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Nutrition in Acute and Chronic Pancreatitis
Published in Mary J. Marian, Gerard E. Mullin, Integrating Nutrition Into Practice, 2017
Endocrine dysfunction is due to loss of alpha and beta cells within the pancreas and can lead to derangements in glucose control, known as type 3c diabetes. Type 3c diabetes makes up about 5%–10% of all diabetes, and 80% of these cases are due to chronic pancreatitis, typically chronic calcific pancreatitis [47,48]. Brittle diabetes can result from impairments in both insulin and glucagon production. It is therefore important to screen chronic pancreatitis patients with fasting blood sugar and hemoglobin A1c [35,49]. Metformin is typically the first drug of choice in patients with type 3c diabetes; however, this may not be tolerated due to its gastrointestinal side effects. Insulin secretagogues can also be used, such as sulfonylureas to help boost insulin secretion. Incretin-based therapies also enhance insulin secretion. Of note, the data on GLP1 agonists and DPP4 inhibitors causing acute pancreatitis is weak—they can cause low-grade amylase and lipase elevations, but this is commonly in asymptomatic patients [50–52]. Many patients will eventually end up on insulin therapy and in cases of severe malnutrition, insulin therapy should be initiated immediately [53]. It is important that MCTs be used with caution in diabetics as they can induce ketogenesis [54].
Long-term changes of pancreatic function in patients with complicated walled-off necrosis
Published in Scandinavian Journal of Gastroenterology, 2022
Camilla Nøjgaard, Mikkel Werge, Astrid Naver, Anne Wilkens Knudsen, Nicolai J. Wewer Albrechtsen, Søren Møller, Lise Lotte Gluud, Srdan Novovic
Four patients developed new-onset diabetes on early follow-up and four on late follow-up (24%). This is also called type 3c diabetes. One patient had endocrine insufficiency before the necrotizing acute pancreatitis. Baseline glucagon levels and cortisol levels were higher at baseline than at early follow-up, both levels probably being driven by acute stress and inflammation (systemic inflammatory response syndrome) which were high at baseline but not after discharge. This is supported by the fact that white blood cell count and CRP levels at both early and late follow-up were within normal limits, suggesting that the inflammatory response is well over after finalized ETDN treatment. In further support to that, cortisol levels were significantly lower on both early and late follow-up as compared to baseline.
Diabetes is an independent predictor of severe acute pancreatitis
Published in Postgraduate Medicine, 2022
Elif Tutku Durmuş, İbrahim Akdağ, Mehmet Yıldız
Diabetes mellitus (DM) and acute pancreatitis (AP) are both health problems with increasing incidence and hospitalization worldwide and they share a close and complex relationship [1,2]. Exocrine pancreatic disorders such as AP can lead to endocrine pancreatic insufficiency and resultant abnormal glucose metabolism [1–4]. Therefore, hyperglycemia due to general pancreatic dysfunction is referred to as ‘type 3c diabetes’ as a disorder separate from other types of DM [5]. In addition, there are studies showing that DM, as a factor independent of other factors such as alcohol, gallstones, and hyperlipidemia, puts patients at a higher risk of developing AP [6–8]. Although the etiological relationships between DM and AP are well defined, there are controversial results about their effects on disease severity and prognosis.
Exploring the link between diabetes and pancreatic cancer
Published in Expert Review of Anticancer Therapy, 2019
Margherita Pizzato, Federica Turati, Valentina Rosato, Carlo La Vecchia
The physiopathology linking type 3c diabetes mellitus to pancreatic cancer is still poorly understood. Diabetes secondary to pancreatic cancer may be the result of a glandular destruction due to tumor infiltration and ductal obstruction. However, diabetes in pancreatic cancer patients is mainly characterized by hyperinsulinemia secondary to insulin resistance. Therefore, diabetes secondary to pancreatic cancer is likely a paraneoplastic effect: mediators released by the cancer interfere with insulin secretion or insulin action [74]. This is supported by the evidence that treatments (resection or chemotherapy) of pancreatic cancer often lead to improvement in hyperglycemia [72]. A direct role of pancreatic cancer in new onset diabetes is also supported by the finding that glucose tolerance improves after tumor treatment in patients with new-onset diabetes secondary to pancreatic cancer, whilst it does not improve in long-standing diabetic patients [75].