Science topics: MedicineInternal MedicineRheumatology
Rheumatology - Science topic
Rheumatology is a rheumatoid arthritis.osteoarthritis,osteoprosis.gout.seronegative
Questions related to Rheumatology
I cannot find any scientific literature about the role of ozone therapy for treating psoriatic arthritis. Can anyone suggest me a bunch of papers on this topic?
Catina Feresin (PhD Experimental Psychology)
Under which disorder category we can put Vasculitis : is it CVS or Rheumatological disorders ?
and Multiple Sclerosis is it Rheumatological or Neurological disorder ?
I can not add the Journal name to my article in my account. The journal name is (Mediterranean Journal of Rheumatology).
How can I do this?
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!
Overwhelmed by a combination of time-consuming administrative work, restricted autonomy and a loss of community, all of which have contributed to burnout throughout the specialty, according to Paula Marchetta, MD, MBA, president of the American College of Rheumatology. One observation was the simple disappearance of the doctors’ lounge in many hospitals.
Do statins have useful roles in rheumatology especially in rheumatoid arthritis?
Osteoarthritis is the second most common rheumatologic problem and it is the most frequent joint disease with a prevalence of 22% to 39% in India. OA is more common in women than men, but the prevalence increases dramatically with age.
As we all Know that Medicine get better, Technology get better, Diagnosis tool get better, Physiotherapy Prevention and management get better still the prevalence increases year by year..........
Thats mean all this get fail for reducing the prevalence of Knee OA among world.
What are the reasons for this?
Now I am doing my study but unfortunately my result is a negative or no any change from baseline in rheumatologic field. However, my study is an experimental study, last studies were only cross-sectional study but I did not believe their concepts. So, I developed my trail to reject their concepts. Please members in research gate suggest me. As when I will choose yo submit, it is very difficult to accept in many journal
Dear collagues from all over the world,
As Izmir Katip Çelebi University, Physiotherapy and Rehabilitation Department, we are looking for ERASMUS+ partners (both for student exchange and researcher exchange). Our university is in West Turkey and our memebers mostly work in the fields of sports physiotherapy, aquatherapy exercises, rheumatologic rehabilitation and multiple sclerosis rehabilitaton. If you/your institute are interested with a collaboration, please feel free to contact with me for more details.
Thank you for your time and consideration.
I need to find a publisher in Rheumatology case reports
Nowadays IVIG is prescribed in many rheumatologic and immunologic diseases like GBS and SLE. In some texts, aseptic meningitis is one of the rare side effect of IVIG... I want to collect some new related case reports... who can help me?
Can headache caused by temporal arteritis be relieved by NSAIDS and analgesics? How long does an episode last? How can someone differentiate between temporal arteritis associated headache and other types of headaches?
Any paper or help that can assist with predicting the life course of primary vasculitis of the skin if left untreated ?
Is presence of ANCA positivity in pulmonary tuberculous patient an indication for concomitant steroid therapy?
Gives h/o bilateral K-nailing for femoral shaft #s in 1988 (asymptomatic now) and Right patellectomy for comminuted patellar # subsequently in 1997.
Liposteroid (dexamethasone palmitate), a lipid emulsion containing dexamethasone, was developed in Japan.
This agent poses greater efficacy and much less risk for systemic adverse effects than dexamethasone sodium phosphate, because the lipid emulsion is easily taken up by phagocytes, and retained in macrophages.
The article of liposteroid was firstly presented in 1982 (1).
Lliposteroid therapy has been used to treat rheumatoid arthritis in Japan.
Recently, Japanese researchers reported the clinical utility of liposteroid in the treatment of diseases associated with macrophage activation (2-6).
On the other hand, only the three countries outside of Japan currently have the marketing approval: Germany, Korea, and China.
I would like to know the efficacy and side effects of liposteroid therapy in various rheumatic diseases worldwide.
1. Mizushima Y, et al. Tissue distribution and anti-inflammatory activity of corticosteroids incorporated in lipid emulsion. Ann Rheum Dis. 1982;41:263-7.
2. Doi T, et al. Long-term liposteroid therapy for idiopathic pulmonary hemosiderosis. Eur J Pediatr. 2013;172:1475-81.
3. Nishiwaki S, et al. Dexamethasone palmitate ameliorates macrophages-rich graft-versus-host disease by inhibiting macrophage functions. PLoS One. 2014;9:e96252.
4. Wakiguchi H, et al. Successful control of juvenile dermatomyositis-associated macrophage activation syndrome and interstitial pneumonia: distinct kinetics of interleukin-6 and -18 levels. Pediatr Rheumatol. 2015;13:49.
5. Nakagishi Y, et al. Successful therapy of macrophage activation syndrome with dexamethasone palmitate. Mod Rheumatol. 2016;26:617-20.
6. Otsubo K, et al. Hemophagocytic lymphohistiocytosis caused by systemic herpes simplex virus type 1 infection: Successful treatment with dexamethasone palmitate. Pediatr Int. 2016;58:390-3.
Lupus nephritis may present with abnormal urinary findings (overt lupus nephritis) or be apparent only upon renal biopsy (silent lupus nephritis).
I would like to know the pathophysiology of silent lupus nephritis, especially, the reason why it has pathological findings of immune complex-mediated glomerulonephritis but does not have abnormal urinalysis findings of proteinuria and hematuria.
Any suggestions will be greatly appreciated.
A 20 y.o male, his height was about 190 cm, positive of wrist and thumb sign, kyphosis, and arachnoidactili. He also had chronic liver disease. ANA test and rheumathoid factor was negative, but anti-dsDNA was positive. What is autoimmune disorder which is possible in this patient?
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 ?
What is the difference between collagenase D and collagenase II? Does anyone know the optimal collagenase for digestion of human cartilage?
I am doing flow cytometry and would like to verify whether the neutrophil influx I am seeing in my sample is from neutrophils within the tissue or from the increased blood present in the inflamed sample. I can check by histology but ideally I was hoping for a flow cytometry method to differentiate. Thank you!
He has hypothyroidism, diabetes, and hypertension. Last summer he was admitted to the ICU for severe hyponatremia (after a 4 day period of febrile illness). Several investigations we done, no specific cause was found (no infection, no malignancies and no adrenal insufficiency). It was decided it was caused by malnutrition and colonic irrigation that was done 4 days in a row.
This summer he has been complaining of fatigue for 4 days associated with worsened back pain. Routine investigations were done, including electrolytes. His Na is 132 mEq/L.
The patient complains frequently that he feels cold. He is always overdressed. The past few days have been extremely hot, temperatures ranged between (33-36C). According to his family he has been overdressed, and covers himself with heavy blankets. The bed and blankets are wet with sweat. He almost drinks 2.5L of water daily.
*40 days ago his Na level was 134 mEq/L, his water intake was restricted and his Na levels became within normal range within a few days.
*His antihypertensive medication has no diuretic. He has a sessile colonic polyp discovered almost a year ago.
Could his hyponatremia possibly be caused by excessive sweating and high water intake? (Mimicking Exercise-Associated hyponatremia in athletes).
Can other clinical manifestations of polymyalgia rheumatica be more suggestive for a paraneoplastic syndrome ?
I'm planning to set-up an in-vitro osteoclastogenesis assay from mouse bone marrow culture, followed by TRAP staining. Could someone share a detailed, working protocol for that? Any suggestions for suppliers of RANKL and MCSF are also appreciated. Thanks.
Is it safe to use anti-TNF during pregnancy or lactation?
I mean while diagnosing my case ?
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.
According to one of Garin Sahip's studies, Rheumatology International 28(3):289-91 · January 2008, the safest combination of Colchicine is with Simvastatin.
My question is: does anybody have any life-experience to confirm this?
Effect of smoking on disease activity and patients functions in ankylosing spondylitis patients
I would like to know what is the appropriate immunosuppressive drug for treatment of pediatric mixed connective tissue disease (MCTD).
I already know the following articles.
1. Tiddens HA, et al. J Pediatr 1993.
2. Nakata S, et al. Nihon Rinsho Meneki Gakkai Kaishi 1997.
3. Mier RJ, et al. Rheum Dis Clin North Am 2005.
By the way, our patient with pediatric MCTD has arthritis, and myositis-like symptoms are main.
I believe that administration of methotrexate may be the appropriate treatment for our case.
Any suggestions will be greatly appreciated.
We are currently performing primary osteoblasts cultures obtained from human trabecullar bone. Although we have not problems to isolate them, it has been described that phenotype reversion occurs after several culture passages. Given that we need sufficient amount of these cells for protein extraction and other studies my question is: How can we supplement the medium to grant the maintenance of osteoblast phenotype during a reasonable time period?
Alternative medical practitioners love to make this claim, as seen in many YouTube videos.
We have a patient who was diagnosed for rheumatoid arthritis (anti-ccp antibodies positive). At the same time patient’s echocardiography revealed dilated cardiomyopathy and initially he was considered for cardioverter-defibrillator implantation. Meanwhile we started our treatment with methotrexate and low-dose glucocorticoids. And now after treatment in control echocardiography cardiomyopathy is not observed. Is it possible that it was only extraarticular manifestation of rheumatoid arthritis?
Young woman with fibromyalgia syndrome presented with significant postural hypotension and severe intractable headache and anxiety.
I need this questionnaire for investigate the low back pain in adolescents. Please send me suggestions for a reliable questionnaire.
I plan to evaluate the expression of Wnt signaling extracellular modulators in FLS of patients with inflammatory joint disease
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.
As a general practitionner mostly, and holding a vacation in a pain unit in hospital, I frequently ask myself which is the impact of telling to a patient "you have fribomyalgia" on further care, knowing that there is no specific treatment for this syndrome about which we have no proof of a specific disease reality.
I found only one study on Pubmed :http://www.ncbi.nlm.nih.gov/pubmed/12115155?log$=activity
One of our student want to make his end of studies research on this theme, but we don't have the capacity of making a cohort. We are searching if there is a study design that would allows us to help to answer this question, may be somebody here has an idea ?
What is your experience with anti-CCP in other diseases besides rheumatoid arthritis?
Is there any method to distinguish auto antibodies from non-auto antibodies. Please answer with reference to some specific peptide sequence defined by commercial kits.
A lot of patients with a history of gout disease have a normal lab in acute attack . What should we do?
I am going to grow mouse BMSCs in-vitro and I want to differentiate them into osteoclasts. I am very new to this so I have been looking around for various protocols and publications for this kind of assay and I have found a good one that suggests alpha-MEM (with 10%FBS) + MCSF (50ng/ml) + RANKL (50ng/ml). Now I am looking for suppliers of alpha-MEM like sigma and Gibco but they have so many varieties that I am confused which one should be ordered. They have alpha-MEM with and without L-glutamine, also with and without ribonucleosides and nucleosides. Can someone mention what these elements are required for the assay and which one should fit my needs?
I am giving a lecture to a audience of sports physicians, physiotherapists and physical trainers on the topic.
I'm looking for a system to score the severity and extension of DISH radiologically.
I only found Mata's et al. score, which I find is confusing.
Does anyone have experience with Mata's scoring system for DISH or use another scoring system to radiologically compare the severity of patients diagnosed with DISH?
Mata S and her colleagues (1998) developed a scoring system for DISH. They described the morphology of the ossified mass and obtained measurements. The Morphological description includes: Ossified anterior longitudinal ligament without osteophytes or with non-bridging / bridging osteophytes with scores of: 1, 2 and 3 points respectively. Score 4 was described for bridging osteophytes larger than 10 mm?!
The article describes that the measurements are taken twice at the superior and inferior end plates of opposing vertebrae at each disc level.
I have these queries:
1. It is not clear if one score will be given for each disc level (averaging the measurements at the opposing upper and lower vertebral end plates), or if each vertebra is given a score by adding the measurements of its upper and lower end-plates.
2. The grading of Mata's scoring of DISH is not clear. what are the scores of mild or severe DISH?
3. Is Mata's system used also for diagnosis?
4. I found very few studies in the literature that used Mata's score. However, the impact of using the scoring system was not clear.
5. Is there another scoring system or method to describe and compare severity of DISH using mainly radiographic criteria not clinical?
(Mata S, Chhem RK, Fortin PR, Joseph L, Esdaile JM. Comprehensive radiographic evaluation of diffuse idiopathic skeletal hyperostosis: development and interrater reliability of a scoring system. Semin Arthritis Rheum 1998:28:88-96)
We used the adherence 8-items morisky medication adherence scale (a validated Arabic version) to assess the medication, and we found that 90% of all rheumatoid arthritis participants (126) were medium to non adherent!
What are the possible causes of non-adherence? What can we do to improve the adherence to medication in both RA patients and other patients?
RA has a preclinical phase of disease development. Seropositive and seronegative RA have significant differences in genetic and environmental risk factors. Is it possible to predict who will get RA? Is it possible to prevent Rheumatoid Arthritis?
CV disease is the leading cause of mortality in these diseases, CAN occurs in these diseases (though often not recognised) & CAN is a significant risk predictor for sudden cardiac death.
Considering using taping to correct ulnar deviation in a patient where the bulkiness of conventional UD splints prevents their use
Whether the estimation of C-reactive protein is enough to predict inflammation and its intensity. What's the role of Anti CCP or RF. Is there any correlation between these three?
ESR is usually elevated in chronic inflammatory conditions like autoimmune disease. Sometimes it is elevated with no obvious cause.
Does anyone know if there is a relationship between ankylosing spondylitis and chronic prostatitis? How often does non-bacterial chronic prostatitis occur in AS? Is it more often in when compared to RA patients or patients without rheumatic disease? If yes, what is the reason of that?
My research is about gouty arthritis. So I want to evaluate the anti-inflammatory and anti-hyperuricemic activity of some medicinal plants: An in vitro and in vivo. Initially, I thought that I'll do evaluation of inflammatory mediators using the blood of an animal. Lately, I think it will be better if I use synovial fluid that represents the gouty arthritis. But, I am not sure if I can collect enough synovial fluid for what I would need to conduct this research. Could anybody explain and help me for this problem of mine?
Is there a consensual quantitative or qualitative definition? Where is the treeshold between a normal vertebral height and a limited loss of height?
How can we differentiate acute SLE pneumonitis from infectious pneumonia in a SLE patient if lavage fluid is negative for microbiology before starting methylprednisolone therapy?
Why all drugs are monoclonal antibodies and not polyclonal antibodies?
Are there polyclonal antibodies?
What is the difference between monoclonal and polyclonal antibodies?
She suffered from intermittent episodes of this unknown vasculitis for 3 years. ANA(-), Anti-dsDNA(-), anti-phosholipid Ab (-), C3, C4: normal; RA factor(-)
I just joined research-gate in the course of researching for a case report that I am writing. I am a 4th yr med student interested in a career in rheumatology. Will begin my rotation next month. Till then, any advice regarding the field, or application for fellowships?