Vitamin C is a powerful antioxidant that supports lung function.
In chicken, supplementation of the feed with vitamin C increased resistance to the coronavirus that causes infectious bronchitis. In an old study on chick embryo lung cultures, exposure to vitamin C increased the resistance to avian coronavirus infection.
The new coronavirus or COVID-19 can compromise the immune system and lung function. This fact has sparked the public interest in drugs and supplements that support the respiratory system and fight-off viral infections.
Vitamin C or ascorbic acid is one of the essential antioxidants that protect our body from oxidative stress and free radicals. Its role in the lungs is particularly important, where it reaches up to 30 times higher level than in the blood.
Once ingested, vitamin C instantly reaches the lining of our airways, acting as the first life of defense against harmful oxidation caused by microbes, smoking, and other stressors.
Viral infections activate our immune cells and cause oxidative stress, depleting vitamin C levels. Increased intake under such conditions can ensure antioxidant protection, support the immune response, and suppress viral replication.
Like COVID-19, the influenza A virus infection or flu can compromise lung function and lead to pneumonia. Vitamin C is essential for the antiviral response in the early stage of flu infection, and a deficiency may worsen lung damage.
It's believed that older people are more susceptible to die from COVID-19 because lowered immunity, especially B- and T- cell numbers.
Because vitamin C can increase B- and T-cells, it may help fight off infections in general.
Vitamin C is a crucial antioxidant that protects the lungs and combats viral infections, but scientists haven't yet tested it against the new coronavirus.
Respiratory Infections
A study on over 1,500 women associated high vitamin C intake with a reduced incidence of upper respiratory tract infections.
In over 19,000 men, high blood vitamin C levels correlated with a reduced incidence of different respiratory conditions, including chronic respiratory disease, pneumonia, and lung cancer.
Vitamin C supplementation decreased the duration and severity of respiratory infections in male swimmers but not in women. It wasn't able to prevent infections in either group.
A 2019 meta-analysis including 3,135 children found that vitamin C didn't prevent upper respiratory tract infections but reduced their duration.
A meta-analysis of three small studies found that vitamin C reduced airway narrowing in response to exercise.
Vitamin C supplementation may reduce the severity and duration of different respiratory conditions, while the effects on prevention are less conclusive.
Common Cold
The common cold is a viral infection of the upper respiratory tract (sinuses, nose, and throat). It's usually caused by rhinoviruses, but the potential threats include influenza and coronaviruses, too.
Vitamin C may function as a weak antihistamine agent to provide relief from flu‐like symptoms such as sneezing, a running or stuffy nose, and swollen sinuses.
In a clinical trial of 715 students, megadoses of vitamin C (3g/day prevention, 6g/day treatment) reduced cold and flu symptoms by 85%.
A comprehensive meta-analysis gathered the data from 44 trials on vitamin C for the common cold and came to the following conclusions for preventive supplementation:
It doesn't lower the risk in adults
It cuts the risk in half in people exposed to intense exercise
It reduces the cold duration by 8% in adults and 14-18% in children
It decreases the severity of colds in all populations
Therapeutic supplementation (once the symptoms begin) didn't significantly impact the cold duration or severity.
Preventive vitamin C supplementation may reduce the severity and duration of a common cold. In people who exercise intensively, it may also lower the risk of catching a cold.
Pneumonia
Pneumonia stands for lung inflammation leading to persistent cough and shortness of breath. Although typically caused by bacterial infections, pneumonia is a potential complication of the COVID-19 infection, too.
A meta-analysis investigated the effects of vitamin C supplementation on pneumonia prevention (2,335 patients) and treatment (197 patients).
According to their results, preventive supplementation may reduce the incidence of pneumonia by 80%. When it comes to treatment, vitamin C may reduce the duration, severity, and mortality of pneumonia. That said, the authors emphasized the poor quality of most included studies.
In a clinical trial of 30 severe pneumonia patients, vitamin C supplementation reduced:
Oxidative stress
DNA damage
Inflammation (TNF-a and IL-6)
Preventive vitamin C supplementation may lower the risk of pneumonia. The treatment may reduce pneumonia severity and duration by combating oxidative stress and inflammation in the lungs. The same may not go for pneumonia caused by COVID-19.
Lung Failure
The worst thing about the new coronavirus is that susceptible patients can develop severe pneumonia that progresses into the severe acute respiratory syndrome (SARS) or lung failure.
Infused vitamin C failed to reduce lung inflammation and failure in a clinical trial on 167 people with sepsis (blood poisoning) and acute lung failure (ARDS), but it did reduce the death rate.
The same therapy was effective in two young women with ARDS caused by viral and bacterial infections.
A meta-analysis of 5 studies found that intravenous vitamin C may reduce the need for mechanical ventilation in the critically ill.
Based on the above findings, a recent study published in The Lancet journal listed vitamin C infusion as potential rescue therapy for critical cases of a COVID-19 infection.
Cytokine Storm
It's believed that many people die from COVID-19 as a result of a cytokine storm.
Patients with COVID-19 who were admitted to the ICU had higher levels of TNF-alpha and other inflammatory cytokines.
In a clinical trial on 30 people with pneumonia, supplementation with vitamin C reduced cytokines such as TNF-α & IL-6.
Summary
Vitamin C supplementation may reduce the duration and severity of different respiratory infections, while its role in prevention is less conclusive and requires further research.
The beneficial effects on pneumonia, a common complication of the COVID-19 infection, are particularly encouraging. However, none of the above studies examined the effects of vitamin C supplementation on this particular virus.
Scientists have announced multiple clinical trials investigating vitamin C supplementation in COVID-19 patients.
https://www.ncbi.nlm.nih.gov/pubmed/18670976 -
Ascorbic acid and infectious bronchitis infections in broilers.
Abstract
The effect of supplementing the feed of broiler chicks with different levels of ascorbic acid on the resistance against infectious bronchitis virus was investigated. Resistance was measured by the severity of tracheal lesions and the development of airsacculitis after challenge. The effect of ascorbic acid was dose dependent. Addition of 300 to 330 ppm ascorbic acid to the feed gave the best results. High concentrations (>600 ppm) had a less beneficial effect.
https://www.ncbi.nlm.nih.gov/pubmed/205194 -
The effect of ascorbic acid on infection chick-embryo ciliated tracheal organ cultures by coronavirus.
Chick embryo tracheal organ cultures showed increased resistance to infection by a coronavirus after exposure to ascorbate, while chick respiratory epithelium and allantois-on-shell preparations showed no increase in resistance to infection by an influenza virus or a paramyxovirus.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4363347/
The effect of vitamin C on bronchoconstriction and respiratory symptoms caused by exercise: a review and statistical analysis
Abstract
Physical activity increases oxidative stress and therefore the antioxidant effects of vitamin C administration might become evident in people undertaking vigorous exercise. Vitamin C is involved in the metabolism of histamine, prostaglandins, and cysteinyl leukotrienes, all of which appear to be mediators in the pathogenesis of exercise-induced bronchoconstriction (EIB). Three studies assessing the effect of vitamin C on patients with EIB were subjected to a meta-analysis and revealed that vitamin C reduced postexercise FEV1 decline by 48% (95% CI: 33% to 64%). The correlation between postexercise FEV1 decline and respiratory symptoms associated with exercise is poor, yet symptoms are the most relevant to patients. Five other studies examined subjects who were under short-term, heavy physical stress and revealed that vitamin C reduced the incidence of respiratory symptoms by 52% (95% CI: 36% to 65%). Another trial reported that vitamin C halved the duration of the respiratory symptoms in male adolescent competitive swimmers. Although FEV1 is the standard outcome for assessing EIB, other outcomes may provide additional information. In particular, the mean postexercise decline of FEF50 is twice the decline of FEV1. Schachter and Schlesinger (1982) reported the effect of vitamin C on exercise-induced FEF60 levels in 12 patients suffering from EIB and their data are analyzed in this paper. The postexercise FEF60 decline was greater than 60% for five participants and such a dramatic decline indicates that the absolute postexercise FEF60 level becomes an important outcome in its own right. Vitamin C increased postexercise FEF60 levels by 50% to 150% in those five participants, but had no significant effect in the other seven participants. Thus, future research on the effects of vitamin C on EIB should not be restricted to measuring only FEV1. Vitamin C is inexpensive and safe, and further study on those people who have EIB or respiratory symptoms associated with exercise is warranted.
https://www.ncbi.nlm.nih.gov/pubmed/15454278/ -
Ascorbic acid in nasal and tracheobronchial airway lining fluids.
Abstract
Ascorbic acid (AA) is thought to be an important antioxidant in the respiratory tract, whose regulation is yet to be fully characterized. We investigated whether AA in respiratory tract lining fluids (RTLFs) can be augmented by oral supplementation with AA. Plasma, nasal lavage fluids (NLFs), induced sputum (IS), and saliva were analyzed for AA immediately before and 2 h after ingestion of 2 g of AA in 13 healthy subjects. Concentrations of AA (median and range) were 52.5 (16.0-88.5), 2.4 (0.18-4.66), 2.4 (0.18-6.00), and 0.55 (0.18-18.90) micromol/l, respectively. Two hours after ingestion of AA, plasma AA increased 2-fold (p = .004), NLF AA increased 3-fold (p = .039), but IS and saliva AA did not increase. As AA concentrations in saliva and tracheobronchial secretions were low compared with other common extracellular components (such as urate), we evaluated the fate of AA in these fluids. Addition of AA to freshly obtained saliva or IS resulted in rapid depletion, which could be largely prevented or reversed by sodium azide or dithiothreitol. These findings suggest that oxidant-producing systems in saliva and airway secretions, such as heme peroxidases and other oxidizing substances, rapidly consume AA. Whereas oral supplementation resulted in detectable increases of AA in NLFs, its levels in tracheobronchial lining fluid, as measured by IS, were unaffected and remained relatively low, suggesting that AA may play a less significant antioxidant role in this compartment as compared with most other extracellular compartments.
https://www.ncbi.nlm.nih.gov/pubmed/19009458/ -
Augmentation of respiratory tract lining fluid ascorbate concentrations through supplementation with vitamin C.
Abstract
Low molecular weight antioxidants within human respiratory tract lining fluids (RTLFs) have been proposed to confer protection against the damaging action of inhaled oxidant gases. There is therefore considerable interest in augmenting the concentrations of these moieties at the air-lung interface to protect against injury to the airway epithelium, the induction of inflammation, and declines in lung function. To determine whether RTLF ascorbate concentrations could be augmented through vitamin C supplementation, 24 healthy subjects with low plasma ascorbate (< 50 microM) were recruited into a double-blinded study. Subjects were divided into two groups, one receiving 60 mg/day of vitamin C for 14 days, the other placebo. On days 8 and 15 of this protocol, plasma, urine, and nasal lavage were obtained for ascorbate determination. After a 7-14-day non-intervention period, subjects previously on placebo received supplements containing 125 mg ascorbate, whilst the group previously on supplements received the placebo compound. This "switching" protocol was repeated three more times utilizing 250, 500, and 1000 mg/day ascorbate dosage regimens. Plasma ascorbate increased incrementally with vitamin C dose, as did its urinary excretion. Despite this, nasal lavage concentrations remained unaltered 24 h after the final supplement at all doses. Closer examination of this issue demonstrated that nasal lavage ascorbate concentrations increased acutely after ingestion of a high dose (1000 mg) supplement, peaking at 2-4 h (p < 0.05) before returning to baseline concentrations 24 h post-supplement. In the absence of a quantitative association between plasma and lavage ascorbate concentrations we contend that this response does not simply reflect ascorbate transudation from the plasma and interstitial space into the lavage medium. We therefore conclude that RTLF ascorbate can be augmented, albeit transiently, by oral vitamin C supplementation, with the transient nature of this response likely reflecting oxidative losses within the RTLF or its sequestration into airway cells.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2099400/ ** -
Vitamin C may affect lung infections
https://onlinelibrary.wiley.com/doi/abs/10.1002/rmv.303 * -
Role of free radicals in viral pathogenesis and mutation
Abstract
Oxygen radicals and nitric oxide (NO) are generated in excess in a diverse array of microbial infections. Emerging concepts in free radical biology are now shedding light on the pathogenesis of various diseases. Free‐radical induced pathogenicity in virus infections is of great importance, because evidence suggests that NO and oxygen radicals such as superoxide are key molecules in the pathogenesis of various infectious diseases. Although oxygen radicals and NO have an antimicrobial effect on bacteria and protozoa, they have opposing effects in virus infections such as influenza virus pneumonia and several other neurotropic virus infections. A high output of NO from inducible NO synthase, occurring in a variety of virus infections, produces highly reactive nitrogen oxide species, such as peroxynitrite, via interaction with oxygen radicals and reactive oxygen intermediates. The production of these various reactive species confers the diverse biological functions of NO. The reactive nitrogen species cause oxidative tissue injury and mutagenesis through oxidation and nitration of various biomolecules. The unique biological properties of free radicals are further illustrated by recent evidence showing accelerated viral mutation by NO‐induced oxidative stress. NO appears to affect a host's immune response, with immunopathological consequences. For example, NO is reported to suppress type 1 helper T cell‐dependent immune responses during infections, leading to type 2 helper T cell‐biased immunological host responses. NO‐induced immunosuppression may thus contribute to the pathogenesis of virus infections and help expansion of quasispecies population of viral pathogens. This review describes the pathophysiological roles of free radicals in the pathogenesis of viral disease and in viral mutation as related to both nonspecific inflammatory responses and immunological host reactions modulated by NO. Copyright © 2001 John Wiley & Sons, Ltd.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2538426/ -
Inflammation in the Vascular Bed - Importance of Vitamin C
Abstract
Despite decreases in atherosclerotic coronary vascular disease over the last several decades, atherosclerosis remains a major cause of mortality in developed nations. One possible contributor to this residual risk is oxidant stress, which is generated by the inflammatory response of atherosclerosis. Although there is a wealth of in vitro, cellular, and animal data supporting a protective role for antioxidant vitamins and nutrients in the atherosclerotic process, the best clinical trials have been negative. This may be due to the fact that antioxidant therapies are applied "too little and too late." This review considers the role of vitamin C, or ascorbic acid in preventing the earliest inflammatory changes in atherosclerosis. It focuses on the three major vascular cell types involved in atherosclerosis: endothelial cells, vascular smooth muscle cells, and macrophages. Ascorbate chemistry, recycling, and function are described for these cell types, with emphasis on whether and how the vitamin might affect the inflammatory process. For endothelial cells, ascorbate helps to prevent endothelial dysfunction, stimulates type IV collagen synthesis, and enhances cell proliferation. For vascular smooth muscle cells, ascorbate inhibits dedifferentiation, recruitment, and proliferation in areas of vascular damage. For macrophages, ascorbate decreases oxidant stress related to their activation, decreases uptake and degradation of oxidized LDL in some studies, and enhances several aspects of their function. Although further studies of ascorbate function in these cell types and in novel animal models are needed, available evidence generally supports a salutary role for this vitamin in ameliorating the earliest stages of atherosclerosis.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5707683/
Vitamin C and Immune Function
Abstract
Vitamin C is an essential micronutrient for humans, with pleiotropic functions related to its ability to donate electrons. It is a potent antioxidant and a cofactor for a family of biosynthetic and gene regulatory enzymes. Vitamin C contributes to immune defense by supporting various cellular functions of both the innate and adaptive immune system. Vitamin C supports epithelial barrier function against pathogens and promotes the oxidant scavenging activity of the skin, thereby potentially protecting against environmental oxidative stress. Vitamin C accumulates in phagocytic cells, such as neutrophils, and can enhance chemotaxis, phagocytosis, generation of reactive oxygen species, and ultimately microbial killing. It is also needed for apoptosis and clearance of the spent neutrophils from sites of infection by macrophages, thereby decreasing necrosis/NETosis and potential tissue damage. The role of vitamin C in lymphocytes is less clear, but it has been shown to enhance differentiation and proliferation of B- and T-cells, likely due to its gene regulating effects. Vitamin C deficiency results in impaired immunity and higher susceptibility to infections. In turn, infections significantly impact on vitamin C levels due to enhanced inflammation and metabolic requirements. Furthermore, supplementation with vitamin C appears to be able to both prevent and treat respiratory and systemic infections. Prophylactic prevention of infection requires dietary vitamin C intakes that provide at least adequate, if not saturating plasma levels (i.e., 100–200 mg/day), which optimize cell and tissue levels. In contrast, treatment of established infections requires significantly higher (gram) doses of the vitamin to compensate for the increased inflammatory response and metabolic demand.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3659258/ - **
Vitamin C Is an Essential Factor on the Anti-viral Immune Responses through the Production of Interferon-α/β at the Initial Stage of Influenza A Virus (H3N2) Infection
Abstract
L-ascorbic acid (vitamin C) is one of the well-known anti-viral agents, especially to influenza virus. Since the in vivo anti-viral effect is still controversial, we investigated whether vitamin C could regulate influenza virus infection in vivo by using Gulo (-/-) mice, which cannot synthesize vitamin C like humans. First, we found that vitamin C-insufficient Gulo (-/-) mice expired within 1 week after intranasal inoculation of influenza virus (H3N2/Hongkong). Viral titers in the lung of vitamin C-insufficient Gulo (-/-) mice were definitely increased but production of anti-viral cytokine, interferon (IFN)-α/β, was decreased. On the contrary, the infiltration of inflammatory cells into the lung and production of pro-inflammatory cytokines, tumor necrosis factor (TNF)-α and interleukin (IL)-α/β, were increased in the lung. Taken together, vitamin C shows in vivo anti-viral immune responses at the early time of infection, especially against influenza virus, through increased production of IFN-α/β.
https://www.ncbi.nlm.nih.gov/pubmed/16988135 - *
Vitamin C deficiency increases the lung pathology of influenza virus-infected gulo-/- mice.
Abstract
This study was designed to determine the effects of vitamin C deficiency on the immune response to infection with influenza virus. l-Gulono-gamma-lactone oxidase gene-inactivated mice (gulo-/- mice) require vitamin C supplementation for survival. Five-wk-old male and female gulo-/- mice were provided water or water containing 1.67 mmol/L vitamin C for 3 wk before inoculation with influenza A/Bangkok/1/79. There were no differences in lung influenza virus titers between vitamin C-adequate and -deficient mice; however, lung pathology in the vitamin C-deficient mice was greater at 1 and 3 d after infection but less at d 7 compared with vitamin C-adequate mice. Male vitamin C-deficient mice had higher expression of mRNA for regulated upon activation normal T expressed and secreted (RANTES), IL-1beta, and TNF-alpha in the lungs at d 1 after infection compared with male controls. However, at d 3 after infection, male vitamin C-deficient mice had less expression of mRNA for RANTES, monocyte chemotactic protein-1 (MCP-1), and IL-12 compared with male controls. None of these differences were observed in female mice. Vitamin C-deficient male mice also had greater nuclear factor-kappaB activation as early as 1 d after infection compared with male controls. These data suggest that vitamin C is required for an adequate immune response in limiting lung pathology after influenza virus infection.
https://www.ncbi.nlm.nih.gov/pubmed/28074891 -
Intake of vitamin C, vitamin E, selenium, zinc and polyunsaturated fatty acids and upper respiratory tract infection-a prospective cohort study.
https://www.ncbi.nlm.nih.gov/pubmed/30705384-
Plasma vitamin C concentrations and risk of incident respiratory diseases and mortality in the European Prospective Investigation into Cancer-Norfolk population-based cohort study.
https://www.ncbi.nlm.nih.gov/pubmed/30465062 -
Efficacy of vitamin C for the prevention and treatment of upper respiratory tract infection. A meta-analysis in children.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3686214/ -
Vitamin C may alleviate exercise-induced bronchoconstriction: a meta-analysis
https://www.ncbi.nlm.nih.gov/pubmed/11781377 -
Nutrients and their role in host resistance to infection.
Abstract
Almost all nutrients in the diet play a crucial role in maintaining an "optimal" immune response, such that deficient and excessive intakes can have negative consequences on immune status and susceptibility to a variety of pathogens. Iron and vitamin A deficiencies and protein-energy malnutrition are highly prevalent worldwide and are important to the public health in terms of immunocompetence. There are also nutrients (i.e., glutamine, arginine, fatty acids, vitamin E) that provide additional benefits to immunocompromised persons or patients who suffer from various infections. The remarkable advances in immunology of recent decades have provided insights into the mechanisms responsible for the effects of various nutrients in the diet on specific functions in immune cells. In this review, we will present evidence and proposed mechanisms for the importance of a small group of nutrients that have been demonstrated to affect host resistance to infection will be presented. An inadequate status of some of these nutrients occurs in many populations in the world (i.e., vitamin A, iron, and zinc) where infectious disease is a major health concern. We will also review nutrients that may specifically modulate host defense to infectious pathogens (long-chain polyunsaturated n-3 fatty acids, vitamin E, vitamin C, selenium, and nucleotides). A detailed review of the effect of long-chain polyunsaturated n-3 fatty acids on host defense is provided as an example of how the disciplines of nutrition and immunology have been combined to identify key mechanisms and propose nutrient-directed management of immune-related syndromes.
https://www.ncbi.nlm.nih.gov/pubmed/10543583 - **
The effectiveness of vitamin C in preventing and relieving the symptoms of virus-induced respiratory infections.
https://www.ncbi.nlm.nih.gov/pubmed/23440782 -
Vitamin C for preventing and treating the common cold.
https://www.ncbi.nlm.nih.gov/pubmed/23925826/ -
Vitamin C for preventing and treating pneumonia.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4165740/ **
Vitamin C Mitigates Oxidative Stress and Tumor Necrosis Factor-Alpha in Severe Community-Acquired Pneumonia and LPS-Induced Macrophages
Abstract
Oxidative stress is an important part of host innate immune response to foreign pathogens. However, the impact of vitamin C on oxidative stress and inflammation remains unclear in community-acquired pneumonia (CAP). We aimed to determine the effect of vitamin C on oxidative stress and inflammation. CAP patients were enrolled. Reactive oxygen species (ROS), DNA damage, superoxide dismutases (SOD) activity, tumor necrosis factor-alpha (TNF-α), and IL-6 were analyzed in CAP patients and LPS-stimulated macrophages cells. MH-S cells were transfected with RFP-LC3 plasmids. Autophagy was measured in LPS-stimulated macrophages cells. Severe CAP patients showed significantly increased ROS, DNA damage, TNF-α, and IL-6. SOD was significantly decreased in severe CAP. Vitamin C significantly decreased ROS, DNA damage, TNF-α, and IL-6. Vitamin C inhibited LPS-induced ROS, DNA damage, TNF-α, IL-6, and p38 in macrophages cells. Vitamin C inhibited autophagy in LPS-induced macrophages cells. These findings indicated that severe CAP exhibited significantly increased oxidative stress, DNA damage, and proinflammatory mediator. Vitamin C mitigated oxidative stress and proinflammatory mediator suggesting a possible mechanism for vitamin C in severe CAP.
https://www.ncbi.nlm.nih.gov/pubmed/31573637 ** -
Effect of Vitamin C Infusion on Organ Failure and Biomarkers of Inflammation and Vascular Injury in Patients With Sepsis and Severe Acute Respiratory Failure: The CITRIS-ALI Randomized Clinical Trial.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5295174/ *
Intravenous vitamin C as adjunctive therapy for enterovirus/rhinovirus induced acute respiratory distress syndrome
Abstract
We report a case of virus-induced acute respiratory distress syndrome (ARDS) treated with parenteral vitamin C in a patient testing positive for enterovirus/rhinovirus on viral screening. This report outlines the first use of high dose intravenous vitamin C as an interventional therapy for ARDS, resulting from enterovirus/rhinovirus respiratory infection. From very significant preclinical research performed at Virginia Commonwealth University with vitamin C and with the very positive results of a previously performed phase I safety trial infusing high dose vitamin C intravenously into patients with severe sepsis, we reasoned that infusing identical dosing to a patient with ARDS from viral infection would be therapeutic. We report here the case of a 20-year-old, previously healthy, female who contracted respiratory enterovirus/rhinovirus infection that led to acute lung injury and rapidly to ARDS. She contracted the infection in central Italy while on an 8-d spring break from college. During a return flight to the United States, she developed increasing dyspnea and hypoxemia that rapidly developed into acute lung injury that led to ARDS. When support with mechanical ventilation failed, extracorporeal membrane oxygenation (ECMO) was initiated. Twelve hours following ECMO initiation, high dose intravenous vitamin C was begun. The patient's recovery was rapid. ECMO and mechanical ventilation were discontinued by day-7 and the patient recovered with no long-term ARDS sequelae. Infusing high dose intravenous vitamin C into this patient with virus-induced ARDS was associated with rapid resolution of lung injury with no evidence of post-ARDS fibroproliferative sequelae. Intravenous vitamin C as a treatment for ARDS may open a new era of therapy for ARDS from many causes.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5116502/ *
Abstract
This case report summarizes the first use of intravenous vitamin C employed as an adjunctive interventional agent in the therapy of recurrent acute respiratory distress syndrome (ARDS). The two episodes of ARDS occurred in a young female patient with Cronkhite-Canada syndrome, a rare, sporadically occurring, noninherited disorder that is characterized by extensive gastrointestinal polyposis and malabsorption. Prior to the episodes of sepsis, the patient was receiving nutrition via chronic hyperalimentation administered through a long-standing central venous catheter. The patient became recurrently septic with Gram positive cocci which led to two instances of ARDS. This report describes the broad-based general critical care of a septic patient with acute respiratory failure that includes fluid resuscitation, broad-spectrum antibiotics, and vasopressor support. Intravenous vitamin C infused at 50 mg per kilogram body weight every 6 hours for 96 hours was incorporated as an adjunctive agent in the care of this patient. Vitamin C when used as a parenteral agent in high doses acts "pleiotropically" to attenuate proinflammatory mediator expression, to improve alveolar fluid clearance, and to act as an antioxidant.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6196621/
Vitamin C supplementation in the critically ill: A systematic review and meta-analysis
https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(20)30127-2/fulltext **
Treatment for severe acute respiratory distress syndrome from COVID-19
https://www.nature.com/articles/s41418-020-0530-3 -
COVID-19 infection: the perspectives on immune responses
https://www.ncbi.nlm.nih.gov/pubmed/31986264
Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China.
https://www.paho.org/journal/sites/default/files/2020-03/40-20-249-Rosa-prelim.pdf?ua=1 -
Vitamin C has antioxidant activity and may reduce oxidative stress and inflammation (57,62), effects that improve vasopressor synthesis, enhance immune cell function, improve endovascular function, and provide epigenetic immunologic modifications. Clinical trials have demonstrated promising data on mortality improvement in sepsis, but more extensive studies are necessary to validate these conclusions
https://clinicaltrials.gov/ct2/show/NCT04264533 **
Vitamin C, also known as ascorbic acid, has antioxidant properties. When sepsis happens, the cytokine surge caused by sepsis is activated, and neutrophils in the lungs accumulate in the lungs, destroying alveolar capillaries. Early clinical studies have shown that vitamin C can effectively prevent this process. In addition, vitamin C can help to eliminate alveolar fluid by preventing the activation and accumulation of neutrophils, and reducing alveolar epithelial water channel damage. At the same time, vitamin C can prevent the formation of neutrophil extracellular traps, which is a biological event of vascular injury caused by neutrophil activation. Vitamins can effectively shorten the duration of the common cold. In extreme conditions (athletes, skiers, art workers, military exercises), it can effectively prevent the common cold. And whether vitamin C also has a certain protective effect on influenza patients, only few studies have shown that vitamin C deficiency is related to the increased risk and severity of influenza infections. In a controlled but non-randomized trial, 85% of the 252 students treated experienced a reduction in symptoms in the high-dose vitamin C group (1g / h at the beginning of symptoms for 6h, followed by 3 * 1g / day). Among patients with sepsis and ARDS, patients in the high-dose vitamin group did not show a better prognosis and other clinical outcomes. There are still some confounding factors in the existing research, and the conclusions are different.
Therefore, during the current epidemic of SARI, it is necessary to study the clinical efficacy and safety of vitamin C for viral pneumonia through randomized controlled trials.