Evidence map›Paper›PMID 32562915›Full record

ArticleMedical hypotheses2020

A new pharmacological approach based on remdesivir aerosolized administration on SARS-CoV-2 pulmonary inflammation: A possible and rational therapeutic application.

Carlo Contini, Carla Enrica Gallenga, Giampiero Neri, Martina Maritati, Pio Conti

Open access · greenAbstract read
In one paragraph

Article in Medical hypotheses, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.5field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Remdesivir: Quo vadis?Biochemical pharmacology · 2021
    Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Letter to the editor: Possible role of topical povidone iodine in case of accidental ocular exposure to SARS-CoV-2.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2020
    Article
  10. Review
  11. Potential Use of Alpha-1 Anti-trypsin in the Covid-19 Treatment.Frontiers in cell and developmental biology · 2020
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

Carlo ContiniDepartment Medical Sciences, Infectious Diseases and Dermatology Section, University of Ferrara, Italy. Electronic address: carlo.contini@unife.it.
Carla Enrica GallengaDept. Morphology, Surgery, Exp. Medicine, PhDs Molecular Medicine, University of Ferrara, Italy.
Giampiero NeriENT, Dept Neuroscience, Imaging & Clinical Sciences, G d'Annunzio University, Chieti, Italy.
Martina MaritatiDept. Morphology, Surgery, Exp. Medicine, PhDs Molecular Medicine, University of Ferrara, Italy.
Pio ContiMolecular Immunopharmacology & Drug Discovery Lab, Tufts University, Boston, MA 02111, USA.
University of Ferrara · ITTufts University · USUniversity of Chieti-Pescara · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The new zoonotic coronavirus (SARS-CoV-2) responsible for coronavirus disease (COVID-19) is a new strain of coronavirus not previously seen in humans and which appears to come from bat species. It originated in Wuhan, Hubei Province, China, and spread rapidly throughout the world, causing over 5,569,679 global cases and 351,866 deaths in almost every country in the world, including Europe, particularly Italy. In general, based on existing data published to date, 80.9% of patients infected with the virus develop mild infection; 13.8% severe pneumonia; 4.7% respiratory failure, septic shock or multi-organ failure; 3% of these cases are fatal. Critical patients have been shown to develop acute respiratory distress syndrome (ARDS) and hospitalization in intensive care units. The average age of patients admitted to hospital is 57-79 years, with one third half with an underlying disease. Asymptomatic infections have also been described, but their frequency is not known. SARS-CoV-2 transmission is mainly airborne from one person to another via droplets. The data available so far seem to indicate that SARS-CoV-2 is capable of producing an excessive immune reaction in the host. The virus attacks type II pneumocytes in the lower bronchi through the binding of the Spike protein (S protein) to viral receptors, of which the angiotensin 2 conversion enzyme (ACE2) receptor is the most important. ACE2 receptor is widely expressed in numerous tissues, including the oropharynx and conjunctiva, but mostly distributed in ciliated bronchial epithelial cells and type II pneumocytes in the lower bronchi. The arrival of SARS-CoV-2 in the lungs causes severe primary interstitial viral pneumonia that can lead to the "cytokine storm syndrome", a deadly uncontrolled systemic inflammatory response triggered by the activation of interleukin 6 (IL-6), whose effect is extensive lung tissue damage and disseminated intravascular coagulation (DIC), that are life-threatening for patients with COVID-19. In the absence of a therapy of proven efficacy, current management consists of off-label or compassionate use therapies based on antivirals, antiparasitic agents in both oral and parenteral formulation, anti-inflammatory drugs, oxygen therapy and heparin support and convalescent plasma. Like most respiratory viruses can function and replicate at low temperatures (i.e. 34-35 °C) and assuming viral thermolability of SARS-CoV-2, local instillation or aerosol of antiviral (i.e. remdesivir) in humid heat vaporization (40°-41 °C) in the first phase of infection (phenotype I, before admission), both in asymptomatic but nasopharyngeal swab positive patients, together with antiseptic-antiviral oral gargles and povidone-iodine eye drops for conjunctiva (0,8-5% conjunctival congestion), would attack the virus directly through the receptors to which it binds, significantly decreasing viral replication, risk of evolution to phenotypes IV and V, reducing hospitalization and therefore death.

Indexed as

AerosolsCOVID-19 Drug TreatmentAdenosine MonophosphateAlanineAnimalsAntiviral AgentsHumansInflammationLungModels, TheoreticalPhenotypePovidone-IodineSARS-CoV-2Adenosine MonophosphateAerosolsAlanineAntiviral AgentsPovidone-IodineremdesivirAerosol vaporization and nebulizationAlcoholic gargleCOVID-19Cytokine stormIL-1/IL-6Monoclonal antibodyPovidone-iodine gargle and eye dropRemdesivirSARS-CoV-2Viral pneumonia

Identifiers

PMID32562915
PMCPMC7246020
OpenAlexW3026524308

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.