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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Concentrations of serum cholesterol, triglyceride, and free glycerol were neasured, and serum lipoprotein electrophoresis was performed in normal dogs and in dogs with hypothyroidism, diabetes mellitus, and acute pancreatitis. Twelve privately owned dogs and 20 Basset Hounds from a research colony served as normal subjects. Privately owned had higher serum lipid concentrations than did research dogs. On electrophorisis of normal dog serum, lipoprotein bands were detected at the beta, pre-beta, alpha-2, and alpha-1 positions. Hypercholesterolemia was associated with increased intensity of the alpha-2-lipoprotein band, and hypertriglyceridemia occurred with increased lipoprotein at the origin, or the beta or pre-beta positions. Hypothyroid dogs had normal lipid values and lipoprotein electrophoretic patterns, hypercholesterolemia with increased intensity of the alpha-2-lipoprotein band, or hypercholesterolemia and hypertiglyceridemia with prominent beta-, pre-beta, and alpha-2-lipoprotein electrophoretic patterns were changed to near-normal values after levothyroxine administration. Diabetic dogs had increased serum cholesterol and triglyceride content and a predominance of lower density lipoproteins, as detected by electrophoresis. Insulin therapy caused the lipid concentrations to decrease and the electrophoretic pattern to revert to near normal. Dogs with acute pancreatitis had moderately increased serum lipid content and electrophoretic patterns characterized by increased intensity of the beta-lipoprotein band and by altered migration of alpha-1-lipoproteins.
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PMID:Lipids and lipoproteins in normal dogs and in dogs with secondary hyperlipoproteinemia. 16 57

A renal transplant patient in whom acute pancreatitis developed 2 1/2 years after surgery is presented. Pancreatisis was accompanied by hyperlipaemia, diabetes mellitus and acute renal failure possibly due to acute tubular necrosis. Pancreatic abscesses necessitated subtotal pancreatectomy 2 months later. Because of generalized tuberculosis finally the patient succumbed 6 weeks thereafter. As aetiological factors cytomegalovirus disease, disorders in lipid metabolism and immunosuppressive therapy must be discussed. It is concluded that prophylactic measures as well as early diagnosis, intensive care and therapy are necessary for reducing the high risks of pancreatis in renal transplant recipients.
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PMID:[Pancreatitis after renal transplantation (author's transl)]. 20 57

A case of diabetic lipemia is reported in a 27 year-old man admitted for acute pancreatitis. Initial investigations revealed gross hyperlipoproteinemia and ketoacidosis. Hyperlipoproteinemia was progressively corrected up to normalization in four weeks under insulin-therapy; the metabolic control of diabetes was obtained in parellel. This feature is caracteristic of "diabetic lipemia". The following sequence could be suggested: onset of diabetes, occurence of diabetic lipemia and then acute pancreatitis.
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PMID:[Acute pancreatitis during "diabetic lipemia": unusual disclosure of insulin-dependent diabetes (author's transl)]. 22 21

The role of surgery in the treatment of acute hemorrhagic or necrotizing pancreatitis is discussed on the basis of a series of 996 patients with all types of acute pancreatitis who were treated in the years 1967--1976. Pancreatic resection was performed in 29 patients with hemorrhagic or necrotizing pancreatitis during the past 3 years. The extent of resection ranged from 60 to 100% of the pancreas. Eight patients died, for a mortality rate of 28%. Eight of 21 surviving patients developed diabetes requiring substitution therapy. During a follow-up period of 6 to 36 months, 17 patients were able to resume work, 3 are still convalescing, and 1 has retired.
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PMID:Resection of the pancreas for acute hemorrhagic and necrotizing pancreatitis. 31 36

Follow-up of 25 cases of pancreatitis in childhood ascertained from the Hospital Activity Analysis in Newcastle and Wales showed that the majority of the children thrived after their illness. Only one child died. Only 2 children developed diabetes mellitus and 3 had significant malabsorption. There were 13 idiopathic cases (9 acute, 4 chronic relapsing), 3 of which were obese girls of pubertal age. It is speculated that obesity, puberty and female sex together may predispose to acute pancreatitis.
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PMID:Pancreatitis in childhood. 46 Dec 79

The five major diseases of the pancreas together make a significant contribution to morbidity and mortality among the people of the United States. These diseases are diabetes, cystic fibrosis, acute and chronic pancreatitis, and carcinoma of the exocrine pancreas. Four of these diseases can be modeled in laboratory animals by acute or chronic administration of chemical poisons or carcinogens. Human pancreatic diseases attributed to the effect of chemical agents including alcohol and drugs include many cases of chronic pancreatitis and some cases of acute pancreatitis. The cause is not known in many cases of human pancreatitis, including interstitial, acute, and chronic clinical forms. Epidemiologic studies suggest that the increasing incidence of carcinoma of the exocrine pancreas in the United States may reflect chemical carcinogenesis. On the basis of experimental observations, we know that pancreatic islet cells can be damaged directly by toxic chemicals, and that islet cell tumors can be chemically induced. Thus, there is adequate background data to conclude that several pancreatic diseases of obscure etiology may be due in part to hitherto unidentified toxic effects of chemical agents encountered in personal or general environments.
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PMID:Environmental factors and diseases of the pancreas. 59 42

Glucagon is secreted not only by A2-cells of the pancreatic islets but also by A cells in the gastric fundus and duodenum. Several reports have demonstrated that the glucagon plasma concentration is increased in genetic diabetes as well as in many conditions associated with a decreased glucose tolerance such as hepatic cirrhosis, myocardial infarction, infectious diseases, burns, taumatic shock, glucagonomas, acute pancreatitis, acromegaly, pheochromacytoma and Cushing's syndrome. Hyperglucagonemia is particularly important in diabetic ketoacidosis and in non-ketotic hyperosmolar coma. The mechanisms responsible for the diabetic's hyperglucagonemia remain controversial. According to several authors, the increased glucagon secretion is, for its main part, secondary to a prolonged defect in insulin secretion and thus relatively insensitive to an acute insulin administration. According to others, the A cell abnormality is of primary origin, independant from insulin deficiency and its effects are cumulative with those of the insulin lack. Several reports dealing with induced or spontaneous experimental diabetes are in favor of the first or the second hypothesis. It appears likely that glucagon plays a role in the metabolic derangments of diabetes. Indeed, hepatic glucose production is closely related to the ratio of molar concentrations of insulin and glucagon. Finally, in insulin-dependant diabetics, somatostatin infusion reduces plasma glucagon concentration and blood glucose and prevents the development of ketosis after withdrawal of insulin therapy. These results illustrate the contribution of glucagon in the pathogenesis of hyperglycemia and ketosis. Several arguments have been accumulated in favor of the following concept: diabetes hyperglycemia results both from glucose under-utilization secondary to insulin lack and from hepatic glucose over-production due to glucagon excess. Although controversial, the role of glucagon in ketogenesis appears likely.
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PMID:[The role of glucagon in hyperglycemia. A review (author's transl)]. 79 28

Acute pancreatitis was experimentally produced in dogs to study the effect of the disease on glucose tolerance. The k value (glucose disappearance coefficient measured in percentage decrease of glucose/min) calculated from the high-dose intravenous glucose-tolerance test was used to evaluate the glucose tolerance of each dog. Thirty dogs were allotted to 3 groups of 10 dogs each as follows: group I--nonsurgical control dogs; group II--surgical control dogs; and group III--pancreatitis-affected dogs. To increase their susceptibility to diabetes, 50% partial pancreatectomies and ductal catheterizations were performed on group II and III dogs. Saline solution was infused into the ductal systems of group II dogs, and staphylococcal alphatoxin was infused into the ductal systems of group III dogs to produce pancreatitis. The results indicated that (1) high-dose intravenous glucose-tolerance test was an effective tool for determining decreased glucose tolerance in dogs; (2) glucose tolerance of group III dogs was markedly decreased compared with that of group I and II dogs; (3) staphylococcal alpha-toxin produced signs of moderately severe pancreatitis; and (4) 50% partial pancreatectomy and saline solution infusion produced clinical and clinicopathologic signs of mild pancreatitis. To determine if a simplified k value (calculated using 2 or 3 blood samples) could closely approximate the standard k value (calculated using 6 blood samples), simplified k values were derived from the 5- and 60-minute blood sample values. These values closely approximated the standard k values, indicating the simplified value may be used in the clinical situation. The standard k value, however, is preferred for investigative work.
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PMID:Effect of staphylococcal alpha-toxin pancreatitis on glucose tolerance in the dog. 94 22

New tests and test methods aid in the diagnosis of pancreatic disorders. Pancreatic carcinoma, especially, may have an improved prognosis with earlier detection as a result of refinements in arteriography, cytology, pancreatic radioisotopic scanning, and endoscopic retrograde cholangiopancreatography. Acute pancreatitis results most commonly from alcoholism, biliary tract disease, and trauma. Management is directed primarily at decreasing pancreatic exocrine secretion. Surgery is usually best avoided in the acute phase. Chronic pancreatitis is most often a result of recurrent attacks of acute pancreatitis. Diabetes and malassimilation become manifest as pancreatic destruction progresses. Management consists of replacement of pancreatic enzymes and diet supplements. Once chronic pancreatitis is established, surgery can only be directed at complications of the disease. Pancreatic ascites is usually associated with a break in the pancreatic ductal system. Ascites caused by trauma responds well to surgical intervention, but the alcoholic type is less amenable to treatment.
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PMID:Pancreatic disease. 107 54

Pancreatico-jejunostomy end to side after resection of the pancreatic tail, or side to side following longitudinal cleaving of the pancreatic duct, was performed in 29 patients suffering from chronic relapsing or acute recurring pancreatitis. A follow-up study with observation time ranging from 6 months to 10 years is presented. The patients were allotted to three groups according to the severity and extent of the inflammatory involvement at operation. The diagnostic findings obtained at the preoperative evaluation correlated well to these groupings. In some patients, however, the inflammatory process was mainly confined to the ductal system, as revealed by pancreatography, while in others the changes were most marked in the parenchyma, as found at histologic examination. 21 caudal pancreatico-jejunostomies and 8 longitudinal anastomoses were performed. Overall results were excellent in 20 patients, good in 6, fair in 3, and poor in none. The rate of postoperative complications was low; no mortality, one spontaneously healed anastomosis insufficiency, subphrenic abscess developed in 2 instances and postoperative diabetes in 5. Only one patient had a recurrent attack of acute pancreatitis postoperatively. Re-anastomosis was successfully performed.
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PMID:Pancreatico-jejunostomy in chronic pancreatitis. An appraisal of 29 cases. 115 67


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