Dna Methylation Data For Ra
In this study, we obtained RA methylation data from the NCBI GEO database. The platform was GPL13534 . GSE42861 contains 354 RA samples and 335 normal control samples. Bisulphite converted DNA was from PBLs. The matrix file of GSE42861 includes the information for samples and normalized beta values for each sample.
Availability Of Data And Materials
All the data is underlying the present study from the National Health Insurance Research database and Management Office for Health Data, China Medical University Hospital, Taichung, Taiwan. Local interested researchers or cooperators can obtain the data through formal application to the Ministry of Health and Welfare, Taiwan.
What Are The Signs And Symptoms Of Ra
With RA, there are times when symptoms get worse, known as flares, and times when symptoms get better, known as remission.
Signs and symptoms of RA include:
- Pain or aching in more than one joint
- Stiffness in more than one joint
- Tenderness and swelling in more than one joint
- The same symptoms on both sides of the body
- Weight loss
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Pd Cases And Matched Controls
Out of approximately 3.6 million people in our data source cohort, we identified 30,032 PD patients . After various steps of exclusion and matching, 8,256 cases were used in the inclusive analysis and 4,738 PD cases were included in the conservative branch of the study . The first step of exclusions involving the five PD comorbidities is shown in Supplementary Figure 4.
The two branches of analytical pipeline differ in reliability of the first date of PD diagnosis and sample size. The inclusive branch includes all PD patients, while the conservative branch includes only those who had their first PD diagnosis assigned to them in the outpatient register as the main diagnosis . In the conservatively constructed cohort, the age-at-first-diagnosis distribution is significantly shifted towards the younger age . This implies that this method better captures the earliest date of PD symptom manifestation as the main diagnosis in the outpatient register is likely to be assigned earlier in a PD patients life compared to PD diagnoses assigned in the in-patient registry. A breakdown of the four classes of patients based on the type of their first PD diagnosis is included in Table 1.
Parkinson And Rheumatoid Arthiritis
My mom has been using Enbrel biologic injection once a year and has recently diagnosed with Parkinson. These kind of Rheumatoid Arthritis biologic treatments have a lot of possible side effects. Also this medication controls her immune system as well as her RA. On the other hand, I was wondering is controlling her immune system with that medicine bad for the progression of Parkinson? Should she stop that kind of treatment for her RA and choose something else? What kind of treatments can she get without effecting her Parkinson in a bad way? Thank you!
Hi : I dont know anything about Enbrel and how it might impact a Parkinsons diagnosis and treatment. This is something that you will need to address with your mothers doctor. Probably her doctor who is treating her RA might be able to help you with an answer to that question. Her health situation seems complicated I certainly appreciate the interest you are taking in your moms health situation I know how difficult that can be. In the meantime, here is a Mayo website that addresses Rheumatoid Arthritis, , perhaps the information there will help you.
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Gene Ontology And Kegg Pathway Analysis Of Shared Gene Pairs
To further analyze the functional characteristics of the shared gene pairs, we extracted 220 unique genes from the 337 gene pairs by removing duplicate genes, and then annotated them to GO categories and KEGG pathways using DAVID. This found 70 GO categories and four KEGG pathways that were significantly annotated. Among them, 11 immune-related GO categories included GO: 0002250: adaptive immune response, GO: 0050853: B cell receptor signaling pathway, GO: 0006952: defense response, GO: 0031295: T cell co-stimulation, GO: 0006955: immune response, GO: 0042832: defense response to protozoan, GO: 0030183: B cell differentiation, GO: 0050900: leukocyte migration, GO: 0070671: response to interleukin-12, GO: 0019815: B cell receptor complex and GO: 0001772: immunological synapse. Two GO categories related to brain development were GO: 0030901: midbrain development and GO: 0022029: telencephalon cell migration. In addition, these genes were also annotated into two immune-related KEGG pathways . As discussed above, 220 unique genes from the 337 gene pairs play important roles in autoimmune regulation and brain development.
The Incidence Of Referral To Fcp After The First Hospital Diagnosis
Patients with PD and MS were the quickest to begin FCP with 20% of PD patients and 13% of MS patients starting FCP within 2 months of their diagnosis. FCP was mainly initiated within 2 years of the first hospital diagnosis. The overall CIP of FCP 2 years after the first hospital diagnosis was 8% , 89%)) for stroke, 53% for PD, 49% for MS, and 16% for RA . The CIP among patients not receiving FCP before the hospital diagnosis was lower .
Table 2 Cumulated Incidence Proportion of FCP 6 Months to 5 Years After Incident Hospital Diagnoses of Stroke, Parkinsons Disease , Multiple Sclerosis and Rheumatoid Arthritis Between 2007 and 2016
Patients with mild Stroke had the lowest CIP within sub-diagnoses of stroke .
The overall CIP from 2011 to 2016 was similar or higher compared with the CIP from 2007 to 2010 ). Looking only at patients not receiving FCP before the hospital diagnosis, only PD patients had higher CIP in the later period compared with the earlier period .
Figure 1 Cumulative incidence proportion of FCP after incident hospital diagnoses of stroke, Parkinson’s Disease , Multiple Sclerosis and Rheumatoid Arthritis by calendar year of diagnosis. Overall. Among those not receiving FCP before the hospital diagnosis.
The CIP among RA patients diagnosed between 2015 and 2016 was lower compared with previous years . The CIP among those diagnosed with RA or PD in 2007 was lower compared with later years .
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What Are The Complications Of Ra
Rheumatoid arthritis has many physical and social consequences and can lower quality of life. It can cause pain, disability, and premature death.
- Premature heart disease. People with RA are also at a higher risk for developing other chronic diseases such as heart disease and diabetes. To prevent people with RA from developing heart disease, treatment of RA also focuses on reducing heart disease risk factors. For example, doctors will advise patients with RA to stop smoking and lose weight.
- Obesity. People with RA who are obese have an increased risk of developing heart disease risk factors such as high blood pressure and high cholesterol. Being obese also increases risk of developing chronic conditions such as heart disease and diabetes. Finally, people with RA who are obese experience fewer benefits from their medical treatment compared with those with RA who are not obese.
- Employment. RA can make work difficult. Adults with RA are less likely to be employed than those who do not have RA. As the disease gets worse, many people with RA find they cannot do as much as they used to. Work loss among people with RA is highest among people whose jobs are physically demanding. Work loss is lower among those in jobs with few physical demands, or in jobs where they have influence over the job pace and activities.
Identifying Large Change Gene Pairs For Ra
We divided the PCC into eight intervals, named strongest negative correlation , strong negative correlation , weak negative correlation , weakest negative correlation , weakest positive correlation , weak positive correlation , strong positive correlation , and strongest positive correlation . For each interval of the RA controls, we analyzed the changes in the co-methylation relationship from controls to cases. The results are presented in Table 1.
Table 1. The number of gene pairs in eight sections for RA cases and controls.
For RA, there were five gene pairs where the PCC changed from a strong negative correlation to a weak positive correlation, and 13 gene pairs where the PCC changed from a weak negative correlation to a strong positive correlation. These 18 gene pairs crossed four intervals and recorded significant changes. There was also a total of 1,893 gene pairs crossing no less than three intervals with large changes of the co-methylation relationship from controls to cases. These are shown in Supplementary File S1.
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Inflammation May Contribute To Both Joint And Nerve Degeneration
byNancy Walsh, Contributing Writer, MedPage Today June 9, 2021
Patients with osteoarthritis are at increased risk for developing Parkinson’s disease, a longitudinal Taiwanese study found.
Incidence rates for developing Parkinson’s disease were 0.99 per 1,000 person-years among patients with osteoarthritis compared with 0.71 per 1,000 for controls, reported Shin-Liang Pan, MD, PhD, and colleagues from the National Taiwan University in Taipei.
Accordingly, the risk among patients with osteoarthritis was 41% higher compared with controls, with an adjusted HR of 1.41 , the researchers wrote online in Arthritis Care & Research.
It is now recognized that inflammation plays a major role in the development of osteoarthritis, while neuroinflammation is characteristic of Parkinson’s disease.
“Because a growing body of literature reports that peripheral inflammation may induce neuroinflammation in the brain, leading to neurodegeneration, we hypothesized that having osteoarthritis may increase people’s risk of later developing Parkinson’s disease,” Pan and colleagues wrote.
Therefore, they analyzed data from Taiwan’s National Health Insurance system, which covers more than 97% of the population, identifying 33,360 individuals ages 50 to 64 who were diagnosed with osteoarthritis during the years 2002 to 2005, matching them by age and sex with the same number of controls.
- Knee or hip osteoarthritis, HR 1.55
- Non-knee or hip, HR 1.42
- Uncategorized, HR 1.32
Pitfalls Limitations And Alternative Interpretations
Given that the Swedish health care system typically offers everyone a life-long follow-up, it is unlikely that RA remains undiagnosed in RA-affected individuals or that PD remains undiagnosed in PD-affected individuals. It is impossible to fully exclude that the association we detected was caused by a confounder, however, we took great care to match PD cases and controls in order to make the groups as similar as possible. A potential confounder that we did not account for could be, for example, educational attainment. Shorter education is associated with increased prevalence of RA in Sweden . Since it has conversely been shown that men attaining higher IQ scores during military conscription in Sweden exhibit higher risk of developing PD , education level is potentially a confounder that could influence the risk for both diseases.
It is important to highlight that our working dataset was limited to only individuals who were first-degree relatives of a person diagnosed with diabetes mellitus or celiac disease. While this dataset was limited, it still allowed us to include 3.6 million individuals, or more than 20% of the entire population followed in the registry. We took precautions to ensure that PD cases and controls were also matched based on the exact type of a relative who had PD and RA. The matching was intended to prevent potential fictitious associations that could arise, due to unequal distribution of family-size affecting factors between PD case and control groups.
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Dopaminergic Agents And Their Effects In Ra: Evidences From The Clinic
Dopaminergic agents were analyzed in the past for the treatment of RA, based on the fact that the stimulation of D2-like DR leads to the inhibition of prolactin, a proinflammatory hormone that is released by the anterior pituitary gland and that is present at high concentration in the serum and synovial fluid of RA patients . In these studies, the effect of dopaminergic agonists on the inflammatory process was supposed to be indirect and mediated by prolactin. However, the results of the studies were not congruent .
Table 2 Clinical evidences of dopaminergic modulation on RA disease
The in vivo D1-like DR blockade showed proinflammatory effects on arthritis in mice . In vitro, blockade of D1-like DR led to reduced osteoclast differentiation in CIA mice, but no alteration of inflammatory cytokines was observed .
Due to the effects of dopaminergic drugs on the immune system, drugs used for the treatment of Parkinson can also alter arthritis onset and progression, as recently described by Zhu et al. . In this study, Zhu et al. investigated the effect of carbidopa, a drug able to block the conversion of levodopa to dopamine in the periphery and therefore used in combination with levodopa in Parkinsons patients. Their results showed that the intake of carbidopa decreased joint inflammation and arthritis score in CIA mice .
Mapping Of Methylation Positions To Genes
In this study, we analyzed genes on a one-to-one basis to compare the global co-methylation landscapes. We used the same data processing for RA and PD. We mapped 485,577 probes in the GPL13534 platform to 21,225 genes. If there were multiple probes in a gene, we calculated the average beta value of those probes as the methylation value of the gene. The final RA dataset used for subsequent analysis consisted of 21,225 genes and 689 samples , and the final PD dataset included 21,225 genes, 335 PD samples, and 237 normal control samples.
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Rheumatoid Arthritis Dysbiosis And Leaky Gut:
Posted on September 15, 2021 by biomebuzz
The last time I wrote about research on the biome and rheumatoid arthritis was last February so its about time for something new and exciting. A paper was just published by researchers at the University College London that shows that bacterial dysbiosis may lead to damage to the lining of the gut, which correlates to joint inflammation and the severity of arthritic disease: in arthritis, there is profound damage to the gut lining, which fails to work properly as a barrier, as well as an accumulation in the gut of white blood cells that cause inflammation. The authors show that, in arthritis, bacteria cross the prohibited border of the intestinal lining and that repairing gut permeability defects with specific drugs inhibits joint inflammation.
Science has already shown that those with RA have abnormal gut bacteria. For example, high levels of Collinsella aerofaciens, bacteria which is known to increase gut permeability, has been found in the population. The mice in these experiments had markedly increased Prevotella and reduced Lactobacillus, which, interestingly, became more pronounced as the disease progressed. Also of note: some treatments currently used for RA, including NSAIDS , are known to increase gut permeability.
Now for some good and genuinely hopeful news:
Osteoarthritis Linked To Higher Parkinson’s Disease Risk
A study published in Arthritis Care & Research has uncovered an elevated risk of Parkinson’s disease in individuals with osteoarthritis.
The retrospective study using Taiwan’s Longitudinal Health Insurance Database 2005 included 33,360 patients who were 50-64 years old and had osteoarthritis in 2002-2005. A comparison group consisted of 33,360 age- and sex- matched individuals without osteoarthritis. The osteoarthritis group had a 41% higher risk of developing Parkinson’s disease, after adjustments. Patients with knee or hip osteoarthritis appeared to have a higher risk of Parkinson’s disease than patients with non-knee and non-hip osteoarthritis or with uncategorized osteoarthritis.
Although the mechanisms behind a potential link between osteoarthritis and Parkinson’s disease are unknown, both conditions involve inflammation.
“Coexisting osteoarthritis and Parkinson’s disease can additively increase the risk of falling. Moreover, osteoarthritis-related mobility impairments may mask early motor symptoms of Parkinson’s disease,” said senior author Shin-Liang Pan, MD, Ph.D., of National Taiwan University. “Health professionals need to be alert to the potential link between these two diseases.”
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Matching Cases With Controls
All PD patients were labeled with a matching type constructed from a combination of three study-related variables and eight technical variables. The three study-related variables were: birth year, sex, birth location. The remaining technical variables were not related to our research question but were used to ensure that the cohort used did not interfere nor bias the study results . In total there were 8404 unique matching types.
For each matching type, the following procedure was done:
1) PD case individuals of this type were extracted and ordered randomly, forming a pool of cases, named A. PD control individuals of this type were extracted and ordered randomly, forming a much larger pool of controls, named B.
2) To find matches for individuals in the pool A, a sub-pool b was formed by selecting individuals from pool B using the following procedure. For each individual in sub-pool b, their personal follow-up end date must supersede the date of PD diagnosis for each individual in pool A. Individual b1, who is the first person in sub-pool b, is assigned to the first person in pool A . Individual b1 is permanently eliminated from pools b and B.
3) The step 2) is repeated sequentially with all individuals in A.
4) The step 3) is repeated maximum 200 times, or until the pool B is depleted, or until none of the individuals in A is assigned a new match.
How Is Ra Treated
RA can be effectively treated and managed with medication and self-management strategies. Treatment for RA usually includes the use of medications that slow disease and prevent joint deformity, called disease-modifying antirheumatic drugs biological response modifiers are medications that are an effective second-line treatment. In addition to medications, people can manage their RA with self-management strategies proven to reduce pain and disability, allowing them to pursue the activities important to them. People with RA can relieve pain and improve joint function by learning to use five simple and effective arthritis management strategies.
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