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Chakravarty-Vartak U, Vartak S, Neelakantan A, Mutha K. Spectrum of diabetic lesions: An autopsy study. JOURNAL OF DIABETOLOGY 2021. [DOI: 10.4103/jod.jod_71_20] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/04/2022] Open
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Alexandre-Heymann L, Mallone R, Boitard C, Scharfmann R, Larger E. Structure and function of the exocrine pancreas in patients with type 1 diabetes. Rev Endocr Metab Disord 2019; 20:129-149. [PMID: 31077020 DOI: 10.1007/s11154-019-09501-3] [Citation(s) in RCA: 35] [Impact Index Per Article: 5.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
In the last 10 years, several studies have shown that the pancreas of patients with type 1 diabetes (T1D), and even of subjects at risk for T1D, was smaller than the pancreas from healthy subjects. This arose the question of the relationships between the endocrine and exocrine parts of the pancreas in T1D pathogenesis. Our review underlines that histological anomalies of the exocrine pancreas are common in patients with T1D: intralobular and interacinar fibrosis, acinar atrophy, fatty infiltration, leucocytic infiltration, and pancreatic arteriosclerosis are all frequent observations. Moreover, 25% to 75% of adult patients with T1D present with pancreatic exocrine dysfunction. Our review summarizes the putative causal factors for these structural and functional anomalies, including: 1/ alterations of insulin, glucagon, somatostatin and pancreatic polypeptide secretion, 2/ global pancreatic inflammation 3/ autoimmunity targeting the exocrine pancreas, 4/ vascular and neural abnormalities, and 5/ the putative involvement of pancreatic stellate cells. These observations have also given rise to new theories on T1D: the primary event of T1D pathogenesis could be non-specific, e.g bacterial or viral or chemical, resulting in global pancreatic inflammation, which in turn could cause beta-cell predominant destruction by the immune system. Finally, this review emphasizes that it is advisable to evaluate pancreatic exocrine function in patients with T1D presenting with gastro-intestinal complaints, as a clinical trial has shown that pancreatic enzymes replacement therapy can reduce the frequency of hypoglycemia and thus might improve quality of life in subjects with T1D and exocrine failure.
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Affiliation(s)
- Laure Alexandre-Heymann
- Service de Diabétologie, Hôpital Cochin, 123 boulevard de Port-Royal, 75014, Paris, France
- Département Hospitalo Universitaire, INSERM U 1016, Université Paris Descartes, Paris, France
| | - Roberto Mallone
- Service de Diabétologie, Hôpital Cochin, 123 boulevard de Port-Royal, 75014, Paris, France
- Département Hospitalo Universitaire, INSERM U 1016, Université Paris Descartes, Paris, France
| | - Christian Boitard
- Service de Diabétologie, Hôpital Cochin, 123 boulevard de Port-Royal, 75014, Paris, France
- Département Hospitalo Universitaire, INSERM U 1016, Université Paris Descartes, Paris, France
| | - Raphaël Scharfmann
- Service de Diabétologie, Hôpital Cochin, 123 boulevard de Port-Royal, 75014, Paris, France
- Département Hospitalo Universitaire, INSERM U 1016, Université Paris Descartes, Paris, France
| | - Etienne Larger
- Service de Diabétologie, Hôpital Cochin, 123 boulevard de Port-Royal, 75014, Paris, France.
- Département Hospitalo Universitaire, INSERM U 1016, Université Paris Descartes, Paris, France.
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The prevalence of pancreatic morphological abnormalities detected by digital autopsy. Pancreatology 2018; 18:717-720. [PMID: 30072207 DOI: 10.1016/j.pan.2018.07.002] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/14/2018] [Accepted: 07/06/2018] [Indexed: 12/11/2022]
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Zsóri G, Illés D, Terzin V, Ivány E, Czakó L. Exocrine pancreatic insufficiency in type 1 and type 2 diabetes mellitus: do we need to treat it? A systematic review. Pancreatology 2018; 18:559-565. [PMID: 29779830 DOI: 10.1016/j.pan.2018.05.006] [Citation(s) in RCA: 24] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/16/2017] [Revised: 05/11/2018] [Accepted: 05/12/2018] [Indexed: 12/11/2022]
Abstract
The exocrine and endocrine pancreata are very closely linked both anatomically and physiologically. Abdominal symptoms such as nausea, bloating, diarrhea, steatorrhea, and weight loss can often occur in diabetic patients. Impairments of the exocrine pancreatic function seem to be a frequent complication of diabetes mellitus; however, they are largely overlooked. The aim of this paper is to provide an overview of the current concepts of exocrine pancreatic insufficiency (PEI) in diabetes mellitus. The prevalence and symptoms of PEI in diabetes mellitus, the pathomechanism, and difficulties of diagnosis and therapy of PEI are summarized in this systematic review.
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Affiliation(s)
- Gábor Zsóri
- University of Szeged, Faculty of Medicine, Albert Szent-Györgyi Medical and Pharmaceutical Center, First Department of Medicine, Szeged, Korányi Fasor 8-10, H-6720, Hungary.
| | - Dóra Illés
- University of Szeged, Faculty of Medicine, Albert Szent-Györgyi Medical and Pharmaceutical Center, First Department of Medicine, Szeged, Korányi Fasor 8-10, H-6720, Hungary
| | - Viktória Terzin
- University of Szeged, Faculty of Medicine, Albert Szent-Györgyi Medical and Pharmaceutical Center, First Department of Medicine, Szeged, Korányi Fasor 8-10, H-6720, Hungary
| | - Emese Ivány
- University of Szeged, Faculty of Medicine, Albert Szent-Györgyi Medical and Pharmaceutical Center, First Department of Medicine, Szeged, Korányi Fasor 8-10, H-6720, Hungary
| | - László Czakó
- University of Szeged, Faculty of Medicine, Albert Szent-Györgyi Medical and Pharmaceutical Center, First Department of Medicine, Szeged, Korányi Fasor 8-10, H-6720, Hungary
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Ata N, Dal K, Kucukazman M, Yeniova AÖ, Karakaya S, Unsal O, Dagdeviren M, Akın KO, Baser S, Beyan E, Ertugrul DT. The effect of glycemic control on CEA, CA 19-9, amylase and lipase levels. Open Med (Wars) 2014; 10:8-13. [PMID: 28352671 PMCID: PMC5152950 DOI: 10.1515/med-2015-0002] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/30/2014] [Accepted: 07/29/2014] [Indexed: 12/22/2022] Open
Abstract
Background Diabetes mellitus is closely related to pancreas cancer. In this study we aimed to investigate the effect of hyperglycemia on tumor and inflammation markers, as well as pancreatic exocrine functions. Methods A total of 98 consecutive diabetic patients with poor glycemic control, and 50 healthy controls were included in the study. We measured hsCRP, erythrocyte sedimentation rate (ESR), CA19-9, CEA, amylase and lipase in addition to routine biochemistry tests, before and after euglycemia was achieved. Results Fasting blood glucose, HbA1c, CA19-9, CEA, hsCRP, ESR, triglycerides, AST, ALT, GGT, ALP, total cholesterol and LDL-C levels decreased significantly with the regulation of glycemic control. Amylase and lipase levels increased with the regulation of glycemic control. After glycemic control, CA19-9 and CEA levels were still higher, whereas amylase and lipase levels were still lower in the diabetic group compared with the control group. Basal HbA1c showed significant correlation with CA19-9, CEA, amylase and lipase. Conclusions We propose to repeat observations of tumor markers after hyperglycemia is resolved, in order to avoid unnecessary invasive tests. Our data also suggest that pancreatic exocrine function was improved with lowering blood glucose in a short period of time.
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Affiliation(s)
- Naim Ata
- Kecioren Training and Research Hospital, Department of Internal Medicine. Ardahan street. No:2506380 Keçiören, Ankara, Turkey
| | - Kürşat Dal
- Kecioren Training and Research Hospital, Department of Internal Medicine. Ardahan street. No:2506380 Keçiören, Ankara, Turkey
| | - Metin Kucukazman
- Kecioren Training and Research Hospital, Department of Internal Medicine. Ardahan street. No:2506380 Keçiören, Ankara, Turkey
| | - Abdullah Ö Yeniova
- Kecioren Training and Research Hospital, Department of Internal Medicine. Ardahan street. No:2506380 Keçiören, Ankara, Turkey, Tel: +90 312 3569000
| | - Serdar Karakaya
- Kecioren Training and Research Hospital, Department of Internal Medicine. Ardahan street. No:2506380 Keçiören, Ankara, Turkey
| | - Oktay Unsal
- Kecioren Training and Research Hospital, Department of Internal Medicine. Ardahan street. No:2506380 Keçiören, Ankara, Turkey
| | - Murat Dagdeviren
- Kecioren Training and Research Hospital, Department of Internal Medicine. Ardahan street. No:2506380 Keçiören, Ankara, Turkey
| | - Kadir O Akın
- Kecioren Training and Research Hospital, Department of Clinical Biochemistry. Ardahan street. No:2506380 Keçiören, Ankara, Turkey
| | - Salih Baser
- Kecioren Training and Research Hospital, Department of Internal Medicine. Ardahan street. No:2506380 Keçiören, Ankara, Turkey
| | - Esin Beyan
- Kecioren Training and Research Hospital, Department of Internal Medicine. Ardahan street. No:2506380 Keçiören, Ankara, Turkey
| | - Derun T Ertugrul
- Kecioren Training and Research Hospital, Department of Internal Medicine. Ardahan street. No:2506380 Keçiören, Ankara, Turkey
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Ewald N, Hardt PD. Diagnosis and treatment of diabetes mellitus in chronic pancreatitis. World J Gastroenterol 2013; 19:7276-7281. [PMID: 24259958 PMCID: PMC3831209 DOI: 10.3748/wjg.v19.i42.7276] [Citation(s) in RCA: 125] [Impact Index Per Article: 10.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/10/2013] [Revised: 08/13/2013] [Accepted: 09/05/2013] [Indexed: 02/06/2023] Open
Abstract
Diabetes secondary to pancreatic diseases is commonly referred to as pancreatogenic diabetes or type 3c diabetes mellitus. It is a clinically relevant condition with a prevalence of 5%-10% among all diabetic subjects in Western populations. In nearly 80% of all type 3c diabetes mellitus cases, chronic pancreatitis seems to be the underlying disease. The prevalence and clinical importance of diabetes secondary to chronic pancreatitis has certainly been underestimated and underappreciated so far. In contrast to the management of type 1 or type 2 diabetes mellitus, the endocrinopathy in type 3c is very complex. The course of the disease is complicated by additional present comorbidities such as maldigestion and concomitant qualitative malnutrition. General awareness that patients with known and/or clinically overt chronic pancreatitis will develop type 3c diabetes mellitus (up to 90% of all cases) is rather good. However, in a patient first presenting with diabetes mellitus, chronic pancreatitis as a potential causative condition is seldom considered. Thus many patients are misdiagnosed. The failure to correctly diagnose type 3 diabetes mellitus leads to a failure to implement an appropriate medical therapy. In patients with type 3c diabetes mellitus treating exocrine pancreatic insufficiency, preventing or treating a lack of fat-soluble vitamins (especially vitamin D) and restoring impaired fat hydrolysis and incretin secretion are key-features of medical therapy.
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Serum CA19-9 level associated with metabolic control and pancreatic beta cell function in diabetic patients. EXPERIMENTAL DIABETES RESEARCH 2012; 2012:745189. [PMID: 22778715 PMCID: PMC3384953 DOI: 10.1155/2012/745189] [Citation(s) in RCA: 26] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Subscribe] [Scholar Register] [Received: 01/10/2012] [Revised: 03/15/2012] [Accepted: 04/15/2012] [Indexed: 01/21/2023]
Abstract
CA19-9 is a tumor-associated antigen. It is also a marker of pancreatic tissue damage that might be caused by diabetes. Long-term poor glycemic control may lead to pancreatic beta cell dysfunction which is reflected by elevated serum CA19-9 level. Intracellular cholesterol accumulation leads to islet dysfunction and impaired insulin secretion which provide a new lipotoxic model. This study firstly found total cholesterol was one of the independent contributors to CA19-9. Elevated serum CA19-9 level in diabetic patients may indicate further investigations of glycemic control, pancreatic beta cell function, and total cholesterol level.
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Affiliation(s)
- Philip D Hardt
- Medizinische Klinik und Poliklinik III, Universitätsklinikum Giessen und Marburg GmbH Standort Giessen.
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Ewald N, Kaufmann C, Raspe A, Kloer HU, Bretzel RG, Hardt PD. Prevalence of diabetes mellitus secondary to pancreatic diseases (type 3c). Diabetes Metab Res Rev 2012; 28:338-42. [PMID: 22121010 DOI: 10.1002/dmrr.2260] [Citation(s) in RCA: 184] [Impact Index Per Article: 14.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
BACKGROUND Diabetes mellitus secondary to pancreatic diseases is a condition seldom thought of in clinical practice. Yet, a high percentage of exocrine pancreatic insufficiency has been reported for the general population and especially for diabetic subjects. Thus, we investigated the prevalence of diabetes mellitus due to pancreatic diseases. METHODS In this study, we investigated 1868 patients diagnosed with diabetes mellitus who had been admitted to our hospital during the last 24 months. Patient data were diligently studied, and patients were reclassified according to the diabetes classification as proposed by the American Diabetes Association. RESULTS Among 1868 subjects, 172 patients could be classified as type 3c diabetes mellitus (9.2%). Among these were 135 diagnosed with chronic pancreatitis (78.5%), 12 with hereditary haemochromatosis, 14 with pancreatic cancer and 7 with cystic fibrosis. Thus, diabetes mellitus due to chronic pancreatitis occurred in this collective in 7.2% of all diabetic subjects. Misclassification of these patients was very common. Only 51.2% (88/172) were initially classified correctly. Most type 3 diabetes patients were initially misclassified as type 2 diabetes (69/84). CONCLUSIONS Diabetes mellitus secondary to pancreatic diseases (especially chronic pancreatitis) seems more common than generally believed with a prevalence of 9.2% among the subjects studied here. Because the awareness of this diabetes type is poor, misclassification is quite frequent. A common problem seems to be the differentiation between type 2 and type 3. Yet, the right classification of diabetes mellitus is important, because there are special therapeutic options and problems in patients with diabetes secondary to pancreatic diseases.
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Affiliation(s)
- N Ewald
- Third Medical Department and Policlinic, University Hospital Giessen and Marburg, Giessen Site, Klinikstrasse 33, Giessen, Germany.
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Exocrine pancreatic insufficiency in diabetes mellitus: a complication of diabetic neuropathy or a different type of diabetes? EXPERIMENTAL DIABETES RESEARCH 2011; 2011:761950. [PMID: 21822421 PMCID: PMC3148449 DOI: 10.1155/2011/761950] [Citation(s) in RCA: 74] [Impact Index Per Article: 5.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Subscribe] [Scholar Register] [Received: 03/27/2011] [Accepted: 05/25/2011] [Indexed: 02/08/2023]
Abstract
Pancreatic exocrine insufficiency is a frequently observed phenomenon in type 1 and type 2 diabetes mellitus. Alterations of exocrine pancreatic morphology can also be found frequently in diabetic patients. Several hypotheses try to explain these findings, including lack of insulin as a trophic factor for exocrine tissue, changes in secretion and/or action of other islet hormones, and autoimmunity against common endocrine and exocrine antigens. Another explanation might be that diabetes mellitus could also be a consequence of underlying pancreatic diseases (e.g., chronic pancreatitis). Another pathophysiological concept proposes the functional and morphological alterations as a consequence of diabetic neuropathy. This paper discusses the currently available studies on this subject and tries to provide an overview of the current concepts of exocrine pancreatic insufficiency in diabetes mellitus.
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Hardt PD, Brendel MD, Kloer HU, Bretzel RG. Is pancreatic diabetes (type 3c diabetes) underdiagnosed and misdiagnosed? Diabetes Care 2008; 31 Suppl 2:S165-9. [PMID: 18227480 DOI: 10.2337/dc08-s244] [Citation(s) in RCA: 130] [Impact Index Per Article: 7.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/03/2023]
Abstract
Exocrine pancreatic insufficiency is frequently associated with diabetes, with high prevalence in both insulin-dependent or insulin-independent patients. Exocrine pancreatic failure has often been perceived as a complication of diabetes. In contrast, recent clinical observations lead to the notion that nonendocrine pancreatic disease is a critical factor for development rather than a sequel to diabetes. The incidence of diabetes caused by exocrine pancreatic disease appears to be underestimated and may comprise 8% or more of the general diabetic patient population. Nonendocrine pancreas disease can cause diabetes by multiple mechanisms. Genetic defects have been characterized, resulting in a syndrome of both exocrine and endocrine failure. Regulation of beta-cell mass and physiological incretin secretion are directly dependent on normal exocrine function. Algorithms for diagnosis and therapy of diabetes should therefore address both endocrine and exocrine pancreatic function.
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Affiliation(s)
- Philip D Hardt
- Third Medical Department and Policlinic, University Hospital Giessen and Marburg, Giessen, Rodthohl 6, D-35385 Giessen, Germany.
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Canaway S, Phillips I, Betts P. Pancreatic exocrine insufficiency and type 1 diabetes mellitus. BRITISH JOURNAL OF NURSING (MARK ALLEN PUBLISHING) 2000; 9:2030-2. [PMID: 11868210 DOI: 10.12968/bjon.2000.9.18.12461] [Citation(s) in RCA: 12] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Accepted: 09/01/2000] [Indexed: 11/11/2022]
Abstract
Studies in adults suggest that some patients with type 1 diabetes mellitus have pancreatic exocrine insufficiency (PEI). The primary aim of this study was to explore the association between pancreatic exocrine function and type 1 diabetes in young people under 17 years. The secondary aim was to evaluate the relationship between PEI in patients with diabetes, their clinical symptoms and blood glucose control. The importance of providing a highly trained multidisciplinary support network are also discussed.
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Affiliation(s)
- S Canaway
- Paediatric Medical Unit, Southampton General Hospital, Southampton
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Nakano S, Mugikura M, Endoh M, Ogami Y, Otsuki M. Acute pancreatitis with diabetic ketoacidosis associated with hypermyoglobinemia, acute renal failure, and DIC. J Gastroenterol 1996; 31:623-6. [PMID: 8844491 DOI: 10.1007/bf02355070] [Citation(s) in RCA: 16] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/04/2023]
Abstract
We report a case of acute pancreatitis with diabetic ketoacidosis associated with increased serum myoglobin concentration, acute renal failure, and disseminated intravascular coagulation. A 49-year-old man suffering from diarrhea, vomiting, and somnolence was admitted to the hospital. He had had flu-like symptoms for 4 days prior to the onset of these symptoms. He was a habitual drinker and had been consuming 360 ml-900 ml of the drink "shochu" (distilled spirits containing 28% alcohol) daily for 30 years. Laboratory data on admission revealed elevated serum levels of pancreatic enzymes, including amylase, trypsin, lipase, pancreatic secretory trypsin inhibitor (PSTI), phospholipase A2 (PLA2), and elastase-1, as well as elevated levels of glucose (373 mg/dl), ketone bodies (3675 mumol/l), and myoglobin (229.8 ng/ml). Treatment with subcutaneous insulin and intravenous administration of electrolyte fluid and the systemic protease inhibitor, gabexate mesilate, was begun immediately. Early after the initiation of treatment, there was an increase in serum creatinine (4.9 mg/dl), and thromobocytopenia (15000/microliters) was observed. The patient completely recovered from renal failure and acute pancreatitis, but required insulin therapy. Alcohol ingestion and dehydration are thought to have played a major role in the triggering of the acute pancreatitis. We examined the relationship among acute pancreatitis, diabetic ketoacidosis, and hypermyoglobinemia in the literature.
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Affiliation(s)
- S Nakano
- Third Department of Internal Medicine, University of Occupational and Environmental Health, School of Medicine, Kitakyushu, Japan
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Kawamori R, Katsura M, Ishida S, Yamasaki Y, Tujii M, Kawano S, Kamada T. Subclinical exocrine pancreatic derangement in human diabetic patients evaluated from pure pancreatic juice. J Diabetes Complications 1995; 9:69-73. [PMID: 7541259 DOI: 10.1016/1056-8727(94)00006-a] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/25/2023]
Abstract
To elucidate the mechanism responsible for histological derangement of pancreas in diabetic patients, pure pancreatic juice (PPJ) aspirated directly from pancreatic duct was analyzed before and after strict glycemic control on poorly controlled diabetic patients without clinical exocrine pancreatic dysfunction. PPJ obtained from 18 diabetics showed a significantly decreased amylase activity compared with ten healthy subjects (109 +/- 4 versus 168 +/- 9 U/mg protein, p < 0.005) in spite of negligible changes in lipase activity, protein concentration, bicarbonate concentration, and its volume. PPJ showed higher concentrations of prostanoids in diabetic patients than in healthy subjects (TXB2, 259 +/- 48 versus 118 +/- 30 pg/mL, p < 0.05; 6-keto-PGF1 alpha, 52.6 +/- 11.5 versus 38.5 +/- 7.5 pg/mL, p > 0.05). Ratio of 6-keto-PGF1 alpha/TXB2 of PPJ in diabetic patients was significantly lower than in healthy subjects (0.195 +/- 0.016 versus 0.422 +/- 0.041, p < 0.005). After strict glycemic control for 1-3 months on nine of 18 diabetic patients, amylase activity of PPJ was significantly higher than that before the control (112 +/- 4 versus 128 +/- 7 U/mg protein, p < 0.01), but still significantly lower than that of healthy subjects (p < 0.005). Lipase activity showed no significant difference between before and after the control. TXB2 and 6-keto-PGF1 alpha concentrations were decreased.(ABSTRACT TRUNCATED AT 250 WORDS)
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Affiliation(s)
- R Kawamori
- First Department of Medicine, Osaka University Medical School, Japan
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Renner IG, Savage WT, Pantoja JL, Renner VJ. Death due to acute pancreatitis. A retrospective analysis of 405 autopsy cases. Dig Dis Sci 1985; 30:1005-18. [PMID: 3896700 DOI: 10.1007/bf01308298] [Citation(s) in RCA: 302] [Impact Index Per Article: 7.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
A large retrospective autopsy study of patients was analyzed to evaluate the major etiologic and pathologic factors contributing to fatal acute pancreatitis (AP). From an autopsy population of 50,227 patients, 405 cases were identified where AP was defined as the official primary cause of death. AP was classified according to morphological and histological, but not biochemical, criteria. Patients with AP died significantly earlier than a control autopsy population of 38,259 patients. Sixty percent of the AP patients died within 7 days of admission. Pulmonary edema and congestion were significantly more prevalent in this group, as was the presence of hemorrhagic pancreatitis. In the remaining 40% of patients surviving longer than 7 days, infection was the major factor contributing to death. Major etiologic groups in AP were chronic alcoholism; postabdominal surgery; common duct stones; a small miscellaneous group including viral hepatitis, drug, and postpartum cases; and a large idiopathic group comprising patients with cholelithiasis, diabetes mellitus, and ischemia. The prevalence of established diabetes mellitus in the AP group was significantly higher than that observed in the autopsy control series, suggesting that this disease should be considered as an additional risk factor influencing survival in AP. Pulmonary complications, including pulmonary edema and congestion, appeared to be the most significant factor contributing to death and occurred even in those cases where the pancreatic damage appeared to be only moderate in extent. Emphasis placed on the early recognition and treatment of pulmonary edema in all cases of moderate and severe AP should contribute significantly to an increase in survival in this disease.
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Affiliation(s)
- A K Foulis
- Department of Pathology, Royal Infirmary, Glasgow, Scotland
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Honoré LH. The lack of a positive association between symptomatic cholesterol cholelithiasis and clinical diabetes mellitus: a retrospective study. JOURNAL OF CHRONIC DISEASES 1980; 33:465-9. [PMID: 7380980 DOI: 10.1016/0021-9681(80)90071-5] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/24/2023]
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Abstract
Exocrine pancreatic function was studied in 20 juvenile-onset diabetics, seven maturity-onset diabetics, and five patients with diabetes secondary to chronic pancreatitis. The results were compared with 13 non-diabetic controls. The outputs of bicarbonate, trypsin, and amylase were reduced in the diabetic patients in response to intravenous secretin and CCK-PZ. In the juvenile-onset group, exocrine pancreatic secretory capacity was reduced in 80% of the patients, and the severity of the reduction was related to the duration of the diabetes. The reduction in pancreatic secretory capacity must be taken into consideration when interpreting pancreatic exocrine function in patients with diabetes.
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Abstract
Three children presented as acute surgical emergencies due to undiagnosed diabetes mellitus. Where diabetic ketoacidosis mimicks the acute abdomen three clinical features are important in reaching the right diagnosis-namely, a history of polydipsia, polyuria, and anorexia preceding the abdominal pain, the deep sighing and rapid respirations, and severe dehydration.
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Penny R, Thompson RG, Polmar SH, Schultz RB. Pancreatitis, malabsorption, and IgA deficiency in a child with diabetes. J Pediatr 1971; 78:512-6. [PMID: 5101447 DOI: 10.1016/s0022-3476(71)80238-x] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/13/2023]
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Siperstein MD, Unger RH, Madison LL. Studies of muscle capillary basement membranes in normal subjects, diabetic, and prediabetic patients. J Clin Invest 1968; 47:1973-99. [PMID: 5675423 PMCID: PMC297361 DOI: 10.1172/jci105886] [Citation(s) in RCA: 416] [Impact Index Per Article: 7.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/16/2023] Open
Abstract
A technique is described for the measurement of muscle capillary basement membranes by electron microscopic examination of needle biopsies of the quadriceps muscle. With this procedure it has been possible to obtain an objective evaluation of the significance of capillary basement membrane hypertrophy in diabetic microangiopathy. The results of such studies of muscle capillary basement membrane thickness in 50 normal, 51 diabetic, and 30 prediabetic patients have demonstrated the following. First, that the average capillary basement membrane width of diabetic patients is over twice that of normal subjects; moreover, such basement membrane thickening is a very constant finding among overtly diabetic patients, in that approximately 98% of individual diabetic subjects demonstrated this lesion. The degree of basement membrane thickening in diabetic patients is, however, unrelated to age, weight, severity, or duration of diabetes. Second, capillary basement membrane hypertrophy has been found in approximately 50% of patients who are genetically prediabetic but who have not yet demonstrated evidence of the manifest carbohydrate disturbances of diabetes mellitus. Third, in contrast to the results obtained in genetically diabetic patients, subjects with severe hyperglycemia due to causes other than genetic diabetes only infrequently show basement membrane hypertrophy. These results indicate that thickening of the muscle capillary basement membranes is a characteristic of genetic diabetes mellitus, and further, that the hyperglycemia of diabetes is probably not the factor responsible for the microangiopathy characteristic of diabetes mellitus. Finally, the discovery of thickened capillary basement membranes in prediabetic patients suggests that basement membrane hypertrophy is a relatively early lesion of the diabetic syndrome and provides further support for the conclusion that this vascular defect is independent of carbohydrate derangements of diabetes mellitus.
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Affiliation(s)
- R. J. Corlett
- Monash University Department of MedicinePrince Henry's HospitalMelbourne
| | - A. Sali
- Monash University Department of MedicinePrince Henry's HospitalMelbourne
| | - J. Hansky
- Monash University Department of MedicinePrince Henry's HospitalMelbourne
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