Science topic

Rheumatoid Arthritis - Science topic

Topic including all aspects of clinical and experimental rheumatoid arthritis research
Questions related to Rheumatoid Arthritis
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Is there a review paper in arthritis just like "Hallmarks of cancer" in Cancer research?
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I RECOMMEND THIS PAOER FOR U
PADI4 (rs2240340), PDCD1 (rs10204525), and CTLA4
(231775) gene polymorphisms and polyarticular
juvenile idiopathic arthritis
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Dear colleagues, our lab is having a new project in synovial fluid processing. We need filtered from all the cells SF.
Does anyone have experience in filtering the SF sample through 0.22 um filters? If it is possible to isolate the cells and keep them (maybe in case of filtering via a vacuum system, not via just syringe and filter).
One more question: what is your typical protocol to get synovial fluid cells spun?
Best regards,
Mariia, PhD in Biology, Ukraine
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Please check the following references :-
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I need to measure IL-6 and tumor necrosis factor-alpha (TNFa) concentrations in blood samples of rheumatoid arthritis patients. What anticoagulants (heparin, citrate and EDTA) will not interfere with the levels of (IL-6 and TNFa).
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thank you Malcolm Nobre for your answer and attached article,
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I need some articles on the incidence and prevalence of rheumatoid arthritis in the world and also in Denmark.
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Very vague question as it varies from region to region.
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Why did Dr. Fauci wait 2 months to recommend an expensive patented nucleic acid analog produced by an American Company when he had proof that Chloroquine was effective as both an antiviral and immune regulator to prevent the lethal effect of Covid19??
PUBLISHED IN NATURE, 04 FEBRUARY 2020
Cell Reseach
“Chloroquine, a widely-used anti-malarial and autoimmune disease drug, has recently been reported as a potential broad-spectrum antiviral drug.8,9 Chloroquine is known to block virus infection by increasing endosomal pH required for virus/cell fusion, as well as interfering with the glycosylation of cellular receptors of SARS-CoV.10 Our time-of-addition assay demonstrated that chloroquine functioned at both entry, and at post-entry stages of the 2019-nCoV infection in Vero E6 cells (Fig. 1c, d). Besides its antiviral activity, chloroquine has an immune-modulating activity, which may synergistically enhance its antiviral effect in vivo. Chloroquine is widely distributed in the whole body, including lung, after oral administration. The EC90 value of chloroquine against the 2019-nCoV in Vero E6 cells was 6.90 μM, which can be clinically achievable as demonstrated in the plasma of rheumatoid arthritis patients who received 500 mg administration.11 Chloroquine is a cheap and a safe drug that has been used for more than 70 years and, therefore, it is potentially clinically applicable against the 2019-nCoV.”
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Because despite the fact that "chloroquine is efficient in limiting the transmission of SARS-CoV," the study was done in cell cultures rather than humans or animals.
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The AtoMs
Newly discovered cell involved in rheumatoid arthritis could serve as treatment target
Join the discussion on the RHEUMATOLOGY group on facebook
Researchers at Osaka University in Japan have made an important discovery about a class of cells involved in rheumatoid arthritis (RA) that could pave the way for new treatments. The team discovered a NEW SUBTYPE of osteoclasts within affected joints that could serve as a potentially therapeutic target.
ARTHRITIS refers to a group of more than 100 chronic diseases characterized by inflammation in the joints that can eventually lead to irreparable damage and debilitating pain and stiffness. Rheumatoid arthritis is an autoimmune form of the disease, where immune cells mistakenly target tissue that lines the joints, causing pain, swelling, and stiffness. Over time, this can damage the joints, cartilage, and surrounding bone.
There is currently no cure for RA, and treatment approaches are limited to drugs to alleviate symptoms or at best delay disease progression, thus scientists are researching the condition in efforts to find potential new treatment targets.
In RA, two main CELL TYPES contribute to the disease progression. Firstly, immune cells release inflammatory cytokines that aggravate tissue lining the joints. Secondly, specialized cells called osteoclasts secrete enzymes and acids that "dissolve" bone.
In a healthy, non-disease state, osteoclasts remodel the bone, but in RA, their ability to breakdown bone is ramped up, which damages joints instead.
Currently, treatments for RA mainly target the immune cells. Treatments that target osteoclasts are limited because we do not know enough about how they are involved in RA. Understanding how these cells are different from the osteoclasts involved in normal physiological processes is persuasive.
Osteoclasts usually line the bone surface underneath layers of cartilage and tissue, which makes them difficult to isolate. A NEW TECHNIQUE for isolating osteoclasts was introduced by the team.
While normal osteoclasts are derived from stem cells in the bone marrow, osteoclasts involved in RA come from blood-borne precursors. The circulating precursors enter the joint and differentiate into a unique sub-type of osteoclasts, which are larger and have distinct markers that are not seen in other osteoclasts !
The NEW SUBTYPE of osteoclasts had properties that could be manipulated: The newly found cells, which the team has dubbed "AtoMs" (Arthritis-associated osteoclastogenic Macrophages), possess properties that could be manipulated in approaches to developing new treatments. For example, the AtoMs have an abundance of the protein FoxM1, which is known to make cells invade tissue. The team hypothesized that eliminating this protein may reduce its arthritis-inducing ability. As reported in "Nature Immunology" the researchers confirmed that this was, in fact, the case. When they genetically or chemically disabled FoxM1 in AtoMs, the destruction of the bone was reduced in the animals' joints.
OSTEOCLASTS IN RA HAVE DISTINCT PROPERTIES THAT MAKE THEM AMENABLE TO THERAPEUTIC TARGETING
THERE IS STILL A LOT TO LEARN ABOUT THIS CLASS OF CELLS, YET THE DISCOVERY COULD OPEN DOOR TO NEW AVENUES OF TREATMENT
Source: Researchers split the 'AtoM' in search of a treatment for rheumatoid arthritis. Eurekalert. Available at: https://www.eurekalert.org/emb_rel…/2019-11/ou-rst111219.php
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Causal treatments for rheumatoid arthritis
Dear Mrs Gheita,
I have described the mechanism of the development and chronification of inflammation by harmful substances in a book using the example of rheumatoid arthritis in accordance with the laws of physics and have thus scientifically proven it. The book is an original work of approx. 56,000 characters including spaces. According to the laws of physics, especially thermodynamics, inflammation is primarily caused physically by heat conduction and only secondarily by harmful bacteria. A change in thinking is required.
Heat conduction, which everyone knows from everyday life, always occurs where temperature differences exist and continues to do so until the temperature difference is equalised. Heat conduction is always taken into account in science and technology, but not in medicine. This is a serious mistake, because heat conduction occurs everywhere, including in the living body. Heat conduction is a physical mechanism that always occurs with external and internal temperature differences and cannot be controlled organically. Therefore, the organism is exposed to the damage caused by heat conduction. If the temperature differences are too great, inflammation of joints and organs can occur.
The book is entitled: Physics of the Origin of Inflammation by Pollutants and subtitled: Causal Treatments that Cure Inflammation and Prevent Antibiotic Resistance.
The link to the publication by Cuvillier Publishing is:
Here you can read an abstract, a reading sample, the table of contents and the keywords for free. I will be happy to answer any questions.
Yours sincerely
Frank Mitter (Author)
99428 Weimar, Germany
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One of student is studying the methylation pattern of certain interleukins from the patients of rheumatoid arthritis. In start of process, he is using Histopaque-1077 based method to extract mononuclear cell layer. But even after following exact protocol (Image attached of protocol used), layers are not being formed? Can anyone guide to make it work?
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Dear Azam Ali, the protocol in general looks fine to me - Particularly because it is provided by the manufacturer. Common problems with PBMC isolation are disturbing the gradient when not carefully handling it, centrifuging without break, and pipetting too much of the supernatant (= plasma) after the centrifugation step.
As an alternative, I can provide you with our protocol for PBMC isolation from RA patients using Ficoll Histopaque too. It is based on 50 ml Falcon tubes with a filter (available e.g., by Greiner bio-one). But of course, it also works with 50 ml Falcons without filter. This then only requires careful pipetting of the blood on top of the ficoll. The last to steps in our protocol are only required if you want to submit your cells to FACS analysis.
Please do not hesitate to contact me in case of further questions about it.
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I'm working on a retrospective study to asses the QOL in adhered rheumatoid arthritis patients, I didn't have any issues with measuring the adherence using PDC Retrospectively but im planning on assessing the Quality of life prospectively by giving the patients questioners in their next follow up , any ideas on how to do that and is it a correct way or there are other preferred methods.
also is there a way on how can I measure the QOL retrospectively ?
thank you
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Abdulsatar Mathkhor Thank you very much for your help , but if our disease is rheumatoid arthritis and we want to asses the QOL depending on ADHERENCE , what do you suggest as a method ? we have the tools such as PDC,AND WHOQOL-BREF questionnaire But we are having a problem on how can we utilize these tools, when do we give them , how we will follow up , and in your answer do you mean depression as an example? but how it will correlate with adherence ? since it is our focus and our objective is that we aim that people with better adherence have a better QOL.
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Hi guys!
I am advancing in the empirical design of my next project about regimes of knowledge production on Adverse Drug Reactions (ADRs) and I would like to know if you have any suggestions of literature about this topic in STS, Medical Sociology of related fields.
I am interested in the perspective of the coproduction of biomedical evidence which emerges in the circuit of pathologization/diagnostic/medicalization/evaluation/new research agenda, specially addressed to the diffusion of immunotherapies and artificial antibodies in Oncology and Rheumatology.
Keep safe and cheers!
Renan
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Wow, Barry, Renan can now go wild.
Those are the most important references.
I recall the frustrations of a US doctor who penned that as:
Death by Prescription - Dr Ray D Strand
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prolonged use of conventional anti-rheumatoid is detrimental hence need for alternative therapy
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Dear Mwihia Stephen,
Propolis has a complex composition. Many of its pharmacological affects are believed to be related to phenolic compounds. Caffeic acid phenethyl ester (CAPE) is among the most active compounds with antiinflammatory activity. Here we have reviewed of the pharmacology of CAPE and clinical trials: https://www.academia.edu/40588958
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I am doing a project related in rheumatoid arthritis and want the correct cell line for studying anti-arthritic activity, what kind of cell lines are generally used for study?
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RAW 264.7 cell line.
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I'm looking reference paper for RA that, if any one have worked using cell lines, but everyone have performed their research using human  primary cells isolated from patients or tissue from RA induced mice models. Please suggest me some solution since we don't have access for getting human patients sample.
Thank you And Regards
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Most of the researchers preferred the human samples or animal model (Rat or Mice) for the rheumatoid arthritis research. Because, it is a bone related disease. If you need cell line related studies on RA, you can use NIH-3T3 mouse embryo fibroblast cell line or sarcoma cell line (SW982). But animal model is much better than cell line studies. Because we easily observe the bone destruction, bone re-modelling, swelling and inflammation
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During pregnancy observable changes in symptoms of autoimmune diseases like Multiple sclerosis (MS), Rheumatoid arthritis (RA), SLE used to occur. eg. in some cases of RA or SLE there are improvement of symptoms in pregnancy. Why these changes occur? Is there any role of fetal cells to make these changes in symptoms?
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Mediators of modified immunity in pregnancy are the polyclonal activation of B cells, the unbalanced T cell regulation in the immune response. The lupus flares up in 40 to 60% of pregnancies. This happens at every stage of pregnancy and childbirth. With little evidence, lupus occurs more often postpartum. It is recommended to plan the pregnancy with a minimum of 6 months afterflares of nephritis. Risk indicators for the mother and fetus are
  • anti-Rho / La
  • anti-phospholipid syndrome
  • renal impairment
  • hypertension.
[Tayseer, G. H., Chaudhary, P., Clowse, M.E.B.: Systemic lupus erythematosus in pregnant patients an neonatal lupus. In: Rheumatology. Ed. Hochberg, M. C. et al. Elsevier Philadelphia 2019;1208-1211.]
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How to find a protocol for Etiological factors of RA ?
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thanks a lot Kathy.
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Do statins have useful roles in rheumatology especially in rheumatoid arthritis?
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Could the determination of a serum cytokines profile during/ at the end of the disease-modifying anti-rheumatic drugs (DMARDs) mono-therapy period be used for the selection of a certain biologic DMARDs for the following treatment in non-responsive rheumatoid arthritis patients ? e.g. anti-TNF versus anti-IL-6?
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ideally.. you would think so. But there has never been a successful panel, or even an inkling of what these biomarkers could even be. There are several reasons why... and I can probably list an entire page or more of them.
While I can tell you that there are clinical trials that are looking at this question... But my own personal opinion... serum/plasma biomarkers, which are kind of static... isn't going to give you the answer. I'm more of a proponent of a function assay.
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patient with rheumatoid arthritis experience several complications related to disease itself or its treatment, one of these morbidity is ILD. how to detect it early using serum markers
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For research purpose there are bio-markers that could be studied, like lung epithelium specific proteins (associated to surfactant, mucin, clara-cell) and also chemo/cytokines MCP-1, glutathione, IL2-R. For clinical use, I don't think we have yet bio-markers for ILD in RA.
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I am a researcher in medicinal chemistry wanted to work on rheumatoid arthritis.
I want to know from where (preferably in India) I can get the pharmacological activity of my compounds???
It's very important as my whole research depends on it....
Please help me....
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NSAIDs are not the only medication for rheumatoid arthtitis. A link to an elementary explanation of the disease, diagnosis and treatment for a start:
Best wishes, Lars-Erik
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Does somebody know that the expression of STAT5 in rheumatoid arthritis synovial fibroblasts (RASFs)? Although some report indicated that the expression of STAT5 in RASFs, we can not detect any signals of STAT5 in RASFs using Western blot.
Please give me your opinions.
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Hi Jack,
Thank you for your opinions.
We always perform WB using T-cell lysates as positive control of STAT5. We can get signal of STAT5 in T-cell lysates, but not in RASFs.
We use polyclonal antibody for STAT5 which can bind both STAT5A and B. This antibody was purchased from CST.
We checked your recommended article. However, there are not so many study to investigate the expression of STAT5 in RASF.
Best wishes,
Kunihiko
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How does the progression of seronegative RA vary with that of seropositive RA
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Determining a prognosis or outcome for any rheumatoid arthritis (RA) patient is difficult; seronegative patients are no different. The disease itself may start out with mild symptoms and involve into more severe ones that make treatment more difficult. Seronegative patients are often regarded as having a milder set of symptoms compared to seropositive . Generally, seronegative patients don’t develop rheumatoid nodules, which are commonly displayed in seropositive patients. This is never a certainty, however, and each patient’s individual symptoms and disease progression will differ. Treatments for seronegative RA are approached the same way as seropositive patients. The goal of treatment is to mitigate pain and prevent the disease’s progression. Focusing on reducing pressure and deterioration of joints is very important in delaying the disease. Treatment should be started as early as possible to prevent the disease from worsening.
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A friend suffers from Rheumatoid arthritis. Can I suggest him to use Voltaren gel, Cataflam or Cambia? Or is there other option?
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These are all add on therapies for temporary pain relief and would work at various degrees. You definitely need non biologic DEMARDs or biologic ones guided by a rheumatologist
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I'm using hyaluronidase (HA) to isolate cells from synovial fluid. I use a concentration of 200 U per millilitre of synovial fluid. For particularly viscous samples, I have read that this can be increased to 400U.
After 30 min incubation at 37oC, I centrifuge the samples at 1000 xg for 10 min. If the synovial fluid remains cellular, I dilute 1:2 with PBS-EDTA and spin again.
My questions:
1. Are there any known negative effects on cell viability/function when using HA?
2. Other researchers want to put the synovial fluid through the mass spectrometer. Are there considerations to be taken into account given that HA has been used on it?
Many thanks for your answers.
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yes
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These patients have typical symmetric joint pain, hardly erosions of the MCP or PIP joints, but radiographic destruction of the dominant hand's wrist. I haven't found anything in the literature on this particular phenomenon. Have others similar patients?
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no problem, happy to contribute patients to a case series.
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I have read interesting work by Dr. Gabe Mirkin about nanobacters and curing Rheumatoid Arthritis with doxcycline. He also was a pioneer in pointing out germs in relation to stomach ulcers which proved to be true in some cases (helobacter)
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amazing
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Interleukin 17 (IL-17) is a class of closely related molecules known to be increased in the human body by exposure to Fluoride by ingestion from water and food, or metabolism of Fluorocarbon anaesthetics and propellants. IL-17 causes Autoimmune Diseases including Psoriasis, Rheumatoid Arthritis, Asthma, Lupus, Multiple Sclerosis, Inflammatory Bowel Disease, Transplant rejection, and destruction of Liver and Heart Cells. IL-17 is also implicated in Skin Cancer.
Other Interleukins are known to be elevated by Fluoride, leading to attacks on other critical cellular and organ systems. Australia's National Health and Medical Research Council actively suppresses this Interleukin science while promoting Water Fluoridation using industrial waste. Can the science community influence this behaviour?
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Dear Michael after reading your answer i did look up to the internet and started reaading bout flouride in water.
I am now able to get some insight about the big problem the humans are facing.
Lets hope that the council for water management will take up the issue in a more seroius manner.
It also has made a difference to my understnading of the disease patterns of autoimmunity.
Thank you for the insights.
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We don't have option of Synovectomy so we have to do HFLS culture from Synovial Fluid. I am trying to culture FLS from synovial fluid of the patients with RA but as this process of drawing SF from patients are taking place in open enviroment, contamination is taking place every time .How can I avoid it ? Secondly I want to know what is the chance of getting the fibroblast like properties of this synoviocytes cultured from Synovial fluid. Is this a good target to study the inflammatory pathway?
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Thanks Subhash.
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I want to evaluate the therapeutic and prophylactic of a drug on RA model in rat. when i should started to administration of drug in therapeutic and prophylactic group? in some studies they started administration few days before RA onset and others initiated at the time the RA onset for therapeutic group
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hallo i already worked on collagen induced arthritis in rat, if this model is want you wont to use i can help you.
arthritis onset is around 14 days after the first immunisation (there is a second immunisation on day 7) bay day 20 all the animals should develop arthritis (any animal not yet arthritic after 20 days will remain non arthritic).
if you want the prophylactic effect you should start drug administration from day 0 (a day before the immunisation). for the therapeutic effect you can start from day 14 or wait until all animals develop arthritis around day 20.
i personally recommand to start with the prophylactic effect especially if you are working with new drug, this model is a sever arthritis and if the drug have a mild effect it will not be seen in therapeutic treatment
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Hello
I want to ask about dietary pattern for rheumatoid arthritis patients
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There have been many studies looking at dietary manipulation in the treatment of RA. The first thing to be said is that diet is an adjunct to the pharmacological treatment of RA with disease-modifying drugs. It does not replace drugs.
Having said that, the only dietary modifications that have been consistently shown to have a (usually very modest) effect on RA are omega-3 supplements (more omega-3 containing foods are usually associated with a Mediterranean diet) and vitamin D, especially if you are vitamin D deficient. Probiotics to modulate the gut microbiome is a more recent supplement that has been shown to improve cytokine levels but not the clinical symptoms, but more research is needed.
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Synovial fluid was already collected from knee joint and firboblast cells were cultured from the collected synovial fluid. What will be the control of synovial fibroblast cells of rheumatoid patient?
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OA SF fibroblasts can be one controls esp if you are evaluating inflammation pathways.
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Hello! I just came across with an article (Mullan et al., 2006 Arthritis and Rheumatism) where the reseaschers showed expression of VCAM-1 in synovial cells of joints in patients with rheumatoid arthritis. I thought that VCAM-1 is expressed exclusively in endothelial cells. Tried to search, but found only in Wikipedia about smooth muscle cells as a sourse for VCAM-1, but without referense. Please, if someone could help to provid the information with references whether there are other researchers showing the presence of VCAM-1 in other cells, that would be fantastic. Thank you in advance.
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If you look at the 4th paragraph of the discussion of Carter et al., 2001, Immunology and Cell Biology, doi:10.1046/j.1440-1711.2001.01019.x, they state: "Vascular cell adhesion molecule-1 is also constitutively expressed on several other non-vascular cell types including type B SLC, bone marrow-derived stromal cells, thymic macrophages, thymic epithelial cells and follicular dendritic cells in tonsils." , with references to each. Hope this helps.
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How to exclude paraneoplastic neuropathy in rheumatoid arthritis patients without autonomic dysfunction?
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Hi,
I would like to help but I don't quite understand the question.  Please elaborate on the neurological condition of your RA patient?  Why do you think paraneoplastic?
HM
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In many countries, many patients with joint pain have to wait for several weeks or months until their first encounter with a rheumatologist. This impedes the EULAR recommendation, that pts with early arthritis should be seen by a rheumatologist within 6 weeks. 
Are there - apart from history taking and physical examination (which may be difficult for the untrained GP) - any useful screening tests to detect (or exclude) a rheumatic disease such as rheumatoid arthritis or CTD? 
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This is the normal test that I order to diagnose or rule out RA:  RA Factor, HLA B27, CRP, ESR
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Someone can help me? I have listened informally, but I can not find really formal and conclusive answers on the following questions: 1- Are there well-established and consolidated scientifical data about the efficacy of the use of rolipram, thalidomide, pentoxifylline or rupatadine, alone or combined, in the treatment of rheumatoid arthritis? 2- Are the existing data obtained in studies with experimental models of rheumatoid arthritis sufficient to point out conclusively and clearly the possible beneficial or deleterious effects arising from the use of each one of these drugs in this disease? 3- Would such eventual data be sufficient to justify clinical trials of each one of these drugs in patients with rheumatoid arthritis whose conventional therapeutic drugs are withdrawn?
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I understand. Thanks for your contribution.
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Can small increase in serum uric acid level (for example 20 units over the maximum reference range) causes
1- Swollen hand fingers only
2- Inflammation on the hand joint only (fingers or palm joint)
3- Difficulties in moving hand fingers only
4- Increase blood ESR level
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From the clinical pain of view, gout usually debuts as monoarticular disease and later on it takes a polyarticular form. initially, the joints of the lower limbs are predominantly affected.
A noninvasive usefull diagnostic tool is ultrasound, that may display double contour sign in the case of gout and some other elementary lesions in the case of rheumatoid arthritis, psoriatic arthritis or osteoarthritis. Thus, i suggest including ultrasound in the initial diagnostic work-up of this patient. 
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I am using Real time PCR with Taq man Chemistry in Rheumatoid arthritis patients. My gene of interest is ROR yT. I am using Beta Actin as a house keeping gene. Now I have one query. Actually I am getting CT value more than 30 (32-37) in case of ROR but normal CT values (18-20) in case of beta actin. Can anyone suggest me regarding this?? Because I hear from somewhere that more than 30 CT value is not valid !!! is it true? or any suggestion regarding this??
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Hey Amit, 
In my opinion, having high Ct values is not a problem as long as your housekeeping gene has a good expression (Ct~20). Make sure that the amplification reaction has a good efficiency and that there is no amplification of your negative control. 
Good luck!
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I have a patient with RA and active MS that unfortunately failed treatment on combination therapy with Methotrexate, Abatacept and Tecfidera. She had an allergic reaction to Rituximab. We could consider monotherapy with Alemtuzumab for MS, but would not like to decompensate her relatively stable RA. 
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Thank you for the great suggestions and all the given references. I am tempted to retry IV Rituximab but using much slower infusion in our own infusion unit instead of using rheumatology community infusion centre and have some antihistamines and steroids ready for use if necessary. If this fails, I might give it a go with Alemtuzumab monotherapy. 
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Could you please share protocol to culture primary macrophages from synovial  fluid/tissue of Rheumatoid Arthritis patients.
And it will extend up to how many passages. 
thanks 
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Thank you so much sir for your kind reply and suggestion.
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Hi, during last months I have been trying to get osteoclast's culture from bone marrow derived macrophages. I did exactly the same as it is described in different papers and protocols. For example, I flushed the bone marrow of 6 week old mouse, perform the erylysis, then culture them for 24h in a petri dish with 30ng/ml of M-CSF, then I transferred all nonadherent cells into a new petri dish for the next 48 h again with 30ng/ml of M-CSF. Afterwards I either took all adherent or nonadherent cells (I found both options in different protocols) and seeded them into 24 well plate (or 96 well plate) with 30ng/ml of M-CSF and 100 (30 and 60 have been tested as well) ng/ml of RANKL for the next 5-7 days. However, I always hardly observe any fusion (see photo after 6 days). I was waiting for 12 days as well. I have also tried different cell numbers per well, but nothing worked out. I would be so happy if someone could share with me his experience and protocol, which will really give the culture as people usually put in papers.
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There are many, many methods out there. This is ours: We take the flushed marrow from 4-6 bones (tibias, femurs and sometimes humerus) from 8wk mice, wash one time, (do not do any cell lysis), put into a 100mm tissue culture dish (no MCSF) overnight. The next day, we take the non-adherent cells and layer that 10ml cell suspension over 15ml Ficoll Hypaque in a 50ml conical tube and spin at RT 400xg (not RPM) 35 min with no brake. Remove cells at the interface (mostly free of RBCs, which pellet during the spin). Add PBS  or serum free media (5x volume of cells) (5ml up to 50ml) Spin 1500RPM 5min to wash, wash one more time (10ml), resuspend in MEM alpha +10% heat inactivated FBS +pen/strep + glutamine, count and plate 5000 cells/well of 96MW plate. We plate cells in 100ul, then add in our reagents. To get OCs, add MCSF 30ng/ml and RANKL 30ng/ml in 100ul, but make up at 2X. Because everyone counts a little differently and stocks of MCSF and RANKL can vary depending on your source, I would plate at 4000, 5000, 6000 and add MCSF 30 and RANKL 20, 30, 40. We feed on Day 3 by gently removing media and replacing with MEM + MCSF30ng/ml +RANKL 30ng/ml. Then watch daily for OCs at Day 4, 5 and 6. Fix in 2.5% glutaraldehyde in PBS for 10min. Can store in PBS til you TRAP stain (We use SIGMA Kit 387A) Be sure your media and water are LPS free. We use Hyclone Defined FBS and buy our media ready made to avoid LPS contamination from water filtered systems. In your picture it looks like your cells are too dense. They need room to move around in order to fuse.
Hope this helps, good-luck.
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What are the targets for Rheumatoid Arthritis other than Chemo kine and Cytokines?
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Indeed, I think María is right. And I think the mistake must be made by a B cell because of the epidemiology - increasing incidence with age and stochastic sporadic pattern. T cell diseases should have an incidence skewed to the age of T cell repertoire development - as the seronegative spondarthropathies do. B cells go on making random changes throughout life. RA is very neatly explained by accumulation of B cell clones that can self perpetuate through bystander T cell help and recruit further clones with time.
Inducing remission in 3 months is all very well but the real target is removal of the disease memory cells, as Jakob says. There is a very nice recent paper from the Radbruch group looking at a mechanism for deleting specific B cells using complex ligands. It may be tough to do that for diseases where auto reactive B cells recognise ubiquitous proteins like IgG Fc but somebody should be able to think up a trick for knocking them out specifically. Targeting mediators I think is unlikely to give long term remission. Metalloproteinase inhibition works in animal models of cartilage resorption but has no effect on RA. I thin that is because cartilage is resorbed in RA only when it has already been killed by intra-articular hypoglycaemia induced by TNF. I doubt metalloproteinases damage living cartilage in man.
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What folate supplements are available and the dose that should be administered.
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Grazie, Ciro, sono d'accordo; saluti!
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Some of the most commonly proposed measures or composites (e.g. RAPID3) have limited correlation to other well-known scales. But if you work with RA patients regularly, I'd like to know if you find a certain group of PROs clinically useful—particularly for making treatment decisions.
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After much clinical research and clinical experience I find myself in total agreement with Dr. Edwards,  One needs measures for trials, FDA, etc, but most are not very relevant for patient care.  I agree that patients should be "doing well" and will generally tell you if they are not.  I have also found that what we consider to be "doing well" often is not the same as what a patient is thinking/feeling.  Listening and dealing with expectations vs outcomes can be very important.  
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In my experience, patients with PMR can have a good response to 6-methyl-prednisolone and not to prednisone, or to classical prednisone (Deltacortene) and not to modified-release prednisone (Lodotra). Obviously with the same dosages (or equivalent). Is it so also for you ? Why is it possible ? 
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There are no solid data. Since glucorticosteroids there is no modern research (no funding, no interest.
A quite possible explanation might be found in different the biodynamic and pharmacodynamic effect and in the effective potency (that is certainly different from that in old  published data). Also, at least in some research data, some glucocorticosteroids have a positive impact on the cardiovascular system while other are neutral. Data are rather uncertain and often conflicting. Anyhow, enjoy the following:
There are known knowns. There are things we know that we know. There are known unknowns. That is to say, there are things that we know that we don't know. But there are also unknown unknowns. There are things we don't know we don't know. Donald Rumsfeld
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I am working on rheumatoid arthritis for which my test results are in International unit in one deciliter. i want to know the value equivalent to 1IU of RA factor in terms of concentration units.
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I don't think this is a matter of concentration. Rheumatoid factor assays measure binding and that depends both on concentration and a profile of affinity going from very high to not so high. One patient may have a small amount of high affinity RF and another a large amount of medium affinity RF and the same amount may bind in the assay. Binding may vary with lab conditions, so you need to calibrate against a standard. It's a bit like fishing for crabs with bacon. If the crabs are hungry you will get a good catch when there are only a few. If they are not so hungry, you need more in the sea to get the same catch. 
If you had a standardised monoclonal rheumatoid factor you could probably work out the relation of IU to concentration, but not for polyclonal RF in sera. 
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We are using 5 targets of folate pathway and 1 house keeping gene for gene expression assay by taq man chemistry in rheumatoid arthritis patients.
is there is any need of standard curve if we are using relative quantification,because i think we are just comparing fold change .. if so then we can only compare this fold change with respect to house keeping gene.
we can add equal quantity of template in each (target as well as house keeping) and change in the cT value may used for fold change.
is this ok ?? 
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You need to do a standard curve to determine the efficiency of primers. 
Another standard curve to determine if there are inhibitors in your cDNA using primers you know that work.
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Can other clinical manifestations of polymyalgia rheumatica be more suggestive   for a paraneoplastic syndrome ? 
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The role of VEGF in the pathogenesis of RS3PE syndrome (and not in the pathogenesis of PMR) would speculate that the presence of RS3PE during PMR is not only a manifestation of the same PMR.
Is PMR + RS3PE a clinical entity in its own right ?   
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Does anyone have a good review, profound knowledge or reasonable expert opinion on how to define the cut-off values of (at baseline) poor prognostic features in rheumatoid arthritis?
More exactly definitions of:
Laboratory:
- a positive CCP-titer (or is it just dichotome?)
- earliness of RF seropositivity (how early?)
Disease-activity:
- DAS28-ESR / CRP (> 3.2 or > 5.1?)
- functional limitation (e. g. through SDAI (>10 ?)
Erosion / Functionality:
- a high number of swollen / tender joint counts (> 6 ?)
- extraarticular features ( number of nodes ?, severity?)
- earlyness of erosion (at which time point?)
Thank You for any input on prognostic factors in RA (not risk factors, though!)
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I don't think that there are cut-off values for CCP titers and earliness of erosions to be considered determinants of bad prognosis.
Seropositive rheumatoid arthritis and erosions are simply considered factors of poor prognosis no matter the earliness for erosions or the titer for CCP. This is both are associated with more co-morbid conditions and thus with a higher mortality risk.
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50 year old patient with past history of rheumatoid arthritis, hx of mexotrexate and humira has large necrotizing lesions to lower leg.  How can this be treated most effectively?
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Thank you
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I’m planning to investigate some plant for healing Rheumatoid arthristis. I read about various papers about it, i would like some advice about this question . I’m really looking to find out what you’d consider to be the most efficient plant compound for therapying rheumatoid arthristis.
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Localized inflammation in RA could be reduced by inhibiting plant products that inhibit the activity of Nf-kB transcription factor. To start, one can use curcumin, a plant product routinely used in Indian food. The plan product is very potent inhibitor of inflammation and relives symptoms of inflammation-associated human diseases in long-term.
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1) What is the prevalence of cervical arthrosis/athritis in Germany ?
2) What are the treatment guidelines for cervical arthrosis/arthritis ?
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Thank you so much.
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Last opd i came across a patient of 5 years with polyarthritis for 6 months. Excruciating pain was there in almost all joints associated with limitation of movements. Knee joint was swollen and tender. No h/o enthuses, pain in hip joint and uveitis. It was diagnosed to be polyarticular JIA. But he had done one HLA B27 screening. It was positive. Now my doubt is should we stamp it as Enthesis related JIA or polyarticular JIA. How frequently we are supposed to get HLA B27 positive in polyarticular JIA? 
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Dear Dr. Shubhankar,
ERA appears infrequently below 5 years, and it is usually associated with: male gender, oligoarticular involvement, mostly asymmetrical, over lower limbs large joints, enthesitis, sacroiliac pain or lumbar spine limitation (this may be a late finding), dactylitis, elevation of APRs and HLA B27 positivity. Your patient does not seem to present any of these except for the HLA allele.
Polyarticular JIA, especially the Rheumatoid Factor negative type, is commonly seen during the early years of age, commonly involves large and small joints of both upper and lower limbs, upper spine (cervical), while lower spine and entheses are usually spared. Your patient resembles this latter picture. However, the HLAB27 positivity prevents us from classifying your patient as Polyarthritis, while he does not meet enough criteria for ERA (I assume his family history was negative for spondyloarthropathy or other B27-related diseases).Naturally, should find a repeatedly positive Rheumatoid Factor your patient is clearly a RF-positive Polyarthritis.
Today your patient seems to fit under the "Undifferentiated Arthritis" type of the ILAR criteria. Nevertheless, given his B27 positivity (and thus an increased risk of developing lower spine invovement later on) I would follow him closely with clinical/imaging techniques to eventually detect sacroiliac impact early.
Answering your question: HLA-B27 frequency in Polyarthritis seems to be similar to the one in the general population: 3-10 % (Thompson et al. Juvenile idiopathic arthritis classified by the ILAR criteria: HLA associations in UK patients. Rheumatology 200241:1183-1189). The frequency in the patient´s particular ethnic background could give you a better estimation.
Best wishes,
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how can i find recent information and results for gene activated matrices for cartilage regeneration in rheumatoid artritis?
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thank you so much Alan!
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how frequent are the existence of RA and psoriasis.  Is HCQS or hydroxychloroquine justified in the condition?
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Dear Satyaprasad,
I think you are asking for the frequency of coexistence of true rheumatoid arthritis with psoriasis, rather than psoriatic arthropathy? There may be literature on this but the problem is that ascertaining the existence of true RA in the presence of psoriasis is not straightforward. Rheumatoid factors and ACPA occur in a small percentage of normals so could occur alongside psoriatic arthropathy. 
The only time I have been convinced that I knew that an arthritis was true RA in the presence of psoriasis was in a case with typical rheumatoid nodulosis and RF. I only saw the one case in thirty odd years.
In practical terms relating to hydroxychloroquine, I think you are entitled to go on probabilities. If an inflammatory arthritis is associated with RF and or ACPA and does not have DIP involvement then if you feel hydroxychloroquine is a reasonable choice for RA (I was never very convinced) then it is probably still reasonable if the patient also has psoriasis. Without autoantibodies or nodules the chances must be that you are dealing with psoriatic arthropathy and I know of no theoretical or practical evidence for hydroxychloroquine being useful there.
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Should I stop methotrexate? or continue with follow up?
and if MTX is stopped, what other drugs can be used?
Finally, how can I differentiate the cause of IPF? I mean it is related to MTX? Due to disease activity? or isolated IPF?  
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As a referral centre for interstitial lung diesease we are regularly confronted with this dilemma. The differential diagnostic possibilities in patients with rheumatic disease developing an interstitial lung disease (ILD) during treatment with MTX include infection (especially PCP), MTX associated lung disease, RA-associated ILD and MTX-associated lymphoproliferative disorder. According to the ATS/ERS guidelines, IPF in terms of UIP can be confirmed or excluded based on clinical presentation and HRCT only. The possibility of an infectious disease requires microbiological analyses of e.g. BAL fluid. In addition FACS analysis of peripheral blood may reveal a decrease in CD4+ T-cells indicating MTX-induced immunsuppression. To my experience it is difficult to distinguish MTX-associated ILD from RA-associated ILD based on clinical-radiological data only. In such cases an open lung biopsy is helpful to tell the difference: EAA-like pattern with or without fibrosis is compatible with MTX induced ILD, whereas RA-associated ILD is characterized by NSIP/OP-like pattern with or without rheuma nodules. MTX-induced lymphoproliferative disorders can be diagnosed either on periprheral lung tissue and /or by demonstrating increased EBV virusload in peripheral blood.
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As the patients do exercises,Can they use drugs less than other patients that they do not exercise???
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Physical exercises are necessary for the Rheumatoid patients as the joints remain flexible and soft tissues mobile. Despite this it will be better to do them when the inflammation is better (so better not during acute inflammatory phases where the patient will be benefitted by rest). Medication has to be monitored and controlled by having regular follow up reviews and the regime has to be changed accordingly.
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Are these different in male and female?
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Patients with RA, male or female in the same degree, will be benefited with exercises that are improving the ROM of the joints and fight against the stiffness. These are wrist rotational movements, wrist resisting (palms and dorsal areas of the hands against each other), side to side movements, stretching exercises and the use of a ball in the palm and squeeze it. Some people apply Yoga exercises.
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Please guide me regarding the above question, if possible please give the reference. Regards.  
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Dear Chetan,
please go through this link. 
here the dose mentioned is 150 microgram.
This might be useful for your research study.
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We have a 21 year old girl who has been symptomatic for last 3 months with polyarthritis and multiple cutaneous ulcers over lower limbs with hemorrhagic blisters. She thereafter developed multiple episodes of transient ischemic attacks (amaurasis fugax 5 times and monoparesis right hand twice) lasting just a few minutes each followed by bluish discolouration of 2 toes (early gangrenous changes). She also had multiple episodes of mucosal bleeds in the last month (7 episodes of epistaxis and 1 episode of melena). Current examination shows symmetrical sensory neuropathy in addition to above findings. There is no renal or pulmonary involvement.
She tested positive for ANA, anticardiolipin antibodies (both IgG and IgM), nRNP, anti Sm and anti dsDNA. Interestingly she tested positive for p ANCA by IIF too and her nasal examination showed a few granulomas in her septum. 
She is being managed as SLE with secondary APLS with pulse steroids followed by oral steroids, Hydroxychloroquin and anticoagulation. A skin biopsy has been taken and we await the results.
I was wondering about the association of the 2 antibodies in the same patient.
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The clinical and laboratory picture reminds me to Wegener granulomatosis. Anti Sm are found in less then 30% of SLE and anti dsDNA even if specific for SLE can be found in other disease. It is not the presence but the titer to consider the final diagnosis. Could you tell us more about that ?
p ANCA has sadly the bad reputation of being of low sensitivity and low specificity in rheumatic diseases. Ex: only 10% of Wegener are postive  and 25 % of Churg strauss shows p ANCA. 
Pulmonary and renal involvement can be insidious and appear later in Wegener granulomatosis. 
Has IF been combined with ELISA study for p ANCA  ? this will be increase sensitivity and specificity. 
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For the last 2 decades we have seen a spate of clinical trials for different biologic agents  starting from anti TNF agents (etanercept/Infliximab/adalimumab/golimumab), T cell costimulation blockade (Abatacept), IL-6 inhibition, or B cell blockade (anti CD20: Rituximab). All the trials targeted 2 kinds of patients. The initial ones looked at "Failures" either MTX failures or anti TNF failures. While the latter ones targeted "Early disease" and took MTX naive patients.
Almost all trials had the following 3 features in common
1. They invariably compared 'MTX + Biologics' with MTX alone
2. They invariably almost always used "Oral methotrexate" in modest doses (under 15 mg/week). Even those that used slightly higher doses (say unto 25-30 mg) had a significant number of patients in modest doses.
3. Those who included "Methotrexate failures" invariably defined it as failing to respond to oral methotrexate of 15 mg.
All 3 points have serious concerns. 
1. Using MTX alone in comparator arm did not reflect the best possible therapy. Trials had started emerging right from the 90's that combining 3 conventional DMARDs with (or without) low dose steroids was better than methotrexate alone.  So, choosing to use methotrexate alone, especially in the latter trials, does not seem very justified.
2. Evidence has existed again since 90's that parenteral methotrexate has a much better bioavailability at higher doses. The percentage absorption of oral MTX reduces further as dose is increased to more than 15 mg (bioavailability is < 65% after 15 mg). So the efficacy might have been under estimated.
3. Defining MTX failure again had the same definition problem. With the same logic given above, it is again very likely that at least some patients (if not many)  labelled as MTX failures and included in various trials were never failures, but just inadequately treated patients. This might have resulted in pumping up the efficacy statistics of the biologics arm.
The seminal paper by O'Dell et al in NEJM 2013 comparing triple therapy of 'MTX, Sulphasalazine and HCQS' with 'MTX + Etanercept' showed an equisimilarity in response at a significantly lower costs (US $ 10200 lesser per patient year). Of course, many issues have been raised about the paper and debate continues to rage but facts are facts.
In a resource limited setting like India, many of us routinely use Triple therapy + low dose steroids with excellent results. Using 25 mg MTX in an subcutaneous route is routinely practiced and we definitely do not find as many drug failures in RA as is reported in literature (unpublished data) with this usage.
Maybe it is time to have a second wave of clinical trials comparing Biologics with "Triple therapy" and steroids instead of with MTX alone and using MTX in higher dose routinely (unto 25 mg SC). I believe that much of the sheen from many of the trials might get taken off and a truer picture of biologics efficacy will emerge.
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To Cari, RA drug trials don't consider just symptoms in the final evaluation of the potential efficacy or lack of it thereof of a given drug; there are validated measuring instruments such as the ACR20, 50, and 70, DAS28, etc, and these include objective measures such as swollen joint count and blood inflammatory markers, e.g., sed rates and CRP. Almost all biologic drug trials also include radiographic data of involved joints over time,
To Daniel: the treatment of RA and of any disease for that matter is best done on a individual basis, stemming from and based on an optimal doctor-patient relationship. Healthcare mandates and huge databases should have no place in the evaluation and treatment of individual patients. We are presently being inundated with non-sense health mandates that add nothing to the quality of the care provided; insurance companies for years have been trying to practice medicine without a license. I understand trying to save money; however, the real value of a given medical approach should be discussed and evaluated with the patient in front of you, based on individual patient response. Different people react differently to different medications. It is the treating physician who would know best that a given individual patient responds better to this particular TNF inhibitor and not to the next one or a biosimilar. Clinicians deal with this problem on a daily basis. I understand that administrators and CEOs of insurance companies would not know this (do they care?), but then again, they are not physicians treating patients. In the end, we don't treat just diseases; we treat human beings suffering from diseases; not two patients are the same,    
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The effect of high-intensity strength training as compared to standard medical care on muscle strength, physical function and health status, in patients with Rheumatoid Arthritis Functional Class II. Which one is more effective?
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Dear Shadab,
see the following paper…
Biggs M, Yap C. The effect of high-intensity strength training as compared to standard medical care on muscle strength, physical function and health status, in patients with Rheumatoid Arthritis Functional Class II (2014). PT Critically Appraised Topics. Paper 44. http://commons.pacificu.edu/cgi/viewcontent.cgi?article=1039&context=ptcats
Best wishes from Germany
Martin
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Do you prescribe corticotherapy and change methotrexate treatment even if there are no articular signs of activity? 
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Good evening Dr Kechida,
first, I would like to recognize the thoughtful contribution of Dr M Khoury to rule out viral or amebic infections in the clinical problem you raised.  I further want to assure her of our best wishes during the hardship and turmoil that her country is going through.  We all hope for a solution if that is still a possibility.
Ulcerative keratitis is not part of run-of-the-mill RA in an adult.  So the first thing to establish is that the patient really has RA and second, if so, that the keratitis is due to RA.  So, be sure of the correct rheum and ophthalm diagnoses.
If the patient has RA,
1.  Clinically, severe keratitis may be part of either RA vasculitis, secondary sicca or associated with peripheral ulcerative keratitis (see PUK in Google for differential diagnosis).  In the former, scleromalacia perforans is more expected than deep keratitis and in the first two, there should be evidence of vasculitis and severe sicca elsewhere, respectively. To be noted, that arthritis and vasculitis are often reciprocally active/inactive in RA.  So here, the "MTX-controlled arthritis" does not necessarily mean that the rheumatoid process is controlled.
2.  Serologically,  the only (high titer) specific marker for RA vasculitis is the Euroimmun anti-Sa (citrullinated-vimentin) ELISA and that for severe sicca, the more likely, if not entirely specific, is anti-La/SS-B.  RF, anti-CCP and other ANA-sub-specificities can be positive in both.  PUK is a clinical diagnosis that can be either sero-RA +, sero-SS + or sero-negative.  ANCA and APLA should be negative.
3.  Local treatment is best left to Ophthamologists.  I would not push for any kind of medicated drops like steroids or cyclosporine and favour natural tears or gels with/without antibiotics.  Just for comfort!  R/O infection...
4.  Systemic treatment is that of vasculitis: IV or PO cyclophosphamide, IV and/or PO corticosteroid boluses and RTX.  ANTI-TNF ARE BEST AVOIDED IN RA VASCULITIS OR SS.
5.  Empirically, once, I used successfully in PKU, long term (1y) treatment with a low dose daily tetracycline (for its anti-collagenase action).  It allowed the acceptance of a corneal graft after an unsuccessful attempt.
That is a complex problem and for everybody to learn, you should give us 6-mth follow-ups. 
Sorry for the length of that response but most of it is not found in textbooks.  Bonne chance!
Henri A. Ménard MD, FRCP (C)
Emeritus Professor of Medicine, McGill U.
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If RA prevalence in North India is indeed 0.75% (similar to the prevalence of developed countries) this would be evidence against the Hygiene / Biome Depletion Theory. The Hygiene / Biome Depletion Theory proposes that the rise of allergic and autoimmune diseases observed in the developed countries throughout the last century was due to the improvement of sanitary conditions and depletion of symbiotic and pathogen microorganisms infection.
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This article might be of value to your question that looks at community prevalence (>51000 people from 12 sites) of RA in India and pegs it closer to 0.34% in India.
Chopra A. Disease burden of rheumatic diseases in India:COPCORD perspective. Indian journal of Rheumatology 10 (2015) 70-77
The hygiene/biome theory might still hold.
About RA being a newly described disease, I am not too sure of that. Though European and Greek medical literature before Sydenham's time may have confused gout and other forms of polyarthritis as manifestations of the same disease, but Indian literature does have excellent description of RA from Atharva Veda (1000 BC)
Caraka described the site of manifestation of rheumatoid arthritis in the following
words. (I have attached an article and highlighted the description in page 3, reads in Sanskrit with translation)
"The sites of its manifestation are hands, feet, fingers, toes and all the joints. It establishes its base first in the hands and feet and then spreads in the entire body"
I would also refer you to the article in Arthritis and Rheumatism that touches upon this issue
Sturrock, R. D., Sharma, J. N. and Buchanan, W. W. (1977), Evidence of rheumatoid arthritis in ancient india. Arthritis & Rheumatism, 20: 42–44. doi: 10.1002/art.1780200107
Is it possible that the chosen patient selection method have selected a more educated sample and thus one living in better sociocultural standards? - ResearchGate. Available from: https://www.researchgate.net/post/Is_it_possible_that_the_chosen_patient_selection_method_have_selected_a_more_educated_sample_and_thus_one_living_in_better_sociocultural_standards [accessed Sep 25, 2015].
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I need to know in real-life practice, that conduct taken rheumatologists and oncologists in patients who enrolled in concurrent cancer and active arthritis, or in patients who had cancer previously and now need biological or who develop cancer during biological treatment. In addition, they prefer some biological agent in particular?
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In fact, I think the theoretical arguments are too weak to guide clinical decision here, Bijit. We know almost nothing about immunosurveillance of tumours and in patients who have or have had overt cancer adaptive immune responses have failed anyway. There is a theoretical issue with blocking TNF since it can cause tumour cell death under  certain experimental conditions but that is not enough to base clinical practice on. There is limited evidence from post marketing surveillance that TNF inhibition is indeed a problem for some cancers. What I think is also important in practice is that TNF inhibitors have been marked as contraindicated in cancer patients and if cancer occur or re-occurs during TNF blockade there can be serious problems with feelings of guilt and anger for patients. If TNF inhibitor trials had not excluded cancer patients at the outset things might be easier.
When I introduced rituximab for RA in 1998 I made sure that we did not exclude cancer patients. As far as I know that has proved the right policy. 
In fact we have found that rituximab gives best results for patients with moderate (not high) autoantibody levels - probably because with very high levels it is harder to clear away enough antibody and disease is more severe and more difficult to get into complete remission. As far as I am concerned all RA is B cell driven. The few completely seronegative cases probably have different diseases - they rarely get a useful response to rituximab.
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Is it possible to change to ilaris? Are there more results and tests?
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Thankyou for sharing this case. What is her ethnic origin? Has sustained Colchicine plus Aza allowed you to taper the steroids successfully?
I have found Anakinra to induce ISRs and other local skin reactions commonly. In the 3 weeks during which you used it, did you note any response or was it too difficult to tell? Use of alternate daily or thrice weekly Anakinra plus or minus concomitant antihistamines or potent topical corticosteroids may help attenuate the adverse skin response. Canakinumab might be better tolerated, but it is very expensive. Rilonacept development has unfortunately been discontinued.
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We received blood from a patient with rheumatoid arthritis and after centrifuging the sample we realized the plasma was yoghurt white in color. Is this a defected tube? It appeared too white to be due to hypercholesterolemia but perhaps it's possible. 
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Immunoglobulins. These patients have reversal of A/G ratio. Serum Protein Electrophoresis is advised.
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Is there any literature regarding safety profile of DMARDs for seropositive (CCP) rheumatoid arthritis in a lactating female? Prednisone and hydroxychloroquine alone are likely not going to work...
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NSAIDS, Hydroxychloroquine, Sulphasalazine and prednisolone
if biologics needed TNF inhibitors may be used
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Does anyone have a patient with AIDS associated with rheumatoid arthritis?
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Dear Dr Carlos Augusto De Andrade,
Though RA is possible, the likelihood is a bit low.  A number of rheumatic manifestations have been described with HIV infection .These include arthralgia, painful articular syndrome, Psoriatic arthropathy, Reiter’s syndrome, reactive arthritis, HIV-associated arthritis, undifferentiated spondyloarthropathy, soft tissue rheumatism, septic arthritis, avascular bone necrosis, osteomyelitis, hypertrophic osteoarthropathy, myalgias, polymyositis, dermatomyositis, Sjogren’s like syndrome – DILS, vasculitis like Schonlein-Henoch purpura, polyarteritis nodosa (PAN), giant cell arteritis (GCA), Wegener’s granulomatosis (WG), Raynaud’s phenomenon, and Behcet’s syndrome. RA is conspicuous by its near absence.
There are actually reports of RA improving with development of HIV. This has been our experience too in a big cohort of over 6000 patients which we followed up at Pune, India, I do not recall a single RA patient, though many had other musculoskeletal complaints. 
Autoimmunity is common in HIV and over 20% of all patients might be positive for RF. Your patient has early arthritis of just 2 weeks with raised acute phase reactants. It might be worth looking for Sjogrens (both clinically and with autoantibodies ) as it can mimic RA. A post viral arthritis syndrome (where the fever might not be remembered vividly) too is a possibility. RA of course can occur but the pretest probability is low. 
I would be curious to know the outcome of your patient over time.
regards
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This topic is related to an academic research project, including a literature review, and research plan. Any insights will be very helpful, as there is a range of variables related to this topic.
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HI Phil
I suggest you to select some major rheumatic diseases to study.  As the diseases are different you have different physioterapic options... Best regards
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What would be effect of inhibition of osteoblast proliferation when Rheumatoid arthritis patient is administered with DMARD capable of inhibiting osteoblast proliferation?
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In Rheumatoid arthritis, the inflammatory cytokines (TNF alpha, IL1, IL17 etc)  inhibit osteoblast proliferation and promote osteoclast differentiation. This causes bone erosions & periarticular osteopenia locally and generalised osteoporosis at distant sites.
The effect of inflammation in negatively affecting bone loss is very high. Almost all DMARDs have a salutatory effect on bone health by reducing this inflammation. Though invitro studies show that there is some deleterious effect on osteoblast proliferation, this effect is very small compared to the deleterious effects of inflammation itself. Thus, in clinical terms, the net effect is positive by stopping the bone loss or at least reducing the rate significantly.
The newer Biologic DMARDs like the TNF inhibitors (Infliximab, etanercept etc) have even shown reversal of bone erosions in a few studies (by MRI imaging) and possibly have a more positive effect on bone health than the non Biologic DMARDs like methotrexate. 
Hope this helps
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Few cases of rheumatoid like arthritis has been recorded with interferon alpha treatment 
Is there any published or personal experience about initiating Interferon based regimen with a DAA for HCV patient with rheumatoid arthritis? 
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There are 3 dimensions to this question1. Does the patient indeed have RA? Over 70% of HCV patients are positive for Rheumatoid factor. HCV itself can cause a form of non erosive arthritis. Cryoglobulinemia , often associated with HCV can present with arthritis. If the patient does not have RA, the arthritis will actually resolve with IFN.
2. Choice of RA therapy on HCV: One needs to avoid methotrexate, lefluniomide and NSAIDs. Hydroxychloroquin and Sulphasalazine might be acceptable DMARDs. In case of choosing biologics, TNF inhibitors are by and large not recommended. Rituximab, though not recommended, is sometimes given as it does have benefial effects on cryoglobulinemia related arthritis of HCV and might cause lesser harm. Abatacept might be an alternative worth exploring.
3. Effect of DAA interferon/ribavirtin on RA: This is a tough one. IFN/ribavirin is known to precipitate autoimmune diseases including RA. 4 cases of RA have been described with IFN therapy. The best I can say is, make your own judgement and monitor patient more frequently.
all the best
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Do you have a detailed protocol for Zymosan A preparation ??
This is what I can find in the literature.....
Zymosan A from Saccharomyces cerevisiae  was resuspended in 10 ml of endotoxin-free saline, boiled and homogenized by sonic emulsification. The suspension was autoclaved and stored in aliquots at -20°C. Arthritis was induced by intra-articular injection of 180 μg (6 μl) of zymosan through the suprapatellar ligament into the joint cavity.
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My protocol includes injection of a fine suspension (not a solution) 500 µg/25µL/paw Sigma Zimosan in saline. Homogenize carefully between animals.
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I would like to know how the IL-2, IL-6 and FAS/APO-1 regulate the auto immune diseases like rheumatoid arthritis? How could we know the toxicity level of protein using the concentration level of IL-2, IL-6 and FAS/APO-1 from T cell?
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Toxicity can be measure by cell death by annexine V staining flow cytometry and stimulation of your antigen can be measure by increasing /decreasing of specific cytokines.
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Most labs measure titers of IgM RF in rheumatoid arthritis patients.  Interestingly, IgE RF was detected in a low percentage of RA patients (9%) [1]. IgE RF correlated better with extra articular manifestations than IgM RF in at least one study [2]. Have other laboratories investigated the potential association between IgE RF and extra articular manifestations?  If so, what are your findings? Is there any association between IgE RF and allergies or sensitivities in RA patients? 
1              Banchuin N, Janyapoon K, Sarntivijai S,  Parivisutt L. Re-evaluation of ELISA and latex agglutination test for rheumatoid factor detection in the diagnosis of rheumatoid arthritis. Asian Pacific journal of allergy and immunology 1992;10(1):47-54.
2              Herrmann D, Jager L, Hein G, Henzgen M,  Schlenvoigt G. IgE rheumatoid factor. Occurrence and diagnostic importance in comparison with IgM rheumatoid factor and circulating immune complexes. J. Investig. Allergol. Clin. Immunol. 1991;1(5):302-307.
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Thank you all for responding with your invaluable insights and perspectives!  In regards to the testing of all the isotypes of RF, the Banchuin et al article investigated the epidemiology of IgM RF, IgA RF, IgG RF, IgD RF and IgE RF. The Hermann et al article only reported on IgM and the IgE RF factor titers. Thank you very much, Maria for your potential explanations / mechanisms for an association between IgE and extraarticular manifestations. Some RA patients self-report sensitivity to various compounds that affect their joint flexibility, tenderness, and inflammation. I wonder if IgE RF could potentially contribute to the phenomena.
Thanks for your insights!  Kathy
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Rheumatoid arthritis patients are potentially at higher risk to develop cardiovascular risk, but studies have shown reverse correlation of lipids and RA with different opinion. What is actual relationship and if lipids are low, how Statin helps in RA?
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It has been demonstratted that the prevalence of cardiovascular complications (CVC) in rheumatoid arthrtits (RA) is increased to an extent comparable to type 2 diabetes mellitus. However, the increased incidence of CVC CANNOT be explained by traditional CV risk factors. Various disease-related mechanisms contribute to CVC. Especially important, the increases synthesis of pro-inflammatory mediators, autoantibodies and perturbation in some lymphocytes. The systemic inflammation seems to be the predominant factor FOR cvc. CurRent pharmacology for RA has different effects on CV risks in RA. There is a special SCORE - European Risk Chart for RA. Briefly, the same inntervention strategies for lowering of LDL in the normal population with elevated CV risk should be used in RA patients.
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I am planning to run a kinetic CIA experiment using male DBA1/J mice and I would like to see change in expression of gene of interest at various stages of disease. I have been reading about the appropriate antigen for induction of disease and found that people use both bovine CII and chicken CII for immunizing this strain. Could anyone suggest if one is better than the other or if it is context dependent. Please suggest appropriate concentration for induction and booster, as well.
Thanks in advance!
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Hello Samra,
You may find this protocol in the below link useful, because I used the same company's protocol for CIA induction in Wistar rats successfully... 
Although I also purchased the collagen from the same company as well, I believe that this may work irrespective of the source of collagen..
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I have conducted a case-control study to detect the association between 8 SNPs with Rheumatoid Arthritis disease using Dominant, Co-dominant, Recessive and Multiplicative models in the Egyptian population. the no. of cases was 105. the no. of controls was 80. The statistical power was measured using G*Power 3.1 assuming medium effect size (0.3), and the α was set to 0.05. The power of the study was 98.3% for the multiplicative, dominant, and recessive models (1 degree of freedom). The power was 96.34% for the co-dominant model (2 degree of freedom). I want to know if these power results are sufficient to prove that my study results are reliable (not just random fluctuations) or not?  
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I would really suggest to work on a larger sample if possible. I guess you will want to publish the data and if you want it to be accepted, I barely see the option with the current size. Get at least the same size of control sample, it should not be a problem. Your current sample might be taken as the preliminary data, but not enough to perform association analysis. For such a case I agree with Gerard`s comment. Hundreds or thousands. Depending what you want, I would start at 300 cases + same control match.
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I have conducted a case-control study to detect the association between 8 SNPs with Rheumatoid Arthritis disease using Dominant, Co-dominant, Recessive and Multiplicative models in the Egyptian population. when more than one model returns a significant association for a given SNP, What is the interpretation of such cases? Will the association with that SNP become stronger or it has no effect on association strength?
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