title: Characteristics of patients with ketosis-prone diabetes (KPD) presenting with acute pancreatitis: implications for the natural history and etiology of a KPD subgroup.
abstract: OBJECTIVE
  Reports of concomitant diabetic ketoacidosis (DKA) and acute pancreatitis (AP) are lacking among emerging forms of diabetes. This longitudinal study characterized ketosis-prone diabetes (KPD) in patients presenting with concomitant AP and DKA.
  
  
  METHODS
  Multi-ethnic KPD patients (N = 755) were followed prospectively for 1 year from the time of index DKA using repeated metabolic and beta cell functional reserve measures. Baseline and longitudinal characteristics were compared between KPD patients whose index DKA was associated with (n = 54) or without (n = 701) AP.
  
  
  RESULTS
  The AP group had significantly higher baseline serum amylase, lipase, and triglyceride levels and significantly lower bicarbonate levels than the non-AP group. AP patients had significantly greater C-peptide area-under-the-curve with glucagon stimulation shortly after the index DKA, and higher fasting C-peptide (FCP) levels 6 to 12 months later. Using the validated "Aβ" KPD classification, 85% of AP patients had β+ status (preserved beta cell functional reserve), compared to 60% of non-AP patients (P = .04). Multivariate analysis revealed that among the β+ KPD subgroup with an identifiable precipitating factor for DKA ("provoked" DKA), patients with AP had worse long-term glycemic outcomes than patients whose DKA was associated with other factors.
  
  
  CONCLUSIONS
  Despite greater clinical severity at presentation, KPD patients with AP have better preserved beta cell function than those without AP. β+ KPD patients presenting with AP have worse long-term glycemic control than those with other causes of provoked DKA. Factors other than beta cell function negatively impact glycemic control in KPD patients presenting with AP.
authors.affiliation: Division of Diabetes, Endocrinology, and Metabolism, Baylor College of Medicine, Houston, TX 77030, USA.
authors.forename: Ramiro
authors.initials: R
authors.lastname: Fernandez
authors.forename: Ranjita
authors.initials: R
authors.lastname: Misra
authors.forename: Ramaswami
authors.initials: R
authors.lastname: Nalini
authors.forename: Christiane S
authors.initials: CS
authors.lastname: Hampe
authors.forename: Kerem
authors.initials: K
authors.lastname: Ozer
authors.forename: Ashok
authors.initials: A
authors.lastname: Balasubramanyam
mesh_terms: D000328:Adult; D000437:Alcoholism / Q000150:complications / Q000503:physiopathology; D000681:Amylases / Q000097:blood; D001639:Bicarbonates / Q000097:blood; D015415:Biomarkers / Q000097:blood; D015992:Body Mass Index; D002096:C-Peptide / Q000097:blood; D015331:Cohort Studies; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000150:complications* / Q000175:diagnosis / Q000628:therapy; D016883:Diabetic Ketoacidosis / Q000150:complications* / Q000209:etiology / Q000276:immunology / Q000503:physiopathology; D005260:Female; D006801:Humans; D015228:Hypertriglyceridemia / Q000150:complications / Q000503:physiopathology; D050417:Insulin-Secreting Cells / Q000276:immunology / Q000378:metabolism*; D008049:Lipase / Q000097:blood; D008137:Longitudinal Studies; D008297:Male; D050177:Overweight / Q000150:complications; D010195:Pancreatitis / Q000150:complications* / Q000209:etiology / Q000276:immunology / Q000503:physiopathology; D011379:Prognosis; D011446:Prospective Studies; D012720:Severity of Illness Index
chemical_list: D001639:Bicarbonates; D015415:Biomarkers; D002096:C-Peptide; D008049:Lipase; D000681:Amylases