Background: COVID-19, an infectious viral disease, has caused a global health crisis. Most cases remain asymptomatic. The majority of patients have mild symptoms while about 15% develop a severe form. The clinical spectrum of SARS-CoV-2 infection appears broad, encompassing asymptomatic infection, upper respiratory tract symptoms, and severe viral pneumonia with respiratory failure that can lead to death. Laboratory tests play an important role in the management of COVID-19 patients. In addition to being essential for the diagnosis, several biological analyses make it possible to identify the inflammatory processes and the potential complications of this disease. This study attempted to identify biochemical assays that could help in the prognosis of the disease to ensure early management. Methods: This was a descriptive study. It focused on patients hospitalized for COVID-19 from March 19, 2020, to January 26, 2021, at the Infectious Disease Management Centre in Lomé (Togo). Medians were compared using the (Mann-Whitney and Wilcoxon) test and frequencies were compared using the Chi-square test or Fisher’s exact test. Results: We included 782 patients. The median age was 41 years IQR from 32 to 55. We observed several biochemical abnormalities in varying proportions for all biochemical parameters studied. Compared to non-serious patients, critically ill patients at admission had more frequently elevated urea, creatinine, transaminases, TG, GGT, CRP and blood glucose. Also, they had more frequent decreases in total cholesterol, HDL-c, blood chloride, and blood calcium. As for patients who died during hospitalization, compared with healed patients, they had more frequent elevations of urea, creatinine, AST, ALT, GGT. CRP and blood glucose. They also had a more frequent decrease in total cholesterol, HDL-c, blood chloride, blood calcium, and blood glucose (p = 0.025). Conclusion: This study shows that COVID-19 is a multi-organ systemic inflammatory viral disease that should be systematically investigated once the diagnosis is confirmed.
Coronaviruses (CoV) are viruses known to cause generally mild respiratory infections in humans and animals. Some strains may be more virulent to humans, such as those of severe acute respiratory syndrome (SARS) and MERS (Middle East respiratory syndrome). SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) is the official name of the new coronavirus identified in the city of Wuhan, the capital of Hubei province in China. It is the etiological agent of the infectious lung disease epidemic that spread around the world in late December 2019. This disease has been named COVID-19 (Coronavirus Disease 2019) by the World Health Organization (WHO) on February 11, 2020. On January 30, 2020, WHO declared the situation a public health emergency of international concern. On March 11, it declared a global pandemic [
To date, to our knowledge, there is no data in Togo on the biochemical profile of patients hospitalized for COVID-19. However, since the creation of the Centre for the Management of Infectious Diseases, several patients have been admitted to this structure. Most of them have benefited from a biochemical assessment on admission, some as part of a systematic pre-therapeutic assessment, and others depending on the clinical picture. This study attempts to identify biochemical analyses whose measurement could help in the prognosis of the disease to ensure early management. The general objective is to describe the biochemical profile of the admission of adult patients hospitalized for COVID-19 at the Infectious Disease Management Centre in Lomé in 2020.
This was a descriptive study that focused on patients hospitalized from March 19, 2020, to January 26, 2021, at the Infectious Disease Management Centre in Lomé, Togo. In this facility, all symptomatic patients diagnosed as COVID-19 positive by RT-PCR on nasal or oropharyngeal swabs were admitted. On admission, most patients had routine blood sampling for blood glucose, renal, and liver function tests. Others, depending on the clinical picture, benefited from a lipid profile, an electrolyte panel, and a C-reactive protein (CRP) test.
We performed an exhaustive sampling of these patients with the inclusion criteria of being 18 years or older and having performed a biochemical test of interest.
The blood tests were performed at the biochemistry laboratory of the “Institut National d’Hygiène (INH)”. These results were obtained from fasting blood samples taken once on admission only.
The Roche-Hitachi Cobas C311 chemical analyzer was used to analyze the blood samples.
Uremia
Reagent: Urea/BUN.
Principle: a kinetic test using urease and glutamate dehydrogenase.
Reference values: 0.15 - 0.45 g/L.
Creatinine
Reagents: creatinine plus ver.2 (CREP2).
Principle: enzymatic method with creatininase, creatinase, and sarcosine oxidase.
Reference values: Female: 5.1 - 9.5 mg/L, Male: 6.7 - 11.7 mg/L.
Aspartate Aminotransferase/Alanine Aminotransferase (AST/ALT)
Reagent: ASTLP/ALTLP: Aspartate/Alanine aminotransferase according to International Federation of Clinical Chemistry (IFCC).
Principle: according to IFCC/standard method 94 with pyridoxal phosphate activation, measured at 37˚C [
Reference values: Female: 10 - 35 IU/L; Male: 10 - 50 IU/L.
Ƴ-Glutamyl Transferase (GGT)
Reagent: GGT-2: ƴ-Glutamyl transferase ver.2 standardization IFCC/Szasz.
Principle: enzymatic colorimetric test.
Reference value: Male: <60 IU/L; Female: <40 IU/L.
Alkaline Phosphatase (ALP)
Reagent: Alkaline Phosphatase acc. to IFCC Gen.2 (ALP2).
Principle: colorimetric test according to a standardized method (measurement at 37˚C).
Reference values: Male: 40 - 129 U/L, female: 35 - 104 U/L.
Total Cholesterol (TC)
Reagent: Cholesterol Gen.2 (CHOL2).
Principle: enzymatic colorimetric method.
Reference value: <0.2 g/L .
High-Density Lipoprotein (HDL-c)
Reagent: HDL-c-cholesterol Gen.4 (HDL-C4).
Principle: enzymatic colorimetric test in homogeneous phase.
Reference value: female: 0.45 - 0.65 g/L.
Low-Density Lipoprotein (LDL-c)
Reagent: LDL-c-Cholesterol Gen.3 (LDL C3).
Principle: enzymatic colorimetric test in homogeneous phase.
Reference value: <0.1 g/L.
Triglycerides (TG)
Reagent: triglycerides (TRIGL).
Principle: enzymatic colorimetric test.
Reference value: <1.5 g/L.
Natremia (Na+), Kalemia (K+) and Chloremia (Cl−)
Reagent: Indirect ion-selective electrode (ISE) Na-K-Cl for Gen.2.
Principle: Electromotive force (EMF) using an ISE.
Reference value: Na+ 136 - 145 mmol/L; K+ 3.5 - 5.1 mmol/L; Cl− 98 - 107 mmol/L.
Reagent: Calcium Gen.2.
Principle: Colorimetric test.
Reference value: 8.6 - 10.0 mg/dL.
Reagent: Magnesium Gen.2.
Principle: Colorimetric test, endpoint method.
Reference value: 1.6 - 2.6 mg/dL.
Reagent: Glucose HK (GLUC3).
Principle: Ultraviolet (UV) test, hexokinase enzymatic reference method.
Reference value: 0.7 - 1.09 g/L.
Reagent: C-reactive Protein Gen.3 (CRPL3).
Principle: Immunoturbidimetric test on latex particles.
Reference value: <5 mg/L.
Hyperuremia of urea was considered when urea value > 0.45 g/L, a high level of creatinine was considered when creatinine level > 12 mg/L in women and >14 mg/L in men.
Elevated transaminases were considered when AST values >1.5 N (>57 IU/L) in men (46.5 IU/L) in women, and ALT >1.5 N (60 IU/L) in men and 48 IU/L in women.
Alkaline phosphatase (ALP) was considered elevated when the level was >1.5 N (418.5 IU/L).
Gamma-glutamyl transferase (GGT) were considered elevated when > 1.5 N (78 IU/L).
Kalemia (K+): Hypo- and hyperkalemia were considered when kalemia levels were, respectively, < 3.3 mmol/L and > 5.1 mmol/L.
Natremia (Na+): Hypo and hypernatremia were considered for natremia < 135 mmol/L and > 145 mmol/L, respectively.
Hypo and hypercalcemia were defined for blood calcium < 90 mg/L and >110 mg/L respectively.
Hypo and hypermagnesemia were considered for magnesemia < 16 mg/L and >27 mg/L respectively.
Total cholesterol (TC): Hypo and hypercholesterolemia were defined for cholesterol levels < 1.4 g/L and >2.2 g/L respectively.
HDL-c was considered decreased if <0.4 g/L in men and <0.35 g/L in women; increased if >0.60 g/L in men and >0.65 g/L in women.
LDL-c was considered increased if it was greater than 1.5 g/L.
Triglycerides (TG): Hypo and hypertriglyceridemia were defined for triglyceride levels < 0.60 g/L and >1.65 g/L respectively.
Hypo and hyperglycemia were defined for blood glucose levels < 0.5 g/L and >1.10 g/L respectively.
CRP was considered increased if >6 mg/L.
D-dimer was considered increased if >500 µg/L.
HbA1c was considered increased if >6.5%.
Patient data were entered into an electronic xlsform deployed through the KoboToolbox platform. Variables of interest were secondarily extracted and analyzed.
We collected:
Socio-demographic characteristics data: Age, gender.
Anamnestic data: Patient medical history or co-morbidities such as hypertension, diabetes, heart diseases, asthma, lung disease, allergies...
Clinical data: Symptoms on admission such as cough, fever, dyspnea, myalgia, anosmia, ageusia...
We used WHO clinical classification of COVID-19.
Biochemical data:
Renal function tests: urea (g/L), creatinine (mg/L).
Liver function tests: transaminases (IU/L), ALP (IU/L), GGT (IU/L).
Electrolyte panel (Na+, Cl−, K+, Ca2+, Mg2+).
Lipid profile (TC, LDL-c, HDL-c, TG) in g/L.
Other biological parameters: CRP (mg/L), blood glucose (g/L), D-dimer, glycated hemoglobin (HbA1c).
WHO Clinical Classification
There are five stages:
Asymptomatic stage: No clinical signs with a positive SARS-CoV-2 PCR test.
Mild stage: Symptoms of acute upper respiratory infection, including fever, fatigue, myalgia, cough, sore throat, runny nose, and sneezing without pneumonia.
Moderate stage: With pneumonia, fever, and frequent coughing some may have wheezing, but no obvious hypoxemia such as shortness of breath.
Severe stage: Rapid progression within 1 week, dyspnea, with central cyanosis, oxygen saturation below 92% on room air, with other manifestations of hypoxemia.
Critical stage: Patients with acute respiratory distress syndrome (ARDS) or respiratory failure, shock, multi-organ dysfunction referral [
For this study we considered patients classified as severe and critical to be serious and asymptomatic, mild and moderate patients to be non-serious.
The data of interest were extracted from the electronic xlsform deployed through the KoboToolbox platform. The data were then cleaned by removing duplicates and correcting outliers. The database was then analyzed using R 4.0.4 software (R Core Team, Vienna) in the RStudio1.4 environment.
The qualitative variables were presented according to their respective numbers and percentages, the quantitative variables according to their medians and interquartile ranges. Medians were compared using non-parametric tests (Mann-Whitney, Wilcoxon) and frequencies using the Chi-square test or Fisher’s Exact test when indicated. The threshold of significance was p < 0.05. Missing data were not included in the analysis.
A password-protected computer was used for data entry and analysis. The data were processed anonymously. We also got an authorization of the centre to collect these data.
The median age was 41 years with an IQR [32 - 55]. The elderly (≥60 years) accounted for 17.6% (n = 138). More than half, 63.6% (n = 497) were male, with a sex ratio of 1.7. Comorbidities were observed in 49.00% (n = 383). The main comorbidities were hypertension (HTN) and diabetes in 45.9% (n = 176), and 31.0% (n = 119) respectively. On admission, 64.8% (n = 502) had at least one symptom. Cough and fever accounted for 31.1% (n = 244) and 26.6% (n = 209) respectively. On admission, serious forms accounted for 14.2% (n = 111). We recorded 10.2% (n = 80) deaths during hospitalization, while the majority, 89.8% (n = 702) were cured. Demographic and clinical characteristics are summarized in
| Characteristic | Size (N = 782) | Proportion (%) |
|---|---|---|
| Age | ||
| <60 | 138 | 17.6 |
| ≥60 | 644 | 82.4 |
| Sex | ||
| Men | 497 | 63.6 |
| Women | 285 | 36.4 |
| Comorbidities | 383 | 49.0 |
| HTN | 176 | 45.9 |
| Diabetes | 119 | 31.0 |
| HTN and Diabetes | 72 | 18.7 |
| Obesity | 40 | 5.1 |
| Asthma | 25 | 3.2 |
| Peptic ulcer | 25 | 3.2 |
| HIV | 21 | 2.7 |
| Atopic terrain | 21 | 2.7 |
| Heart disease | 6 | 0.7 |
| Tuberculosis | 6 | 0.7 |
| Veinous thromboembolic disease | 5 | 0.6 |
| Cancer | 5 | 0.6 |
| Chronic renal failure | 3 | 0.3 |
| Symptoms | 502 | 64.8 |
| Cough | 244 | 31.1 |
| Fever | 209 | 26.6 |
| Dyspnea | 179 | 22.8 |
| Headache | 156 | 19.9 |
| Asthenia | 105 | 13.4 |
| Myalgia | 70 | 8.9 |
| Rhinitis | 62 | 7.9 |
| Anosmia | 52 | 6.6 |
| Chest pain | 48 | 6.1 |
| Arthralgia | 42 | 5.3 |
| Aguesia | 36 | 4.6 |
| Diarrhoea | 20 | 2.5 |
| Abdominal pain | 20 | 2.5 |
| Vomiting | 20 | 2.5 |
| Sore throat | 15 | 1.9 |
| Severity stage | ||
| Not serious | 671 | 85.8 |
| Asymptomatic | 274 | 35.0 |
| Slight | 296 | 37.9 |
| Moderate | 101 | 12.9 |
| Serious | 111 | 14.2 |
| Severe | 84 | 10.7 |
| Critical | 27 | 3.5 |
| Outcome of the disease | ||
| Healed | 702 | 89.8 |
| Deceased | 80 | 10.2 |
| Characteristic | Size n (%) | Reference value | Median [IQR] | Low n (%) | Normal n (%) | High n (%) |
|---|---|---|---|---|---|---|
| Renal function tests | ||||||
| Uremia (g/L) | 561 (71.6) | <0.45 | 0.2 [0.2 - 0.3] | NA | 484 (86.3) | 77 (13.7) |
| Serum creatinine (mg/L) | 506 (64.8) | <14 | 10.0 [9.0 - 12.0] | NA | 449 (88.7) | 57 (11.3) |
| Hepatic function panel | ||||||
| AST (IU/L) | 565 (72.1) | <57 | 38.0 [28.0 - 56.7] | NA | 423 (74.9) | 142 (25.1) |
| ALT (IU/L) | 565 (72.1) | <60 | 30.0 [20.2 - 45.0] | NA | 474 (83.9) | 91 (16.1) |
| GGT (IU/L) | 391 (49.9) | <78 | 39.0 [24.0 - 76.0] | NA | 296 (75.7) | 95 (24.3) |
| ALP (IU/L) | 74 (9.5) | <418.5 | 91.0 [69.0 - 163.0] | NA | 71 (95.9) | 03 (4.1) |
| Lipid profile | ||||||
| Total Cholesterol (g/L) | 374 (47.8) | 1.4 - 2.2 | 1.7 [1.4 - 2.0] | 79 (21.1) | 243 (65) | 52 (13.9) |
| HDL-cholesterol (g/L) | 205 (26.2) | 0.40 - 0.65 | 0.5 [0.4 - 0.6] | 42 (20.5) | 163 (79.5) | 12 (5.9) |
| LDL-cholesterol (g/L) | 208 (26.6) | ≤1.5 | 1.1 [0.7 - 1.3] | NA | 181 (87) | 27 (13.0) |
| Triglycerides (g/L) | 352 (44.9) | 0.6 - 1.65 | 0.9 [0.7 - 1.4] | 29 (8.2) | 265 (75.3) | 58 (16.5) |
| Electrolyte panel | ||||||
| Natremia (mmol/L) | 180 (23.1) | 135 - 155 | 140.0 [136.2 - 143.6] | 22 (12.2) | 158 (87.8) | 0 |
| Chloremia (mmol/L) | 192 (24.7) | 98 - 107 | 102.0 [98.0 - 105.0] | 46 (24.0) | 111 (57.8) | 35 (18.2) |
| Kalemia (mmol/L) | 192 (24.7) | 3.3 - 5.3 | 4.4 [4.0 - 4.8] | 10 (5.2) | 164 (85.4) | 18 (9.4) |
| Calcemia (mg/L) | 114 (14.6) | 90 - 110 | 91.0 [86.0 - 98.5] | 47 (41.2) | 63 (55.3) | 04 (3.5) |
| Magnesemia (mg/L) | 98 (12.6) | 16 - 27 | 20.0 [18.0 - 22.0] | 15 (15.3) | 77 (78.6) | 01 (01.1) |
| Other | ||||||
| CRP (mg/L) | 134 (17.3) | <6 | 12.0 [6.0 - 48.0] | NA | 54 (40.3) | 80 (59.7) |
| Blood glucose (g/L) | 548 (70.3) | 0.5 - 1.1 | 0.9 [0.8 - 1.2] | 05 (0.9) | 360 (65.7) | 183 (33.4) |
| HbA1c (%) | 71 (9.0) | <6.5 | 7.3 [5.8 - 9.4] | NA | 30 (42.3) | 41 (57.7) |
| D-dimer (µg/L) | 7 (0.9) | <500 | 1700.0 [1330.9 - 3246.1] | NA | 00 | 07 (100) |
IQR= interquartile range; g = gram; mg = milligram; µg = microgram; L = litre; IU = international unit; mmol = millimole; n= size; (%) proportion estimated as a percentage; The percentages reported are percentages in rows; NA = not applicable. AST = aspartate aminotransferase; ALT = alanine aminotransferase; GGT = gamma-glutamyl transferase; ALP = alkaline phosphatase.
The Biochemical characteristics according to the stage of severity are summarized in
| Characteristic | Total | Severity stage | p | Outcome of the disease | p | ||
|---|---|---|---|---|---|---|---|
| Not serious | Serious | Healed | Deceased | ||||
| Uremia (n) | 561 | 465 | 96 | 499 | 62 | ||
| Median (g/L) [IQR] | 0.2 [0.2 - 0.3] | 0.2 [0.2 - 0.3] | 0.4 [0.3 - 0.9] | <0.001 | 0.2 [0.2 - 0.3] | 0.6 [0.3 - 1.5] | <0.001 |
| High n (%) | 77 (13.7) | 35 (7.5) | 42 (43.8) | <0.001 | 42 (8.4) | 35 (56.5) | <0.001 |
| Serum creatinine (n) | 506 | 413 | 93 | 447 | 59 | ||
| Median (mg/L) [IQR] | 10 [9 - 12] | 10 [8 - 12] | 12.2 [9 - 22] | <0.001 | 10 [8 - 12] | 14 [9 - 48] | <0.001 |
| High n (%) | 57 (11.3) | 23 (5.6) | 34 (36.6) | <0.001 | 28 (6.3) | 29 (49.2) | <0.001 |
| AST | 565 | 482 | 83 | 514 | 51 | ||
| Median (IU/L) [IQR] | 38 [28.0 - 56.7] | 36 [27 - 50] | 62 [44 - 108] | <0.001 | 36 [28 - 52] | 65 [43 - 173] | <0.001 |
| High n (%) | 142 (25.1) | 96 (19.9) | 46 (55.4) | <0.001 | 112 (21.8) | 30 (58.8) | <0.001 |
| ALT (n) | 565 | 482 | 83 | 514 | 51 | ||
| Median (IU/L) [IQR] | 30 [20.2 - 45.0] | 28.5 [20 - 44] | 41 [26 - 74] | <0.001 | 29 [20 - 45] | 41 [24 - 71] | <0.001 |
| High n (%) | 91 (16.1) | 62 (12.9) | 29 (34.9) | <0.001 | 74 (14.4) | 17 (33.3) | 0.040 |
| GGT (n) | 391 | 340 | 51 | 359 | 32 | ||
| Median (IU/L) [IQR] | 39 [24 - 76] | 35 [23 - 62.5] | 79 [49 - 177] | <0.001 | 36 [23 - 66] | 80.5 [58.5 - 195] | <0.001 |
| High n (%) | 95 (24.3) | 69 (20.3) | 26 (51.0) | <0.001 | 77 (21.4) | 18 (56.3) | <0.001 |
| ALP (n) | 74 | 48 | 26 | 61 | 13 | ||
| Median (IU/L) [IQR] | 91 [69 - 163] | 91 [67.5 - 159.5] | 95.5 [75 - 164] | 0.575 | 91 [73 - 163] | 100 [65 - 163] | 0.847 |
| High n (%) | 3 (4.1) | 2 (4.2) | 1 (3.8) | 0.946 | 1 (1.6) | 2 (15.4) | 0.052 |
| TC (n) | 374 | 317 | 57 | 342 | 32 | ||
| Median (g/L) [IQR] | 1.7 [1.4 - 2.0] | 1.8 [1.5 - 2.1] | 1.7 [1.3 - 2.0] | 0.065 | 1.8 [1.5 - 2.1] | 1.5 [1.2 - 2.0] | 0.016 |
| Hypo-TC n (%) | 79 (21.1) | 61 (19.2) | 18 (31.6) | 0.035 | 64 (18.7) | 15 (46.9) | 0.020 |
| Hyper-TC n (%) | 52 (13.9) | 47 (14.8) | 5 (8.8) | 0.224 | 48 (14) | 4 (12.5) | 0.810 |
| HDL-c (n) | 205 | 174 | 31 | 190 | 18 | ||
| Median (g/L) [IQR] | 0.5 [0.4 - 0.6] | 0.5 [0.4 - 0.6] | 0.4 [0.2 - 0.6] | 0.006 | 0.5 [0.4 - 0.6] | 0.3 [0.2 - 0.4] | <0.001 |
| Hypo-HDL-c n (%) | 42 (20.5) | 26 (14.9) | 16 (51.6) | <0.001 | 1.1 [0.8 - 1.4] | 0.7 [0.4 - 1.0] | <0.001 |
| LDL-c (n) | 208 | 177 | 31 | 190 | 18 | ||
| Median (g/L) [IQR] | 1.07 [0.7 - 1.3] | 1.1 [0.7 - 1.3] | 0.8 [0.4 - 1.2] | 0.001 | 1.1 [0.8 - 1.4] | 0.7 [0.4 - 1.0] | <0.001 |
| Hyper-LDL-c n (%) | 27 (13) | 25 (14.1) | 2 (6.5) | 0.241 | 25 (14.1) | 2 (6.5) | 0.241 |
| TG (n) | 352 | 297 | 55 | 320 | 32 | ||
| Median (g/L) [IQR] | 0.9 [0.7 - 1.4] | 0.9 [0.7 - 1.3] | 1.4 [0.9 - 2] | <0.001 | 1 [0.7 - 1.4] | 1.3 [0.9 - 2.3] | <0.001 |
| Hypo-TG n (%) | 29 (8.2) | 25 (8.4) | 4 (7.3) | 0.776 | 27 (8.4) | 2 (6.3) | 0.667 |
| High n (%) | 58 (16.5) | 37 (12.5) | 21 (38.2) | <0.001 | 43 (13.4) | 15 (46.9) | <0.001 |
| Natremia (n) | 180 | 115 | 65 | 140 | 40 | ||
| Median (mmol/L) [IQR] | 140 [136.2 - 143.6] | 141 [137 - 144] | 139 [136 - 142.4] | 0.268 | 140 [137 - 143] | 140 [135 - 146] | 0.558 |
| Hyponatremia n (%) | 22 (12.2) | 13 (11.3) | 9 (13.8) | 0.617 | 13 (9.3) | 9 (22.5) | 0.024 |
| Chloremia (n) | 192 | 123 | 69 | 151 | 41 | ||
| Median (mmol/L) [IQR] | 102 [98 - 105] | 102 [99 - 105] | 100 [94 - 105] | 0.022 | 102 [98 - 105] | 101.5 [95 - 106] | 0.773 |
| Hypochloremia n (%) | 46 (24%) | 22 (17.9) | 24 (34.8) | 0.008 | 33 (21.9) | 13 (31.7) | 0.189 |
| Hyperchloremia n (%) | 35 (18.2) | 23 (18.7) | 12 (17.4) | 0.821 | 25 (16.6) | 10 (24.4) | 0.249 |
| Kalemia (n) | 192 | 123 | 69 | 151 | 41 | ||
| Median (mmol/L) [IQR] | 4.4 [3.99 - 4.8] | 4.4 [4 - 4.8] | 4.3 [3.9 - 4.8] | 0.450 | 4.4 [3.9 - 4.7] | 4.6 [4 - 5.1] | 0.094 |
| Hypokalemia n (%) | 10 (5.2) | 4 (3.3) | 6 (8.7) | 0.103 | 8 (5.3) | 2 (4.9) | 0.914 |
| Hyperkalemia n (%) | 18 (9.4) | 12 (9.8) | 6 (8.7) | 0.808 | 11 (7.3) | 7 (17.1) | 0.056 |
| Calcemia (n) | 114 | 97 | 17 | 104 | 10 | ||
| Median (mg/L) [IQR] | 91 [86 - 98.5] | 93 [88 - 99] | 85 [83 - 90] | 0.001 | 92 [87 - 99] | 82.5 [81 - 89] | <0.001 |
| Hypocalcemia n (%) | 47 (41.2) | 35 (36.1) | 12 (70.6) | 0.007 | 39 (37.5) | 8 (80) | 0.009 |
| Hypercalcemia n (%) | 4 (3.5) | 4 (4.1) | 0 (0) | 0.394 | 4 (3.8) | 0 (0) | 0.527 |
| Magnesemia (n) | 98 | 88 | 10 | 96 | 02 | ||
| Median (mg/L) [IQR] | 20 [18 - 22] | 19.5 [17 - 22] | 19.5 [18 - 22] | 0.953 | 19 [17 - 22] | 20.5 [20 - 21] | 0.659 |
| Hypomagnesemia n (%) | 15 (15.3) | 13 (14.8) | 8 (80) | 0.663 | 15 (15.6) | 0 (0) | 0.543 |
| Hypermagnesemia n (%) | 1 (1) | 1 (1.1) | 0 (0) | 0.734 | 1(1) | 0 (0) | 0.884 |
| CRP (n) | 134 | 92 | 42 | 113 | 21 | ||
| Median (mg/L) [IQR] | 12 [6 - 48] | 6 [6 - 25.5] | 36 [12 - 96] | <0.001 | |||
| High n (%) | 80 (59.7) | 44 (47.8) | 36 (85.7) | <0.001 | 63 (55.8) | 17 (81.0) | 0.036 |
| Blood glucose (n) | 548 | 464 | 84 | 493 | 55 | ||
| Median (g/L) [IQR] | 0.9 [0.8 - 1.2] | 0.9 [0.8 - 1.2] | 1.2 [0.9 - 1.9] | <0.001 | |||
| Hypoglycemia n (%) | 5 (0.9) | 3 (0.3) | 2 (2.4) | 0.124 | 3 (0.6) | 2 (3.6) | 0.025 |
| Hyperglycemia n (%) | 183 (33.4) | 133 (28.7) | 50 (59.7) | <0.001 | 149 (30.2) | 34 (61.8) | <0.001 |
| HbA1c (n) | 71 | 52 | 19 | 59 | 12 | ||
| Median (mg/L) [IQR] | 7.3 [5.8 - 9.4] | 7.4 [5.8 - 9.6] | 6.4 [5.9 - 9.1] | 0.550 | 7.4 [6 - 9.6] | 6.3 [5.2 - 9.2] | 0.211 |
| High n (%) | 41 (57.7) | 32 (61.5) | 9 (47.4) | 0.284 | 36 (61.0) | 5 (41.7) | 0.216 |
n = size; (%) proportion estimated as a percentage. The percentages reported are percentages in columns; IQR = interquartile range; AST = aspartate aminotransferase; ALT = alanine aminotransferase; GGT = gamma-glutamyl transferase; ALP = alkaline phosphatase. TC = total cholesterol; HDL-c = high density lipoprotein cholesterol; LDL-c = low density lipoprotein cholesterol; TG = triglycerides; CRP = C-reactive protein; HbA1c = glycated hemoglobin.
serious forms with (p < 0.001). A significant increase in transaminases (ASAT, ALAT) and GGT was observed in patients with serious forms compared with non-serious forms, in the respective proportions of (55.4% vs. 19.9%: p < 0.001) (34.9% vs. 12.9%: p < 0.001) and (51% vs. 20.3%: p < 0.001). As for the lipid profile, a decrease in median HDL-c and LDL-c was observed in patients with serious forms with (p = 0.006) and (p = 0.001) respectively, while median triglycerides were elevated (p < 0.001). Compared to non-serious cases, the seriously ill had hypocholesterolemia (31.6% vs. 19.2%: p = 0.035), hypo-HDL-c (51.6% vs. 14.9%: p < 0.001), and hypertriglyceridemia (38.2% vs. 12.5%: p < 0.001). For the electrolyte panel, the medians for chloremia and calcemia were lower in patients with serious forms, with (p = 0.022) and (p = 0.001) respectively. Hypochloremia and hypocalcemia predominated in the serious forms, with (34.8% vs. 17.9%: p = 0.008) and (70.6% vs. 36.1%: p = 0.007) respectively. CRP and blood glucose levels were also elevated in the serious form, with (85.7% vs. 47.8%: p < 0.001) and (59.7% vs. 28.7%: p < 0.001) respectively.
We included 782 patients, hospitalized at the Infectious Disease Management Centre in Lomé between March 19, 2020, and January 26, 2021. The median age was 41 years IQR [32 - 55]. More than half (63.5%) were male. Nearly half (48.5%) had comorbidities. More than half (64.8 %) had at least one symptom. One hundred and eleven patients (14.2%) had a serious form on admission. Eighty patients (10.2%) died during hospitalization.
We observed biochemical abnormalities in varying proportions. These abnormalities concerned all the biochemical parameters studied. Compared to non-serious patients, seriously affected patients on admission had more frequently elevated urea, creatinine, transaminases, TG, GGT, CRP and blood glucose. There was also a decrease in TC, HDL-c, blood chloride, blood calcium. As for patients
who died during hospitalization, compared with cured patients, they showed an increase in urea, creatinine, ASAT, GGT, ALAT, CRP and blood glucose. They also had a decrease in TC, HDL-c, blood chloride, blood calcium and blood glucose.
The various biochemical abnormalities observed allowed us to identify potential organ damage such as impaired renal and hepatic function in patients infected with SARS-CoV-2. The increase in serum urea and creatinine, relatively frequent in this study, could suggest disturbances of renal function in these patients. Indeed, the kidney expresses 100 times more ACE2 than the lungs. Therefore, it could be an ideal target for viral replication during infection. However, the cytokine storm would be more responsible for these lesions than the cytopathic effects of the virus [
The elevation of liver enzymes (transaminases and GGT) as well as a decrease in certain substances synthesized by the liver, notably lipoproteins (HDL-c and LDL-c), suggest an impairment of liver function, which is all the more marked in the serious forms of the disease. In contrast to the kidney, ACE2 is weakly expressed in hepatocytes, except in the bile ducts. Thus, liver damage, especially in serious forms, seems to be related less to viral cytotoxicity than to sepsis. It has been reported that pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β modulate lipid metabolism by modifying liver function and decreasing cholesterol efflux and transport as observed in some human immunodeficiency virus (HIV) infected patients [
Hypocalcemia, hyponatremia, and hypochloremia are the electrolyte panel abnormalities frequently observed in this study with a predominance in serious forms and deceased patients. Hypocalcemia could be related to hypoalbuminemia which has been frequently reported in COVID-19 [
CRP was elevated in more than half of patients in whom it was performed and was even more marked in the serious forms. This indicates the inflammatory nature of the disease. This inflammation would be responsible for the multisystemic lesions observed in several studies such as this one [
Hyperglycemia was common in serious forms of the disease. This suggests disturbances in glycemic regulation that are more marked in serious forms. However, it would have seemed useful to correlate the patients with hyperglycemia with the existence or not of diabetes mellitus.
Some of the results deserve attention, however. Indeed, renal, liver functions, and blood sugar tests were performed by about seven out of ten patients. This could be explained by the fact that these tests are part of the systematic pre-therapeutic check-up performed on all hospitalized patients. However, in about 20% of patients, at least one of these tests was missing. Some patients transferred from other health facilities had in their possession the results of paraclinical examinations including the biochemical tests of interest. In addition, the more expensive lipid profile and serum electrolyte tests were particularly prescribed for patients with serious forms of the disease. Only 17.3% (n = 134) had a CRP test, of which 37.8% (n = 42) had a serious form. Also, the deceased patients who had a CRP test on admission represented only 26.2% (n = 21). These low proportions of CRP testing could be explained by the fact that patients routinely have a blood count and sedimentation rate (ESR) on admission, the results of which are readily available compared to CRP. However, the CRP remains more sensitive and more specific in assessing inflammatory phenomena than the ESR [
It should be noted that in the absence of pre-disease findings and post-cure monitoring it would be presumptuous to associate these abnormalities exclusively with COVID-19. Also, a significant proportion of patients were being treated for comorbidities such as diabetes and hypertension. Self-medication, a common practice in Togo [
The first limitation of this study is that several patients admitted to the centre were transferred from hospital facilities. Some had benefited from therapeutic protocols including rehydration, use of potentially hepatotoxic and nephrotoxic drugs. This may have altered some biochemical parameters before admission. Also, some patients were admitted with pre-admission tests, therefore they did not benefit from certain tests as the focus was on checking these results a few days after admission.
Another limitation concerns missing data, affecting the completeness of the data collection. Indeed, the biochemical results of some patients were not found.
The third limitation concerns the application of different thresholds for classifying certain biological parameters as abnormal. Several factors, including the different assay techniques used, could explain this.
In the literature, there is the heterogeneity of data regarding biochemical abnormalities in COVID-19 positive patients.
The frequencies of hyperuremia (13.7%) and high levels of serum creatinine (11.3%) are similar to those of Kefti et al. [
The frequency of liver function abnormalities, particularly elevated transaminases (AST: 25.1%) (ALT: 16.1%), was similar to those of Guan et al. [
Our results were similar to those of Wei et al. [
The electrolyte panel abnormalities observed in this study were similar to those of Teczan et al. in [
CRP
The frequency of CRP elevation (59.7%) in this study was similar to those of Kefti et al. [
Blood Glucose
Very few data have been reported on the admission blood glucose profile of COVID-19 patients. The frequency of hyperglycemia in the serious forms and among the deceased patients is similar to the study by Wu et al. who reported that patients with hyperglycemia on admission had a higher risk of developing the serious forms of the disease and even of having an unfavorable outcome [
This study aimed to identify biochemical assays which could help to predict the prognosis of the disease, to ensure early and appropriate management and to promote optimal resource allocation in developing countries.
Several abnormalities were observed in varying proportions in all the biochemical parameters studied. These abnormalities were the most predominant in patients who presented serious forms of COVID-19 and those who died. However, a non-negligible proportion of patients admitted a priori with no clinical signs of severity had biochemical abnormalities, notably elevated CRP. This suggests that, like the renal and liver function tests, CRP should be systematically monitored on admission, to optimize management. Biochemical tests thus play an important role in the management of SARS-COV-2 infection, through early identification and monitoring of disease complications.
In addition, a prospective study over the entire hospitalization period would enable changes in biochemical parameters to be monitored and would help to better identify biochemical abnormalities predictive of severity or death.
The staff of Biochemistry Laboratory at Institut National d’Hygiène.
The staff of Infectious Diseases Management Centre in Lomé.
The authors declare that they have no competing interests.
Feteke, L., Halatoko, W.A., Prateaux, M.A., Kotosso, A., Bara, F.D., Adjoh, K.S., Salou, M., Ekouevi, K.D. and Djibril, M. (2023) Biochemical Profile of Patients Hospitalized for COVID-19 at the Infectious Disease Management Centre in Lomé in 2020. Open Journal of Internal Medicine, 13, 271-294. https://doi.org/10.4236/ojim.2023.134026