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1.
Front Cell Infect Microbiol ; 12: 935280, 2022.
Article in English | MEDLINE | ID: covidwho-2154687

ABSTRACT

The use of non-steroidal anti-inflammatory drugs (NSAIDs) in patients with coronavirus disease 2019 (COVID-19) has raised great concerns. The effect of NSAIDs on the clinical status of COVID-19 remains in question. Therefore, we performed a post-hoc analysis from the ORCHID trial. Patients with COVID-19 from the ORCHID trial were categorized into two groups according to NSAID use. The 28-day mortality, hospitalized discharge, and safety outcomes with NSAIDs for patients with COVID-19 were analyzed. A total of 476 hospitalized patients with COVID-19 were included; 412 patients (86.5%) did not receive NSAIDs, while 64 patients (13.5%) took NSAIDs as regular home medication. Patients who took NSAIDs did not have a significant increase in the risk of 28-day mortality (fully adjusted: hazard ratio [HR]: 1.12, 95% CI: 0.52-2.42) in the Cox multivariate analysis. Moreover, NSAIDs did not decrease hospital discharge through 28 days (fully adjusted: HR: 1.02, 95% CI: 0.75-1.37). The results of a meta-analysis including 14 studies involving 48,788 patients with COVID-19 showed that the use of NSAIDs had a survival benefit (summary risk ratio [RR]: 0.70, 95% CI: 0.54-0.91) and decreased the risk of severe COVID-19 (summary: RR: 0.79, 95% CI: 0.71-0.88). In conclusion, the use of NSAIDs is not associated with worse clinical outcomes, including 28-day mortality or hospital discharge in American adult hospitalized patients with COVID-19. Based on current evidence, the use of NSAIDs is safe and should not be cautioned against during the COVID-19 pandemic. Ongoing trials should further assess in-hospital treatment with NSAIDs for patients with COVID-19.


Subject(s)
COVID-19 , Adult , Humans , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , COVID-19/drug therapy , Hospitalization , Pandemics , Meta-Analysis as Topic
3.
Biomolecules ; 12(10)2022 10 13.
Article in English | MEDLINE | ID: covidwho-2071206

ABSTRACT

Microbial products have been used for the treatment of different diseases for many centuries. The serratiopeptidase enzyme provides a new hope for COVID-19-infected patients. Nowadays, anti-inflammatory drugs are easy to obtain at minimal expenditure from microbial sources. Serratia sp. is identified as one of the most efficient bacteria produced from serratiopeptidase. Screening for new and efficient bacterial strains from different sources has been of interest in recent years. Serratiopeptidase remains the most well-known anti-inflammatory drug of choice. Serratiopeptidase is a cheaper and safer anti-inflammatory drug alternative to NSAIDs. The multifaceted properties of serratiopeptidase may lead towards arthritis, diabetes, cancer and thrombolytic treatments. Existing serratiopeptidase treatments in combination with antibiotics are popular in the treatment of postoperative swelling. Although an exclusive number of serratiopeptidase-producing strains have been derived, there is an urge for new recombinant strains to enhance the production of the enzyme. This review explores the properties of serratiopeptidase, different therapeutic aspects, industrial production, and various analytical techniques used in enzyme recovery. In addition, the review highlights the therapeutic and clinical aspects of the serratiopeptidase enzyme to combat COVID-19-induced respiratory syndrome.


Subject(s)
COVID-19 , Humans , COVID-19/drug therapy , Peptide Hydrolases , Anti-Bacterial Agents/therapeutic use , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Anti-Inflammatory Agents
4.
J Dtsch Dermatol Ges ; 20(10): 1289-1302, 2022 10.
Article in English | MEDLINE | ID: covidwho-2063672

ABSTRACT

A fixed drug eruption (FDE) is a common cutaneous adverse drug reaction which occurs following administration of an offending drug. The aim of this review is to provide an update on the list of drugs causing FDE, with a focus on emerging drug culprits reported since the start of the century. Across published literature, triggers for FDE are widely varied. The most frequently implicated drugs include analgesics (nonsteroidal anti-inflammatory drugs [NSAIDs] and paracetamol) and antibiotics. Co-trimoxazole is perhaps the most well described single agent. Since the start of the century there have been over 200 drugs named in case reports on FDE. Newer, novel agents of note include cyclooxygenase-2 specific inhibitors, fluconazole, and phosphodiesterase 5 inhibitors. Other implicated drugs include vaccines, such as various SARS-CoV-2 vaccines. Drugs incriminated in FDE vary based on the geographical region studied and prescribing patterns at a given time. Newer drugs continue to enter the market and are playing an increasing role in the field of FDE. Awareness of rarer culprits and emerging novel agents can help identify a trigger, allowing for prompt withdrawal of the causative agent, preventing recurrence.


Subject(s)
COVID-19 Vaccines , COVID-19 , Drug Eruptions , Humans , Acetaminophen/therapeutic use , Anti-Bacterial Agents/therapeutic use , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , COVID-19 Vaccines/adverse effects , Cyclooxygenase 2/therapeutic use , Drug Eruptions/diagnosis , Drug Eruptions/drug therapy , Drug Eruptions/etiology , Fluconazole/therapeutic use , Phosphodiesterase 5 Inhibitors/therapeutic use , SARS-CoV-2 , Trimethoprim, Sulfamethoxazole Drug Combination/adverse effects
5.
Lancet Infect Dis ; 20(11): e276-e288, 2020 11.
Article in English | MEDLINE | ID: covidwho-2062013

ABSTRACT

As severe acute respiratory syndrome coronavirus 2 continues to spread worldwide, there have been increasing reports from Europe, North America, Asia, and Latin America describing children and adolescents with COVID-19-associated multisystem inflammatory conditions. However, the association between multisystem inflammatory syndrome in children and COVID-19 is still unknown. We review the epidemiology, causes, clinical features, and current treatment protocols for multisystem inflammatory syndrome in children and adolescents associated with COVID-19. We also discuss the possible underlying pathophysiological mechanisms for COVID-19-induced inflammatory processes, which can lead to organ damage in paediatric patients who are severely ill. These insights provide evidence for the need to develop a clear case definition and treatment protocol for this new condition and also shed light on future therapeutic interventions and the potential for vaccine development. TRANSLATIONS: For the French, Chinese, Arabic, Spanish and Russian translations of the abstract see Supplementary Materials section.


Subject(s)
Betacoronavirus , Coronavirus Infections/epidemiology , Coronavirus Infections/immunology , Pneumonia, Viral/epidemiology , Pneumonia, Viral/immunology , Systemic Inflammatory Response Syndrome/epidemiology , Systemic Inflammatory Response Syndrome/immunology , Adolescent , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Antiviral Agents/therapeutic use , COVID-19 , Child , Child, Preschool , Coronavirus Infections/drug therapy , Coronavirus Infections/virology , Female , Humans , Immunoglobulins, Intravenous/therapeutic use , Infant , Infant, Newborn , Male , Mucocutaneous Lymph Node Syndrome/drug therapy , Mucocutaneous Lymph Node Syndrome/immunology , Pandemics , Pneumonia, Viral/drug therapy , Pneumonia, Viral/virology , Risk Factors , SARS-CoV-2 , Systemic Inflammatory Response Syndrome/drug therapy , Systemic Inflammatory Response Syndrome/virology , Young Adult
6.
NPJ Prim Care Respir Med ; 32(1): 35, 2022 09 21.
Article in English | MEDLINE | ID: covidwho-2036825

ABSTRACT

Early in the COVID-19 pandemic, anecdotal reports emerged suggesting non-steroidal anti-inflammatory drugs (NSAIDs) may increase susceptibility to infection and adversely impact clinical outcomes. This narrative literature review (March 2020-July 2021) attempted to clarify the relationship between NSAID use and COVID-19 outcomes related to disease susceptibility or severity. Twenty-four relevant publications (covering 25 studies) reporting original research data were identified; all were observational cohort studies, and eight were described as retrospective. Overall, these studies are consistent in showing that NSAIDs neither increase the likelihood of SARS-CoV-2 infection nor worsen outcomes in patients with COVID-19. This is reflected in current recommendations from major public health authorities across the world, which support NSAID use for analgesic or antipyretic treatment during COVID-19. Thus, there is no basis on which to restrict or prohibit use of these drugs by consumers or patients to manage their health conditions and symptoms during the pandemic.


Subject(s)
Antipyretics , COVID-19 , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Antipyretics/therapeutic use , Humans , Pandemics , Retrospective Studies , SARS-CoV-2
7.
RMD Open ; 8(2)2022 09.
Article in English | MEDLINE | ID: covidwho-2020255

ABSTRACT

SARS-CoV-2 has been recognised as a potential trigger of inflammatory arthritis in individuals with inflammatory rheumatic diseases as well as in previously unaffected individuals. However, new-onset arthritis after COVID-19 is a heterogeneous phenomenon that complicates differential diagnosis. For example, acute arthritis with features of viral arthritis has been reported after COVID-19, as has crystal-induced arthritis. Arthritides mimicking reactive arthritis (ReA) have also been described, but these patients often do not fulfil the typical features of ReA: several reports describe cases of patients older than 45 years at the onset of arthritis, and the characteristic genetic feature of ReA, HLA-B27, is rarely found. Because viral infections are much less likely to cause ReA than bacterial infections, and respiratory infections are rarely the cause of ReA, it is currently unknown whether SARS-CoV-2 can cause true ReA. Here, we report the case of a 30-year-old patient who presented with acute pain, swelling and redness in the left metatarsophalangeal (MTP) joint and ankle 7 days after resolution of a SARS-CoV-2 infection. Diagnostics revealed arthritis of the MTP2, synovitis of the upper ankle with significant joint effusion and peritendinitis of the flexor tendons. Based on the clinical manifestations and diagnostic test results, ReA appeared to be the most likely cause. A screening for typical ReA-associated infections was negative. The patient was treated with NSAIDs and intra-articular and systemic glucocorticoids. At a follow-up visit after discontinuation of glucocorticoids, the patient was symptom-free. Overall, we observed a ReA with typical clinical, genetic and patient characteristics after SARS-CoV-2 infection, and we conclude that a direct association with COVID-19 is highly plausible.


Subject(s)
Arthritis, Reactive , COVID-19 , Adult , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Arthritis, Reactive/diagnosis , Arthritis, Reactive/drug therapy , Arthritis, Reactive/etiology , COVID-19/complications , COVID-19/diagnosis , HLA-B27 Antigen , Humans , SARS-CoV-2
8.
PLoS One ; 17(5): e0267462, 2022.
Article in English | MEDLINE | ID: covidwho-1910600

ABSTRACT

Non-steroidal anti-inflammatory drugs (NSAIDs) and acetaminophen are among the most-frequently used medications. Although these medications have different mechanisms of action, they have similar indications and treatment duration has been positively correlated with cardiovascular risk although the degree of risk varies by medication. Our objective was to study treatment effects of chronic use of individual NSAID medications and acetaminophen on all-cause mortality among patients who tested positive for COVID-19 while accounting for adherence. We used the VA national datasets in this retrospective cohort study to differentiate between sporadic and chronic medication use: sporadic users filled an NSAID within the last year, but not recently or regularly. Using established and possible risk factors for severe COVID-19, we used propensity scores analysis to adjust for differences in baseline characteristics between treatment groups. Then, we used multivariate logistic regression incorporating inverse propensity score weighting to assess mortality. The cohort consisted of 28,856 patients. Chronic use of aspirin, ibuprofen, naproxen, meloxicam, celecoxib, diclofenac or acetaminophen was not associated with significant differences in mortality at 30 days (OR = 0.98, 95% CI: 0.95-1.00; OR = 0.99, 95% CI: 0.98-1.00; OR = 1.00, 95% CI: 0.98-1.01; OR = 0.99, 95% CI: 0.98-1.00; OR = 1.00, 95% CI: 0.98-1.01; OR = 0.99, 95% CI: 0.97-1.01; and OR = 1.00, 95% CI: 0.99-1.02, respectively) nor at 60 days (OR = 0.97, 95% CI: 0.95-1.00; OR = 1.00, 95% CI: 0.99-1.01; OR = 0.99, 95% CI: 0.98-1.01; OR = 0.99, 95% CI: 0.97-1.00; OR = 0.99, 95% CI: 0.97-1.01; OR = 0.99, 95% CI: 0.97-1.01; and OR = 1.01, 95% CI: 0.99-1.02, respectively). Although the study design cannot determine causality, the study should assure patients as it finds no association between mortality and chronic use of these medications compared with sporadic NSAID use among those infected with COVID-19.


Subject(s)
COVID-19 , Veterans , Acetaminophen/adverse effects , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , COVID-19/drug therapy , Humans , Retrospective Studies , United States/epidemiology
9.
EBioMedicine ; 76: 103856, 2022 Feb.
Article in English | MEDLINE | ID: covidwho-1894987

ABSTRACT

BACKGROUND: Many repurposed drugs have progressed rapidly to Phase 2 and 3 trials in COVID19 without characterisation of Pharmacokinetics /Pharmacodynamics including safety data. One such drug is nafamostat mesylate. METHODS: We present the findings of a phase Ib/IIa open label, platform randomised controlled trial of intravenous nafamostat in hospitalised patients with confirmed COVID-19 pneumonitis. Patients were assigned randomly to standard of care (SoC), nafamostat or an alternative therapy. Nafamostat was administered as an intravenous infusion at a dose of 0.2 mg/kg/h for a maximum of seven days. The analysis population included those who received any dose of the trial drug and all patients randomised to SoC. The primary outcomes of our trial were the safety and tolerability of intravenous nafamostat as an add on therapy for patients hospitalised with COVID-19 pneumonitis. FINDINGS: Data is reported from 42 patients, 21 of which were randomly assigned to receive intravenous nafamostat. 86% of nafamostat-treated patients experienced at least one AE compared to 57% of the SoC group. The nafamostat group were significantly more likely to experience at least one AE (posterior mean odds ratio 5.17, 95% credible interval (CI) 1.10 - 26.05) and developed significantly higher plasma creatinine levels (posterior mean difference 10.57 micromol/L, 95% CI 2.43-18.92). An average longer hospital stay was observed in nafamostat patients, alongside a lower rate of oxygen free days (rate ratio 0.55-95% CI 0.31-0.99, respectively). There were no other statistically significant differences in endpoints between nafamostat and SoC. PK data demonstrated that intravenous nafamostat was rapidly broken down to inactive metabolites. We observed no significant anticoagulant effects in thromboelastometry. INTERPRETATION: In hospitalised patients with COVID-19, we did not observe evidence of anti-inflammatory, anticoagulant or antiviral activity with intravenous nafamostat, and there were additional adverse events. FUNDING: DEFINE was funded by LifeArc (an independent medical research charity) under the STOPCOVID award to the University of Edinburgh. We also thank the Oxford University COVID-19 Research Response Fund (BRD00230).


Subject(s)
Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Benzamidines/therapeutic use , COVID-19/drug therapy , Guanidines/therapeutic use , Administration, Intravenous , Adult , Aged , Aged, 80 and over , Anti-Inflammatory Agents, Non-Steroidal/pharmacokinetics , Benzamidines/adverse effects , Benzamidines/pharmacokinetics , Biomarkers/blood , Biomarkers/metabolism , COVID-19/mortality , COVID-19/virology , Drug Administration Schedule , Female , Guanidines/adverse effects , Guanidines/pharmacokinetics , Half-Life , Humans , Immunophenotyping , Kaplan-Meier Estimate , Male , Middle Aged , SARS-CoV-2/isolation & purification , SARS-CoV-2/physiology , Treatment Outcome , Viral Load
10.
Immunobiology ; 227(3): 152224, 2022 05.
Article in English | MEDLINE | ID: covidwho-1819510

ABSTRACT

The COVID-19 pandemic has set back progress made on antimicrobial resistance (AMR). Without urgent re-focus, we risk slowing down drug discovery and providing treatment for drug resistant Mycobacterium tuberculosis. Unique in its immune evasion, dormancy and resuscitation, the causal pathogens of tuberculosis (TB) have demonstrated resistance to antibiotics with efflux pumps and the ability to form biofilms. Repurposing drugs is a prospective avenue for finding new anti-TB drugs. There are many advantages to discovering novel targets of an existing drug, as the pharmacokinetic and pharmacodynamic properties have already been established, they are cost-efficient and can be commercially accelerated for the new development. One such group of drugs are non-steroidal anti-inflammatory drugs (NSAIDs) that are originally known for their ability to supress the host proinflammatory responses. In addition to their anti-inflammatory properties, some NSAIDs have been discovered to have antimicrobial modes of action. Of particular interest is Carprofen, identified to inhibit the efflux mechanism and disrupt biofilm formation in mycobacteria. Due to the complexities of host-pathogens interactions in the lung microbiome, inflammatory responses must carefully be controlled alongside the in vivo actions of the prospective anti-infectives. This critical review explores the potential dual role of a selection of NSAIDs, as an anti-inflammatory and anti-tubercular adjunct to reverse the tide of antimicrobial resistance in existing treatments.


Subject(s)
Anti-Infective Agents , COVID-19 , Mycobacterium tuberculosis , Tuberculosis , Anti-Infective Agents/therapeutic use , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Antitubercular Agents/pharmacology , Antitubercular Agents/therapeutic use , COVID-19/drug therapy , Humans , Immunomodulating Agents , Pandemics , Tuberculosis/drug therapy
11.
Expert Opin Pharmacother ; 23(6): 681-691, 2022 Apr.
Article in English | MEDLINE | ID: covidwho-1769033

ABSTRACT

INTRODUCTION: Aspirin or non-steroidal anti-inflammatory drugs (NSAIDs) and colchicine are first-line treatments for acute and recurrent pericarditis. Drugs blocking the NACHT, leucine-rich repeat, and pyrin domain-containing protein 3 (NLRP3) inflammasome/interleukin-1ß (IL-1ß) axis are beneficial in patients with multiple recurrences. AREAS COVERED: In this review, the role of the NLRP3 inflammasome/IL-1ß axis in the pathophysiology of pericarditis is discussed. Updates about novel therapies targeting IL-1 for recurrent pericarditis (RP) and practical considerations for their use are provided. EXPERT OPINION: IL-1 inhibitors have been increasingly studied for RP in recent years. NLRP3 inflammasome is a key mediator in the pathophysiology of RP. IL-1ß, its main product, can sustain its own production and feeds local and systemic inflammation. Randomized clinical trials testing anakinra (a recombinant form of the IL-1 receptor antagonist blocking IL-1α and IL-1ß) and rilonacept (an IL-1α and IL-1ß trap) have shown that IL-1 blockade reduces recurrences. These trials also helped in phenotyping patients with RP. Patients with multiple recurrences and signs of pericardial and/or systemic inflammation might benefit from IL-1 blockers in order to interrupt cyclic flares of auto-inflammation. Given this evidence, guidelines should consider incorporating IL-1 blockers.


Subject(s)
Pericarditis , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Colchicine/therapeutic use , Humans , Inflammasomes/metabolism , Inflammasomes/therapeutic use , Inflammation/drug therapy , Pericarditis/diagnosis , Pericarditis/drug therapy
12.
Brain Behav Immun ; 87: 59-73, 2020 07.
Article in English | MEDLINE | ID: covidwho-1719339

ABSTRACT

As of April 15, 2020, the ongoing coronavirus disease 2019 (COVID-2019) pandemic has swept through 213 countries and infected more than 1,870,000 individuals, posing an unprecedented threat to international health and the economy. There is currently no specific treatment available for patients with COVID-19 infection. The lessons learned from past management of respiratory viral infections have provided insights into treating COVID-19. Numerous potential therapies, including supportive intervention, immunomodulatory agents, antiviral therapy, and convalescent plasma transfusion, have been tentatively applied in clinical settings. A number of these therapies have provided substantially curative benefits in treating patients with COVID-19 infection. Furthermore, intensive research and clinical trials are underway to assess the efficacy of existing drugs and identify potential therapeutic targets to develop new drugs for treating COVID-19. Herein, we summarize the current potential therapeutic approaches for diseases related to COVID-19 infection and introduce their mechanisms of action, safety, and effectiveness.


Subject(s)
Coronavirus Infections/therapy , Pneumonia, Viral/therapy , Adrenal Cortex Hormones/therapeutic use , Angiotensin-Converting Enzyme 2 , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Antibodies, Monoclonal, Humanized/therapeutic use , Anticoagulants/therapeutic use , Antimalarials/therapeutic use , Antiviral Agents/therapeutic use , Betacoronavirus , Bevacizumab/therapeutic use , COVID-19 , COVID-19 Vaccines , Chloroquine/therapeutic use , Coronavirus Infections/drug therapy , Coronavirus Infections/prevention & control , Humans , Hydroxychloroquine/therapeutic use , Immunization, Passive , Immunoglobulins, Intravenous/therapeutic use , Immunologic Factors/therapeutic use , Interferons/therapeutic use , Janus Kinase Inhibitors/therapeutic use , Killer Cells, Natural , Medicine, Chinese Traditional , Mesenchymal Stem Cell Transplantation , Nitric Oxide/therapeutic use , Pandemics , Peptidyl-Dipeptidase A , SARS-CoV-2 , Spike Glycoprotein, Coronavirus , Trace Elements/therapeutic use , Viral Vaccines/therapeutic use , Vitamins/therapeutic use , Zinc/therapeutic use
13.
Br J Clin Pharmacol ; 88(7): 3114-3131, 2022 07.
Article in English | MEDLINE | ID: covidwho-1714131

ABSTRACT

Understanding how pharmaceutical opioids and antipyretic analgesics interact with the immune system potentially has major clinical implications for management of patients with infectious diseases and surgical and critical care patients. An electronic search was carried out on MEDLINE, EMBASE, PsycINFO, CENTRAL and the Cochrane library to identify reports describing the immunomodulatory effects of opioid analgesics and antipyretic analgesics, and their effects in infectious diseases. In adaptive immunity, nonsteroidal anti-inflammatory drugs have divergent effects: augmenting cell-mediated immunity but inhibiting humoral immunity. Nonsteroidal anti-inflammatory drugs have demonstrated a beneficial role in Mycobacterium tuberculosis infection and histoplasmosis in animals, and may be plausible adjuvants to antimicrobial agents in these diseases. There is a need to evaluate these findings rigorously in human clinical trials. There is preliminary evidence demonstrating antiviral effects of indomethacin in SARS CoV-2 in vitro; however, uncertainty regarding its clinical benefit in humans needs to be resolved in large clinical trials. Certain opioid analgesics are associated with immunosuppressive effects, with a developing understanding that fentanyl, morphine, methadone and buprenorphine suppress innate immunity, whilst having diverse effects on adaptive immunity. Morphine suppresses key cells of the innate immunity and is associated with greater risk of infection in the postsurgical setting. Efforts are needed to achieve adequate analgesia whilst avoiding suppression of the innate immunity in the immediate postoperative period caused by certain opioids, particularly in cancer surgery.


Subject(s)
Antipyretics , COVID-19 , Communicable Diseases , Analgesics , Analgesics, Opioid/pharmacology , Analgesics, Opioid/therapeutic use , Animals , Anti-Inflammatory Agents, Non-Steroidal/pharmacology , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Antipyretics/pharmacology , Antipyretics/therapeutic use , COVID-19/drug therapy , Humans , Morphine , Pharmaceutical Preparations
14.
Pharmacol Res Perspect ; 10(2): e00925, 2022 04.
Article in English | MEDLINE | ID: covidwho-1712174

ABSTRACT

In this systematic review, we aimed to assess the efficacy and safety of nonsteroidal anti-inflammatory drugs (NSAIDs) in treating respiratory tract infections in adults and children. PubMed, Scopus, Web of Science, Cochrane, and Embase databases were searched. A total of 34 randomized clinical trials were included in this systematic review. We assessed the risk of bias of all included studies using the Cochrane tool for risk of bias assessment. The evidence on ibuprofen, naproxen, aspirin, diclofenac, and other NSAIDs were rated for degree of uncertainty for each of the study outcomes and summarized using the grading of recommendations assessment, development, and evaluation (GRADE) approach. Our findings suggest that high-quality evidence supports the use of NSAIDs to reduce fever in both adults and children. However, the evidence was uncertain for the use of NSAIDs to reduce cough. Most studies showed that NSAIDs significantly relieved sore throat. The evidence for mortality and oxygenation is limited. Regarding the adverse events, gastrointestinal discomfort was more frequently reported in children. For adults, our overall certainty in effect estimates was low and the increase in gastrointestinal adverse events was not clinically significant. In conclusion, NSAIDs seem to be beneficial in the outpatient management of fever and sore throat in adults and children. Although the evidence does not support their use to decrease mortality nor improve oxygenation in inpatient settings, the use of NSAIDs did not increase the rate of death or the need for ventilation in patients with respiratory tract infections. Further studies with a robust methodology and larger sample sizes are recommended.


Subject(s)
Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Respiratory Tract Infections/drug therapy , Virus Diseases/drug therapy , Ambulatory Care , COVID-19/drug therapy , Hospitalization , Humans , Randomized Controlled Trials as Topic , SARS-CoV-2
15.
Allergy ; 77(8): 2337-2354, 2022 08.
Article in English | MEDLINE | ID: covidwho-1691634

ABSTRACT

Non-steroidal anti-inflammatory drugs (NSAIDs) and other eicosanoid pathway modifiers are among the most ubiquitously used medications in the general population. Their broad anti-inflammatory, antipyretic, and analgesic effects are applied against symptoms of respiratory infections, including SARS-CoV-2, as well as in other acute and chronic inflammatory diseases that often coexist with allergy and asthma. However, the current pandemic of COVID-19 also revealed the gaps in our understanding of their mechanism of action, selectivity, and interactions not only during viral infections and inflammation, but also in asthma exacerbations, uncontrolled allergic inflammation, and NSAIDs-exacerbated respiratory disease (NERD). In this context, the consensus report summarizes currently available knowledge, novel discoveries, and controversies regarding the use of NSAIDs in COVID-19, and the role of NSAIDs in asthma and viral asthma exacerbations. We also describe here novel mechanisms of action of leukotriene receptor antagonists (LTRAs), outline how to predict responses to LTRA therapy and discuss a potential role of LTRA therapy in COVID-19 treatment. Moreover, we discuss interactions of novel T2 biologicals and other eicosanoid pathway modifiers on the horizon, such as prostaglandin D2 antagonists and cannabinoids, with eicosanoid pathways, in context of viral infections and exacerbations of asthma and allergic diseases. Finally, we identify and summarize the major knowledge gaps and unmet needs in current eicosanoid research.


Subject(s)
Asthma , COVID-19 , Hypersensitivity , Anti-Inflammatory Agents, Non-Steroidal/pharmacology , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Antiviral Agents/pharmacology , Antiviral Agents/therapeutic use , Asthma/drug therapy , COVID-19/drug therapy , Consensus , Eicosanoids/metabolism , Humans , Hypersensitivity/drug therapy , Inflammation/drug therapy , SARS-CoV-2
16.
Curr Rheumatol Rev ; 18(4): 346-351, 2022.
Article in English | MEDLINE | ID: covidwho-1686283

ABSTRACT

BACKGROUND: It has been over a year since the first documented case of the COVID-19 virus was recorded. Since then, our understanding of this virus has continually evolved, however, its wide-ranging effects are still unfolding. Similar to previously studied viral infections, severe acute respiratory syndrome-associated coronavirus-2 (SARS-CoV-2) has been shown to lead to a degree of autoimmunity in patients who are recovering from its effects. Due to its effects on the innate immune system, such as the toll-like receptors and complement system, a varying degree of proinflammatory markers can become widespread in those who continue to recover from the virus. This case series offers a unique perspective on how COVID-19 has had dramatic effects on those already suffering from inflammatory rheumatic conditions, such as rheumatoid arthritis, systemic lupus erythematosus, or fibromyalgia. As the ever-lasting effects of COVID-19 are still unfolding, this case series is one of few to discuss the development and changes of patients with rheumatic conditions. This study hopes to encourage larger studies to be conducted on the effects of COVID- 19 on autoimmune conditions. CASE PRESENTATION: Seven patients were identified with new manifestations of rheumatic conditions, which included 3 cases of rheumatoid arthritis, 2 cases of polymyalgia rheumatica, 1 case of reactive arthritis, and 1 case of cutaneous lupus. Post-COVID syndrome was also diagnosed in 7 other patients. Patients with rheumatoid arthritis presented with symptoms 4-5 weeks after being diagnosed with COVID-19. Symptoms of polyarticular joint pain, swelling, and morning stiffness were reported in this group. These patients were treated with disease-modifying anti-rheumatic drugs and experienced an improvement in symptoms on follow-up. Two cases of polymyalgia rheumatica were identified in patients that were previously diagnosed with COVID-19 six weeks prior. One patient had no significant past medical history and the other patient had a history of rheumatoid arthritis, which was well controlled. These patients experienced weakness and tenderness in the proximal joints with elevated levels of ESR and CRP. They were treated with prednisone and showed improvement. Reactive arthritis was diagnosed in 1 patient who presented with swelling in both hands and wrists 2 days after being diagnosed with COVID-19. This patient began to experience symptoms of reactive arthritis 2 days after resolution of initial COVID-19 symptoms and this persisted for 3 months. The patient was managed with methylprednisolone injections and NSAIDs, which improved her symptoms. Post-COVID syndrome was identified in 7 patients. All patients were female and had a history of well-controlled fibromyalgia. Patients generally experienced fatigue, headaches, and memory fog, which had variable onset from a few days and up to 4 weeks after being diagnosed with COVID-19. One patient had a complete recovery of her symptoms at follow-up 3 months after the initial presentation. The other 6 patients continued to report symptoms of post-COVID syndrome at follow-up. Patients were managed with lifestyle modifications and their previous fibromyalgia treatment. CONCLUSION: While cases of COVID-19 continue to rise, complications of this disease are still being discovered. Those who initially recover from COVID-19 may experience new-onset rheumatic conditions, worsening of previously diagnosed rheumatic conditions, or post-COVID syndrome. As we continue to learn more about the effects of COVID-19, the awareness of these manifestations will play a key role in the appropriate management of these patients.


Subject(s)
Antirheumatic Agents , Arthritis, Reactive , Arthritis, Rheumatoid , COVID-19 , Fibromyalgia , Polymyalgia Rheumatica , Rheumatic Diseases , Humans , Female , Male , COVID-19/complications , Polymyalgia Rheumatica/complications , Polymyalgia Rheumatica/diagnosis , Polymyalgia Rheumatica/drug therapy , SARS-CoV-2 , Fibromyalgia/complications , Arthritis, Reactive/drug therapy , Prednisone/therapeutic use , Antirheumatic Agents/therapeutic use , Arthritis, Rheumatoid/drug therapy , Rheumatic Diseases/drug therapy , Methylprednisolone/therapeutic use , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use
18.
Int J Mol Med ; 49(3)2022 Mar.
Article in English | MEDLINE | ID: covidwho-1625254

ABSTRACT

Mefenamic acid is a non­steroidal anti­inflammatory drug exhibiting a wide range of anti­inflammatory, antipyretic, analgesic and probable antiviral activities. The present study evaluated the efficacy of treatment with mefenamic acid combined with standard medical care vs. standard medical care plus a placebo in ambulatory patients with coronavirus disease 2019 (COVID­19; nasal/oropharyngeal swabs reverse transcription­PCR test results positive for severe acute respiratory syndrome coronavirus 2). The present study is a phase II prospective, two­arm, parallel­group, randomized, double­blind placebo­controlled clinical trial which analyzed 36 patients. Two aspects were evaluated during the 14­day follow­up period: i) The time for reaching a patient acceptable symptom state (PASS), and ii) the last day of each COVID­19 symptom presentation. Adverse effects were evaluated. The clinical severity for all the patients in the study was mild (88.9%) and moderate (11.1%). The control (placebo) group achieved PASS on day 8.0±1.3, compared with day 4.4±0.8 in the mefenamic acid group (P=0.020, Kaplan­Meier analyses using log­rank tests). Patients that received mefenamic acid plus standard medical care had a ~16­fold higher probability of achieving PASS on day 8 (adjusted RR, 15.57; 95% CI, 1.22­198.71; P=0.035), compared with the placebo plus standard medical care group. All symptoms lasted for fewer days in the mefenamic acid group, compared with the placebo group; however, only the symptoms of headache (P=0.008), retro­orbital eye pain (P=0.049), and sore throat (P=0.029) exhibited statistically significant differences. The experimental treatment produced no severe adverse effects. On the whole, the present study demonstrates that the administration of mefenamic acid markedly reduced the symptomatology and time to reach PASS in ambulatory patients with COVID­19. Due to its probable antiviral effects and potent anti­inflammatory mechanisms, mefenamic acid may prove to be useful in the treatment of COVID­19, in combination with other drugs, including the new antivirals (remdesivir, molnupiravir, or favipiravir). However, future studies are also required to confirm these findings.


Subject(s)
Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , COVID-19/drug therapy , Mefenamic Acid/therapeutic use , Ambulatory Care , Antiviral Agents/therapeutic use , COVID-19/complications , COVID-19/therapy , Combined Modality Therapy , Double-Blind Method , Eye Pain/etiology , Headache/etiology , Humans , Pharyngitis/etiology , Prospective Studies , Treatment Outcome
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