The current study assessed fasting blood glucose and lipid profiles among asthmatic patients on corticosteroid therapy and non-asthmatic control participants at Bahir Dar public hospitals. The mean fasting blood glucose level in the asthmatic patients on corticosteroid therapy (107.57 ± 21.78) was significantly higher than in the control group (95.51 ± 15.14) (p < 0.001). This result supports findings from studies in Pakistan and Turkey [31, 32]. Corticosteroids can increase insulin resistance and hepatic gluconeogenesis, decrease glucose utilization by peripheral tissues, and cause beta-cell dysfunction. This increase in hepatic gluconeogenesis is due to the direct effects of glucocorticoids on the hepatic expression of genes that code for enzymes required for glucose and glycogen biosynthesis [33, 34]. The mean serum total cholesterol level in asthmatic patients on corticosteroid therapy (187.32 ± 55.68) was significantly higher than in the control group (135.32 ± 49.88) (p < 0.001). This finding is consistent with studies done in San Francisco, Italy, and India [35-37]. However, it is inconsistent with studies from Turkey and Pakistan [31, 32], However, it is inconsistent with studies from Turkey and Pakistan [31, 32]. These discrepancies could be due to differences in sample size, socioeconomic health services, study design, and participants' physical exercise habits.
The prevalence of hyperglycemia in asthmatic patients on corticosteroid therapy was 20.39% (95% CI: 14.3–27.7). This is consistent with the findings of studies conducted in Korea (14.7%) and Spain (18%) [31, 32, 38]. This was consistent with the findings of studies conducted in Korea (14.7%) and Spain (18%) [23, 39]. This result was higher than the findings of the studies done in Britain (10%) and Jimma, (11.11%) [40, 41]. This difference might be due to variations in sample size, corticosteroid types used, exposure time, study design, and sociodemographic characteristics. The prevalence of hyperglycemia in controls was 4.6% (95% CI: 1.9–9.3 which is similar to findings from studies conducted in Sweden (4.8%) [42], and Spain (10 %) [23]. The prevalence of total cholesterol was 32.23% (95% CI: 25–40) and 7.9% (95% CI: 4.6–13) in asthmatic patients using steroid drug therapies and controls, respectively. This finding is in contrast to reports from studies in Britain [40]. This difference may be due to variations in health services, methodology, steroid dose and duration, socioeconomic factors, and access to healthcare.
The prevalence of hypertriglyceridemia was 19.07% and 12.5% in asthmatic patients and controls, respectively. Similarly, the prevalence of increased LDL cholesterol was 22.37% and 12.5% in asthmatic patients and controls, while the prevalence of decreased HDL was 18.42% and 8.5% in asthmatic patients and controls. Steroid drugs, particularly systemic corticosteroids, can lead to lipolysis in adipose tissues, lipogenesis in the liver, and increased levels of these lipid profiles [9]. The prevalence of dyslipidemia was 45.4% (95% CI: 37.3-53.7) and 26.31% (95% CI: 20-34) in asthmatic participants and controls, respectively. The prevalence of dyslipidemia was 45.4% (95% CI: 37.3-53.7) and 26.31% (95% CI: 20-34) in asthmatic participants and controls, respectively [23, 43]. The possible reasons for this could be the difference in socioeconomics and health services, the dose of medications, the duration of time on medication, and the types of corticosteroids used, which include inhalational, oral, and parenteral corticosteroids. Inhaled corticosteroids are known to produce relatively fewer systemic adverse effects, and their effect on carbohydrate and lipid metabolism is less compared to other corticosteroids [7, 44]. Female participants had 2.19 times the odds of developing dyslipidemia (AOR = 2.19; 95% CI: 1.25–3.82) (p = 0.006).
With menopause, women experience a worsening of their lipid profile, with a transition to higher and more atherogenic dyslipidemia [45]. The odds of having dyslipidemia were 4.22 (AOR= 4.22; 95% CI: (1.90–9.39) with p < 0.001) and 5.21 (AOR=5.21; 95% CI: (1.81–15.03) with p = 0.002) times higher in overweight and obese study participants compared to normal weight. Overweight and obesity contribute to insulin resistance in peripheral tissues, leading to an enhanced hepatic flux of fatty acids from dietary sources, intravascular lipolysis, and adipose tissue resistant to the antilipolytic effects of insulin [46].
The odds of having dyslipidemia in physically inactive study participants was 2.59 (AOR= 2.59; 95%CI: 1.41-4.77), P=0.002 times higher than active physical exercising study participants. Sedentary lifestyles are known to be predisposing factors for the development of overweight and obesity. When individuals engage in minimal physical activity and spend a significant amount of time sitting or lying down, their energy expenditure decreases. This reduced energy expenditure, coupled with the consumption of excess calories, can lead to weight gain and an increased risk of overweight and obesity, which are risk factors for the development of abnormal lipid profiles [47]. The odds of having dyslipidemia were 7 (AOR = 7.04 (95% CI: (2.01-24.61), P = 0.002), and 4.74 (95% CI: (1.40-16.02), p = 0.012), times higher in asthmatic patients taking high doses of corticosteroids for a long period compared to who took a low dose and for a shorter period. Studies in Korea and Germany support this finding, demonstrating that higher corticosteroid doses and longer durations increase the occurrence of dyslipidemia [26, 48]. Overweight, obesity, and physical activity lasting less than two hours and a half per week had 7.28, 6.81, and 4.7 times the odds of having dyslipidemia (AOR = 7.28; 95% CI: (1.74–30.53) with p = 0.007, 6.81; 95% CI: (1.83–25.24) with p = 0.004, and 4.70; 95% CI: (1.69–13.06) with p = 0.003, respectively). Having a family history of diabetes mellitus (DM) increases the occurrence of hyperglycemia 6.41 times (AOR=6.41; 95% CI: (2.05-20.07), p<0.001) compared to those who had no family history of DM.
Certain environmental factors, such as the intrauterine environment, and genetic ones, including mitochondrial DNA mutations, have been linked to the increased maternal transmission of hyperglycemia to the next generation [49]. The risk of having hyperglycemia was 8.87 (AOR= 8.87; 95%CI: (2.05-38.27), p= 0.003) and 6.47 (AOR= 6.47; 95%CI: 1.66-25.23), p=0.007 times higher in high dose corticosteroid users, and long period corticosteroid users compared to low dose and short time users. This result is inconsistent with findings from a study in Jimma, which reported no statistically significant associations. This difference might be due to variations in sample size, corticosteroid dose, and duration of treatment [41]. The study also showed that the blood glucose of the study participants was positively correlated with total cholesterol, triglyceride, and LDL, and negatively correlated with HDL cholesterol. Liver glucocorticoids cause hyperglycemia, enhance hepatic lipogenesis, inhibit fatty acid β-oxidation, and increase total cholesterol, triglyceride, and low-density lipoprotein [50].
Limitations of the study
Although this study was conducted on case-control, the cross-sectional nature of the study limits the ability to determine causal relationships between the use of asthmatic steroid drugs and the health outcomes.