Dr. Steinberg’s secondary analyses of SCALE trial show that saxenda/liraglutide raises reversibly the blood levels of amalyse and lipase. The incidence of acute pancreatitis was rare, but more common in those receiving liraglutide (n=12, 0.3%) than placebo (n=1, 0.1%). About 5,000 participants were followed for one year.
Roughly 50% of acute pancreatitis cases were felt to be gallstone-mediated. No correlation between amylase/lipase levels, gallstone formation and anticipation of pancreatitis was seen. Findings suggest no need of measuring pancreatic markers in patients receiving liraglutide 1.8 or 3.0 mg daily.
GT
Also see:
Saxenda/Victoza, lipase and pacreatitis (part 1)
Diabetes Care
Secondary analyses (SCALE)
May 2017
Objective: To describe amylase/lipase activity levels and events of acute pancreatitis (AP) in the SCALE (Satiety and Clinical Adiposity—Liraglutide Evidence in individuals with and without diabetes) weight-management trials.
Research Design and Methods: Secondary analyses were performed on pooled data from four trials (N = 5,358 with BMI ≥30, or 27-30 kg/m2 with ≥1 comorbidity). Of these, 1,723 had normoglycemia, 2,789 had prediabetes, and 846 had type 2 diabetes. Participants were randomized to liraglutide 3.0 mg (n = 3,302), liraglutide 1.8 mg (n = 211, only type 2 diabetes), or placebo (n = 1,845). Relationships between characteristics and amylase/lipase activity at baseline and during treatment were investigated.
Results:
Over 56 weeks, liraglutide 3.0 mg versus placebo was associated with increases in mean levels of 7% (amylase) and 31% (lipase), respectively. Similar changes in amylase/lipase levels were observed with liraglutide 1.8 mg.
More participants receiving liraglutide 3.0 mg versus placebo experienced amylase (9.4% vs. 5.9%) and lipase (43.5% vs. 15.1%) elevations greater than or equal to the upper limit of normal (ULN); few had elevations ≥3 × ULN for amylase (<0.1% with liraglutide 3.0 mg or placebo) or lipase (2.9% vs. 1.5%). After liraglutide discontinuation, enzymes returned to baseline levels.
Thirteen participants developed acute pancreatitis: 12 on (n = 9, 0.3%) or after (n = 3, 0.1%) liraglutide 3.0 mg treatment and one (0.1%) with placebo.
A total of 6/13 participants with acute pancreatitis (5/12 liraglutide; 1 placebo) had gallstone disease evident at AP onset.
Amylase/lipase elevations either 1 × ULN or ≥3 × ULN before AP onset had very low positive predictive value (PPV) for acute pancreatitis (<1%).
Conclusions:
Liraglutide resulted in dose-independent, reversible increases in amylase/lipase activity, unrelated to baseline characteristics, not predicting onset of acute pancreatitis.
Gallstones possibly contributed to 50% of acute pancreatitis cases.
Data provide no basis for amylase/lipase level monitoring in liraglutide treatment except in suspected acute pancreatitis.
