Zdenek Vrozina Profile picture
May 28 16 tweets 2 min read Read on X
Another study where long COVID does not look like a small residual problem after infection, but like broad chronic illness scattered across everyday medicine.
And that is exactly why the system often fails to see it🧵
The study analyzed data from 58 US hospitals.
The algorithm identified PASC in 16.28% of patients after COVID.
Roughly 1 in 6!
The most important part is not only how many people have long COVID.
It is that most of the detected manifestations were not short acute episodes.
They were mostly chronic or potentially chronic conditions.
The more important number is this -
14.54% of all post-COVID patients had chronic PASC burden!
That is not a few weeks of cough after a virus.
That means long-term care, follow-ups, specialists, tests, medication, and work limitations.
The cumulative prevalence of PASC did not decline.
It slightly increased through mid-2024.
The authors interpret this as an accumulating burden, not just the fading tail of early pandemic waves.
Long COVID often does not appear in the system as long COVID.
Instead, the patient shows up
to primary care with fatigue,
to cardiology with dysautonomia or palpitations,
to endocrinology with a new metabolic problem,
to neurology with cognitive symptoms.
And this is the coding problem.
Many of these patients are not coded as long COVID/PASC. They are coded under the specific diagnosis they present with. Fatigue, palpitations, dysautonomia, cognitive symptoms, respiratory problems, abnormal glucose, prediabetes, or other chronic conditions.
Without a connecting code, the burden fragments into many ordinary diagnoses.
The system then fails to see it as post-infectious chronic disease, even while it is already carrying it clinically.
That is the real strength of this study.
It challenges the illusion we don’t see long COVID, so it isn’t there.
The opposite is true.
Part of the burden is already inside the system, just split across diagnoses and specialties.
Healthcare does not need to report a collapse of long COVID clinics to be under pressure.
The burden can show up as more prediabetes/diabetes, more fatigue syndromes, more neurology visits, more cardiology complaints, and more respiratory problems.
The system is treating it.
It just often cannot see the common denominator.
Long COVID does not have to overwhelm healthcare under one label.
It can burden it as thousands of ordinary diagnoses without a shared code.
There was no COVID-negative control group, and some variation may reflect coding practices.
But the signal is large.
After COVID, we are seeing broad, long-term, poorly coded illness.
And if we cannot name it properly, that does not mean it does not exist.
It means we are measuring it badly.
And it may also mean we are treating it poorly.
If post-COVID illness is fragmented across specialties without a shared framework, patients may receive treatment for isolated symptoms while the underlying post-infectious process remains unrecognized. @szupraha @ZdravkoOnline @adamvojtech86
Fragmented recognition often leads to fragmented care.
Tian at al., Long COVID Persistence and Surveillance Gaps Across 58 US Hospitals. jamanetwork.com/journals/jaman…

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More from @ZdenekVrozina

Jun 8
A genuinely interesting study.
Researchers from Johns Hopkins looked at how SARS2 infection changes the cardiac autonomic nervous system - how the heart is regulated through the sympathetic and parasympathetic branches.
It’s not one fixed state.
It’s a process.
In three phases🧵
Why does this matter?
Because dysautonomia is one of the common features of Long COVID -
palpitations, dizziness, fatigue, orthostatic intolerance, POTS etc
The autonomic nervous system helps regulate heart rate, blood pressure, breathing, digestion, the body’s ability to adapt to stress.
This wasn’t a human study.
It was a hamster model of COVID-19.
So researchers can follow the infection very closely, repeatedly, at precise time points.
Translation to humans is always limited.
A hamster is not a human - even if some models would like to be.
Read 25 tweets
Jun 6
Viral proteins can activate the same pathways after infection that connect neuroinflammation, synapse loss, tau, alpha-synuclein, and broken cellular cleanup.
That’s why parallels with other viruses, including HIV, matter.
A new review tries to put this whole story together. 🧵
The main point is not that SARS2 has to keep massively replicating in the brain.
The authors suggest a protein-as-pathogen model.
Viral proteins themselves may act as long-term triggers, keeping nervous tissue stuck in innate immune activation, stress, and poor cellular cleanup.
The core pathway looks like this -
viral protein
TLR2/TLR4
microglia and astrocytes
NLRP3/interferon signaling
synapse loss
tau and alpha-synuclein
impaired autophagy and proteostasis!
That convergence is the heart of the review.
Read 22 tweets
Jun 5
Does the brain always return to baseline after COVID?
A new multimodal MRI study suggests the answer may be - not always.
After infection, some brains may remain in a different network state - and we still do not know if that state is temporary, compensatory, or maladaptive🧵
The important part is not one single MRI finding.
The strength of this study is that it combines three MRI layers
structural MRI - grey matter volume,
diffusion MRI - white-matter microstructure,
resting-state fMRI - functional connectivity.
The study included 76 people recovered from COVID-19 and 51 healthy controls.
The authors looked at the whole recovered group, and then stratified COVID participants by severity
non-hospitalized vs hospitalized.
That matters, because some effects only became visible when severity was taken into account.
Read 20 tweets
Jun 4
Almost one year after SARS2 infection, children with Long COVID showed measurable changes in the tiny blood vessels of the retina.
Wider arterioles.
Wider venules.
A shifted arteriole-to-venule ratio.
This was not just a symptom survey.
It was an objective microvascular signal🧵
The authors looked at retinal blood vessels in the eye - because the retina offers a non-invasive window into the body’s microcirculation.
And this was not just a few weeks after infection.
The first examination happened roughly 44-50 weeks after SARS2 infection.
So, basically, around one year later.
Read 19 tweets
Jun 3
Child can recover from COVID.
Their routine tests can look normal.
Yet more sensitive testing may still detect abnormalities in the lungs, immune system, quality of life, and possibly even the heart.
A new review from Taiwan's DISCOVER cohort helps explain why🧵
This is not a single study.
It is a summary of findings from the DISCOVER program, the largest Taiwanese research project focused on pediatric Long COVID (PASC), covering more than 500 children and adolescents after SARS-CoV-2 infection.
An important detail.
Taiwan largely avoided the Alpha and Delta waves.
Most children in this cohort were infected during Omicron surge.
That makes this one of the clearest looks at pediatric post Omicron Long COVID.
Read 19 tweets
May 31
This study is important because it captures a small, systematic shift in a marker of cardiac injury across the population after COVID-19.
And that is exactly the signal that can be easily missed in an individual, but may matter in public health🧵
The authors had an unusually valuable situation. People had their troponin I measured before the pandemic, and then again after a period during which some of them had SARS2 infection.
The result is fairly consistent. Previous SARS2 infection was associated with higher cTnI after the pandemic and with a higher probability of troponin rising between the two measurements.
Read 14 tweets

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