Association Between Famotidine Use and Clinical Outcomes in Patients With COVID-19: Assessment of Available Evidence.
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ABSTRACT:
SUBMITTER: Ma T
PROVIDER: S-EPMC7553027 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:IntroductionTo compare outcomes in patients hospitalized with coronavirus (COVID-19) receiving famotidine therapy with those not receiving famotidine.MethodsRetrospective, propensity-matched observational study of consecutive COVID-19-positive patients between February 24, 2020, and May 13, 2020.ResultsOf 878 patients in the analysis, 83 (9.5%) received famotidine. In comparison to patients not treated with famotidine, patients treated with famotidine were younger (63.5 ± 15.0 vs 67.5 ± 15.8 years, P = 0.021), but did not differ with respect to baseline demographics or preexisting comorbidities. Use of famotidine was associated with a decreased risk of in-hospital mortality (odds ratio 0.37, 95% confidence interval 0.16-0.86, P = 0.021) and combined death or intubation (odds ratio 0.47, 95% confidence interval 0.23-0.96, P = 0.040). Propensity score matching to adjust for age difference between groups did not alter the effect on either outcome. In addition, patients receiving famotidine displayed lower levels of serum markers for severe disease including lower median peak C-reactive protein levels (9.4 vs 12.7 mg/dL, P = 0.002), lower median procalcitonin levels (0.16 vs 0.30 ng/mL, P = 0.004), and a nonsignificant trend to lower median mean ferritin levels (797.5 vs 964.0 ng/mL, P = 0.076). Logistic regression analysis demonstrated that famotidine was an independent predictor of both lower mortality and combined death/intubation, whereas older age, body mass index >30 kg/m, chronic kidney disease, National Early Warning Score, and higher neutrophil-lymphocyte ratio were all predictors of both adverse outcomes.DiscussionFamotidine use in hospitalized patients with COVID-19 is associated with a lower risk of mortality, lower risk of combined outcome of mortality and intubation, and lower levels of serum markers for severe disease in hospitalized patients with COVID-19.(Equation is included in full-text article.).
| S-EPMC7473796 | biostudies-literature
Project description:BackgroundRecent evidence has established a beneficial effect of systemic corticosteroids for treatment of moderate-to-severe COVID-19.ObjectiveTo determine if inhaled corticosteroid use is associated with COVID-19 outcomes.MethodsIn a nationwide cohort of hospitalized SARS-CoV-2 test-positive individuals in Denmark, we estimated the 30-day hazard ratio of intensive care unit (ICU) admission or death among users of inhaled corticosteroids (ICS) compared with users of bronchodilators (β2 -agonist/muscarinic-antagonists), and non-users of ICS overall, with Cox regression adjusted for age, sex, and other confounders. We repeated these analyses among influenza test-positive patients during 2010-2018.ResultsAmong 6267 hospitalized SARS-CoV-2 patients, 614 (9.8%) were admitted to ICU and 677 (10.8%) died within 30 days. ICS use was associated with a hazard ratio of 1.09 (95% CI [CI], 0.67 to 1.79) for ICU admission and 0.78 (95% CI, 0.56 to 1.11) for death compared with bronchodilator use. Compared with no ICS use overall, the hazard ratio of ICU admission or death was 1.17 (95% CI, 0.87-1.59) and 1.02 (95% CI, 0.78-1.32), respectively. Among 10 279 hospitalized influenza patients, of which 951 (9.2%) were admitted to ICU and 1275 (12.4%) died, the hazard ratios were 1.43 (95% CI, 0.89-2.30) and 1.11 (95% CI, 0.85-1.46) for ICU admission, and 0.80 (95% CI, 0.63-1.01) and 1.03 (95% CI, 0.87-1.22) for death compared with bronchodilator use and no ICS use overall, respectively.ConclusionOur results do not support an effect of inhaled corticosteroid use on COVID-19 outcomes, however we can only rule out moderate-to-large reduced or increased risks.Study registrationThe study was pre-registered at encepp.eu (EUPAS35897).
| S-EPMC8441753 | biostudies-literature
Project description:BackgroundAlthough there are several efficacious vaccines against COVID-19, vaccination rates in many regions around the world remain insufficient to prevent continued high disease burden and emergence of viral variants. Repurposing of existing therapeutics that prevent or mitigate severe COVID-19 could help to address these challenges. The objective of this study was to determine whether prior use of bisphosphonates is associated with reduced incidence and/or severity of COVID-19.MethodsA retrospective cohort study utilizing payer-complete health insurance claims data from 8,239,790 patients with continuous medical and prescription insurance January 1, 2019 to June 30, 2020 was performed. The primary exposure of interest was use of any bisphosphonate from January 1, 2019 to February 29, 2020. Bisphosphonate users were identified as patients having at least one bisphosphonate claim during this period, who were then 1:1 propensity score-matched to bisphosphonate non-users by age, gender, insurance type, primary-care-provider visit in 2019, and comorbidity burden. Main outcomes of interest included: (a) any testing for SARS-CoV-2 infection; (b) COVID-19 diagnosis; and (c) hospitalization with a COVID-19 diagnosis between March 1, 2020 and June 30, 2020. Multiple sensitivity analyses were also performed to assess core study outcomes amongst more restrictive matches between BP users/non-users, as well as assessing the relationship between BP-use and other respiratory infections (pneumonia, acute bronchitis) both during the same study period as well as before the COVID outbreak.ResultsA total of 7,906,603 patients for whom continuous medical and prescription insurance information was available were selected. A total of 450,366 bisphosphonate users were identified and 1:1 propensity score-matched to bisphosphonate non-users. Bisphosphonate users had lower odds ratios (OR) of testing for SARS-CoV-2 infection (OR = 0.22; 95%CI:0.21-0.23; p<0.001), COVID-19 diagnosis (OR = 0.23; 95%CI:0.22-0.24; p<0.001), and COVID-19-related hospitalization (OR = 0.26; 95%CI:0.24-0.29; p<0.001). Sensitivity analyses yielded results consistent with the primary analysis. Bisphosphonate-use was also associated with decreased odds of acute bronchitis (OR = 0.23; 95%CI:0.22-0.23; p<0.001) or pneumonia (OR = 0.32; 95%CI:0.31-0.34; p<0.001) in 2019, suggesting that bisphosphonates may protect against respiratory infections by a variety of pathogens, including but not limited to SARS-CoV-2.ConclusionsPrior bisphosphonate-use was associated with dramatically reduced odds of SARS-CoV-2 testing, COVID-19 diagnosis, and COVID-19-related hospitalizations. Prospective clinical trials will be required to establish a causal role for bisphosphonate-use in COVID-19-related outcomes.FundingThis study was supported by NIH grants, AR068383 and AI155865, a grant from MassCPR (to UHvA) and a CRI Irvington postdoctoral fellowship, CRI2453 (to PH).
| S-EPMC10691801 | biostudies-literature
Project description:Famotidine has been considered to be a potential treatment for COVID-19 but the current data is conflicting. This retrospective study was conducted by utilizing data of 9565 COVID-19 hospitalized patients. Patients treated with and without famotidine were matched by propensity score using a 1:1 matching scheme. A total of 1593 patients (16.7%) received famotidine. In-hospital mortality was similar in patients treated with and without famotidine in the propensity-matched cohorts (28.3% vs. 28.2%, p = 0.97), which remains similar irrespective of severity or concomitant treatment by steroids. Famotidine treatment was not associated with a lower risk of in-hospital mortality of COVID-19 patients.
| S-EPMC8662098 | biostudies-literature
Project description: Not available
| S-EPMC7242191 | biostudies-literature
Project description:We investigated the association between endogenous vitamin D and the severity of COVID-19 as well as the mechanisms of action of vitamin D supplementation. Vitamin D deficiency and insufficiency were associated with increased severity and unfavourable outcome after 28 days. Vitamin D levels were negatively associated with biomarkers of COVID-19 severity. Vitamin D supplementation after challenge of mice with COVID-19 plasma led to reduced levels of TNFα, IL-6, IFNγ and MPO in the lung, as well as down-regulation of pro-inflammatory pathways as derived from RNA-seq experiments. Thus, vitamin D demonstrates a protective effect against severity and unfavorable outcome in COVID-19, possibly through attenuation of tissue-specific hyperinflammation.
2024-01-16 | GSE222471 | GEO
Project description:AimPrevious studies have reported inconsistent results regarding the association between metformin use and clinical outcomes in diabetes mellitus (DM) patients with coronavirus disease 2019 (COVID-19). This study aimed to evaluate the association between metformin use and clinical outcomes in DM patients with COVID-19.MethodsThis retrospective study was based on claims data. All diseases, including COVID-19, were defined using International Classification of Diseases 10th Revision (ICD-10) codes. Patients were divided into three groups depending on metformin use: CON (those not taking DM medication); N-MFOM (those taking DM medications other than metformin); and MFOM (those taking metformin for DM). Ultimately, 1865 patients were included; CON, N-MFOM and MFOM groups comprised 1301, 95 and 469 patients, respectively.ResultsKaplan-Meier analyses showed that MFOM patients had poorer survival rates than those in the CON group, but there were no significant differences in survival rates between MFOM and N-MFOM groups. Multivariate Cox regression analyses revealed more favourable survival in CON than in N-MFOM patients, but there was no statistically significant difference in MFOM vs the other groups. Also, there were no significant differences in rates of use of inotropes, extracorporeal membrane oxygenation, conventional oxygen therapy, high-flow nasal cannulas or mechanical ventilators, nor in the rates of acute kidney injury or cardiac events across all study groups.ConclusionNo definite association could be found between metformin use and clinical outcomes, including survival. However, given the disproportionate participant numbers in our groups and small number of events, further studies are needed to determine whether the use of metformin has favourable or unfavourable effects in DM patients with COVID-19.
| S-EPMC7640920 | biostudies-literature
Project description:SARS-CoV-2 infection is required for COVID-19, but many signs and symptoms of COVID-19 differ from common acute viral diseases. SARS-CoV-2 infection is necessary but not sufficient for development of clinical COVID-19 disease. Currently, there are no approved pre- or post-exposure prophylactic COVID-19 medical countermeasures. Clinical data suggest that famotidine may mitigate COVID-19 disease, but both mechanism of action and rationale for dose selection remain obscure. We have investigated several plausible hypotheses for famotidine activity including antiviral and host-mediated mechanisms of action. We propose that the principal mechanism of action of famotidine for relieving COVID-19 symptoms involves on-target histamine receptor H2 activity, and that development of clinical COVID-19 involves dysfunctional mast cell activation and histamine release. Based on these findings and associated hypothesis, new COVID-19 multi-drug treatment strategies based on repurposing well-characterized drugs are being developed and clinically tested, and many of these drugs are available worldwide in inexpensive generic oral forms suitable for both outpatient and inpatient treatment of COVID-19 disease.
| S-EPMC8021898 | biostudies-literature
Project description:SARS-CoV-2 infection is required for COVID-19, but many signs and symptoms of COVID-19 differ from common acute viral diseases. Currently, there are no pre- or post-exposure prophylactic COVID-19 medical countermeasures. Clinical data suggest that famotidine may mitigate COVID-19 disease, but both mechanism of action and rationale for dose selection remain obscure. We explore several plausible avenues of activity including antiviral and host-mediated actions. We propose that the principal famotidine mechanism of action for COVID-19 involves on-target histamine receptor H 2 activity, and that development of clinical COVID-19 involves dysfunctional mast cell activation and histamine release.
| S-EPMC9793841 | biostudies-literature
Project description:SARS-CoV-2 infection is required for COVID-19, but many signs and symptoms of COVID-19 differ from common acute viral diseases. Currently, there are no pre- or post-exposure prophylactic COVID-19 medical countermeasures. Clinical data suggest that famotidine may mitigate COVID-19 disease, but both mechanism of action and rationale for dose selection remain obscure. We explore several plausible avenues of activity including antiviral and host-mediated actions. We propose that the principal famotidine mechanism of action for COVID-19 involves on-target histamine receptor H 2 activity, and that development of clinical COVID-19 involves dysfunctional mast cell activation and histamine release.
| S-EPMC7336703 | biostudies-literature