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ORIGINAL ARTICLE
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COVID-19 and Underlying Comorbidities: A Population-Based Study on 3109 Patients in North India


1 MBBS Student in the 2nd Professional Year in Maulana Azad Medical College, New Delhi, India
2 Department of Biochemistry, Maulana Azad Medical College, New Delhi, India
3 District Civil Hospital, Sonipat, Haryana, India

Date of Submission20-Apr-2021
Date of Decision26-Aug-2021
Date of Acceptance09-Sep-2021
Date of Web Publication11-Oct-2021

Correspondence Address:
Vatsala Khurana,
Department of Biochemistry, Maulana Azad Medical College, New Delhi-110002
India
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/mamcjms.mamcjms_39_21

  Abstract 


Context: The world witnessed the emergence of a new disease, coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) which is now a global pandemic. Studies have shown that people with pre-existing conditions are more vulnerable to the virus compared to people with no comorbidities. Aims: The present study has been conducted to evaluate the prevalence of comorbidities among patients with COVID-19 admitted to a district hospital in Sonipat, Haryana. Materials and methods: An epidemiologic, questionnaire-based cross-sectional study was conducted on consecutive patients with COVID-19 admitted to a civil hospital in Sonipat, Haryana between May 13, 2020 to November 13, 2020 over a period of 6 months. Statistical analysis: The data were analyzed using SPSS version 20.0 (IBM Corp., Armonk, New York, USA). Results: The results show that men (65.4%) were affected more than women with maximum prevalence in the age group of 21 to 30 years (28.8%). Only 10.7% of the volunteers showed no signs of any chronic ailment in contrast to 89.3% volunteers who were already suffering from some underlying health condition. The data also revealed that people suffering from type 2 diabetes (40.9%) and hypertension (33.5%) are more susceptible to develop SARS-CoV-2. About 55.9% of the participants were asymptomatic at presentation. Conclusion: People with chronic conditions were more susceptible to COVID-19, may be due to an increased inflammation leading to weakening of the immune system. As prevention is better than cure, so by following basic principles of sanitization, social distancing, and use of proper face masks, people with comorbidities can protect themselves from the virus.

Keywords: Comorbidity, COVID-19, diabetes, hypertension, SARS-CoV-2



How to cite this URL:
Lamba M, Khurana V, Lamba G, Goswami B. COVID-19 and Underlying Comorbidities: A Population-Based Study on 3109 Patients in North India. MAMC J Med Sci [Epub ahead of print] [cited 2021 Dec 3]. Available from: https://www.mamcjms.in/preprintarticle.asp?id=328062

Key Messages: People with underlying chronic medical conditions are reported to be at a higher risk of contracting COVID-19. They therefore need to be more cautious and can reduce their risk of infection by following basic principles of sanitization, social distancing, and use of proper face masks.




Key Messages: People with underlying chronic medical conditions are reported to be at a higher risk of contracting COVID-19. They therefore need to be more cautious and can reduce their risk of infection by following basic principles of sanitization, social distancing, and use of proper face masks.


  Introduction Top


Coronavirus disease 2019 (COVID-19) started as an epidemic in mainland China with the focus initially being reported in the city of Wuhan, Hubei province. The etiologic agent of COVID-19 was isolated and identified as a novel coronavirus, initially designated as 2019-nCoV. Later, the virus genome was sequenced and because it was genetically related to the coronavirus outbreak responsible for the severe acute respiratory syndrome (SARS) outbreak of 2003, the virus was named as SARS coronavirus-2 (SARS-CoV-2) by the International Committee for Taxonomy of Viruses. The initial cases have been associated with the Huanan South China Seafood Market where snakes, birds, and other animals such as bats were sold. A suspected bat origin was suggested after 96% genome sequence identity was demonstrated between SARS-CoV-2 and another coronavirus named Bat-CoV-RaTG13 isolated from bat species which colonized a province nearly 2000 km away from Wuhan.

But now, this disease, triggered by SARS-CoV-2, which hit India in January 2020, has turned into a global pandemic. The cases of COVID-19 have been soaring around the globe over the past months. As of November 2020, 60 million cases have reportedly been confirmed and 1.5 million have died all over the world.

In a Chinese retrospective study, patients with diabetes had more severe pneumonia, higher concentrations of lactate dehydrogenase, α-hydroxybutyrate dehydrogenase, alanine aminotransferase, and γ-glutamyl transferase, and fewer lymphocytes with a higher neutrophil count. Patients with COVID-19 with diabetes had an increased risk of intensive care unit admission. In a retrospective study of 191 patients with COVID-19 admitted to hospital, compared with survivors, those who died had a higher prevalence of hypertension (23% vs. 48%), diabetes (14% vs. 31%), and coronary heart disease (1% vs. 24%).[1],[2]

The most prevalent comorbidity in patients hospitalized for COVID-19 was hypertension, which was also a risk factor for acute kidney injury and mortality in these patients, researchers found in two separate studies. Hypertension alone was linked to increased rates of mortality. Researchers found several less prevalent comorbidities, including chronic kidney disease (CKD; 6%), nonhypertensive cardiovascular disease (11%), chronic obstructive pulmonary disease (COPD; 4.3%), and cerebrovascular accident (5%). A weaker immune system is one reason people with high blood pressure and other health problems are at higher risk for coronavirus. Long-term health conditions and aging weaken the immune system so it is unable to fight off the virus. Another possibility is that the higher risk comes not from high blood pressure itself, but from certain drugs used to treat it ‒ angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs). The theory is based on the fact that ACE inhibitors and ARBs raise levels of an enzyme called ACE2 in the body. And to infect cells, the COVID-19 virus must attach itself to ACE2.[3]

The COVID-19 mostly affects patients with grades 4 to 5 CKD. Patients with CKD have several conditions that make them a target population for the virus, that is, an older age, comorbidities, and a frail immunological system. Distinctively, outpatient advanced grades 4 to 5 CKD recipients may have a higher risk of acquiring the infection as they have more contact with hospital facilities.[4]

Patients with COPD have increased risk of severe pneumonia and poor outcomes when they develop COVID-19. This may be related to poor underlying lung reserves or increased expression of ACE2 receptor in small airways. But findings have led to speculation that treatments for respiratory disease, specifically inhaled corticosteroids, might have a protective effect against SARS-CoV-2.[5]

The present study has been conducted to evaluate the prevalence of comorbidities among patients with COVID-19 admitted to a civil hospital in in Sonipat, Haryana.


  Materials and method Top


Study

The World Health Organization global influenza surveillance standards define the surveillance case definitions for influenza-like illness (ILI) and severe acute respiratory infections (SARI). Key messages when using the case definitions:
  1. Influenza infection causes a clinical syndrome not easily distinguished from other respiratory infections.
  2. The case definitions for ILI and SARI are not necessarily intended to capture all cases but to describe trends over time.
  3. Using one common case definition globally will allow national health authorities to interpret their data in an international context.


ILI case definition: An acute respiratory infection with measured fever of ≥38°C and cough; with onset within the last 10 days.

SARI case definition: An acute respiratory infection with history of fever or measured fever of ≥38°C and cough; with onset within the last 10 days; and requires hospitalization.[6]

Study participants

This study included 3109 consecutively admitted patients to a civil hospital in Sonipat, Haryana between May 13, 2020 to November 13, 2020 over a period of 6 months. An epidemiologic, questionnaire-based cross-sectional study was conducted. Chronic condition was diagnosed on the basis of conventional criteria of the disease. All patients were invited to anonymously complete a questionnaire given to them in physical form. The questionnaire was validated by three faculty members of the institute, Maulana Azad Medical College, New Delhi.

A suspected patient with COVID-19 was defined as someone fulfilling both of the following criteria: (1) having at least one of the following symptoms or signs, including fever, respiratory symptoms, such as cough, sore throat, or dyspnea or radiographic evidence of pneumonia, and reduced counts of white blood cell or lymphocytes and (2) recently having lived in or paid visit to or gone to cities where community transmission of SARS-CoV-2 virus was reported, including Wuhan city, or recently having close contact with a confirmed patient with COVID-19 or patients with fever/respiratory symptoms within 14 days before illness onset.

A confirmed case was defined as a patient testing positive for SARS-CoV-2 by polymerase chain reaction detection of upper respiratory specimen. In particular, respiratory symptoms mainly included stuffy nose, nasal discharge, cough, sputum production, and chest pain. Systemic symptoms involved fever, fatigue, debility, muscle pain, headache, and palpitations.

Questionnaire

Sociodemographic information of patients mainly included age, gender, place of residence during the COVID-19 epidemic, symptoms present, and their chronic disease. Chronic condition was diagnosed on the basis of conventional criteria of the disease. All patients were invited to anonymously complete a questionnaire.

Statistical analysis

The data were analyzed using SPSS version 20.0 (IBM Corp., Armonk, New York, USA).

Ethics

Ethical approval was not required for this project as per the Institutional Ethics Committee as this was an anonymous questionnaire-based study based on medical education.


  Results Top


  1. Subjects: In a total of 3109 patients, the average age was 34.3 years, with a body mass index (BMI) of 20.57 ± 8.01 kg/m2 on an average. There were 2031 men and 1076 women.
  2. Variation of COVID-19 with respect to sex: From [Figure 1], this can be deduced that males are more susceptible for COVID-19. The data were reported till November 13, 2020. Out of 3109 patients admitted to a civil hospital in Sonipat, Haryana, 2031 were males and 1076 were females.
    Figure 1 Risk of developing disease in people based on sex.

    Click here to view
  3. Variation of COVID-19 with respect to age: As depicted in [Figure 2], people in the age group between 21 and 40 years are under greater risks in developing the disease, maybe because of increased exposure. Neonates and infants are the least prone to contact the virus. This might be due to the protective nature of the parents.
    Figure 2 Risk of developing disease in people based on age group.

    Click here to view
  4. Morbidity of COVID-19 with other chronic ailments: The data in [Figure 3] reveal that people suffering from type 2 diabetes non-insulin-dependent diabetes mellitus (NIDDM) (40.9%) and hypertension (33.5%) are more susceptible to develop SARS-CoV-2. People suffering from other heart conditions such as heart block or myocardial infarction are less likely to develop the disease (5.6%). Patients with chronic bronchitis (3.8%) and chronic renal failure (3.7%) are somehow equally prone for the virus. Lastly, tuberculosis patients were found to be the least liable (1.8%) for SARS-CoV-2 among all the comorbidities observed in this study. This composed the comorbidity pattern of patients admitted with COVID-19 in the civil hospital, Sonipat, Haryana as reported till November 13, 2020.
    Figure 3 Severity of viral infection in patients with other diseases.

    Click here to view
  5. Symptoms at presentation: According to the [Figure 4], 1735 volunteers out of 3109 appeared asymptomatic whereas 1368 out of 3109 appeared symptomatic. This reveals that 55.9% of the participants showed no symptoms and can spread the virus further unknowingly. Rest 44.1% participants showed symptoms of varying degrees as reported in the data from patients admitted with COVID-19 in civil hospital, Sonipat, Haryana till November 13, 2020.
    Figure 4 Symptomatic and asymptomatic spread of disease through volunteers.

    Click here to view



  Discussion Top


In this study, 3109 consecutively admitted patients with COVID-19 were chosen from a civil hospital in Sonipat, Haryana and their comorbid conditions studied. It was found that people irrespective of age and sex are an easy target to get infected with SARS-CoV-2. Still, some citizens are more liable to contact the virus. Children between 11 and 20 are moderately likely to get the disease. One factor contributing to this can be school closures during epidemics and pandemics which aim to decrease transmission among children and might also have whole-population effects if children are major contributors to community transmission rates.[7] Lastly, old age individuals are also less vulnerable to contact the virus due to less exposure. However, patients over 60 years showed profound clinical manifestations, greater severity, and longer disease courses compared with those under 60 years.[8]

Males are comparatively at a greater risk, may be due to higher expression of ACE2, high CD200R signaling, sex hormones, and lifestyle. The reason for this variation can be:
  1. Asian males had higher expression of ACE2 than females. ACE2 receptor encoded by ACE2 gene has been proved to be the receptor for both the SARS-CoV and the human respiratory coronavirus NL63.[9] There is a positive correlation of ACE2 expression and the infection of SARS-CoV. This means that an organism whose expression of ACE2 protein is high has a facilitated environment for pathogenesis of coronavirus.
  2. To generate an appropriately controlled response during infections, immunologic checkpoints, such as the inhibitory CD200 receptor (CD200R), greatly play a great role in balancing the immune system during microbial infection by stimulating and controlling hyperimmune-mediated response. A study by Karnam and colleagues revealed that CD200-CD200R and sex are host factors that together determine the outcome of viral infection. Organisms with high CD200R signaling have an enhanced clearance of viral infection. A review which looked on association between sex differences in immune responses concluded that sex-based immunologic differences contribute to variations in the susceptibility to infectious diseases and responses to vaccines in males and females.
  3. A large part of this difference is also driven by gender behavior (lifestyle), such as far higher levels of smoking and drinking among men compared to women. Further, the recent study conducted in Spain (one of the hardest hit countries in Europe) reported that women had more responsible attitude towards the COVID-19 pandemic than men. This may reversibly affect their undertaking of preventive measures such as frequent hand washing, face masking, and stay at home orders.
  4. Females are more resistant to infections than men, and this is possibly mediated by several factors including sex hormones.[10]


Individuals aged between 21 and 40 years are also more likely to get the disease because of increased exposure. Citizens presenting with long-standing illnesses are also more vulnerable to get infected with the virus because of reduced immunity due to increased inflammation. People with chronic steroid intake, alcohol consumption, or smoking are also liable. Finally, it can be concluded that more than 50% of the patients came out to be asymptomatic showing no signs of the virus. These people, if not isolated, can spread the virus further.[2]

In addition, [Figure 3] shows that people with other chronic conditions are more vulnerable to the virus. The reason can be increased inflammation leading to weakening of the immune system, making it harder for people living with the condition to fight off the disease in general. Only 10.7% of all the volunteers showed no signs of any other chronic ailment along with COVID-19 in contrast to 89.3% volunteers who were already agonized with other atrocious maladies.

In another study, conducted by Tadic et al., the authors found that the percentage of patients with COVID-19 with diabetes varies from 3% to 21%. In two largest meta‐analyses that included 46,248 and 76,993 patients with COVID‐19, respectively, diabetes was detected in 8.6% and 7.9% of the patients. In one of the largest studies published (n = 1099) so far, diabetes was present in 7.4% of patients with COVID‐19 and it was significantly more prevalent in patients with severe form of disease and those who experienced primary outcome end point (admission to an intensive care unit, the use of mechanical ventilation, or death). The same group of authors in a larger group of patients with COVID‐19 (n = 1590) reported diabetes in 8.2%, and it was significantly more prevalent among patients with COVID‐19 with severe form than in patients with nonsevere form of disease (34.6% vs. 14.3%). The difference in results can be due to the higher fat–lean ratio, indicating a greater load–capacity ratio, increase in BMI in Indian population which elevate diabetes risk to a greater extent than they do in European population, raising the susceptibility to insulin resistance. Environmental and lifestyle changes resulting from industrialization and migration to urban environment from rural settings may be responsible to a large extent, for this epidemic of type 2 diabetes in Indians. In addition, diabetes is a hyperinflammatory condition and it seems that it may increase susceptibility for COVID‐19 independently of other underlying diseases. There are several possible mechanisms: (a) inflammation, (b) hypercoagulable state, and (c) activation of renin‐angiotensin‐aldosterone system and dysregulation of sympathetic nervous system. There is evidence that SARS‐CoV-2, the novel coronavirus responsible for COVID‐19, uses ACE2 on the surfaces of epithelial cells to bind and enter to infected cells. ACE2 is located in cardiac, kidney, lung, and intestinal tissues and converts angiotensin II to angiotensin I, which promotes vasodilation.[11] Henceforth, genetic factors come to play when describing susceptibility differences to the virus.

People with diabetes are more likely to experience severe symptoms and complications when infected with the virus. When people with diabetes do not manage their disease well and experience fluctuating blood sugars, they are generally at risk for a number of diabetes-related complications. Having heart disease or other complications in addition to diabetes could worsen the chance of getting seriously ill from COVID-19, like other viral infections, because your body’s ability to fight off an infection is compromised. Viral infections can also increase inflammation, or internal swelling, in people with diabetes. This is also caused by above-target blood sugars, and both could contribute to more severe complications.[12]

In addition, analysis of early data from both China and the United States shows that high blood pressure is another most commonly shared pre-existing condition among those hospitalized, affecting between 30% and 50% of the patients. Other health conditions included cancer, diabetes, or lung disease. In Italy, a report said that more than 99% of people who had died from the virus had one of these conditions and 76% of them had high blood pressure. A weaker immune system is one reason people with high blood pressure and other health problems are at higher risk for coronavirus. Long-term health conditions and aging weaken your immune system so it is less able to fight off the virus. Nearly two-thirds of people over 60 have high blood pressure. Another possibility is that the higher risk comes not from high blood pressure itself, but from certain drugs used to treat it ‒ ACE inhibitors and ARBs. The theory is based on the fact that ACE inhibitors and ARBs raise levels of an enzyme called ACE2 in your body. And to infect cells, the COVID-19 virus must attach itself to ACE2.[12]

The results of this study correlate well with observations made in studies conducted previously, suggesting that people with chronic conditions are indeed more susceptible to acquire COVID-19. This may be due to an increased inflammation leading to weakening of the immune system. Practicing COVID-19 appropriate behavior is thus even more important for people with comorbidities.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Apicella M, Campopiano MC, Mantuano M, Mazoni L, Coppelli A, Del Prato S. COVID-19 in people with diabetes: understanding the reasons for worse outcomes. Lancet Diabetes Endocrinol 2020;8:782-92.  Back to cited text no. 1
    
2.
Dos Santos WG. Natural history of COVID-19 and current knowledge on treatment therapeutic options. Biomed Pharmacother 2020;129:110493.  Back to cited text no. 2
    
3.
American Heart Association [Internet]. Dallas; c2021.Research on the impact of ACE-i and ARBs for patients with COVID-19 continues to evolve. Available at https://newsroom.heart.org/news/research-on-the-impact-of-ace-i-and-arbs-for-patients-with-covid-19-continues-to-evolve. Accessed December 2, 2020.  Back to cited text no. 3
    
4.
Collado S, Arenas MD, Barbosa F et al. COVID-19 in grade 4–5 chronic kidney disease patients. Kidney Blood Press Res 2020;45:768-74.  Back to cited text no. 4
    
5.
Schultze A, Walker AJ, MacKenna B et al. Risk of COVID-19-related death among patients with chronic obstructive pulmonary disease or asthma prescribed inhaled corticosteroids: an observational cohort study using the OpenSAFELY platform. Lancet Respir Med 2020;8:1106-20.  Back to cited text no. 5
    
6.
Fitzner J, Qasmieh S, Mounts AW et al. Revision of clinical case definitions: influenza-like illness and severe acute respiratory infection. Bull World Health Organ 2018;96:122-8.  Back to cited text no. 6
    
7.
Omori R, Matsuyama R, Nakata Y. The age distribution of mortality from novel coronavirus disease (COVID-19) suggests no large difference of susceptibility by age. Sci Rep 2020;10:1-9.  Back to cited text no. 7
    
8.
Dhochak N, Singhal T, Kabra SK, Lodha R. Pathophysiology of COVID-19: why children fare better than adults? Indian J Pediatr 2020;87:537-46.  Back to cited text no. 8
    
9.
Pradhan A, Olsson PE. Sex differences in severity and mortality from COVID-19: are males more vulnerable? Biol Sex Differ 2020;11:53.  Back to cited text no. 9
    
10.
Bwire GM. Coronavirus: why men are more vulnerable to Covid-19 than women? SN Compr Clin Med 2020;2:874-6.  Back to cited text no. 10
    
11.
Tadic M, Cuspidi C, Sala C. COVID‐19 and diabetes: Is there enough evidence? J Clin Hypertens (Greenwich) 2020;22:943-8.  Back to cited text no. 11
    
12.
American Diabetes Association [Internet]. Virginia; c1995-. How COVID-19 Impacts People with Diabetes. Available at https://www.diabetes.org/coronaviruscovid-19/how-coronavirus-impacts-people-with-diabetes. Accessed November 30, 2020.  Back to cited text no. 12
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]



 

 
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