Category: Knee Arthritis

Tips for Parenting with Rheumatoid Arthritis

Parenting is hard at first – but rewarding. Add a chronic condition like RA to the mix, and that delicate balance between your self-care and your role as a parent can easily get lost. These tips and strategies can help you get through difficult days, manage your energy, and make meaningful memories with your family.

I was recently interviewed for the WebMD article below, which provides tips for parenting while living with rheumatoid arthritis. Although the article focuses on RA, many of the tips mentioned would apply to other chronic diseases as well!

I’ve always believed that parents with chronic illness deserved more recognition and support – that’s why I started Mamas Facing Forward in the first place! So it’s exciting to see this topic being addressed in a more mainstream health publication. Hopefully this article will help other parents realize they are not alone – and find their way to us where we can continue to support them!

Tips for Parenting with Rheumatoid Arthritis

WebMD

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October 25, 2023
Tapering and discontinuation of glucocorticoids in patients with rheumatoid arthritis treated with tofacitinib

This study aimed to evaluate the steroid-sparing effect of tofacitinib in patients with RA. To the best of our knowledge, this is the first prospective study that evaluated the feasibility of a predetermined schedule for GCs discontinuation in patients initiating tofacitinib treatment. This showed that already 12 weeks after starting treatment, 30% of patients were able to stop their daily dose of GCs. The most recent recommendations for the treatment of RA suggest that the dosage of GCs should be reduced to discontinuation as soon as possible¹. In fact, the dose and duration of steroid treatment influence the safety profile and there is no agreement on the definition of the ‘safe’ dose.¹⁷. The optimal dose and duration of GC therapy and the best strategy to taper off and withdraw GCs are still scarce. A recent systematic literature review reported 14 different regimens proposed to reduce and/or stop oral GCs¹⁸. Randomized clinical trials with RA drugs do not provide sufficient information on GC therapy during treatment with biologics and do not allow to displace definitive conclusions on GC discontinuation, also considering that the steroid-sparing effect never appears as a secondary endpoint¹⁹.

A subanalysis of the ACTION (AbataCepT In rOutiNe Clinical Practice) study showed that over a 24-month period from the start of abatacept, approximately 40% of the 734 patients taking GCs at the start of the study were able to control their prednisone levels to lower. dose, usually within the first 3 months of treatment, and that the median GC dose decreased from 7.5 mg/day to 5 mg/day after 24 months of treatment²⁰. The need to evaluate the steroid-sparing effect of RA medications is real and relevant, as evidenced by real-world studies. Most real-world evidence comes from retrospective studies evaluating the effect of bDMARDs on GC therapy in patients with long-standing RA, such as those enrolled in our study. Many years ago, Naumann et al. described dose reduction of GCs that was associated with reduced disease activity as early as 3 months after starting a TNF inhibitor in 87 patients with RA; during 5 years of follow-up, 81% of patients reduced the dose of GCs and 32% of patients discontinued treatment²¹.

In a French retrospective study published in 2009, the authors noted an overall 30% reduction in the dose of oral GCs in the first year of treatment with TNF inhibitors, starting as early as 3 months; on the other hand, 61% of patients were still using low-dose prednisone after 1 year⁷. More recently, analysis of the TReasure database found that after a median of 59 months, 28.4% of 1936 patients receiving GCs at registry entry discontinued concomitant steroid treatment.²². The retrospective nature of the study explains the lack of prespecified criteria for GC tapering. The SPARE-1 study included RA patients treated with tocilizumab (TCZ) and an oral prednisone dose > 5 mg/day and aimed to evaluate the percentage of patients who reduced their GC dose to less than 5 mg/day after 12 months of TCZ²². At the end of follow-up, 40% of patients reached the target dose; RA duration not more than 5 years, daily prednisone dose <7.5 mg, and low baseline ESR were predictive of PDN reduction to less than 5 mg/day²³.

Fernandez-Nebro et al. prospectively followed for 24 months 161 patients starting infliximab, etanercept, or adalimumab, showing that almost 60% of patients taking GCs at baseline were able to discontinue and the remaining patients significantly reduced the daily dose²⁴. In a previous paper published by our group, we demonstrated a 56% reduction in the percentage of RA patients treated with baricitinib who were taking glucocorticoids after 24 weeks; In addition, we registered a significant reduction in the daily dose of prednisone from an average of 5 mg/day to 0 mg/day, simultaneously with a significant reduction in pain after just 4 weeks.²⁵. Similarly, in the current study, the rapid effect of tofacitinib on pain and disease activity certainly contributed to the rapid reduction of the dose of GCs, to complete discontinuation; Indeed, approximately one-third of included patients discontinued daily GCs within 12 weeks of starting tofacitinib.

The initial adjunctive GCs therapy on a DMARD background would allow rapid control of disease activity, also guaranteeing long-term structural benefits, which persist even after GCs withdrawal; doses ranging from 5 to 10 prednisone per day appear to be associated with significantly slower radiographic progression². A post hoc analysis of 6 randomized, controlled phase III trials of tofacitinib suggested that concomitant use of GCs did not affect either the clinical or radiographic efficacy of the drug.²⁶. In a prospective evaluation of the efficacy of tofacitinib according to discontinuation of GCs, we observed no difference in the reduction of disease activity as assessed by DAS28_CRP, CDAI and SDAI; furthermore, low disease activity or remission was achieved regardless of the concomitant use of GCs. In contrast, data from a Turkish registry showed a significantly higher DAS28_CRP score and a significantly lower proportion of patients achieving low disease activity or remission in patients who continued GCs concurrently with bDMARDs or tsDMARDs.²⁰. Data on the effect of GCs on clinical response to TNF inhibitors are also conflicting and have shown that a higher or lower percentage of patients achieve the treatment goal.^27,28. In the SEMIRA (The Steroid EliMination In Rheumatoid Arthritis) trial, patients were randomly assigned to the regimen of continued prednisone or tapered prednisone; two-thirds of patients who achieved low disease activity with tocilizumab tapered the steroid dose in the 24-week study, but contrary to what we observed in our patients, patients who continued with prednisone had better control of disease activity²⁹.

In our study, age at enrollment and disease duration were negatively associated with GC discontinuation. This is not surprising, as results from a recent double-blind, placebo-controlled study showed that elderly patients (over 70 years at baseline) with established and severe RA had long-term beneficial effects in both disease and disease activity. and joint damage resulting from taking a low dose of prednisolone as an addition to basic treatment³⁰. However, this study did not include patients taking tsDMARDs. Recently, data from the Veterans Affairs Rheumatoid Arthritis Registry showed that 54% of patients tapered and 33% discontinued oral GCs; younger age, positive rheumatoid factor, higher ESR at enrollment, a greater number of prior csDMARDs, and a higher mean glucocorticoid dose during the 30 days before the index date were all significantly associated with GC tapering and discontinuation³¹.

The 2013 EULAR recommendations on the treatment of moderate to high doses of glucocorticoids in rheumatic diseases state that “When deciding to initiate glucocorticoid treatment, comorbidities and risk factors for adverse effects should be evaluated and treated where indicated […]”³². Particularly at medium to high doses, GCs are often associated with the occurrence of adverse events, including osteoporosis, diabetes, hypertension, cardiovascular events, and recurrent infections. Sparing GCs – as suggested by our results – may be beneficial in terms of short-term safety (risk of infection, especially reactivation of herpes Zoster) and long-term safety (metabolic and cardiovascular events, as well as osteoporotic fractures ). A large study of RA patients from the CorEvitas registry showed that GCs increased the risk of cardiovascular events after just six months of treatment, at a daily dose of more than 5 mg³³.

Some of these side effects – mainly infections and cardio-metabolic effects – raise concerns in patients treated with both bDMARDs and tsDMARDs; in particular, the results of the ORAL Surveillance study raised a warning about cardiovascular safety in patients treated with tofacitinib³⁴.

The current study has some limitations. The small sample size did not allow stratification of patients based on concurrently administered MTX. However, the MTX dose remained stable and the logistic regression did not identify the co-medication as a factor influencing the ability to discontinue GCs. The long disease duration and failure of previous treatments probably caused the steroid-sparing effect of tofacitinib to be underestimated. Still, 30% of patients stopping GCs after just three months is an impressive result.

The strength of the study lies in its prospective nature and interventional design, which allowed the GC dose reduction schedule to be predefined to homogenize the outcome.

In conclusion, in our cohort of patients with long-standing RA treated with tofacitinib, discontinuation of glucocorticoids was feasible in up to 30% of patients. The results of the study should encourage rheumatologists to consider GC tapering and withdrawal as a possible goal in the daily management of RA patients on long-term treatment with oral GC.

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October 25, 2023
Genetic markers can help women with rheumatoid arthritis make informed decisions about pregnancy

When women with rheumatoid arthritis (RA) plan to become pregnant, many worry about whether they should stop their medications, risking a flare-up of their disease, or continue taking medications and risk possible damage to the baby.

About 50% to 75% will see their disease improve naturally during pregnancy for reasons yet unknown, while others may see a worsening of their RA. But they couldn’t have known what would happen to them.

Now, for the first time, Northwestern Medicine scientists have identified pre-pregnancy genetic markers that can predict who will get better and who will get worse.

The research was published this week in Research and therapy for arthritis.

RA is an incurable disease that affects 1% of the world’s adult population and is three times more common in women. It leads to significant disability due to inflammation of the joints and destruction of cartilage and bones.

“When women with RA become pregnant, there is often a natural improvement,” said lead researcher Damini Jawaheer, associate professor of medicine in rheumatology at Northwestern University Feinberg School of Medicine. “They describe it as ‘a miracle.’ They say, “I’ve never felt better with the medicine I’ve been taking.” But the cause of this improvement is a complete mystery.

“If women with RA can know in advance whether their disease is likely to resolve during pregnancy, they know they can stop taking their medications. Some RA medications are toxic and affect the fetus, while others are considered safe. But some women with RA don’t want to take RA medications during pregnancy, even those that are considered safe.”

Being able to predict who will get better and who will get worse will help women in their pregnancy planning and will also help ensure that treatment during pregnancy is targeted only to those women who are predicted to get worse, Jawaheer said . In addition, women who are predicted to improve, and their fetuses, will not be unnecessarily exposed to medications.

Jawaheer and her team found that before pregnancy, a group of white blood cells called neutrophils were highly expressed among the women who improved during pregnancy, and that some genes related to B cells were highly expressed among women who deteriorated.

This field hasn’t been well studied, in part because it’s difficult to find women for pregnancy screenings before they become pregnant, Jawaheer said.

She and colleagues were able to conduct the study because they had previously established a unique pregnancy cohort in Denmark, which enrolled women with RA and healthy women before pregnancy and followed them over time to determine who improved and who deteriorated. Using blood samples taken from these women before pregnancy, they examined the levels of several genes expressed in the blood. Blood samples were collected before pregnancy from 19 women with RA and 13 healthy women participating in the prospective pregnancy cohort.

Next, Jawaheer plans to conduct a study on a larger cohort of women to validate these findings. Additionally, her lab is trying to figure out why RA improves during pregnancy.

How does nature ensure that an incurable disease disappears? If we can understand how pregnancy produces natural improvement, we can use that as a model to develop a new drug that would be safer and could improve the lives of women and men living with this terrible disease.”

Damini Jawaheer, associate professor of medicine in rheumatology at Northwestern University Feinberg School of Medicine

The name of the paper is: “Pre-pregnancy gene expression traits are associated with subsequent improvement/worsening of rheumatoid arthritis during pregnancy.”

The other Northwestern author is Matthew Wright.

The study was funded by grants R21AR057931 and R01AR073111 from the National Institute of Arthritis, Musculoskeletal and Skin Diseases of the National Institutes of Health and by Gigtforeningen and Juliane Marie Center in Denmark.

Source:

Magazine reference:

Wright, M., et al. (2023). Pre-pregnancy gene expression signatures are associated with subsequent improvement/worsening of rheumatoid arthritis during pregnancy. Research and therapy for arthritis. doi.org/10.1186/s13075-023-03169-6.

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October 25, 2023
From this moment on. Ahead.: Rheumatoid Arthritis and Sex: Tips to Improve Intimacy

Rheumatoid arthritis (RA) can find its way into every aspect of your life, including your sex life… You can still have a healthy sex life if you have RA… But you may need to find other ways that work best for you and your partner .

WebMD

I was recently interviewed for the WebMD article below, which provides tips for improving intimacy while living with rheumatoid arthritis. I speak from personal experience when I say that this is a topic where it used to be impossible to find positive, uplifting advice. That’s why I started speaking out on this very personal topic in the first place! It’s exciting to see this topic covered in a more mainstream health publication! Hopefully the article will help raise awareness that couples facing these challenges are not alone or unusual – and encourage people to contact their doctor for help if necessary.

Rheumatoid Arthritis and Sex: Tips to Improve Intimacy

WebMD

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October 25, 2023
Is there a connection between the onset of psoriasis and the risk of autoimmune diseases?

In a recent study published in the Scientific Reports Journal, researchers evaluated the risk of new autoimmune diseases in individuals with early psoriatic disease.

Study: Risk of incident autoimmune diseases in patients with newly diagnosed psoriatic disease: a national population-based study. Image credits: Flystock/Shutterstock.com

Background

Psoriatic disease, which often includes psoriasis and psoriatic arthritis, is a systemic inflammation-related disease with serious clinical consequences.

Autoreactive T lymphocytes, which express proinflammatory cytokines such as interleukins (ILs)-17 and 22, and interferon-gamma (INF-γ) characterize psoriatic diseases.

Studies have linked the autoimmune component of psoriasis to several autoimmune diseases, including autoimmune thyroid diseases, inflammatory bowel disease, alopecia areata, and autoimmune rheumatic diseases.

About the study

In the national population study, researchers evaluated the link between autoimmune diseases and psoriatic diseases.

Patients with newly diagnosed psoriatic disease between January 2007 and December 2019 were included in the study, using the Korean National Health Insurance Service (NHIS) database.

The team used previously established diagnostic algorithms for psoriatic disease in Korea to identify people with the condition. Patients with psoriatic disease had one or more recorded visits with psoriatic diseases such as psoriasis and psoriatic arthritis as their primary diagnostic code and vitamin D prescriptions.

Autoimmune diseases such as CD, UC, Graves’ disease, Hashimoto’s disease, SLE, RA, Sjögren’s syndrome, systemic sclerosis, AS, type 1 diabetes and alopecia areata were studied.

Comparators who had no diagnostic code for psoriatic diseases between January 2005 and December 2019 and no diagnostic code for autoimmune diseases during the washout were randomly selected and matched on sex and age at a 1:1 ratio.

In addition to the diagnostic codes, the researchers also added relevant prescription information for medications and RID codes for all diseases to the diagnostic algorithms for outcomes.

The team added follow-up information on newly identified autoimmune diseases from 2007 to 2020. Multivariate Cox regression modeling was performed to determine adjusted risk ratios (aHRs).

The Charlson Comorbidity Index (CCI) values for comorbidities such as hypertension, diabetes, dyslipidemia, chronic obstructive pulmonary disease (COPD), liver cirrhosis, chronic kidney disease, alcoholic liver disease, and heart failure were determined. The team conducted subgroup analyzes based on gender, age and severity of psoriatic disease.

Patients who received diagnostic codes for psoriatic disease between January 2005 and December 2006 were excluded from the study.

Additionally, the team excluded individuals diagnosed with autoimmune diseases [Crohn’s disease (CD), ulcerative colitis (UC), Graves’ disease, Hashimoto’s disease, systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), Sjögren’s syndrome, ankylosing spondylitis (AS), systemic sclerosis, alopecia areata, and diabetes type 1] before diagnosis of psoriatic disease and those followed for less than one year.

Results

The study included 321,354 individuals in the psoriatic and control groups with a mean age of 43 years, and 59% were men.

Patients with psoriasis showed a significantly increased risk of ankylosing spondylitis, systemic lupus erythematosus, ulcerative colitis, Crohn’s disease, alopecia areata, type 1 diabetes and rheumatoid arthritis, with aHR values of 2.3, 1.9, 1.7 , 2.0, 1.4, 1.2 and 1.6. respectively.

On the other hand, the risks for Hashimoto’s disease, Graves’ disease, systemic sclerosis and Sjögren’s syndrome did not differ significantly between the groups. Type 1 diabetes, alopecia areata, AS, RA, SLE, UC, and CS had NNH values of 9,567, 1,295, 9,946, 3,256, 47,987, 17,899, and 39,988 individual years, respectively.

With the exception of type 1 diabetes, all autoimmune diseases showed a significantly increased risk in psoriatic subjects compared to controls after controlling for CCI and insurance type. After controlling for CCI and insurance type, the risk of type 1 diabetes (aHR, 1.1) was not significant in men with psoriatic disease compared with male controls.

After adjusting for type of insurance and CCI, all autoimmune diseases showed significantly greater risks in younger psoriatic individuals under 40 years of age and in individuals 40 years of age and older compared with controls.

After controlling for insurance type and CCI, CD risk (aHR, 1.4) was not significantly greater in older psoriatic subjects than in controls.

Mild and moderate psoriatic disease occurred in 79% (n=255,285) and 21% (n=66,069) of patients with psoriatic disease, respectively, including the incidence of UC, CD, RA, SLE, alopecia areata, and type diabetes. 1, and AS were greater compared to controls.

After controlling for age, gender, CCI, and insurance type, patients with moderate to severe psoriatic disease showed a significantly increased risk of rheumatoid arthritis, AS, and type 1 diabetes, with aHR values of 1.5, 1.5, and 1.2, respectively.

Conclusion

Based on the study results, patients with psoriatic conditions have a greater chance of developing autoimmune diseases.

This study also found the occurrence of autoimmune diseases unrelated to psoriasis, such as Graves’ disease, Hashimoto’s disease, Sjögren’s syndrome, and systemic sclerosis. Due to the low absolute risk, routine screening for these conditions may not be recommended.

However, appropriate investigations may be necessary in individuals with psoriatic disease to determine the existence of concomitant alopecia areata and provide tailored therapy.

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October 24, 2023
COVID-19 increases the risk of autoimmune diseases

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.

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October 24, 2023
Understanding the genetics of rheumatoid arthritis and its implications

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.

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October 24, 2023
3 tips for achieving big life goals while living with a chronic illness

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

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October 24, 2023
You don’t look sick – Living with rheumatoid arthritis: VEGAN PAN DINNER

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…

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October 23, 2023
Inflammatory diseases do not increase the risk of clotting after COVID, research shows
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.
Magazine reference:

Khan, R., Ellen, K. M., Tang, F., James, Widdifield, J., McCurdy, J. D., Kaplan, GG, & Benchimol, E. I. (2023). Venous thromboembolism after COVID-19 infection in people with and without immune-mediated inflammatory diseases. JAMA network opened, 6(10), e2337020–e2337020. https://doi.org/10.1001/jamanetworkopen.2023.37020
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October 23, 2023