Mudr. Jan Machač

Léčba dlouhého COVIDU dle FLCCC

Dosavadní zkušenosti s léčbou „long-Covidu“:

Pomáhá (bohužel ne vždy) na 3-5 dní Ivermectin -dávka jak při léčbě akutního onemocnění+ Montelucast 10mg 1-0-1, držet nízkohistaminovou dietu. Kde dominují neurolopsychiatrické symptomy – deprese, úzkosti, bolesti hlavy, nevýkonnost, nesoustředěnost, „mozková mlha“, tak nasadit Fevarin 50mg 1-0-1 – do ustoupení potíží, minimálně 15 dní. U nespavosti Melatonin 1Omg aspoň měsíc.

Trvá-li kašel, dušnost, zadýchávání se a nevýkonnost, vhodné podat Budiar 1-0-1 + Ventolin inh 1-1-1. Vyloučit reinfekci/reaktivaci chorob jako je Chlamydophila pneumoniae, Mykoplazma pneumonie, Borrelióza…tam jsou vhodná antibiotika, např. Klarithromycin 500mg 1-0-1 (U chronické Borreliózy přidat ke Klacidu i Cefuroxim 500mg á 12 hod.)

U dětí nevím.

Níže protokol  I-RECOVERY




If presenting with shortness of breath or low oxygen levels:
Initial therapy of Long Haul COVID-19 Syndrome:
Management Protocol for Long Haul COVID-19 Syndrome (LHCS) I-RECOVER

The approach outlined below is a consensus protocol based on a collaboration led by Dr. Mobeen Syed (“Dr. Been”), Dr. Ram Yogendra,
Dr. Bruce Patterson, Dr. Tina Peers, and the FLCCC Alliance. Given the lack of clinical treatment trials of Long Haul COVID-19 Syndrome, these recommendations are based on the pathophysiologic mechanisms of COVID-19 and post-viral illnesses along with our
collective experience observing profound and sustained clinical responses achieved with the treatment approaches below.
This protocol has also been used to treat post-vaccine inflammatory syndromes with similar success. As with all FLCCC Alliance protocols, the components, doses, and durations will evolve as more clinical data accumulates. For the most up-to-date information on optional treatments,

go to: (see LHCS section).


0.2–0.4mg/kg dose – once daily with meals* for 3–5 days
(higher doses are sometimes needed in anosmia).
* Take on empty stomach if presenting with nausea/diarrhea/anorexia.
After 3–5 days, change to once or twice weekly depending on the time to symptom recurrence/persistence.
Discontinue after 2–4 weeks if all symptoms have resolved and do not recur.
Relative Contraindications:
– Patients on Warfarin require close monitoring and dose adjustment.
– Pregnant or lactating women require a more in-depth risk/benefit


if presenting with neurologic symptoms, i.e. poor concentration, forgetfulness, mood disturbance:
50mg – twice daily for 15 days. Reduce dose or discontinue if side effects develop. Doses as low as 9mg
twice daily have shown efficacy. Monitor closely as some patients may respond poorly. Some individuals can
experience acute anxiety; monitor and treat carefully to prevent rare escalation to suicidal or violent behavior.

CORTICOSTEROID THERAPY A tapering dose of prednisone as follows:
1. 0.5mg/kg daily for 5 days
2. 0.25mg/kg daily for 5 days
3. 0.12mg/kg daily for 5 days
Take in morning to lessen impact on sleep. Side effects may include: Increased appetite, mood changes, insomnia,
raised blood glucose, dyspepsia.

If symptoms still unresolved or recur after ivermectin and corticosteroid regimens:


If not all symptoms resolve with ivermectin: Refer to lung specialist if available, otherwise perform chest imaging (CT
preferred) to assess for secondary organizing Pneumonia (OP). If findings consistent with secondary OP found, initiate Corticosteroid Therapy. May need to repeat or prolong course of treatment if symptoms or oxygen needs persist.


Choose a Type I and a Type II antihistamine along with a mast cell stabilizer –
for example, Loratadine, Famotidine, and Rupatadine (v Česku není). Change medicines if poor response. United States FDA approved doses of many of the below medicines are once daily but can use up to three times daily with caution and close monitoring if poor response or side effects.
First-line Therapy
Low histamine diet
Type l antihistamines: Loratadine 10mg, or Cetirizine 10mg, or Fexofenadine 180mg (v Česku není)– three times daily as tolerated.
Type ll antihistamines: Famotidine 20mg, or Nizatidine 150mg (v Česku není) – twice daily as tolerated.
Mast cells stabilizers:
– Rupatadine 10mg (v Česku není) – once daily, or Ketotifen 1mg – once daily at night (increase as tolerated).
– May add: Sodium Cromoglycate 200mg – three times daily (increase slowly), or Quercetin 500mg – three times daily.
Second-line Therapy
Montelukast 10mg (beware depression in some) – once daily.
Low Dose Naltrexone (LDN) (v Česku není) – start with 0.5mg daily, increasing by 0.5mg weekly up to 4.5mg daily. Avoid if on opiates.
Diazepam 0.5–1mg twice daily.
SSRIs – antidepresiva

For use in all patients:

Vitamin C — 500mg twice daily
Omega-3 Fatty Acids — 4gm/daily (Vascepa, Lovaza, or DHA/EPA)
Atorvastatin — 40mg daily
Melatonin — 2–10mg nightly, start with low dose, increase as tolerated in absence of sleep disturbance.
Additional Supplement Vitamin D3 — 2,000–4,000 IU daily

The Long Haul COVID-19 Syndrome (LHCS) is characterized by prolonged malaise, headaches, generalized fatigue, sleep difficulties, hair loss, smell disorder, decreased appetite, painful joints, dyspnea, chest pain and cognitive dysfunction[400-411] Up to 80% of patients experience prolonged illness after COVID-19. LHCS is not only seen after the COVID-19 infection but it is being observed in some people that have received vaccines (likely due to monocyte activation by the
spike protein from the vaccine). LHCS may persist for months after the acute infection and almost half of patients report reduced quality of life. Patients may suffer prolonged neuropsychological symptoms, including multiple domains of cognition.[409,412] A puzzling feature of LHCS is that it is not predicted by initial disease severity; post-COVID-19 frequently affects mild-to-moderate cases and younger adults that did not require respiratory support or intensive care. [411] The symptom set of LHCS is in majority of the cases very similar to the chronic inflammatory response syndrome (CIRS)/myalgic encephalomyelitis/ chronic fatigue syndrome.[411] An important differentiating factor from CIRS is the observation that LHCS continues to improve on its own albeit slowly in majority of the cases. Another important
observation is that LHCS includes more young people compared to severe COVID-19 that affects older people or persons with comorbidities. Furthermore, the similarity between the mast cell activation syndrome and LHCS has been observed, and many consider postCOVID-19 to be a variant of the mast cell activation syndrome.[413] The LHCS syndrome in highly heterogenous and likely results from a variety of pathogenetic mechanisms Furthermore, it is likely that delayed treatment (with ivermectin) in the early symptomatic phase will results in a high viral load which increase the risk and severity of LHCS. The following theories have been postulated to explain LHCS: [411]
1. Ongoing respiratory symptoms (SOB, cough, reduced effort tolerance) may be related to unresolved organizing pneumonia (activate pulmonary macrophages).
2. Monocyte activation syndrome. Persistence of viral debris in monocytes results in an ongoing immune response in an attempt by the immune system to clear the offending protein(s) and viral RNA fragments.
3. The neurological symptoms may be related micro- and/or macrovascular thrombotic disease which appears to be common in severe COVID-19 disease.[414] Brain MRIs’ 3 months post-infection demonstrated micro-structural changes in 55% of patients. [415] In addition, features of encephalopathy may be related to encephalitis and auto-reactive brain antibodies [416] as well as severe cerebral vasoconstriction. [417] The brain microvasculature expresses ACE-2 receptors and SARS-CoV-2 “pseudovirons” may bind to the microvascular endothelium causing cerebral microvascular inflammation and clotting.[418].
4. An unmasking of mast cell activation syndrome (MCAS), or triggering of mast cell activation syndrome. Mast cells are present in the brain, especially in the median eminence of the hypothalamus, where they are located perivascularly close to nerve endings positive for corticotrophin releasing hormone.[419] Following stimulation, mast cells release inflammatory mediators such as histamine, tryptase, chemokines and cytokines which may result in
neurovascular inflammation.[419] The “brain-fog”, cognitive impairment and general fatigue reported in long-COVID-19 may be due to mast cell related neurovascular inflammation. Clinical signs and symptoms can be grouped in the following clusters.
The reason for this grouping is to allow organ specific targeted therapy/individualized therapy.
1. Respiratory: shortness of breath, congestion, persistent cough, etc.
2. Neurological/psychiatric: brain fog, malaise, tiredness, headaches, migraines, depression, inability to focus/concentrate, altered cognition, insomnia, vertigo, panic attacks, tinnitus, anosmia, phantom, smells, etc.
3. Musculoskeletal: myalgias, fatigue, weakness, joint pains, inability
to exercise, post-exertional malaise, inability to perform normal activities of daily life (ADL’s).
4. Cardiovascular: Palpitations, arrhythmias, Raynaud like syndrome, hypotension, and tachycardia on exertion.
5. Autonomic: Postural tachycardia syndrome (POTs), abnormal sweating.
6. GIT disturbance: Anorexia, diarrhea, bloating, vomiting, nausea, etc.
7. Dermatologic: Itching, rashes, dermatographia
8. Mucus membranes: Running nose, sneezing, Burning and itchy eyes.

Approach to Treatment
The treatment approach should be individualized according to the grouping of clinical signs and symptoms. However, in general, it is likely that patients who received inadequate antiviral treatment (ivermectin) during the acute symptomatic phase and inadequate anti-inflammatory/macrophage repolarization therapy (corticosteroids, statins, omega-3 fatty acids, fluvoxamine, ivermectin, etc) during the acute phase of COVID-19 are much more likely to develop the PostCOVID-19 Syndrome. In patients with ongoing respiratory symptoms chest imaging is suggested (preferably a chest CT scan). Those withunresolved pulmonary inflammation (organizing pneumonia) should be treated with a course of corticosteroids (prednisone) and closely followed. A CRP should be measured, and extended corticosteroids
(titrated to the CRP) offered to these patients. Similar to patients who have recovered from septic shock, [420] a prolonged (many months) immune disturbance with elevated pro- and anti-inflammatory cytokines may contribute to the LHCS. This is likely the consequence of monocyte activation syndrome and monocyte repolarization therapy
is therefore indicated. In addition, a cytokine panel may allow targeted anti-inflammatory therapy (Maraviroc in patients with high CCR5 levels). It should be noted that much like omega-3 fatty acids, corticosteroids have been demonstrated to increase expression of pro-resolving lipids including Protectin D1 and Resolvin D4.[421] An unknown number of patients who have recovered from COVID-19 organizing pneumonia will develop pulmonary fibrosis with associated limitation of activity. Pulmonary function testing demonstrates a restrictive type pattern with decreased residual volume and DLCO.
[406] These patients should be referred to a pulmonologist with expertise in pulmonary fibrosis. Anti-fibrotic therapy may have a role in these patients, [380-383] however additional data is required before this therapy can be more generally recommended. As discussed above, the serotonin receptor blocker cyproheptadine may reduce the risk of pulmonary fibrosis. [256]

The I-RECOVER protocol is borne of clinical experience only and thus is meant solely for educational purposes to health care providers regarding potentially beneficial empiric treatment approaches for Long Haul COVID-19 Syndrome. Never disregard professional medical advice because of something you have read on our website and releases. This is not intended to be a substitute for professional medical advice, diagnosis, or treatment in regards to any patient. Treatment for an individual patient is determined by many factors and thus should rely on the judgement of your
physician or qualified health care provider. Always seek their advice with any questions you may have regarding your medical condition or health.

Please check our homepage regularly for updates of our COVID-19 Protocols! – New medications may be added and/or dose
changes to existing medications may be made as further scientific studies emerge!
256. Skurikhin EG, Andreeva TV, Khnelevskaya ES et al. Effect of antiserotonin drug on the development of lung fibrosis and blood system reactions after intratracheal administration of
bleomycin. Bull Exp Biol Med 2012; 152:519-23.
380. Seifirad S. Pirfenidone: A novel hypothetical treatment for COVID-19. Medical Hypotheses
2020; 144:11005.
381. Saba A, Vaidya PJ, Chavhan VB et al. Combined pirfenidone, azithromycin and prednisolone
in post-H1N1 ARDS pulmonary firbosis. Sarcoidosis Vasc Diffuse Lung Dis 2018; 35:85-90.
382. Spagnolo P, Balestro E, Aliberti S et al. Pulmonary fibrosis secondary to COVID-19: a call to
arms? Lancet Resp Med 2020; 8:750-752.
383. George PM, Wells AU, Jenkins RG. Pulmonary fibrosis and COVID-19: the potential role for
antibibrotic therapy. Lancet Resp Med 2020; 8:807-15.
400. Carfi A, Bernabei R, Landi F. Persistent symptoms in patients after acute COVID-19. JAMA 2020.
401. Prescott HC, Girard TD. Recovery from Severe COVID-19. Leveraging the lessons of survival
from sepsis. JAMA 2020.
402. Greenhalgh T, Knight M, A’Court C et al. Management of post-acute COVID-19 in primary
care. BMJ 2020.
403. Chopra V, Flanders SA, O’Malley M. Sixty-day outcomes among patients hospitalized with
COVID-19. Ann Intern Med 2020.
404. Mandal S, Barnett J, Brill SE et al. ‘Long-COVID’: a cross-sectional study of persisting symptoms, biomarker and imaging abnormalities following hospitalization for COVID-19. Thorax 2020.
405. Michelen M, Manoharan L, Elkheir N et al. Characterising long-term COVID-19: a rapid living systematic review. medRxiv 2020.
406. Huang C, Huang L, Wang Y et al. 6-month consequences of COVID-19 in patients discharged feom hospital: a cohort study. Lancet 2021.
407. Logue JK, Franko NM, McCulloch DJ et al. Sequelae in adults at 6 months after COVID-19
infection. JAMA Network Open 2021; 4:e210830.
408. Janiri D, Carfi A, Kotzalidis GD et al. Posttraumatic stress disorder in patients after severe
COVID-19 infection. JAMA Psychiatry 2021.
409. Voruz P, Allali G, Benzakour L et al. Long COVID neuropsychological deficits after severe,
moderate or mild infection. medRxiv 2021.
410. Al-Aly Z, Xie Y, Bowe B. High-dimensional characterization of post-acute sequalae of COVID-19. Nature 2021.
411. Yong SJ. Long-haul COVID-19: Putative pathophysiology, risk factors, and treatments. medRxiv 2020.
412. Taquet M, Geddes JR, Husain M et al. 6-month neurological and psychiatric outcomes in
236 379 survivors of COVID-19: a retrospective cohort study using electronic health records. Lancet Psychiatry 2021.
413. Afrin LB, Weinstock LB, Molderings GJ. COVID-19 hyperinflammation and post-Covid-19
illness may be rooted in mast cell activation syndrome. Int J Infect DIs 2020.
414. Bryce C, Grimes Z, Pujadas E et al. Pathopysiology of SARS-CoV-2: targeting of endothelial
cells renders a complex disease with thrombotic microangiopathy and aberrant immune
response. The Mount Sinai COVID-19 autopsy experience. medRxiv 2020.
415. Lu Y, Li X, Geng D et al. Cerebral micro-structutal changes in COVID-19 patients – An MRIbased 3-month follow-up study. EClinicalMedicine 2020.
416. Franke C, Ferse C, Kreye J et al. High frequency of cerebrospinal fluid autoantibodies in
COVID-19 patients with neurological symptoms. Brain,Behavior, and Immunity 2021.
417. Sirous R, Taghvaei R, Hellinger JC et al. COVID-19-associated encephalopathy with fulminant cerebral vasoconstriction: CT and MRI findings. Radiology Case Reports 2020;
418. Magro CM, Mulvey JJ, Laurence J et al. Docked severe acute respiratory syndrome coronavirus 2 proteins within the cutaneous and subcutaneous microvasculature and their role in
the pathogenesis of severe coronavirus disease 2019. Human Pathology 2020; 106:106-16.
419. Theoharides TT, Cholevas C, Polyzoidis K et al. Long-COVID syndrome-associated brain fog
and chemofog: Luteolin to the rescue. Biofactors 2021; 47:232-41.
420. Riche F. Protracted immune disorders at one year after ICU discharge in patients with septic shock. Crit Care 2018; 22:42.
421. Andreakos E, Papadaki M, Serhan CN. Dexamethasone, pro-resolving lipid mediators and
resolution of inflammation in COVID-19. Allergy 2020.
422. COVID-19 rapid guideline: managing the long-term effects of COVID-19.
guidance/ng188 . 2020. National Institute for Health and Care Excellence. 4-26-2021.
423. Sanabria-Mazo JP, Montero-Marin J, Feliu-Soler A et al. Mindfulness-based program plus
amygdala and inusla retraining (MAIR) for the treatment of women with fibromyalgia: A
pilot ramdomized controlled trial. J Clin Med 2020; 9:3246.
424. Theoharides TC. COVID-19, pulmonary mast cells, cytokine storms, and beneficial actions
of luteolin. Biofactors 2020; 46:306-8.
425. Bawazeer MA, Theoharides TC. IL-33 stimulates human mast cell release of CCL5 and CCL2
via MAPK and NF-kB, inhibited by methoxyluteolin. Eur J Pharmacol 2019; 865:172760.
426. Weng Z, Patel AB, Panagiotidou S et al. The novel flavone tetramethoxyluteolin is a potent
inhibitor of human mast cells. J Allergy Clin Immunol 2015; 135:1044-52.
427. Patel AB, Theoharides TC. Methoxyluteolin inhibits neuropeptide-stimulated proinflammatory mediator release via mTOR activation from human mast cells. J Pharmacol Exp
Ther 2017; 361:462-71.
428. Calis Z, Mogulkoc R, Baltaci AK. The roles of flavonols/flavonoids in neurodegeneration and
neuroinflammation. Mini Rev Med Chem 2020; 20:1475-88.
For updates and more information on the treatment protocols of the FLCCC Alliance please see: I-RECOVER · Version 1 · June 16, 2021 · Page 3/3