Category: Knee Arthritis

Although chronic diseases are quite common (the Centers for Disease Control and Prevention says that 6 in 10 adults in the US have one chronic disease, and 4 in 10 have two or more chronic diseases), I’ve always had trouble finding tools that address the impact that chronic illness can have on relationships and intimacy.

Now there’s a book that addresses exactly that problem: Sex – Interrupted: Fostering Intimacy While Living with Illness or Disability. Iris Zink, rheumatology nurse, and Jenny Thorn Palter, former editor of Lupus now magazine, have written a book that recognizes the intimacy issues that patients with chronic diseases often face and offers helpful suggestions for both healthcare providers and patients.

Click below to read my review of the book!

Book review: Sex – Interrupted: Fostering Intimacy While Living with Illness or Disability

Moms facing forward

You can also visit www.intimacyandillness.com For more information. The first 50 people to purchase the book through their website will receive a free sample copy of Pure Romance.

From a recent study published in JAMA network openedresearchers analyzed the incidence and risk of autoinflammatory and autoimmune diseases following the coronavirus disease 2019 (COVID-19).

Study: Autoimmune and autoinflammatory connective tissue disorders after COVID-19. Image credits: Kateryna Kon / Shutterstock.com

COVID-19 and autoimmunity

The causative agent of COVID-19, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), can trigger autoimmune reactions and, as a result, contribute to autoimmunity. In fact, several studies have described the development of vitiligo, alopecia areata, vasculitis, and systemic lupus erythematosus (SLE) after recovery from COVID-19.

Respiratory and cardiovascular outcomes after COVID-19 have been extensively evaluated due to the potential role of SARS-CoV-2 in heart failure. Similarly, similarities have been reported between autoimmune diseases and COVID-19; However, autoimmune diseases have not been extensively investigated as post-acute consequences of COVID-19.

About the study

In the current study, researchers evaluate the risk and incidence of various autoinflammatory and autoimmune connective tissue disorders after recovery from COVID-19. To this end, data from the Korean COVID-19 National Health Insurance Service (NHIS) registry were collected for people with a COVID-19 diagnosis and general health assessment from October 8, 2020 to December 31, 2021.

Individuals who underwent a general health examination and were not diagnosed with COVID-19 were identified as a control group. All study participants were followed until outcome diagnosis, death, emigration, or study end date. The risk and incidence of autoinflammatory and autoimmune diseases were estimated in study participants without these conditions before COVID-19.

The occurrence of these disorders was defined as having three or more medical visits with associated clinical diagnosis codes. Cardiovascular outcomes reported to be associated with COVID-19 were positive control outcomes, while outcomes less likely to be associated with COVID-19 were negative control outcomes.

Demographics, lifestyle factors, socio-economic status and comorbidity data were obtained from the NHIS database. Propensity scores and inverse probability weights were also estimated.

Risk of outcomes was assessed for COVID-19 and control cohorts. A multivariable Cox proportional hazards analysis was performed, with adjustments for covariates. Subgroup analyzes were conducted based on gender, age, COVID-19 severity, and vaccination status.

Findings of the study

The study included 354,527 and 6.13 million individuals with and without COVID-19, respectively, with well-balanced covariates. The mean follow-up duration was 119.7 days for the COVID-19 cohort and 121.4 days for the control group.

The COVID-19 cohort had a significantly higher risk of Crohn’s disease, sarcoidosis, alopecia areata, alopecia totalis and anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis, while the risk of SLE was lower.

The overdetection bias was minimal in the COVID-19 cohort. Women in the COVID-19 cohort were at greater risk of subsequently developing vitiligo, Crohn’s disease, sarcoidosis, alopecia totalis, alopecia areata, and ANCA-associated vasculitis.

By comparison, men in the COVID-19 cohort were at greater risk of developing ankylosing spondylitis, systemic sclerosis, adult-onset Still’s disease, Crohn’s disease, psoriasis and alopecia totalis. The risks of ANCA-associated vasculitis and alopecia totalis were much higher in those aged 40 years or older.

The risks of sarcoidosis, adult-onset Still’s disease, rheumatoid arthritis and Crohn’s disease were also higher in people under 40. The overall risk of incidents increased as the severity of COVID-19 increases.

Unvaccinated individuals were at greater risk of developing Crohn’s disease, alopecia totalis, alopecia areata, and positive control results. This additional risk of positive control results and autoimmune diseases was not identified in vaccinated individuals.

In sensitivity analyses, the researchers compared demographic and clinical data between individuals with a general health examination and those without. The group studied consisted mainly of adults, as the health research focuses on workers and households. Both groups showed similar COVID-19 positivity rates; however, more examined individuals were vaccinated than unexamined individuals.

Conclusions

The current study compared the risks of autoinflammatory and autoimmune diseases in individuals with a history of COVID-19 versus non-COVID-19 controls. These risk estimates in the predominantly Asian sample were likely lower than in other ethnic groups, which may be due to delayed disease development/progression.

Some limitations of the current study include the primarily adult population and the fact that the sample consisted entirely of Asians, limiting the generalizability of these findings to other ethnic groups and adolescents/children. In addition, the researchers were unable to determine whether some individuals were more susceptible to autoimmunity than others.

Overall, the study’s findings suggest that SARS-CoV-2 infection may be associated with autoimmune diseases. Thus, long-term management of COVID-19 patients should also include autoimmunity assessments.

Introduction

Rheumatoid arthritis (RA) is an autoimmune disease that affects millions of people worldwide. Although the exact cause of RA remains unknown, research has shown that the genetics of rheumatoid arthritis play an important role in its development. In this article, we will delve deeper into the genetics of RA, examining the key genetic markers associated with the disease and their implications.

Genetic markers associated with RA

HLA-DR4: Revealing the dominant gene

The HLA-DR4 human leukocyte antigen gene stands out as the gene most closely linked to RA. Individuals who possess this gene are more predisposed to developing the disease and often experience more severe symptoms. The HLA-DR4 gene encodes proteins responsible for distinguishing between self and foreign cellular materials, including viral and bacterial proteins.

STAT4: The immune system regulator

Another important genetic marker associated with RA is STAT4. This gene plays a crucial role in regulating and activating the immune system. Abnormalities in STAT4 function have been observed in individuals with RA, underscoring its significance in disease development.

TRAF1 and C5: key players in chronic inflammation

The genes TRAF1 and C5 have been identified as major contributors to chronic inflammation, a feature characteristic of RA. These genes play a crucial role in initiating and perpetuating the inflammatory response that leads to joint damage in individuals with RA.

PTPN22: Influencing the progression of RA

PTPN22 is a gene that influences the progression and expression of RA. Although the precise mechanisms by which it affects the disease are not yet fully understood, researchers have identified its involvement. Further studies are underway to unravel the complexity of PTPN22’s role in the development of RA.

The complexity of genetic heredity and RA

Although some of the genetics of rheumatoid arthritis are known and the above genetic markers are strongly associated with RA, it is essential to note that not everyone who possesses these genes will develop the disease, and conversely, not all individuals with RA have these genetic possess markers. This complexity suggests that other genetic and environmental factors may also contribute to the development of RA.

The need for further research

Although significant progress has been made in identifying genetic markers associated with RA, there is still much to learn. Researchers have discovered more than 100 regions in the genome that are linked to the risk of developing RA in different ethnicities. To understand why some individuals with these genetic markers develop the disease while others require no further investigation.

Conclusion

Genetics undoubtedly plays a crucial role in the development of rheumatoid arthritis. The HLA-DR4 gene is emerging as the primary genetic marker associated with RA, alongside other notable genes such as STAT4, TRAF1, C5 and PTPN22. However, the complexity of genetic inheritance suggests that additional factors contribute to the development of this debilitating autoimmune disease. Continued research in this area will provide valuable insights into the underlying mechanisms of RA, ultimately leading to improved diagnostic tools and targeted therapies for those affected.

Related

The uncertainty associated with the diagnosis of a lifelong chronic disease can make it very difficult to make plans in advance. But living with a chronic illness shouldn’t mean giving up life goals that are really important to you… As an example of how to approach big life goals while living with a chronic illness, I’m going to use what seemed like: a pretty outrageous goal I set for myself in 2016: ride in the Arthritis Foundation’s California Coast Classic.

Mary Leach

In this article, I’ll share some of the strategies I used to achieve my goal of cycling 525 miles in the Arthritis Foundation’s California Coast Classic – and how you can apply the same strategies to achieve big life goals while dealing with a chronic illness lives.

3 tips for achieving big life goals while living with a chronic illness

Moms facing forward

I made a vegan pan dinner. It has tofu, green beans and Japanese sweet potatoes. You season everything and throw it in a pan and put it in the oven. It’s a very easy dinner and it made so much that I will be eating it for a few days.

My friend’s kid came over to help me. He drove me to the computer store to have my laptop checked. You know, on the laptop I spilled tea on the keyboard. The place he took me to wouldn’t look at it, but later that day I took a taxi to another store. They send it in to have it looked at. For $30, it’s worth having it reviewed.

The boy also drove me to the dog food store to get some new food for Lucky. She is losing weight and not eating as much. I thought some tempting foods would help. Later she ate a little bit of it. Lucky eats, but not as much as he used to. She ran 2 miles yesterday, so she’s doing great!

See you tomorrow…

This is evident from a recent study published in the journal JAMA network openedResearchers in Canada investigated whether coronavirus disease 2019 (COVID-19) patients with immune-mediated inflammatory diseases (IMIDs) were at higher risk of experiencing venous thromboembolism after recovery from severe acute respiratory syndrome coronavirus 2 (SARS-CoV- 2) infections compared to COVID-19 patients without IMIDs.

Study: Venous thromboembolism after COVID-19 infection in people with and without immune-mediated inflammatory diseases. Image credits: Kateryna Kon / Shutterstock

Background

Immune-mediated inflammatory diseases are heterogeneous chronic diseases resulting from an abnormally activated immune system. Approximately 5% to 7% of the population of the Western world is affected by IMIDs, and individuals with IMIDs have a higher risk of venous thromboembolism compared to individuals without IMIDs. Rheumatoid arthritis, multiple sclerosis, vasculitis, inflammatory bowel disease, and psoriasis are IMIDs known to increase the risk of venous thromboembolism.

The inflammation in IMID patients causes platelet abnormalities, endothelial dysfunction, fibrinolysis disorders, and abnormal activation of clotting factors. Recent evidence also indicates that the widespread inflammation and endothelial dysfunction caused by COVID-19 is associated with a higher risk of venous thromboembolism and multi-organ failure in patients who have recovered from moderate to severe SARS-CoV-2 infections. However, whether COVID-19 increases the risk of venous thromboembolism in patients with IMIDs remains unknown.

About the study

In the current study, the researchers used population-based healthcare data from Ontario, Canada, to evaluate whether the risk and incidence of venous thromboembolism were higher in individuals with IMIDs who had recovered from COVID-19 compared to COVID-19 . patients without IMIDs.

The data includes all interactions Ontario residents with valid health cards had with the health care system, including emergency room visits, hospital admissions, outpatient surgeries and single-day hospital admissions. In addition, physician billings for all patient interactions were included in the data. The administrative health information was also linked to databases containing demographic information and data on COVID-19 testing and vaccination status.

In the retrospective matched cohort analysis, researchers matched individuals who had IMIDs and tested positive for COVID-19 with up to five individuals who tested positive for COVID-19 but did not have IMIDs. Controls were compared based on factors such as age, gender, urban or rural residence, and average income quantile of the neighborhood. Individuals with a diagnosis of malignant neoplasm five years after a positive COVID-19 test were excluded from the study.

Positive cases of COVID-19 were identified based on polymerase chain reaction (PCR) results, while individuals with IMIDs were identified based on physician billings, records of endoscopy procedures, and medication prescriptions specific to IMIDs. Data on hospital admissions and emergency department visits were used to identify events of venous thromboembolism. The primary outcome examined was venous thromboembolism of any type, with secondary outcomes including pulmonary embolism and deep venous thrombosis.

A modified Charlson Comorbidity Index was used to include comorbidities such as diabetes, chronic obstructive pulmonary disease, or congestive heart failure before the positive diagnosis of COVID-19. Individuals with at least two vaccination doses before positive diagnosis of COVID-19 were considered vaccinated. In addition, socio-demographic factors such as residential areas in urban or rural areas, gender, age, socio-economic status and death before the conclusion of follow-up were also taken into account during the analysis.

Results

The findings suggested that individuals with IMIDs did not have a significantly higher risk of venous thromboembolism after recovery from SARS-CoV-2 infections compared to individuals without IMIDs. Among the 28,440 individuals with IMIDs included in the study, the incidence of venous thromboembolism was 2.64 per 100,000 person-days, while in the matched cohorts of individuals without IMIDs it was 2.18 per 100,000 person-days.

However, when the analysis was not adjusted for comorbidities, those with IMIDs had a greater risk of venous thromboembolism after recovery from COVID-19 than those without IMIDs. Furthermore, findings were similar when the risk of deep venous thrombosis and pulmonary embolism was examined separately.

The presence of other comorbidities was found to confound the association between venous thromboembolism and IMIDs after SARS-CoV-2 infections. These findings highlight the need for physicians to consider factors such as comorbidities and individual risk factors when prescribing venous thromboembolism prophylactics to IMID patients who have recovered from COVID-19.

Conclusions

Overall, the findings reported that patients with IMIDs are not at greater risk of venous thromboembolism after SARS-CoV-2 infections compared to COVID-19 patients without IMIDs. However, some comorbidities may confound the association between IMIDs and venous thromboembolism associated with COVID-19, and physicians should consider individual risk factors when treating IMID patients for COVID-19 complications.

Introduction

Rheumatoid arthritis (RA) is an autoimmune disease that causes chronic inflammation of the joints, leading to pain, stiffness and swelling. Although the exact cause of RA remains unknown, research suggests that both genetic and environmental factors of rheumatoid arthritis play an important role in its development. No single trigger will cause RA, but rather there is a complex interplay of genetics and environmental triggers that can ‘initiate’ the development of rheumatoid arthritis. Each of these factors is unique to the person and all contribute to the onset and progression of this condition.

Understanding rheumatoid arthritis

Before we delve into the environmental factors, it is important to have a basic understanding of rheumatoid arthritis. RA is a chronic inflammatory disease that mainly affects the joints, but can also affect other organs. It is characterized by the immune system mistakenly attacking the body’s own tissues, especially the synovium, which lines the joints.

Environmental triggers of rheumatoid arthritis

Although genetics contribute to a person’s susceptibility to RA, environmental factors can trigger the disease in individuals with a genetic predisposition. These triggers can be external factors that interact with the body’s immune system and potentially lead to the development of RA. Several environmental factors have been identified and studied in association with rheumatoid arthritis.

Genetic predisposition and environmental factors

Individuals with certain genetic variations are more likely to develop rheumatoid arthritis. However, genetic predisposition alone is not sufficient to cause the disease. Environmental factors play a crucial role in the onset of RA in genetically susceptible individuals. Factors such as infections, smoking, diet, air pollution, stress, hormonal changes, weather conditions and exposure to chemicals are mentioned as possible triggers.

The role of infections in causing rheumatoid arthritis

Infections, especially those caused by certain bacteria and viruses, have been linked to the development of rheumatoid arthritis. It is believed that these infections can trigger an abnormal immune response, leading to the production of antibodies that attack the body’s own tissues. This process can eventually cause the onset of RA in susceptible individuals.

The impact of smoking on rheumatoid arthritis

Smoking has long been recognized as a major environmental cause of rheumatoid arthritis. Research has shown that smokers have a higher risk of developing RA than non-smokers. The chemicals in tobacco smoke can activate immune cells and promote inflammation, contributing to the development and progression of the disease.

Diet and rheumatoid arthritis

Although the relationship between diet and rheumatoid arthritis is complex and not yet fully understood, certain dietary factors have been linked to the risk and severity of RA. For example, diets rich in omega-3 fatty acids, found in oily fish and flaxseed, have shown potential anti-inflammatory effects and may help reduce symptoms of RA. On the other hand, diets high in saturated fats and processed foods can promote inflammation and worsen the condition.

The influence of air pollution

Air pollution, especially particulate matter (PM2.5) and diesel exhaust, has been identified as a potential environmental trigger for rheumatoid arthritis. Inhalation of these pollutants can lead to oxidative stress, inflammation and immune system dysfunction. Long-term exposure to air pollution has been linked to an increased risk of developing RA and worsening symptoms in individuals already diagnosed with the condition.

Stress and rheumatoid arthritis

Chronic stress has been implicated as a trigger for rheumatoid arthritis. Stress can compromise the immune system and promote inflammation, potentially worsening RA symptoms. Although stress alone does not cause the disease, it can contribute to its onset and influence its progression.

Hormonal factors

Hormonal changes, especially in women, have been linked to an increased risk of rheumatoid arthritis. The fluctuation of hormones, such as estrogen, during the reproductive phase and menopause can affect the immune response and contribute to the development or worsening of RA symptoms.

Weather and rheumatoid arthritis

Many people with rheumatoid arthritis report that changes in weather conditions, especially cold and damp weather, can worsen their symptoms. Others say humidity increases swelling and pain in their joints. Although the exact mechanisms behind this association are not yet fully understood, it is thought that changes in temperature and barometric pressure may influence joint inflammation and pain perception in some individuals with RA.

Chemical exposure and rheumatoid arthritis

Exposure to certain chemicals, such as solvents, pesticides and heavy metals, has been linked to an increased risk of developing rheumatoid arthritis. These chemicals can disrupt the immune system and promote inflammation, potentially triggering the onset of RA or worsening its symptoms.

Preventive measures and lifestyle changes

While it may not be possible to completely prevent rheumatoid arthritis, certain preventative measures and lifestyle changes can help reduce the risk and control symptoms. These include maintaining a healthy diet, avoiding smoking and exposure to secondhand smoke, managing stress levels, staying physically active, protecting oneself from infections and minimizing exposure to environmental pollutants and chemicals.

Conclusion

In conclusion, rheumatoid arthritis is a complex disease influenced by both genetic and environmental factors. Environmental factors of rheumatoid arthritis, such as infections, smoking, diet, air pollution, stress, hormonal changes, weather conditions, and chemical exposure may contribute to the onset and progression of RA in genetically predisposed individuals. Understanding these triggers and taking preventative measures can play an important role in controlling the disease and improving the quality of life for people with rheumatoid arthritis.

Frequently Asked Questions

1. Can rheumatoid arthritis be completely prevented?

Rheumatoid arthritis cannot be completely prevented, but certain lifestyle changes can help reduce the risk and manage symptoms effectively.

2. Are all infections associated with rheumatoid arthritis?

Although certain infections have been linked to the development of rheumatoid arthritis, not all infections have been linked to the disease.

3. Is there a specific diet for rheumatoid arthritis?

There is no one-size-fits-all diet for rheumatoid arthritis. However, a balanced and healthy diet that is rich in nutrients and low in processed foods can support overall health and possibly alleviate symptoms.

4. How does air pollution affect rheumatoid arthritis?

Air pollution, especially particulate matter and diesel exhaust, can promote inflammation and oxidative stress, potentially worsening symptoms and increasing the risk of developing rheumatoid arthritis.

5. Can stress alone cause rheumatoid arthritis?

Stress alone may not cause rheumatoid arthritis, but it can contribute to its onset and influence its progression by affecting the immune system and promoting inflammation.

Related

Perhaps one of the most challenging aspects of motherhood with a chronic illness is helping your children understand what’s going on with your body and encouraging acceptance about how your illness affects them. How can you help them develop empathy for what you are experiencing, especially if your illness is invisible? Where is the line between being honest and worrying them? What’s the best way to address their concerns in child-friendly language? This is a topic that will probably need to be an ongoing conversation in your family – and sometimes reading a book together can help!

Click below to read a review of “How Many Marbles Do You Have? Helping Children Understand the Limitations of People with Chronic Fatigue Syndrome and Fibromyalgia” by Melinda Malott.

Children’s book review: How many marbles do you have?

Moms facing forward

Researchers from Keele University’s School of Medicine have found that painkilling drugs – commonly known as ‘analgesics’ – are being widely prescribed across England to people with inflammatory arthritis, despite little research evidence that they improve pain in these patients, and studies which show that they can cause serious side effects. -Effects.

The study, funded by the National Institute for Health and Care Research (NIHR) and published in the journal RheumatologyResearch found that all types of painkillers were widely prescribed: About two-thirds of patients with inflammatory arthritis received a prescription painkiller in 2020, and one in four patients received long-term prescription opioids. Many of these long-term prescriptions for opioids started around the time people were diagnosed with inflammatory arthritis.

Worryingly, many types of painkillers were more likely to be prescribed to people with inflammatory arthritis who were older (and therefore most at risk of side effects from medicines), were women, lived in deprived areas and in the north of England. This suggests there is unfairness about pain, or the way pain is managed in people with inflammatory arthritis in the NHS.

Inflammatory arthritis groups together conditions that cause joint pain and swelling. Its three main types – rheumatoid arthritis, psoriatic arthritis and axial spondyloarthritis – affect more than 1% of adults in England. Pain is a major challenge for patients with inflammatory arthritis, with most patients suffering daily pain and viewing pain as the area of ​​their health they most want to see improved.

The crucial first step in improving NHS pain care for these patients is understanding how it is managed. To address this, the research team looked at data from a large GP database – the Clinical Practice Research Datalink Aurum – which currently contains information from more than 1,400 GP practices across England.

They looked at data from 2004 to 2020 to understand how different types of painkillers are prescribed to patients with inflammatory arthritis, and how this varies between people based on their age, gender, ethnicity and where they live.

Lead author Dr Ian Scott said the findings show there is an urgent need to improve the way pain is treated in patients with inflammatory arthritis in the English NHS. He described the fact that one in four patients were prescribed long-term opioids, and in 2020, one in ten patients were prescribed gabapentinoids, despite these medications having many potential side effects and no clinical trials showing they help when taken on be used this way. , as “very worrying”.

There are better ways to treat pain in patients with inflammatory arthritis that have been shown to help in clinical trials. These include reducing joint inflammation using specialized disease-modifying medications and exercise. We need to shift the focus of pain care from the long-term use of ineffective painkillers to the use of treatments that have been shown to help.”

Dr. Ian Scott, lead author