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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A female with premary hyperparathyroidism and secondary renal lesions, as well as lesions of the stomach and pancreas is described. The initial illness was manifested by repeated renal crises. Later, gastroenterological complaints appeared--epigastralgia, vomiting, frequent hematemesis with melena. That was the cause for a gastric resection, diffuse erosive gastritis being found. After the operation, the pains and the vomiting of hematin matter repeatedly recidivated. Clinically and at the laboratory, data were formed for a chronic recidivating pancreatitis with the presence of primary hyperparathyroidism. The postoperative treatment of the parathyroid adenoma led to an improvement of the gastroenterological complaints.
Vutr Boles 1976 Dec
PMID:[Chronic recurrent pancreatitis with erosive gastritis in a patient with primary hyperparathyroidism]. 101 31

Using a two stages screening method the prevalence in the general population of hyperlipoproteinemias (HLP), separated in the five types proposed by Fredrickson, Levy and Lees, and adopted by WHO has been studied. The study included 7,085 subjects of both sexes, aged 25-65 years, representing 84,52 % of a population taken at random within a district of Bucarest. HLP was found in 1,013 cases, i.e. 14,29 % of the investigated population. 48.37 % were men and 51.63 % women. The prevalence of HLP was lowest in the first decace of age studied (25-35 years) and highest in the last two decades (45-65 years). Overweight was more frequently encountered in these patients (64.46 %) than in the total population (32.3 %). Of the 1,013 cases with HLP, 42.35 % (6.05 % of the total population) were of type IV, 27.05 % (3.86 % of the total population) of type II-b, 22.80 % (3.26 % of the total population) of type II-a, 4.74 % (0.67 % of the total population) of the type III and 3.06 % (0.43 % of the total population) of the type V. 22.70 % of the HLP patients were considered primary familial HLP, 66.54 % primary non-familial HLP and 10.76 % secondary HLP; IN 109 secondary HLP, the most frequently encountered disease was diabetes mellitus (42.20 %), followed by hypothyroidism (24.77 %), alcoholism (12.84 %), obstructive liver diseases (9.17 %), pancreatitis (5.50 %), nephrotic syndrome (2.75 %) and treatment with estrogens and steroids (2.75 %).
Diabete Metab 1976 Dec
PMID:The epidemiology of hyperlipoproteinemia in a Rumanian general population sample. Study of 7,085 cases. 101 36

Neuropsychiatric and psychosomatic disorders occurring the exocrine pancreatic diseases are not rare, nevertheless didn't it seem to be very interesting in research and there exists no summarizing work of this disorders. Therefore we tried to give a comprehensive representation of those neuropsychiatric problems which are connected with the function of this organ. At first we give a description of psychopathology and pathogenesis of the functional pancreatic psychosis. The problematic of the reciprocal relationship of nervous system and pancreatitis, alcoholism and pancreatitis are demonstrated as well as the psychic disorders occurring the pancreas insufficiency, cystes of pancreas and congenital pancreatic diseases. Psychosomatic and mental disorders of pancreas carcinoma and mucoviscidosis are shown in detail. The question of the interrelation between pancreatic function and amyotrophic lateral sclerosis or parathyreotic diseases are discussed just as themes of neuropsychiatric pharmacotherapie and pancreatic function and mental disorders in pancreatic treatment.
Fortschr Neurol Psychiatr Grenzgeb 1976 Dec
PMID:[Neuropsychiatric disorders of the diseases of exocrine pancreas (author's transl)]. 105 12

A case of pancreatic ascites is reported and compared with 55 previously reported cases. A 42-year-old black male chronic alcoholic presenting with abdominal pain was found at operation to have chronic pancreatitis with no pseudocyst formation or overt duct disruption, in contrast to the majority of cases reported. The diagnosis and differentiation from cirrhosis of the liver were based on the operative findings, elevated serum amylase level, ascitic fluid amylase value, and protein content. Surgical exploration alone has proven beneficial--the patient has done well in the past 2 years with no recurrence of the ascites and continued weight gain. The clinical course was compatible with pancreatitis although the radiographic and angiographic studies were not diagnostic. It is suggested that the clinical entity of pancreatic ascites occurs more often than reported and a workup for it should be done even in the face of unconvincing radiographic and angiographic evidence.
Am J Dig Dis 1975 Dec
PMID:Pancreatic ascites. A case report and review of the literature. 120 11

Plasma pancreatic glucagon concentrations were determined in the basal state and after the infusion of alanine in 10 patients with acute pancreatitis (5 in an initial episode of pancreatitis), in 10 patients with chronic pancreatic insufficiency, and in 21 healthy controls. In acute pancreatitis, basal glucagon levels were nine times normal but were higher during the initial attack than with a history of previous attacks. The glucagon response to alanine was also increased threefold to fourfold in initial attacks. In contrast, after recovery from the initial attack of acute pancreatitis, during acute episodes of pancreatitis in patients with a history of previous attacks, and in patients with pancreatic insufficiency, alanine failed to elicit a consistent rise in plasma glucagon. The data suggest that hyperglucagonemia may contribute to the hyperglycemia of acute pancreatitis, particularly during the initial episode. Loss of alpha cell responsiveness to alanine provides a sensitive index of previous pancreatitis.
Ann Intern Med 1975 Dec
PMID:Glucagon secretion in acute and chronic pancreatitis. 120 May 23

Within a few hours after one injection of fresh human serum by the intraperitoneal route only, mice developed pancreatic acinar cell necrosis and inflammation, fat necrosis, elevated serum amylase and a shocklike state. The extent of these lesions and mortalities were roughly dose dependent and were not noticeably modified by either different fasting cycles or pilocarpine. Acinar cell changes and necrosis usually developed first in subserosal acini. The earliest ultrastructural change detected was nonspecific swelling of cytoplasmic compartments which was reversible but also preceded the cytoplasmic degradation that developed in cells undergoing necrosis. Notably, zymogen granule dissolution neither preceded nor accompanied this swelling, but developed pari passu with cell degradation. Occasionally, intact granules were found in necrotic cells. Serum was cytotoxic for isolated acinar cells in vitro, even in the presence of soybean trypsin inhibitor. These results (1) indicate that the injury mechanism in vivo is directly initiated through contact of serum with acinar cell surfaces and is independent of zymogen secretions and trypsin activation, and (2) suggest that a rapid disturbance in cell membrane permeability results, the magnitude of which being the primary determinant of cell death. Pancreatic toxicity of human serum was abolished by aging, heating, ethylenediaminetetraacetic acid, heparin, zymosan, cobra venom factor, and absorptions with mouse red blood cells, against which fresh, unabsorbed serum was hemolytic. Pancreatic toxicity in vitro and, to a much lesser extent, in vivo was reconstituted by combining the red blood cell-absorbed serum with either heated serum, or with IgM-enriched, but not IgG serum fractions. Fresh cord serum was virtually nontoxic and could substitute for absorbed serum in such reconstitutions. These results indicate that the injury mechanism involves at least two serum components. By both circumstance and analogy, other results and a review of other examples of foreign sera toxicity suggest that they are components of a complement-dependent, cytotoxic heterophile antibody system. The relevance of this odd phenomenon is that it offers a simple model of acute pancreatitis, contributes to the debunking of traditional notions of the pivotal role of zymogens in the initiation of acute pancreatitis, and hints at a potential pathogenetic connection between pancreatitis and products of immune or related reactions.
Lab Invest 1975 Dec
PMID:Foreign serum-induced pancreatitis in mice. I. A new model of acute pancreatitis. 120 81

Gray scale scanners allow the demonstration of much more anatomical detail than was possible with the older type scanners. The initial step in the ultrasonic examination of the pancreas is display of the anatomical detail of the portal vasculature which provides a guidepost to the pancreas. Pancreatitis is characterized by a diffusely enlarged echo-free pancreas. Pancreatic pseudocyst is almost always an echo-free unilocular fluid collection. The size of a pancreatic pseudocyst can be measured so that progress can be assessed. Pseudocysts located in the region of the tail of the pancreas may be best demonstrated by scanning from the back over the left kidney. Pancreatic pseudocysts may be partly solid. Pancreatic carcinoma appears as a localized relatively echo-free, poorly defined solid mass which attenuates the ultrasound beam. Pancreatic carcinoma smaller than 2 cm in diameter are particularly difficult to diagnose by ultrasonic examination. Pancreatic carcinoma may be difficult to distinguish from chronic pancreatitis. Dilated bile ducts can be demonstrated and point to extrahepatic biliary obstruction. Serial ultrasonic scans have been suggested as a means of monitoring the response of pancreatic tumors to therapy. The relative diagnostic value of endoscopic retrograde cannulation of the pancreatic ducts and ultrasound has not as yet been established. Ultrasonic examination is easier to perform and less expensive than any other pancreatic imaging procedure other than the upper gastrointestinal barium examination.
Radiol Clin North Am 1975 Dec
PMID:Ultrasonic examination of the pancreas. 120 74

The authors report 6 cases of chronic familial pancreatitis. They review the literature on this disease which is still little recognised and seek the specific characteristics, early onset, transmission as an autosomic dominant with incomplete penetrance, relatively favourable prognosis, together with the suggestive signs, pancreatic lithiasis and certain complications. Apart from these signs, chronic familial pancreatitis differs very little from common chronic pancreatitis. The only cause is apparently genetic. Etiopathogenesis is thus still obscure. Treatment should be started early, but surgical methods are the same as in primary chronic pancreatitis.
J Chir (Paris) 1975 Dec
PMID:[Chronic familial pancreatitis (6 cases, 3 families)]. 122 33

To determine whether the lipase:amylase ratio differentiates alcoholic from nonalcoholic pancreatitis, we conducted a retrospective review of charts with the diagnosis of acute pancreatitis at the George Washington University Medical Center between January 1988 and July 1990. A total of 446 charts were reviewed. For a patient to be included in the subsequent analysis, the following criteria were met: 1) the patient had typical symptoms of pancreatitis, 2) serum amylase and lipase were analyzed on admission, and 3) a computerized tomographic (CT) scan or ultrasound of the abdomen was obtained within 72 h of admission. Forty-seven charts satisfied the requirements for inclusion in the study. Data collected from the charts included history of alcohol consumption, age, sex, race, admission serum amylase and serum lipase (from this the amylase:lipase ratio was calculated), peak serum amylase and serum lipase, and number of days of abdominal pain before admission. Patients with alcoholic pancreatitis had significantly lower serum amylase levels and significantly higher lipase:amylase ratios than those with nonalcoholic pancreatitis (p < 0.01). There was no difference in the serum lipase between the groups. The higher the lipase:amylase ratio, the greater the specificity of alcohol as the etiology of acute pancreatitis. Only patients with alcoholic acute pancreatitis had lipase:amylase ratios > 5.0 (sensitivity 31%, specificity 100%). Our data point to the clinical utility of the lipase:amylase ratio in differentiating alcoholic from nonalcoholic acute pancreatitis. Prospective studies will be needed to confirm the clinical utility of this ratio.
Am J Gastroenterol 1992 Dec
PMID:The admission serum lipase:amylase ratio differentiates alcoholic from nonalcoholic acute pancreatitis. 128 Apr 5

To clarify a possible cause of hyperamylasemia in end-stage renal disease (ESRD), histological studies were performed on the pancreatic glands of twenty-seven autopsied patients with ESRD who had received long-term hemodialysis. The findings were compared with those in a similar number of age-matched control subjects. Histological evidence of pancreatitis was found in 51.9% of the ESRD patients as compared with 14.8% in the controls (p < 0.005). The pancreatitis was chronic in nature in 85.7% of the ESRD patients showing changes of pancreatitis. Secretin administration to an additional group of twelve patients with ESRD induced an elevation in the activities of both total and P-type serum amylase in only one patient. These findings suggest that although histological pancreatic alterations are common in patients with ESRD, they are probably not responsible for the P-type hyperamylasemia frequently found in such patients.
Int J Pancreatol 1992 Dec
PMID:Histological pancreatitis in end-stage renal disease. 128 64


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