RESUMO
PURPOSE: Diabetes mellitus (DM) has been reported to be associated with a worse outcome of COVID-19 infection. The evidence is scarce in the Middle East and Saudi Arabia. We aimed to evaluate the impact of diabetes mellitus and hyperglycemia in non-diabetic individuals on the severity and outcome of COVID-19 infection. METHODS: This is a retrospective observational study, which included patients with confirmed COVID-19 infection [RT-PCR positive for SARS-CoV2] who were admitted to King Fahd Hospital of the University-Khobar-Eastern Province-Saudi Arabia from March to September 2020. Baseline demographic data, laboratory investigations, and markers of the severity of COVID-19 were analyzed. The collected data were categorized according to the Saudi Arabian Ministry of Health COVID-19 infection severity criteria. Patients were divided into three groups as follows: patients in Group 1 had pre-existing DM, patients in Group 2 did not have DM but were documented to have hyperglycemia at presentation, and patients in Group 3 were neither diabetics nor hyperglycemics at presentation and served as the control group. The severity and outcome of the control group were compared with the other two groups. The effect of risk factors on the severity and outcome of COVID-19 infection was studied in the DM group. RESULTS: A total of 414 patients were included (70.5% males and 29.5% females). The mean age (SD) of patients was 52.3 (±15.5) years. Compared to the control group, pre-existing DM was found to be significantly associated with severe (OR 3.61), critical disease (OR 4.32), intensive care unit (ICU) admission (OR 2.0), and death (OR 2.0) from COVID-19 infection. Hyperglycemia without known DM was also found to be associated with critical COVID-19 pneumonia (P 0.001), and had longer duration of hospitalization (P 0.014), higher ICU admission, mechanical ventilation, and death from COVID-19 infection (P < 0.0001). CONCLUSION: Diabetes mellitus and hyperglycemia at presentation, even in the absence of pre-existing DM, are independent risk factors for disease severity and worse outcome of COVID-19 infection. These patients should be identified and managed accordingly. The COVID-19 vaccination program should also target those populations to improve their outcomes.
RESUMO
The regions of AlQatif and AlAhssa in the Eastern Province of Saudi Arabia are known for their high prevalence of hemoglobinopathies, including ßthalassemia and sickle cell anemia. Previously, the αgene deletion has been demonstrated as highly prevalent among populations residing in these two regions. The present study was conducted in order to investigate the implications of the αglobin gene deletion on fetal hemoglobin (HbF) and hemoglobin α2 (HbA2) concentrations in patients with transfusiondependent ßthalassemia. A total of 166 Saudi patients with transfusiondependent ßthalassemia and 337 healthy Saudi patients were included in the study. The α3.7, α4.2, -FIL, -SEA, -MED and -(20.5) gene deletions were identified using multiplex αglobin deletion polymerase chain reaction. The present study revealed that the α3.7 gene deletion is the most prevalent (43.5%) in the Saudi populations that were analyzed and is characterized by the deletion of 3,804 base pairs. Numerous genotypes, namely 3.7α2/α1α2, 3.7α2/α1α12, 3.7α2/3.7α2, 3.7α2HphI/α1α2HphI, 3.7α2/α14.2, 3.7α2/α1polyA1α2, 3.7α12/α1α12, FIL/3.7α2 and 3.7α2/3.7α2Hb Villiers le Bel were also identified in the investigated population. Furthermore, a gradual increase in the concentration of HbF and HbA2 in patients with ßthalassemia and the number of αgene deletions was demonstrated; whereas in healthy patients the level of HbA2 was demonstrated to decrease as the number of αgene deletions increased. Therefore, it can be concluded that the high HbF concentration in the present study is predominantly associated with other mutations associated with ßthalassemia rather than αglobin deletions. Furthermore, the results of the present study also revealed novel αgene deletion genotypes prevalent in the population studied, namely α1α2/α1α2HphI, α1α2HphI/α1α2HphI, α1α2/α1α2Hb Handsworth, 3.7α2HphI/α1α2HphI, 3.7α2/3.7α2Hb Villiers le Bel and -MED/α1α2HphI.