severe erosive ra | Arthritis Information

 

any one else got this diagnosis.. how you fairing out..

Boney   Hi Boney, my RD says I have severe RA but not erosive so far as we know.  But it is relentless pain and flares, badly controlled due to allergies and intolerances!  Is yours erosive?  Janie. hi janie .. my diagnosise is severe erosive.. i am yet to speak whith
someone whith same diagnose.. im begining to wonder if it is a uk.
type diagnosise. you seem to have the same prob as me whith  meds..
but whilst i was able to take the  dmrds combined whith pred
controlled my ra fairly well.. i hope you stay erosion free..
Boney      Hi Boney,

I have severe RA, but I've also have had RA for 31 yrs now.  I'm not familiar w/the term "severe erosive RA."  Isn't all RA potentially "erosive" if the inflammation is uncontrolled?

My RA wasn't well controlled, plus I had a lot of stress when both my parents became sick and passed away, but once I began on the biologics I had more control of the inflammation, but by that point I already had joint damage.

I hope you find a treatment program that helps you.  Take care. 

hi joi really sorry to be reding about your parents..
ra is a complex disease whith different forms and outcomes.. i have now
scoured the web to get info to try peice it together..the problem is finding info
that is easily understood.. here goes
Boney
setDOI("ADOI=10.1002/art.20720");setISSN("1529-0131")setISSN("0004-3591")setEarlyView("-----")  Research Articles
Use of mass spectrometry to identify protein biomarkers of disease severity in the synovial fluid and serum of patients with rheumatoid arthritisTo identify a panel of candidate protein biomarkers of rheumatoid arthritis (RA) that can predict which patients will develop erosive, disabling disease.A 2-step proteomic approach was used for biomarker discovery and verification. In the first step, 2-dimensional liquid chromatography-coupled tandem mass spectrometry was used to generate protein profiles of synovial fluid (SF) from patients with either erosive RA (n = 5) or nonerosive RA (n = 5). In the second step, the selected candidate markers were verified using quantitative multiple reaction monitoring mass spectrometry in sera of patients with erosive RA (n = 15) or nonerosive RA (n = 15) and of healthy controls (n = 15).Through differential profiling of proteins in the <40-kd portion of the SF proteome, we selected 33 prospective candidate biomarkers from a total of 418 identified proteins. Among the proteins that were elevated in the SF of patients with erosive RA were C-reactive protein (CRP) and 6 members of the S100 protein family of calcium-binding proteins. Significantly, levels of CRP, S100A8 (calgranulin A), S100A9 (calgranulin B), and S100A12 (calgranulin C) proteins were also elevated in the serum of patients with erosive disease compared with patients with nonerosive RA or healthy individuals.Several potential protein marker candidates have been identified for prognosis of the erosive form of RA. This study demonstrates the facility of using protein mass spectrometry in SF and serum for global discovery and verification of clinically relevant sets of disease biomarkers.Department of Radiology, Rosalind Russell Medical Research Center for Arthritis, University of California, San Francisco, California, ETATS-UNIS
⁽³⁾ Department of Epidemiology and Biostatistics, Erasmus MC, University Medical Center Rotterdam, Rotterdam, PAYS-BAS
⁽⁴⁾ Department of Medicine, Rosalind Russell Medical Research Center for Arthritis, University of California, San Francisco, California, ETATS-UNIS

Résumé / Abstract

Objective. To investigate the influence of individual patient risk profiles on the value of the HLA-DRB 1 shared epitope (SE) as a predictor of severe erosive damage in rheumatoid arthritis (RA). Methods. Patient characteristics, clinical signs and symptoms, rheumatoid factor (RF) status, and HLA-DRB 1 genotypes were available for 154 Caucasian women with RA. Risk profiles were defined by non-genetic factors that predict severe erosive disease. The additional value of the SE was defined by the likelihood ratios (LR) of SE presence and absence, which were calculated at the individual patient level. Results. In the total population, the LR of SE presence was 1.42 and the LR of SE absence was 0.37, corresponding to an odds ratio of 3.9, indicating a substantially higher risk of severe erosive disease in those with the SE compared to those without. The LR of SE presence and absence varied depending on the risk profile of the women, from 1.01 to 2.25 for SE presence and 0.22 to 0.49 for SE absence. Considering all the patient characteristics, SE status was most significantly related to RF status. Consequently, the LR of SE presence and absence were higher for RF-negative women compared to RF-positive women (SE presence 1.77 vs 1.40, p < 0.001 and SE absence 0.38 vs 0.30, p < 0.001). Conclusion. The additional value of SE testing for predicting severe erosive disease varies according to patient risk profiles. Given the likely availability of genetic and other novel tests in the future, information about the additional value of test results is needed to ensure the optimal use of such testing in the management of RA.

Associations between the HLA-DRB1*04 allele and its subtypes
0401–0409, and severe erosive rheumatoid arthritis (RA) were
evaluated in 222 patients from different ethnic groups and 110
healthy control subjects resident in the Tshwane (Pretoria) region
of South Africa. Patients were screened serologically for HLA-DR4,
followed by genotyping of DRB1*04 using SSP-PCR procedures.
Patients of Caucasian and African origin had significantly
increased frequencies of HLA-DR4 (P < 0.0001, and P < 0.00001,
respectively), the respective increases in relative risk for RA being
7.3 (P < 0.0001) and 6.1 (P < 0.0001). HLA-DRB1*0401 and *0404
were identified as the most common alleles in these RA patients,
with respective P values of 0.0081 and 0.0012 for African patients
and <0.0001 and 0.0352 for Caucasians. These observations
underscore the association between RA and HLA-DR4, particularly
with the *0401 and *0404 alleles, in the South African setting.
Results and discussion
The frequencies of HLA-DRB1*04 in the total group of patients
and control subjects, as well as in the sub-groups of patients, are
shown in Table 1. A significant increase in the frequency of
DRB1*04 was observed in RA patients relative to that of control
subjects (48.2% versus 11.8%, respectively), with an attendant
increase in relative risk. The breakdown by race reveals that the
trend is consistent across the individual race groups, although
the small number of Indian patients precludes meaningful
statistical analysis of the data for this sub-group.
Molecular analysis of HLA-DRB1*04 alleles was then performed
on 92/96 of those patients found to be DR4+ using the microlymphocytotoxicity
procedure. HLA-DRB1*0401 and *0404
were the only alleles represented at high frequency in RA
patients, with respective frequencies of 51.4% and 20.6% in
the total HLA-DRB1*04+ RA population. The corresponding frequencies
in the Caucasian group were 73.3% and 16.0%, while
both alleles were equally represented (35.0%) in the group of
African patients. The relative risk (RR) and P values are shown in
Table 2. Because of small numbers, allele frequencies were not
calculated for the sub-group of Indian patients with RA; nevertheless,
these results were included in analyses of the total
group. Although seven patients were homozygous for HLADRB1*
04, none was homozygous for a specific allele. Four, 2 and
1 of these were DRB1*0401/02, *0403/05 and *0401/03, respectively.
The results of the current study have clearly demonstrated a
strong relationship between severe erosive RA and the HLADRB1*
04 alleles *0401 and *0404 in patients resident in the
Tshwane region and are consistent with data reported from
studies conducted in other geographical regions, including
Europe, North America, Asia2–6 and elsewhere in southern
Africa.14,15 Nevertheless, the exact role of HLA-DRB1*04 allele
typing in the early identification and clinical management of
those patients who are likely to progress to severe, erosive
disease remains to be established. At present, it seems unlikely
that this procedure will be used in isolation, but rather in combination
with other recent diagnostic and prognostic innovations,
including the detection of circulating antibodies to cyclic
citrullinated peptides16 and glucose-6-phosphate isomerase.17
Together, these procedures may contribute significantly to the
improved management of RA.

Clinical Haematology and Medical Oncology Unit, Royal Hobart Hospital, Hobart, Tasmania, Australia.

We describe the induction of sustained remissions and possible cure of severe erosive rheumatoid arthritis (RA) by bone marrow transplantation (BMT) in 2 patients. BMT was used to treat severe aplastic anemia which was caused by gold in one case and D-penicillamine in the other. In the 8 and 6 years since the transplants (representing 8 and 4 years since cessation of all immunosuppressive therapy, respectively), the RA in each case has been completely quiescent. Although short term remission of severe RA following BMT has been reported, these are the first cases for which prolonged followup has been available. This experience raises the question of the role of BMT itself as a therapeutic option for patients with uncontrolled destructive synovitis.

Abstract

Stored samples from within the first year of disease of 119 patients with rheumatoid arthritis (RA) enrolled in a long-running prospective study have been studied for the presence of IgM and IgA rheumatoid factors (RF), using agglutination of rabbit IgG coated red blood cells to detect IgMRF and an ELISA technique using rabbit IgG coated on the microtitre plates and labelled F(aB)₂ fragment of goat anti-IgA. Outcome measures at a mean follow-up of 10.1 years (range 3-20) included the Steinbrocker functional grade and grading of erosive changes on hand and feet Xrays using a modification of Lawrence's method. Both IgA and IgG levels at presentation correlated significantly with outcome measured by erosive changes and functional grade at a mean of 10 years and with the time of first appearance of erosions. In patients who are IgMRF negative early in the disease, IgARF positivity indicates a greater chance of developing both erosions and impaired function than when both tests are negative. IgARF positivity seems to precede IgMRF Hmmmm, verrrrry interesting. Snooooozzzzzzzzzzze.  :-) I can't make too much sense out of this, but noticed this at the end:

 

"In patients who are IgMRF negative early in the disease, IgARF positivity indicates a greater chance of developing both erosions and impaired function than when both tests are negative. IgARF positivity seems to precede IgMRF"

 

I googled rheumatoid factor (see wikipedia site below) and RF (rheumatoid factor) "is an antibody against the Fc portion of IgG, which is itself an antibody; rheumatoid factor and IgG join to form immune complexes which contribute to rheumatological diseases."

 

When I was diagnosed back in 1977, I tested positive for rheumatoid factor, though I have no idea if it was IgMRF or IgARF.  I have joint damage, but not until 23 yrs after being diagnosed did I need joint replacement, and now that I am on enbrel and mtx, the inflammation is much better controlled,

 

In my muddled way, I guess I'm trying to say that even if you do test positive for RF, I feel with appropriate drug treatment, joint damage can be prevented or minimized.  There is much more hope for someone recently diagnosed, more successful outcomes, so don't be discouraged or disheartened by these medical terminologies.

 

 http://en.wikipedia.org/wiki/Rheumatoid_factor

 

 

 

 

my RA has been severely erosive.  I have joint damage everywhere and have had 7 joint replacements.  I've had it for about 23-24 years now with very little control.  My rheumatoid factor was majorly positive but its been so long don't ask me what type was done or what the actual number was.  [QUOTE=Joie] Isn't all RA potentially "erosive" if the inflammation is uncontrolled?[/QUOTE]