ice9 Profile picture
23 Oct, 5 tweets, 4 min read
Terguride (5-HT2A/B antagonist) for prevention of PAH and ventricular or pulmonary fibrosis in conditions of acutely elevated plasma 5-HT @farid__jalali

hindawi.com/journals/bmri/…

pubmed.ncbi.nlm.nih.gov/28821451/

researchgate.net/publication/51…
This might complement the effects of cyproheptadine and/or famotidine in the treatment of acute serotonin syndrome:

Precedex (dexmedetomidine) has also drawn favorable commentary recently for ICU cases, and likewise has a history of use in serotonin syndrome.

Linking for reference--

Thread discussing evidence that plasma 5-HT is generally highly elevated in moderate to severe COVID-19 cases, including direct confirmation from blood tests in a sample of such patients, as well as practical consequences:

Pimethixene is also a 5-HT2B antagonist, though it isn't very widely available. It also has antipsychotic properties.

Might be useful in serotonin syndrome. It is fairly similar to cyproheptadine, but may be marginally more potent.

Brands listed for Brazil, France, Tunisia.

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More from @__ice9

23 Oct
@Longco191 That is a more complex question.

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.
Read 6 tweets
22 Oct
Further thoughts on post-viral ME/CFS after more literature review.

Initial suspicions about infected leukocytes were too narrow.

Persistently, latently, or formerly infected cells in tissues with low turnover are a more likely culprit.
Clearance of such cells in ME/CFS patients is impaired.

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):

Read 9 tweets
22 Oct
Mask tests, worst-case short-distance pure-aerosol:

- increased distance somewhat protective

- cotton and surgical masks somewhat protective if worn by spreader, limited if recipient

- N95 masks highly protective on spreader, moderately highly on recipient; fit also matters
Important:

- this is a worst-case test

- none of the masks fully protected

- hospital staff should use PAPR/CAPR if possible

- limit proximity/duration of contact

- if you think you may be infected, avoid others; wear good quality mask otherwise

msphere.asm.org/content/msph/5…
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:

Read 7 tweets
22 Oct
First pass:

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.
Not sure how to correct.

Perhaps more apoptosis? Steroids then.

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
Read 4 tweets
21 Oct
@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.
@GemzME @sickanddamned Questions:

- What is the mechanism of indomethacin-induced mitochondrial fragmentation and ROS increase, and does it occur in a relevant immune response also?

- What is mechanism of COVID-19 myalgia? Is it related?

- What about myalgia in other viruses, esp w/ high lactate?
@GemzME @sickanddamned Indomethacin activates PKCζ-p38-DRP1 pathway, causing rapid mitochondrial fission and risking apoptosis.
jbc.org/content/early/…

Blocked by mitochondrial fission inhibitor mdivi-1

DRP1 is also induced by p53 in some viral infections, interestingly.
solvecfs.org/hhv-6-mediated…
Read 59 tweets
13 Oct
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.
Used:
- alcoholic mouthwash gargling 3x/day, ended odd sensations in throat quickly
- vitamin D 2000 IU 2x/day
- vitamin C 1g 3x/day
- nitazoxanide 500mg 3x/day
- umifenovir 200mg 3x/day
- bromhexine 8mg 3x/day
- ambroxol 15mg 3x/day
- hydroxychloroquine 200mg 2x/day
...
Read 7 tweets

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