Here’s the Data: Endocrine Insufficiency After Acute Pancreatitis in Children

M Abu-El-Haija et al. Clin Gastroenterol Hepatol 2024; 22: 2033-2043. Open Access! The Role of Pancreatitis Risk Genes in Endocrine Insufficiency Development After Acute Pancreatitis in Children

In this observational prospective cohort with 114 children (after excluding 6), outcomes following the first episode of acute pancreatitis (AP) were determined. In addition, pancreatitis risk genes (CASRCELCFTRCLDN2CPA1CTRCPRSS1SBDSSPINK1, and UBR1) were sequenced. A genetic risk score was derived from all genes with univariable P < .15.

Pre-DM was defined as follows: fasting blood glucose ≥100 mg/dL and <126 mg/dL, or hemoglobin A1C ≥5.7% and <6.5%

Key findings:

  • 95/114 (83%) remained normoglycemic and 19/114 (17%) developed endocrine insufficiency (4 DM, 15 pre-DM) 12 months after the first episode of AP
  • Sixty-three subjects (52.5%) had at least 1 reportable variant identified
  • Severe AP (58% vs 20%; P = .001) and at least 1 gene affected (79% vs 47%; P = .01) were enriched among the endocrine-insufficient group
  • CFTR (53%), SPINK1 (13%), PRSS1 (10%), and UBR1 (9%) accounted for the majority of variants identified

My take: 3.5% of this cohort developed diabetes and 13% developed prediabetes. The risk is increased in those with severe acute pancreatitis and underlying genetic variants. As noted recently with Dr. Freeman’s lecture (summarized on prior blog posts), it is worthwhile for patients to follow-up after an episode of acute pancreatitis.

Related blog posts: