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Monika Fekete Department of Public Health, Semmelweis University, Faculty of Medicine, Budapest, Hungary

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Zsofia Szarvas Department of Public Health, Semmelweis University, Faculty of Medicine, Budapest, Hungary

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Vince Fazekas-Pongor Department of Public Health, Semmelweis University, Faculty of Medicine, Budapest, Hungary

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Agnes Feher Department of Public Health, Semmelweis University, Faculty of Medicine, Budapest, Hungary

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Norbert Dosa Department of Public Health, Semmelweis University, Faculty of Medicine, Budapest, Hungary

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Andrea Lehoczki Department of Hematology and Stem Cell Transplantation, National Institute for Hematology and Infectious Diseases, South Pest Central Hospital, Budapest, Hungary

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Stefano Tarantini Department of Public Health, Semmelweis University, Faculty of Medicine, Budapest, Hungary
Department of Biochemistry and Molecular Biology at University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA

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Janos Tamas Varga Department of Pulmonology, Semmelweis University, Budapest, Hungary

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https://orcid.org/0000-0002-8552-1336
Open access

Abstract

Introduction

Patients with chronic obstructive pulmonary disease (COPD) are a vulnerable group in terms of the outcome of coronavirus infection in relation to their disease or its treatment, with a higher risk of developing serious complications compared to the healthy population.

Aim

The aim of our summary study is to review the background and health outcomes of chronic obstructive pulmonary disease and COVID-19 infection in the presence of both diseases.

Methods

Review of national and international medical databases (PubMed, MEDLINE, and MOB) with keywords COPD, COVID-19, disease risk, cause, prevention, complications, and prognosis.

Results

Meta-analyses show that COPD is one of the most common underlying conditions in patients hospitalized for COVID-19. Such patients are five times more likely to develop a serious complication due to oxygen supply problems therefore they are more likely to be admitted to intensive care units, where they may require mechanical ventilation. In the case of underlying COPD, the usual care plan for COVID-19 infection should be followed, as well as all public health recommendations to minimize the risk of developing and transmitting COVID-19.

Conclusion

Coronavirus infection is especially dangerous for COPD patients, who are much more likely to become seriously ill, so increased surveillance, prevention, early detection, adequate treatment and rehabilitation of the disease group are of paramount importance.

Abstract

Introduction

Patients with chronic obstructive pulmonary disease (COPD) are a vulnerable group in terms of the outcome of coronavirus infection in relation to their disease or its treatment, with a higher risk of developing serious complications compared to the healthy population.

Aim

The aim of our summary study is to review the background and health outcomes of chronic obstructive pulmonary disease and COVID-19 infection in the presence of both diseases.

Methods

Review of national and international medical databases (PubMed, MEDLINE, and MOB) with keywords COPD, COVID-19, disease risk, cause, prevention, complications, and prognosis.

Results

Meta-analyses show that COPD is one of the most common underlying conditions in patients hospitalized for COVID-19. Such patients are five times more likely to develop a serious complication due to oxygen supply problems therefore they are more likely to be admitted to intensive care units, where they may require mechanical ventilation. In the case of underlying COPD, the usual care plan for COVID-19 infection should be followed, as well as all public health recommendations to minimize the risk of developing and transmitting COVID-19.

Conclusion

Coronavirus infection is especially dangerous for COPD patients, who are much more likely to become seriously ill, so increased surveillance, prevention, early detection, adequate treatment and rehabilitation of the disease group are of paramount importance.

Introduction

COVID-19 (coronavirus disease 2019) is an acute respiratory infection caused by SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), which is currently causing a pandemic [1]. The clinical manifestations of COVID-19 are diverse. The majority of people infected with COVID-19 have mild or no symptoms, but in 20 percent of cases the condition can become severe or critical and a fraction of infected patients progress to respiratory failure, multi-organ disease and even death [1–4]. As of February 5, 2022, over 390 million individuals have been contracted SARS-CoV-2 worldwide, of whom over 5.7 million patients have succumbed to the disease.

Chronic obstructive pulmonary disease (COPD) is a progressive lung disease that is characterized by persistent respiratory symptoms, low-grade lung inflammation and airflow obstruction. The two most common conditions of COPD are emphysema and chronic bronchitis, often caused by tobacco smoking. Epidemiological studies show that COPD is a risk factor for poor clinical outcomes in established COVID-19 [5].

In this review, the interactions between COPD and SARS-CoV-2 infection are considered [6–9]. The pathophysiological mechanisms contributing to poor outcomes in COPD patients with COVID-19 are discussed. Specific recommendations for the care of COPD patients during the pandemic are described.

COPD exacerbates severity of COVID-19

Based on currently available data, COPD patients have a much higher rate of severe COVID-19 infection [6–9]. A recent meta-analysis reported a high odds ratio (OR = 5.69) for the development of severe COVID-19 (defined as acute respiratory failure and/or admission to intensive care) in COPD patients [5], while another meta-analysis reported an OR = 4.38 [10]. One review, which focused specifically on comorbidities, described that COPD had the highest odds ratio for severe COVID-19 (OR = 5.97), while hypertension (OR = 2.29), diabetes (OR = 2.47), cardiovascular disease (OR = 2.93) and cerebrovascular disease (OR = 3.89) had lower ORs [11]. In these studies, severe COVID-19 infection was defined as acute respiratory failure and/or admission to intensive care.

The mechanisms by which COPD exacerbates severity of COVID-19 are likely multifaceted. COPD is an inflammatory disease of the bronchi, which is associated with narrowing of the airways, increased secretion and reduced airway reserve [12]. Due to the constant inflammation, the lung tissue is remodeled, damaged and gradually destroyed, causing a gradual deterioration in breathing, difficulty breathing and then respiratory failure. At this stage, oxygen treatment is often necessary [13]. Severe pneumonia at this stage can lead to respiratory collapse in a matter of hours. Chronic obstructive airway disease and treatment with oral corticosteroids render COPD patients more susceptible to infections, including COVID-19. The reduced respiratory reserve, which is further compromised by a possible pneumonia, makes patients particularly vulnerable and prone to severe complications [1]. In addition, COPD is associated with increased expression of angiotensin-converting enzyme 2 (ACE-2), the entry receptor of SARS-CoV-2, in the lower airway epithelial cells, which further increases the risk and severe outcome of COVID-19 infection [14]. COPD develops most often in people who are 40 or older. It has also been shown that COVID-19 can affect individuals in all age groups, yet it mostly causes severe disease in older adults. The mechanisms by which aging exacerbate the severity of COVID-19 include age-related immunosenescence, aging-induced impairment of organismal and cellular stress resilience and a greater prevalence of comorbidities in older adults [2, 12–24]. COPD patients who are former smokers tend to exhibit the highest mortality associated with COVID-19 infection [15–17]. The pathophysiological mechanisms by which smoking increases the risk of developing complications from COVID-19 include impaired innate and adaptive immune responses and impairment of the lungs’ self-cleansing defense mechanisms [25, 26] (Table 1). Inhaled steroids in COPD do not increase susceptibility to viral infection and that in any case; the prescribed basal therapy should not be abandoned during a coronavirus pandemic.

Table 1.

Changes in the lungs due to cigarette smoke and SARS-CoV-2 mediated injury in COPD

Smoker lung
  •  ➢ Mucous metaplasia

  •  ➢ Loss of club cells

  •  ➢ ↑B cells, antibodies increase

  •  ➢ ↑Alveolar macrophages

  •  ➢ ↑Cytotoxic CD8+cells, ↑cytokines, ↑chemokines

  •  ➢ ↑Neutrophil granulocytes

  •  ➢ ↑Proteases

  •  ➢ Exhausted T cells and ↓Regulatory T cells

  •  ➢ Loss of alveolar type 2 progenitor cells (AT2)

  •  ➢ Endothelial injury

  •  ➢ ↑Secretion production

  •  ➢ ↓Ability of the lungs to self-clean

  •  ➢ Impaired immune response


Evidence for factors critical in COVID-19 severity
  •  ➢ Smoke-induced changes in numbers of the main ACE-2-producing cells

  •  ➢ SARS-CoV-2 S protein cleavage by proteinases

  •  ➢ Smoke-induced altered antiviral responses

  •  ➢ Smoke-induced inflammation

  •  ➢ Smoke-induced altered lung structure and endothelial damage

  •  ➢ Other smoke-induced unknown factors


SARS-CoV-2 mediated injury
  •  ➢ Vasoconstriction

  •  ➢ Vascular permeability↑

  •  ➢ Oedema

  •  ➢ Lung injury

  •  ➢ Pulmonary inflammation

  •  ➢ Respiratory failure

  •  ➢ ACE-2 activity reduced

  •  ➢ Angiotensin II levels increased

ACE-2 = angiotensin-converting enzyme 2; CD = cluster of differentiation; SARS-CoV-2 = severe acute respiratory syndrome coronavirus 2.

COPD, cigarette smoking and ACE-2 expression

On the basis of the available evidence it can be hypothesized that changes in the expression of ACE-2 play an important role in increased susceptibility to severe COVID-19 infection. ACE-2 is implicated in the entry of the virus into the host’s airway epithelium to establish an active infection [18, 19]. A recent clinical trial was conducted to explore the association between ACE-2 expression and COVID-19 mortality in COPD patients [20]. COPD was defined as cases where the ratio of forced expiratory volume in 1 s (FEV1) to forced vital capacity (FVC) (FEV1/FVC) was less than 70% or where a computed tomography (CT) scan showed clear signs of emphysema. All patients also had a sub-segmental airway sampled by brush cytology and ribonucleic acid (RNA) sequencing was performed. In addition, ACE-2 protein expression was determined from resected lung tissue samples. The results of the aforementioned study showed significantly elevated ACE-2 expression in airway epithelial cells in COPD patients compared to controls (COPD: 2.52 ± 0.66 AU vs. control: 1.70 ± 0.51 AU) [20]. Smoking status was also significantly associated with airway ACE-2 expression, with significantly higher gene expression in active smokers than in controls who never smoked (active smokers: 2.77 ± 0.91 AU vs. never smokers: 1.78 ± 0.39 AU) [20]. Another important observation was that ACE-2 gene expression was inversely correlated with FEV1 values, a correlation that was confirmed in three different cohorts [20].

The virus enters the cell by binding to the ACE-2 receptor expressed on the type II epithelial cells. Additionally, ACE-2 is also expressed on the surface of epithelial and endothelial cells in the heart, kidney, esophagus, stomach, intestine and blood vessels and in certain white blood cells [21]. It is important to highlight the pathogenic role of endothelitis associated with diffuse infection and inflammation of the endothelium, which can lead to activation of the coagulation system and the complement cascade, resulting in vascular injury and thromboembolism, ischemia, thus increasing further organ damage in patients [22, 23]. A recently recognized important feature of COVID-19 is the abnormal activation of the coagulation system, which clinically predisposes to arterial and venous thromboembolism [24–28]. The degree of coagulopathy is proportional to the severity of the disease and thromboinflammatory biomarkers predict worse outcomes [29]. The pathophysiological mechanisms promoting thrombogenesis in COVID-19 patients include hyperactive coagulation and complement systems induced associated with excessive inflammation, platelet activation and endothelial dysfunction and injury [30]. Because of the exacerbated pro-thrombotic state, anti-coagulation therapies may be most effective in patients with chronic illness [31].

Treatment of COPD patients infected with COVID-19

Specific data and research evaluating the specific treatment of COPD patients with COVID-19 are not available. However, it is essential that chronic lung patients adhere to medication and medication monitoring instructions, with regular preventive inhaled bronchodilator medication being of particular importance [32]. It is important to avoid smoking completely and to maintain regular physical activity [33, 34]. Most patients are given long-acting bronchodilators or a combination of different types of bronchodilators in their inhalers (so-called “sprays” or “dry powder inhalers”), and abandoning these preparations is particularly dangerous [35]. In the case of acute deterioration, aerosol or dry powder inhaler formulations are recommended instead of mechanical nebulizers. If necessary, oxygen therapy should be used to maintain Sp02 levels above 88–90% [36]. All patients with COPD showing signs of respiratory failure should have arterial blood gas monitoring. If the pH < 7.35 (hypercapnic acidosis), ventilatory support, i.e. non-invasive ventilation (NIV) invasive ventilation or high-flow oxygen therapy, should be considered. The effect of systemic corticosteroids on COVID-19 is still controversial [37], but due to COPD-induced deterioration, oral or intravenous corticosteroid administration may be used in the setting of COVID-19 infection. As with other COVID-19 patients, low molecular weight heparin should be used prophylactically to prevent thromboembolic complications unless there are other contraindications.

In COPD, on the one hand, the body’s defense system does not work properly, and on the other hand, the breathing surface is reduced, decreasing the respiratory reserve, which in the case of pneumonia quickly leads to respiratory failure [38]. Some patients already require oxygen therapy on a daily basis and may be particularly at risk from coronavirus infection [39]. Of particular interest for COPD research will be the ongoing COPD follow-up studies after the COVID-19 pandemic to assess the potential interactions between COVID-19 and COPD, with particular focus on its symptoms, exacerbations, respiratory function, consequences of reduced physical activity, mental, social and societal effects [40].

Pulmonary rehabilitation programs for patients with COPD

During the coronavirus outbreak, several pulmonary rehabilitation programs were suspended to reduce the risk of SARS-CoV-2 spreading [41]. Therefore, patients should be encouraged and supported to remain active at home, participating in self-monitored pulmonary rehabilitation. It may be worth using a home respiratory trainer to improve inhalation muscle strength, thereby reducing breathing difficulties and increasing endurance [42]. New technologies and increased individual internet connectivity also provide opportunities to develop a suitable telerehabilitation strategy for patients [43]. Telerehabilitation is also used to treat chronic diseases, including heart disease [44], stroke [45], and multiple sclerosis [46]. Self-monitored home exercise has been shown to improve patient outcomes in many diseases, including respiratory function and quality of life in COPD [47], and home tele-rehabilitation has been shown to be as effective as hospital rehabilitation in reducing the risk of acute exacerbations and hospitalizations, as well as emergency department admissions [48, 49]. Using digital tools can also improve medication adherence in chronic respiratory patients and, thanks to real-time data analysis, it is possible to detect symptoms at an early stage of exacerbation and, if necessary, change medication with a doctor [50, 51]. Global Initiative for Chronic Obstructive Lung Disease (GOLD) has developed a device to support the remote monitoring of COPD patients by enabling home measurement of peak expiratory flow (PEF) [52, 53]. The professional spirometry system for monitoring lung disease is a smart device consisting of a portable spirometer, a built-in heart rate monitor and an online management interface that can be downloaded to a smartphone. The spirometer monitors the exhalation and inhalation curves and displays the most important parameters in real time on the smartphone screen, measures FEV1, FVC, PEF, heart rate, provides high accuracy flow measurement, respiratory function analysis and, if the user wishes, a training plan. Once the measurement is complete, that can be easily shared with the physician via the internet. From this data, the GP or pulmonologist can determine whether the medication needs to be changed. Given the accuracy, predictability and personalization of digital remote monitoring devices, there is a strong case for current and future technologies to be incorporated into the management of chronic respiratory patients.

Disease-specific recommendations for COPD patients on the COVID-19 pandemic [53]

  • If the possibility of coronavirus infection arises, the prescribed epidemiological procedure is justified (use of masks, keeping distance, observance of hygiene rules). Only one patient may use an inhalation device.

  • If a coronavirus infection is suspected or confirmed, the patient can be treated at home if symptoms are mild, it is important to control fever and drink plenty of fluids.

  • If, during home treatment of a mild illness, underlying condition cause exacerbation of choking symptoms, immediate help should be obtained from the appropriate hospital ward, as hospital admission is necessary for severe symptoms. These include choking, dyspnea or pneumonia in addition to fever (above 38 °C).

  • The patient should make sure that they have enough medication and/or prescriptions for several weeks of inhaled medicines for the preventive treatment of COPD.

  • As discontinuation or dose reduction of justified maintenance treatment for COPD may cause adverse health effects, there is no reason to stop or adjust the dose of therapy used.

  • If home oxygen therapy is needed, discuss in advance with the supplier how to ensure continuous oxygen supply.

  • If the patient is using a long-acting bronchodilator inhaler, it is important and necessary to maintain the same dose. Discontinuation of these preparations is particularly dangerous in COPD.

  • In addition to bronchodilators, some patients are also given a medicine called inhaled corticosteroid. These drugs have been shown to be safe even in the presence of confirmed COVID infection, but their omission may increase the likelihood of acute exacerbations as COPD worsens.

Conclusion

The coronavirus pandemic has dramatically shifted the landscape of the healthcare sector, which did not adapt rapidly enough to limit the initial number of doctor-patient encounters, resulting in numerous avoidable deaths of individuals with comorbidities such as COPD. Patients with COPD are more likely to develop severe complications from COVID-19 disease due to oxygen supply problems, thus are more likely to be admitted to intensive care units, where they may require mechanical ventilation. Active smokers and patients with COPD have increased ACE-2 expression in the lower airways, which may partly explain why COVID-19 is an increased risk in this population. The available evidence highlights the importance of smoking cessation and the particular importance of increased surveillance, prevention, early detection, treatment and rehabilitation of this patient group.

Consent for publication

Not applicable.

Competing interests

The authors declare that they have no competing interests.

Funding

This research did not receive any specific grant from funding agencies in the public, commercial, or non-profit sectors.

List of abbreviations

ACE-2

angiotensin-converting enzyme 2

COPD

chronic obstructive pulmonary disease

COVID-19

coronavirus disease 2019

CT

computed tomography

FEV1

forced expiratory volume in 1 second

FVC

forced vital capacity

GOLD

Global Initiative for Chronic Obstructive Lung Disease

OR

odds ratio

PEF

peak expiratory flow

RNA

ribonucleic acid

SARS

severe acute respiratory syndrome

SARS-CoV-2

severe acute respiratory syndrome coronavirus 2

MOB

Hungarian Medical Bibliography (Magyar Orvosi Bibliográfia)

WHO

World Health Organization

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    Chen J , Jin W , Zhang X-X , Xu W , Liu X-N , Ren C-C . Telerehabilitation approaches for stroke patients: systematic review and meta-analysis of randomized controlled trials. J Stroke Cerebrovasc Dis 2015; 24(12): 26602668. https://doi.org/10.1016/j.jstrokecerebrovasdis.2015.09.014.

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    Amatya B , Galea MP , Kesselring J , Khan F . Effectiveness of telerehabilitation interventions in persons with multiple sclerosis: a systematic review. Mult Scler Relat Disord 2015; 4(4): 358-369. https://doi.org/https://doi.org/10.1016/j.msard.2015.06.011.

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    Ma S , Hecht A , Varga J , Rambod M , Morford S , Goto S , et al. Breath-by-breath quantification of progressive airflow limitation during exercise in COPD: a new method. Respir Med 2010; 104(3): 389396. https://doi.org/10.1016/j.rmed.2009.10.014.

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    Holland AE , Hill CJ , Rochford P , Fiore J , Berlowitz DJ , McDonald CF . Telerehabilitation for people with chronic obstructive pulmonary disease: feasibility of a simple, real time model of supervised exercise training. J Telemed Telecare 2013; 19(4): 222226. https://doi.org/10.1177/1357633x13487100.

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    Vitacca M , Bianchi L , Guerra A , Fracchia C , Spanevello A , Balbi B , et al. Tele-assistance in chronic respiratory failure patients: a randomised clinical trial. Eur Respir J 2009; 33(2): 411418. https://doi.org/10.1183/09031936.00005608.

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    Sillanpää E , Stenroth L , Bijlsma AY , Rantanen T , McPhee JS , Maden-Wilkinson TM , et al. Associations between muscle strength, spirometric pulmonary function and mobility in healthy older adults. Age (Dordr) 2014; 36(4): 9667. https://doi.org/10.1007/s11357-014-9667-7.

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    • Search Google Scholar
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    Criner GJ , Cole T , Hahn KA , Kastango K , Eudicone JM , Gilbert I . Use of a digital chronic obstructive pulmonary disease respiratory tracker in a primary care setting: a feasibility study. Pulm Ther 2021; 7(2): 533547. https://doi.org/10.1007/s41030-021-00168-3.

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    Jackson H , Hubbard R . Detecting chronic obstructive pulmonary disease using peak flow rate: cross sectional survey. BMJ 2003; 327(7416): 653654. https://doi.org/10.1136/bmj.327.7416.653.

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    • Export Citation
  • 53.

    Halpin DMG , Criner GJ , Papi A , Singh D , Anzueto A , Martinez FJ , et al. Global initiative for the diagnosis, management, and prevention of chronic obstructive lung disease. The 2020 GOLD science committee report on COVID-19 and chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2021; 203(1): 2436. https://doi.org/10.1164/rccm.202009-3533SO.

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Editor-in-Chief

László ROSIVALL (Semmelweis University, Budapest, Hungary)

Managing Editor

Anna BERHIDI (Semmelweis University, Budapest, Hungary)

Co-Editors

  • Gábor SZÉNÁSI (Semmelweis University, Budapest, Hungary)
  • Ákos KOLLER (Semmelweis University, Budapest, Hungary)
  • Zsolt RADÁK (University of Physical Education, Budapest, Hungary)
  • László LÉNÁRD (University of Pécs, Hungary)
  • Zoltán UNGVÁRI (Semmelweis University, Budapest, Hungary)

Assistant Editors

  • Gabriella DÖRNYEI (Semmelweis University, Budapest, Hungary)
  • Zsuzsanna MIKLÓS (Semmelweis University, Budapest, Hungary)
  • György NÁDASY (Semmelweis University, Budapest, Hungary)

Hungarian Editorial Board

  • György BENEDEK (University of Szeged, Hungary)
  • Zoltán BENYÓ (Semmelweis University, Budapest, Hungary)
  • Mihály BOROS (University of Szeged, Hungary)
  • László CSERNOCH (University of Debrecen, Hungary)
  • Magdolna DANK (Semmelweis University, Budapest, Hungary)
  • László DÉTÁRI (Eötvös Loránd University, Budapest, Hungary)
  • Zoltán GIRICZ (Semmelweis University, Budapest, Hungary and Pharmahungary Group, Szeged, Hungary)
  • Zoltán HANTOS (Semmelweis University, Budapest and University of Szeged, Hungary)
  • Zoltán HEROLD (Semmelweis University, Budapest, Hungary) 
  • László HUNYADI (Semmelweis University, Budapest, Hungary)
  • Gábor JANCSÓ (University of Pécs, Hungary)
  • Zoltán KARÁDI (University of Pecs, Hungary)
  • Miklós PALKOVITS (Semmelweis University, Budapest, Hungary)
  • Gyula PAPP (University of Szeged, Hungary)
  • Gábor PAVLIK (University of Physical Education, Budapest, Hungary)
  • András SPÄT (Semmelweis University, Budapest, Hungary)
  • Gyula SZABÓ (University of Szeged, Hungary)
  • Zoltán SZELÉNYI (University of Pécs, Hungary)
  • Lajos SZOLLÁR (Semmelweis University, Budapest, Hungary)
  • Gyula TELEGDY (MTA-SZTE, Neuroscience Research Group and University of Szeged, Hungary)
  • József TOLDI (MTA-SZTE Neuroscience Research Group and University of Szeged, Hungary)
  • Árpád TÓSAKI (University of Debrecen, Hungary)

International Editorial Board

  • Dragan DJURIC (University of Belgrade, Serbia)
  • Christopher H.  FRY (University of Bristol, UK)
  • Stephen E. GREENWALD (Blizard Institute, Barts and Queen Mary University of London, UK)
  • Osmo Otto Päiviö HÄNNINEN (Finnish Institute for Health and Welfare, Kuopio, Finland)
  • Helmut G. HINGHOFER-SZALKAY (Medical University of Graz, Austria)
  • Tibor HORTOBÁGYI (University of Groningen, Netherlands)
  • George KUNOS (National Institutes of Health, Bethesda, USA)
  • Massoud MAHMOUDIAN (Iran University of Medical Sciences, Tehran, Iran)
  • Tadaaki MANO (Gifu University of Medical Science, Japan)
  • Luis Gabriel NAVAR (Tulane University School of Medicine, New Orleans, USA)
  • Hitoo NISHINO (Nagoya City University, Japan)
  • Ole H. PETERSEN (Cardiff University, UK)
  • Ulrich POHL (German Centre for Cardiovascular Research and Ludwig-Maximilians-University, Planegg, Germany)
  • Andrej A. ROMANOVSKY (University of Arizona, USA)
  • Anwar Ali SIDDIQUI (Aga Khan University, Karachi, Pakistan)
  • Csaba SZABÓ (University of Fribourg, Switzerland)
  • Eric VICAUT (Université de Paris, UMRS 942 INSERM, France)
  • Nico WESTERHOF (Vrije Universiteit Amsterdam, The Netherlands)

 

Editorial Correspondence:
Physiology International
Semmelweis University
Faculty of Medicine, Institute of Translational Medicine
Nagyvárad tér 4, H-1089 Budapest, Hungary
Phone/Fax: +36-1-2100-100
E-mail: pi@semmelweis-univ.hu

Indexing and Abstracting Services:

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  • Medline
  • Referativnyi Zhurnal
  • SCOPUS
  • WoS - Science Citation Index Expanded

 

2022  
Web of Science  
Total Cites
WoS
335
Journal Impact Factor 1.4
Rank by Impact Factor

Physiology (Q4)

Impact Factor
without
Journal Self Cites
1.4
5 Year
Impact Factor
1.6
Journal Citation Indicator 0.42
Rank by Journal Citation Indicator

Physiology (Q4)

Scimago  
Scimago
H-index
33
Scimago
Journal Rank
0.362
Scimago Quartile Score

Physiology (medical) (Q3)
Medicine (miscellaneous) (Q3)

Scopus  
Scopus
Cite Score
2.8
Scopus
CIte Score Rank
Physiology 68/102 (33rd PCTL)
Scopus
SNIP
0.508

2021  
Web of Science  
Total Cites
WoS
330
Journal Impact Factor 1,697
Rank by Impact Factor

Physiology 73/81

Impact Factor
without
Journal Self Cites
1,697
5 Year
Impact Factor
1,806
Journal Citation Indicator 0,47
Rank by Journal Citation Indicator

Physiology 69/86

Scimago  
Scimago
H-index
31
Scimago
Journal Rank
0,32
Scimago Quartile Score Medicine (miscellaneous) (Q3)
Physiology (medical) (Q3)
Scopus  
Scopus
Cite Score
2,7
Scopus
CIte Score Rank
Physiology (medical) 69/101 (Q3)
Scopus
SNIP
0,591

 

2020  
Total Cites 245
WoS
Journal
Impact Factor
2,090
Rank by Physiology 62/81 (Q4)
Impact Factor  
Impact Factor 1,866
without
Journal Self Cites
5 Year 1,703
Impact Factor
Journal  0,51
Citation Indicator  
Rank by Journal  Physiology 67/84 (Q4)
Citation Indicator   
Citable 42
Items
Total 42
Articles
Total 0
Reviews
Scimago 29
H-index
Scimago 0,417
Journal Rank
Scimago Physiology (medical) Q3
Quartile Score  
Scopus 270/1140=1,9
Scite Score  
Scopus Physiology (medical) 71/98 (Q3)
Scite Score Rank  
Scopus 0,528
SNIP  
Days from  172
submission  
to acceptance  
Days from  106
acceptance  
to publication  

2019  
Total Cites
WoS
137
Impact Factor 1,410
Impact Factor
without
Journal Self Cites
1,361
5 Year
Impact Factor
1,221
Immediacy
Index
0,294
Citable
Items
34
Total
Articles
33
Total
Reviews
1
Cited
Half-Life
2,1
Citing
Half-Life
9,3
Eigenfactor
Score
0,00028
Article Influence
Score
0,215
% Articles
in
Citable Items
97,06
Normalized
Eigenfactor
0,03445
Average
IF
Percentile
12,963
Scimago
H-index
27
Scimago
Journal Rank
0,267
Scopus
Scite Score
235/157=1,5
Scopus
Scite Score Rank
Physiology (medical) 73/99 (Q3)
Scopus
SNIP
0,38

 

Physiology International
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Physiology International
Language English
Size B5
Year of
Foundation
2006 (1950)
Volumes
per Year
1
Issues
per Year
4
Founder Magyar Tudományos Akadémia
Founder's
Address
H-1051 Budapest, Hungary, Széchenyi István tér 9.
Publisher Akadémiai Kiadó
Publisher's
Address
H-1117 Budapest, Hungary 1516 Budapest, PO Box 245.
Responsible
Publisher
Chief Executive Officer, Akadémiai Kiadó
ISSN 2498-602X (Print)
ISSN 2677-0164 (Online)

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