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home:diseases:rheumatoid_arthritis [07.10.2019] – [Gout] sallieqhome:diseases:rheumatoid_arthritis [09.14.2022] (current) – external edit 127.0.0.1
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 =====Management ===== =====Management =====
  
-Managing Rheumatoid Arthritis with Dietary Interventions    (({{pubmed>long:29167795}}))+Managing Rheumatoid Arthritis with Dietary Interventions    (({{pmid>long:29167795}}))
  
 ==== Pain medications ==== ==== Pain medications ====
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 ===== Evidence of infectious cause ===== ===== Evidence of infectious cause =====
  
-Scher's and Abramson's 2011 review "The microbiome and rheumatoid arthritis" offers a variety of evidence pointing to a key role of microbes in RA.(({{pubmed>long:21862983}}))+Scher's and Abramson's 2011 review "The microbiome and rheumatoid arthritis" offers a variety of evidence pointing to a key role of microbes in RA.(({{pmid>long:21862983}}))
  
  
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 <relatedarticle> [[home:alternate:autoimmunity|Autoimmune theory of disease]] </article> <relatedarticle> [[home:alternate:autoimmunity|Autoimmune theory of disease]] </article>
  
-An increasing number of studies are providing support for the view that “autoantibodies” can be generated in response to the persistent presence of a pathogenic microbiota. While high titers of rheumatoid factor (RF) are associated with severe rheumatoid arthritis, they also appear in a number of other diseases including viral, bacterial, and parasitic infections.(({{pubmed>long:9198668}})) Maturation of RF can be initiated by chronic infections.(({{pubmed>long:8898963}}))+An increasing number of studies are providing support for the view that “autoantibodies” can be generated in response to the persistent presence of a pathogenic microbiota. While high titers of rheumatoid factor (RF) are associated with severe rheumatoid arthritis, they also appear in a number of other diseases including viral, bacterial, and parasitic infections.(({{pmid>long:9198668}})) Maturation of RF can be initiated by chronic infections.(({{pmid>long:8898963}}))
  
  
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 ==== Development during IRIS ==== ==== Development during IRIS ====
  
-During IRIS, HIV/AIDS patients experience the worsening or onset of systemic inflammatory clinical signs and symptoms following treatment with highly active antiretroviral therapy (HAART). This syndrome results when HAART allows for partial recovery of the immune response. This causes renewed and exuberant host immunological responses towards opportunistic infectious agents, agents that the host accumulated during prior periods of immunosuppression.(({{pubmed>long:20507930}}))+During immune reconstitution inflammatory syndrome, HIV/AIDS patients experience the worsening or onset of systemic inflammatory clinical signs and symptoms following treatment with highly active antiretroviral therapy (HAART). This syndrome results when HAART allows for partial recovery of the immune response. This causes renewed and exuberant host immunological responses towards opportunistic infectious agents, agents that the host accumulated during prior periods of immunosuppression.(({{pmid>long:20507930}}))
  
-A number of well-known readily cultured pathogens have been conclusively linked to IRIS: the herpes viruses, cytomegalovirus, hepatitis B and C, //M. tuberculosis//, //Mycobacterium avium// complex and //Cryptococcus neoformans//.(({{pubmed>long:17488505}})) However, many more microbes likely contribute to the reaction since AIDS clinicians do not yet have access to the metagenomic tools. Certainly, the existence of IRIS in culture-negative HAART patients suggests that more microbes may be present than the few that have already been isolated.(({{pubmed>long:19365271}}))+A number of well-known readily cultured pathogens have been conclusively linked to IRIS: the herpes viruses, cytomegalovirus, hepatitis B and C, //M. tuberculosis//, //Mycobacterium avium// complex and //Cryptococcus neoformans//.(({{pmid>long:17488505}})) However, many more microbes likely contribute to the reaction since AIDS clinicians do not yet have access to the metagenomic tools. Certainly, the existence of IRIS in culture-negative HAART patients suggests that more microbes may be present than the few that have already been isolated.(({{pmid>long:19365271}}))
  
-Interestingly, patients experiencing IRIS often "develop" autoimmune conditions as a manifestation of immune restoration including rheumatoid arthritis,(({{pubmed>long:12194745}})) This suggests that patients with RA accumulated microbes that are directly involved in the pathogenesis of this disease state.+Interestingly, patients experiencing IRIS often "develop" autoimmune conditions as a manifestation of immune restoration including rheumatoid arthritis,(({{pmid>long:12194745}})) This suggests that patients with RA accumulated microbes that are directly involved in the pathogenesis of this disease state.
  
 ==== Other evidence ==== ==== Other evidence ====
  
-  * **Gut-joint axis** – One excellent example gut–joint axis hypothesis is represented by classic Whipple disease, in which the presence of a single bacterium in the small intestine, //Tropheryma whipplei//, is sufficient for the development of joint inflammation in predisposed individuals.(({{pubmed>long:21461659}})) A 2008 comparison of the composition of intestinal microbiota of 101 patients with early rheumatoid arthritis with those diagnosed with fibromyalgia. In comparison to patients with fibromyalgia patients, RA patients had significantly less //Bifidobacteria// and bacteria of the //Bacteroides-Porphyromonas-Prevotella// group, //Bacteroides fragilis// subgroup, and //Eubacterium rectale//--//Clostridium coccoides// group.(({{pubmed>long:18528968}}))  +  * **Gut-joint axis** – One excellent example gut–joint axis hypothesis is represented by classic Whipple disease, in which the presence of a single bacterium in the small intestine, //Tropheryma whipplei//, is sufficient for the development of joint inflammation in predisposed individuals.(({{pmid>long:21461659}})) A 2008 comparison of the composition of intestinal microbiota of 101 patients with early rheumatoid arthritis with those diagnosed with fibromyalgia. In comparison to patients with fibromyalgia patients, RA patients had significantly less //Bifidobacteria// and bacteria of the //Bacteroides-Porphyromonas-Prevotella// group, //Bacteroides fragilis// subgroup, and //Eubacterium rectale//--//Clostridium coccoides// group.(({{pmid>long:18528968}}))  
-  * **Presence of microbes in the synovium** – Several reports have associated RA with bacterial overgrowth and deposition of resultant immune complexes in the synovial fluid.(({{pubmed>long:2670259}}))  +  * **Presence of microbes in the synovium** – Several reports have associated RA with bacterial overgrowth and deposition of resultant immune complexes in the synovial fluid.(({{pmid>long:2670259}}))  
-  * **Periodontal disease comorbidity** – Patients with RA often exhibit periodontal disease, which is associated with pathogens like //Porphyromonas gingivalis//. A 2010 study showed that //P. gingivalis// promotes early and later stages of apoptosis of primary human chondrocytes, which might contribute to the joint damage seen in the pathogenesis of RA.(({{pubmed>long:20582408}}))+  * **Periodontal disease comorbidity** – Patients with RA often exhibit periodontal disease, which is associated with pathogens like //Porphyromonas gingivalis//. A 2010 study showed that //P. gingivalis// promotes early and later stages of apoptosis of primary human chondrocytes, which might contribute to the joint damage seen in the pathogenesis of RA.(({{pmid>long:20582408}}))
  
  
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 <mainarticle> [[home:pathogenesis:vitamind:metabolism|Metabolism of vitamin D and the Vitamin D Receptor]] </article> <mainarticle> [[home:pathogenesis:vitamind:metabolism|Metabolism of vitamin D and the Vitamin D Receptor]] </article>
  
-Consistent with the Marshall Pathogenesis, patients with RA tend to have higher than normal levels of 1,25-D. Mawer //et al.// found that 1,25-D levels were particularly elevated in the synovial fluid surrounding the joints of patients with rheumatoid arthritis (RA).(({{pubmed>long:1950677}})) In this study, median serum levels of 1,25-D at baseline was not elevated in the RA patients — only 24 pg/ml. Thus, the extrarenal synthesis of 1,25-D was not obvious from the routine blood test for 1,25-D. There is no reason to think that the metabolism of other diseases is any different. Mice without functional Vitamin D Receptor signaling develop arthritic symptoms.(({{pubmed>long:22064970}}))+Consistent with the Marshall Pathogenesis, patients with RA tend to have higher than normal levels of 1,25-D. Mawer //et al.// found that 1,25-D levels were particularly elevated in the synovial fluid surrounding the joints of patients with rheumatoid arthritis (RA).(({{pmid>long:1950677}})) In this study, median serum levels of 1,25-D at baseline was not elevated in the RA patients — only 24 pg/ml. Thus, the extrarenal synthesis of 1,25-D was not obvious from the routine blood test for 1,25-D. There is no reason to think that the metabolism of other diseases is any different. Mice without functional Vitamin D Receptor signaling develop arthritic symptoms.(({{pmid>long:22064970}}))
  
  
-1,25-dihydroxyvitamin D3 (1,25(OH)2D3), has potent anti-inflammatory effects on T-cells. However the efficacy of vitamin-D in an inflammatory setting is unclear. [[http://ard.bmj.com/content/75/Suppl_1/A29.1?utm_source=TrendMD&utm_medium=cpc&utm_campaign=ARD_TrendMD-1|D 1,25]]+1,25-dihydroxyvitamin D3 (1,25(OH)2D3), has potent anti-inflammatory effects on T-cells. However the efficacy of vitamin-D in an inflammatory setting is unclear. [[https://ard.bmj.com/content/75/Suppl_1/A29.1?utm_source=TrendMD&utm_medium=cpc&utm_campaign=ARD_TrendMD-1|D 1,25]]
  
  
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 <mainarticle> [[home:alternate:genetic_predisposition|Genetic predisposition to disease]] </article> <mainarticle> [[home:alternate:genetic_predisposition|Genetic predisposition to disease]] </article>
  
-Evidence as to how human genes contribute to the development of RA has been weak. Genome-wide associations studies explain only 16% of disease variance.(({{pubmed>long:10643697}})) Moreover, the prevalence of RA concordance in monozygotic twins in European studies is ≤15%,(({{pubmed>long:3820198}})) (({{pubmed>long:8402000}})) and it is unclear whether this level actually exceeds the risk of developing RA that exists in the general population.(({{pubmed>long:11823356}}))+Evidence as to how human genes contribute to the development of RA has been weak. Genome-wide associations studies explain only 16% of disease variance.(({{pmid>long:10643697}})) Moreover, the prevalence of RA concordance in monozygotic twins in European studies is ≤15%,(({{pmid>long:3820198}})) (({{pmid>long:8402000}})) and it is unclear whether this level actually exceeds the risk of developing RA that exists in the general population.(({{pmid>long:11823356}}))
  
  
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-//**Proal**, et al., "Immunostimulation in the era of the metagenome"//(({{pubmed>long:21278764}}))</blockquote>+//**Proal**, et al., "Immunostimulation in the era of the metagenome"//(({{pmid>long:21278764}}))</blockquote>
  
  
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-//**Proal**, et al., "Immunostimulation in the era of the metagenome"//(({{pubmed>long:21278764}}))</blockquote>+//**Proal**, et al., "Immunostimulation in the era of the metagenome"//(({{pmid>long:21278764}}))</blockquote>
  
 ===== Data ===== ===== Data =====
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 sarcoidosis, rheumatoid arthritis sarcoidosis, rheumatoid arthritis
  
-Read the [[http://bacteriality.com/2008/06/03/interview21/|interview]]+Read the [[https://bacteriality.com/2008/06/03/interview21/|interview]]
  
 <html></div></div></html> <html></div></div></html>
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 rheumatoid arthritis, dyslexia rheumatoid arthritis, dyslexia
  
-Read the [[http://bacteriality.com/2007/09/01/interview2/|interview]]+Read the [[https://bacteriality.com/2007/09/01/interview2/|interview]]
  
 <html></div></div> <html></div></div>
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 ===== Childhood ===== ===== Childhood =====
  
-Do infections trigger juvenile idiopathic arthritis?  (({{pubmed>long:000}}))+Do infections trigger juvenile idiopathic arthritis?  (({{pmid>long:000}}))
  
 ===== Gout ===== ===== Gout =====
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  I drink about an extra 2.2 L (outside of meals) of water daily and I haven't had a major flare since doing so.  I drink about an extra 2.2 L (outside of meals) of water daily and I haven't had a major flare since doing so.
  
-I recently heard that phytic acid is able to inhibit the enzyme xanthine oxidase that causes a build up of uric acid(({{pubmed>long:14738912}})). The supplement IP6 Gold is a good source of phytic acid but I have not tried it though. I am concerned that this supplement might be immunosuppressive as it works like Allopurinol which also blocks xanthine oxidase - we know that Allopurinol to be immunosuppressive.  +I recently heard that phytic acid is able to inhibit the enzyme xanthine oxidase that causes a build up of uric acid(({{pmid>long:14738912}})). The supplement IP6 Gold is a good source of phytic acid but I have not tried it though. I am concerned that this supplement might be immunosuppressive as it works like Allopurinol which also blocks xanthine oxidase - we know that Allopurinol to be immunosuppressive.  
 //David//</blockquote> //David//</blockquote>
  
-Herein, we report a positive relationship between serum UA and acute-phase reactants, such as high-sensitivity C-reactive protein, fibrinogen, ferritin, complement C3, and erythrocyte sedimentation rate, in a cohort of 2731 nondiabetic adults. The relationship remains significant after adjustment for several confounders, including age, sex, adiposity, anti-hypertensive treatments or diuretics use. To confirm the existence of a causal relationship, we examined the effect of UA on the expression of inflammatory biomarkers in human hepatoma HepG2 cells and characterized the signaling pathway by which UA acts. +Herein, we report a positive relationship between serum UA and acute-phase reactants, such as high-sensitivity C-reactive protein, fibrinogen, ferritin, complement C3, and erythrocyte sedimentation rate, in a cohort of 2731 nondiabetic adults. The relationship remains significant after adjustment for several confounders, including age, sex, adiposity, anti-hypertensive treatments or diuretics use. To confirm the existence of a causal relationship, we examined the effect of UA on the expression of inflammatory biomarkers in human hepatoma HepG2 cells and characterized the signaling pathway by which UA acts.  .......The effect of UA was completely blocked by the antioxidant N-acetylcysteine.  (({{pmid>long:28408375}}))
- +
-The effect of UA was completely blocked by the antioxidant N-acetylcysteine. +
-(({{pubmed>long:28408375}}))+
  
  
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 +<nodisp>
 ===== Notes and comments ===== ===== Notes and comments =====
  
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 If we ever have an article on JIA: If we ever have an article on JIA:
-<blockquote>Do infections trigger juvenile idiopathic arthritis?(({{pubmed>long:20012631}}))+<blockquote>Do infections trigger juvenile idiopathic arthritis?(({{pmid>long:20012631}}))
  
 Aslan M, Kasapcopur O, Yasar H, Polat E, Saribas S, Cakan H, Dirican A, Torun MM, Arısoy N, Kocazeybek B. Aslan M, Kasapcopur O, Yasar H, Polat E, Saribas S, Cakan H, Dirican A, Torun MM, Arısoy N, Kocazeybek B.
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 Rheumatology International, published online before print December 13, 2009. Rheumatology International, published online before print December 13, 2009.
  
-http://dx.doi.org/10.1007/s00296-009-1253-4+https://dx.doi.org/10.1007/s00296-009-1253-4
  
 Abstract Abstract
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 jejuni come forward and seen common in JIA cases. We also suggest that the pre-diagnosis of microorganisms, which can play a role as primarily or by intervening in the etiopathogenesis of JIA and adding specific antimicrobial therapy to the standard JIA therapy, it is possible to perform new, extended, especially molecular based serial case studies. jejuni come forward and seen common in JIA cases. We also suggest that the pre-diagnosis of microorganisms, which can play a role as primarily or by intervening in the etiopathogenesis of JIA and adding specific antimicrobial therapy to the standard JIA therapy, it is possible to perform new, extended, especially molecular based serial case studies.
  
-http://dx.doi.org/10.1007/s00296-009-1253-4+https://dx.doi.org/10.1007/s00296-009-1253-4
 </blockquote> </blockquote>
  
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-===== References =====+===== References =====</nodisp> 
home/diseases/rheumatoid_arthritis.1562747864.txt.gz · Last modified: 07.10.2019 by sallieq
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