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Query: UMLS:C0149521 (chronic pancreatitis)
 7,199 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this work was: a) the prospective study of the prevalence of hyperamylasemia in 100 patients with chronic alcoholism; b) the determination of the serum isoamylase distribution in patients with hyperamylasemia by an inhibitor assay; c) the search of the origin of elevated serum isoamylase S. Moderate hyperamylasemia was found in 15 patients. The importance of alcohol abuse, the prevalences of cirrhosis and smokers were not statistically different from those observed in normoamylasemic patients. After one week of hospitalization, serum amylase was still elevated in 11 of 14 alcoholic patients. Hyperamylasemia was due to an increase in the isoamylase P in 5 cases, in the isoamylase S in 7 cases, and in both forms in 3 cases. Activities of serum lipase and isoamylase P were roughly parallel. Only two out of 8 patients with elevated isoamylase P had chronic pancreatitis. The salivary origin of elevated isoamylase S was suspected in only one out of 10 patients. This work shows that the origin of moderate hyperamylasemia, observed in alcoholic patients, is often extrapancreatic. It is suggested that the dosage of serum lipase simpler than that of isoamylases, may be routinely used in chronic alcoholic patients for diagnostic purposes.
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PMID:[Occurrence and nature of hyperamylasemia in chronic alcoholics]. 608 28

The present investigation defined the pattern of pancreatic, pituitary and adrenal responses after insulin-induced hypoglycemia in chronic calcific pancreatitis (CCP) related to alcohol abuse, and assessed the role of some of these hormones in the counterregulation of blood glucose. We studied 6 Black men with recently diagnosed CCP, all showing radiological evidence of pancreatic calcification and normal glucose tolerance, as well as 7 matched nonobese male controls. After a standard iv insulin tolerance test inducing marked hypoglycemia, patients with CCP showed significantly impaired mean plasma pancreatic glucagon and pancreatic polypeptide responses compared to the controls. Mean basal plasma somatostatin levels tended to be higher in chronic pancreatitis and remained so throughout the test without altering consistently; in the controls somatostatin peaked significantly at 30 min. Concerning extrapancreatic hormonal changes, plasma growth hormone, prolactin and total catecholamines responded normally in CCP, but plasma cortisol rose to significantly higher levels than controls at 60 and 120 min after the injection of insulin. This, coupled with the brisk output of catecholamines, may have prevented the heightened sensitivity to insulin anticipated because of their hypoglucagonemia. We conclude that patients with CCP show impaired pancreatic hormone release after insulin hypoglycemia with the exception of somatostatin; there is also an excessive rise in plasma cortisol, possibly related to the long standing abuse of alcohol in the past.
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PMID:Hormonal profile after insulin-induced hypoglycemia in chronic calcific pancreatitis. Pancreatic, pituitary and adrenal responses. 639 52

Of 81 patients with chronic pancreatitis admitted to the Ottawa Civic Hospital over a 5-year period, 40 had conditions that were thought to be amenable to various operations. Good results were obtained in 70%. Of note were the 75% good results of pancreaticojejunostomy. Several patients needed further operations. The proportion of good results leaves no room for complacency, but it is difficult to envisage how a damaged gland can be expected to make a full recovery from either internal or external drainage procedures. Two patients died of carcinoma within 2 years of their initial operation and may have had carcinoma of the pancreas from the outset, although their mode of presentation and results of investigation were those of chronic pancreatitis. Alcohol abuse was thought to be responsible for the condition in 72% of these patients.
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PMID:Chronic pancreatitis: a 5-year experience. 646 1

Examination of 124 pancreatico-duodenal preparations obtained during surgery and of 250 pancreatic preparations at post-mortem has shown, that patients with chronic pancreatitis do have rather frequently cysts of the duodenal wall (38,5%). These cysts have a diameter of 2-100 mm. They are located in most cases in the submucosal layer as well as in the muscularis propria layer of the duodenal wall between pylorus and papilla. They lead to stenoses of the duodenum in 27% of the cases and they may be considered as a drainage barrier for pancreatic juice in 48.6% of the cases. They are lined with a single layer cylindrical or cubical epithelium; below the epithelium there are located rather frequently tubular glands (49.1%) and sometimes residues of Brunner's glands (7%) as well as ectopical pancreatic tissue (8.8%). The type of epithelial lining points to the fact, that these cysts may be considered as heterotopic formations of pancreatico-ductal tissue. On comparing the groups of patients with chronic pancreatitis with and without cysts of the duodenal wall it turned out that there was no difference between these groups in regard to histology of the disease, alcohol abuse, age and sex. Single cases described in the literature and 4 own cases show however, that chronic pancreatitis may be caused by primary cysts of the duodenal wall.
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PMID:[Duodenal wall cysts and diseases of the pancreas]. 667 17

A group of 73 patients suffering from painful alcoholic, chronic pancreatitis, hospitalized from 1971 to 1981, has been analyzed retrospectively. The aim was to assess the effects of alcohol withdrawal and pancreatic surgery on the course of pancreatic pain. The mean number of years during which the patients complained of pain was 3.5 +/- 0.5 (m +/- SEM). At the end of follow-up, 70 p. 100 of the patients did no longer suffer, alcohol withdrawal was obtained in 45 p. 100 and surgery had been performed in 41 p. 100. Continued alcohol abuse did not prevent pain relief: 60 p. 100 of patients continuing to drink at the end of follow-up, did not suffer any longer. One year after pancreatic surgery, pain relief was more frequent, if alcohol abstinence had been obtained before surgery (p less than 0.01). Among the 53 patients followed up to 5 years after the start of pain: a) the cumulative actuarial probability of disappearance of pain was 17 p. 100 at 2 years, 52 p. 100 at 5 years, 62 p. 100 at 8 years after the start of pain. Alcohol abstinence and surgery were observed during the first five years of pain; b) the mean number of years of pain was lower among the patients who became abstinent early (less than 4 years after the beginning of pain) than among those who did not (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Chronic alcoholic pancreatitis: relation of pain to withdrawal and pancreatic surgery]. 673 54

Chronic pancreatitis is an infrequently considered cause of gastrointestinal bleeding. Four cases are described who presented to a surgical unit in a year. One patient bled down the main pancreatic duct from a splenic artery pseudoaneurysm, one had a fatal haemorrhage from a superior mesenteric artery aneurysm which ruptured into the duodenum, and two were considered to have bled from vessels in the stomach or colon which were involved in the peripancreatic inflammatory tissues. The difficulties in diagnosing these patients are described and the report emphasises that the diagnosis should be considered in obscure cases of gastrointestinal bleeding especially where there is a history of alcohol abuse and left upper quadrant or epigastric pain.
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PMID:Chronic pancreatitis as a cause of gastrointestinal bleeding. 697 76

Ethanol is easily absorbed from the intestine and diffuses quickly throughout body water. The bulk of ethanol is metabolized in the liver, where alcohol dehydrogenase, a complex mixture of isoenzymes, oxidizes ethanol to acetaldehyde. Ethanol abuse produces functional and structural changes in the gastrointestinal tract, such as in the stomach, small intestine, liver, and pancreas. Accumulating evidence suggests direct toxicity of ethanol and possibly of acetaldehyde. Fatty liver, alcoholic hepatitis, liver cirrhosis, acute and chronic gastritis, deranged structure and function of the small intestine, acute and chronic pancreatitis, and pancreatic lithiasis are some of the sequelae of ethanol abuse. Recent investigations have enhanced our understanding of the functional and structural changes of the gastrointestinal tract produced by the abuse of ethanol.
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PMID:Ethanol, the liver, and the gastrointestinal tract. 719 92

Intramural hematoma of the duodenum is usually caused by blunt abdominal injury. Sometimes this lesion occurs in patients with coagulation disturbances or pancreatic disease such as chronic pancreatitis. There also appears to be a link with alcohol abuse. We describe the case-history of a 45-year-old male with chronic pancreatitis who presented with abdominal pain. The diagnosis of a space-occupying process of the duodenum was made and subsequently a pancreatico-duodenectomy was performed. The duodenum revealed an intramural hematoma, the pancreas showed signs of mild chronic pancreatitis.
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PMID:Intramural hematoma of the duodenum in a patient with chronic pancreatitis. 729 15

In the prospective clinical long-term study of 246 patients with chronic pancreatitis, 26 patients (24 men) developed 27 histologically proved malignant tumors (11%). Four additional patients with neoplasia were excluded (papilloma, two; Bowen's disease of the tonsils, one; and seminoma, one, occurring 8 years before onset of pancreatitis). In six patients pancreatic cancer was diagnosed (2.4%), which indicates a slightly increased risk over the general population. Interestingly, 21 patients developed extrapancreatic cancer (8.5%), including a very high incidence that has not been noted previously. The cancers were located in the oral cavity (in six), larynx (three), bronchus (eight), and gastrointestinal tract (four). The data suggest a causal relationship between chronic pancreatitis and cancer. As possible factors, smoking, alcohol abuse, diabetes, malnutrition, immune deficiency, and high dietary fat intake are discussed. There is, however, no definite evidence for any single known factor.
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PMID:High incidence of extrapancreatic carcinoma in chronic pancreatitis. 743

Forty patients underwent total pancreatoduodenectomy for end-stage chronic pancreatitis. There were 34 men and six women of median age 39 (range 21-66) years. Alcoholism was the major aetiological agent (30 patients), and five patients had had previous acute idiopathic pancreatitis. The overwhelming indication for operation was severe abdominal pain, complicated by failing exocrine and endocrine function. Resection was performed in one (17 patients) or two (23) stages, following previous proximal (seven) or distal (16) pancreatectomy; progression from partial to total pancreatectomy occurred over an interval of 8-96 (median 15) months. A further six patients had undergone previous pseudocyst or duct drainage procedures. The pylorus was preserved in 28 patients and the spleen in ten. Median operating time was 6 (range 2.5-8.5) h and median blood loss 2000 (range 500-16,000) ml. There were two hospital deaths and three patients required reoperation. Of 38 survivors, 30 obtained complete or substantial relief of pain. There were 15 late deaths at 2.5-120.0 months after operation, 13 in the alcohol group and 11 disease-related. Total pancreatectomy can relieve the intractable pain of chronic pancreatitis at the cost of possible premature death from continuing alcohol abuse.
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PMID:Role of total pancreatectomy in the treatment of patients with end-stage chronic pancreatitis. 748 80


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