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Biomedical subjects

M Plebani

Publications and source records attributed to M Plebani.

At least 253 records · Page 14Linked to original sources
PubMed1993

Serum malondialdehyde and mitochondrial aspartate aminotransferase activity as markers of chronic alcohol intake and alcoholic liver disease.

Since lipid peroxidation is a well-know mechanism of alcohol-related liver damage, the aim of the present study was to assess the role of serum malondialdehyde (MDA), a secondary product of lipoperoxidation, in the detection of alcoholism and different stages of alcoholic liver disease and to correlate serum levels of malondialdehyde with other markers. Sixty-five patients with a mean alcohol intake of 151 gr/day, were divided into three groups: alcoholics with normal liver function (ANLF, 7 pts), non-cirrhotic alcoholic liver disease (NCALD, 26 pts) and alcoholic cirrhosis (ALC, 32 pts). The control group consisted of 15 healthy subjects. Serum MDA was measured by the thiobarbituric acid reaction test, and mitochondrial aspartate aminotransferase (mAST) with immunochemical assay. MDA had a higher sensitivity (70% vs 37.5%) and specificity (100% vs 93%) than mAST in detecting alcohol abuse, irrespective of the presence of liver disease. Serum MDA levels were significantly higher in all three groups than in controls (2.3 +/- 0.1 nmol/ml), the highest value being found in NCALD (4.6 +/- 0.4). Serum MDA levels were correlated with prothrombin time (p < 0.005) and blood alcohol levels (p < 0.05). mAST serum activity was also significantly higher in all three groups than in controls. A significant correlation was found between serum MDA and mAST only when the whole group was considered.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[Alcohol-dependent mast cell activation in ulcer].

Numerous studies have shown that alcohol causes both acute and chronic damage to gastroduodenal mucosa. The methods of damage differ however, and experimental studies in animals have shown that the degranulation of mast cells in gastric mucosa causes acute hemorrhagic lesions after the consumption of alcohol. It is not known whether this mechanism also operates in man. The aim of the present study was therefore to evaluate whether there is a correlation between mast-cell activation, determined by assaying tryptase levels in gastric mucosa, and the consumption of alcohol in patients with ulcerative diseases. Thirty-one patients with cicatrized ulcerative lesions (13 gastric ulcers, 18 duodenal ulcers) were included in the study. Biopsies at the level of the gastric fundus and antrum and the duodenal bulb were performed in all patients to determine tryptase levels. Biopsy material was frozen and subsequently homogenized; the enzyme was assayed in the supernatant using a radioimmunometric method. The mean daily alcohol consumption was calculated in clinical terms for each patient over the past 5 years and patients were subdivided into non-drinkers and moderate (< 60 g alcohol/day) and excessive (> 60 g alcohol/day) drinkers. It was found that tryptase concentrations were higher in the fundus compared to the gastric antrum and duodenal bulb, irrespective of alcohol consumption both in patients with gastric ulcer and duodenal ulcer. The importance of mast cells in provoking alcohol-dependent damage was studied at a gastric level. Alcohol leads to their degranulation and therefore contributes to the formation of gastric lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Esaprazole effect on acid, peptic and alkaline secretion in duodenal ulcer patients.

To study the effect of Esaprazole, a new antiulcer drug, on acid, peptic and alkaline secretion a modified gastric acid test was performed in 18 duodenal ulcer patients. Pentagastrin was administered as bolus 30' and 75' after the beginning of the test, followed by Esaprazole 300 mg i.v. at 90'. Gastric juice was collected every 15' for determination of: total volume, volume of non parietal secretion, acid, bicarbonate and pepsin output. Serum pepsinogen group I was determined by radioimmunoassay. Esaprazole had a significant inhibitory effect on the total volume of gastric secretion and on volume of non parietal secretion. Pepsin output and serum pepsinogen group I were not affected by Esaprazole, while bicarbonate secretion was reduced. Antiulcer activity of Esaprazole seems to be due to the reduction of total volume of gastric secretion.

Adult↗
PubMed1992

Theophylline inhibits late asthmatic reactions induced by toluene diisocyanate in sensitised subjects.

Toluene diisocyanate (TDI)-induced asthma is a frequent occupational airway disease. To determine whether a calibrated dosage of oral slow-release theophylline inhibits asthmatic reactions and the associated increase of airway responsiveness to methacholine induced by TDI, we examined six asthmatic subjects who developed a late or a dual asthmatic reaction after TDI inhalation challenge. We administered oral slow-release theophylline or placebo to each subject for 7 days according to a double-blind, randomized, cross-over study design. When the subjects received a placebo, TDI caused a late or a dual asthmatic reaction. When the subjects received theophylline. TDI caused significantly reduced late asthmatic reactions. Mean serum theophylline concentrations were within the therapeutic range. Theophylline neither modified the baseline airway responsiveness to methacholine, nor the increase of airway responsiveness to methacholine induced by TDI. These results suggest that slow-release theophylline may improve TDI-induced late asthmatic reactions, but it does not change the baseline airway responsiveness to methacholine and the increase of airway responsiveness to methacholine induced by TDI.

Administration, Inhalation↗
PubMed1992

Glutathione, protein sulfhydryls and cysteine proteases in gastric mucosal injury and protection.

Glutathione is one of the endogenous protective chemicals, like prostaglandins, in the gastric mucosa. Depletion of these agents aggravate the chemical- or stress-induced gastric erosions and ulcers. However, gastroprotection can be achieved even in the presence of low mucosal concentration of glutathione and prostaglandins, indicating the presence of other protective chemicals (e.g. polyamines, growth factors, neurotransmitters, steroids) in the stomach. Protein sulfhydryls were also implicated in the mechanism of action of gastroprotective drugs. We recently tested the hypothesis that cysteine proteases might be a target of gastroprotective and antiulcer agents, and decided to look for the presence of proteases and protease inhibitors (PI) in the gastric mucosa and juice. Protease activity and PI were measured with general substrates hemoglobin, azocasein and albumin at optimal pH (2.0, 5.6, 7.4) of aspartic, cysteine and serine proteases. Homogenates of glandular stomach mucosa and gastric juice from fasted rats were incubated in the presence or absence of specific inhibitors and gastroprotective SH alkylators such as NEM or iodoacetate. PI was measured after acid and heat inactivation of endogenous proteinases and addition of pepsin, cysteine proteinase papain, or trypsin. Our results indicate that of the proteases found in the stomach 98% was pepsin at pH 2.0, and up to 56% or 24% was SH-sensitive at pH 5.6 or 7.4, respectively. Intragastric administration of SH alkylators such as NEM or iodoacetate exerted a dose- and time-dependent gastroprotection against chemically induced acute erosions and ulcers. Thus, in addition to glutathione, proteinases and their specific endogenous inhibitors may also be involved in gastric mucosal injury and protection.

Animals↗
PubMed1992

Measurement of tryptase in endoscopic gastroduodenal biopsies: distribution and relationship with ulcer disease.

Tryptase, a serine endoprotease, was determined in mucosal biopsies from fundus, corpus, antrum and corpus-fundus of the stomach and from the duodenum in 15 controls, 66 patients with duodenal ulcer, 22 with gastric ulcer and 9 with duodenitis. Intra- and inter-assay coefficients of variation ranged from 3.3% to 8.0% and from 3.5% to 8.6%, respectively. In controls, the highest values for tryptase were found in the fundus and progressively decreased in the corpus, antrum and duodenum. Analysis of variance of data from repeated measurements, performed in six subjects having multiple determinations, achieved statistical significance (F = 16.85, P less than 0.001). Data from the corpus-fundus area documented a significant difference among patient groups (F = 2.70, P less than 0.05). Patients with an active gastric ulcer had higher mean values when compared to controls and to patients with healed gastric ulcer. A similar trend was found in patients with active duodenal ulcer. Furthermore, corpus-fundus tryptase evaluated longitudinally in three patients with an active ulcer (point A) and after healing (point B), showed significant decrease from point A to point B. By contrast it remained elevated or showed only minor decrease in two patients with a persistent active ulcer.

Adult↗
PubMed1992

Alterations in bilirubin metabolism during extra- and intrahepatic cholestasis.

This study was performed to investigate modifications in the serum bilirubin forms, hepatobiliary enzymes, and some glycoproteic substances in patients during the course of extrahepatic cholestasis (stage A) and following its clinical resolution (stage B). The series consisted of 16 patients: 11 had main bile duct stones; two, benign stenosis of the main bile duct; and three, main bile duct cancer. Cholestasis resolved spontaneously in one case, under endoscopy in two, and following surgery in 13. Five patients with liver cirrhosis and a picture of intrahepatic cholestasis following anesthesia were also investigated. Serum bilirubin forms were measured using van den Bergh's method and the alkaline methanolysis-HPLC procedure; the mono- and di-conjugated forms were considered together in the overall evaluation of the results. The hepatobiliary enzymes (ALP, GGT, and AST) were increased at stage A and significantly decreased at stage B. Similar patterns were observed in total (TB), unconjugated (UB), and conjugated bilirubin (CB) and in the percentage of CB out of TB (% CB). In the majority of patients, % CB at stage B was lower than at stage A, whereas in subjects with a high initial UB value, a different % CB pattern was observed. The direct bilirubin percentage (% DB), on the other hand, had a different pattern, and the variations between stages A and B were not significant. The pathophysiological bilirubin pattern was similar in patients with intrahepatic cholestasis. At stage A, in a number of patients the levels of glycoproteic substances (CA 19-9, TPA and ferritin) were raised, but at stage B they tended to decrease towards the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Acute reflux pancreatitis in rats: a comparison between two experimental models.

This study was undertaken in order to compare the reliability of two acute reflux pancreatitis models in rats, one performed by positioning a silicon tube in the duodenum and the other by creating a gastro-jejunal anastomosis. In two groups (A = 10 and B = 10 rats) a silicon tube was positioned in the duodenum; in the remaining two groups (C = 12 and D = 6 rats) a latero-lateral antecolic anisoperistaltic gastro-jejunal anastomosis was performed 30 days before surgery. A closed duodenal loop was created for 12 hours in groups A and C but not in B and D. Rats in both groups A and C developed acute pancreatic inflammation of a mild degree. Sham operated rats with silicon tube placement had higher histological damage scores than those with gastro-jejunal anastomosis. The difference found between the two groups of rats which underwent gastro-jejunal anastomosis was more marked than that between the two groups which had silicon tube placement. It was concluded that the creation of a gastro-jejunal anastomosis is probably the safer procedure to allow gastro-intestinal flow in acute reflux pancreatitis in rats.

Amylases↗
PubMed1992

Urinary phospholipase A2 excretion in chronic pancreatic diseases.

This study was performed to investigate the behavior of phospholipase A2 (PLA2) in serum and urine of patients with chronic pancreatic diseases and to ascertain whether any factors influenced the results. In 30 controls, 45 patients with pancreatic cancer, 54 with chronic pancreatitis, and 64 with extrapancreatic diseases, serum and urinary PLA2, pancreatic isoamylase and RNase, and urinary N-acetylglucosaminidase (NAG) were measured. Serum PLA2 levels were higher in patients with chronic pancreatitis than in all the other groups. In our patients, only occasionally was urinary PLA2 elevated, the increase occurring almost exclusively in the presence of an acute inflammatory disease, e.g., relapsed chronic pancreatitis or active inflammatory bowel disease. A correlation was found between serum PLA2 and serum RNase, an indicator of tissue damage, but not between serum PLA2 and pancreatic isoamylase. Urinary PLA2 output was correlated with its renal input and with RNase output. No correlation was found between PLA2 output and pancreatic isoamylase or NAG urinary excretion. In conclusion, (1) the determination of serum PLA2 activity may be an aspecific test of pancreatic disease; (2) PLA2 urinary excretion occasionally increases, especially in the presence of severe phlogosis, which occurs in chronic pancreatitis, in particular during relapse; and (3) irrespective of the tissue origin of urinary PLA2, its increased excretion may be accounted for in part by its increased circulating levels. It is, however, more likely the consequence of a renal tubular dysfunction, which is sometimes found in patients with pancreatic diseases.

Adult↗
PubMed1992

Role of serum fasting gastrin in screening for hypergastrinemic syndromes in duodenal ulcer disease.

Basal serum gastrin levels were measured in 237 patients with endoscopically confirmed duodenal ulcer and were higher than normal in 16 cases. Protein meal gastrin stimulation was performed on this group of 16 patients and on a control group of 48 patients with normal basal gastrin concentrations but high rates of either ulcer recurrence or of complications (e.g., bleeding or perforation); 21 patients from the two groups were also tested for serum gastrin inhibition with secretin. Four cases (25%) of antral G-cell hyperfunction were found in the first group, plus 1 case compatible with Zollinger-Ellison syndrome (6.2%). Only 1 case (2%) of antral G-cell hyperfunction was found among the 48 controls. These results suggest the clinical utility of routine basal gastrin measurement in screening for hypergastrinemic patients with duodenal ulcer disease.

Adult↗
PubMed1992

Extra-hepatic cholestasis determines a reversible increase of glycoproteic tumour markers in benign and malignant diseases.

This study was performed in order to assess the relative role of cholestasis in increasing some serum glycoproteic markers of malignancy (CA 19-9, TPA, CEA). 30 Patients with benign and 16 with malignant extra-hepatic cholestasis were studied on admission (stage A) and after the operative or spontaneous resolution of the cholestatic picture (stage B). CA 19-9 and TPA were found to be lower in stage B than in stage A benign diseases. A similar behaviour was found in malignant diseases, although findings were significant only for CA 19-9. In neither of the patient groups was CEA found to present a significant trend. Extra-hepatic cholestasis appears able to increase per se serum glycoproteic markers in benign diseases, with variations proportional to the severity of the clinical picture. The same considerations can apply to malignancies, even if in these situations the production of tumour markers by the neoplastic growth should also be considered. We should therefore be cautious in assessing the diagnostic usefulness of new tumour markers when cholestasis is present.

Adult↗
PubMed1992

Antigliadin antibody classes in chronic liver disease.

Antigliadin antibody (AGA) subtypes (IgG and IgA class) were tested in sera from 67 patients with chronic liver disease of different aetiology (29 with primary biliary cirrhosis (PBC), 31 with chronic non-A non-B hepatitis, and 7 with autoimmune chronic active hepatitis (CAH) compared with 23 subjects with inflammatory bowel disease (IBD). Nineteen patients with coeliac disease served as positive controls. IgA-AGA alone were found in 3.4% of patients with primary biliary cirrhosis and in 3.2% of non-A, non-B CAH. IgG-AGA alone were found in 1.3% of patients with IBD, in 6.8% of primary biliary cirrhosis and in 14.2% of autoimmune CAH. IgA-AGA and IgG-AGA together were found in 6.8% of PBC and in 1 patient with autoimmune CAH. Jejunal biopsy, performed in 7 out of the 2 patients with both IgA and IgG-AGA, showed the characteristic features of coeliac disease in one subject with autoimmune CAH. The same patient had the highest titre of AGA. In conclusion, these results indicate that AGA (either IgG and IgA) can be present at low titre in chronic liver disease and their presence may be secondary to the liver damage per sè. High titres of AGA in chronic liver disease may suggest a real association with coeliac disease.

Adult↗
PubMed1992

Pathophysiology of the gastric microcirculation.

Mucosal blood flow performs an extremely important role in microcirculation wherein alterations necessarily lead to severe gastric and duodenal mucosal lesions. The removal of back-diffused H+ ions through the adaptation of microcirculatory flow represents a valid defence mechanism. The blood flow's inability to contain H+ back-diffusion lies at the bottom of rapid-onset acute mucosal lesions; moreover, it probably contributes to the onset of chronic ulcer in certain areas already precariously supplied, because of the breakdown of the mucosal barrier or a further reduction in blood supply. Portal hypertension leads to altered blood flow in the gastric microcirculation. This haemo-dynamic condition brings about a series of endoscopically evident changes which are probably a consequence of the conspicuous increase in mucosal and submucosal vascular area. This haemodynamic situation may be an aetiopatho-genetic factor in the cirrhotic subject's marked sensitivity to gastric mucosal damage.

Animals↗
PubMed1992

The natural history of duodenal ulcer disease.

With a view to describing the natural history of duodenal ulcer, currently linked with powerful and widely used drugs, we retrospectively reviewed all patients followed-up at our unit between 1978 and 1989. All DU subjects with at least 5 years of clinical-endoscopic follow-up were admitted to the study. Concomitant gastric ulcer, previous gastrointestinal surgery and treatment other than with H2-blockers (where necessary) were considered exclusion criteria. Forty-four patients (35 males, 9 females, mean age 44.5) proved eligible for this study. At monthly intervals in the patients' history of ulcer disease (starting from a baseline month 0 when ulcer symptoms first appeared), we compared all cases in which the duration of disease coincided, i.e. for each month of the clinical course of the ulcer there was a certain number of patients at the same point in time; patients' histories coincided variously over a period ranging from 0 to 15 years. We considered endoscopically-diagnosed relapses (both symptomatic and asymptomatic) and hemorrhages as marker events for the activity of DU disease. A year-by-year duodenal ulcer activity rate was obtained for both treated and untreated subjects, as follows: No. of events/mean No. of patients followed-up per month x 100. Fisher's exact test and multivariate analysis (stepwise logistic regression) were used to investigate risk factors of poor outcome. We found that the years between the 1st and 5th and between the 10th and 15th from the onset of duodenal ulcer disease had higher peaks of activity, mostly in untreated subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗