| Literature DB >> 35206976 |
Jose Roberto Gutierrez-Camacho1, Lorena Avila-Carrasco1, Alberto Murillo-Ruíz-Esparza2, Idalia Garza-Veloz1, Roxana Araujo-Espino3, Maria Calixta Martinez-Vazquez1, Perla M Trejo-Ortiz3, Iram Pablo Rodriguez-Sanchez4, Iván Delgado-Enciso5, Maria E Castañeda-López1, Araceli Gamón-Madrid1, Margarita L Martinez-Fierro1.
Abstract
Background: The pandemic of COVID-19 has represented a major threat to global public health in the last century and therefore to identify predictors of mortality among COVID-19 hospitalized patients is widely justified. The aim of this study was to evaluate the possible usefulness of Charlson Comorbidity Index (CCI) as mortality predictor in patients hospitalized because COVID-19.Entities:
Keywords: COVID-19; SARS-CoV-2; charlson index; comorbidity; obesity
Year: 2022 PMID: 35206976 PMCID: PMC8872141 DOI: 10.3390/healthcare10020362
Source DB: PubMed Journal: Healthcare (Basel) ISSN: 2227-9032
Comparison of findings between patients with COVID-19 with and without obesity (n = 377).
| Variable | Patients with | Patients with | Odds Ratio | |
|---|---|---|---|---|
| Risk factors | ||||
| Type 2 diabetes mellitus | 49 (31.2) | 49 (22.2) | 1.583 (0.996–2.517) |
|
| COPD | 10 (6.3) | 16 (10.1) | 0.867 (0.383–1.965) | 0.733 |
| Tobaccoism | 12 (7.6) | 28 (12.7) | 0.567 (0.279–1.154) | 0.114 |
| Chronic renal disease | 6 (3.8) | 3(1.3) | 2.874 (0.708–11.671) | 0.123 |
| Heart disease | 3 (1.9) | 10 (4.5) | 0.409 (0.111–1.511) | 0.167 |
| HIV/AIDS | 0 (0.0) | 1(0.4) | N.A. | - |
| Asthma | 4 (2.5) | 4 (1.8) | 1.412 (0.348–5.732) | 0.628 |
| Immunosuppression | 10 (6.3) | 12 (5.4) | 1.179 (0.496–2.802) | 0.709 |
| Hypertension | 72 (45.8) | 71 (32.2) | 1.778 (1.165–2.712) |
|
| Symptoms | ||||
| Anosmia | 62 (39.4) | 83 (37.7) | 1.077 (0.708–1.640) | 0.729 |
| Dysgeusia | 62 (39.4) | 72 (32.7) | 1.342 (0.876–2.055) | 0.176 |
| Cyanosis | 42 (26.7) | 50 (22.7) | 1.242 (0.773–1.994) | 0.370 |
| Conjunctivitis | 8 (5.0) | 17 (8.5) | 0.641 (0.270–1.525) | 0.311 |
| Abdominal pain | 39 (24.8) | 44 (20.0) | 1.322 (0.810–2.158) | 0.263 |
| Vomiting | 23 (14.6) | 25 (11.3) | 1.339 (0.729–2.458) | 0.345 |
| Polypnea | 101 (64.3) | 110 (50.0) | 1.804 (1.185–2.745) |
|
| Fever | 136 (86.6) | 179 (81.3) | 1.483 (0.838–2.626) | 0.174 |
| Myalgia | 113 (71.9) | 154 (70.0) | 1.101 (0.700–1.730) | 0.678 |
| Arthralgia | 102 (64.9) | 136 (61.8) | 1.145 (0.748–1.754) | 0.532 |
| Rhinorrhea | 37 (23.5) | 61 (27.7) | 0.804 (0.501–1.289) | 0.364 |
| Attack to the general state | 137 (87.2) | 176 (80.0) | 1.713 (0.965–3.040) | 0.064 |
| Headache | 126 (80.2) | 186 (84.5) | 0.743 (0.434–1.271) | 0.277 |
| Calophries | 83 (52.8) | 110 (50.0) | 1.122 (.744–1.690) | 0.583 |
| Diarrhea | 40 (25.4) | 53 (24.0) | 1.077 (0.671–1.730) | 0.758 |
| Thoracic pain | 103 (65.6) | 120 (54.4) | 1.590 (1.041–2.426) |
|
| Cough | 140 (89.1) | 189 (85.9) | 1.351 (0.719–2.538) | 0.349 |
| Odynophagia | 83 (52.8) | 115 (52.2) | 1.024 (.680–1.543) | 0.909 |
| Dyspnea | 132 (84.0) | 158 (71.8) | 2.072 (1.233–3.480) |
|
| Irritability | 11 (7.0) | 13 (5.9) | 1.200 (0.523–2.752) | 0.667 |
| Mechanical ventilation (Intubation) | 28 (17.8) | 17 (7.7) | 2.592 (1.364–4.924) |
|
Data are displayed as frequency and percentage. p-values < 0.05 are highlighted in bold. NA = Not applicable.
Figure 1Charlson comorbidity index analysis. (A) Comparison between Charlson comorbidity index values between patients who died because of COVID-19 complications and of those who survived. (B) Value of Charlson comorbidity index as predictor of mortality between patients hospitalized because COVID-19. CCI: Charlson comorbidity index. A: Area under ROC curve.
Comparison of the Charlson comorbidity index by age group in hospitalized patients who did and did not die because of COVID-19 complications.
| Age Group (Years) | Patients Who Died of COVID-19 ( | Charlson Comorbidity Index * | COVID-19 Survivors ( | Charlson Comorbidity Index * | |
|---|---|---|---|---|---|
| 18–30 | 4 | 2.9 ± 0.65 | 10 | 1.7 ± 0.86 |
|
| 31–40 | 4 | 3.3 ± 1.40 | 35 | 1.75 ± 0.37 |
|
| 41–50 | 21 | 7.1 ± 3.46 | 43 | 4.8 ± 0.73 |
|
| 51–60 | 34 | 30.02 ± 7.55 | 53 | 10.11 ± 1.4 |
|
| 61–70 | 30 | 42.12 ± 5.58 | 48 | 25.4 ± 4.15 |
|
| 71–80 | 22 | 63.5 ± 11.37 | 17 | 29.4 ± 11.03 |
|
| 81–90 | 15 | 61.5 ± 14.30 | 11 | 62.22 ± 11.33 | 0.661 |
| 91–100 | 2 | 88.19 ± 55.46 | 3 | 78.54 ± 10.30 |
|
* Charlson comorbidity index data are represented as mean of percentage by age group ± standard deviation. p-value was obtained from the comparison of the average of CCI score of the patients who died because COVID-19 complications and COVID-19 survivors using t-test. p-values < 0.05 are highlighted in bold.
Figure 2Pathophysiological mechanisms related with severe COVID-19 in patients with and without comorbidities. Following SARS-CoV-2 infection, the acquired and innate immune responses to that of people without comorbidities are effectively activated to eliminate the pathogen and infected cells with minimal inflammation and lung damage. The integrity of their vascular endothelial cells is well maintained, and the vessels possess normal functions of contraction and dilation, anti-inflammation, anticoagulation, and antioxidant capacity. However, patients with comorbidities such as hypertension, cardiovascular disease, obesity, and/or diabetes have an increased viral load when exposed to an amount of virus equivalent to those people without comorbidities. Impaired antiviral immunity, leaky SARS-CoV-2 infections, and excessive macrophage infiltration together contribute to uncontrolled cytokine storm, promoting the development of immunopathology such as pulmonary edema and hyaline membrane. The predisposition to a prothrombotic state in COVID-19 is associated with chronical conditions, driven largely by endothelial damage, platelet hyperactivation, hypercoagulability, hyperinflammation, and impaired fibrinolysis and poor outcomes [9,30,31,32,57]. CHO: cholesterol; G: glycosylated; SARS-CoV-2: severe acute respiratory syndrome coronavirus 2; COVID-19: coronavirus disease 2019.