ILLUSTRATION BY KIMBERLY MARTENS FOR OBG MANAGEMENT

Hypertension in pregnancy is a major challenge in current obstetric practice. Based on an analysis of the National Inpatient Sample, the Centers for Disease Control and Prevention (CDC) recently reported that from 2017 to 2019 the prevalence of hypertensive disorders in pregnancy increased from 13.3% to 15.9% of hospital deliveries.¹ During that same time period, the prevalence of pregnancy-associated hypertension, which includes preeclampsia, eclampsia, and gestational hypertension, increased from 10.8% to 13.0%.¹ The prevalence of chronic hypertension increased from 2.0% to 2.3%.¹ In 2017 and 2019, unspecified maternal hypertension was diagnosed in 0.5% and 0.6% of the sample, respectively.¹

Bruno and colleagues reported a 3-fold increase in the prevalence of HDPs from 1989 to 2020, with an acceleration in the rate of increase from 2010 to 2020.² The increase in prevalence of HDPs may be caused by an increase in the prevalence of advanced maternal age, obesity, and diabetes. Black patients are disproportionately impacted by both pregnancy-associated hypertension and chronic hypertension.¹ In 2019, the prevalence of pregnancy-associated hypertension was greater among Black patients (15.6%), than White (12.1%), Hispanic (10.6%), or Asian or Pacific Islander patients (7.7%).¹ Similarly, the prevalence of chronic hypertension was greater among Black patients (4.3%) than among White (2.0%), Hispanic (1.5%), or Asian or Pacific Islander patients (1.2%).¹ Racial/ethnic differences in HDPs may be influenced by poverty; structural racism; or lack of access to care, diet, and obesity.^3,4

HDPs are major contributors to maternal morbidity and mortality. The CDC reported that among maternal deaths occurring during the delivery hospitalization, 32% of the decedents had documented hypertension.¹ HDPs are associated with an approximately 2.5-fold increased risk of a severe morbidity, a composite measure that includes blood transfusion, acute kidney injury, disseminated intravascular coagulation, sepsis, shock, and pulmonary edema.⁵ A history of HDPs is associated with an approximately 67% increase in the lifetime risk of cardiovascular disease, including coronary artery disease, stroke, peripheral vascular disease, and heart failure.^6,7

What are the best antihypertensive medications for pregnancy?

All clinicians know that the use of angiotensin-converting-enzyme inhibitors (ACE-Is) and angiotensin-receptor-blockers (ARBs) are contraindicated in pregnancy because they cause major congenital anomalies, with an odds ratio of 1.8 (95% confidence interval [CI], 1.42-2.34), compared with no exposure.⁸ In addition, ACE-Is and ARBs increase the risk of stillbirth, with an odds ratio of 1.75 (95% CI, 1.21-2.53).⁸ No increase in congenital anomalies were detected for patients exposed to other antihypertensive medications.⁸ Prior to attempting conception, patients with chronic hypertension should discontinue ACE-Is and ARBs and initiate an alternative medication.

The most commonly used antihypertensive medications in pregnancy are labetalol, nifedipine, and methyldopa.⁹ Labetalol blocks the beta-1, beta-2, and alpha-1 adrenergic receptors.¹⁰ Nifedipine blocks calcium entry into cells through the L-type calcium channel.¹¹ Methyldopa is a central nervous system alpha-2 adrenergic agonist.¹² The dose range for these commonly used medications are labetalol 400 mg to 2,400 mg daily in divided doses every 8 to 12 hours, nifedipine extended-release 30 mg to 120 mg daily, and methyldopa 500 mg to 2 g daily in 2 to 4 divided doses. Some clinicians recommend prescribing divided doses of nifedipine extended release at doses ≥ 60 mg for patients who have bothersome adverse effects, hypotension following a single daily dose, or hypertension between single daily doses. The nifedipine extended release tablets should not be divided. If monotherapy with the maximal daily dose of labetalol does not achieve the blood pressure (BP) target, adding nifedipine as a second agent is an option.⁹ Similarly, if monotherapy with the maximal daily dose of nifedipine extended release does not achieve the BP target, adding labetalol as a second agent is an option.⁹

In a network meta-analysis of antihypertensive medications used in pregnancy, that included 61 trials and 6,923 participants, all the medications studied reduced the risk of developing severe hypertension by 30% to 70%.¹³ Sufficient data was available to also report that labetalol used to treat hypertension in pregnancy reduced the risk of developing proteinuria.¹³ Given similar efficacy among antihypertensive medications, patient comorbidities may influence the medication choice. For example, labetalol may not be the optimal medication for a patient with poorly controlled asthma due to its ability to cause bronchospasm.^14,15 Methyldopa may not be the optimal medication for a patient with depression.¹⁶ Based on the available data, labetalol, nifedipine, and methyldopa are the best antihypertensive medications for pregnant patients.

Continue to: What is an optimal BP target when treating chronic hypertension in pregnancy?...

What is an optimal BP target when treating chronic hypertension in pregnancy?

When treating chronic hypertension in pregnant patients, a concern is that reducing maternal BP may decrease uteroplacental perfusion and result in fetal growth restriction. However, a recent trial reported that a BP treatment target < 140/90 mm Hg is associated with better outcomes for both mother and newborn than withholding antihypertension medications. In the trial, 2,408 women with chronic hypertension diagnosed before 20 weeks of gestation were randomly assigned to an active treatment group with prescription of antihypertension medicines to achieve a BP target of < 140/90 mm Hg; or to a control group where no antihypertension or no additional antihypertension treatment was prescribed unless BP was ≥ 160 mm Hg systolic or ≥ 105 mm Hg diastolic.⁹ The hypertension medications prescribed to the patients in the active treatment group were labetalol (63.2%), nifedipine (33.4%), amlodipine (1.7%), methyldopa (0.5%), hydrochlorothiazide (0.3%), metoprolol (0.2%), and missing/unknown/other (0.7%).⁹

If a patient in the control group developed severe hypertension, they were started on an antihypertension medicine and the BP treatment target was < 140/90 mm Hg. Compared with the control regimen, active treatment resulted in a significant decrease in the development of preeclampsia (24.4% vs 31.1%; risk ratio [RR], 0.79; 95% CI, 0.69-0.89), severe hypertension (36.1% vs 44.3%; RR, 0.82; 95% CI, 0.74-0.90), preterm birth < 37 weeks’ gestation (27.5% vs 31.4%; RR, 0.87; 95% CI, 0.77-0.99), preterm birth < 35 weeks’ gestation (12.2% vs 16.7%; odds ratio [OR], 0.69; 95% CI, 0.55-0.88), and low birth-weight (< 2,500 g) newborns (19.2% vs 23.1%; RR, 0.83; 95% CI, 0.71-0.97).⁹ The percentage of small for gestational age birth weight below the 10th percentile was similar in the treatment and control groups, 11.2% and 10.4%, respectively (adjusted RR, 1.04; 95% CI, 0.82-1.31).⁹ The number of patients who would need to be treated to prevent one primary-outcome event was 15.⁹ The investigators concluded that for pregnant patients with chronic hypertension, the optimal BP target is < 140/90 mm Hg.⁹

When does BP reach a postpartum peak?

In pregnant patients with hypertension, BP may decrease immediately after birth. Following birth, BP tends to increase, reaching a peak 3 to 6 days postpartum.^17,18 This pattern was observed in patients with and without preeclampsia in the index pregnancy. Among 136 patients without antepartum preeclampsia, the prevalence of a diastolic BP > 89 mm Hg was 5% and 15% on postpartum days 1 and 3, respectively.¹⁷ The postpartum rise in BP may be due to mobilization of water from the extravascular to the intravascular space and excretion of total body sodium that accumulated during pregnancy.¹⁹ In one study of 998 consecutive singleton cesarean births, 7.7% of the patients with no recorded elevated BP before delivery developed de novo hypertension postpartum.²⁰ Compared with patients without antepartum or new onset postpartum hypertension, the patients who developed postpartum hypertension had a higher body mass index, were more likely to be Black and to have a history of type 2 diabetes. Compared with patients without antepartum or postpartum hypertension, the patients who developed de novo postpartum hypertension, had significantly elevated soluble fms-like tyrosine kinase-1 and significantly decreased placental growth factor, a pattern seen with preeclampsia.²⁰ These results suggest that de novo postpartum hypertension may have molecular causes similar to preeclampsia.²⁰

Postpartum hypertension should be treated with a medication that is thought to be safe for breastfeeding patients, including labetalol, nifedipine, or enalapril.^21-23 The relative infant dose of labetalol, nifedipine, and enalapril is approximately 3.6%, ≤ 3.2%, and 1.1%, respectively.²⁴ If the relative infant dose of a medication is < 10% it is generally considered to be compatible with breastfeeding.²⁵

Many obstetricians have seldom prescribed enalapril, an ACE-I. The initial dose of enalapril is 5 mg or 10 mg daily. After initiation of treatment, the dose can be adjusted based on BP measurement. The maximal daily dose is 40 mg daily in one dose or two divided doses. Similar to other hypertension medicines, enalapril therapy may cause hypotension and dizziness. Enalapril should not be used by pregnant patients because it is associated with an increased risk of congenital anomalies and fetal demise.

Does a HDP increase the risk of developing chronic hypertension?

All obstetricians know that a patient with a history of a HDP is at an increased risk for developing chronic hypertension treated with a medication, but the magnitude of the risk is less well known. In a nationwide study in Denmark, the prevalence of chronic hypertension treated with medication 10 years after delivery among patients with a history of a HDP in their first pregnancy, was 14%, 21%, and 32%, if the first pregnancy occurred in the patient’s 20s, 30s, or 40s, respectively.²⁶ The corresponding prevalence of chronic hypertension in patients without a history of a HDP was 4%, 6%, and 11%, if the first pregnancy occurred in the 20s, 30s, or 40s, respectively.²⁶ Maternal age is an important predictor of who will develop chronic hypertension within 10 years following a pregnancy with a HDP.

In modern obstetric practice, the hypertensive disorders of pregnancy are prevalent and associated with increased maternal and newborn morbidity. Appropriate treatment of hypertension with labetalol, nifedipine, or methyldopa improves maternal and newborn health. Available evidence suggests that maintaining BP < 140/90 mm Hg during pregnancy for most patients is a practical goal with significant benefit. A significant public-health concern is that an increase in the prevalence of HDPs will eventually translate into an increase in chronic hypertension and the attendant complications of heart attack, heart failure, stroke, and renal insufficiency. Recognizing the increased prevalence of HDPs, ObGyns will need to alert patients to their long-term health risks and coordinate appropriate follow-up and treatment to optimize the future health of their patients. ●

ILLUSTRATION BY KIMBERLY MARTENS FOR OBG MANAGEMENT

Hypertension in pregnancy is a major challenge in current obstetric practice. Based on an analysis of the National Inpatient Sample, the Centers for Disease Control and Prevention (CDC) recently reported that from 2017 to 2019 the prevalence of hypertensive disorders in pregnancy increased from 13.3% to 15.9% of hospital deliveries.¹ During that same time period, the prevalence of pregnancy-associated hypertension, which includes preeclampsia, eclampsia, and gestational hypertension, increased from 10.8% to 13.0%.¹ The prevalence of chronic hypertension increased from 2.0% to 2.3%.¹ In 2017 and 2019, unspecified maternal hypertension was diagnosed in 0.5% and 0.6% of the sample, respectively.¹

Bruno and colleagues reported a 3-fold increase in the prevalence of HDPs from 1989 to 2020, with an acceleration in the rate of increase from 2010 to 2020.² The increase in prevalence of HDPs may be caused by an increase in the prevalence of advanced maternal age, obesity, and diabetes. Black patients are disproportionately impacted by both pregnancy-associated hypertension and chronic hypertension.¹ In 2019, the prevalence of pregnancy-associated hypertension was greater among Black patients (15.6%), than White (12.1%), Hispanic (10.6%), or Asian or Pacific Islander patients (7.7%).¹ Similarly, the prevalence of chronic hypertension was greater among Black patients (4.3%) than among White (2.0%), Hispanic (1.5%), or Asian or Pacific Islander patients (1.2%).¹ Racial/ethnic differences in HDPs may be influenced by poverty; structural racism; or lack of access to care, diet, and obesity.^3,4

HDPs are major contributors to maternal morbidity and mortality. The CDC reported that among maternal deaths occurring during the delivery hospitalization, 32% of the decedents had documented hypertension.¹ HDPs are associated with an approximately 2.5-fold increased risk of a severe morbidity, a composite measure that includes blood transfusion, acute kidney injury, disseminated intravascular coagulation, sepsis, shock, and pulmonary edema.⁵ A history of HDPs is associated with an approximately 67% increase in the lifetime risk of cardiovascular disease, including coronary artery disease, stroke, peripheral vascular disease, and heart failure.^6,7

What are the best antihypertensive medications for pregnancy?

All clinicians know that the use of angiotensin-converting-enzyme inhibitors (ACE-Is) and angiotensin-receptor-blockers (ARBs) are contraindicated in pregnancy because they cause major congenital anomalies, with an odds ratio of 1.8 (95% confidence interval [CI], 1.42-2.34), compared with no exposure.⁸ In addition, ACE-Is and ARBs increase the risk of stillbirth, with an odds ratio of 1.75 (95% CI, 1.21-2.53).⁸ No increase in congenital anomalies were detected for patients exposed to other antihypertensive medications.⁸ Prior to attempting conception, patients with chronic hypertension should discontinue ACE-Is and ARBs and initiate an alternative medication.

The most commonly used antihypertensive medications in pregnancy are labetalol, nifedipine, and methyldopa.⁹ Labetalol blocks the beta-1, beta-2, and alpha-1 adrenergic receptors.¹⁰ Nifedipine blocks calcium entry into cells through the L-type calcium channel.¹¹ Methyldopa is a central nervous system alpha-2 adrenergic agonist.¹² The dose range for these commonly used medications are labetalol 400 mg to 2,400 mg daily in divided doses every 8 to 12 hours, nifedipine extended-release 30 mg to 120 mg daily, and methyldopa 500 mg to 2 g daily in 2 to 4 divided doses. Some clinicians recommend prescribing divided doses of nifedipine extended release at doses ≥ 60 mg for patients who have bothersome adverse effects, hypotension following a single daily dose, or hypertension between single daily doses. The nifedipine extended release tablets should not be divided. If monotherapy with the maximal daily dose of labetalol does not achieve the blood pressure (BP) target, adding nifedipine as a second agent is an option.⁹ Similarly, if monotherapy with the maximal daily dose of nifedipine extended release does not achieve the BP target, adding labetalol as a second agent is an option.⁹

In a network meta-analysis of antihypertensive medications used in pregnancy, that included 61 trials and 6,923 participants, all the medications studied reduced the risk of developing severe hypertension by 30% to 70%.¹³ Sufficient data was available to also report that labetalol used to treat hypertension in pregnancy reduced the risk of developing proteinuria.¹³ Given similar efficacy among antihypertensive medications, patient comorbidities may influence the medication choice. For example, labetalol may not be the optimal medication for a patient with poorly controlled asthma due to its ability to cause bronchospasm.^14,15 Methyldopa may not be the optimal medication for a patient with depression.¹⁶ Based on the available data, labetalol, nifedipine, and methyldopa are the best antihypertensive medications for pregnant patients.

Continue to: What is an optimal BP target when treating chronic hypertension in pregnancy?...

What is an optimal BP target when treating chronic hypertension in pregnancy?

When treating chronic hypertension in pregnant patients, a concern is that reducing maternal BP may decrease uteroplacental perfusion and result in fetal growth restriction. However, a recent trial reported that a BP treatment target < 140/90 mm Hg is associated with better outcomes for both mother and newborn than withholding antihypertension medications. In the trial, 2,408 women with chronic hypertension diagnosed before 20 weeks of gestation were randomly assigned to an active treatment group with prescription of antihypertension medicines to achieve a BP target of < 140/90 mm Hg; or to a control group where no antihypertension or no additional antihypertension treatment was prescribed unless BP was ≥ 160 mm Hg systolic or ≥ 105 mm Hg diastolic.⁹ The hypertension medications prescribed to the patients in the active treatment group were labetalol (63.2%), nifedipine (33.4%), amlodipine (1.7%), methyldopa (0.5%), hydrochlorothiazide (0.3%), metoprolol (0.2%), and missing/unknown/other (0.7%).⁹

If a patient in the control group developed severe hypertension, they were started on an antihypertension medicine and the BP treatment target was < 140/90 mm Hg. Compared with the control regimen, active treatment resulted in a significant decrease in the development of preeclampsia (24.4% vs 31.1%; risk ratio [RR], 0.79; 95% CI, 0.69-0.89), severe hypertension (36.1% vs 44.3%; RR, 0.82; 95% CI, 0.74-0.90), preterm birth < 37 weeks’ gestation (27.5% vs 31.4%; RR, 0.87; 95% CI, 0.77-0.99), preterm birth < 35 weeks’ gestation (12.2% vs 16.7%; odds ratio [OR], 0.69; 95% CI, 0.55-0.88), and low birth-weight (< 2,500 g) newborns (19.2% vs 23.1%; RR, 0.83; 95% CI, 0.71-0.97).⁹ The percentage of small for gestational age birth weight below the 10th percentile was similar in the treatment and control groups, 11.2% and 10.4%, respectively (adjusted RR, 1.04; 95% CI, 0.82-1.31).⁹ The number of patients who would need to be treated to prevent one primary-outcome event was 15.⁹ The investigators concluded that for pregnant patients with chronic hypertension, the optimal BP target is < 140/90 mm Hg.⁹

When does BP reach a postpartum peak?

In pregnant patients with hypertension, BP may decrease immediately after birth. Following birth, BP tends to increase, reaching a peak 3 to 6 days postpartum.^17,18 This pattern was observed in patients with and without preeclampsia in the index pregnancy. Among 136 patients without antepartum preeclampsia, the prevalence of a diastolic BP > 89 mm Hg was 5% and 15% on postpartum days 1 and 3, respectively.¹⁷ The postpartum rise in BP may be due to mobilization of water from the extravascular to the intravascular space and excretion of total body sodium that accumulated during pregnancy.¹⁹ In one study of 998 consecutive singleton cesarean births, 7.7% of the patients with no recorded elevated BP before delivery developed de novo hypertension postpartum.²⁰ Compared with patients without antepartum or new onset postpartum hypertension, the patients who developed postpartum hypertension had a higher body mass index, were more likely to be Black and to have a history of type 2 diabetes. Compared with patients without antepartum or postpartum hypertension, the patients who developed de novo postpartum hypertension, had significantly elevated soluble fms-like tyrosine kinase-1 and significantly decreased placental growth factor, a pattern seen with preeclampsia.²⁰ These results suggest that de novo postpartum hypertension may have molecular causes similar to preeclampsia.²⁰

Postpartum hypertension should be treated with a medication that is thought to be safe for breastfeeding patients, including labetalol, nifedipine, or enalapril.^21-23 The relative infant dose of labetalol, nifedipine, and enalapril is approximately 3.6%, ≤ 3.2%, and 1.1%, respectively.²⁴ If the relative infant dose of a medication is < 10% it is generally considered to be compatible with breastfeeding.²⁵

Many obstetricians have seldom prescribed enalapril, an ACE-I. The initial dose of enalapril is 5 mg or 10 mg daily. After initiation of treatment, the dose can be adjusted based on BP measurement. The maximal daily dose is 40 mg daily in one dose or two divided doses. Similar to other hypertension medicines, enalapril therapy may cause hypotension and dizziness. Enalapril should not be used by pregnant patients because it is associated with an increased risk of congenital anomalies and fetal demise.

Does a HDP increase the risk of developing chronic hypertension?

All obstetricians know that a patient with a history of a HDP is at an increased risk for developing chronic hypertension treated with a medication, but the magnitude of the risk is less well known. In a nationwide study in Denmark, the prevalence of chronic hypertension treated with medication 10 years after delivery among patients with a history of a HDP in their first pregnancy, was 14%, 21%, and 32%, if the first pregnancy occurred in the patient’s 20s, 30s, or 40s, respectively.²⁶ The corresponding prevalence of chronic hypertension in patients without a history of a HDP was 4%, 6%, and 11%, if the first pregnancy occurred in the 20s, 30s, or 40s, respectively.²⁶ Maternal age is an important predictor of who will develop chronic hypertension within 10 years following a pregnancy with a HDP.

In modern obstetric practice, the hypertensive disorders of pregnancy are prevalent and associated with increased maternal and newborn morbidity. Appropriate treatment of hypertension with labetalol, nifedipine, or methyldopa improves maternal and newborn health. Available evidence suggests that maintaining BP < 140/90 mm Hg during pregnancy for most patients is a practical goal with significant benefit. A significant public-health concern is that an increase in the prevalence of HDPs will eventually translate into an increase in chronic hypertension and the attendant complications of heart attack, heart failure, stroke, and renal insufficiency. Recognizing the increased prevalence of HDPs, ObGyns will need to alert patients to their long-term health risks and coordinate appropriate follow-up and treatment to optimize the future health of their patients. ●

ILLUSTRATION BY KIMBERLY MARTENS FOR OBG MANAGEMENT

Hypertension in pregnancy is a major challenge in current obstetric practice. Based on an analysis of the National Inpatient Sample, the Centers for Disease Control and Prevention (CDC) recently reported that from 2017 to 2019 the prevalence of hypertensive disorders in pregnancy increased from 13.3% to 15.9% of hospital deliveries.¹ During that same time period, the prevalence of pregnancy-associated hypertension, which includes preeclampsia, eclampsia, and gestational hypertension, increased from 10.8% to 13.0%.¹ The prevalence of chronic hypertension increased from 2.0% to 2.3%.¹ In 2017 and 2019, unspecified maternal hypertension was diagnosed in 0.5% and 0.6% of the sample, respectively.¹

Bruno and colleagues reported a 3-fold increase in the prevalence of HDPs from 1989 to 2020, with an acceleration in the rate of increase from 2010 to 2020.² The increase in prevalence of HDPs may be caused by an increase in the prevalence of advanced maternal age, obesity, and diabetes. Black patients are disproportionately impacted by both pregnancy-associated hypertension and chronic hypertension.¹ In 2019, the prevalence of pregnancy-associated hypertension was greater among Black patients (15.6%), than White (12.1%), Hispanic (10.6%), or Asian or Pacific Islander patients (7.7%).¹ Similarly, the prevalence of chronic hypertension was greater among Black patients (4.3%) than among White (2.0%), Hispanic (1.5%), or Asian or Pacific Islander patients (1.2%).¹ Racial/ethnic differences in HDPs may be influenced by poverty; structural racism; or lack of access to care, diet, and obesity.^3,4

HDPs are major contributors to maternal morbidity and mortality. The CDC reported that among maternal deaths occurring during the delivery hospitalization, 32% of the decedents had documented hypertension.¹ HDPs are associated with an approximately 2.5-fold increased risk of a severe morbidity, a composite measure that includes blood transfusion, acute kidney injury, disseminated intravascular coagulation, sepsis, shock, and pulmonary edema.⁵ A history of HDPs is associated with an approximately 67% increase in the lifetime risk of cardiovascular disease, including coronary artery disease, stroke, peripheral vascular disease, and heart failure.^6,7

What are the best antihypertensive medications for pregnancy?

All clinicians know that the use of angiotensin-converting-enzyme inhibitors (ACE-Is) and angiotensin-receptor-blockers (ARBs) are contraindicated in pregnancy because they cause major congenital anomalies, with an odds ratio of 1.8 (95% confidence interval [CI], 1.42-2.34), compared with no exposure.⁸ In addition, ACE-Is and ARBs increase the risk of stillbirth, with an odds ratio of 1.75 (95% CI, 1.21-2.53).⁸ No increase in congenital anomalies were detected for patients exposed to other antihypertensive medications.⁸ Prior to attempting conception, patients with chronic hypertension should discontinue ACE-Is and ARBs and initiate an alternative medication.

The most commonly used antihypertensive medications in pregnancy are labetalol, nifedipine, and methyldopa.⁹ Labetalol blocks the beta-1, beta-2, and alpha-1 adrenergic receptors.¹⁰ Nifedipine blocks calcium entry into cells through the L-type calcium channel.¹¹ Methyldopa is a central nervous system alpha-2 adrenergic agonist.¹² The dose range for these commonly used medications are labetalol 400 mg to 2,400 mg daily in divided doses every 8 to 12 hours, nifedipine extended-release 30 mg to 120 mg daily, and methyldopa 500 mg to 2 g daily in 2 to 4 divided doses. Some clinicians recommend prescribing divided doses of nifedipine extended release at doses ≥ 60 mg for patients who have bothersome adverse effects, hypotension following a single daily dose, or hypertension between single daily doses. The nifedipine extended release tablets should not be divided. If monotherapy with the maximal daily dose of labetalol does not achieve the blood pressure (BP) target, adding nifedipine as a second agent is an option.⁹ Similarly, if monotherapy with the maximal daily dose of nifedipine extended release does not achieve the BP target, adding labetalol as a second agent is an option.⁹

In a network meta-analysis of antihypertensive medications used in pregnancy, that included 61 trials and 6,923 participants, all the medications studied reduced the risk of developing severe hypertension by 30% to 70%.¹³ Sufficient data was available to also report that labetalol used to treat hypertension in pregnancy reduced the risk of developing proteinuria.¹³ Given similar efficacy among antihypertensive medications, patient comorbidities may influence the medication choice. For example, labetalol may not be the optimal medication for a patient with poorly controlled asthma due to its ability to cause bronchospasm.^14,15 Methyldopa may not be the optimal medication for a patient with depression.¹⁶ Based on the available data, labetalol, nifedipine, and methyldopa are the best antihypertensive medications for pregnant patients.

Continue to: What is an optimal BP target when treating chronic hypertension in pregnancy?...

What is an optimal BP target when treating chronic hypertension in pregnancy?

When treating chronic hypertension in pregnant patients, a concern is that reducing maternal BP may decrease uteroplacental perfusion and result in fetal growth restriction. However, a recent trial reported that a BP treatment target < 140/90 mm Hg is associated with better outcomes for both mother and newborn than withholding antihypertension medications. In the trial, 2,408 women with chronic hypertension diagnosed before 20 weeks of gestation were randomly assigned to an active treatment group with prescription of antihypertension medicines to achieve a BP target of < 140/90 mm Hg; or to a control group where no antihypertension or no additional antihypertension treatment was prescribed unless BP was ≥ 160 mm Hg systolic or ≥ 105 mm Hg diastolic.⁹ The hypertension medications prescribed to the patients in the active treatment group were labetalol (63.2%), nifedipine (33.4%), amlodipine (1.7%), methyldopa (0.5%), hydrochlorothiazide (0.3%), metoprolol (0.2%), and missing/unknown/other (0.7%).⁹

If a patient in the control group developed severe hypertension, they were started on an antihypertension medicine and the BP treatment target was < 140/90 mm Hg. Compared with the control regimen, active treatment resulted in a significant decrease in the development of preeclampsia (24.4% vs 31.1%; risk ratio [RR], 0.79; 95% CI, 0.69-0.89), severe hypertension (36.1% vs 44.3%; RR, 0.82; 95% CI, 0.74-0.90), preterm birth < 37 weeks’ gestation (27.5% vs 31.4%; RR, 0.87; 95% CI, 0.77-0.99), preterm birth < 35 weeks’ gestation (12.2% vs 16.7%; odds ratio [OR], 0.69; 95% CI, 0.55-0.88), and low birth-weight (< 2,500 g) newborns (19.2% vs 23.1%; RR, 0.83; 95% CI, 0.71-0.97).⁹ The percentage of small for gestational age birth weight below the 10th percentile was similar in the treatment and control groups, 11.2% and 10.4%, respectively (adjusted RR, 1.04; 95% CI, 0.82-1.31).⁹ The number of patients who would need to be treated to prevent one primary-outcome event was 15.⁹ The investigators concluded that for pregnant patients with chronic hypertension, the optimal BP target is < 140/90 mm Hg.⁹

When does BP reach a postpartum peak?

In pregnant patients with hypertension, BP may decrease immediately after birth. Following birth, BP tends to increase, reaching a peak 3 to 6 days postpartum.^17,18 This pattern was observed in patients with and without preeclampsia in the index pregnancy. Among 136 patients without antepartum preeclampsia, the prevalence of a diastolic BP > 89 mm Hg was 5% and 15% on postpartum days 1 and 3, respectively.¹⁷ The postpartum rise in BP may be due to mobilization of water from the extravascular to the intravascular space and excretion of total body sodium that accumulated during pregnancy.¹⁹ In one study of 998 consecutive singleton cesarean births, 7.7% of the patients with no recorded elevated BP before delivery developed de novo hypertension postpartum.²⁰ Compared with patients without antepartum or new onset postpartum hypertension, the patients who developed postpartum hypertension had a higher body mass index, were more likely to be Black and to have a history of type 2 diabetes. Compared with patients without antepartum or postpartum hypertension, the patients who developed de novo postpartum hypertension, had significantly elevated soluble fms-like tyrosine kinase-1 and significantly decreased placental growth factor, a pattern seen with preeclampsia.²⁰ These results suggest that de novo postpartum hypertension may have molecular causes similar to preeclampsia.²⁰

Postpartum hypertension should be treated with a medication that is thought to be safe for breastfeeding patients, including labetalol, nifedipine, or enalapril.^21-23 The relative infant dose of labetalol, nifedipine, and enalapril is approximately 3.6%, ≤ 3.2%, and 1.1%, respectively.²⁴ If the relative infant dose of a medication is < 10% it is generally considered to be compatible with breastfeeding.²⁵

Many obstetricians have seldom prescribed enalapril, an ACE-I. The initial dose of enalapril is 5 mg or 10 mg daily. After initiation of treatment, the dose can be adjusted based on BP measurement. The maximal daily dose is 40 mg daily in one dose or two divided doses. Similar to other hypertension medicines, enalapril therapy may cause hypotension and dizziness. Enalapril should not be used by pregnant patients because it is associated with an increased risk of congenital anomalies and fetal demise.

Does a HDP increase the risk of developing chronic hypertension?

All obstetricians know that a patient with a history of a HDP is at an increased risk for developing chronic hypertension treated with a medication, but the magnitude of the risk is less well known. In a nationwide study in Denmark, the prevalence of chronic hypertension treated with medication 10 years after delivery among patients with a history of a HDP in their first pregnancy, was 14%, 21%, and 32%, if the first pregnancy occurred in the patient’s 20s, 30s, or 40s, respectively.²⁶ The corresponding prevalence of chronic hypertension in patients without a history of a HDP was 4%, 6%, and 11%, if the first pregnancy occurred in the 20s, 30s, or 40s, respectively.²⁶ Maternal age is an important predictor of who will develop chronic hypertension within 10 years following a pregnancy with a HDP.

In modern obstetric practice, the hypertensive disorders of pregnancy are prevalent and associated with increased maternal and newborn morbidity. Appropriate treatment of hypertension with labetalol, nifedipine, or methyldopa improves maternal and newborn health. Available evidence suggests that maintaining BP < 140/90 mm Hg during pregnancy for most patients is a practical goal with significant benefit. A significant public-health concern is that an increase in the prevalence of HDPs will eventually translate into an increase in chronic hypertension and the attendant complications of heart attack, heart failure, stroke, and renal insufficiency. Recognizing the increased prevalence of HDPs, ObGyns will need to alert patients to their long-term health risks and coordinate appropriate follow-up and treatment to optimize the future health of their patients. ●

Vidyard Video

 Additional videos from SGS are available here, including these recent offerings:

• Tips for navigating the altered retroperitoneum

• A guide to understanding your anatomy

• Resection of five-centimeter cesarean scar ectopic pregnancy and isthmocele repair
  using vascular clamps

Vidyard Video

 Additional videos from SGS are available here, including these recent offerings:

• Tips for navigating the altered retroperitoneum

• A guide to understanding your anatomy

• Resection of five-centimeter cesarean scar ectopic pregnancy and isthmocele repair
  using vascular clamps

Vidyard Video

 Additional videos from SGS are available here, including these recent offerings:

• Tips for navigating the altered retroperitoneum

• A guide to understanding your anatomy

• Resection of five-centimeter cesarean scar ectopic pregnancy and isthmocele repair
  using vascular clamps

A claim that drinking tea might protect people against developing type 2 diabetes has been met with caution from multiple experts ahead of the annual meeting of the European Association for the Study of Diabetes.

The claim is that people who drink four or more cups of tea every day – specifically green, Oolong, or black tea – are 17% less likely to develop type 2 diabetes than those who do not drink tea. Drinking fewer cups of tea per day was not found to confer any benefit.

“Our results are exciting because they suggest that people can do something as simple as drinking four cups of tea a day to potentially lessen their risk of developing type 2 diabetes,” Xiaying Li of Wuhan (China) University of Science and Technology is quoted as saying in an official EASD press release.

NataliTerr/Fotolia.com

“It is possible that particular components in tea, such as polyphenols, may reduce blood glucose levels, but a sufficient amount of these bioactive compounds may be needed to be effective,” Dr. Li added.

“The words ‘suggest’ and ‘potentially’ are crucial here,” said Kevin McConway, PhD, MSc, MBA, emeritus professor of applied statistics at The Open University, said in a separate statement to the press that reeled in Dr. Li’s enthusiasm.

“Tea drinking would only be useful for reducing diabetes risk if the tea drinking causes reductions in risk, that is, if the risk is reduced if you drink the tea and not if you don’t – and this study simply can’t show whether it does this or not,” Dr. Conway stressed.

Naveed Sattar, FMedSci FRCPath FRCPGlas FRSE, professor of metabolic medicine at the University of Glasgow, was also cautiously critical. “There is no good trial evidence whatsoever that the chemicals in tea prevent diabetes,” he observed separately.

“So, I suspect its more about tea being healthier (less calorific) than many alternative drinks or tea drinkers leading healthier lives more generally.”

Dr. Sattar added that it could be that people who drink tea might also be avoiding drinking more harmful sugary drinks and have other health behaviors that might lead them to have a lower risk for type 2 diabetes.

Time for tea?

Dr. Li will present the findings of two analyses on Sept. 21 at the EASD meeting: the first a large observational cohort study and the second an updated systematic review and meta-analysis.

For the cohort study, Dr. Li and her coauthors took data on more than 5,100 adults who had participated in the long-running and ongoing China Health and Nutrition Survey (CHNS). Information on tea drinking behavior was extracted from questionnaires that had been filled out at two time points – 1997 and 2009 – and they determined whether people had developed type 2 diabetes according to American Diabetes Association criteria.

Nearly half, 45.8%, were found to be tea drinkers, and 10% of the population they sampled had developed type 2 diabetes. No association between tea drinking and type 2 diabetes development was found, however, with the hazard ratio comparing tea drinkers and non–tea drinkers sitting firmly at 1.02. Moreover, a sensitivity analysis that excluded participants who had developed type 2 diabetes in the first 3 years of follow-up did not change the result.

Things were slightly different when Dr. Li and associates performed their meta-analysis that involved analyzing data on more than 1 million participants in 19 studies conducted in eight countries that had been published up to September 2021.

Here, they found there was a significant (P < .003) linear association between tea consumption and having type 2 diabetes, with the relative risk of developing type 2 diabetes decreasing by 0.986 for every additional cup of tea that was drunk.

HRs for the development of type 2 diabetes in tea drinkers versus non–tea drinkers were 1.00 for those who drank less than one cup per day, 0.96 for those who had one to two cups, and 0.84 for those who drank four or more cups.

“While more research needs to be done to determine the exact dosage and mechanisms behind these observations, our findings suggest that drinking tea is beneficial in reducing the risk of type 2 diabetes, but only at high doses (at least 4 cups a day)”, said Dr. Li.

Perhaps, “we did not find an association between tea drinking and type 2 diabetes in our cohort study because we did not look at higher tea consumption,” she added.

Tempest in a teacup

“This is large, observational data. It’s not a randomized controlled trial so there’s plenty of room for data to be misunderstood,” warned Matt Sydes, MSc, professor of clinical trials & methodology at the MRC Clinical Trials Unit, University College London.

“Everyone drinks fluids. If there is an effect here (and that’s a big if), it might be not about the tea they drink, but about what they don’t drink. One can’t tell at the moment. It seems unlikely that a large randomized controlled trial could be done to disambiguate” added Dr. Sydes

“Being only a conference abstract, it is difficult to assess the quality of this research,” Baptiste Leurent, PhD, a medical statistician also working at University College London, said. Not only was the cohort study observational, so were all the other studies included in the meta-analysis, he pointed out.

“Therefore, no cause-effect conclusions can be drawn. The association could simply be due to other factors, such as those drinking more tea having a healthier lifestyle. It does not seem that the authors tried to control for confounders, which is usually difficult in meta-analysis,” Dr. Leurent said.

“There is reason to be a bit skeptical at this point; we really need to have the full details to assess it properly,” said Jonathan Cook of the Centre for Statistics in Medicine at the University of Oxford (England). “It’s a fair attempt to look at this, but not cutting edge, [using] fairly standard approaches.”

Similar studies have shown a reduced risk associated with coffee drinking, noted Duane Mellor, PhD, a registered dietitian and senior teaching fellow at Aston University in Birmingham.

“The important take-home message is that lifestyle is important in managing risk of developing type 2 diabetes,” Dr. Mellor said.

“That includes choosing low-calorie drinks including mainly water as well as unsweetened tea and coffee as your drinks of choice as part of a healthy lifestyle.”

The study was funded by the Young Talents Project of Hubei Provincial Health Commission, the Science and Technology Research Key Project of Education Department of Hubei Province, the Sanuo Diabetes Charity Foundation, and the Xiangyang Science and Technology Plan Project, all based in China. Dr. Li had no conflicts of interest to disclose. Dr. McConway is a Trustee and on the advisory committee of The Science Media Centre.  Dr. Sattar has consulted for many companies that make diabetes and cardiovascular drugs and has been involved in multiple trials of lifestyle approaches for the prevention and remission of diabetes. Dr. Sydes, Dr. Leurent, Dr. Cook, and Dr. Mellor had no conflicts of interest to report.

A claim that drinking tea might protect people against developing type 2 diabetes has been met with caution from multiple experts ahead of the annual meeting of the European Association for the Study of Diabetes.

The claim is that people who drink four or more cups of tea every day – specifically green, Oolong, or black tea – are 17% less likely to develop type 2 diabetes than those who do not drink tea. Drinking fewer cups of tea per day was not found to confer any benefit.

“Our results are exciting because they suggest that people can do something as simple as drinking four cups of tea a day to potentially lessen their risk of developing type 2 diabetes,” Xiaying Li of Wuhan (China) University of Science and Technology is quoted as saying in an official EASD press release.

NataliTerr/Fotolia.com

“It is possible that particular components in tea, such as polyphenols, may reduce blood glucose levels, but a sufficient amount of these bioactive compounds may be needed to be effective,” Dr. Li added.

“The words ‘suggest’ and ‘potentially’ are crucial here,” said Kevin McConway, PhD, MSc, MBA, emeritus professor of applied statistics at The Open University, said in a separate statement to the press that reeled in Dr. Li’s enthusiasm.

“Tea drinking would only be useful for reducing diabetes risk if the tea drinking causes reductions in risk, that is, if the risk is reduced if you drink the tea and not if you don’t – and this study simply can’t show whether it does this or not,” Dr. Conway stressed.

Naveed Sattar, FMedSci FRCPath FRCPGlas FRSE, professor of metabolic medicine at the University of Glasgow, was also cautiously critical. “There is no good trial evidence whatsoever that the chemicals in tea prevent diabetes,” he observed separately.

“So, I suspect its more about tea being healthier (less calorific) than many alternative drinks or tea drinkers leading healthier lives more generally.”

Dr. Sattar added that it could be that people who drink tea might also be avoiding drinking more harmful sugary drinks and have other health behaviors that might lead them to have a lower risk for type 2 diabetes.

Time for tea?

Dr. Li will present the findings of two analyses on Sept. 21 at the EASD meeting: the first a large observational cohort study and the second an updated systematic review and meta-analysis.

For the cohort study, Dr. Li and her coauthors took data on more than 5,100 adults who had participated in the long-running and ongoing China Health and Nutrition Survey (CHNS). Information on tea drinking behavior was extracted from questionnaires that had been filled out at two time points – 1997 and 2009 – and they determined whether people had developed type 2 diabetes according to American Diabetes Association criteria.

Nearly half, 45.8%, were found to be tea drinkers, and 10% of the population they sampled had developed type 2 diabetes. No association between tea drinking and type 2 diabetes development was found, however, with the hazard ratio comparing tea drinkers and non–tea drinkers sitting firmly at 1.02. Moreover, a sensitivity analysis that excluded participants who had developed type 2 diabetes in the first 3 years of follow-up did not change the result.

Things were slightly different when Dr. Li and associates performed their meta-analysis that involved analyzing data on more than 1 million participants in 19 studies conducted in eight countries that had been published up to September 2021.

Here, they found there was a significant (P < .003) linear association between tea consumption and having type 2 diabetes, with the relative risk of developing type 2 diabetes decreasing by 0.986 for every additional cup of tea that was drunk.

HRs for the development of type 2 diabetes in tea drinkers versus non–tea drinkers were 1.00 for those who drank less than one cup per day, 0.96 for those who had one to two cups, and 0.84 for those who drank four or more cups.

“While more research needs to be done to determine the exact dosage and mechanisms behind these observations, our findings suggest that drinking tea is beneficial in reducing the risk of type 2 diabetes, but only at high doses (at least 4 cups a day)”, said Dr. Li.

Perhaps, “we did not find an association between tea drinking and type 2 diabetes in our cohort study because we did not look at higher tea consumption,” she added.

Tempest in a teacup

“This is large, observational data. It’s not a randomized controlled trial so there’s plenty of room for data to be misunderstood,” warned Matt Sydes, MSc, professor of clinical trials & methodology at the MRC Clinical Trials Unit, University College London.

“Everyone drinks fluids. If there is an effect here (and that’s a big if), it might be not about the tea they drink, but about what they don’t drink. One can’t tell at the moment. It seems unlikely that a large randomized controlled trial could be done to disambiguate” added Dr. Sydes

“Being only a conference abstract, it is difficult to assess the quality of this research,” Baptiste Leurent, PhD, a medical statistician also working at University College London, said. Not only was the cohort study observational, so were all the other studies included in the meta-analysis, he pointed out.

“Therefore, no cause-effect conclusions can be drawn. The association could simply be due to other factors, such as those drinking more tea having a healthier lifestyle. It does not seem that the authors tried to control for confounders, which is usually difficult in meta-analysis,” Dr. Leurent said.

“There is reason to be a bit skeptical at this point; we really need to have the full details to assess it properly,” said Jonathan Cook of the Centre for Statistics in Medicine at the University of Oxford (England). “It’s a fair attempt to look at this, but not cutting edge, [using] fairly standard approaches.”

Similar studies have shown a reduced risk associated with coffee drinking, noted Duane Mellor, PhD, a registered dietitian and senior teaching fellow at Aston University in Birmingham.

“The important take-home message is that lifestyle is important in managing risk of developing type 2 diabetes,” Dr. Mellor said.

“That includes choosing low-calorie drinks including mainly water as well as unsweetened tea and coffee as your drinks of choice as part of a healthy lifestyle.”

The study was funded by the Young Talents Project of Hubei Provincial Health Commission, the Science and Technology Research Key Project of Education Department of Hubei Province, the Sanuo Diabetes Charity Foundation, and the Xiangyang Science and Technology Plan Project, all based in China. Dr. Li had no conflicts of interest to disclose. Dr. McConway is a Trustee and on the advisory committee of The Science Media Centre.  Dr. Sattar has consulted for many companies that make diabetes and cardiovascular drugs and has been involved in multiple trials of lifestyle approaches for the prevention and remission of diabetes. Dr. Sydes, Dr. Leurent, Dr. Cook, and Dr. Mellor had no conflicts of interest to report.

A claim that drinking tea might protect people against developing type 2 diabetes has been met with caution from multiple experts ahead of the annual meeting of the European Association for the Study of Diabetes.

The claim is that people who drink four or more cups of tea every day – specifically green, Oolong, or black tea – are 17% less likely to develop type 2 diabetes than those who do not drink tea. Drinking fewer cups of tea per day was not found to confer any benefit.

“Our results are exciting because they suggest that people can do something as simple as drinking four cups of tea a day to potentially lessen their risk of developing type 2 diabetes,” Xiaying Li of Wuhan (China) University of Science and Technology is quoted as saying in an official EASD press release.

NataliTerr/Fotolia.com

“It is possible that particular components in tea, such as polyphenols, may reduce blood glucose levels, but a sufficient amount of these bioactive compounds may be needed to be effective,” Dr. Li added.

“The words ‘suggest’ and ‘potentially’ are crucial here,” said Kevin McConway, PhD, MSc, MBA, emeritus professor of applied statistics at The Open University, said in a separate statement to the press that reeled in Dr. Li’s enthusiasm.

“Tea drinking would only be useful for reducing diabetes risk if the tea drinking causes reductions in risk, that is, if the risk is reduced if you drink the tea and not if you don’t – and this study simply can’t show whether it does this or not,” Dr. Conway stressed.

Naveed Sattar, FMedSci FRCPath FRCPGlas FRSE, professor of metabolic medicine at the University of Glasgow, was also cautiously critical. “There is no good trial evidence whatsoever that the chemicals in tea prevent diabetes,” he observed separately.

“So, I suspect its more about tea being healthier (less calorific) than many alternative drinks or tea drinkers leading healthier lives more generally.”

Dr. Sattar added that it could be that people who drink tea might also be avoiding drinking more harmful sugary drinks and have other health behaviors that might lead them to have a lower risk for type 2 diabetes.

Time for tea?

Dr. Li will present the findings of two analyses on Sept. 21 at the EASD meeting: the first a large observational cohort study and the second an updated systematic review and meta-analysis.

For the cohort study, Dr. Li and her coauthors took data on more than 5,100 adults who had participated in the long-running and ongoing China Health and Nutrition Survey (CHNS). Information on tea drinking behavior was extracted from questionnaires that had been filled out at two time points – 1997 and 2009 – and they determined whether people had developed type 2 diabetes according to American Diabetes Association criteria.

Nearly half, 45.8%, were found to be tea drinkers, and 10% of the population they sampled had developed type 2 diabetes. No association between tea drinking and type 2 diabetes development was found, however, with the hazard ratio comparing tea drinkers and non–tea drinkers sitting firmly at 1.02. Moreover, a sensitivity analysis that excluded participants who had developed type 2 diabetes in the first 3 years of follow-up did not change the result.

Things were slightly different when Dr. Li and associates performed their meta-analysis that involved analyzing data on more than 1 million participants in 19 studies conducted in eight countries that had been published up to September 2021.

Here, they found there was a significant (P < .003) linear association between tea consumption and having type 2 diabetes, with the relative risk of developing type 2 diabetes decreasing by 0.986 for every additional cup of tea that was drunk.

HRs for the development of type 2 diabetes in tea drinkers versus non–tea drinkers were 1.00 for those who drank less than one cup per day, 0.96 for those who had one to two cups, and 0.84 for those who drank four or more cups.

“While more research needs to be done to determine the exact dosage and mechanisms behind these observations, our findings suggest that drinking tea is beneficial in reducing the risk of type 2 diabetes, but only at high doses (at least 4 cups a day)”, said Dr. Li.

Perhaps, “we did not find an association between tea drinking and type 2 diabetes in our cohort study because we did not look at higher tea consumption,” she added.

Tempest in a teacup

“This is large, observational data. It’s not a randomized controlled trial so there’s plenty of room for data to be misunderstood,” warned Matt Sydes, MSc, professor of clinical trials & methodology at the MRC Clinical Trials Unit, University College London.

“Everyone drinks fluids. If there is an effect here (and that’s a big if), it might be not about the tea they drink, but about what they don’t drink. One can’t tell at the moment. It seems unlikely that a large randomized controlled trial could be done to disambiguate” added Dr. Sydes

“Being only a conference abstract, it is difficult to assess the quality of this research,” Baptiste Leurent, PhD, a medical statistician also working at University College London, said. Not only was the cohort study observational, so were all the other studies included in the meta-analysis, he pointed out.

“Therefore, no cause-effect conclusions can be drawn. The association could simply be due to other factors, such as those drinking more tea having a healthier lifestyle. It does not seem that the authors tried to control for confounders, which is usually difficult in meta-analysis,” Dr. Leurent said.

“There is reason to be a bit skeptical at this point; we really need to have the full details to assess it properly,” said Jonathan Cook of the Centre for Statistics in Medicine at the University of Oxford (England). “It’s a fair attempt to look at this, but not cutting edge, [using] fairly standard approaches.”

Similar studies have shown a reduced risk associated with coffee drinking, noted Duane Mellor, PhD, a registered dietitian and senior teaching fellow at Aston University in Birmingham.

“The important take-home message is that lifestyle is important in managing risk of developing type 2 diabetes,” Dr. Mellor said.

“That includes choosing low-calorie drinks including mainly water as well as unsweetened tea and coffee as your drinks of choice as part of a healthy lifestyle.”

The study was funded by the Young Talents Project of Hubei Provincial Health Commission, the Science and Technology Research Key Project of Education Department of Hubei Province, the Sanuo Diabetes Charity Foundation, and the Xiangyang Science and Technology Plan Project, all based in China. Dr. Li had no conflicts of interest to disclose. Dr. McConway is a Trustee and on the advisory committee of The Science Media Centre.  Dr. Sattar has consulted for many companies that make diabetes and cardiovascular drugs and has been involved in multiple trials of lifestyle approaches for the prevention and remission of diabetes. Dr. Sydes, Dr. Leurent, Dr. Cook, and Dr. Mellor had no conflicts of interest to report.

Key clinical point: Increased mean glycated hemoglobin (A1c) level and A1c variability were associated with a significantly higher risk for diabetes-related complications in patients with type 2 diabetes (T2D).

Major finding: Elevated mean A1c level was associated with a significantly higher risk for urine albumin-to-creatinine ratio [UACR] of >300 mg/g (adjusted hazard ratio [aHR] 1.308; P < .001), any retinopathy (aHR 1.274; P < .001), and advanced retinopathy (aHR 1.237; P = .036); similarly, increased standard deviation of A1c was associated with an increased risk for UACR of >300 mg/g (aHR 1.478; P < .001), doubling of serum creatinine (aHR 2.133; P < .001), and all-cause (aHR 1.880; P < .001) and cardiovascular (aHR 1.431; P = .016) mortality.

Study details: Findings are from a prospective study including 1869 patients with T2D who were followed-up for a median of 9.5 years.

Disclosures: This study was supported by grants from the Taipei Veterans General Hospital. The authors declared no conflicts of interest.

Source: Wu TE et al. Mean HbA1c and HbA1c variability are associated with differing diabetes-related complications in patients with type 2 diabetes mellitus. Diabetes Res Clin Pract. 2022 (Sep 2). Doi: 10.1016/j.diabres.2022.110069

Key clinical point: Increased mean glycated hemoglobin (A1c) level and A1c variability were associated with a significantly higher risk for diabetes-related complications in patients with type 2 diabetes (T2D).

Major finding: Elevated mean A1c level was associated with a significantly higher risk for urine albumin-to-creatinine ratio [UACR] of >300 mg/g (adjusted hazard ratio [aHR] 1.308; P < .001), any retinopathy (aHR 1.274; P < .001), and advanced retinopathy (aHR 1.237; P = .036); similarly, increased standard deviation of A1c was associated with an increased risk for UACR of >300 mg/g (aHR 1.478; P < .001), doubling of serum creatinine (aHR 2.133; P < .001), and all-cause (aHR 1.880; P < .001) and cardiovascular (aHR 1.431; P = .016) mortality.

Study details: Findings are from a prospective study including 1869 patients with T2D who were followed-up for a median of 9.5 years.

Disclosures: This study was supported by grants from the Taipei Veterans General Hospital. The authors declared no conflicts of interest.

Source: Wu TE et al. Mean HbA1c and HbA1c variability are associated with differing diabetes-related complications in patients with type 2 diabetes mellitus. Diabetes Res Clin Pract. 2022 (Sep 2). Doi: 10.1016/j.diabres.2022.110069

Key clinical point: Increased mean glycated hemoglobin (A1c) level and A1c variability were associated with a significantly higher risk for diabetes-related complications in patients with type 2 diabetes (T2D).

Major finding: Elevated mean A1c level was associated with a significantly higher risk for urine albumin-to-creatinine ratio [UACR] of >300 mg/g (adjusted hazard ratio [aHR] 1.308; P < .001), any retinopathy (aHR 1.274; P < .001), and advanced retinopathy (aHR 1.237; P = .036); similarly, increased standard deviation of A1c was associated with an increased risk for UACR of >300 mg/g (aHR 1.478; P < .001), doubling of serum creatinine (aHR 2.133; P < .001), and all-cause (aHR 1.880; P < .001) and cardiovascular (aHR 1.431; P = .016) mortality.

Study details: Findings are from a prospective study including 1869 patients with T2D who were followed-up for a median of 9.5 years.

Disclosures: This study was supported by grants from the Taipei Veterans General Hospital. The authors declared no conflicts of interest.

Source: Wu TE et al. Mean HbA1c and HbA1c variability are associated with differing diabetes-related complications in patients with type 2 diabetes mellitus. Diabetes Res Clin Pract. 2022 (Sep 2). Doi: 10.1016/j.diabres.2022.110069

Key clinical point: Use vs no use of sodium-glucose cotransporter-2 (SGLT2) inhibitors was associated with a lower risk for new-onset stroke (NOS) among patients with type 2 diabetes (T2D), with risk reductions being greater among those receiving concurrent statins, biguanides, thiazolidinediones, and glucagon-like peptide-1 receptor agonists (GLP-1 RA).

Major finding: The risk for NOS was significantly lower among SGLT2 inhibitor users vs nonusers (adjusted hazard ratio [aHR] 0.85; 95% CI 0.82-0.88), with similar results being reported in patients receiving statins (aHR 0.84; 95% CI 0.81-0.86), biguanides (aHR 0.77; 95% CI 0.75-0.79), thiazolidinediones (aHR 0.89; 95% CI 0.85-0.93), and GLP-1 RA (aHR 0.84; 95% CI 0.71-0.98).

Study details: The data come from a retrospective population-based cohort study including 232,101 patients with T2D using an SGLT2 inhibitor who were matched with 464,202 patients with T2D not using an SGLT2 inhibitor.

Disclosures: This study was supported by grants from Chung Shan Medical University Hospital. The authors declared no competing interests.

Source: Lin TK et al. Sodium-glucose co-transporter-2 inhibitors reduce the risk of new-onset stroke in patients with type 2 diabetes: A population-based cohort study. Front Cardiovasc Med. 2022;9:966708 (Aug 9). Doi: 10.3389/fcvm.2022.966708

Key clinical point: Use vs no use of sodium-glucose cotransporter-2 (SGLT2) inhibitors was associated with a lower risk for new-onset stroke (NOS) among patients with type 2 diabetes (T2D), with risk reductions being greater among those receiving concurrent statins, biguanides, thiazolidinediones, and glucagon-like peptide-1 receptor agonists (GLP-1 RA).

Major finding: The risk for NOS was significantly lower among SGLT2 inhibitor users vs nonusers (adjusted hazard ratio [aHR] 0.85; 95% CI 0.82-0.88), with similar results being reported in patients receiving statins (aHR 0.84; 95% CI 0.81-0.86), biguanides (aHR 0.77; 95% CI 0.75-0.79), thiazolidinediones (aHR 0.89; 95% CI 0.85-0.93), and GLP-1 RA (aHR 0.84; 95% CI 0.71-0.98).

Study details: The data come from a retrospective population-based cohort study including 232,101 patients with T2D using an SGLT2 inhibitor who were matched with 464,202 patients with T2D not using an SGLT2 inhibitor.

Disclosures: This study was supported by grants from Chung Shan Medical University Hospital. The authors declared no competing interests.

Source: Lin TK et al. Sodium-glucose co-transporter-2 inhibitors reduce the risk of new-onset stroke in patients with type 2 diabetes: A population-based cohort study. Front Cardiovasc Med. 2022;9:966708 (Aug 9). Doi: 10.3389/fcvm.2022.966708

Key clinical point: Use vs no use of sodium-glucose cotransporter-2 (SGLT2) inhibitors was associated with a lower risk for new-onset stroke (NOS) among patients with type 2 diabetes (T2D), with risk reductions being greater among those receiving concurrent statins, biguanides, thiazolidinediones, and glucagon-like peptide-1 receptor agonists (GLP-1 RA).

Major finding: The risk for NOS was significantly lower among SGLT2 inhibitor users vs nonusers (adjusted hazard ratio [aHR] 0.85; 95% CI 0.82-0.88), with similar results being reported in patients receiving statins (aHR 0.84; 95% CI 0.81-0.86), biguanides (aHR 0.77; 95% CI 0.75-0.79), thiazolidinediones (aHR 0.89; 95% CI 0.85-0.93), and GLP-1 RA (aHR 0.84; 95% CI 0.71-0.98).

Study details: The data come from a retrospective population-based cohort study including 232,101 patients with T2D using an SGLT2 inhibitor who were matched with 464,202 patients with T2D not using an SGLT2 inhibitor.

Disclosures: This study was supported by grants from Chung Shan Medical University Hospital. The authors declared no competing interests.

Source: Lin TK et al. Sodium-glucose co-transporter-2 inhibitors reduce the risk of new-onset stroke in patients with type 2 diabetes: A population-based cohort study. Front Cardiovasc Med. 2022;9:966708 (Aug 9). Doi: 10.3389/fcvm.2022.966708

Key clinical point: In patients with type 2 diabetes (T2D), increased visit-to-visit variability in glycated hemoglobin (A1c) and fasting plasma glucose (FPG) was associated with a higher risk for severe hypoglycemia; however, FPG variability better predicted severe hypoglycemic events than A1c variability.

Major finding: Each standard deviation (SD) increase in the variability in A1c and FPG significantly increased the risk for hypoglycemia requiring any third-party assistance (adjusted hazard ratio [aHR] 1.10 and aHR 1.40, respectively; both P < .01) and hypoglycemia requiring medical assistance (aHR 1.11 and aHR 1.46, respectively; both P < .01). However, FPG variability better predicted severe hypoglycemic events than A1c variability (P < .01).

Study details: Findings are from a post hoc analysis of the ACCORD trial including patients with T2D and a high risk for cardiovascular disease, of which 10,052 and 10,068 patients were included in A1c and FPG variability analyses, respectively.

Disclosures: This study was partly supported by the National Science Foundation of China project. The authors declared no conflicts of interest.

Source: Long C et al. Association of long-term visit-to-visit variability of HbA1c and fasting glycemia with hypoglycemia in type 2 diabetes mellitus. Front Endocrinol (Lausanne). 2022;13:975468 (Aug 11). Doi: 10.3389/fendo.2022.975468

Key clinical point: In patients with type 2 diabetes (T2D), increased visit-to-visit variability in glycated hemoglobin (A1c) and fasting plasma glucose (FPG) was associated with a higher risk for severe hypoglycemia; however, FPG variability better predicted severe hypoglycemic events than A1c variability.

Major finding: Each standard deviation (SD) increase in the variability in A1c and FPG significantly increased the risk for hypoglycemia requiring any third-party assistance (adjusted hazard ratio [aHR] 1.10 and aHR 1.40, respectively; both P < .01) and hypoglycemia requiring medical assistance (aHR 1.11 and aHR 1.46, respectively; both P < .01). However, FPG variability better predicted severe hypoglycemic events than A1c variability (P < .01).

Study details: Findings are from a post hoc analysis of the ACCORD trial including patients with T2D and a high risk for cardiovascular disease, of which 10,052 and 10,068 patients were included in A1c and FPG variability analyses, respectively.

Disclosures: This study was partly supported by the National Science Foundation of China project. The authors declared no conflicts of interest.

Source: Long C et al. Association of long-term visit-to-visit variability of HbA1c and fasting glycemia with hypoglycemia in type 2 diabetes mellitus. Front Endocrinol (Lausanne). 2022;13:975468 (Aug 11). Doi: 10.3389/fendo.2022.975468

Key clinical point: In patients with type 2 diabetes (T2D), increased visit-to-visit variability in glycated hemoglobin (A1c) and fasting plasma glucose (FPG) was associated with a higher risk for severe hypoglycemia; however, FPG variability better predicted severe hypoglycemic events than A1c variability.

Major finding: Each standard deviation (SD) increase in the variability in A1c and FPG significantly increased the risk for hypoglycemia requiring any third-party assistance (adjusted hazard ratio [aHR] 1.10 and aHR 1.40, respectively; both P < .01) and hypoglycemia requiring medical assistance (aHR 1.11 and aHR 1.46, respectively; both P < .01). However, FPG variability better predicted severe hypoglycemic events than A1c variability (P < .01).

Study details: Findings are from a post hoc analysis of the ACCORD trial including patients with T2D and a high risk for cardiovascular disease, of which 10,052 and 10,068 patients were included in A1c and FPG variability analyses, respectively.

Disclosures: This study was partly supported by the National Science Foundation of China project. The authors declared no conflicts of interest.

Source: Long C et al. Association of long-term visit-to-visit variability of HbA1c and fasting glycemia with hypoglycemia in type 2 diabetes mellitus. Front Endocrinol (Lausanne). 2022;13:975468 (Aug 11). Doi: 10.3389/fendo.2022.975468

Key clinical point: Sodium-glucose cotransporter-2 inhibitor (SGLT2i) vs dipeptidyl peptidase-4 inhibitor (DPP4i) use at discharge was associated with a lower risk for 1-year all-cause mortality and heart failure (HF) readmission in hospitalized patients with HF and type 2 diabetes (T2D) in a superaged society.

Major finding: Overall, 71.91% of patients were ≥75 years old. SGLT2i vs DPP4i significantly reduced the risk for 1-year all-cause mortality (adjusted hazard ratio [aHR] 0.70; 95% CI 0.56-0.89) and HF readmission (aHRk 0.52; 95% CI 0.45-0.61), with findings being similar among very elderly patients (age, ≥75 years).

Study details: Findings are from a retrospective study including patients hospitalized with the first episode of acute HF and T2D, of which 2101 patients with T2D receiving SGLT2i were propensity score-matched with 2101 of those receiving DPP4i.

Disclosures: This work was supported by Labor Research Grants from the Ministry of Health, Labour, and Welfare of Japan. The authors declared no conflicts of interest.

Source: Nakai M et al. Contemporary use of SGLT2 inhibitors in heart failure patients with diabetes mellitus: A comparison of DPP4 inhibitors in a nationwide electric health database of the superaged society. Cardiovasc Diabetol. 2022;21:157 (Aug 13). Doi: 10.1186/s12933-022-01586-6

Key clinical point: Sodium-glucose cotransporter-2 inhibitor (SGLT2i) vs dipeptidyl peptidase-4 inhibitor (DPP4i) use at discharge was associated with a lower risk for 1-year all-cause mortality and heart failure (HF) readmission in hospitalized patients with HF and type 2 diabetes (T2D) in a superaged society.

Major finding: Overall, 71.91% of patients were ≥75 years old. SGLT2i vs DPP4i significantly reduced the risk for 1-year all-cause mortality (adjusted hazard ratio [aHR] 0.70; 95% CI 0.56-0.89) and HF readmission (aHRk 0.52; 95% CI 0.45-0.61), with findings being similar among very elderly patients (age, ≥75 years).

Study details: Findings are from a retrospective study including patients hospitalized with the first episode of acute HF and T2D, of which 2101 patients with T2D receiving SGLT2i were propensity score-matched with 2101 of those receiving DPP4i.

Disclosures: This work was supported by Labor Research Grants from the Ministry of Health, Labour, and Welfare of Japan. The authors declared no conflicts of interest.

Source: Nakai M et al. Contemporary use of SGLT2 inhibitors in heart failure patients with diabetes mellitus: A comparison of DPP4 inhibitors in a nationwide electric health database of the superaged society. Cardiovasc Diabetol. 2022;21:157 (Aug 13). Doi: 10.1186/s12933-022-01586-6

Key clinical point: Sodium-glucose cotransporter-2 inhibitor (SGLT2i) vs dipeptidyl peptidase-4 inhibitor (DPP4i) use at discharge was associated with a lower risk for 1-year all-cause mortality and heart failure (HF) readmission in hospitalized patients with HF and type 2 diabetes (T2D) in a superaged society.

Major finding: Overall, 71.91% of patients were ≥75 years old. SGLT2i vs DPP4i significantly reduced the risk for 1-year all-cause mortality (adjusted hazard ratio [aHR] 0.70; 95% CI 0.56-0.89) and HF readmission (aHRk 0.52; 95% CI 0.45-0.61), with findings being similar among very elderly patients (age, ≥75 years).

Study details: Findings are from a retrospective study including patients hospitalized with the first episode of acute HF and T2D, of which 2101 patients with T2D receiving SGLT2i were propensity score-matched with 2101 of those receiving DPP4i.

Disclosures: This work was supported by Labor Research Grants from the Ministry of Health, Labour, and Welfare of Japan. The authors declared no conflicts of interest.

Source: Nakai M et al. Contemporary use of SGLT2 inhibitors in heart failure patients with diabetes mellitus: A comparison of DPP4 inhibitors in a nationwide electric health database of the superaged society. Cardiovasc Diabetol. 2022;21:157 (Aug 13). Doi: 10.1186/s12933-022-01586-6

Key clinical point: Dipeptidyl peptidase-4 (DPP4) inhibitors were more effective than other oral antidiabetic drugs (OAD) in reducing glycemic variability in patients with type 2 diabetes (T2D) receiving no concurrent insulin treatment.

Major finding: The mean amplitude of glycemic excursions reduced significantly in patients receiving DPP4 inhibitors vs other OAD (mean difference [MD] −0.69 mmol/L; P < .001), insulin secretagogues (MD −0.92 mmol/L; P < .001), non-secretagogues (MD −0.43 mmol/L; P = .02), sulfonylureas (MD −0.91 mmol/L; P < .001), and sodium-glucose cotransporter-2 inhibitors (MD −0.67 mmol/L; P = .03).

Study details: The data come from a meta-analysis of 14 randomized controlled trials including 855 patients with T2D.

Disclosures: This study was funded by MSD China Holding Co. Ltd. Four authors declared being employees of MSD China, and one author declared being an employee of Merck Sharp & Dohme LLC.

Source: Chai S et al. Influence of dipeptidyl peptidase-4 inhibitors on glycemic variability in patients with type 2 diabetes: A meta-analysis of randomized controlled trials. Front Endocrinol (Lausanne). 2022;13:935039 (Aug 9). Doi: 10.3389/fendo.2022.935039

Key clinical point: Dipeptidyl peptidase-4 (DPP4) inhibitors were more effective than other oral antidiabetic drugs (OAD) in reducing glycemic variability in patients with type 2 diabetes (T2D) receiving no concurrent insulin treatment.

Major finding: The mean amplitude of glycemic excursions reduced significantly in patients receiving DPP4 inhibitors vs other OAD (mean difference [MD] −0.69 mmol/L; P < .001), insulin secretagogues (MD −0.92 mmol/L; P < .001), non-secretagogues (MD −0.43 mmol/L; P = .02), sulfonylureas (MD −0.91 mmol/L; P < .001), and sodium-glucose cotransporter-2 inhibitors (MD −0.67 mmol/L; P = .03).

Study details: The data come from a meta-analysis of 14 randomized controlled trials including 855 patients with T2D.

Disclosures: This study was funded by MSD China Holding Co. Ltd. Four authors declared being employees of MSD China, and one author declared being an employee of Merck Sharp & Dohme LLC.

Source: Chai S et al. Influence of dipeptidyl peptidase-4 inhibitors on glycemic variability in patients with type 2 diabetes: A meta-analysis of randomized controlled trials. Front Endocrinol (Lausanne). 2022;13:935039 (Aug 9). Doi: 10.3389/fendo.2022.935039

Key clinical point: Dipeptidyl peptidase-4 (DPP4) inhibitors were more effective than other oral antidiabetic drugs (OAD) in reducing glycemic variability in patients with type 2 diabetes (T2D) receiving no concurrent insulin treatment.

Major finding: The mean amplitude of glycemic excursions reduced significantly in patients receiving DPP4 inhibitors vs other OAD (mean difference [MD] −0.69 mmol/L; P < .001), insulin secretagogues (MD −0.92 mmol/L; P < .001), non-secretagogues (MD −0.43 mmol/L; P = .02), sulfonylureas (MD −0.91 mmol/L; P < .001), and sodium-glucose cotransporter-2 inhibitors (MD −0.67 mmol/L; P = .03).

Study details: The data come from a meta-analysis of 14 randomized controlled trials including 855 patients with T2D.

Disclosures: This study was funded by MSD China Holding Co. Ltd. Four authors declared being employees of MSD China, and one author declared being an employee of Merck Sharp & Dohme LLC.

Source: Chai S et al. Influence of dipeptidyl peptidase-4 inhibitors on glycemic variability in patients with type 2 diabetes: A meta-analysis of randomized controlled trials. Front Endocrinol (Lausanne). 2022;13:935039 (Aug 9). Doi: 10.3389/fendo.2022.935039

Key clinical point: Sodium-glucose cotransporter-2 (SGLT-2) inhibitors did not have any significant beneficial effects on cardiac autonomic neuropathy (CAN) indices in patients with type 2 diabetes (T2D).

Major finding: SGLT-2 inhibitors had no significant effect on the low-frequency-to-high-frequency ratio (mean difference [MD] −0.11; P = .36), change in standard deviation of all 5-minute mean normal RR intervals (MD −2.83; P = .23), and change in the square root of the mean of the sum of the squares of differences between adjacent RR intervals (MD −0.14; P = .94).

Study details: Findings are from a meta-analysis of four randomized controlled trials including 247 patients with T2D who were randomly assigned to receive SGLT-2 inhibitors or placebo/active comparator.

Disclosures: This study did not receive any funding. The authors declared no conflicts of interest.

Source: Patoulias D et al. Effect of SGLT-2 inhibitors on cardiac autonomic function in type 2 diabetes mellitus: A meta-analysis of randomized controlled trials. Acta Diabetol. 2022 (Aug 19). Doi: 10.1007/s00592-022-01958-0

Key clinical point: Sodium-glucose cotransporter-2 (SGLT-2) inhibitors did not have any significant beneficial effects on cardiac autonomic neuropathy (CAN) indices in patients with type 2 diabetes (T2D).

Major finding: SGLT-2 inhibitors had no significant effect on the low-frequency-to-high-frequency ratio (mean difference [MD] −0.11; P = .36), change in standard deviation of all 5-minute mean normal RR intervals (MD −2.83; P = .23), and change in the square root of the mean of the sum of the squares of differences between adjacent RR intervals (MD −0.14; P = .94).

Study details: Findings are from a meta-analysis of four randomized controlled trials including 247 patients with T2D who were randomly assigned to receive SGLT-2 inhibitors or placebo/active comparator.

Disclosures: This study did not receive any funding. The authors declared no conflicts of interest.

Source: Patoulias D et al. Effect of SGLT-2 inhibitors on cardiac autonomic function in type 2 diabetes mellitus: A meta-analysis of randomized controlled trials. Acta Diabetol. 2022 (Aug 19). Doi: 10.1007/s00592-022-01958-0

Key clinical point: Sodium-glucose cotransporter-2 (SGLT-2) inhibitors did not have any significant beneficial effects on cardiac autonomic neuropathy (CAN) indices in patients with type 2 diabetes (T2D).

Major finding: SGLT-2 inhibitors had no significant effect on the low-frequency-to-high-frequency ratio (mean difference [MD] −0.11; P = .36), change in standard deviation of all 5-minute mean normal RR intervals (MD −2.83; P = .23), and change in the square root of the mean of the sum of the squares of differences between adjacent RR intervals (MD −0.14; P = .94).

Study details: Findings are from a meta-analysis of four randomized controlled trials including 247 patients with T2D who were randomly assigned to receive SGLT-2 inhibitors or placebo/active comparator.

Disclosures: This study did not receive any funding. The authors declared no conflicts of interest.

Source: Patoulias D et al. Effect of SGLT-2 inhibitors on cardiac autonomic function in type 2 diabetes mellitus: A meta-analysis of randomized controlled trials. Acta Diabetol. 2022 (Aug 19). Doi: 10.1007/s00592-022-01958-0

Key clinical point: In patients with type 2 diabetes (T2D) advancing from basal insulin (BI) therapy, a once-daily insulin glargine 100 U/mL and lixisenatide (iGlarLixi) injection regimen showed similar glycemic control to multiple injections with BI plus rapid-acting insulin (RAI), without weight gain.

Major finding: At 6 months, the mean reduction in glycated hemoglobin with iGlarLixi was noninferior to BI+RAI (mean difference [MD] 0.1%; 1-sided P = .0032), with weight gain being significantly lower with iGlarLixi vs BI+RAI (MD −0.8 kg; 2-sided P = .0069). The incidence of hypoglycemia was similar between the treatment groups.

Study details: Findings are from a retrospective study that used propensity score matching to evaluate therapy advancement with iGlarLixi (n = 814) or BI+RAI (n = 814) in patients with T2D on BI therapy.

Disclosures: This study was funded by Sanofi, Paris, France. Some authors declared receiving honoraria for speaking or consulting or research support or serving as advisory board members or speakers for various sources, including Sanofi. Three authors reported being employees of Sanofi.

Source: McCrimmon RJ et al. iGlarLixi versus basal plus rapid-acting insulin in adults with type 2 diabetes advancing from basal insulin therapy: The SoliSimplify real-world study. Diabetes Obes Metab. 2022 (Aug 19). Doi: 10.1111/dom.14844

Key clinical point: In patients with type 2 diabetes (T2D) advancing from basal insulin (BI) therapy, a once-daily insulin glargine 100 U/mL and lixisenatide (iGlarLixi) injection regimen showed similar glycemic control to multiple injections with BI plus rapid-acting insulin (RAI), without weight gain.

Major finding: At 6 months, the mean reduction in glycated hemoglobin with iGlarLixi was noninferior to BI+RAI (mean difference [MD] 0.1%; 1-sided P = .0032), with weight gain being significantly lower with iGlarLixi vs BI+RAI (MD −0.8 kg; 2-sided P = .0069). The incidence of hypoglycemia was similar between the treatment groups.

Study details: Findings are from a retrospective study that used propensity score matching to evaluate therapy advancement with iGlarLixi (n = 814) or BI+RAI (n = 814) in patients with T2D on BI therapy.

Disclosures: This study was funded by Sanofi, Paris, France. Some authors declared receiving honoraria for speaking or consulting or research support or serving as advisory board members or speakers for various sources, including Sanofi. Three authors reported being employees of Sanofi.

Source: McCrimmon RJ et al. iGlarLixi versus basal plus rapid-acting insulin in adults with type 2 diabetes advancing from basal insulin therapy: The SoliSimplify real-world study. Diabetes Obes Metab. 2022 (Aug 19). Doi: 10.1111/dom.14844

Key clinical point: In patients with type 2 diabetes (T2D) advancing from basal insulin (BI) therapy, a once-daily insulin glargine 100 U/mL and lixisenatide (iGlarLixi) injection regimen showed similar glycemic control to multiple injections with BI plus rapid-acting insulin (RAI), without weight gain.

Major finding: At 6 months, the mean reduction in glycated hemoglobin with iGlarLixi was noninferior to BI+RAI (mean difference [MD] 0.1%; 1-sided P = .0032), with weight gain being significantly lower with iGlarLixi vs BI+RAI (MD −0.8 kg; 2-sided P = .0069). The incidence of hypoglycemia was similar between the treatment groups.

Study details: Findings are from a retrospective study that used propensity score matching to evaluate therapy advancement with iGlarLixi (n = 814) or BI+RAI (n = 814) in patients with T2D on BI therapy.

Disclosures: This study was funded by Sanofi, Paris, France. Some authors declared receiving honoraria for speaking or consulting or research support or serving as advisory board members or speakers for various sources, including Sanofi. Three authors reported being employees of Sanofi.

Source: McCrimmon RJ et al. iGlarLixi versus basal plus rapid-acting insulin in adults with type 2 diabetes advancing from basal insulin therapy: The SoliSimplify real-world study. Diabetes Obes Metab. 2022 (Aug 19). Doi: 10.1111/dom.14844