi-dx (never been officially dx'd). I have since then become RF+. SSA/SSB/ANA-. Never had a lip biopsy.
Yet my symptoms are Sjs, not RA! I have autonomic symptoms but have had (some of) those since childhood and think those are not caused by Sjs but not sure since they worsened with the onset of my other symptoms. I have had some weird sensory symptoms but they have been episodic. I also drop things now. I never dropped things before.
So I'll just hang out here and wait for research to come along that sheds some light on... What the Heck? ::)
Quote from: Nymph on February 10, 2017, 03:48:27 AM
So, I am weird specimen, as I have always known. ;)
I am anti-CCP+ since time of semi-dx (never been officially dx'd). I have since then become RF+. SSA/SSB/ANA-. Never had a lip biopsy.
Yet my symptoms are Sjs, not RA! I have autonomic symptoms but have had (some of) those since childhood and think those are not caused by Sjs but not sure since they worsened with the onset of my other symptoms. I have had some weird sensory symptoms but they have been episodic. I also drop things now. I never dropped things before.
So I'll just hang out here and wait for research to come along that sheds some light on... What the Heck? ::)
Interesting - so you aren't actually officially even seronegative for SJS then? From one weird specimen to another - I think so many of us have a sort of MCTD rather than one seropositve disease. My neuro symptoms are so closely tied up with dryness but also with systemic inflammation that is more vascular than has ever been properly acknowledged yet I believe. But also so very like MS - and yet I don't have MS, despite some white matter and paired o bands in my CSF and Serum. The pattern of my +ANA points to Scleroderma or Polymyositis and yet I don't appear to have either.
Maybe, as my opthamologist suggests, our doctors should name our unique versions of autoimmunity after each of their patients - having first identified that we do have established autoimmunity rather than something else of a more "functional" nature going on? And let up on which specific disease they are treating. After all most connective tissue diseases are treated with roughly the same modifying treatments.
Actually MCTD is defined by high titres of anti RNP and ANA which is my case and diagnosis. I got sjogren's dx to go with it from having positive ss-b. Patients who have a clear autoimmune process, but no positive blood work or lip biopsy are put into the Undifferentiated Connective Tissue Disease catagory until positive blood work.
Yes Tharrell but what about people like me who do have very positive lip biopsy with +ANA and high titres of inflammation - but who don't have the more specific serum markers of any CTDs? But on the other hand I do have multiple extraglandular symptoms that indicate neurological involvement and crossover with other rheumatic diseases including vasculitis, Scleroderma and RA? This isn't classed as UCTD for me because the Sjogrens has been histologically confirmed so it is differentiated.
So would you call this Sjogrens plus UCTD or just UCTD, or perhaps seronegative MCTD - or simply seronegative primary Sjogrens? I'm inclined to the latter but I then need seronegative primary Sjogrens to be better acknowledged and understood when it has become a multisystem CTD
I've just been discussing this on the phone with someone deeply knowledgeable and with medical training and she calls it MCTD rather than UCTD.
PS and UCTD also has to have serum markers to be diagnosed as in +ANA
My personal opinion is that we can call the individual diseases anything we want. The bottom line is they are autoimmune and hard to diagnose and require treatment much of the time for comfort and continuing ability to carry out daily activities of living.
I read an interesting article many years ago and did not document anything from it---I didn't know I would want the info later!!! This article went on to say that many researchers felt that all the autoimmune diseases were actually the same disease that showed up in different ways. This really makes a lot of sense to me due to the cross over of all many of the symptoms. Just may thoughts. Irish
I think this is very true Irish. The only thing that I would add is that some people have chronic symptoms as part of conditions that aren't autoimmune - so that's why criteria matter or otherwise they might be treated the wrong way. For example Lyme is treated by boosting the immune system so dmards or steroids could do a lot of harm. Otherwise I think that each of us has our own version of autoimmunity - and I'd say mine is called "Sjögren's Mat". ;)
this for me is quite difficult to understand bec english is not my language. and i also wonder if someone who is negative for some tests can change the result with time passing. or if one is negative for ssb or any other can become positive after a while? bec if it is so all the general "landscape" changes.
Or not??
Mine have changed a lot blurgardenia. But I have no idea if this is because of drugs I was taking around the time of testing. My ANA wasn't tested at first, only my RF - which was a weak positive. Then I was diagnosed with RA. Then after that I was tested for ANA and all the rest and it was equivocal - don't know more than that. Then last year, off all RA meds and steroids, I was retested and my ANA was clear positive with a different pattern to Sjogren's. But my RF and ENA panel were all negative. So on the strength of this and small fibre neuropathy, plus raised immunoglobulins and high inflammatory bloods (always) I was advised to have lip biopsy - which was entirely positive.
Could my ENA panel change and become positive over time? Not sure but I think it's only the less specific ones that can change? Could be wrong though.
Your English reads very well to me.
Hi bluegardenia, yes, blood work can change over time. I was positive for ana and ss-b first. It took two years for the anti- rnp to become positive, but now my ana and ss-b is negative. My rheumatologist attributes the negative ana and ss-b to treatment. It can all get so confusing!
The more important matter is that a rheumatologist recognizes what is going on and treats your symptoms. Thos rheumatologists are unfortunately few and far between.
Yes, we can be positive or negative with our autoimmune blood work and then "convert" to just the opposite. My immunologist tells me that just because we convert from positive to negative doesn't mean that we are cured. Our body can still have all the symptoms but change from positive to negative.
Then there are the people who have positive blood work all the time and never have any symptoms. It is just the way our bodies are. People can have the positive blood work and no symptoms--ever-- or negative and have lots of symptoms. We just have to accept things for the way they are. It doesn't work to place all our hopes and dreams on our blood work. We have to take the symptoms and treatment, if possible or necessary, and live life the best we can. Good luck. Irish
Yes, in my medical file it says "undifferentiated inflammatory polyarthrophy" or something like that. Basically UCTD. And "sicca". I was first told I had RA. Then she retracted that a year later. According to the research I have a strong chance of still developing RA, exactly what chance is hard to tell. I feel that with every year that goes by without it I get a little bit safer! I seem to have mostly stabilized in that my disease does not appear to be progressing.
BTW, anti-CCP is actually considered seropositive for Sjogren's in a small cohort of studies, although not in any official capacity. Apparently it occurs in ~5% of Sjs patients without RA. Thus I cannot say that I am seropositive OR seronegative, but rather that the serology of this disease is in the baby stages yet. Clearly I have autoimmunity. Yet I believe that some of my problems may stem from a genetic connective tissue disorder (EDS-H). I will probably never qualify for any study since I cross too many boundaries. Those of us who have a complex diagnostic picture will probably be forever putting the pieces together for ourselves, and seeking outside-the-box docs who will work with us.