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Biomedical subjects

C Florent

Publications and source records attributed to C Florent.

At least 73 records · Page 4Linked to original sources

Influence of chronic lactulose ingestion on the colonic metabolism of lactulose in man (an in vivo study).

The effects of a chronic load of nonabsorbable sugars on intracolonic bacterial metabolism of carbohydrates and on H2 breath excretion are disputed. However, most of the discussion relies on indirect evidence or on results of in vitro studies. Thus, we attempted to assess directly and in vivo the effects on intracolonic metabolism of lactulose of a chronic oral load of this nonabsorbable disaccharide. 20 g of lactulose was given orally twice daily during 8 d to eight normal volunteers. In all, breath H2 concentration was measured on days 1 and 8 after ingestion of the morning lactulose dose. In four subjects, stools were collected during 2 d at the beginning and at the end of the lactulose maintenance period to measure fecal pH and daily outputs of carbohydrates and beta-galactosidase. The four other subjects were intubated on days 1 and 8 to measure the pH and the concentrations of carbohydrates, lactic acid, and volatile fatty acids (VFA) in the distal ileum and cecal contents. Moreover, 14C-lactulose was added to cold lactulose and 14CO2 breath outputs determined. Pulmonary H2 excretion fell from day 1 to day 8 (P less than 0.05), whereas 14CO2 excretion increased (P less than 0.01). Fecal water pH, lactic acid, and VFA concentrations did not vary between the two stool collection periods. 24-h fecal weight, fecal water, and carbohydrate outputs showed a trend to decrease between days 1 and 2 and days 7-8, whereas beta-galactosidase activity rose markedly (P less than 0.01). No significant variations were observed for all parameters measured in ileal fluid. In the cecum, areas under the concentration curves decreased from day 1 to day 8 for lactulose, galactose, and fructose (P less than 0.01), while an increase was found for lactic acid (P less than 0.001), acetic acid (P less than 0.0001), and total VFA (P less than 0.001). Cecal fluid pH dropped faster (P less than 0.05) and to a lower level (P less than 0.05) on day 8 than on day 1. These data clearly show that a chronic load of a nonabsorbable sugar induces changes in colonic bacterial metabolic pathways resulting in a better efficiency of the flora to digest the carbohydrate.

Adult↗

[Effect of pentagastrin and cimetidine on gastric protein loss in exudative gastropathies].

The effectiveness of cimetidine in decreasing protein loss in protein-losing gastropathies has recently been questioned. The present investigation was designed to test the effects of pentagastrin and cimetidine on gastric protein loss in 6 patients with this type gastropathy: 4 with Ménétrier's disease and 2 with Stempien's disease. Fecal and gastric loss of 51Cr-labelled proteins were measured and expressed as ml of plasma per unit of time +/- SEM. Gastric protein loss was measured during intravenous infusion of normal saline, pentagastrin alone (6 microgram/kg/h), combined pentagastrin and cimetidine (1.5 mg/kg/h), and cimetidine alone. Each solution was perfused during 105 min to obtain a steady state effect upon gastric protein loss during one hour. Fecal clearance was increased in all patients: 193 +/- 16 ml/day (N less than 40 ml/day). Gastric 51Cr albumin loss was increased by pentagastrin stimulation (15.9 +/- 1.2 ml/h); cimetidine resulted in a reduction of the pentagastrin induced loss (7.0 +/- 3.8 ml/h) while cimetidine alone had no effect (3.8 +/- 0.6 ml/h) on basal loss. Our results suggest that cimetidine therapy may be of benefit in decreasing protein loss in patients with this type of gastropathy.

Blood Proteins↗

[Effects of a shielding antacid on changes in the gastric potential difference induced by aspirin in man].

Acetyl salicylic acid (AAS) disrupts the gastric mucosal barrier, causing a drop in the transmural potential difference (PD) and mucosal injuries. The decrease of PD correlates with endoscopic assessment and mucosal damage. The gastric PD may be used as a sensitive model for the assessement of drug-induced damage to the gastric mucosa. We have studied the effects of a shielding antacid ( Gelox ) on PD modifications induced by 500 mg of AAS in 12 healthy volunteers. Measures were performed after administration of one unit of Gelox and after a 3 day treatment period (1 unit, three times daily). Gelox induced a significant decrease of maximal PD drop (10.7 +/- 3.1 mV and 7.5 +/- 2.8 mV respectively; p less than 0.001) and of PD recovery time (p less than 0.05). After the 3 day treatment period and 14 h after the last intake, there was an increase of basal PD values and a very significant decrease (p less than 0.001) of maximal PD drop induced by AAS alone and AAS + Gelox (5.33 +/- 2.42 mV and 3.66 +/- 2.18 mV, respectively). Since the antacid effect had disappeared 14 h after the last intake of Gelox ; these results suggest an increase of the gastric mucosal barrier and a real "shielding effect".

Adult↗

[Serum pepsinogen: its value as index of basal and stimulated gastric acid secretion (author's transl)].

Group I pepsinogen serum levels (PG I) and gastric acid outputs were determined before ("basal") and after pentagastrin or insulin stimulation in 13 patients with active duodenal ulcer and in 4 patients with hyperselective vagotomy. There was a statistically significant correlation between basal PG I serum level and basal acid output (r = 0,88, p less than 0,01) and between PG I serum level 45 min after stimulation and peak acid output (r = 0,68, p less than 0,01). However, the scattering of individual values was such that serum PG I cannot be used as an index of gastric acid secretion in clinical practice.

Adult↗

Intestinal clearance of alpha 1-antitrypsin. A sensitive method for the detection of protein-losing enteropathy.

Gastrointestinal loss of plasma is usually measured with radiolabeled macromolecules. These methods are expensive and cumbersome. The use of alpha 1-antitrypsin as an endogenous marker and the determination of alpha 1-antitrypsin fecal clearance enable the diagnosis of protein-losing enteropathy. alpha 1-Antitrypsin is measured in feces and blood by radial immunodiffusion, and the results are expressed as clearance. There is a significant correlation between alpha 1-antitrypsin fecal clearance and 51Cr-plasma protein clearance (r = 0.96, p less than 0.001). The sensibility of alpha 1-antitrypsin test compared to [51Cr] is 93.3%, the specificity is 90%. The positive predictive value is 97.7%, the negative predictive value 75%. We found no alpha 1-antitrypsin in gastric juice of pH below 3. In vitro studies confirmed the destruction of alpha 1-antitrypsin in gastric juice of pH below 3. There is a slight decrease of alpha 1-antitrypsin concentration when stools are incubated at 37 degrees C. In duodenal juice there is a small lessening of alpha 1-antitrypsin concentration after an incubation at 37 degrees C for 1 h. In conclusion, the fecal clearance of alpha 1-antitrypsin seems to be an inexpensive and quite reliable test of protein-losing enteropathy.

Humans↗