Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum Deoxyribonuclease (DNase) of normal persons and of patients with chronic pancreatitis, pancreatic cancer, Diabetes Mellitus, or other malignant diseases was determined with (32P) DNA as substrate. Serum DNase activity was much lower in patients with chronic pancreatitis, pancreatic cancer, or other malignant diseases than in control subjects, and serum DNase activity was almost normal in patients with Diabetes Mellitus. There was no correlation between serum DNase and serum amylase, but there was a good correlation between serum DNase and DNase I output in duodenal juice. There was an inverse correlation between serum DNase and serum RNase. These results imply that in the diagnosis of possible pancreatic disorders serum DNase may be a good indicator and thus may be useful for the detection of malignant diseases.
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PMID:Clinical investigation of serum deoxyribonuclease: II. Clinical studies of serum deoxyribonuclease activity in pancreatic disease. 52 Jul 66

The authors discuss the main features of the complex pathophysiology of patients subjected to duodenocephalopancreatectomy, and particularly the difficulties inherent in clinical assessment of the digestive and metabolic impairment consequent upon the duodeno-gastro-pancreatic mutilation. Out of a total of 57 cases of this description, they singled out for recheck 23 patients who had undergone duodenocephalopancreatectomy not less than six months and not more than seven years before (chronic pancreatitis, 11 cases; various malignancies of the periampullar area, 10 cases; Zollinger-Ellison syndrome, 1 case; retroperitoneal lymphoma, 1 case). Seventy-six per cent of patients who had been gainfully employed were able to resume their jobs after surgery. Steatorrhea, assessed in terms of fecal fats, was present in all cases; notwithstanding, 70% of the patients gained weight (average increase 7 kg). All patients were on enzyme replacement therapy. Only 4% developed diabetes, and none developed postoperative peptic ulcers. Conversely there was a high incidence (65%) of bone structure reshuffling, signally osteoporosis, probably imputable to steatorrhea and vitamin D malabsorption, plus the often associated increase of serum alkaline phosphatase activity.
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PMID:[The biological results of duodenocephalopancreatectomy. Clinical evaluations based on a long-term follow-up]. 53 2

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

Secretin releasing response to intraduodenal acid infusion was investigated in 15 cases of diseased control, 7 cases of duodenal ulcer, 5 cases of chronic pancreatitis, and 6 cases of diabetes mellitus. Plasma secretin levels in response to duodenal acidification were less in duodenal ulcer and the appearance of the maximal peak was delayed compared with that found in control. It is suggested that the secretin release was impaired in duodenal ulcer in spite of hypersecretion of gastric acids. In chronic pancreatitis, secretin releasing response to acidification was markedly impaired, in addition, inhibition of secretin release by bicarbonate was diminished due to a lack of bicarbonate flow from the pancreas. On the other hand, although the response of secretin release in diabetes mellitus was also lower compared with that in control group, the capacity of secretin response showed values in-between control subjects and chronic pancreatitis. This research was supported in part by grant from the Ministry of Education, Science and Culture in Japan.
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PMID:Secretin secretion in patients with duodenal ulcer, chronic pancreatitis and diabetes mellitus. 64 3

An analysis of 89 cases with chronic pancreatitis revealed 56% of chronic alcoholic pancreatitis (AP). The sex ratio was 47 males to 3 females and the mean age at onset was 42.4 years in AP and 49.3 years in chronic non-alcoholic pancreatitis (NAP). The 'total amount' of alcohol consumption was correlated to the onset. In AP, the abdominal pain was apt to relapse and severe in nature, furthermore painless pancreatitis was seen in 6%. The association with diabetes or calcification (38%) were more frequently seen in AP. The calcifications in AP appeared to be smaller in size and distributed diffusely or localized in cephalic portion. A striking frequency of liver dysfunctions (39 cases) were demonstrated, however, cirrhosis was rare in AP. The P-S test dysunctions in NAP were frequently reversible in the follow up study, while even some of chronic asymptomatic alcoholics developed clinical signs of pancreatitis during the observed period and proceeded to definite AP, of whom pancreatic dysfunctions showed fluctuation and eventual progression. In other words, even pain free intervals the pancreatic inflammation in susceptible persons may proceed to ultimated destruction of the pancreas. The fatality from chronic pancreatitis was rare (12.3%), which was related diabetes mellitus.
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PMID:A clinical investigation of chronic pancreatitis--comparative study between alcoholic pancreatitis and non-alcoholic pancreatitis--. 66 97

Information from 72 patients from 7 families in England and Wales confirms that hereditary pancreatitis is inherited as an autosomal dominant conditions with limited penetrance. The degree of penetrance is approximately 80%. These patients have had recurrent attacks of abdominal pain starting from childhood or young adult life. The mean age of onset in the 7 families studied was 13.6 years. There were two peaks, with maximum numbers at 5 years and 17 years. The second peak was thought to represent genetically susceptible individuals having pain brought on by alcohol rather than representing evidence of genetic heterogeneity. Five of the 7 families had members with both childhood and adult ages of onset. Only 4 patients out of 72 had life-threatening disease and in the majority of cases the attacks of pain were of nuisance value only. Hereditary pancreatitis was implicated in only 1 patient's death and this was not definite. Patients appear to get better after a period of symptoms usually as they approach middle age, or after a severe attack. In older patients alcohol, emotional upsets, and fatty food appear to precipitate attacks. Pancreatic insufficiency (5.5%), diabetes mellitus (12.5%), pseudocysts (5.5%), and haemorrhagic pleural effusion are uncommon complications. Portal vein thrombosis occurred definitely in 2 patients and was suspected in 3 others. Carcinoma of the pancreas was not found in any of 72 patients studied in detail; however, 2 members from a family not visited personally had chronic pancreatitis and malabsorption going on to carcinoma. They may have suffered from a different disease. Genetic linkage information was too slight for many definite conclusions. However, there was no suggestion of linkage with any of the markers tested.
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PMID:Hereditary pancreatitis in England and Wales. 67 83

In order to study the disposition which is thought to be latent in chronic pancreatitis, we investigated the sweat chloride concentration of 95 normal subjects, 43 cases of chronic pancreatitis, 12 cases of cholelithiasis, 15 cases of peptic ulcers, 16 cases of hepatic diseases and 23 cases of diabetes mellitus with the sweat test, using the method of pilocarpine iontophoresis. We obtained the following results. (1) In normal subjects, the sweat chloride concentration was inclined to rise gradually with age from childhood to adulthood; the mean value of sweat chloride concentration was 30.0 mEq/liter in adults from 20 years old, and the upper limit was about 60 mEq/liter. (2) The mean value of sweat chloride concentration was 60.0 mEq/liter in chronic calcifying pancreatitis; this value was markedly higher than that of control subjects of the same age (p is less than 0.001). (3) The mean value of sweat chloride concentration in cholelithiasis, peptic ulcer and hepatic diseases did not differ significantly from control subjects. The mean value of sweat chloride concentration in diabetes mellitus was significantly higher than that of control subjects (p is less than 0.01), but was significantly lower than that in chronic pancreatitis (p is less than 0.01). (4) It was supposed that some cases of chronic pancreatitis have a congenital disposition toward abnormal secretion of sweat glands and epithelium in the pancreatic duct, resembling cystic fibrosis, and this disposition leads easily to pancreatic disorders when the individual is exposed to various external factors.
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PMID:The significance of the sweat test in chronic pancreatitis. 67 78

We found abnormal glucose tolerance curves in 45 of 47 patients with chronic pancreatitis and observed secondary diabetic retinopathy in eight of 45 cases showing slight changes in the fundus. Abnormal glucose tolerance curves were somewhat related to the exocrine dysfunction of the pancreas. Slightly abnormal glucose tolerance curves were observed frequently in patients with chronic pancreatitis, and both insulin and glucagon responses were decreased. We could not explain the cause of the low frequency of secondary diabetic retinopathy in pancreatic diabetes from the results of insulin and glucagon response tests.
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PMID:Secondary diabetic retinopathy in chronic pancreatitis. 67 11

In 394 consecutive autopies, tissue from the body of the pancreas showed chronic inflammation in 52 cases (13%); 32 were mild, 11 moderate and 9 severe. Only two of these cases had the clinical diagnosis chronic pancreatitis. The incidence of inspissated plugs of protein in the ducts, dilated ducts and acinar ectasia was significantly higher when chronic inflammation was present. There was a significant higher incidence of chronic inflammation in the pancreas in patients with diabetes mellitus. No significant correlation was noted between chronic inflammation in the pancreas and cholelithiasis, previous cholecystectomy, peritonitis, gastric and duodenal ulcer, abdominal operations, ascites and liver metastases.
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PMID:The incidence and clinical relevance of chronic inflammation in the pancreas in autopsy material. 71 98

Various parameters of the insulin secretion in man may be appreciated and calculated by studying the insulin response to an intravenous pulse of glucose followed 120 minutes later by one of tolbutamide. The relative insensitivity of the B cell to glucose, probable marker of a constitutional pancreatic predisposition to diabetes may be assessed in a given individual whatever his age and body weight. The glucose intolerance per se is due to, or accompagnied by various B cell dysfunctions according to its etiology. This is illustrated by the results observed in chronic pancreatitis, liver cirrhosis, aged or obese subjects.
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PMID:[A method of studying insulin secretion in humans: the glucose stimulation test, followed by tolbutamide]. 79 23


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