Int J. Pharm. Drug. Anal, Vol: 8, Issue: 10, 2020; 1-4
Review Article
Prevalence of comorbidities associated with COVID19 in Andhra Pradesh, India
Poojitha.D, Dr.J.Bhargava Narendra
Department of Pharmacy Practice, QIS College of Pharmacy, Vengamukkapalem, Ongole, Andhra Pradesh, India
Abstract
The covid-19,caused by a newly discovered corona virus, known as severe acute respiratory syndrome(corona Virus 2 ).The outbreak of corona virus pandemic has affected the lives of billions of individuals, It affects not only on public health but also social and economic activities. The main aim of the study is to describe the association comorbidities in covid-19 patients and their complications .The highly effected comorbid conditions are Hypertension, Diabetes, CVD, malignancies, HIV, Renal diseases, Asthma, COPD, Obesity and liver diseases.
Keywords: SARS-CoV-2, pandemic, comorbidities, Risk factors, Hypertension, Diabetes, CVD, HIV.
Article History: Received on: 24-08-2020 Accepted on: 15-10-2020 Published: 27-10-2020
Corresponding Author:
Dr.J.Bhargava Narendra
E-Mail: jbn53@gmail.com
This article is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. Copyright © 2020 Author(s) retain the copyright of this article.
Introduction
A pneumonia of unknown cause detected in Wuhan city, was reported to the WHO country office in China on December 31 ,2019.The new virus is officially called as severe acute respiratory syndrome -CoV-2-(SARSCoV-2) due to its similarity to SARS -CoV-2 of 2003,the disease caused by it is named as COVID -19 by WHO on February 11 2020 and declared as world pandemic on 11March, 2020.Although related CoVs, SARS-CoV and middle east respiratory syndrome (MERS -CoV) are both closely related to SARS -CoV-2 ,the biological differences between these two viruses are striking SARS -CoV-2 is more infectious It is having 79% similarity to SARS -CoV-2 at nucleotide level. COVID -19,is the seventh covid in human population .SARS-COV-2 utilises ACE-2 receptors found at the surface of the host cells to get inside the cell which is facilitated by furin cleavage [1]. Physicians around the world learning new things about this virus everyday, so far, we know that COVID -19 may not initially cause any symptoms for some people later fewer are experiencing mild to severe pneumonia like symptoms.
Doctors around the world treating the affected individuals during pandemic, in their findings have said
that over 48% of patients undergone death are due to comorbid conditions. Out of 48%,more than 30%are diagnosed with Hypertension, 19%with diabetes and <8% with cardiovascular conditions [2].
Role of Angiotensin-Converting Enzyme Inhibitors and angiotensin Receptor blockers
ACE2 is a homolog of angiotensin-converting enzyme that converts angiotensin II to angiotensin 1 to 7, thereby diminishing vasoconstriction mediated by the renin angiotensin system. The use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers is common in cardiovascular disorders (hypertension, coronary artery disease, congestive heart failure, and
DM). There are conflicting data on whether these drugs increase or have minimal effect on ACE2 levels.SARS-CoV-2 entry into cells is ACE2 dependent however, ACE2 appears to be protective against acute lung injury. In a murine model, binding of the SARS-CoV spike protein to ACE2 caused ACE2 down regulation, leading to an increase in angiotensin II and ultimately increased pulmonary vascular permeability, inducing pulmonary oedema and reduced lung function. Treatment with recombinant ACE237 and losartan38 mitigated the degree of lung injury [3].
Hypertension versus covid 19
The hypertension reduces the immunity of a patient significantly due to which virus enter your body and cause fatal damage. Spike protein of corona virus binds to the receptors in the body called ACE-2 receptors and brings down the level of ACE -2 receptors which are already down regulated in hypertensive patients. When the receptor level gets down regulated due to corona virus, lots of adverse effects happen in the body. The virus may cause inflammation of the heart muscle called myocarditis, which makes it harder for the heart to pump. Atherosclerosis patients are also at risk the virus may make those plaques more likely to break apart and cause a heart attack. Past studies have shown that people with heart disease who get a respiratory illness like the flu or earlier types of coronavirus are at higher risk for a heart attack [4].
DIABETES versus COVID-19
High plasma glucose levels and diabetes mellitus (DM) are known risk factors for pneumonia.
In general, people with diabetes are more likely to experience severe symptoms and complications when infected with a virus. People may experience complications such as diabetic kidney disease and ischaemic heart disease which further increases the severity of COVID-19 disease and the need for care such as acute dialysis. Some findings indicate that COVID-19 could cause acute cardiac injury Chinese study compared 39 SARS-CoV patients without previous diabetes, who did not receive steroid treatment, with 39 matched healthy siblings and showed that 20 of the 39 SARS-CoV patients developed diabetes during hospitalization. Some studies suggested that SARS-CoV might have damaged islets and caused acute insulin dependent diabetes mellitus Therefore, although further evidence is needed, pancreatic damage may also be present in COVID-19 patients, possibly contributing to worse outcomes in subjects with diabetes.
Lastly, late diabetic complications such as diabetic kidney disease and ischaemic heart disease may complicate the situation for people with diabetes, making them frailer and further increasing the severity of COVID-19 disease and the need for care such as acute dialysis. Some findings indicate that COVID-19 could cause acute cardiac injury with heart failure, leading to deterioration of circulation [5].
Obesity versus COVID-19
The team, from the University of North Carolina, looked at data from 75 studies from around the world for their research, including nearly 400,000 patients.
They found that people with obesity and Covid-19 were twice as likely to end up in hospital and 74% more likely to be admitted to intensive care. They were also more at risk of dying from the disease caused by coronavirus.
It can also lead to more inflammation in the body, reduce the body's ability to fight off infections and put more strain on other organs, as well as the breathing. Obesity has been shown to alter immune function and increase the susceptibility to infection from different pathogens. Elevated circulating pro-inflammatory cytokines, as well as reduced adiponectin levels, may impair the immunological response to infection [6] This entails disruption in the lymphoid tissue structure and shifts in leukocyte populations and inflammatory phenotypes. Also, B and T cell responses are impaired in Patient with obesity , and this causes an increased susceptibility and delay of resolution of viral infections.
Obesity is associated with decreased pulmonary function, including decreased expiratory reserve volume and respiratory system compliance, which may place patient with obesity at a higher risk of COVID-19 complications .
COPD versus COVID -19
COVID-19 affects the respiratory system. Existing lung disorders means it is more difficult for the lungs to fight against infection .If a person with COPD contracts the COVID-19 virusthey may be more likely to experience breathlessness and also require hospitalisation [7]. Virus also cause Acute respiratory distress syndrome [8] which fills your lungs with fluid so you can’t breath enough oxygen which some times leads to put on ventilation.
ASTHMA versus COVID-19
Asthmatic patients are more prone to develop viral infection due to their delayed innate immune response and impaired secretion of IFN-lambda. Asthma with other respiratory disease induce severe symptoms .people with different types of asthma are affected differently by COVID -19. Both allergic asthmatics and non -allergic asthmatics experience similar symptoms but both are separate risk factors, few studies suggest that Non-allergic asthma significantly heightened the likelihood of severe COVID -19 while allergic asthma did not [9]. According to the researchers the possible mechanism involved is. The ACE-2receptors are embedded in certain cells in lungs which acts as binding sites for SARS -CoV-2.SARS-CoV-2 after entering lungs causes damage to tissues essential for oxygen absorption. ACE-2expression is higher in case of Non-allergic asthmatics and lower in case of allergic asthmatics. Some studies also suggest that asthmatics who are using corticosteroids are safe because of corticosteroids capacity to suppress COVID -19 replication and cytokine production.
30%of the COVID-19 patients are died with CVD . The mechanism of these associations remain unclear. Potential include CVD more prevalent in patients with advance in age. A functionally impaired immune system, or elevated levels of ACE 2,a patients with CVD having a predisposition to COVID-19. Myocardial injury evidenced by elevated cardiac biomarkers, was recordered in several patients. According to a study of 138 hospitalised patients in china, cardiac injury was present in 7.2patients and 2.2% of the require they ICU care. National health care commission reported that 12% of the patients with out known CVD had elevated troponin levels are cardiac arrest during hospitalisation .In one study stated that a 4 days after symptom onset median hs-cTnl were 8.8pg/ml in non Survivors versus 2.5pg/ml survivors. Notably the median time to death from the onset of symptoms was 18.5 days the rise in hs-CTnl trades with other inflammatory biomarkers like D-dimer ,ferritin ,lnterleukin,lactate dehydrogenase may reflect cytokine storm or secondary hemophagyocytic lymphohistiocytosis more than isolated Myocardial injury in some other patients suggests a different pattern to injure some other patients experience coronary obstruction where as others do not . In another report from China, a 63year old man with no cardiac history presented with both severe respiratory manifestation and evidenced of fulminant myocarditis with an enlarged left ventricle and his ejection fraction is 32% the patient had an elevated troponin 1and NT-proDNP he was treated with intravenous immunoglobulin steroids anti viral therapy and was placed on extra corporeal membrane oxygenation. The exact mechanism of cardiac involvement in COVID- 19 remains investigation .one potential mechanism is direct myocardial involvement mediated by ACE-2. More over, an increased rate of inflammatory cytokines in covid -19 cases mediate atherosclerosis, procoagulant activation on, and hemodynamic instability leading to ischemia and thrombosis [3].
The SARS-CoV-2 S protein is expressed in tissues during the viral replication cycle and causes inflammation in most tissues, including the liver. This inflammatory response facilitates viral clearance from the tissues and promotes an adaptive immune response to viral infection. The liver is a highly intricate filtration machine that detoxifies portal blood of the xenobiotics that originate from the intestines. This liver function can be disrupted by extreme physiological stress. Cytokine storm is one of the most potent physiological stresses that result in a hyper-inflammatory condition and leads to organ damage. High levels of IL-2, IL-6, IL-7, IL-10, TNF-α, GM-CSF, IP-10, MCP-1, and MIP-1α were observed in patients with severe COVID-19. Reactive oxygen species, ischemia-reperfusion injury, sepsis-induced cholestasis, and drug toxicity injury are some of the mechanisms that could cause sepsis-induced liver injury. Furthermore, hypo-perfusion and a hyper-inflammatory state result in an unfavourable microenvironment that leads to liver injury The main COVID-19 liver damages are moderate micro vesicular steatosis and mild inflammation at the lobules and portal region, which reflects drug toxicity Although evidence is lacking, patients with chronic liver diseases may be more susceptible to SARS-CoV-2 infection. Biologic drugs used to treat COVID-19, such as tocilizumab and baricitinib, can result in the reactivation of diseases, such as HBV infections However, three other patients who did not have a history of liver disease exhibited signs of hepatic damage, such as nuclear glycogen deposition, micro vesicular steatosis, zone 3 sinusoidal dilatation, patchy hepatic necrosis, and minimal lymphocytic infiltration [1].
Patients suffering from any malignancy are at a higher risk of developing COVID-19 infection due to their weak immune response. In recent Chinese study suggest the people who had undergone radiation therapy, chemotherapy or undergone surgery are in the past one month are at higher risk (10).It has been found that 58.3% of the COVID-19 patients in a study had, Lung Carcinoma and 41.7% of them were taking Immunotherapy, chemotherapy, or Radiation therapy . A total of 2% fatality rate observed among the COVID-19 cases who already had malignancies. According to the recent study done in August 2020 by a team of researchers at the university of Birmingham, people suffering from Hematologic malignancies are at 57% higher risk of developing severe covid-19 infection [11]. The study was published in the lancet, stated that among those with blood or bone marrow cancers, Leukaemia patients were most likely to develop severe covid complications and were twice as more likely to die from covid than general population
HIV versus covid 19
People with HIV have a high risk of developing covid 19 due to immuno compromised immune system. HIV is also a vulnerable comorbidity .Mortality was increased in patients with HIV to with out HIV patients .In another study stated that patient with HIV and other covid 19 are at much higher risk than patients with only HIV infection [12]. The risk for HIv patient getting Very sick in covid is high in people with out effective HIV treatment and also people with less CD4 count (<50) are at higher risk. [13]. Some studies also concluded that anti retroviral therapy has potential effect of SARS-CoV-2 which could be a reason for having fewer cases of SARS Cov-2 in HIV patients
Beyond respiratory cells, other organs might be affected with SARS-CoV-2 various cells of kidney have higher ACE-2receptors. Thus cultured renal proximal Tubular epithelial cells glomerular mesangial cells and podocytes express ACE-2 on their surface which is a target for SARS-CoV-2. Studies suggest that Covid -19 can directly infect kidney tubular cells, inducing acute tubular damage. New onset of protesters and increased serum creatinine levels are observed in some patients. However, complement -mediated micro vascular injury, rhabdomylosis -associated kidney injury and collapsing glomerulopathy associated with apolipoprotein L1 risk variants have been observed. SARS-CoV-2 affects the kidneys by direct cellular injury or sepsis, leading to a Cytokine storm. There are chances of Mortalities in addition to the risk of AKI in Covid -19 [14].
A study by researchers at Princeton University’s Center for Disease Dynamics, Economics and Policy, the Johns Hopkins Bloomberg School of Public Health and other institutions — published in the journal Science — showed that in 18 per cent of cases in these two states, patients were diagnosed either less than 24 hours before death or posthumously. The study looked at cases recorded until 1 August.Reflecting India’s status as the diabetes capital of the world, the study found that diabetes was the most common comorbidity among patients who died of Covid-19 in Tamil Nadu and Andhra Pradesh. “Among decedents in the two Indian states, the most prevalent comorbid conditions were diabetes (45.0 per cent), sustained hypertension (36.2 per cent), coronary artery disease (12.3 per cent), and renal disease (8.2 per cent). “While prevalence of any comorbidity was highest among decedents at older ages, this pattern differed across conditions; diabetes was most prevalent among decedents ages 50-64 years, and liver disease and renal disease were most prevalent in fatal cases at ages 0-17 years and 18-29 years, respectively. At least one comorbid condition was noted among 62.5 per cent of fatalities, in comparison to 22 per cent of fatalities in the United States as of 30 May 2020, [26]. The first case of the COVID- 19 pandemic in the Indian state of Andhra Pradesh was reported in Nellore on 12 march 2020.A 24 year-old ,who was confirmed positive for covid19,was also it’s first victim .He had travel history to Italy. The Andhra Pradesh health department has confirmed a total of 687351cases, including 5780 deaths and 622136 recoveries ,as of 30 September the virus has spread in 13districts of the state, of which East Godavari has the highest number of cases [15].
SARS-CoV-2 affected globally a large population with pneumonia-like symptoms, and the patients with other comorbidities are utmost at the risk of infection. Critical situations develop in individuals with hypertension, diabetes, COPD, heart diseases, malignancies, and HIV COPD patients develop substantially severe symptoms and comparatively higher mortality rates. The comorbid individuals must undertake preventive measures to protect themselves during the pandemic. The SARS-CoV-2 infection becomes detrimental when it confronts a person with comorbidity, and the management of these patients with appropriate medical care is an imperative step towards their survival.
References