In vivo diagnosis of feline infectious peritonitis by comparison of protein content, cytology, and direct immunofluorescence test on peritoneal and pleural effusions.
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Biomedical subjects
Publications and source records attributed to M C Parodi.
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4-Methylpyrazole (4-MP), a specific inhibitor of alcohol dehydrogenase, exerts gastroprotection of unusually long duration in rats. We tested the hypothesis that pretreatment with 4-MP might protect the human gastric mucosa against alcohol-induced acute injury. Fourteen healthy volunteers received pretreatment with either 4-MP, 15 mg/kg body weight dissolved in 50 ml of orange juice, or placebo and 2 hr later 100 ml of 40% ethanol. The endoscopic appearance of the gastric mucosa was evaluated and scored (scale 0-5) and mucosal biopsies were obtained just before pretreatment and 30 min after ethanol for histologic examination and prostaglandin E2 measurement. In the 4-MP group the mean endoscopic injury score was significantly lower than that in placebo group, in both the body and the antrum. Histologically, 4-MP significantly reduced disruption of surface epithelium and completely prevented the deep hemorrhagic mucosal lesions. In the 4-MP group no changes in gastric mucosal PGE2 levels were detected. In rats, 4-MP did not inhibit gastric acid output, whereas it markedly increased the adherent gastric mucus evaluated by the alcian blue recovery method. When lipid peroxidation was induced by carbon tetrachloride in hepatic microsomes, 4-MP caused significant inhibition of malondialdehyde generation. We conclude that 4-MP provides significant protection of the human stomach against alcohol-induced acute mucosal injury. 4-MP, besides inhibiting the conversion of alcohol to acetaldehyde, might protect the gastric mucosa by increasing adherent gastric mucus and by scavenging free radicals.
Aim of this experience has been to evaluate the current diagnostic potentiality of the endoscopy in the framework of the gastric ulcerous pathology. On the total of the gastric ulcers 17.9% have resulted to be neoplastic with the hystologic examination. The diagnostic accurracy of the endoscopy has resulted to be of the 87% compared to hystology. From our data it is evidenced how the endoscopy examination has a relevant diagnostic accuracy in defining the nature of the gastric ulcer which however has to be confirmed by the histology which seems to be diriment.
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In the present study we evaluated the contents of endogenous prostaglandins type E2 and F2 alpha in the antral mucosa, and the type E2 in the duodenal mucosa in a group of thirty non-ulcer dyspeptics in comparison with a group of thirty duodenal ulcer patients. A significantly reduced concentration of duodenal and antral PGE2 was found in ulcer patients as compared with dyspeptic subjects. A significantly increased concentration of antral PGE2 was observed in cases with active superficial antral gastritis, either in dyspeptics or in duodenal ulcer patients, as compared with normal antrum cases. A significantly increased level of PGF2 alpha was found in active superficial gastritis of the dyspeptic group.
This study was conducted to assess the behavior of various parameters involved in mucosal protection (mucus and prostaglandins) and of presumed aggressive factors (hydrochloric acid and Helicobacter (Campylobacter) pylori in 20 patients with chronic liver disease, with or without clinical and instrumental signs of portal hypertension. The two groups of patients showed no difference from controls with respect to gastric acid secretion and the presence of antral Helicobacter pylori. The amount of gastric soluble mucus was reduced and the quality altered in cirrhotic patients with portal hypertension. The mucus of subjects with chronic active liver disease with no gross signs of portal hypertension showed significant qualitative differences from that of normal controls. The prostaglandin E2 concentration in the gastric mucosa was lower than normal in both groups of liver disease patients, but prostaglandin F2 alpha did not appear to differ between patients and controls.
The actions of cimetidine are well known: an inhibitor of gastrin hydrochloric secretion, cimetidine modifies neither the motility nor any of the other functional factors. Numerous authors also attribute a cytoprotective role to cimetidine, one that is apparently carried out independently of the inhibitory effect on hydrochloric secretion. The cytoprotective mechanism itself is not yet fully understood. Numerous hypotheses have been made, including increased production of bicarbonates, inhibition of cyclic AMP, increased mucosal blood flow, and increased mucous production. However, all these hypotheses have not been fully explained, hence the problem remains open to further contributions. Well accepted, instead, is the possibility that the drug may not only intervene in acid-hydrochloric inhibition but may also, by broadening its mechanisms, enhance the powers of the mucosal barrier.
Acute upper gastrointestinal bleeding remains a difficult emergency problem, and, despite recent pharmacological advances, the choice and results of medical treatment are the subject of debate. To determine the effectiveness of two potent inhibitors of gastric acid secretion, somatostatin and cimetidine, in the control of upper gastrointestinal bleeding of non-variceal origin, we initiated a multicentric, randomized, prospective therapeutic trial in 56 patients presenting with acute hemorrhage due to gastric and duodenal ulcers and erosions defined by uniform and precise criteria. The two drugs were administered i.v. for 48 hours at a dose of 250 mcg/h (somatostatin) and 1,600 mg/24 h (cimetidine). Vital signs, laboratory values, and gastric aspirate were checked frequently in accordance with a strict schedule; the number of blood transfusions was also noted. Endoscopy for the assessment of bleeding before admission to the trial and the end of treatment was performed in every patient. Bleeding stopped in 28 of the 30 (93.3%) patients treated with somatostatin, and in 16 of the 26 (61.5%) of those receiving cimetidine (p less than 0.01). The blood requirement of the patients treated with somatostatin and cimetidine was, on average, 1.10 +/- 1.16 and 2.46 +/- 4.03 units per patient, respectively (p less than 0.05). Somatostatin was also significantly superior - in the patients in whom the treatments were successful - with respect to the time taken to achieve this result. In conclusion, our results, together with those already published, point to a definite therapeutic effectiveness of somatostatin in upper gastrointestinal bleeding as here defined, and would appear to justify a more extensive clinical use under controlled conditions.
The presence of estradiol (E) and progesterone (Pg) receptors (R) has been demonstrated also in normal and neoplastic tissues known to be hormone-independent and in particular in primitive colonic cancer, and, possibly, in healthy colonic mucosa. In this study endoscopic and surgical colonic mucosa specimens from 55 subjects were analyzed and divided as follows: 21 samples from healthy subjects, 12 normal mucosa samples from subjects affected with colonic cancer, 8 adenomatous polyps specimens, 5 samples from ulcerative colitis drawn on areas showing macroscopic lesions and 9 colonic cancer specimens. In the control group we have observed 6 cases positive for ER (28.6%) and 2 positive for PgR (14.3%). Six normal mucosa specimens from subjects affected with colonic cancer were found to be positive for ER (50%) and 2 for PgR (16.7%). Five colonic cancers resulted ER positive (55.5%) and 4 PgR positive (44.4%). Four polyps were ER positive (50%) and 3 PgR positive (37.5%); in this group only one subject showed positive binding in the surrounding normal tissue. These data confirm the presence of ER and PgR in colonic cancer and colonic adenomas (so-called precancerous disease); in these subjects the finding of steroid receptors also in normal mucosa suggests that the presence of steroid binding could be considered as a marker of a precancerous condition.
We have studied gastric mucus secretion after carbenoxolone, zolimidine and prostanoic acid short term treatment (28 days) in patients with endoscopically demonstrated peptic gastric ulcer of the lesser curvature. Six patients were treated with carbenoxolone (300 mg/day), 6 with zolimidine (1200 mg/day) and 6 with prostanoic acid (2 g/day). All of them were submitted to gastric juice collection, before and after treatment, during 1 h at fast. On the samples of gastric juice, taken at 15 min intervals, the protein component (PC), glucosamine (GL), fucose (FU), the free N-acetyl-neuraminic acid (NANA) and sulphate groups (SG), were determined by biochemical methods. We have observed a significant increase of PC after zolimidine (P less than 0.02) and prostanoic acid (P less than 0.05) treatment, without significant variations of the other mucus components. No significant variations of mucus secretion after carbenoxolone treatment. If we compare the three drugs, we can see a significant increase of PC after zolimidine (P less than 0.005) and after prostanoic acid (P less than 0.001), compared with the results obtained after carbenoxolone. There are no significant variations of basal and stimulated (pentagastrin 6 mcg/Kg i.v.) secretory volume and acid output before and after treatment in the three groups of patients.
We have studied gastric soluble mucus behaviour in 58 patients with histological evidence of chronic gastritis and without circumscribed lesions of the upper gastrointestinal tract endoscopically demonstrated, compared with a control group of 8 normal subjects. As mucus secretion parameters, the protein component of mucosubstances, glucosamine, fucose, the free NANA and sulphate groups content were determined with biochemical methods. In cases of superficial gastritis, either diffuse or limited to fundus or to antrum with normal remaining mucosa, we have observed a significant decrease of fucomucines and a significant increase of sulphomucines compared with a control group, without significant quantitative variations of total soluble mucus. In cases of diffuse and limited atrophic gastritis there were more significant qualitative variations of soluble mucus characterized by a higher decrease of neutral mucosubstances with a high increase of the acid ones than in cases of superficial gastritis. Quantitative variations of total soluble mucus were present only in the situation of diffuse to fundus and antrum atrophic gastritis.
The effect of somatostatin (250 mcg. by i.v. bolus injection) on serum gastrin behaviour was studied in 12 dyspeptic subjects. In 6 of them, seven gastrin levels were determined in the basal conditions and after somatostatin injection. In the remaining 6 patients, the gastrinemic profile was evaluated after histamine injection (0.5 mg/i.m.) and after the injection of histamine plus somatostatin (24 h later). Gastric acid secretion was also determined in all the cases. The results obtained demonstrate that somatostatin reduces the gastrin release: this reduction appears 30 minutes after its administration and persists until the 60th minute: after the 75th minute the serum gastrin returns to the basal level. The contemporaneous injection of somatostatin and of histamine does not modify the gastrinemic profile as compared to what was observed in the basal condition or after histamine alone.
The therapeutic efficacy of ranitidine, pirenzepine, cimetidine and placebo in the 28 day treatment of duodenal ulcer was evaluated through an open randomized study performed in 120 patients. At the end of treatment, ranitidine, pirenzepine and cimetidine demonstrated a significantly higher efficacy on ulcer healing as well as on symptom relief in comparison with placebo (P less than 0.05). Data regarding cimetidine and ranitidine failed to reveal significant differences: pirenzepine, on the contrary, when compared with both the H2 blockers employed showed a slower effect on symptom disappearance. As far as functional data are concerned, placebo administration did not induce any variation of secretory or gastrinemic behaviour: on the contrary, after the end of ranitidine and cimetidine treatment a significant decrease of BAO and of MAO were found, failing to reveal any serum gastrin variation. After pirenzepine therapy no differences in the acid secretory behaviour were seen, while a significant increase of fasting gastrinemia was observed.
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