Rheumatology - Science topic

Here are some papers related to ozone therapy for psoriatic arthritis

https://en.cnki.com.cn/Article_en/CJFDTotal-NMYZ201211044.htm

Vasculitis in considered group of connective tissue disorders that covered in Rheumatology branch

But multiple sclerosis belongs to neurology branch of medicine

Yes this is absolutely necessary for researchers, and I'm surprised Research Gate has designed this field as an autocomplete. There's no way that RG can index all journals - and I notice it even misses some big notable journals in my field that are indexed. @ResearchGate can you change this to a manual input field?

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

Burnout is a major issue.

Kindly see the following RG links and PDF attachment.

According to your risk factors for knee OA proven by existing peer reviewed research in your paper, I should be explaining to my patients that they should:

· Stop aging

· Stop being female

· Stop being obese

· Stop performing work that involves kneeling, squatting or lifting

· Stop performing high intensity exercises such as running over long periods

· Avoid mineralizing their bones too much

How much money, time and debate did it take to arrive at these conclusions?

I suggest that Sackett’s methodology when used to research knee OA is at the top of the error of your ways.

Your suggestion that “Generally speaking, researchers focus their studies on a very specific risk factor” is the pearl inside the shell of your paper. In future studies, it might be worthwhile for them to examine the impact of the interaction of two or more risk factors. A Stochastic Model of research that utilizes a multimodal treatment plan whose components are symbiotic and safe may produce better, more valid and more applicable clinical outcomes.

Theoretically, any methodology that improves overall foot and postural stability, support, strength, symmetry and balance should reduce the existence, progression and life-altering of knee OA (think foot typing).

The knee joint is akin to the transmission of a car in that it has little functional importance of stabilizing or moving the machine as a whole. It simply translates the motions and moments generated from the hips downward and the foot upwards in order to have a more efficient, more productive, less injured biomachine. While it is important for every car to have a well oiled and functional transmission, it is the ability of a car to resist degeneration, deformity and performance issues by dampening and buffering forces generated by the engine and the ability of the tires and chassis to absorb the impact shock of the road and degenerative forces of gravity, friction, etc.

You conclude that “In the future, it could also be useful to do systematic reviews of the effectiveness of care approaches that combine various treatment modalities”. Biomechanically, I have been doing that successfully for decades in real time. Perhaps with your insightful addition to the literature, more of us will consider your suggestions.

I remain available to assist any or all open minded researchers and clinicians in meeting this challenge.

Good fortune to all our knees.

I suggest you try Plos one Journal. They accept the negative results. Good luck!

i am working as assistant professor, department of physiotherapy school of health sciences with career point university, alaniya, kota, rajasthan india . my speciality is neuro physiotherapy. can you please tell me in detail about it we will be pleased to be a part of it.

thanks and regards.

One alternative is the Journal of Middle East and North Africa Sciences

Check it out.

How rare? Did you see one? Is it restricted to some disease under treatment? There is an aphorism about IVIg: "In a desperate situation (usually atypical/uncertain diagnosis), one has not tried everything, if one has not tried IVIg."

So, incidence vs coincidence? Ideas about mechanism?

Here are my concluding remarks on this matter.

1. Trested PMR/TA has a natural history of 1-2 yrs. The typical headaches shoud disappear in the first 1-2 months on Pred and with adequate dosing, they should not recur. The clinical difficulty is how to interpret recurring symptoms after 5-6 months during prednisone tapering. Those are a mixture of mild inflammatory C-spine/shoulder on OA in an elderly polysymptomatic person. Normal acute phase reactants are reassuring but a mild elevation, is problematic as it can be non specific. Trial of NSAIDs (before Pred) are useful and may be enough.

2. NSAIDs are not the primary trestment but can be useful empirically later in recurring PMR-like atypical symptoms.

3. The typical headaches at onset are easy to identify. The 18-month-recurring headaches are more difficult (vide supra) and it becomes the art of personlized medicine to deal with them according to the « primo non nocere » principle.

Best wishes

HM

This depends upon the cause of skin vasculitis. The most common skin vasculitis is small vessel vasculitis of the variety known as leucocytoclastic vasculitis. This can have varying caused ranging from infections, drugs to associated systemic vasculitis with internal organ involvement. The ones related to drugs and infection might be self limiting. The skin vasculitis associated with systemic vasculitis especially medium vessel vasculitis in the form of large ulcers or pyoderma gangrenosum like lesions or cutaneous infarcts need aggressive immunosuppressive therapy

I believe we need more data in a sequential fashion in this patient, as above-stated. Apparently he had culture-proven TB, and a positive ANCA test, ? pattern and specificity. A diagnosis of true idiopathic vasculitis would require a tissue diagnosis regardless of the ANCA test. There are several questions to be answered, as raised by the other authors,

If computer assistance (CAOS) is available, you can operate both knees without removing the nails. If not, I suggest removing the nails. The screws in the right femur may remain in place. The left knee seems easy, but the right knee is a challenge: Take a true anterior-posterior long hip-knee-ankle x-ray with a calibration object on it. Imagine were you can place the intramedullary rod. Measure the distance from the entry point to the point where the rod will abut on the lateral cortex of the femur. Measure the HKFS-angle (hip-knee-intramedullary rod angle). Then ask your supplier or technician to deliver an intramedullary rod that is not too long. Finally, during the operation, set the distal cut at the HKFS-angle you already measured on the x-ray. The rest should be like a standard procedure.

Dear All, 

Let's discuss the clinical utility of liposteroid in the treatment of rheumatic diseases.

Regards,

Hiroyuki Wakiguchi

Usually, severe forms of lupus nephritis, e.g., DPGN would present with an active urine sediment, with the presence of red cell casts, and proteinuria; often, these patients are also hypertensive, and may have an increased serum creatinine. Pure membranous lupus nephritis would present with significant proteinuria and nephrotic syndrome, however, with a normal serum creatinine. Mixed forms like membrano-proliferative lupus nephritis would have nephrotic and nephritic components, and the urine findings would likely be abnormal in most if not all cases. For the precise histopathologic findings, including the latest WHO classification, including electron microscopy, you may want to consult a pathology book, 

Ok Dr. Gonzales, I will

Thanks for your message.

Collagenase D prepared from Clos. histolyticum ihas high collagenase activityand very low tryptic activity. Collagenase 2 has a highLipolytic activity from fat cells

Dear Paul, in mice blood neutrophils are CD31+. After activation and transendothelial migration, neutrophils are CD31-. 

Urine sodium in this patient is ~ 50 mMol/L. In presence of hyponatremia a urine Na of > 20 mMol/L is suggestive of relative excess of volume due to Inappropriate secretion of Antidiuretic hormone or Hypothyroidism, or Glucolorticoid deficiency or Stress.

In this patient hypothyroidism is already present. Stress also may be a factor. SIADH can't be ruled out at the moment.

If it is purely due of sweating (extrarenal losses) Urine Na should be < 20 mMol/L.

Water restriction to < 1 liter per day should correct hyponatremia in this patient. Also, correction of hypothyroidism will be needed.

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 ?   

The 66/68 joint count is not routinely used in the usual disease activity calculators. Unless your patient group has a lot of feet involvement (which would not be picked up in the commonly used DAS28), then the DAS28 should be sufficient. Unlike the DAS28, I think that there are no accepted cutoff levels for assessing disease activity based on the 66/68 counts. If you need to assess more than 28 joints, there is a Ritchie Articular Index (RAI) that counts 44 joints (including some lower limb joints).

Here is a protocol that we use in my lab using the sigma kit and it works quite nice:

1. Carefully wash the cells 2x with PBS to remove loosely adherent cells

2. Add 500µl fixation buffer and incubate for 3 minutes at room temp

3. Wash the cells 2x with PBS

4. Add 500µl TRAP solution and incubate for 5-15 minutes

(Evaluate under the microscope, to avoid over staining. Cells should be violet-brown. Not too pink)

5. Wash again in PBS

6. Add 500µl Glycerin /PBS 1:1 mixture to keep your cell morphology until you are done taking your beautiful pictures

0,625ml citrate

0,2ml 37% PFA

1,625ml Aceton

First mix:

1,8ml dist water

20µl Naphthalon

80µl Acetat

40µl Tartrate

20µl Sodium Nitrite

20µl Fast garnet

Vortex and incubate 2 min at RT

Add the two mixtures together

 Hope this could help...

Trained in both adult and pediatric rheumatology at HSS over 30 years ago and prior to that, having the privilege of working with the late Professor John Baum, gave me the opportunity and challenge of seeing and managing many children with SS.

As you are likely aware, the EBM in this area is minimal, and one is left with predominantly n of 1 trials.  Certainly, there is no strong data that anyone pharmacological approach works best for all the manifestations of PSS.

Whether the predominant clinical issue is impending ischemia from severe Raynauds, encasement of fibrosing cutaneous involvement, ILD, pulmonary hypertension, microangiopathic anemia, ARF, cardiac involvement or GI involvement - any of these individually or in combination requires empiric therapy and individualized clinical judgement , in my humble opinion, as EBM alone is inadequate to algorithmically address these medical issues or the psychosocial and nutritional issues that are concurrent and important co-morbidities.  Other than the Up To Date Resource available via many Health Science Library licenses or personal subscription, the best (and freely available summary on all classes of interventions is via Medscape's formerly emedicine link I provide you below, I hope you find it useful for your specific needs as a starting point. 

Best!

Alan

I helped develop certolizumab.  The risk of transfer of this pegylated product is low.  Of course avoiding drugs in pregnancy as other have suggested makes sense.  Use depends on how difficult a patient is to manage, i.e. what are the tradeoffs.  You should know that there are OB/GYN doctors who use anti-TNFs as an aid to maintaining risky pregnancies, i.e. risk of spontaneous abortion.  This is not a labeling that any company is likely to pursue, not will anyone likely try to quantify the risks other than as noted by surveillance data.  Reason: even one bad pregnancy outcome will likely lead to a large lawsuit.  Good questions, great answers, good luck with your patient(s).

It is uncommon, but it can happen to have a negative ANA screen and a positive dsDNA specific test.  The main factor that can give this results is: "The Method used for the ANA screening test". Due to newer methods available, the gold standard method (IFA) is being replaced by some labs to other methods that have lower sensitivity but higher throughput. This has become an important point of discussion for some time. 

ANA test is a screening test and is performed by different methods in different laboratories. Some methods are more sensitive (like ANA using HEP2 cells by IFA "the gold standard", but higher false positive rate) and others are less sensitive (but lower false positive rate): ELISA with only a few selected antigens or Multiplex Bead immunoassay testing only 12 different antigens which are either recombinant, native bovine-derived or synthetic (such as dsDNA).

The explanation for your question goes back to you:

What method is being used for ANA screening? that should give you the most likely answer to your question.

ANCA positivity can be seen in SLE patients, 10-20 percent incidence, including our own clinical experience. A positive ANCA can also be drug-induced, as can be antiphospholipid antibodies. A positive ANA by itself is rather non-specific, and can be seen in an number of conditions, including seemingly not autoimmune entities, e.g., IPF, sickle cell disease, etc, 

The answer to the question posed in Sahin's title, "Which statin should be used together with colchicine?" [1] is probably "None, if possible" [2]. Suspected drug-drug interactions with colchicine have been reported with different statins [e.g. 3-8], and there is too little information on which to base firm conclusions. The mechanism is not clear, but it is likely to be primarily pharmacodynamic, since colchicine is myopathic [9]; pharmacokinetic mechanisms will add complications in some cases [10].

If colchicine is used to treat acute gout, the statin can be withdrawn until the acute phase has resolved. There are other therapeutic alternatives to colchicine for long-term therapy of hyperuricaemia in patients taking statins.

If colchicine has to be used, e.g. in patients with familial Mediterranean fever, an alternative lipid-modifying agent could be chosen, but use of the lowest possible dose of colchicine and careful monitoring would in any case always be wise [11].

References

1. Sahin G, Korkmaz C, Yalcin AU.  Which statin should be used together with colchicine? Clinical experience in three patients with nephrotic syndrome due to AA type amyloidosis. Rheumatol Int 2008; 28(3): 289-91.

2. Boonmuang P, Nathisuwan S, Chaiyakunapruk N, Suwankesawong W, Pokhagul P, Teerawattanapong N, Supsongserm P. Characterization of Statin-Associated Myopathy Case Reports in Thailand Using the Health Product Vigilance Center Database. Drug Saf 2013 Apr 25. [Epub ahead of print]

3. Hsu WC, Chen WH, Chang MT, Chiu HC. Colchicine-induced acute myopathy in a patient with concomitant use of simvastatin. Clin Neuropharmacol 2002; 25: 266-8.

4. Phanish MK, Krishnamurthy S, Bloodworth LL. Colchicine-induced rhabdomyolysis. Am J Med 2003; 114: 166-7. [atorvastatin]

5. Atasoyu EM, Evrenkaya TR, Solmazgul E. Possible colchicine rhabdomyolysis in a fluvastatin-treated patient. Ann Pharmacother 2005; 39: 1368-9.

6. Alayli G, Cengiz K, Cantürk F, Durmus D, Akyol Y, Menekse EB. Acute myopathy in a patient with concomitant use of pravastatin and colchicine. Ann Pharmacother 2005; 39: 1358-61.

7. Torgovnick J, Sethi N, Arsura E. Colchicine and HMG Co-A reductase inhibitors induced myopathy—a case report. Neurotoxicology 2006; 27(6): 1126-7. [lovastatin]

8. Tufan A, Dede DS, Cavus S, Altintas ND, Iskit AB, Topeli A. Rhabdomyolysis in a patient treated with colchicine and atorvastatin. Ann Pharmacother 2006; 40(7-8): 1466-9.

9. Altman A, Szyper-Kravitz M, Shoenfeld Y. Colchicine-induced rhabdomyolysis. Clin Rheumatol 2007; 26(12): 2197-9.

10. Davis MW, Wason S. Effect of steady-state atorvastatin on the pharmacokinetics of a single dose of colchicine in healthy adults under fasted conditions. Clin Drug Investig 2014; 34(4): 259-67.

11. Anonymous. Colchicine: serious interactions. Prescrire Int 2008; 17(96): 151-3.

 1. Effect on the inflammatory activity of the disease and the radiologic damage:

A few studies have shown that there is a deleterious effect of smoking in AS:

Smokers have more active disease and further damage on the axial skeleton in AS.

 2. Effect on the lungs:

There already is a restrictive lung disease in AS due to limited chest expansion (secondary to arthritis of the costo-vertebral joints ).

Also, occasionally, there is lung fibrosis, mostly in the apices, causing restrictive disease.

 Smoking adds insult to injury here by causing obstructive lung disease.

I would use CellCept and low dose prednisone for SLE-like symptoms. There is no good data on scleroderma-like symptoms. CellCept and MTX could be considered.

 Thank you very much for your help, Ariana.

I am not aware of any reason to think this. Indeed there is no reason to think that micro-organisms have much to do with autoimmunity. I think one might as well ask if there is any reason to think RA is due to eating bananas. Unfortunately pseudoscience and gossip plays a large part in immunological theory even within high profile journals these days!

I do not think that RA directly causes cardiomyopathy.

We observe that many cases of headache in fibromyalgia patients are caused by the presence of tender points in the fascial region, particularly in cheek, orbital, and occipital region. These tender points often mimic "true" migraine pain. In such cases medical massage performer by experienced in fibromyalgia physiotherapist may markedly improve symptoms. In our opinion in the localization of tender points thermography can be helpful, as it indicates "cold regions". Complementary measures include: cold avoidance and warm (sometimes sleeping in cap may be helpful).

Diagnosing RA includes the following-

a. Clinical - synovitis of the small joints of hand and feet associated with morning stiffness b. Rheumatoid factor and/or Anti CCP positivity c. radiology which shows joint space narrowing and later erosions d. esr and crp are usually positive.titres of these tests are important. no other cause to explain the symptoms especially if tests are negative.

however clinical suspicion and examination is the  most important as 'sero negative' RA is a well known entity.

cuida espalda - spanish  publication

Good question which I can't answer.  However, if you are screening by qPCR, make sure the primers for RSpondin 1,2,3 are good.  See Kabiri Z from Virshup DM (Stroma provides an intestinal stem cell niche in the absence of epithelial Wnts.  Development 2014, 141:2206-2215, doi: 10.1242/dev.104976

Other than the standard DAS 28 OR 66/68 joint counts, the only other assessment types I have come across are ultrasound imaging based. This is currently in development as it takes out the objective nature of the joint assessment and assessors.

Fibromyalgia is very interesting syndrome because treating it combines several knowledge areas such as pain perception physiology and physiopathology, stress response physiology and disorders, emotional aspects of chronic pain, depression and anxiety as comorbitidies, and others. This is a challenge for a good clinician. I am a rheumatologist but I think this syndrome is defying a complete doctor. Fibromyalgia is teaching us to be "doctors" again. 

Approximately half of patients with RA have anti-CCPseveral years before the onset of symptoms and can be detected in about 0.6% of population. In other autoimmune diseases and infections can be also be detected (Nielsen MMJ. Arthritis Rheum 2004;50:380-386)):

• Palindromic rheumatism (Salvador G. Rheumatology 2003;42:972): 56%

• Psoriatic arthritis (Bogliolo L. J Rheumatol 2005:32:511): 12%

• Primary Sjögren syndrome (Gottenberg J. Ann Rheum Dis 2005:64:114): 9%

• JIA polyiarticular (Kasapcopur Ö. Ann Rheum Dis 2005:63:1687): 6%

• SLE (Hoffman IEA. Ann Rheum Dis 2005;64:330): 5%

• Spondiloarthritis (Salvador G. Rheumatology 2003;42:972): 3%

• Hepatitis C (Lienesch D. J Rheumatol 2005;32:489): 2%

In all of this, the most important point remains to identify the reliable autoantigen. one of the modified ways would be to make two aliquots of polyclonal antibody fractions of patient sera; one having only IgG fraction purified by using protein G column and other aliquot should essentially contain all the antibody types accept IgG ( left-out of IgG minus sera). This step increases the chances of specific hit while performing SERPA or MApping. 2nd step should be to equilize the dilution factor while before probing the tissue/cell lysares with (above) purified polyclonal ab fractions. This can be done by checking the conc. of IgG and IgM ( two of the most relevant auto-ab) and accordingly set up the dilution factor, that ideally varies from patient to patient.  All the Best

Determining uric acid level in acute gouty arthritis does not add any information about decision-making. Amdiminister the treatment according to your protocol.

I guess treating the cells with 5% horse serum (in DMEM plus antibiotics) for 5-7 days will promote for differentiation. Also, try by treating with BMP2 (50ng/mL).

Dear Christan,

Good question. Exercises on OA knee has been performing form many decades and it has built strong positive evidence. As you are going to talk in front of experts I would suggest to prepare the material/ slides using recent guidelines/ position statements/ review etc. Below is some of the recent guidelines on Exercise and OA Knee. Hope this will serve the purpose...

1.http://updates.pain-topics.org/2013/06/new-guidelines-for-treating-knee.html

2.http://www.oarsi.org/sites/default/files/docs/2014/non_surgical_treatment_of_knee_oa_march_2014.pdf

3. http://www.guideline.gov/content.aspx?id=46946

4. http://www.bmj.com/content/347/bmj.f5555

5. http://www.hindawi.com/journals/ijcd/2013/845015/

6. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3830983/

Many more recent publication are also there but couldn't attached all of them...

Regards

Maybe this is helpful:

Diffuse idiopathic skeletal hyperostosis (DISH): Forestier's disease with extraspinal manifestations.

Resnick D, Shaul SR, Robins JM

Radiology. 1975 Jun; 115(3):513-24.

The point Kourosh makes with regard to pain is something I think is incredibly valid as patients do not feel HPs are really taking into account the individual needs if they have failed to help alleviate pain and provide guidance, support to achieving effective pain relief . We may know that ultimately DMARDs should improve pain ref lief but a) we fail to explain this to the patient and b) the patient needs something that will relieve their pain promptly. It is the major factor that caused them to seek a medical opinion. We must do better if we are to work with the patient to achieve their ultimate aims.

The study to be done would be in research subjects with no RA (yet), who are HLA-DR positive for the shared epitope, who are also anti-CCP positive, and without clinical symptoms as of study entry. I suppose such groups could be divided in smokers and non-smokers, and then followed in a prospective manner, one group pre-treated with a relatively benign agent, say hydroychloroquine (HCQ), and the other group just observed over time. Such a study will require a large population to be screened first, perhaps people with a family history of RA. Incidentally, HCQ has been documentd to prevent diabetes in RA patients, and also to prevent flare-ups of lupus, and progression of disease. So, to a point, HCQ could be considered a "prophylactic agent" for autoimmune diosrders.

Here comes one more article on the subject

Temporary splinting in RA is advisable for joint rest and relieving of pain but permanent splint is contraindicated to avoid more stiffness and deformities. Functional splinting can be designed with helping of occupational therapy. And

Whatever the type of splinting you are using a pain free range of motion exercise programs should be applied.

Sorry for the late answer

AS you know:

Positivity for RF is a marker for a more serious and more erosive disease. It is also true with anti-CCP. But anti-CCP and RF do not correlate well with activity. A possible explanation that anti-CCP do not correlate with activity is that anti-CCP is designed to be a very a specific diagnostic test. Anti-CCP is either negative or positive in high titers ( usually).

Another ACPA is the leser known anti-MCV test that seems to correlate with DAS and radiologic damage as well. Anti-MCV titers are distributed more homogenously (from low to very high titers) and are better suited than anti-CCP to measure disease activity. Treatment with infliximab has resulted to decreased anti-MCV titers.

You can find under my profile either a pre or post-print of the article published in clinical experimental Rheumatology.

I wish you and your family a happy new year.

The problem with ESR as discussed by others is a lack of specificity. While selected uses can be defended as a disease marker in selected patients with autoimmune disorders followed by one assay platform type, most of the reported clinical uses of ESR as a disease screening tool are better performed by other assays, such as CRP and more recently biomarkers in infection/sepsis such as procalcitonin, neutrophil CD64, soluble CD163, cell free DNA plasma levels, TREM-1, IL-6, and others.

I have attached the International Council for Standardization in Haematology (ICSH) guideline publication for ESR, which some may find useful.

Thank You very much for the asnwer :)

Dear Ms. Rahmi,

Yes. It is possible to estimate the cytokines in synovial fluid. But the major challenge is the collection of synovial fluid from rodent joints. In human, we can collect around 2-3ml per joint in a single time. But in case of laboratory animals, it will be around <0.5-1mL. During my rheumatoid arthritis experiment, I have tried to collect the synovial fluid (I got around <5mL), which was not sufficient to do numbers of cytokine estimation. While collecting synovial fluid some other things also used to come along with it. Which develops a bias of actual fluid. Hence, I have preferred plasma/serum of arthritis animals for all cytokine estimation. I can suggest you for blood plasma or serum of the rodents for cytokine estimation.

Thank you for those valuable answers.

don't forget CRP, which in LES flair does not increase much; if it's infection, it will increase. But I think that BAL safely helps you to rule out infection (y compris tuberculosis).

Very basic question; u need to have drugs specifically targetting and not non specific to be effective.

How do you assume that this is vasculitis? Is there any histology proof? It looks superficial. Dermographism? It doesn't really follow any particular anatomic structure. What does your patient study? Could be patient-induced and how is her mental status? Blood coagulation tests? Illicit-drug use?

Dear David ,This career so interesting ,include autoimmune diseases like Rheumatoid arthritis,SLE,systemic sclerosis ,....also inflammatory muscle disease,sero negative ,osteoprosis,osteoarthritis....,I will add case study and this will help you .