Acute pancreatitis due to diabetes: The role of hyperglycaemia and insulin resistance

• Published in: Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] 2012-05, Vol.12 (3), p.234-239
• Main Authors: Solanki, Nicholas S, Barreto, Savio G, Saccone, Gino T.P
• Format: Article
• Language: English
• Subjects: Acidosis; Acinar Cells - drug effects; Acinar Cells - metabolism; Acute Disease; Animals; Diabetes Mellitus, Type 1 - complications; Diabetes Mellitus, Type 1 - drug therapy; Diabetes Mellitus, Type 2 - complications; Diabetes Mellitus, Type 2 - drug therapy; Endocrinology & Metabolism; Gastroenterology and Hepatology; Glucose - adverse effects; Humans; Hyperglycemia - complications; Hyperglycemia - drug therapy; Hypertriglyceridaemia; Insulin - pharmacology; Insulin Resistance; Obesity; Oral hypoglycaemics; Pancreatitis - etiology; Stellate cells
• ISSN: 1424-3903; 1424-3911
• DOI: 10.1016/j.pan.2012.01.003

Abstract Background The co-existence of diabetes mellitus (DM) in patients with acute pancreatitis (AP) is linked to poor outcomes. Four large epidemiological studies have suggested an aetiological role for DM in AP. The exact nature of this role is poorly understood. Objective To analyse the available clinical and experimental literature to determine if DM may play a causative role in AP. Methods A systematic search of the scientific literature was carried out using EMBASE, PubMed/MEDLINE, and the Cochrane Central Register of Controlled Trials for the years 1965–2011 to obtain access to all publications, especially randomized controlled trials, systematic reviews, and meta-analyses exploring the mechanisms of pathogenesis of AP in patients with DM. Results No clinical studies could be identified directly providing pathogenetic mechanisms of DM in the causation of AP. The available data on DM and its associated metabolic changes and therapy indicate that hyperglycaemia coupled with the factors influencing insulin resistance (tumour necrosis-α, NFκB, amylin) cause an increase in reactive oxygen species generation in acinar cells. Conclusions Complex pathogenetic connections exist between AP and factors involved in the development and therapy of DM. Insulin resistance and hyperglycaemia, hallmarks of DM, are important factors linked to the susceptibility of diabetics to AP. Given the high morbidity associated with an attack of AP in a diabetic patient, targeting these two aspects by therapy may help not only to reduce the risk of development of AP, but may also help reduce the severity of an established attack in a diabetic patient.