Science topics: MedicineInternal MedicineRheumatologyRheumatic Diseases
Rheumatic Diseases - Science topic
Disorders of connective tissue, especially the joints and related structures, characterized by inflammation, degeneration, or metabolic derangement.
Questions related to Rheumatic Diseases
Has anyone studied the effects of rheumatic drugs on the coronavirus?
I read the article
and see that many specialists place great hopes on drugs for rheumatic diseases in the treatment of covid. The article is from the beginning of the pandemic and I am interested in whether there is confirmation of the hopes written in the article. Is there new data and progress in this direction?
I would like to ask your opinions on an interesting case:
46 yr old female patient had an infection of uppper respiratory system in the beginning of September. Shortly afterwards she developed angina pectoris like symptoms. EKG was without pathological signs. In 24h-EKG only a sinus tachycardia showed, when walking slowly (up to 140-160 beats /minute). Echocardiography was without pathological signs as was lab (CRP, troponin, myoglobin, hemoglobin,...). In a cardio-MRI in November a cardiac microvasculatory dysfunction (endothelialitis? small vessel disease?) was diagnosed.
In a blood test, troponin, creatine kinase, creatine kinase-MB, CRP, c-ANCA, p-ANCA, lupus anticoagulant, anti-cardiolipin antibodies... and so on all were negative.
Only antibodies against endothelium could be shown.
Does anybody here have experience with a case like that? At the moment, we think mainly about an autoinflammatory process (e.g. triggered by auto-antibodies). Is there any way to find evidence pro or con?
Why do steroid injections help to relieve pain?
are there any results of the study of coping strategies in adolescents with cancer and rheumatic diseases?
How to differentiate granulomatosis with polyangiitis from microscopic polyangiitis?
Why we do not speak more about focal infections (focalosisi) in ethiopathogenesis of rheumatismus, systemic disease, neuropsychiatric diseases, s.c. "autimmune disease"...
I'm looking for articles about AR and self management tools like ONESELF
It is difficult to differentiate between disease activity and infection in multisystem rheumatic diseases like systemic vasculitis and SLE. I seek the opinion of the experts bout the upcoming biomarkers for the same.
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 ?
We're setting up a study looking at a group of auto-immune/inflammatory/rheumatic diseases that affect women during their reproductive years, and affect the musculoskeletal system (e.g. Rheumatoid Arthritis, Lupus, vasculitis).
I'm wondering what we could call this group of diseases when communicating with patients and the public so that it's clear what we mean? If we describe this as 'arthritis' for example, would women with Lupus or vasculitis identify with this group? Or would auto-immune diseases that affect the joints and muscles make sense?
I'm hoping to talk to some patients about this later in the week, but it would be great to have some ideas to take to them. Any advice from clinicians and researchers working in this area on terminology that we might use would be very welcome.
Can other clinical manifestations of polymyalgia rheumatica be more suggestive for a paraneoplastic syndrome ?
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:
- a positive CCP-titer (or is it just dichotome?)
- earliness of RF seropositivity (how early?)
- 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!)
As the patients do exercises,Can they use drugs less than other patients that they do not exercise???
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.
Please guide me regarding the above question, if possible please give the reference. Regards.
Treatment of young woman with dermatomyositis and has pyoderma gangrenosum
I'm looking for any articles/posters/papers that support this coping trajectories (non in the parents, only in the children/adolescence) in different serious illnesses
In our studies we have found that recency of diagnosis was related to coping strategies used.
Children more recently diagnosed with their chronic disease (0-6 months)
used less cognitive strategies than those children who are in the period
between 1 and 2 years from diagnosis.
We have also found that there are different trajectories between cancer diseases and rheumatic diseases.
e.g., inflammatory, degenerative, metabolic/endocrine...
There is large empirical and observational evidence that medically supervised modified fasting (fasting cure, 200-500 kcal nutritional intake per day) with periods of 7-21 days is efficacious in the treatment of rheumatic diseases, chronic pain syndromes, hypertension, and metabolic syndrome. The beneficial effects of fasting followed by vegetarian diet in rheumatoid arthritis are confirmed by randomized controlled trials. Further beneficial effects of fasting are supported by observational data and abundant evidence from experimental research which found caloric restriction and intermittent fasting being associated with deceleration or prevention of most chronic degenerative and chronic inflammatory diseases. Intermittent fasting may also be useful as an accompanying treatment during chemotherapy of cancer.
does anyone have experience in this area?
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.
I dont understand why i always got higher expression of healthy subject than the patients it self. This time we use autoimmune patients. My control subject ( healthy subject) is always get high expression of M3R elisa. Do you have experience about this M3R Elisa (peptide) ?
We compared it using 7 peptides , we mixed peptide 1-3 than loop1 , loop 2 , loop 3 and negative peptide. but we got control sample was higher than the patient`s.. Can you explain about this?
Kindly tell me how will we measure cost of drug..
Stop therapy or in which circunstances you will continue
I am looking for tools used to measure conflict effect on chronic diseases in general.
DMARDs non responder are considered for biologicals. However this patient can't afford biologicals. Is there any other way to control her disease activity?
Current techniques such as Disease Activity questionnaire are considered to be very out dated and easily affected by the disposition of the subject. Are there other less-known techniques that are used by clinicians and OT's to measure and quantify joint stiffness? These may not be standard techniques used by the NHS.
I am developing a biomarker assay for the detection of aggrecan fragments in patient synovial fluid samples and need to source synovial fluid or at the very least a 'SF like substance' for my standard curve. I am currently only able to compare SF assay results to that of a standard curve in buffer (which needless to say acts considerably differently to SF!)
Citrullin plays a role in the pathogenesis of rheumatoid athritis. But what is the physiological function?
I know a lot of people suffering from rheumatism as a chronic disease; they have started the treatment with non steroidal anti-inflammatory drugs, but the effect does not last for a long time, so they have to be treated all their lives.
Much progress was made to understand better this disease, including immunology and molecular pharmacology studies.
What is the best way to understand the disease of certain subjects and the best strategy to defeat this persistent disease?
Anyone with relevant research experience for discussion?
I am trying to find something interesting about caffeine and rheumatic diseases, because I have to prepare a presentation for other students (I'm in 4th year). All I've found is caffeine/metothrexate/rheumatoidic arthritis. Maybe you can help me?