[Acute-phase proteins in colorectal cancer].
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Biomedical subjects
Publications and source records attributed to D Dumitraşcu.
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We proposed to investigate the following parameters regarding upper gastrointestinal hemorrhage occurring in the patients with acute pancreatitis: incidence, form of manifestation, severity, correlated to the clinical and morpho-pathological form of acute pancreatitis, cause (direct causality or morbid association). The study was carried out on the inpatients of the internal-medicine and surgery units over a period of one year. For sake of accuracy the study also included the cases submitted to necropsy over a period of 5 years. The practical experience has revealed that though gastrointestinal bleeding is not a frequent complication--9.1% in the patients with acute pancreatitis and 36.3% of the necropsied cases--it is often severe, which imposes the early recognition for its adequate management.
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The evacuation time (T1/2) of the stomach was determined in the patients with partial gastric resection by a sequential computerized scintigraphic method. The effect of Salbutamol and Dopamine was followed on T1/2 and the scintigraphic surface of the stomach (appreciated indirectly by measuring the longitudinal and transversal diameters). Salbutamol prolongs significantly T1/2, from 6.41 +/- 2.72 minutes to 12.33 +/- 6.45 minutes. The scintigraphic surface of the resected stomach is not slightly modified by Salbutamol. Dopamine prolongs very much T1/2, from 13.00 +/- 4.01 minutes to 75.03 +/- 24.36 minutes, in parallel with the increase of the scintigraphic image of the stomach. Our investigations lead to the conclusion that Salbutamol, given per os, may become a new therapeutic mean in the dumping syndrome.
The phenomenon of endointestinal protein exudation in acute infectious enterocolitis is studied. Total proteins were determined in 30 cases of acute enterocolitis and 50 of bacillary dysentery in the acute stages of the disease and convalescence. The proteinogram of the jejunal juice was performed in the acute stage and convalescence in 20 patients. In 16 patients and 5 controls endointestinal albumin elimination was determined quantitatively by means of 131I labeled albumin. The results showed increase in the total protein content in the jejunal juice in the course of acute infectious enterocolitis and bacillary dysentery and a return to normal values in convalescence. Electrophoresis of the jejunal juice in acute infectious enterocolitis showed the absence of fraction III with alpha1-globulin migration, and increased fractions I, II and IV probably due to the loss of endointestinal albumin, also confirmed by quantitative albumin determinations with 131I labeled albumin. In conclusion, patients with acute infectious enterocolitis present a marked loss of endointestinal albumins in the acute stage of the disease, with a return to normal values in convalescence.
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The number of biological tumoral markers used in the diagnosis and therapy monitoring of hepatocellular carcinoma has increased, but their separate use is limited as none of them is specific, being only tumour-associated (proteins). But when in abnormal amounts and used in combination, they are of great help in the diagnosis and therapy monitoring. A combination of alpha-fetoprotein (AFP) and alpha 1-antitrypsin (AAT) data raises the diagnostic accuracy in hepatocellular carcinoma from 43% obtained with AFP alone, to 90.5% and if the combination includes the carcinoembryonic antigen (CEA) data too the accuracy increases to 100%, still without strict specificity for hepatocellular carcinoma.
The niphedipine pharmacokinetics was investigated in the patients with hepatic cirrhosis, in comparison with a group of healthy subjects, after administering unique doses of 10 mg per os. The niphedipine concentrations in serum were determined by a gas chromatography method. The niphedipine pharmacokinetics may be described in correspondence with the open pharmacokinetic model. The values of pharmacokinetic parameters of niphedipine in the patients with hepatic cirrhosis are significantly modified in comparison with those noticed in the healthy subjects. An increase in the level of the maximum concentrations (158 ng/ml versus 68 ng/ml), of the biological half time (11.9 hours versus 2.5 hours) and of the area under the curve of the drug concentrations in time (450 ng.ml-1.hour versus 205 ng.ml-1.hour) were found. The relative bioavailability [correction of biodisponibility] of niphedipine was double in the patients with hepatic cirrhosis versus the healthy subjects. The modified pharmacokinetics of niphedipine in the patients with hepatic cirrhosis and the great individual variations found, require a decrease of the dose in this category of patients and a surveillance of the clinical effect.
The Kupffer cells clearance of colloidal 198Au particles with a diameter of 200-300 A was estimated in 14 subjects with different collagen diseases: 7 without previous treatment and 7 under immunodepressive treatment compared to 10 controls. No difference between the subjects with collagen disease and controls was observed. The group with collagen disease under immunodepressive treatment has lower Kupffer cells clearance for colloidal gold particles than non-treated patients, without statistical significance.
In 39 patients the following were assessed: gastric acid secretion (mmol/hour), gastric juice volume (ml/hour), glycemia (mg%), and in 10 of them also pepsinogen I serum concentration (ng/ml). All these parameters were determined in basal conditions and after administration of glucagon. Glucagon induced achlorhydria in 33.3% of the patients, hypochlorhydria in 33.3%, did not influence HCl in 12.8%, and hyperchlorhydria in 20.5%. The gastric juice volume changed in parallel with chlorhydria. The HCl secretion did not correlate with the glycemia levels. Pepsinogen I was not significantly influenced by glucagon. It may be concluded that glucagon had a two-fold action on HCl secretion: (a) in two thirds of the patients studied it induced hypo- or achlorhydria; (b) in about 20% it induced hyperchlorhydria.
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