The SA Journal Diabetes & Vascular Disease Volume 21 No 1 (November 2024)

RESEARCH ARTICLE SA JOURNAL OF DIABETES & VASCULAR DISEASE 24 VOLUME 21 NUMBER 1 • November 2024 gliclazide, glimepiride, repaglinide, pioglitazone), the newer agents (vildagliptin, dapagliflozin, liraglutide, empagliflozin, sitagliptin, exenatide, saxagliptin) and who were on insulin as A10A (insulin and analogues). Those on antihypertensive therapy were identified according to ATC C02 (antihypertensives), C03 (diuretics), C07 (beta-blocking agents), C09 (agents acting on the renin–angiotensin system), C08 (calcium channel blockers) and G04CA03 (alpha-adrenoreceptor antagonist). The choice of selecting antihypertensive medication is based mainly on the patient’s glycaemic and lipid profiles. Patients claiming treatment for dyslipidaemia ATC C10 [lipid-modifying therapy, which are statins (98% claim rate), fibrates, ezetimibe and bile acid sequestrants] were identified. Patients claiming antidepressant ATC (N06A) were characterised according to those on SSRIs (Fluoxetine, Paroxetine, Sertraline, Citalopram, Escitalopram, Fluvoxamine) versus those not on SSRIs, such as, patients on serotonin norepinephrine reuptake inhibitors (Venlafaxine, Desvenlafaxine, Duloxetine), noradrenergic and specific serotonergic antidepressants (Mirtazapine; Mianserin), serotonin receptor antagonists and reuptake inhibitors (Trazodone), norepinephrine dopamine reuptake inhibitor (Bupropion), serotonergic antidepressant (Vortioxetine) or melatonergic agonist (Agomelatine). The class of SSRI was characterised separately as data show that in combination with a statin, it had a larger effect on depressive symptoms than either drug alone.37 Confidentiality was maintained throughout the analysis by using the patients’ unique scheme membership number and dependent code to align patient-level records. The University of the Witwatersrand, Johannesburg, Faculty of Health Sciences Human Ethics Committee (M140326; M1911196) approved the study. Approval was granted by the principal officer of the scheme for the scheme data to be used in the study and by the human resources manager to gather data from the scheme administrative database for the research. Statistical analysis Data extracted from the database were exported to Microsoft Excel 2016 and statistical analysis was performed with Statistica 13.3 (StatSoft Inc, Tulsa, OK) and SAS 9.4. Study patients were those with a total cholesterol level < 4.5 mmol/l; those below target LDL-C < 1.8 mmol/l; those above target high-density lipoprotein cholesterol > 1.0 mmol/l in men and > 1.2 mmol/l in women; those below triglyceride target level < 1.7 mmol/l; and BP in patients with SBP < 140 mmHg. HbA1c and lipid levels are given as median (IQR). Categorical variables such as gender, number of claims for medicines and disease control measures are summarised as frequencies and percentages and were compared using Chi-square or Fisherexact tests. Multiple comparisons were analysed using Bonferroni correction among the three groups and the level of significance was set at p < 0.0166. Stepwise univariate and multivariate logistic regression analyses were performed to determine factors predicting HbA1c and LDL-C control in the study groups of patients with T2DM and MDD only. A sensitivity analysis was performed on patients claiming different classes of antidepressants. Claims were compared between those on SSRIs with those not on SSRIs and equated to their HbA1c targets attained. The significance level was set at p < 0.05. Results Table 1 shows the characteristics of the patients in the T2DM + MDD and T2DM – MDD groups compared to the control (MDD) group. More females and older patients were among the T2DM + MDD (p < 0.001) and MDD groups (p < 0.0001) compared to the T2DM – MDD group. The T2DM groups showed similar claiming patterns for lipid-lowering medications. Over 70% of those with T2DM with or without MDD were on lipid-lowering treatment with statins, and among those, < 7% were on combined therapies such as statin + ezetimibe (2.7, 3.2%) or statin + fibrate (3.6, 3.9%). However, a higher proportion of patients among the T2DM + MDD group versus the T2DM – MDD group claimed antihypertensives (79 vs 68%) (p = 0.0010). A small number (12.5, 10.8%) (p = 0.601) claimed sodium-glucose transport protein 2 inhibitors (SGLT2i). Table 2 depicts the CV indices of glycaemic, BP and lipid profiles of the patients attaining targets. The median (IQR) HbA1c level in patients with T2DM + MDD was higher compared to the T2DM – MDD group [7.4% (6.0–8.2) vs 7.2% (6.2–8.5), p < 0.05]. A higher proportion of patients in the T2DM + MDD group achieved HbA1c levels of < 7% compared to the T2DM – MDD group (p < 0.05). The LDL-C median (IQR) was similar in the T2DM + MDD [2.4 mmol/l (1.8–3.1)] and T2DM – MDD [2.4 mmol/l (1.8–3.1)] groups, but significantly lower when compared to the MDD group [3.0 mmol/l (2.4–3.8), p < 0.001]. Only 24% of patients in the T2DM groups achieved target LDL-C levels of < 1.8 mmol/l. The SBP of patients in the T2DM + MDD, T2DM – MDD and MDD groups was similar and on target. Fig. 1 shows that only 13% of the T2DM + MDD and 7.1% of T2DM – MDD groups achieved simultaneous ABC targets. Table 3 depicts a stepwise multivariate logistic regression analysis, which identified predictors of HbA1c control of the T2DM study groups. Table 1. Characteristics of patients with T2DM + MDD, T2DM – MDD and MDD T2DM + MDD T2DM – MDD MDD control Characteristics (n = 223) (25%) (n = 656) (75%) p-value (n = 332) p-value Age (years) (mean ± SD) 61 ± 13 57 ± 14 0.01 50 ± 17 < 0.0001 Female, n (%) 121 (54) 245 (37) < 0.001 213/332 (64) < 0.0001 Therapy claimed, n (%) Antihypertensives 177/223 (79) 447/656 (68) 0.001 121/332 (36) < 0.0001 Lipid-lowering therapy 173/223 (78) 471/656 (72) 0.092 117/332 (35) < 0.0001 Antidepressant therapy 223/223 (100) – – 262/332 (79) < 0.001 Selective serotonin reuptake inhibitors 108/223 (48) – – 168/332 (51) 0.478 MDD, major depressive disorder; T2DM, type 2 diabetes mellitus.

RkJQdWJsaXNoZXIy NDIzNzc=