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Hypoglycemia: Definition, Identification, Prevention, and TreatmentChronic hyperglycemia and pancreatic dysfunction -
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Academic Content and Language Evaluation of This Article. Answering Reviewers PDF Peer-Review Report PDF. Citation of this article. Ewald N, Hardt PD. Diagnosis and treatment of diabetes mellitus in chronic pancreatitis.
World J Gastroenterol ; 19 42 : [PMID: DOI: Corresponding Author of This Article. Nils Ewald, MD, Associate Professor of Internal Medicine, Department of Internal Medicine, General Hospital Luebbecke-Rahden, Virchowstr.
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Copyright © Baishideng Publishing Group Co. All rights reserved. World J Gastroenterol. Nov 14, ; 19 42 : Published online Nov 14, doi: Nils Ewald , Philip D Hardt. Nils Ewald, Justus-Liebig-University Giessen, Giessen, Germany.
Nils Ewald, Department of Internal Medicine, General Hospital Luebbecke-Rahden, Luebbecke, Germany. Correspondence to : Nils Ewald, MD, Associate Professor of Internal Medicine, Department of Internal Medicine, General Hospital Luebbecke-Rahden, Virchowstr. Received: June 10, Revised: August 13, Accepted: September 4, Published online: November 14, Key Words: Diabetes mellitus , Chronic pancreatitis , Type 3c diabetes , Pancreatogenic diabetes , Pancreatitis.
Citation: Ewald N, Hardt PD. Table 1 Current classification of diabetes mellitus. Source: Ref. Screening for type 3c diabetes mellitus in chronic pancreatitis. Distinguishing type 3c diabetes from other types.
Table 2 Proposed diagnostic criteria for type 3c diabetes mellitus. Major criteria must be present Presence of exocrine pancreatic insufficiency monoclonal fecal elas tase-1 test or direct function tests Pathological pancreatic imaging endoscopic ultrasound, MRI, CT Absence of type 1 diabetes mellitus associated autoimmune markers Minor criteria Absent pancreatic polypeptide secretion Impaired incretin secretion e.
MRI: Magnetic resonance imaging; CT: Computed tomography; GLP Glucagon-like peptide-1; HOMA-IR: Homeostasis model assessment of insulin resistance; HOMA-B: Homeostasis model assessment of beta-cell.
Managing exocrine pancreatic insufficiency. P- Reviewers: Dumitrascu DL, Sakata N S- Editor: Gou SX L- Editor: A E- Editor: Wu HL. Wang W , Guo Y, Liao Z, Zou DW, Jin ZD, Zou DJ, Jin G, Hu XG, Li ZS. Occurrence of and risk factors for diabetes mellitus in Chinese patients with chronic pancreatitis.
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Rothenbacher D , Löw M, Hardt PD, Klör HU, Ziegler H, Brenner H. When individuals with post-pancreatectomy diabetes require exogenous insulin therapy, as explained above, the absence of glucagon renders them very vulnerable to severe hypoglycemia.
In post-pancreatectomy, diabetes hypoglycemia is not easily avoided because without glucagon, it is a daunting task to precisely mimic physiologic insulin secretion, which varies widely throughout the course of a day as a function of carbohydrate ingestion, physical activity, stress and underlying circadian rhythms.
In addition to losses of hormones, post-operative alterations in GI transit time and malabsorption due to exocrine pancreatic insufficiency complicate management. In some cases, post-pancreatectomy diabetes can be prevented or at least ameliorated by auto-transplantation of pancreatic islets from the surgical specimen The strategy preserves at least some insulin and glucagon functionality and is suitable when the underlying disease is not a malignancy.
The isolation procedure is not easy or always successful. However, given the difficulty in managing post-pancreatectomy diabetes, we suggest that auto-transplantation be considered whenever possible.
Hypoglycemia without Diabetes in Patients with an Underlying Pancreatic Disorder. Compared to the common problem of hypoglycemia occurring during insulin therapy, primary hypoglycemic disorders resulting from insulin overproduction in the absence of diabetes are rare.
Essentially all are disorders of the pancreas. The classic example of hypoglycemia due to a pancreatic disorder is insulinoma; its management is discussed at length in another Pancreapedia entry Here we focus on issues relevant to hypoglycemia per se.
Individuals with an insulinoma typically have fasting hypoglycemia but may occasionally also experience postprandial hypoglycemia. Diagnosis requires documentation of hyperinsulinemia during a hypoglycemic episode.
It is usually not possible to obtain laboratory data during a spontaneous event, and for that reason a hour monitored fast is often required to make the diagnosis. Most, but not all, patients with the disease experience hypoglycemia within 72 hours.
Hypoglycemia occurs in less than 24 hours in about two thirds of cases, and in less than 48 hours of fasting in the great majority of affected patients 9. By the time an insulinoma comes to clinical attention, hypoglycemic events are typically characterized by episodes of neuroglycopenia.
This may be due to HAAF since diagnosis is typically delayed. Often patients are given other diagnoses such as seizure disorder, before hypoglycemia due to an insulinoma is considered.
Common neuroglycopenic symptoms include confusion and personality changes or bizarre behavior that may not be recognized as metabolic in origin. Patients may have amnesia for the hypoglycemic events.
This is a rare condition of diffuse hyperplasia of pancreatic islet beta cells leading to hyperinsulinemia and hypoglycemia. It presents in infants and young children as lethargy, irritability, or difficulty feeding. There is potential for serious complications, including seizures and permanent brain damage, when diagnosis is delayed.
It is relatively rare, affecting approximately 1 in 50, newborns. Multiple genetic defects have been found to cause congenital hyperinsulinemia. Second most common are mutations that occur in KCNJ11, which encodes the ATP-dependent potassium K-ATP channel involved in insulin secretion.
There have, however, been reports of successful medical treatment of the condition with calcium channel blockade 3, 19 and octreotide 15 both as monotherapy and in conjunction with surgery. We suggest that a trial of these medications may be warranted before surgery. Figure 1. Characteristic histologic and immunocytochemical features of nesideoblastosis in a patient with neuroglycopenia after Roux-en-Y gastric bypass.
A Extreme variation in islet size and the presence of large lobulated islets center of panel. B Ductulo-insular complexes. Endocrine cell clusters are intimately connected with a small pancreatic duct. C Insulin positive endocrine cell clusters are scattered throughout the acinar parenchyma.
D Insulin positive cells are seen scattered amongst the pancreatic duct epithelium. From Rabiee et al. Roux-en-Y gastric bypass RYGB is a common bariatric procedure for the treatment of obesity and type 2 diabetes.
Hyperinsulinemic hypoglycemia not attributable to dumping is a rare complication of the procedure and typically begins to occur 2 to 4 years after surgery 26, Most cases are characterized by post-prandial symptoms.
The underlying mechanism responsible for hyperinsulinemia is not fully characterized. It has been attributed to the induction of nesidioblastosis 11, 34, 37 Figure 1 , but this pathological diagnosis has been called into question 18, 25 and has not always been observed in pancreatectomy or pancreatic biopsy specimens Another mechanism may involve rapid transit of nutrients into the upper small bowel and the enhanced secretion of incretin hormones, including gastric inhibitory peptide GIP and glucagon-like peptide 1 GLP-1 This concept is supported by the observation that feeding via percutaneous gastrostomy tube placed in the bypassed stomach reduces hypoglycemia Many cases of post-RYGB hypoglycemia occur with dumping syndrome and can be managed with modification of diet to include frequent high protein, low carbohydrate feedings Some cases, however, are severe, intractable, and refractory to dietary management 6, 31, 37, Others, including some that did not respond to banding 43 , have been treated successfully with partial or near-total pancreatectomy 6; 31, 37, 43 , but many of these have developed diabetes Most recently, laparoscopic reversal of the bypass with resolution of hypoglycemia has been reported 5; Successful medical treatment of post-RYGB hypoglycemia has also been reported using acarbose 26 , calcium channel blockade 26 , diazoxide 38 , and combined therapies We suggest that a trial of medical management is indicated in cases of severe post-RYGB hypoglycemia, not only because it can be efficacious and obviate the need for surgery, but also because some cases managed in this way may undergo spontaneous remission Practical guidelines for management of severe acute pancreatitis by integrated traditional Chinese and western medicine protocol specifications.
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Download references. These authors thank all the staff from the pancreas multidisciplinary teams at West China Hospital of Sichuan University for their continuous support.
This study was supported by NZ-China Strategic Research Alliance Award China: YFE, QX, TJ, WH and LD; New Zealand: JAW and AP ; National Science Foundation of China No.
Department and Laboratory of Integrated Traditional Chinese and Western Medicine, Sichuan Provincial Pancreatitis Centre and West China-Liverpool Biomedical Research Centre, West China Hospital, Sichuan University, No.
Liverpool Pancreatitis Research Group, Liverpool University Hospitals NHS Foundation Trust and Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
West China-Washington Mitochondria and Metabolism Center, West China Hospital, Sichuan University, Chengdu, China. Division of Endocrinology and Metabolism, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University and Collaborative Innovation Center of Biotherapy, Chengdu, China.
State Key Laboratory of Oncogenes and Related Genes, Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. Biostatistics and Clinical Trials, Department of Oncology, University of Cambridge, Cambridge, UK.
Surgical and Translational Research Centre, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand. Sayali Pendharkar, Anthony R. Applied Surgery and Metabolism Laboratory, School of Biological Sciences, University of Auckland, Auckland, New Zealand.
Pancreatitis Center, Division of Gastroenterology, Johns Hopkins Medical Institutions, Baltimore, USA. You can also search for this author in PubMed Google Scholar.
XY and RZ contributed equally as co-first authors. XY, RZ, TJ, LY, LL, WC, and LD: acquisition of data. XY and WH: drafting of the manuscript. XY, RZ, PZ, RM, and WH: analysis and interpretation of data. PZ and RMartina: statistical analysis supervision.
DD, XF, TL, and JAW: important intelligence input. SP, ARP, VKS, RS, and JAW: critical revision of the manuscript. WH and QX: study concept and design, obtained funding; study supervision.
Correspondence to Wei Huang. RS has provided consultancy to Abbot Mylan ; no further support from any organization for the submitted work; no financial relationships with any organizations that might have had an interest in the submitted work in the previous 3 years; no other relationship or activities that could appear to have influenced the submitted work.
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Reprints and permissions. Yang, X. et al. Stress Hyperglycemia Is Independently Associated with Persistent Organ Failure in Acute Pancreatitis.
Health benefits of weight management article Hormonal balance after pregnancy only available Chrnic the PDF Fat-burning complexes. Download dyafunction PDF to view the article, as well as pancfeatic associated figures and tables. Pancreatitis can Chronic hyperglycemia and pancreatic dysfunction temporary dyscunction and glycosuria by interfering with islet cell function, a process that is sometimes hypegrlycemia as the pancreatitis subsides. In rare cases pancreatitis also produces permanent diabetes mellitus either by producing sufficient permanent islet cell damage or by precipitating clinical evidence of the disease in the person hereditarily predisposed to it. The treatment of pancreatitis in the diabetic would be the same as in the patient without diabetes. The presence of uncontrolled diabetes, especially with the acute type of pancreatitis, requires additional insulin. Actual coma has been caused by severe acute pancreatitis, and at times resistance to insulin is marked, requiring intensive insulin therapy.
Hpyerglycemia clinical significance of Nutritional strategies for stamina arising in dysfunctiln setting Chronic hyperglycemia and pancreatic dysfunction pancreatic disease also known hhperglycemia diabetes of the exocrine pancreas, DEP has drawn more attention in recent years. Uyperglycemia, significant improvements still need to be made in the recognition, Chronic hyperglycemia and pancreatic dysfunction and treatment of the disorder, and in the knowledge of the pathological mechanisms. The clinical course of DEP is different from type 1 diabetes mellitus T1DM and type 2 diabetes mellitus T2DM. DEP develops in patients with previous existing exocrine pancreatic disorders which damage both exocrine and endocrine parts of pancreas, and lead to pancreas exocrine insufficiency PEI and malnutrition. Therefore, damage in various exocrine and endocrine cell types participating in glucose metabolism regulation likely contribute to the development of DEP.
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