[Instrumental and clinical comparison of films for mammography. Analysis of the characteristic curve and modulation transfer function].
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Biomedical subjects
Publications and source records attributed to L Benini.
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In order to investigate the role of circulating free trypsinogen and renal tubular dysfunction in affecting trypsin plasma-urine transfer, serum immunoreactive trypsin (IRT), its urinary output, IRT molecular size distribution, filtrable immunoreactive trypsin, gamma-glutamyltransferase and alpha-glucosidase outputs were studied in 6 control subjects, 9 patients with pancreatic cancer and 15 with chronic pancreatitis. The majority of immunoreactivity was always eluted at a molecular weight of about 24,000 and might therefore be considered as free trypsinogen. Variable amounts of IRT at higher molecular weights, possibly represented by trypsin-inhibitor complexes, were also detected. Increasing IRT levels were generally accounted for by free trypsinogen, regardless of the nature of the disease. Unlike serum free trypsinogen levels, renal tubular damage, evaluated by means of the excretion of two high-molecular weight urinary enzymes, seems to play a prominent role in explaining trypsin plasma-urine transfer.
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Forty-six subjects (20 chronic pancreatitis, 7 chronic liver disease, 7 recovered from acute pancreatitis, 2 Crohn's disease, and 10 healthy controls) classified by S-C test as having normal pancreatic function (26 subjects), or moderate (10 subjects) and severe (10 cases) pancreatic insufficiency, were given, on different days, 1 g of oral PABA or 348 mg of oral fluorescein dilaurate. At the 1st, 2nd, and 4th hours (PABA) and the 2nd, 4th, and 6th hours (fluorescein) serum samples were taken for assay. In the presence of severe exocrine pancreatic insufficiency, the sensitivity of the fluorescein serum levels was higher than that observed for the PABA (100% and 80%, respectively), and quite similar to that shown by the urinary tests (100% and 70%, respectively). On the contrary, in presence of moderate pancreatic insufficiency, both the urinary test (pancreolauryl and (PABA) give a sensitivity higher than that found in the serum tests (30-40% and 10-30%, respectively). The parallel combination of both the serum or urinary tests does not significantly improve the sensitivity of the single test. These results suggest that the serum PABA and serum fluorescein tests can be valid choice when a prolonged urinary collection is difficult, i.e., in children and in elderly patients. However, the slight diagnostic gain does not justify the routine use of both urinary and serum tests.
Plasma levels of lactoferrin (LF) have been found to be increased in a few patients with cystic fibrosis (CF). This study was aimed at investigating plasma LF levels in children with CF (26 cases) and in controls (C) (19 cases). Plasma LF was measured by a radioimmunoassay method. Plasma LF levels were not significantly different in CF and in C, even though 10 CF patients showed LF levels above the mean + 2 SD value of the controls. Neither the duration of the disease nor the age of the controls was correlated with LF or with the exocrine pancreatic capacity. A significant relationship between the presence of an acute lung inflammation and LF levels was found. This study shows that LF is increased in CF only in the presence of an acute inflammatory state. Further studies are necessary to establish the usefulness of an LF assay as an index of the presence of an acute inflammatory process.
A 14C-triolein breath test was carried out on 49 subjects suffering from chronic pancreatitis or from other digestive diseases, and its results were compared with the daily fecal fat excretion. The 14CO2 peak excretion was abnormal in all the subjects with a fecal fat excretion above 14 g/day, whereas individual values of 14CO2 peak excretion in subjects without steatorrhea and with a fecal fat excretion ranging from 7.1 to 14 g overlapped. The lowest value observed in patients not suffering from steatorrhea was chosen as the lower normal limit of 14CO2 peak excretion. A test sensitivity as high as 64% was attained. The correlation between fecal fat and 14CO2 peak excretion was highly significant (r = 0.802; p less than 0.0001), and it followed a negative exponential function. Therefore, small variations in the 14CO2 peak excretion can be associated with a wide range of fecal fat excretion. Well-compensated diabetes secondary to pancreatitis did not interfere with the results of the test. In conclusion, in our experience this test proved to be a qualitative diagnostic tool with a low sensitivity.
The reliability of the para-aminobenzoic acid (PABA) test (performed in the conventional manner, i.e. without control day) and of the pancreolauryl test was assayed in respect of the exocrine pancreatic capacity measured by using the secretin-caerulein test in 57 subjects, 22 of which were suffering from chronic pancreatitis. When 50 and 20% urinary excretion of the orally administered Bz-Ty-PABA and pancreolauryl, respectively, were chosen as the lower normal limits, the PABA test showed a specificity quite similar to that of the pancreolauryl test (97 and 95%, respectively) despite the lack of a control day test, but a lower sensitivity (39 vs. 83%). The association of both tests was not advantageous compared with the pancreolauryl test alone.
Lactoferrin is present in pancreatic juice, and greatly increased concentrations are found in the pancreatic juice of patients with chronic pancreatitis. It is not known whether these high levels of lactoferrin represent a genetically determined defect predisposing to the later development of chronic pancreatitis or are simply a consequence of the disease. In view of the morphological and functional similarities between the pancreatic and parotid glands, we have measured the immunoreactive lactoferrin concentration in pure parotid saliva of 30 patients with chronic calcific pancreatitis, 26 controls, 5 patients with proven pancreatic cancer, 2 patients with Sjögren's disease and 2 patients with chronic recurrent parotitis. No difference in the lactoferrin concentration was detected between control subjects and patients with chronic pancreatitis or pancreatic cancer. Raised levels were found in the 4 patients with parotid gland disease. These findings suggest that increased lactoferrin secretion is confined to the exocrine pancreas in patients with chronic pancreatitis and is thus probably a phenomenon secondary to the disease.
A group of 191 patients with chronic relapsing pancreatitis was followed for about 10 years. Ninety-three of them were selected for surgery because of incapacitating painful relapses or persistent pain and were submitted to side-to-side pancreaticojejunostomy. Ninety-eight were selected for medical management. Seventeen patients died during the follow-up. The cumulative probability of pain relief, 10 years after clinical onset of the disease was 62.9% in the patients who had been submitted to surgery and 42.8% in the nonoperated patients. In the operated group, no case of further relapse was observed after a 3-year pain-free interval, but in the nonoperated group some patients complained of further painful relapses. Complete and lasting alcohol withdrawal and/or steatorrhea were significantly associated with a more favorable result in the patients who had been submitted to surgery. However, the relationship between alcohol consumption, exocrine pancreatic insufficiency, and pain behavior did not reach statistical significance in the nonoperated patients. In patients selected for and submitted to surgery, whose disease before surgery was severe because of a high frequency of painful relapses, the chance of pain relief was similar to, and to some extent higher than, that observed in patients not selected for surgery and suffering from a mild or moderate disease. Alcohol withdrawal and exocrine pancreatic insufficiency have been confirmed as being adjunctive factors toward lessening pain in patients who had been submitted to pancreaticojejunostomy.
Frequency of duodenal ulcer in patients with chronic pancreatitis is still controversial. This study aims to prospectively investigate the frequency of duodenal ulcer in a group of 190 patients (162 males and 28 females) affected by chronic relapsing pancreatitis admitted to our department between 1970 and 1979. 41 cases (21.5%) were endoscopically observed (22% of the males and 17.9% of the females; male:female ratio 1.2:1). Drinking habits, cigarette consumption, presence of pancreatic calcifications and surgery did not affect the frequency of duodenal ulcer. Exocrine pancreatic insufficiency, as fecal fat excretion higher than 7 g/day, seems to be linked with an increased frequency of duodenal ulcer (exact Fisher's test: p = 0.0586). Moreover, duodenal ulcer was present in about one third of the patients who afterwards died, but it was the cause of death in only 1 case. Even if a prospective control population is lacking, the male:female ratio of duodenal ulcer in chronic pancreatitis seems to be different from that observed in a comparable hospitalized group (1.2:1 vs. 2.4:1) and from that reported in literature in the general adult population.
Controversial data have been reported on gastric acid secretion in patients with chronic pancreatitis. Moreover, studies on gastroduodenal morphological changes in patients with this disease and with other alcohol-related conditions have given different results. Basal and penta-gastrin-stimulated gastric secretion, histological changes of gastric and duodenal mucosa, and basal and meal-stimulated gastrin were measured in 21 patients with chronic alcoholic pancreatitis and in the following pair-matched groups: 21 chronic alcoholics and 21 control subjects (nonulcer dyspepsia), and in 19 patients with proven liver cirrhosis of alcoholic origin. No patient suffered from peptic ulcers. Moreover, gastric secretion was also measured in 51 patients with proven duodenal ulcers and in 34 healthy subjects. Basal acid output in patients with chronic pancreatitis was significantly higher (p less than 0.05) than in the other groups, except for the patients with duodenal ulcers. Peak acid output values in patient with chronic pancreatitis were similar to those measured in patients with duodenal ulcer, and they were higher than in the healthy subject group and in patients with liver cirrhosis, but statistical significance was not attained for patients with nonulcer dyspepsia. An increased frequency of duodenitis was found in patients with chronic pancreatitis, whereas an increased frequency of gastric metaplasia in the duodenal bulb was observed in all the patients with alcohol-related conditions considered. No relevant differences among the considered groups were found relating to gastric histological changes. Basal and meal-stimulated gastrin were similar in all the studied groups. This study suggests that in patients with chronic pancreatitis there is increased gastric secretion and probably an increased capacity for secretion of acid. Moreover, in patients with chronic pancreatitis, duodenitis seems to be frequent, but it probably is not directly related to chronic alcohol consumption.
In two minipigs chronic pancreatic and duodenal fistulas, which allowed the diversion and the intestinal replacement of pancreatic secretion, were prepared. In a third minipig a chronic biliary fistula was also prepared so the bile secretion could be fed back into the intestine through a duodenal catheter. In these animals a chronic gastric fistula was made so gastric secretion could also be collected. Diversion-replacement of pure pancreatic juice and of bile were carried out in the fasting state. This study confirms the presence of a feedback regulatory mechanism in exocrine pancreatic secretion in the pig. Moreover, it suggests that bile can interfere with this phenomenon.
5 healthy volunteers were submitted to i.v. infusion for 45 min of graded doses of commercial GIH secretin (0.01, 0.025, 0.05, 0.5, 1 and 2 CU/kg h-1). Parathormone serum levels were measured before and during the infusion. All the dosages of exogenous secretin were followed by a significant increase in serum PTH levels in a dose-dependent fashion. Commercial GIH secretin, even at low doses, seems to increase circulating parathyroid hormone levels significantly.
Gastrointestinal hormones containing the C-terminal tetrapeptide of gastrin are involved in calcium homeostasis. The aim of this study was to investigate: 1) the effect of a standard meal (schedule a) and of a duodenal infusion of 5% aminoacid solution (schedule b) on calcium, CT and PTH serum levels in man; 2) the behaviour of these parameters during I.V. infusions of pentagastrin (mcg 1.5/Kg-hour), sincalide (mcg 0.04/Kg-hour) and caerulein (ng 75/Kg-hour) (schedule c). In order to avoid any possible interference by endogenous secretin release, schedule c was performed in 5 patients previously submitted to total gastrectomy. Schedule a and b were studied in 5 healthy volunteers. After a standard meal a slight increase of CT and PTH was measured. Duodenal infusion of aminoacid was followed by hypocalcaemia and slight but constant rise of CT levels, without significant variations of circulating PTH. Pentagastrin, sincalide and caerulein induced a slight but significant hypocalcaemia and a rise of serum CT levels, together with a significant increase of serum PTH. These findings suggest that peptides containing the C-terminal tetrapeptide of gastrin directly affect calcium homeostasis in the absence of secretin release.
The behaviour of serum gastrin fasting levels was studied in 39 randomized patients with proven duodenal ulcer, 21 receiving cimetidine (1 g/day) and 18 placebo for 28 days. No significant variations of gastrin fasting values were found, but in four patients given cimetidine a relevant increase was observed at the end of the treatment. One out of 6 patients, previously treated with placebo, showed a marked increase of fasting gastrin levels after a second trial of cimetidine. No increase of G-17 was observed in the patients showing fasting hypergastrinemia after cimetidine. The present study seems to confirm some previous observations and it seems to suggest the possibility that in some patients cimetidine could induce hypergastrinemia.
The clinical and pathological features of 132 patients of North-Eastern Italy with proven chronic pancreatitis (presence of radiological pancreatic calcification and/or surgical and histological data) have been studied. The disease appeared to be associated with chronic and regular alcoholic habits in most cases. Histo-pathological examinations showed calcifying pancreatitis also in patients without radiological pancreatic calcification. Chronic pancreatitis in North-Eastern Italy seems to be similar to that described in France, except for a high frequency of associated gallstones.
This paper gives an example of the use of correspondence analysis in a study of the risk factors of surgery in uncomplicated chronic relapsing alcoholic pancreatitis (UCRAP) where censored observations are present. Ninety-seven patients were admitted to a long-term follow-up project on the clinical evolution of UCRAP. During follow-up 61 patients underwent surgery, while the observations for the remaining 36 patients were censored. Correspondence analysis was performed on three prognostic variables, selected by a preliminary univariate analysis. A supplementary variable indicating the state of each patient at a particular time (still in follow-up, operated on, lost to follow-up), was projected onto the best factor plane chosen by correspondence analysis. Cox's proportional hazards regression model was also used with the scores of patients on the factor axes as independent variables to evaluate their prognostic importance. Both correspondence analysis and the Cox model showed that the first two axes provide important prognostic information. Furthermore, the former suggested a pattern of censorship for patients with observations censored after 5 years of follow-up. The results of this study confirm that correspondence analysis may be useful in follow-up studies by providing graphic display of important information relative both about the event under study and about censored observations.
Serum levels of elastase-1 were measured in 174 patients with pancreatic diseases and in 131 controls and were compared with the circulating levels of trypsin, lipase and amylase and with clinical data. In 48 patients with chronic pancreatitis serum enzyme levels were also compared with the pancreatic exocrine capacity. About 50% of the patients with chronic pancreatic disease showed increased levels of serum elastase, sometimes even in the face of long lasting pain-free periods, and/or of severe pancreatic impairment. On the contrary, serum trypsin and lipase were almost always either normal or below the normal range in the absence of painful relapses and/or in the presence of an impairment of the exocrine pancreatic function. A strict correlation was found between elastase-1 and trypsin (r = 0.778) and lipase (r = 0.834). However, controls and patients with chronic pancreatic diseases behaved differently, an increase in trypsin and in lipase levels being associated in the patients with chronic pancreatitis with an increase in elastase-1 values significantly larger than that observed in controls. These findings raise the hypothesis, at present unproven, that trypsin and lipase serum assays are more reliable indices of pancreatic exocrine function, whereas serum elastase-1 levels may indicate the presence of acute pancreatic episodes, even if subclinical, the importance of which, in the natural history of the disease, remains unknown.