Cureus
Trajectories of Glycemia Following Acute Pancreatitis: A Prospective Longitudinal Study
By Uppati V Krishna, Bommi GowriShankar, Mutyala Trivenu V Chowdary and 3 others.
Abstract
Introduction: Acute pancreatitis (AP) may cause persistent disturbances in glucose metabolism that extend beyond the resolution of acute inflammatory episodes.However, the progression of glycemic abnormalities during the early recovery period remains insufficiently characterized, emphasizing the need for prospective longitudinal evaluation.We aimed to evaluate glycemia trajectories after an episode of AP over a 12-month follow-up by determining the cumulative incidence of new-onset prediabetes and diabetes and assessing longitudinal changes in glycemic parameters.Methods: This prospective longitudinal observational study included 77 adults diagnosed with AP without preexisting diabetes who were followed up for 12 months.We recorded clinical characteristics, pancreatitis severity scores, laboratory investigations, and fasting blood glucose (FBG), postprandial blood glucose (PPBG), and glycated hemoglobin (HbA1c) levels at baseline, six months, and 12 months.Statistical analyses were performed using repeated-measures analysis of variance for longitudinal comparisons, Bonferroniadjusted post hoc tests, and McNemar's test for categorical outcomes.Statistical significance was set at p < 0.05.Results: Among the 77 participants, 45 (58.4%) were male participants, and 39 (50.6%) had biliary pancreatitis.During follow-up, the incidence of prediabetes increased significantly from 12 (15.6%)at six months to 19 (24.7%) at 12 months (p = 0.023), while that of diabetes increased from three (3.9%) to five (6.5%); however, the difference was not statistically significant (p = 0.480).Overall, glycemic abnormalities increased significantly from 15 (19.5%) to 24 (31.2%)(p = 0.008).Repeated-measures analysis demonstrated a significant increase in FBG levels from 96 ± 9.5 to 106 ± 17.0 mg/dL (p < 0.001), PPBG from 127 ± 16.5 to 150 ± 35.0 mg/dL (p = 0.003), and HbA1c from 5.52% ± 0.11% to 6.06 ± 0.40% (p < 0.001) over the 12-month period.Glycemic trajectory analysis showed that 35 (45.5%) participants remained in the normal-stable group, 35 (45.5%) exhibited a moderately stable pattern, and seven (9.1%) demonstrated a high glycemic trajectory.Conclusion: Progressive deterioration in glycemic control occurs during the first year following AP, with nearly one-third of the patients developing prediabetes or diabetes.HbA1c demonstrated the greatest longitudinal increase and may serve as a sensitive marker for identifying patients at risk for post-pancreatitis dysglycemia.These findings support routine metabolic surveillance after AP to facilitate early diagnosis and timely intervention.






