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Query: UMLS:C0011849 (diabetes)
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Early insulin response to rapid intravenous injection of glucose was studied in 7 cases of cystic fibrosis aged 8 months to 9 1/2 years. Plasma insulin was measured with a radioimmunological method. Blood glucose values were determined and the glucose disappearance rate (kG) calculated. In all children except the youngest one the early insulin response values were low compared with normal children. The kG-values were normal and correlated neither to the duration of clinical symptoms, nor to the patients' actual clinical condition measured by means of the Shwachman score. The explanation of the decreased insulin response is probably the progressive fibrosis of the pancreas. This may also explain the reported increased incidence of diabetes mellitus in cystic fibrosis. Comparison is made with the condition in pancreatic fibrosis in rabbits, produced through duct ligation.
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PMID:Insulin release in cystic fibrosis. 114 52

According to the 1988 Marseilles-Rome classification inflammatory pancreatic diseases are represented by acute (AP) and chronic pancreatitis (CP), pancreatic fibrosis and abscesses (due to infection of cystic cavities). Each form is defined by specific etiological, pathomorphological, functional and evolutive aspects. In our experience with 348 AP cases, gallstones and chronic alcohol abuse, alone or together, represent the major causative factors (over 70% of cases). Mortality observed in necrotizing AP only, varies from 26% of idiopathic to 8% of biliary cases. Ductal scars, exocrine and endocrine impairment were observed in about 45% and 20% respectively as sequelae of necrotizing AP, whatever the etiology. As far as CP is concerned, the main etiological factor is chronic alcohol consumption (82% of cases). The clinical evolution of CP may be roughly divided in two phases, the earlier (within 5 years from onset) characterized by frequently recurrent pain, calcifications and cystic cavities and the later when pain spontaneously regresses and steatorrhea and diabetes tend to appear. Heavy alcohol intake, smoking and frequent relapses are related to a less favourable course. About 60% of the patients underwent surgery within 5 years from onset. Pain relief was achieved in the large majority. Reduction in alcohol intake and the natural tendency of the disease to burn out, probably aid pain relief. Mortality in CP is due to diseases secondary to alcohol and smoking abuse (cardiovascular and neoplastic) more than to CP alone. We believe that multiple parameters are required for a complete definition of each pancreatic patient.
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PMID:Acute and chronic pancreatitis: an up-date. 174 47

Chronic pancreatitis is difficult to treat in patients with a nondilated duct. Patients experiencing intractable pain unresponsive to or judged untreatable by lesser procedures must decide between total pancreatectomy and resultant diabetes or a continuation of their pancreatitis. From 1977 through 1990, 26 patients underwent extensive pancreatectomy and dispersed pancreatic islet tissue autotransplantation for treatment of chronic pancreatitis pain and prophylaxis of surgical diabetes. Of these 26 patients, total (Whipple) or near-total (greater than 95%) pancreatectomy was performed in 24 patients. Of these 24 patients, pain relief could be assessed in 21 patients at 5 to 155 months (mean, 5.7 years), and 19 patients (90%) reported partial or complete remission. Of the patients who underwent total or near-total pancreatectomy, islets were injected intraportally in 22 patients and into the renal subcapsule in two patients. The latter two patients have required insulin since surgery. Of the other 22, one patient died from a complication of the pancreatectomy. Nine of the 21 evaluable recipients of intraportal islet autografts were insulin independent for at least several months after surgery. Five patients are currently insulin independent at 6 years, 4 years, 1.5 years, 9 months, and 5 months after surgery. Of the other four patients, one patient died insulin independent at 6 years, and three patients required insulin beginning 8 to 18 months after surgery. Insulin independence correlated with the number of islets recovered, which in turn correlated inversely with the degree of pancreatic fibrosis. Of our four most recent patients, three patients had mildly to moderately fibrotic glands, and higher numbers of islets were obtained. After total (Whipple) pancreatectomy, these three patients are insulin independent. A liver biopsy was performed in one patient 8 months after total pancreatectomy and islet autotransplantation; numerous clusters of islet cells staining strongly for insulin and glucagon were detected within portal triads on both wedge and needle biopsy specimens. Morbidity related to the intraportal-dispersed pancreatic islet tissue transplantation was low (no disseminated intravascular coagulation, significant portal hypertension, or hepatic dysfunction). Islet autotransplantation can be an effective and safe adjunct to extensive pancreatic resection for those patients who risk surgical diabetes for relief of their chronic pancreatitis pain.
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PMID:Autotransplantation of dispersed pancreatic islet tissue combined with total or near-total pancreatectomy for treatment of chronic pancreatitis. 185 51

Chronic pancreatitis is associated with glucose intolerance and resultant pancreatogenic diabetes. Using the canine pancreatic duct-ligated model of pancreatitis, we serially evaluated pancreatic histology and electron microscopy, tolerance to intravenous and oral glucose, and insulin response to glucose loading. Pancreatic duct ligation caused microscopic evidence of acute pancreatitis at 1 week, progressing to acinar loss and fibrosis consistent with chronic pancreatitis at time periods up to 6 months. The islets of Langerhans showed degranulation early and appeared to be structurally preserved late. Calculated K values indicated a progressive significant deterioration in intravenous glucose tolerance, falling significantly from 3.46 +/- 0.23 basally to 1.51 +/- 0.17 at 6 months after duct ligation (p less than 0.0001). Oral glucose tolerance deteriorated significantly, with the integrated glucose response rising from 23.7 +/- 1.2 g/dl.minute basally to 32.3 +/- 2.8 g/dl.minute at 6 months after duct ligation (p less than 0.05). Integrated insulin response to both intravenous and oral glucose deteriorated with pancreatitis. Pancreatitis-induced glucose intolerance is a consistent feature of this duct-ligated model. Glucose intolerance stabilizes between 4 and 6 months after duct ligation and is associated with pancreatic acinar fibrosis and pancreatic endocrine structural preservation. While the mechanism of altered glucose tolerance may involve mechanical, neural, humoral, or vascular events, our data clearly support the conclusion that pancreatic ductal stenosis with resultant pancreatic fibrosis and chronic pancreatitis is associated with abnormal islet responsiveness leading to circulating insulin deficiency and glucose intolerance, despite histologic and ultrastructural evidence of intact islets of Langerhans.
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PMID:Pancreatic structure and glucose tolerance in a longitudinal study of experimental pancreatitis-induced diabetes. 247 67

A fatal case of Yersinia enterocolitica septicemia which was complicated by unique hemosiderosis is reported. On admission, the patient had diabetes and showed unusual hyperferritinemia. Postmortem examination revealed that the liver was studied with abscesses, and Yersinia antigen was expressed in foamy macrophages within these abscesses. Moreover, the cadaver showed generalized hemosiderin deposition, which was mainly observed in the liver and, to lesser degrees, in the pancreas, spleen, lymph nodes, brain, thyroid and kidneys. Since there was no apparent cause of the hyperferritinemia and generalized hemosiderosis, consideration was given to possible primary hemochromatosis. However, no liver or pancreatic fibrosis was demonstrated. Kupffer cells were also loaded with hemosiderin, and therefore it was considered that these cells had lost their ability to phagocytize the microorganism adequately, leading to major liver involvement. Interestingly, hemosiderin deposits in the kidneys were mostly present in glomerular epithelial cells. To our knowledge, this unique presentation has not been previously described in humans.
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PMID:Fatal Yersinia enterocolitica septicemia complicated by unique hemosiderosis. A case report. 306 9

The pancreas and duodenum of 24 beagle dogs were given intraoperative irradiation (IORT) with 6 MeV electrons. The dose range was 17.5 Gy to 40 Gy. Billroth II gastrojejunostomy was performed on all dogs prior to irradiation. Six control dogs received only Billroth II surgery. Starting 2 weeks after surgery, dogs in the irradiation groups were given 50 Gy 6 MV X rays external beam radiation therapy (EBRT) to the pancreas and duodenum. The total dose of 50 Gy was given in 2 Gy fractions over 5 weeks. Dogs were monitored for 135 days then necropsied. Gross and histopathologic changes in the pancreas and duodenum were evaluated and quantitative analysis of pancreatic lesions done. Duodenal ulcers were found following 32.5 Gy and 40 Gy IORT. The pancreases were atrophic in irradiated dogs and exocrine pancreatic insufficiency occurred in one dog given 25 Gy. Gross pancreatic atrophy correlated with IORT dose. Histopathologic evidence of radiation damage to the pancreas was observed in acinar cells. Islet cell lesions were not apparent. There was pancreatic fibrosis and damage to blood vessels and ducts. Dose-response relationships were observed for the index of damage to the pancreas as a whole, for pancreatic fibrosis and a decrease in normal acinar cells. Although 25 Gy IORT plus 50 Gy EBRT was tolerated by the duodenum to 135 days, these doses may cause later pancreatic injury as an expression of damage to blood vessels and ducts. Exocrine pancreatic insufficiency and diabetes mellitus may thus represent potential late complications of IORT following 25 Gy or higher doses.
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PMID:Pathologic response of the pancreas and duodenum to experimental intraoperative irradiation. 338 21

We report the first case of the Pancreatic fibrosis calcification syndrome (PFCS) in a Liberian. The patient presented with the classical features of the syndrome - a history of recurrent abdominal pain, diabetes mellitus, malabsorption and pancreatic calcification on plain abdominal X-ray. The patient also has situs inversus; we believe that this combination is a casual one. Since describing this case, five more cases have been diagnosed; we believe that this condition is not rare in Liberia.
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PMID:Pancreatic fibrosis calcification and situs inversus in a Liberian female; a case report. 373 86

The presentation of diabetes in the young South African Indian is atypical in that insulin-dependent diabetes mellitus is rare, while non-insulin-dependent diabetes mellitus is common. In addition, youthful onset of tropical diabetic syndrome (J-type diabetes) is extremely rare. To date there appear to be no reports on a further tropical malnutrition diabetic syndrome associated with pancreatic fibrosis and calcification (Z-type diabetes). Four Indian patients with features consistent with the diagnosis of Z-type diabetes are described. All were asthenic, came from a poor socio-economic background and developed insulin-requiring diabetes in their youth; 3 of the 4 patients had pancreatic calcification.
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PMID:The occurrence of Z-type diabetes (tropical pancreatic diabetes) in the South African Indian. 382 89

Out of 325 patients with diabetes mellitus 24 (7.4%) suffered from pancreatic fibrosis-calcification. Of these 21 were below the age of 30 years. Sorghum (Jowar) was the staple diet for all. Most patients belonged to the lowest socio-economic strata.
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PMID:Pancreatic fibrosis-calcification with diabetes in South Maharashtra, India. 407 52

A series of 22 patients with cystic fibrosis (CF) of similar clinical severity (9 with normal carbohydrate tolerance and 13 with insulin-treated fasting hyperglycemia) was examined with quantitative vitreous fluorophotometry. All of the CF patients studied had normal fundi on ophthalmoscopy, fundus photographs, and fluorescein angiography. Mean vitreous fluorescein concentration in the CF patients whose hyperglycemia was treated with insulin (11.79 ng/ml) was significantly higher than in CF patients with normal carbohydrate tolerance (6.98 ng/ml, P less than 0.005). Thus, CF patients with fasting hyperglycemia demonstrate a breakdown of the blood-retinal barrier. When CF patients with fasting hyperglycemia were compared with age- and sex-matched type I diabetics, there was no significant difference in mean vitreous fluorescein accumulation. Thus, breakdown of the blood-retinal barrier, one of the earliest detectable functional abnormalities that may be associated with the microangiopathy of diabetes mellitus, also occurs with equal frequency and severity in the diabetes secondary to pancreatic fibrosis associated with CF.
Diabetes 1983 Jun
PMID:Quantitative vitreous fluorophotometry in insulin-treated cystic fibrosis patients. 662 36


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