Increased Risk of Post-Acute Sequalae of COVID-19 in Patients With Immune-Mediated Inflammatory Diseases, 2025, Vitus et al.

SNT Gatchaman

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Increased Risk of Post-Acute Sequalae of COVID-19 in Patients With Immune-Mediated Inflammatory Diseases
Evangelin Shaloom Vitus; Christian Nikolai Sørensen; Anastasia Karachalia Sandri; Rahma Elmahdi; Tine Jess

BACKGROUND AND AIMS
Dysregulation of the immune system and chronic inflammation, the primary drivers of post-acute sequalae of corona virus disease 2019 (COVID-19) (PASC), are at the heart of immune-mediated inflammatory disease (IMID) pathology. As PASC remains underexplored in IMID patients, we explored the risk of PASC in patients with IMIDs including spondylarthritis (SpA), rheumatoid arthritis (RA), hidradenitis suppurativa, ulcerative colitis, Crohn's disease and psoriasis compared to a matched non-IMID population.

METHODS
In this cohort study, all individuals with a recorded positive severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) test (January 2020 to January 2022) were identified from the Danish national registers. Cox regression was used to compare COVID-positive IMID persons with matched COVID-positive non-IMID ones. Subgroup analysis by COVID-related hospitalization, COVID vaccination, IMID medication, and stratification analysis by age, sex, and SARS-CoV-2 variant were carried out.

RESULTS
A total of 753 PASC cases were reported among 25,889 IMID and 51,778 matched individuals. The median age and follow-up time were 48 years (interquartile range: 35–61) and 7.7 months (interquartile range: 7.1–16.1), respectively, and 56% were women. An increased risk of PASC was seen in the IMID group as a whole compared to the non-IMID group (hazard ratio (HR): 1.64, 95% confidence interval (CI): 1.42–1.89), and for SpA (HR: 2.05, 95% CI: 1.30–3.22), RA (HR: 1.90, 95% CI: 1.38–2.61), and psoriasis (HR: 1.62, 95% CI: 1.31–2.01) individually. The risk of PASC remained higher among hospitalized and vaccinated IMID patients.

CONCLUSION
This study showed an increased risk of PASC in individuals with an IMID and in SpA, RA, and psoriasis individually. Results indicate chronic impact of early SARS-CoV-2 infection on IMID patients following acute COVID-19.

Link | PDF | Gastro Hep Advances [Open Access]
 
Fascinating that PASC is increased with ank spond - which basically means HLA-B27. B27 tends to protect against viral problems, which is probably why it survives in the population despite AS. This is the first instance I know of of it having a downside in the context of virus.

Maybe ME/CFS is the price humanity pays for some gain-control setting in an immune response pathway that protects against smallpox or measles encephalitis but has its downside. How that relates to the B27 issue is fascinating.

There are going to be a lot of genes to look for in the DecodeME dataset to see if they are, perhaps surprisingly, unbiased. B27, EDS genes, allergy genes, insulin resistance genes, CRP responsiveness genes...
 
Fascinating that PASC is increased with ank spond - which basically means HLA-B27. B27 tends to protect against viral problems, which is probably why it survives in the population despite AS. This is the first instance I know of of it having a downside in the context of virus.

Maybe ME/CFS is the price humanity pays for some gain-control setting in an immune response pathway that protects against smallpox or measles encephalitis but has its downside. How that relates to the B27 issue is fascinating.

There are going to be a lot of genes to look for in the DecodeME dataset to see if they are, perhaps surprisingly, unbiased. B27, EDS genes, allergy genes, insulin resistance genes, CRP responsiveness genes...
Are there other known examples of diseases that are «the price we have to pay» for a beneficial trait?
 
Maybe ME/CFS is the price humanity pays for some gain-control setting in an immune response pathway that protects against smallpox or measles encephalitis but has its downside. How that relates to the B27 issue is fascinating.
I've been thinking that ME/CFS is the result of the monostability of the immune system that needs to maintain the fine balance between protecting you from the environmental insult and making you sick all the time. It falls, and it can't right itself up easily since it is monostable.
 
I've been thinking that ME/CFS is the result of the monostability of the immune system that needs to maintain the fine balance between protecting you from the environmental insult and making you sick all the time. It falls, and it can't right itself up easily since it is monostable.
I’ve been on a similar track. I actually haven’t gotten sick with an infection at all in the past 6 years, even prior to COVID when I was interacting with people more regularly. I mostly attributed that to being less able to interact in person and then needing to be COVID cautious, but there were a couple instances where I was the only person in the room to walk away without catching an infection.

I’ve heard anecdotes here and there from other pwME reporting something similar—where they seem less likely to catch an infection but if they do catch something, it ends up being hell (though often after a brief period of improvement before infection symptoms start). It’s just hard to disentangle the phenomenon from other confounding factors re: social interaction and exposure.
 
I've been thinking that ME/CFS is the result of the monostability of the immune system that needs to maintain the fine balance between protecting you from the environmental insult and making you sick all the time. It falls, and it can't right itself up easily since it is monostable.
Isn’t it bi- or multistable system if it can get stuck in more than one position?
 
Yes, I was puzzled by monostable.
I think the tradec off between strategies provided by different genes is probably something different from any bistability. Any given individual only has one strategy.
 
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