Rheumatic Diseases - Science topic

Have a look at this useful link.

Thank you for your answers!

I don't have experience with a case like this, but it seems plausible that they could be related with this manifestation. I suggest the following literature:

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- https://www.thelancet.com/action/showPdf?pii=S2352-3964%2820%2930558-2

Best regards

Vitamin D3 is not a vitamin at all, it is actually a POWERFUL  seco-steroid hormone that is involved in bone and joint and tissue remodeling, as well as immune system modulation. It alters the expression of 2,000+ of your genes. If you are low in Vitamin D3, your immune system will be out of focus  and may accidentally attack good tissues (autoimmune disease) or ignore bad actors or defective cells  (infections from bacteria, fungi or viruses,  and cancer cells). Now you might not know this but when tissues need to be repaired in your body, quite often there is a lot of destruction and then rebuilding going on. And the repair mechanisms in your body  borrow many of the components  of your immune system to tear down tissue that needs to be remodeled (macrophages for example). Having low levels of Vitamin D3  can lead to an impaired healing process in addition to immune system problems. This impaired healing process is what causes plantar fasciitis to become a chronic ailment that can last  for many years , even decades. There  are various self reports of people who have cured their plantar fasciitis  simply, quickly, and for a cost of next to nothing by simply  boosting their Vitamin D3 levels including myself.

To make the heel spurs disappear

First Set of Required Nutrients:

Other deficient nutrients that adding will help foot pain:

Vitamin B-1 Deficiency

Scientists discovered vitamin B-1, or thiamine, first. Along with the other B vitamins, it's water-soluble, meaning it isn't stored by your body and is excreted with your urine. You need vitamin B-1 to help digest carbohydrates, use fats and proteins, manufacture red blood cells and assist the proper functioning of your immune and nervous systems. Alcoholics and the elderly are prone to deficiency of vitamin B-1, resulting in beriberi, a disease causing weakness, fatigue, an enlarged heart and confusion. It also causes edema, burning, tingling and stabbing pain in your feet and lower legs.

Vitamin B-12 Deficiency

Vitamin B-12 has the most complex chemical structure of all the B vitamins and the only one that contains the metal cobalt, according to Oregon State University. Vitamin B-12 is an integral part of DNA and enzyme synthesis, nervous system functions and red blood cell production. Unlike the other B vitamins, vitamin B-12 is stored in your liver. Deficiency of vitamin B-12 is prevalent in the Vegetarians and elderly and sometimes results in a condition called pernicious anemia. The symptoms of a vitamin B-12 deficiency include poor appetite, sore tongue, memory loss and dementia, along with difficulty walking and painful tingling sensations and numbness in your feet.

Deficiency of Biotin

Although it's classified in the B vitamin family, AltMD states biotin is actually a coenzyme that works along with the B vitamins. You get biotin through your diet. You need biotin for the synthesis of fatty acids, to build protein from amino acids and obtain energy from the breakdown of carbohydrates. It also helps maintain the health of your nerves, skin, hair and nails. Biotin deficiency causes fatigue, grayish skin color, skin rashes and problems with digestion. It also causes your skin to become painfully sensitive to touch with tingling in your feet and hands.

Dear, if you search with the topics you will get them.

The clinical picture and ANCA pattern may help....

Yes!

follow Peter J. Schulz, he was the project leader. Also check out the publications with data from the project he co-authored with Luca Camerini, Maria Caiata, Zlatina Kostova, Ahmad Allam.

Hello Sir. Assessing expression of CD64 on neutrophils (inducible during infection, vs constitutive expression on monocytes and macrophages) by flow cytometry seems to hold much promise and was presented as an oral paper at the ACR in 2016 in a work from Prof Vikas Agarwal's group. Regards,

 Durga

Thanks for your message.

I agree with Hans that you will muddle your clinical waters if you include conditions such as fibromyalgia, chronic fatigue, etc.  The more specific the group you look at, the fewer outliers.  The best of luck.

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 ?   

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.

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).

Dear Shubhankar

I agree with Dr Edwards...

The duration of arthritis for diagnosis is set at SIX weeks essentially to rule out  infective and post infective (reactive) arthritis. 

One can definitely make a diagnosis of JIA before 6 weeks - in the instance of systemic onset JIA where the diagnostic criteria mentions only 2 weeks of daily temperature spikes (not 6 weeks).

In other subtypes of JIA, one may be able to diagnose earlier (4-5 wks) in some instances going by factors like the pattern of arthritis or associations - for example, if you have extensive polyarthritis affecting multiple small joints or when there is associated psoriasis, in which cases any other pathology is less likely. We have started definitive therapy by 4-5 weeks in some such scenarios. In any case they could be commenced on a rheumatological dose of NSAIDs at the first review which should afford some relief.

The problem most often arises in oligoarthritis affecting large joints especially monoarthritis, in which case waiting for six weeks is unlikely to cause long term damage of joints. They too should be commenced on NSAIDs at the earliest.

In most situations, this period could be used for investigations to rule out alternate pathology like ASO titre, Lyme serology etc, as indicated.

Regards

Kishore.

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.

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, 

Dear Chetan,

please go through this link. 

http://www.ors.org/Transactions/61/0081.pdf. 

here the dose mentioned is 150 microgram.

This might be useful for your research study.

Cyclosporine seems to be helpful. I've also used infliximab successfully. I've used tocilizumab- without success in 1 case.

Thank you all for the contributions,

Alessandro

As Johannes has noted, the ACR has classification systems for inflammatory and non-inflammatory diseases. I guess my question to you would be what is the intellectual purpose or focus of your curiosity. There are primarily inflammatory diseases and then primary non-inflammatory diseases, but then, as you suggest, the multiplicity of pathologies would make for a very difficult categorization system.

Thank you for correcting me:  BMI is indeed Body Mass Index.  Those two  studies provide  results corresponding to daily clinical experience confirming the added burden of obesity on RA.  I will read them again but I do not recall that they help us evaluate the effect of fasting per se which is the issue here.  That being said, I need to do some exercise and work on my own BMI.  Best wishes.

My protocol includes injection of a fine suspension (not a solution) 500 µg/25µL/paw Sigma Zimosan in saline. Homogenize carefully between animals.

The ELISA you use may not be sensitive enough to detect accurately M3R in blood (what fraction do you use?). What you call high expression relative to values for the patients may still  be close to the lower detection limit (do you have a standard curve to refer to?). I have never used these particular ELISA but I know that some other commercial  ELISA do not always work well when used with patients' samples. The following reference may help you: Ann Rheum Dis 2011;70:235-236 doi:10.1136/ard.2010.129049

There is no "best" method for cost-effectiveness, because different jurisdictions consider use different methodologies acceptable. For instance, NICE (www.nice.nhs.uk) uses cost/utility analysis, ie cost per QUALY, whereas IQWIG in Germany does not. A good starting point is the ISPOR website (www.ISPOR.org), which has an overview of the pharmacoeconomic guidelines published by different countries. There is a whole body of literature devoted to this, as there is a lot of money involved.

Some investigators have suggested that TNF-α antagonists do not need to be discontinued if the patient has isolated induction of autoantibodies without any clinical manifestations of lupus (Ramos-Casals, Brito-Zeron etal. 2007; Kerbleski and Gottlieb 2009). In another study, 4 of 5 patients tolerated an alternative TNF inhibitor (adalimumabfor 3 patients, etanercept for 1) without recurrence of ATIL after discontinuation of infliximab (Wetter and Davis 2009).In any case, your position favors the security  in the present real world. We will see in the future. Thanks !

Dear Nour,

Check these papers out:

Using Insights From Behavioral Economics and Social Psychology to Help Patients Manage Chronic Diseases. Braden K. Mogler, Suzanne B. Shu, Craig R. Fox, Noah J. Goldstein, Ronald G. Victor, José J. Escarce, Martin F. Shapiro

J Gen Intern Med. 2013 May; 28(5): 711–718.

Psychological Stress in Childhood and Susceptibility to the Chronic Diseases of Aging: Moving Towards a Model of Behavioral and Biological Mechanisms

Gregory E. Miller, Edith Chen, Karen J. Parker. Psychol Bull. 2011 November; 137(6): 959–997. 

Preterm Birth and Its Long-Term Effects: Methylation to Mechanisms

Sasha E. Parets, Carrie E. Bedient, Ramkumar Menon, Alicia K. Smith

Biology (Basel) 2014 September; 3(3): 498–513.

Beyond Obesity and Lifestyle: A Review of 21st Century Chronic Disease Determinants. Garry Egger, John Dixon Biomed Res Int. 2014; 2014: 731685.

Health-Related Quality of Life in Pediatric Liver Transplant Recipients Compared to Other Chronic Disease Groups

Christine A Limbers, et al. Pediatr Transplant. 2011 May; 15(3): 245–253.

Integrating Co-Morbid Depression and Chronic Physical Disease Management: Identifying and Resolving Failures in Self-Regulation

Jerusha B. Detweiler-Bedell et al. Clin Psychol Rev. 2008 December; 28(8): 1426–1446

Hi

I agree with all the comments. However, I would highlight:

1) Confirm with a rheumatologist the diagnosis and there is not an added complication. 2) To consider or attempt to introduce the patient in a clinical trial of a biologic drug

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.

There is an infrequent condition known as intermittent hydrarthrosis (IH). Its onset is usually seen in childhood or adolescence. It usyally affects the knees, causing considerable effusion of the joints. The synovial fluid may be mildly (no more than 5000 white cells/mL) or non-inflammatory.

Since I see the Institution where you are working, may be you could ask to your clinician colleagues to collect synovial fluid from their IH patients.

I don't know if such substance could be considered "normal" for your purposes, but IH synovial fluids are the closest and most abundant sources of it, to the best of my knowledge.

Dear Robert,

Thanks for the comments. As you say, there are several paradoxes in the RF story. We tried to produce a complete mechanistic theory in our 1999 Immunology paper and earlier in a chapter I have just had to scan in for somebody because there are no copies of the book in the USA! The diagram in that chapter has 25 steps. My memory is that my most complicated diagram had 55 steps, with four positive feedback steps and more negative ones than I could count. Balancing effects from FcgammaRIIb and CR1 and various modes of linking of more than one receptor figured, together with the need for several clones to feed off each others' signals. So your point about IgM RF being perhaps ordinarily T cell independent is a good one, but my guess is that in RA persistent IgM RF production is bound in to the IgG RF and IgA RF production that IS T cell dependent and which generate, at least for IgG RF, complexes that encourage IgM RF B cells.

We failed to get a watertight story, because the number of possibilities are just too great. But maybe that is the lesson - RA may come about in lots of slightly different ways. And of course since that time we have had to reconsider the story in the light of ACPA. Do they feed off RF, or the other way around or are they runners in the same race or what? There is now an embarasse de richesse available for mechanisms. Yet Dr Cambridge and I hang on to the idea that there is a general principle here of 'cheating on the signals'. The 9G4 epitope on VH4-34 increasingly looks to us to be of much wider relevance to this cheating than was realised. It seems to mark a completely different low threshold system that is supposed to 'burn out' maybe by 'overstimulation induced death' but for some reason sometimes does not.

I have had to admit defeat on a tight story, and become a philosopher, but Jo Cambridge has not and the truth will one day emerge I think!

According to Moeez et. al,

" Citrullination normally occurs in cells undergoing apoptosis, and hence, citrullinated proteins are cleared from body and not encountered by immune system. However, in rheumatoid arthritis patients, these are not cleared. Anti-citrullinated protein antibodies are detectable in patients at risk of rheumatoid arthritis long before the onset of the disease."

Rheumatol Int. 2013 Jul;33(7):1669-73. doi: 10.1007/s00296-012-2635-6. Epub 2013 Feb 1.

Anti-citrullinated protein antibodies: role in pathogenesis of RA and potential as a diagnostic tool.

Before asking if rheumatism is a curable disease, we must ask: ”Is rheumatism a disease”.

Rheumatism is not a disease, rheumatic diseases are. They comprise more than 100 different entities with different pathogeneses, symptoms, and treatments.

In medicine in general, apart from infectious diseases, nothing is curable. Metabolic diseases (e.g. diabetes), heart diseases, gastro-intestinal, pulmonary diseases..etc.. are generally chronic or recurrent, with few examples of acute transient problems. The same applies to rheumatic diseases.

Medical doctors do not provide cures: they try to alleviate pain, improve quality of life and increase life expectancy. I think we managed to reach these three goals to a great extent over the past few decades. E.G. we do not treat rheumatoid arthritis as we used to do 40 years ago. Many breakthrough drugs changed the life of patients for the best.

Hi Nectarios

I totally agree with professor Shinichi Kawai. In fact, in 2006 our group determined that RA patients have higher plasmatic levels of these adipokines. As professor Shinichi Kawai says for the synoviocytes, in our lab we could also determine that both adipokines have pro-inflammatory activities in chondrocytes. Therefore, it could be considered that these adipokines have a pro-inflammatory character in joint tissues (the are several papers from different groups supporting this idea). On the contrary, systemically, the actions of these adipokines are not the same. Whilst leptin exhibits the same pro-inflammatory activities, adiponectin is well characterized as an anti-inflammatory factor, mainly at cardiovascular level. According to this, it is necessary to stress that the systemic levels of these adipokines may not be representative of their synovial fluid levels (check the paper of Presle 2006 PMID:16527497). Therefore, to achieve a better understanding of the plasmatic increase of these adipokines in RA patients it should be considered other factors like the inflammatory cachexia, the imbalance between lean mas/fat mass, the cardiovascular alterations of these patients and so on.

The January 2002 issue of "Arthritis and Rheumatism" journal found participants who consumed less than4 cups of decaffeinated coffee per day had an increased risk of developing rheumatoid arthritis, while participants who consumed at least 3 cups of caffeinated tea per day showed a decreased risk of developing RA. These findings suggest caffeine may possibly stop ordelay the onset of rheumatoid arthritis. The November 2003 issue of"Arthritis and Rheumatism" outlines a large-scale study that found little to no evidence linking caffeine and RA risk, which suggests caffeine may not have a direct effect on the development of certain forms of arthritis or joint pain. Further investigation is required to verify the connection of caffeine and arthritis.

Since caffeine is a stimulant, you must carefully monitor your daily consumption to avoid side effects. MayoClinic suggests consuming 200 to 300 mg of caffeine daily to avoide side effect bcz more than 500mg is nt good --thanks