Pancreatic Diabetes after Distal Pancreatectomy: Incidence Rate and Risk Factors

Diabetes of the exocrine pancreas (DEP) is a form of diabetes that occurs due to pancreatic disease. It is far more common than has been previously considered, with a recent study showing 1.8% of adults with new-onset diabetes should have been classified as DEP. The majority is misdiagnosed as type 2 diabetes mellitus (T2DM). Patients with DEP exhibit varying degrees of exocrine and endocrine dysfunction. Damage to the islet of Langerhans effects the secretion of hormones from the β, α, and pancreatic polypeptide cells; the combination of low insulin, glucagon, and pancreatic polypeptide contributes to rapid fluctuations in glucose levels. This form of "brittle diabetes" may result in the poorer glycemic control observed in patients with DEP, when compared with those with T2DM. Diabetes of the exocrine pancreas has a different natural history to other forms of diabetes; patients are more likely to require early insulin initiation compared with those with T2DM. Therefore, individuals with DEP should be advised about the symptoms of decompensated hyperglycemia, although they are less likely to develop ketoacidosis. Clinicians should screen for DEP in patients with acute or chronic pancreatitis, following pancreatic resection, or with co-existing cystic fibrosis or hemochromatosis. Incident diabetes may herald the onset of pancreatic ductal carcinoma in a small subset of patients. Once identified, patients with DEP can benefit from specific lifestyle advice, pancreatic enzyme replacement therapy, metformin treatment, appropriate insulin dosing, and monitoring. Further research is needed to establish the ideal treatment regimens to provide optimal clinical outcomes for this unique form of diabetes.

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“…Over 80% of cases have mutations in the pancreatic transcription factor genes GATA6 and PTF1A. De Franco et al 14 Baumeister et al15 Kim et al16…”

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confidence: 99%

Diabetes of the exocrine pancreas

Wynne

Devereaux

Dornhorst

2018

J of Gastro and Hepatol

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“…It is acknowledged that surgical trauma leads to a local increase of inflammatory cytokines [ 36 ]. Interestingly, hTERT-MSC infusion attenuated the transcription of IFN-γ and TNF-α at the surgical site.…”

Section: Resultsmentioning

confidence: 99%

Mesenchymal stem cells promote pancreatic β-cell regeneration through downregulation of FoxO1 pathway

et al. 2020

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Background Mesenchymal stem cells (MSC) are non-haematopoietic, fibroblast-like multipotent stromal cells. In the injured pancreas, these cells are assumed to secrete growth factors and immunomodulatory molecules, which facilitate the regeneration of pre-existing β-cells. However, when MSC are delivered intravenously, their majority is entrapped in the lungs and does not reach the pancreas. Therefore, the aim of this investigation was to compare the regenerative support of hTERT-MSC (human telomerase reverse transcriptase mesenchymal stem cells) via intrapancreatic (IPR) and intravenous route (IVR). Methods hTERT-MSC were administered by IPR and IVR to 50% pancreatectomized NMRI nude mice. After eight days, blood glucose level, body weight, and residual pancreatic weight were measured. Proliferating pancreatic β-cells were labelled and identified with bromodeoxyuridine (BrdU) in vivo. The number of residual islets and the frequency of proliferating β-cells were compared in different groups with sequential pancreatic sections. The pancreatic insulin content was evaluated by enzyme-linked immunosorbent assay (ELISA) and the presence of hTERT-MSC with human Alu sequence. Murine gene expression of growth factors, β-cell specific molecules and proinflammatory cytokines were inspected by real-time polymerase chain reaction (RT-PCR) and Western blot. Results This study evaluated the regenerative potential of the murine pancreas post-hTERT-MSC administration through the intrapancreatic (IPR) and intravenous route (IVR). Both routes of hTERT-MSC transplantation (IVR and IPR) increased the incorporation of BrdU by pancreatic β-cells compared to control. MSC induced epidermal growth factor (EGF) expression and inhibited proinflammatory cytokines (IFN-γ and TNF-α). FOXA2 and PDX-1 characteristics for pancreatic progenitor cells were activated via AKT/ PDX-1/ FoxO1 signalling pathway. Conclusion The infusion of hTERT-MSC after partial pancreatectomy (Px) through the IVR and IPR facilitated the proliferation of autochthonous pancreatic β-cells and provided evidence for a regenerative influence of MSC on the endocrine pancreas. Moderate benefit of IPR over IVR was observed which could be a new treatment option for preventing diabetes mellitus after pancreas surgery.

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“…Because the resected parenchymal volume is smaller with central pancreatectomy than distal pancreatectomy, postoperative pancreatic function is expected to be better after central pancreatectomy. The incidence rate of new-onset diabetes ranges from 9% to 19.2% after distal pancreatectomy [10,11]. It was reported that the incidence rate of new-onset diabetes/impaired glucose tolerance was 0% after central pancreatectomy versus 16% after spleen-preserving distal pancreatectomy [12], while another study found rates of 14% after central pancreatectomy and 46% after distal pancreatectomy [13].…”

Section: Conflict Of Interestmentioning

confidence: 99%

The Evaluation of the Early and Late Postoperative Pancreatic Function and Nutritional Status: Central Pancreatectomy Versus Distal Pancreatectomy

Izumo¹

2017

Int J Surg Res Pract

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Pancreatic Diabetes after Distal Pancreatectomy: Incidence Rate and Risk Factors

Cited by 18 publications

References 14 publications

Diabetes of the exocrine pancreas

Diabetes of the exocrine pancreas

Mesenchymal stem cells promote pancreatic β-cell regeneration through downregulation of FoxO1 pathway

The Evaluation of the Early and Late Postoperative Pancreatic Function and Nutritional Status: Central Pancreatectomy Versus Distal Pancreatectomy

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