Biomedical subjects
Publications and source records attributed to G Cavallini.
Twenty adult patients affected by atopic dermatitis (AD) were submitted to the p-aminobenzoic acid (PABA) test in order to evaluate the proteolytic pancreatic function. All but one showed a normal PABA test. These results seem to exclude a proteolytic maldigestion as a pathogenetic factor in AD.
The aim of this work was to study the effect of 20% and 40% ethanol, administered acutely, on gastric PGE2 release in normal subjects and alcoholics. Ethanol 20% did not modify the release of PGE2 into the gastric juice, whereas 40% ethanol increased PGE2 release only in healthy subjects. The basal PGE2 levels were higher in alcoholic patients.
Failures in experimental and human pancreatic transplantation are mainly attributable to rejection, graft thrombosis, and technical problems. There are, however, problems related to other causes, such as preservation injuries, which we found to exhibit, at least within the first 6 h, the same histological patterns seen in experimental acute pancreatitis. We performed pancreatic transplantation in 110 syngeneic rats under different preservation techniques and administration of gabexate mesilate, a synthetic protease inhibitor. The results showed that antiprotease treatment reduces graft preservation injuries significantly.
Pancreatic calcifications are particularly frequent in patients with severe pancreatic insufficiency and long-lasting chronic pancreatitis. To clarify whether calcifications point to a more severe form of the disease, irrespective of its duration, we have retrospectively analyzed patients with chronic pancreatitis submitted to the secretin-cerulein test in our center over a six-year period. Out of 120 patients, calcifications were found in 55. Higher alcohol intake and longer duration of the disease were found in patients with calcifications, compared with patients without calcifications (p less than 0.001). In both groups, lipase and chymotrypsin were more severely impaired than bicarbonate; a greater reduction of pancreatic exocrine function was found in patients with calcifications, compared to those without (p less than 0.001, Mann-Whitney U-test). When the patients were classified according to the duration of the disease or the severity of exocrine function impairment, higher percentages of patients with calcifications were found in the classes with more advanced disease. A log-linear analysis showed that the prevalence of calcifications was associated with pancreatic function impairment, even within the same class of duration of the disease. It is likely that calcifications mark more severe forms of chronic pancreatitis, even in the early phases of the disease.
The case of a patient submitted to sonographic abdominal examination because of recent onset of fever, abdominal pain and weight loss, with the finding of multiple enlarged lymph nodes along great vessels, is reported. Because of the negativity of noninvasive procedures, the patient underwent laparatomy and biopsy. The histologic and bacteriologic diagnosis of tuberculous lymphnodes was unexpected, as the patient was unreactive to the tuberculin skin test and had no signs of active pulmonary tuberculosis. Although uncommon, tuberculosis must be included in the differential diagnosis of subdiaphragmatic lymphadenopathies even if symptoms of mycobacterial infection or other signs of the infections are not presented.
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In severe necrotizing pancreatitis, the retroperitoneum is the main site both of autodigestion and of the production of toxins. With the aim of removing necrotic tissues and active enzymes from the retroperitoneum, we developed a surgical approach based on a wide exposure of the pancreas and on the insertion of multiple drainages with postoperative irrigations with hypertonic solutions and antiproteases. We treated 191 patients, and our results correlated with the timing of the operation. The operative mortality rate ranges from 8.1 in patients undergoing our procedure within 48 hours from the onset of the disease to 28.4 per cent when the operation was delayed for more than 96 hours. Our technique is detailed and the indications as to the timing of surgical treatment in instances of pancreatitis are discussed.
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In 27 beagle dogs, acute necrotizing pancreatitis was induced by retrograde injection of autologous bile and trypsin into the main pancreatic duct. Animals were randomly assigned to the following treatments: group 1--(9 dogs) aprotinin 600,000 KIU/d by i.v. route; group 2--(9 dogs) peritoneal dialysis for 6 d plus 500,000 KIU/L of aprotinin in the dialysate fluid; group 3--(9 dogs) peritoneal dialysis without aprotinin in the dialysate fluid. All dogs of the group 1 died within 16 h following the induction of pancreatitis and extensive necrotizing and hemorrhagic changes were seen in the pancreatic and peripancreatic areas. Six dogs of the group 2 survived and no necrotizing changes were observed 30 or 50 d after the induction of pancreatitis. Three dogs of the group 3 survived, but slight necrotizing lesions were found at the autopsy. The survival rate was higher in dogs with peritoneal lavage (p = 0.0129) or with peritoneal lavage plus aprotinin (p less than 0.0001) than in those receiving i.v. aprotinin, indicating that the latter treatment has no beneficiary effect on the course of acute pancreatitis.
Fecal chymotrypsin (FCT) has been measured by a new photometric method (Monotest Chymotrypsin; Boehringer, Mannheim) in 78 patients: 44 with chronic pancreatitis and 34 not affected by any pancreatic disease. The results were compared with those from other tests of pancreatic secretory (secretin-cerulein test) and digestive [serum and urinary p-aminobenzoic acid (PABA) and pancreolauryl] capacity. When FCT values were severely reduced (below 6.7 U/g), from 90 to 100% of the patients also presented abnormal pancreatic secretory and digestive capacity. On the other hand, 87% of the patients with normal FCT (above 20 U/g) presented normal secretory and digestive capacity. Patients with intermediate FCT values (between 6.7 and 20 U/g) showed normal or abnormal pancreatic secretory and digestive capacity with the same probability. Therefore, FCT, carried out as a first test, seems to identify subjects that need no further pancreatic function tests (normal and severely impaired FCT) and patients who need other more complex functional investigations (intermediate FCT values).
Passive intestinal permeability was measured in 15 adult patients with atopic eczema. Values in the patients did not differ significantly from those in 12 healthy control subjects. These results suggest that altered intestinal permeability is not important in the pathogenesis of atopic eczema in adults.
The authors describe an original surgical technique for pancreatic transplantation carried out on an experimental rat model which duplicates as closely as possible the anatomic-functional situation of a pancreatic graft in man (one arterovenous vascular peduncle with one functioning kidney only). The technique entails a microanastomosis between the mesenteric artery and the portal vein of the donor organ with the left renal artery and vein of the recipient. This method appears to be technically encouraging and particularly useful in studying the early phases of ischemic graft injuries, a field in which the authors are particularly interested.
Serum and urine elastase 1, its renal output and clearance and urinary gamma-glutamyltransferase and ribonuclease excretions were measured in 16 patients with pancreatic cancer, 23 with chronic pancreatitis and in 22 healthy controls in order to evaluate elastase 1 plasma-urine transfer in chronic pancreatic disease and to investigate any factors that might influence the clearance of this enzyme. In an additional group of 17 patients with different pancreatic diseases the serum molecular size distribution of elastase 1 after chromatography was ascertained. An increased urinary elastase 1 output was found in 4/16 patients with pancreatic cancer and in 6/23 with chronic pancreatitis. No correlation was found between circulating elastase 1 and its urinary output; a negative correlation was detected between the serum levels of this enzyme and its clearance. The excretion of ribonuclease and gamma-glutamyltransferase was correlated with elastase 1 output and clearance. While the majority of elastase 1 in serum was accounted for by high molecular forms, probably the expression of complexes with serum inhibitors, free circulating enzyme was present in all patients with high serum elastase 1. Our findings suggest that elastase 1 urinary excretion increases in some patients with chronic pancreatic disease regardless of the neoplastic or inflammatory nature of the illness. Although the availability of different amounts of ultrafiltrable enzyme may play a role in influencing elastase 1 plasma-urine transfer, renal tubular damage appears to be the most important factor influencing the increase in the urinary output of elastase 1.
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This study was prospectively carried out to evaluate the frequency and clinical significance of pancreatic impairment in the course of chronic inflammatory bowel disease (CIBD). Twenty-seven patients affected by ulcerative colitis or Crohn's disease were submitted to a secretin-cerulein test, oral glucose test (OGT) and to indirect immunofluorescence (IFL) for detection of autoantibodies against exocrine and endocrine tissue. A bicarbonate plus enzyme or only an enzyme insufficiency was found in 11/27 patients, whereas isolated lipase decrease was observed in 18 subjects. In the results of the OGT and the indirect IFL test there was no difference between patients and controls. These data demonstrate that pancreatic impairment is a far more frequent occurrence than generally recognized in clinical practice. The decrease of lipase secretion could worsen the consequences of malabsorption in Crohn's disease of the small intestine. Therefore we think that a pancreatic assessment is advisable, at least in Crohn's disease patients with steatorrhea.
Unlike previous reports, in 123 patients with abdominal injury or surgery significant and persistent hypokalemia was observed only after traumatic or surgical injuries of the liver. On the contrary, in all other extrahepatic abdominal trauma or operations kalemia was normal. This discrepancy may be related to the much greater abundance, in comparison with other abdominal organs, of adrenergic endings present in the liver. Trauma to or surgery of the liver stimulates such fibers, which locally release proportionally large amounts of norepinephrine. The consequent stimulation of beta-adrenergic receptors enhances the transfer of potassium from the blood into the cells, even if the affinity of norepinephrine for such receptors is less than that of epinephrine. The frequent finding of kaliuria at the upper normal levels may suggest an accessory role of aldosterone in causing and maintaining this hypokalemia.
In order to investigate the role of renal factors in affecting trypsinogen 1 metabolism and excretion in chronic pancreatic disease, serum immunoreactive trypsin (IRT), urinary IRT, gamma-glutamyltransferase (GGT), alpha-glucosidase (AGL) and RNase outputs and the molecular size distribution of serum and urine IRT were studied in 8 control subjects, 18 cases with pancreatic cancer, and 23 cases with chronic pancreatitis. Serum chromatography demonstrated that most immunoreactivity eluted as trypsinogen 1. Smaller amounts of immunoreactivity at higher molecular weights were also observed. Urine chromatography displayed both trypsinogen 1 and heavier molecular forms. An inverse linear correlation was noticed between creatinine clearance and serum trypsinogen 1 levels. Multiple regression analysis (urinary IRT output dependent and GGT, AGL, and RNase predictor variables) showed a significant linear correlation. RNase was found to be the most important parameter in explaining urinary IRT output. Mild variations in the glomerular function seem to be able to influence serum trypsinogen 1 levels. Urinary IRT excretion is principally explained by a disturbance in the tubular reabsorption of low molecular weight proteins, such as RNase.
We measured in 193 patients, admitted to our wards for symptoms and signs suggestive of pancreatic or digestive malignancy, the serum levels of five tumor-associated antigens (CA 19-9, CA 50, CA 125, TPA, CEA) and we evaluated their diagnostic accuracy both when used alone and in combination. For CA 19-9 and CA 50 a sensitivity for pancreatic cancer as high as 92 and 88%, respectively, and specificity of 91.8% were found. A lower sensitivity vs. pancreatic cancer was found for the other tumor markers, and vs. the other digestive and nondigestive malignancies for all tumor markers (apart for CA 19-9 and CA 50 vs. biliary carcinomas). As for the combined assays, the best figures were found vs. pancreatic cancer for CA 19-9 plus CA 50, CA 50 plus CEA, CA 50 plus CA 125; a sensitivity by far worse vs. the other gastrointestinal cancers was found for all the possible combinations. We conclude that in selected symptomatic patients some tumor-marker determinations can be useful in identifying those with a high probability of harboring a pancreatic cancer, to be further studied or operated upon. The clinical relevance of this in patients already symptomatic is at present unclear.