Abstract:
The emergence of COVID-19 has heightened interest in how the illness interacts
with common comorbidities including malaria and type 2 diabetes mellitus (T2DM).
COVID-19 infection has been associated with new-onset hyperglycaemia and
T2DM, as well as a worsening of glycaemic control in non-diabetics without a
history of diabetes and diabetics due to direct pancreatic damage and the cytokine
onslaught in response to the infection. This cross-sectional study evaluated COVID-
19 recovered persons with or without malaria for their likelihood of developing
T2DM. Two hundred and ninety non-COVID-19 and COVID-19 confirmed
participants with or without malaria were recruited from the public health reference
laboratory database in the Northern region of Ghana. Respondents were assessed for
fasting blood glucose (FBG), beta cell function, C-reactive protein (CRP), insulin
resistance (IR), malondialdehyde (MDA), and malaria parasitaemia. Beta cell
function and IR were calculated using the Homeostatic models for assessment of IR
(HOMA-IR) and beta cell function (HOMA-B) formulae. COVID-19 recovered
respondents exhibited significantly higher mean levels for HOMA-IR (7.1 ± 8.1 vs
3.7 ± 2.9 mIU/L; P<0.001), FBG (4.95 ± 1.13 vs 4.26 ± 0.58 mmol/l; P<0.001), and
CRP (1.35 ±1.41 vs 0.99 ± 0.88 mg/dl; P=0.0098) compared to the control
respondents. The total prevalence of HOMA-IR in cases was 38.3% compared to
32.4% in the control respondents. A binary logistic regression analysis of beta cell
activity, insulin, CRP, MDA, and malaria found that study participants with malaria
had a greater risk of developing hyperinsulinemia than participants without malaria
in both groups. Mean values of the other indices were comparable between the
groups. The findings of the study demonstrate that COVID-19, through insulin
resistance, can contribute to the risk of T2DM development in recovered COVID-19
respondents.
