There are various possible post-acute COVID-19 symptoms.
Cardiorespiratory functional capacity may sometimes take a few weeks to months to recover.
Patients who experienced extensive clotting may have longer-lasting damage to affected areas.
@Longco191 There may be a risk of developing an autoimmune or autoinflammatory condition, such as a new joint or connective tissue disorder, potentially requiring assessment by a rheumatologist for diagnosis and treatment. Anecdotally, this often does appear to be treatable to some extent.
@Longco191 Some acutely recovered patients have reported fairly strong indicators of developing POTS, which is usually symptomatically treatable with appropriate medication by e.g. GPs familiarized with the issue. The underlying cause is usually harder to address and may be neurological.
@Longco191 Anosmia usually recovers within months. Treatments for refractory cases are still an area of research.
Reports of Sicca syndrome.
There are also some rarer reported issues, e.g.: new endocrine disorders, hypertension, diabetes, MS, GBS, in one case Parkinson's disorder, etc.
@Longco191 Even after accounting for these, some COVID-19 survivors have symptoms potentially consistent with ME/CFS. Specific cases vary.
It is important to address any other known issues first. Fatigue may arise from something more tractable.
ME/CFS treatments are an area of research.
@Longco191 Overall, post-COVID-19 subchronic or potentially chronic symptoms arise from diverse underlying causes, and are best treated or managed separately as distinct conditions.
There is no unified "long-haul COVID-19" disorder. There are only various possible lasting complications.
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Terguride (5-HT2A/B antagonist) for prevention of PAH and ventricular or pulmonary fibrosis in conditions of acutely elevated plasma 5-HT @farid__jalali
The secretome of such cells is often inflammatory (see first reference above) and has been shown to be metabolically disruptive for at least some viruses (more data on CoVs would be helpful):
Real-world viral load in respiratory secretions is likely a couple orders of magnitude lower than the viral concentrations in the aerosols used in this test:
Converging evidence seems to indicate a common underlying mechanism for ME/CFS of specifically post-viral origin might result from DRP1-inducing warning signals from infected leukocytes.
Should be possible for any virus that can persistently infect leukocytes.
May be more persistent if virus has reached bone marrow. Predict more chronic symptoms in patients w/ bone marrow infection.
Indirect remedial measures: mitochondrial antioxidants, co-factors, e.g. CoQ10, NADH.
Anyway this is still early and speculative. There are other theories too.
But it explains why steroids may help recent cases and not old ones, why rituximab helped in some studies, why mitochondrial ROS is high and glycolysis starts quickly, why ME/CFS plasma *causes it*, etc
@GemzME@sickanddamned I mean yes you will end up with rhabdomyolysis if you push too hard at the limits of dysfunctional mitochondria in muscle tissue.
I will also predict considerable myalgia in ME/CFS patients after little exercise. And yes, this appears to be the case.
Pardon delayed responses. I seem to have contracted a respiratory virus after maintenance staff visited my residence.
On the bright side, treatments discussed seem to work. Mostly feeling better after ~2.5 days of nasal/throat irritation, myalgia, low fever, headache, fatigue.
First symptom was scratchy feeling in oropharynx, then recalcitrant headache and fever and fatigue, then intermittent burning feeling in nasal passages, but only partial loss of olfactory perception.
Still feel a bit unsteady and tired from past fever but otherwise no symptoms.