Abstract
Introduction
Clinical trials have demonstrated greater glycemic control and weight loss with once-weekly (OW) semaglutide versus other anti-diabetes medications, including sodium-glucose co-transporter 2 inhibitors (SGLT2is) in adults with type 2 diabetes (T2D), yet real-world evidence is limited.
Methods
This observational study of adults with uncontrolled T2D (HbA1c ≥ 7.0%) initiating semaglutide OW or SGLT2is (January 2018–February 2022; first prescription = index) utilized linked data from IQVIA PharMetrics® Plus adjudicated claims and Ambulatory Electronic Medical Records databases. Among the all semaglutide OW cohort and subgroups (1: persistent [≤ 60-day gap in semaglutide OW supply]; 2: receiving maximum dose ≥ 1 mg; and 3: persistent and ≥ 1 mg dose), changes in weight, body mass index (BMI), and glycated hemoglobin (HbA1c) outcomes from baseline to 1 year post index were descriptively compared. For the main analysis, changes in weight, BMI, HbA1c, and all-cause healthcare resource utilization (HCRU) after 1 year were compared among adjusted semaglutide OW and comparator SGLT2i cohorts, following inverse probability of treatment weighting (IPTW).
Results
The all semaglutide OW cohort included 772 patients, and IPTW adjusted cohorts included 416 semaglutide OW patients and 1093 SGLT2i patients. Significant (P < 0.0001) mean changes from baseline were observed in the all semaglutide OW cohort and all subgroups, in weight (kg [all: − 4.4; 1: − 5.0; 2: − 4.9; 3: − 5.2]), BMI (kg/m2 [all: − 1.5; 1: − 1.8; 2: − 1.8; 3: − 1.9]), and HbA1c (% [all: − 1.5; 1: − 1.7; 2: − 1.5; 3: − 1.6]). Post-IPTW adjustment, the semaglutide OW cohort had significantly greater mean reductions versus the SGLT2i cohort in weight (− 4.4 versus − 3.4 kg, P = 0.0061), BMI (− 1.5 versus − 1.1 kg/m2, P = 0.0013), and HbA1c (− 1.6 versus − 1.2%, P < 0.0001), with similar all-cause HCRU.
Conclusion
Adults with T2D initiating semaglutide OW in the real-world had significant decreases in weight, BMI, and HbA1c after 1 year, with greater improvements versus SGLT2i, and similar HCRU.
Keywords: BMI, GLP-1 receptor agonist, HbA1c, Healthcare resource utilization, Real-world evidence, Semaglutide, SGLT2i, Type 2 diabetes, Weight
Key Summary Points
| Why carry out this study? |
| Type 2 diabetes (T2D) is a chronic disease, with a high clinical and economic burden, affecting > 90% of adults with diabetes in the USA. |
| The efficacy of semaglutide once weekly (OW) has been demonstrated in previous clinical trials, alone and versus other anti-diabetes medications, but real-world evidence is limited. |
| This study was designed to investigate the real-world impact of semaglutide OW versus sodium-glucose co-transporter 2 inhibitors (SGLT2is) on weight, body mass index (BMI), glycated hemoglobin (HbA1c), and healthcare resource utilization (HCRU) outcomes in patients with T2D. |
| What was learned from the study? |
| Initiating semaglutide OW is associated with significant decreases in weight, BMI, and HbA1c in adults with T2D, and better outcomes versus initiating SGLT2is, but similar all-cause medical HCRU, 1 year after initiating therapy. |
| The results support the use of semaglutide OW in routine clinical practice in adults with T2D in the USA. |
Introduction
More than 38 million people in the United States (USA) have diabetes, of which 90–95% have type 2 diabetes (T2D) [1]. T2D is a chronic, progressive disease with substantial clinical and economic impact [2, 3]. A critical part of diabetes management is adequate glycemic control, which plays an important role in preventing or delaying the complications associated with diabetes [4]. Recent guidelines from the American Diabetes Association (ADA) also emphasize the importance of weight management for people with T2D and overweight or obesity, noting that this should represent a primary goal alongside glycemic management, and that they may benefit from any magnitude of weight loss. It also supports more intensive weight loss goals based on the efficacy of and access to newer medications [5, 6]. Both glucagon-like peptide 1 receptor agonists (GLP-1 RAs) and sodium-glucose co-transporter 2 inhibitors (SGLT2is) are now recommended by the ADA for the treatment of T2D, according to the individual needs of the patient [6]. With respect to glycemic control, GLP-1 RAs activate GLP-1 receptors in the pancreas, leading to glucose-mediated enhancement of insulin release and reduction of glucagon release [7]. A minor delay in gastric emptying in the early postprandial phase is also involved in the mechanism of blood glucose-lowering effect of GLP-1 RAs [8]. SGLT2is reduce blood glucose without stimulating insulin release by reducing renal tubular glucose reabsorption [9]. Weight loss is a second common effect of both GLP-1 RAs and SGLT2is. GLP-1 RAs reduce food intake, appetite and hunger, and promote fullness and satiety, through a complex brain–gut interaction including delaying gastric emptying and gut motility [10]. For SGLT2is, weight loss is the result of glucose excretion from the kidneys, with the glucose-dependent inhibition of SGLT2 receptor leading to a loss of 60–100 g of glucose per day in urine [11].
Over the past decade, these two drug classes have emerged as effective treatments with manageable tolerability and safety profiles for T2D, with the number of available drugs in these drug classes expanding during this time. In 2017, the US Food and Drug Administration (FDA) approved semaglutide once-weekly (OW) injection (Ozempic®; Novo Nordisk) up to 1 mg/week to improve glycemic control in adults with T2D, as an adjunct to diet and exercise. Per the drug label, the dose of semaglutide OW can also be increased to 2 mg/week if additional glycemic control is required, following at least 4 weeks on the 1 mg dose [8]. Semaglutide OW is also approved to reduce the risk of major adverse cardiovascular events in adults with T2D and established cardiovascular disease following studies demonstrating significant improvement in these outcomes [12], which may also result in improved healthcare resource utilization (HCRU) and medical costs [13]. In the SUSTAIN clinical trials, semaglutide OW achieved superior glycemic control and weight loss compared with several other classes of anti-diabetes medications (ADMs) [14–18], including canagliflozin, an SGLT2i [19]. In the multinational double-blind, parallel-group, phase 3b, randomized controlled SUSTAIN 8 trial, patients receiving semaglutide OW had significantly greater reductions in glycated hemoglobin (HbA1c) and weight than those receiving canagliflozin (HbA1c estimated treatment difference [ETD] − 0.49%, P < 0.0001; weight ETD − 1.06 kg, P = 0.0029) [19]. Furthermore, a meta-analysis of eight trials comparing semaglutide OW with SGLT2is found that semaglutide OW, at a dose of 1 mg, was significantly more effective in reducing weight and improving HbA1c than the SGLT2is evaluated (statistically meaningful at the 0.05 significance level) [20].
Although several observational real-world studies of semaglutide OW have been undertaken [21–31], evidence concerning its relative effectiveness versus other interventions (including SGLT2is) in the real-world setting is limited. There are also limited data regarding HCRU in patients treated with GLP-1 RAs and SGLT2is. A real-world retrospective cohort analysis in patients with T2D and cardiovascular disease (CVD) found all-cause HCRU and medical costs to be significantly lower among patients receiving empagliflozin, an SGLT2i, compared with other branded antihyperglycemic agents, including GLP-1 RAs [32]. However, no specific comparison was made directly between empagliflozin and GLP-1 RAs alone.
The current observational study therefore aimed to provide further real-world evidence concerning the comparative effectiveness of semaglutide OW versus SGLT2is in relation to change in weight, body mass index (BMI), HbA1c, and composite outcomes, as well as all-cause HCRU and medical costs, in patients with T2D over a 1-year period. In a separate subgroup analysis, we also assessed how changes in weight, HbA1c, and composite outcomes were impacted by persistence with semaglutide OW treatment and dose.
Methods
Ethics Practices
The study involved use of IQVIA de-identified administrative claims and electronic medical records (EMR) data files. The Department of Health and Human Services does not consider analysis of deidentified secondary data to meet the definition for human subject research. Therefore, this study was exempt from federal regulations covering human subject research and did not require institutional review board review. This is as per exemption (d)4 from 45 CFR 46.104 [33].
Study Design and Patient Population
This real-world, observational study was conducted in US patients receiving semaglutide OW or SGLT2is, utilizing data from July 1, 2017 to February 28, 2023 (study period). Data were obtained for a linked patient population from IQVIA’s PharMetrics® Plus and Ambulatory EMR (AEMR) databases (comprising commercial health plan information from managed care plans and laboratory/vital data, respectively, throughout the USA), with the first claim for the index therapy designated as the index date.
For the all semaglutide OW cohort, eligible adults (aged ≥ 18 years) with ≥ 1 diagnosis on a confirmatory medical claim for T2D (any time prior to and including the index date) who initiated semaglutide OW with ≥ 2 filled prescription claims were identified, with the first claim during the selection window of January 1, 2018 to February 28, 2022, and the second claim during the follow-up period (1-year period after the index date). Patients were required to have continuous enrollment in the baseline period (6 months prior to the index date) and over the follow-up period. Patients were also required to have linkage to AEMR, with available and valid weight and HbA1c values in AEMR at baseline and at the end of the follow-up period. All patients were required to have baseline HbA1c of ≥ 7.0% (indicative of uncontrolled hyperglycemia) in AEMR on the index date or closest available date (between 180 days pre index to 30 days post index). Baseline weight was taken in AEMR between 90 days pre index to 30 days post index, using the value closest to the actual index date. Similar inclusion criteria were applied for the comparator SGLT2i cohort, with ≥ 2 prescription claims for an SGLT2i required.
Exclusion criteria for both cohorts included a type 1 diabetes (T1D) diagnosis, gestational diabetes, metastatic cancer, comorbid conditions related to unintentional weight change, bariatric surgery, pregnancy, and pharmacy claims for anti-obesity medication in the baseline or follow-up periods. In the all semaglutide OW cohort, patients with a pharmacy claim for any GLP-1 RA (drug or combination product for T2D or obesity) during the baseline period were excluded. Patients with a pharmacy claim for any SGLT2i during the baseline or follow-up periods were excluded for the comparison with SGLT2is. In the comparator SGLT2i cohort, those with any prior SGLT2i use during the baseline period or any baseline or follow-up use of any GLP-1 RA were excluded. Full details of the eligibility criteria are provided in Fig. 1.
Fig. 1.
Patient selection criteria and attrition numbers. *Pre-IPTW. AEMR Ambulatory Electronic Medical Records, AOM anti-obesity medication, GLP-1 RA glucagon-like peptide 1 receptor agonist, HbA1c glycated hemoglobin, IPTW inverse probability of treatment weighting, OW once-weekly, sema semaglutide, SGLT2i sodium-glucose co-transporter 2 inhibitor, T2D type 2 diabetes
Demographic characteristics were assessed as of the index date, and clinical characteristics were assessed over the baseline period. The follow-up values for weight were recorded at 1 year post index (360 days post index ± 90 days, taking the value closest to day 360), with change in weight (kg) evaluated by subtracting the baseline value from the follow-up value. BMI data were collected as per the weight data, with height and weight used to calculate BMI if the recorded BMI value was unavailable. In addition, categorical and binary BMI measures based on BMI value were reported for the baseline and follow-up periods. Follow-up HbA1c values were recorded at 1 year post index (360 days post index ± 90 days, taking the value closest to day 360). Change in HbA1c was evaluated by subtracting the baseline value from the follow-up value.
Study Outcomes
All Semaglutide OW Cohort and Subgroup Analysis
The assessed outcomes included change in weight and HbA1c from baseline to end of the follow-up period for the semaglutide OW cohort. In addition, composite outcomes were assessed in terms of the proportion of patients achieving both follow-up HbA1c < 7.0% and ≥ 5% weight loss; both follow-up HbA1c < 7.0% and ≥ 10% weight loss; and both follow-up HbA1c < 7.0% and ≥ 15% weight loss. As an additional analysis, changes in weight and HbA1c, including the composite weight and HbA1c outcomes, were compared over the follow-up period in the following patient subgroups: persistent—patients who were persistent to the index therapy (defined as patients with ≤ 60 days’ gap in supply); ≥ 1 mg—patients receiving maximum dose ≥ 1 mg; or persistent and ≥ 1 mg—patients persistent to the index therapy and receiving maximum dose ≥ 1 mg over the follow-up period.
Main Analysis of Semaglutide OW Comparative Effectiveness with SGLT2is
The subset of patients initiating semaglutide OW who did not have baseline or follow-up use of SGLT2i were identified, characterized, and compared with patients initiating SGLT2i after inverse probability of treatment weighting (IPTW), for changes in weight, BMI, HbA1c, composite weight and HbA1c outcomes, all-cause HCRU, and medical costs. HCRU was assessed over the baseline and follow-up periods (including index date) and expressed as both the proportion of patients with utilization, and as per-patient number of visits averaged across both cohorts. Mutually exclusive HCRU endpoints included inpatient hospitalizations, emergency room (ER) visits, and outpatient medical services (including physician office visits, and other outpatient services). Total medical cost (sum of inpatient costs, ER costs, and outpatient medical costs) was also analyzed. All costs are reported in 2022 US dollars (USD) using the medical component of the Consumer Price Index.
Statistical Analysis
Demographics and clinical characteristics of the all semaglutide OW cohort and subgroups were reported descriptively. Descriptive statistics were reported for all study measures. Appropriate statistical tests were used for within-group comparisons of baseline and follow-up weight and HbA1c outcomes, including paired t test, Wilcoxon signed-rank test, and McNemar’s test.
For the pairwise comparison of semaglutide OW versus SGLT2i cohorts, IPTW was used to adjust for imbalances in selected baseline patient characteristics between the treatment cohorts. Standardized mean difference (SMD) was reported as a measure of balance for baseline characteristics and HCRU/cost both pre and post IPTW. An SMD of ≥ 0.10 (absolute) between groups was considered meaningful. Weights were constructed by estimating each patient’s probability of receiving semaglutide OW treatment based on observed covariates from a logistic regression model. Stabilized IPTW was used as it reduces the type I error by preserving the sample size in pseudo datasets rather than doubling the sample size in traditional IPTW; weight values greater than five were truncated to five because of the potential bias of outliers. Therefore, pseudo datasets using stabilized weights can result in a larger sample size than the original sample size pre IPTW.
All-cause HCRU and medical costs over the follow-up period were also compared post IPTW, as well as changes in weight and HbA1c. Appropriate weighted statistical tests were used for comparison of outcomes post IPTW, including weighted chi-square tests for categorical variables, and weighted t tests (mean) for continuous variables. For comparisons between less frequent independent samples (e.g., patients with ≥ 1 hospitalization), pairwise independent comparisons were conducted using the parametric t test (mean) and non-parametric Wilcoxon rank-sum test (median), because the IPTW adjustment no longer applied to the independent samples which were subgroups of IPTW-adjusted cohorts. Incidence rate ratios of hospitalizations and ER visits were calculated for each exploratory pairwise comparison.
For all statistical analyses, a P value of < 0.05 was considered statistically significant.
Results
After eligibility criteria were applied using linked IQVIA’s PharMetrics® Plus and AEMR databases, 772 patients were identified for inclusion in the analysis of the impact of semaglutide OW from baseline to follow-up (Fig. 1). For the comparison of the semaglutide OW cohort versus the SGLT2i cohort, 439 and 1089 patients, were identified respectively. Following IPTW adjustment, the final cohorts consisted of 416 patients in the semaglutide OW cohort and 1093 in the SGLT2i cohort (empagliflozin, 63.9%; dapagliflozin, 25.2%; canagliflozin, 9.4%; ertugliflozin, 1.5%). Baseline demographics and clinical characteristics are summarized in Table 1 for the all semaglutide OW cohort, for the subgroups (defined by persistence and dose), and for the IPTW-adjusted semaglutide OW and comparator SGLT2i cohorts. Characteristics were generally similar across the semaglutide OW subgroups and between semaglutide OW and comparator SGLT2i cohorts, with the exception of use of oral fixed-dose combinations at baseline, which was higher in the SGLT2i cohort (8.8% versus 5.9% for semaglutide OW; SMD 0.1090).
Table 1.
Baseline demographics and clinical characteristics
| All semaglutide OW cohort and subgroups | Semaglutide OW and comparator SGLT2i cohorts (IPTW-adjusted) | ||||||
|---|---|---|---|---|---|---|---|
| Semaglutide OW cohort (n = 772) | Persistent (n = 508) | ≥ 1 mg (n = 347) | Persistent and ≥ 1 mg (n = 251) | Semaglutide OW cohort (n = 416) | SGLT2i cohort (n = 1093) | SMD | |
|
Age, years (mean, SD) |
54.8 (9.5) | 54.6 (9.1) | 53.9 (9.5) | 54.0 (9.5) | 55.6 (10.1) | 55.8 (9.8) | 0.0226 |
| Male, n (%) | 370 (47.9) | 248 (48.8) | 166 (47.8) | 123 (49.0) | 176 (42.4) | 439 (40.2) | − 0.0444 |
|
HbA1c, % (mean, SD) |
8.9 (1.6) | 8.8 (1.5) | 8.9 (1.6) | 8.9 (1.6) | 8.9 (1.5) | 8.9 (1.6) | − 0.0134 |
|
Weight, kg (mean, SD) |
108.1 (23.0) | 108.2 (22.7) | 110.2 (22.7) | 110.8 (21.9) | 106.1 (21.7) | 105.0 (23.1) | − 0.0466 |
|
BMI, kg/m2 (mean, SD) |
36.9 (7.1) | 37.0 (7.0) | 37.5 (6.9) | 37.9 (6.8) | 36.2 (6.7) | 35.7 (7.2) | − 0.0707 |
| BMI, kg/m2 (categorical), n (%) | |||||||
| Underweight: < 18.5 | 0 (0) | 0 (0) | 0 (0) | 0 (0) | 0 (0) | 0 (0) | 0.0000 |
| Normal weight: 18.5–24.9 | 15 (1.9) | 10 (2.0) | 4 (1.2) | 2 (0.8) | 11 (2.6) | 41 (3.8) | 0.0682 |
| Overweight: 25.0–29.9 | 108 (14.0) | 63 (12.4) | 44 (12.7) | 28 (11.2) | 68 (16.2) | 191 (17.5) | 0.0330 |
| Obesity class I: 30.0–34.9 | 217 (28.1) | 149 (29.3) | 84 (24.2) | 62 (24.7) | 118 (28.5) | 316 (28.9) | 0.0095 |
| Obesity class II: 35.0–39.9 | 186 (24.1) | 121 (23.8) | 89 (25.6) | 66 (26.3) | 110 (26.4) | 276 (25.3) | − 0.0266 |
| Obesity class III: ≥ 40 | 243 (31.5) | 162 (31.9) | 124 (35.7) | 91 (36.3) | 109 (26.3) | 268 (24.6) | − 0.0389 |
| BMI, kg/m2 (binary), n (%) | |||||||
| < 30.0 | 123 (15.9) | 73 (14.4) | 48 (13.8) | 30 (12.0) | 78.2 (18.8) | 232.3 (21.3) | 0.0608 |
| ≥ 30.0 | 646 (83.7) | 432 (85.0) | 297 (85.6) | 219 (87.3) | 337.3 (81.2) | 860.5 (78.7) | − 0.0608 |
| CCI, mean (SD) | 0.7 (1.6) | 0.7 (1.6) | 0.7 (1.6) | 0.8 (1.7) | 0.6 (1.4) | 0.6 (1.4) | − 0.0169 |
| DCSI, mean (SD) | 0.7 (1.2) | 0.7 (1.2) | 0.7 (1.1) | 0.7 (1.0) | 0.8 (1.2) | 0.7 (1.2) | − 0.0456 |
| Pre-index ADM classes, n (%) | |||||||
| Biguanides | 472 (61.1) | 312 (61.4) | 207 (59.7) | 154 (61.4) | 295 (70.2) | 755 (69.1) | − 0.0397 |
| SGLT2i | 222 (28.8) | 146 (28.7) | 104 (30.0) | 75 (29.9) | – | – | – |
| Insulin | 213 (27.6) | 132 (26.0) | 104 (30.0) | 71 (28.3) | 84 (20.2) | 211 (19.3) | − 0.0210 |
| Sulfonylurea | 203 (26.3) | 144 (28.3) | 94 (27.1) | 78 (31.1) | 109 (26.3) | 312 (28.5) | 0.0493 |
| DPP4i | 105 (13.6) | 78 (15.4) | 54 (15.6) | 42(16.7) | 63 (15.2) | 170 (15.5) | 0.0091 |
| Fixed-dose combination orals | 101 (13.1) | 71 (14.0) | 44 (12.7) | 31 (12.4) | 25 (5.9) | 96 (8.8) | 0.1090* |
| TZD | 75 (9.7) | 43 (8.5) | 29 (8.4) | 18 (7.2) | 29 (7.0) | 66 (6.0) | − 0.0379 |
| Other | 6 (0.8) | 6 (1.2) | 2 (0.6) | 2 (0.8) | 2 (0.5) | 9 (0.8) | 0.0369 |
| Pre-index comorbidities | |||||||
| CKD | 61 (7.9) | 35 (6.9) | 30 (8.6) | 16 (6.4) | 33 (7.8) | 77 (7.1) | − 0.0302 |
| Stage V CKD/dialysis/ESKD | 1 (0.1) | 1 (0.2) | 0 (0) | 0 (0) | 0 (0) | 0 (0) | 0.0000 |
| Obesity | 295 (38.2) | 194 (38.2) | 145 (41.8) | 106 (42.2) | 144 (34.7) | 378 (34.6) | − 0.0028 |
| COVID-19 | 26 (3.4) | 16 (3.1) | 17 (4.9) | 10 (4.0) | 11 (2.6) | 32 (2.9) | 0.0201 |
| Cardiac dysrhythmia | 33 (4.3) | 21 (4.1) | 13 (3.7) | 7 (2.8) | 30 (7.2) | 64 (5.9) | − 0.0519 |
| Coronary artery disease | 73 (9.5) | 51 (10.0) | 31 (8.9) | 26 (10.4) | 52 (12.4) | 111 (10.1) | − 0.0726 |
| Myocardial infarction | 6 (0.8) | 4 (0.8) | 2 (0.6) | 1 (0.4) | 6 (1.4) | 21 (2.0) | 0.0402 |
| Stroke/TIA | 15 (1.9) | 10 (2.0) | 9 (2.6) | 5 (2.0) | 12 (2.8) | 31 (2.8) | − 0.0006 |
| Peripheral vascular disease | 30 (3.9) | 22 (4.3) | 12 (3.5) | 10 (4.0) | 18 (4.2) | 45 (4.1) | − 0.0061 |
ADM anti-diabetes medication, BMI body mass index, CCI Charlson Comorbidity Index, CKD chronic kidney disease, DCSI Diabetes Complications Severity Index, DPP4i dipeptidyl peptidase 4 inhibitor, ESKD end-stage kidney disease, HbA1c glycated hemoglobin, IPTW inverse probability of treatment weighting, OW once-weekly, SD standard deviation, SGLT2i sodium-glucose co-transporter 2 inhibitor, SMD standard mean deviation, TIA transient ischemic attack, TZD thiazolidinedione
*Significant SMD value
Pre–Post Analysis of Changes in Weight, BMI, and HbA1c in the All Semaglutide OW Cohort and Subgroups
Changes in weight, BMI, and HbA1c from baseline to follow-up with semaglutide OW are summarized in Fig. 2. Overall, weight decreased by a mean (SD) 4.4 (7.1) kg, BMI decreased by 1.5 (2.6) kg/m2, and HbA1c decreased by 1.5 (1.7)%, all P < 0.0001 (Fig. 2a–c), with significant decreases also seen in all subgroups (P < 0.0001; Fig. 2a–c). Numerically, the greatest decreases in weight (5.2 kg) and BMI (1.9 kg/m2) were observed in the cohort of patients persistent to treatment and receiving ≥ 1 mg.
Fig. 2.
Change from baseline to follow-up in a–c weight, BMI, and HbA1c (all semaglutide OW cohort and subgroups), and d–f weight, BMI, and HbA1c (IPTW-adjusted semaglutide OW and comparator SGLT2i cohorts). *Significant change from baseline (P < 0.0001). BMI body mass index, HbA1c glycated hemoglobin, IPTW inverse probability of treatment weighting, OW once weekly, sema, semaglutide, SD standard deviation, SGLT2i sodium-glucose co-transporter 2 inhibitor
The composite weight and HbA1c outcomes for all cohorts are shown in Fig. 3. In the all semaglutide OW cohort, 25% of patients achieved HbA1c < 7.0% with ≥ 5% weight loss, 11.3% achieved HbA1c < 7.0% with ≥ 10% weight loss, and 4.4% achieved HbA1c < 7.0% with ≥ 15% weight loss (Fig. 3a). Numerically greater achievement of these composite outcomes was observed where persistence was high: 30.1% of patients persistent to treatment achieved HbA1c < 7.0% with ≥ 5% weight loss, and 5.5% achieved HbA1c < 7.0% with ≥ 15% weight loss. Similarly, the largest proportion of patients who achieved HbA1c < 7.0% with ≥ 10% weight loss (14.7%) was in the subgroup of patients persistent and ≥ 1 mg dose.
Fig. 3.
Composite weight and HbA1c outcomes from baseline to follow-up in a all semaglutide OW cohort and subgroups and b IPTW-adjusted semaglutide OW and comparator SGLT2i cohorts. HbA1c glycated hemoglobin, IPTW inverse probability of treatment weighting, OW once-weekly, sema semaglutide, SGLT2i sodium-glucose co-transporter 2 inhibitor
The proportion of patients in each cohort by BMI category at baseline versus follow-up is summarized in Fig. 4. Overall, and in all subgroups of the all semaglutide OW cohort, the total proportion of patients in the obesity classes II and III decreased, while the proportion of patients in the lower weight categories (normal and overweight) increased, reflecting the mean weight loss observed with semaglutide OW (Fig. 4a).
Fig. 4.
BMI distribution at baseline and follow-up in a all semaglutide OW cohort and subgroups and b IPTW-adjusted semaglutide OW and comparator SGLT2i cohorts. Overall proportion of patients with obesity may not equal combined proportions of patients in each obesity class as a result of rounding. BMI body mass index, IPTW inverse probability of treatment weighting, OW once-weekly, sema semaglutide, SGLT2i sodium-glucose co-transporter 2 inhibitor
Main IPTW-Adjusted Comparative Analysis of Semaglutide OW Versus SGLT2is
Significantly greater reductions in all three outcomes of weight, BMI, and HbA1c were observed with semaglutide OW versus SGLT2is (weight, − 4.4 versus − 3.4 kg [P = 0.0061]; BMI, − 1.5 versus − 1.1 kg/m2 [P = 0.0013]; HbA1c, − 1.6 versus − 1.2% [P < 0.0001]; Fig. 2d–f).
With respect to the composite outcomes, a significantly greater composite outcome achievement was observed for semaglutide OW compared with SGLT2is (Fig. 3b).
A similar result to the all semaglutide cohort was observed in the adjusted semaglutide OW and comparator SGLT2i cohorts, with a lower proportion of patients with class II/III obesity and a higher proportion of patients with normal weight at follow-up, compared with baseline in both groups (Fig. 4b).
HCRU data for semaglutide OW versus SGLT2is are summarized in Table 2. Overall, both cohorts had similar all-cause HCRU at follow-up, with few differences observed. A significantly lower proportion of patients in the semaglutide OW cohort had “other outpatient services” (97.8% versus 99.7%, P = 0.0003), but the absolute difference was small. A numerically lower mean (SD) all-cause total medical cost over the follow-up period was observed with semaglutide OW than with SGLT2is ($5852 [$10,113] versus $7547 [$16,865], respectively), but the difference was not statistically significant (P = 0.0538).
Table 2.
IPTW-adjusted all-cause HCRU and medical costs at follow-up
| Semaglutide OW cohort (n = 416) | Comparator SGLT2i cohort (n = 1093) | P value | |
|---|---|---|---|
| Inpatient hospitalization | |||
| Patients with ≥ 1 hospitalization, n (%) | 25 (6.0) | 62 (5.7) | 0.8190 |
| Average LOS per patient for all hospitalizations (days), mean (SD) | 4.5 (3.2) | 4.5 (2.8) | 0.9933 |
| Number of hospitalizations per patient, mean (SD) | 1.0 (0.2) | 1.3 (0.6) | 0.0287* |
| Time from index date to first all-cause hospitalization (days), mean (SD) | 134.8 (84.9) | 182.5 (105.0) | 0.0445* |
| Incidence rate of hospitalization (95% CI) (per person year) | 0.120 (0.078, 0.178) | 0.114 (0.088, 0.146) | N/A |
| Total inpatient cost per patient (USD) | 1299 (6313) | 2246 (11,992) | 0.1242 |
| ER visits | |||
| Patients with ≥ 1 ER visit, n (%) | 63 (15.2) | 192 (17.6) | 0.2658 |
| Number of ER visits per patient, mean (SD) | 1.6 (0.8) | 1.6 (1.7) | 0.7925 |
| Incidence rate of ER visits (per person year) | 0.303 (0.233, 0.388) | 0.352 (0.304, 0.405) | N/A |
| Total ER cost per patient (USD), mean (SD) | 353 (1318) | 328 (1451) | 0.7606 |
| Outpatient medical | |||
| Physician office visits | |||
| Patients with ≥ 1 physician office visit, n (%) | 414 (99.7) | 1083 (99.1) | 0.2134 |
| Number of physician office visits per patient, mean (SD) | 10.8 (11.9) | 10.9 (11.3) | 0.9338 |
| Total physician office visit cost per patient (USD), mean (SD) | 1252 (1369) | 1294 (1515) | 0.6176 |
| Other outpatient services† | |||
| Patients with ≥ 1 other service, n (%) | 406 (97.8) | 1089 (99.7) | 0.0003* |
| Number of other service visits per patient, mean (SD) | 31.4 (25.6) | 32.9 (33.3) | 0.4064 |
| Total other service cost per patient (USD), mean (SD) | 2948 (5594) | 3679 (8090) | 0.0894 |
| Total outpatient medical cost per patient (USD), mean (SD) | 4200 (6112) | 4973 (8775) | 0.0979 |
| Total medical cost per patient (USD), mean (SD) | 5852 (10,113) | 7547 (16,865) | 0.0538 |
All costs are reported in 2022 USD using the medical component of the Consumer Price Index
CI confidence interval, ER emergency room, HCRU healthcare resource utilization, IPTW inverse probability of treatment weighting, LOS length of stay, N/A not applicable, OW once weekly, SD standard deviation, SGLT2i sodium-glucose co-transporter 2 inhibitor, USD US dollars
*Significant P values
†Includes laboratory/pathology tests, radiology, surgical services, and ancillary services
Discussion
This observational database study provides evidence that the weight and HbA1c reductions observed in clinical trials of semaglutide OW are achieved in patients with T2D in the real-world setting. Overall, 1 year after initiating semaglutide OW, there was a mean 4.4 kg weight reduction and a decrease in HbA1c of 1.5% in the all semaglutide OW cohort. Following IPTW, all weight, BMI, and HbA1c outcomes, including composite outcomes, were significantly better in the semaglutide OW cohort, compared with the SGLT2i cohort. This provides evidence for the utilization of GLP-1 RAs over SGLT2i in patients with T2D to help achieve real-world optimal glycemic control, as well as reductions in body weight.
These findings are comparable to the results of the phase 3 SUSTAIN clinical trials of semaglutide OW in which, across trials and ethnicity subgroups, weight reduced from baseline by 2.3–4.7 kg with a dose of 0.5 mg, and by 3.6–6.1 kg with 1 mg [34]. The respective decreases from baseline in HbA1c were by 1.0–1.5% with semaglutide 0.5 mg, and by 1.3–2.0% with 1 mg [34, 35]. These data suggest that the 1 mg dose has a more potent therapeutic effect than the 0.5 mg dose on both weight and HbA1c outcomes. Our data are also consistent with other recent real-world observational studies of semaglutide OW where weight reductions of 2.8–7.8 kg have been reported, together with HbA1c reductions of 0.8–1.5% [21–31]. The RELATE study was a real-world retrospective database study of 1926 adults with T2D, which utilized linked data from IQVIA’s Longitudinal Prescription Claims, Professional Fee Claims and AEMR in the USA. At 12-month follow-up, initiating semaglutide OW was associated with significant (P < 0.001) decreases in mean weight (− 4.1 kg), BMI (− 1.5 kg/m2), and HbA1c (− 1.3%) [36].
Treatment persistence is an important factor in the treatment of T2D. High treatment persistence is associated with good glycemic control and lower HCRU, whereas lower treatment persistence is associated with inadequate glycemic control and a higher risk of mortality and morbidity [37]. In a subgroup analysis of the effectiveness of orally administered semaglutide in a real-world setting, persistence on drug was associated with a significantly greater reduction in HbA1c [38]. Our results are consistent with this finding, albeit with semaglutide OW, whereby persistent patients had greater reductions in weight, BMI, and HbA1c compared with the all semaglutide cohort, as well as better composite outcomes.
Importantly, our study adds to our understanding of the real-world efficacy of semaglutide OW showing that mean improvements in weight, BMI, HbA1c, and composite outcomes are significantly greater with semaglutide OW versus SGLT2i. This provides real-world evidence in addition to the efficacy profile established in the clinical trial setting. A meta-analysis of randomized controlled trials comparing GLP-1 RAs and SGLT2is in patients with obesity and T2D uncontrolled on metformin found that GLP-1 RA use was associated with significantly reduced HbA1c (− 0.40%; 95% CI − 0.54, − 0.25; P < 0.00001) compared to SGLT2i use. With respect to body weight, semaglutide OW was associated with a significant weight loss benefit (mean difference − 0.75 kg; 95% CI − 1.18, − 0.31; P = 0.0007) [39].
The analysis did not show any major difference between semaglutide OW and SGLT2i with respect to HCRU, despite the superior weight- and glucose-lowering effect of semaglutide OW. It is possible that a longer period of follow-up would be required for any differences in HCRU related to therapeutic potency to manifest, and this is a possibility worthy of further study. Nevertheless, these results are not in agreement with those observed by Raju et al. [32], which demonstrated that empagliflozin, an SGLT2i, was associated with significantly lower all-cause HCRU and medical costs compared with other branded antihyperglycemic agents including DPP4is, other SGLT2is besides empagliflozin, GLP-1 RAs, or insulin. However, as the results for patients utilizing other branded antihyperglycemic agents were combined, and there was no specific comparison between empagliflozin and GLP-1 RAs, it cannot be concluded in this study that empagliflozin use was associated with better HCRU outcomes than GLP-1 RA use specifically. Real-world HCRU and medical costs can be important factors in deciding which ADM to initiate, and further research is warranted on these outcomes for patients with T2D.
Limitations of the study related to the study design and data source utilized include the potential for miscoding/misclassification, and that the findings may not be representative of the overall US T2D population. It should also be noted that patients initiating semaglutide OW (and SGLT2i) were empirically selected for this intervention; hence, the results cannot necessarily be extrapolated to a general T2D population. The sample size of the population was relatively small; thus, the statistical power of analyses is likely to be weakened. The analyses presented here should therefore be interpreted with caution. Although IPTW was applied to adjust for confounding in the comparative analysis versus SGLT2i, some residual confounding cannot be ruled out. However, the study analyzed data from a cohort of patients in a real-world setting, without the regular investigator–patient contact and rigorous assessment schedule associated with a clinical trial. Finally, as previously noted, the follow-up only lasted for 1 year, which is a relatively short time in which to compare HCRU. A longer follow-up period might provide better discernment of differences in HCRU, and this should be considered for future studies.
Conclusions
This study demonstrates that initiation of semaglutide OW in adults with T2D in a real-world setting was associated with significant decreases in weight, BMI, and HbA1c after 1 year, further contributing to the real-world evidence of the effectiveness of this intervention. Patients who were persistent to treatment and received a maximum dose of ≥ 1 mg had numerically greater reduction in weight outcomes than patients in other subgroups. Compared with initiating an SGLT2i, semaglutide OW was associated with significantly greater improvements in weight, BMI, and HbA1c, but with similar all-cause HCRU and medical costs after 1 year. Together, these analyses provide further support for the use of semaglutide OW in routine clinical practice for adults with T2D in the USA to aid glycemic and weight control.
Acknowledgments
Medical Writing/Editorial Assistance
The authors acknowledge the medical writing and editorial assistance of Aislinn Harkin and Beverly La Ferla, of Ashfield MedComms, an Inizio company (funded by Novo Nordisk Inc.).
Author Contributions
Conceptualization [James Amamoo, Lin Xie, Josh Noone], Methodology [James Amamoo, Riddhi Doshi, Lin Xie, Victoria Divino, Justin Chen, Josh Noone, Cory Gamble, Mico Guevarra, Aaron King], Formal analysis and investigation [James Amamoo, Riddhi Doshi, Lin Xie, Victoria Divino, Justin Chen, Josh Noone, Cory Gamble, Mico Guevarra, Aaron King], Writing – review and editing [James Amamoo, Riddhi Doshi, Lin Xie, Cory Gamble, Victoria Divino, Justin Chen, Josh Noone, Mico Guevarra, Aaron King], Funding acquisition [James Amamoo, Lin Xie, Josh Noone], Supervision [James Amamoo, Lin Xie, Riddhi Doshi], Resource [Lin Xie].
Funding
Sponsorship for this study was funded by Novo Nordisk Inc. (Plainsboro, NJ, USA). The journal’s Rapid Service Fee was funded by Novo Nordisk Inc. (Plainsboro, NJ, USA).
Data Availability
Original de-identified data used in this analysis were obtained from and are the property of IQVIA. IQVIA has restrictions prohibiting the authors from making the minimal data set publicly available. Interested researchers may contact IQVIA to apply to gain access to the study’s data in the same way the authors obtained the data (https://www.iqvia.com/contact/sf).
Declarations
Conflict of Interest
James Amamoo: Employee of Novo Nordisk Inc. Riddhi Doshi: Employee of IQVIA who received funding from Novo Nordisk Inc. to conduct this study. Joshua Noone: Employee of Novo Nordisk Inc. Lin Xie: Employee of Novo Nordisk Inc. Cory Gamble: Employee of Novo Nordisk Inc. and holds gifted stocks in Novo Nordisk. Mico Guevarra: Employee of Novo Nordisk Inc. and holds gifted stocks in Novo Nordisk. Victoria Divino: Employee of IQVIA who received funding from Novo Nordisk Inc. to conduct this study. New affiliation is Novo Nordisk Inc., Plainsboro, New Jersey, USA. Justin Chen: Employee of IQVIA who received funding from Novo Nordisk Inc. to conduct this study. Aaron King: Paid speaker and clinical advisor for Astellas Pharma, Abbott, Dexcom, Eli Lilly, Mannkind and Novo Nordisk Inc.
Ethical approval
The study involved use of IQVIA de-identified administrative claims and EMR data files. The Department of Health and Human Services does not consider analysis of deidentified secondary data to meet the definition for human subject research. Therefore, this study was exempt from federal regulations covering human subject research and did not require institutional review board review. This is as per exemption (d)4 from 45 CFR 46.104.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
Original de-identified data used in this analysis were obtained from and are the property of IQVIA. IQVIA has restrictions prohibiting the authors from making the minimal data set publicly available. Interested researchers may contact IQVIA to apply to gain access to the study’s data in the same way the authors obtained the data (https://www.iqvia.com/contact/sf).