Efectividad del secnidazol en el tratamiento de escolares asintomáticos parasitados por giardia lamblia y/o entamoeba histolytica / Effectiveness of secnidazol in the treatment of asymptomatic schoolchildren parasited by giardia lamblia and/or entamoeba histolytica

El propósito de la investigación es conocer la eficacia del Secnidazol en el tratamiento de escolares asintomáticos portadores de Giardia lamblia y/o Entamoeba histolytica, así como el evaluar su tolerancia. Se escogieron 50 niños parasitados (totalizando 53 casos con Entamoeba histolytica y/o Giardia lamblia), con edades comprendidas entre 5 y 14 años, de uno u otro sexo, a quienes se les administró el medicamento y tres días después se realizaron exámenes coproparasitológicos controles. La tolerancia del medicamento se evaluó mediante encuesta. De 53 casos parasitados, la relación de protozoarios fue: Giardia lamblia (66,03 por ciento) seguidos de Entamoeba hitolytica (33,97 por ciento). La efectividad parasitológica del Secnidazol contra Giardia lamblia fue del 100 por ciento y de Entamoeba histolytica de 95,45 por ciento. Se obtuvo un solo caso portador que no respondió al tratamiento (4,55 por ciento). El medicamento fue bien tolerado en el 50 por ciento de los casos. Los síntomas más frecuentes fueron: hiporexia, cefalea, dolor abdominal, mareos, náuseas, vómitos, diarrea, fatiga, alteración del gusto y prurito. La eficacia y la relativamente buena tolerancia del Secnidazol fue demostrada en el presente estudio. Se obtuvo cura parasitológica al tercer día de administrado el medicamento

Prevalencia de enteroparasitosis en una escuela urbana en el Municipio San Francisco, Estado Zulia, Venezuela / Prevalence of enteric parasitosis in an urban area school in San Francisco Municipality, Zulia State, Venezuela

El propósito de la investigación es conocer la prevalencia de las enteroparasitosis en una escuela urbana de la parroquia San Francisco. Del total de la población escolar, se escogieron 114 niños, de edades comprendidas entre 5 y 15 años de ambos sexos, donde se les realizó exámenes coproparasitológicos y de recolección de información a través de encuestas epidemiológicas. De los niños seleccionados, 74,56 por ciento reportaron positividad para uno o más enteroparásitos. 40,35 por ciento fueron masculinos y 34,21 por ciento femeninos. Las edades más parasitadas fueron comprendidas entre 8 y 12 años (34,24 por ciento) segudas de 5 a 8 años 30,69 por ciento. Los helmintos más frecuentes fueron: Enterobius vermicularis (45,55 por ciento), Trichus trichuria (27,80 por ciento). Ascaris lumbricoides (23,35 por ciento) e Hymenolepis nana (3,30 por ciento) y los protozoos fueron: Blastocystis hominis (37,28 por ciento), Giardia lamblia (17,79 por ciento). Endolimax nana (16,95 por ciento), Entamoeba coli (15,26 por ciento). El poliparasitismo predominó sobre el monoparasitismo. Las helmintiasis observadas presentaron en su mayoría una infestación leve. Se evidencia acentuados malos hábitos higiénicos en los niños así como en la escuela. Se obtuvo elevada prevalencia parasitaria en la población estudiada. La Enterobiasis fue la helmintiasis más común

Modulation by nitric oxide of gastric acid secretion in toads.

Nitric oxide (NO) is a novel chemical messenger that mediates a variety of biological actions. This study was undertaken to investigate the effects of NO on parietal cell function. The rate of [3H]arginine conversion to [3H]citrulline, a parameter of NO synthase activity, and NO formation (as NO2-), were inhibited by the NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), in a concentration-dependent manner in the non-stimulated toad gastric mucosa. This range of concentrations of L-NAME provoked stimulation of H+ secretion in a similar fashion, which was blocked by L-arginine but not by D-arginine. Pre-treatment with carbachol plus ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetra-acetic acid (EGTA) prevented the effect of L-NAME on H+ secretion and drastically reduced NO synthase activity. L-arginine had an inhibitory effect on H+ secretion in non-stimulated and carbachol-stimulated gastric mucosa, which was reversed by L-NAME. Carbachol and pentagastrin, but not histamine, significantly increased NO formation in the toad gastric mucosa. The results suggest that changes in NO synthesis in the gastric mucosa may modulate parietal cell function and that a calcium-dependent mechanism may be involved.

Interactions between oxoglutarate oxidation and acid secretion in isolated rabbit gastric glands.

The effects of gastric secretagogues, and other agents that modify H+,K(+)-ATPase activity and cell calcium concentration, on the rate of oxoglutarate oxidation were investigated in isolated gastric glands. Oxoglutarate was oxidized in a dose-dependent manner by gastric glands, with an apparent Km for oxoglutarate of 3.9 +/- 0.5 mM. Oxoglutarate progressively inhibited the rate of glucose oxidation. In the presence of 0.5 mM oxoglutarate plus 10 mM glucose, the latter substrate was preferentially oxidized and contributed most to oxygen uptake. With 10 mM oxoglutarate plus 10 mM glucose, the rate of glucose oxidation was greatly inhibited and oxoglutarate oxidation accounted for most of the oxygen consumption. Acid secretion (aminopyrine accumulation) was significantly increased by 0.1 mM histamine in glands oxidizing 10 mM oxoglutarate, although this stimulation was significantly lower than that observed in the presence of 0.5 mM oxoglutarate plus 10 mM glucose. Omeprazole, an inhibitor of the H+,K(+)-ATPase, significantly reduced the oxidation of oxoglutarate, whereas NH4+, an activator of the enzyme, stimulated the oxidation of a submaximal dose of oxoglutarate. Carbachol at 0.1 mM significantly increased the rate of oxidation of non-saturating concentrations of oxoglutarate. The calcium ionophore ionomycin at 10 microM produced a similar effect. Chelation of intracellular calcium by BAPTA AM caused a significant inhibition of oxoglutarate oxidation. The results provide further evidence that changes in the ATP:ADP ratio resulting from activation of the H+,K(+)-ATPase, and calcium ions are involved in the mechanisms of activation of oxidative metabolism in the parietal cell.

Mechanism of cholinergic stimulation of glucose oxidation in isolated gastric glands.

The mechanisms of cholinergic activation of carbohydrate metabolism were investigated in isolated rabbit gastric glands. Carbachol stimulated the rate of glucose oxidation in a dose-dependent fashion with a half-maximal effect occurring at approximately 9 microM. Atropine and omeprazole, but not cimetidine, completely blocked the stimulation induced by carbachol. Direct activation of the H(+)-K(+)-adenosinetriphosphatase by NH+4 caused a significant stimulation of glucose oxidation that was totally abolished by oligomycin and by the mitochondrial uncouplers dinitrophenol and carbonyl cyanide p-trifluoromethoxyphenylhydrazone. These latter agents did not abolish the stimulating effect of carbachol on glucose oxidation. Ionomycin increased the rate of glucose oxidation in a dose-dependent manner, and this effect was not blocked by oligomycin. The metabolic effect of ionomycin was reduced but not abolished by omeprazole. 1,2-Bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid acetoxymethyl ester eliminated the carbachol-induced stimulation of glucose oxidation and partially inhibited the effect of NH+4. The mitochondrial enzymes pyruvate dehydrogenase and oxoglutarate dehydrogenase were activated by physiological concentrations of calcium in the isolated mitochondria. This effect was blocked by incubation with ruthenium red.(ABSTRACT TRUNCATED AT 250 WORDS)

[Effects of hydrocortisone on acid secretion in the isolated toad gastric mucosa]. / Efectos de la hidrocortisona sobre la secreción ácida en la mucosa gástrica aislada del sapo.

The effects of steroids on gastric acid secretion have been studied in different animal species with contradictory results. In the present work we investigated direct effects of hydrocortisone on acid secretion in the isolated toad gastric mucosa (Bufo marinus). The rate of hydrogen ion secretion (QH+) was measured using the pH-stat method of Durbin and Heinz. Hydrocortisone significantly stimulated QH+ in a dose dependent manner. The effect tended to reach a maximum with the concentration of 10mM and lasted for at least one hour. In the mucosa pre-treated with 1mM cimetidine, an specific antagonist of histamine H2 receptors, the addition of 10mM hydrocortisone did not stimulate QH+, but addition of the cholinergic agonist carbachol did produce a significant stimulation in the rate of acid secretion. In the gastric mucosa previously stimulated with 5mM hydrocortisone, the addition of a submaximal dose of histamine increased QH+ and this effect was greater than that provoked by histamine in the absence of the steroid. The results indicate that hydrocortisone significantly stimulates acid secretion in a dose-dependent manner in the isolated toad gastric mucosa. This effect seems to be dependent on the activation of H2 receptors.

Efectos de la hidrocortisona sobre la secreción ácida en la mucosa gástrica aislada del sapo. / [Effects of hydrocortisone on acid secretion in the isolated toad gastric mucosa]

The effects of steroids on gastric acid secretion have been studied in different animal species with contradictory results. In the present work we investigated direct effects of hydrocortisone on acid secretion in the isolated toad gastric mucosa (Bufo marinus). The rate of hydrogen ion secretion (QH+) was measured using the pH-stat method of Durbin and Heinz. Hydrocortisone significantly stimulated QH+ in a dose dependent manner. The effect tended to reach a maximum with the concentration of 10mM and lasted for at least one hour. In the mucosa pre-treated with 1mM cimetidine, an specific antagonist of histamine H2 receptors, the addition of 10mM hydrocortisone did not stimulate QH+, but addition of the cholinergic agonist carbachol did produce a significant stimulation in the rate of acid secretion. In the gastric mucosa previously stimulated with 5mM hydrocortisone, the addition of a submaximal dose of histamine increased QH+ and this effect was greater than that provoked by histamine in the absence of the steroid. The results indicate that hydrocortisone significantly stimulates acid secretion in a dose-dependent manner in the isolated toad gastric mucosa. This effect seems to be dependent on the activation of H2 receptors.

Secretory and metabolic effects of ethanol in the isolated amphibian gastric mucosa.

The effects of pure ethanol and some alcoholic beverages on acid secretion and metabolism were examined in the isolated toad gastric mucosa. Pure ethanol applied to the luminal side or to the submucosal side at low concentrations (2%-10%) was a potent stimulant of acid secretion, whereas high concentrations (greater than or equal to 20%) were inhibitory. Cimetidine and calcium-free solutions did not abolish the secretory effect of ethanol. Beer and wine, but not rum and whisky, caused a significant stimulation of acid secretion. Respiration was progressively increased by ethanol at concentrations between 2% and 20%. This effect was not affected by cimetidine or by SCH 28080, an inhibitor of the gastric hydrogen-potassium-stimulated adenosine triphosphatase. Ethanol (10%) significantly increased by 46% the tissue lactate-pyruvate ratio. The oxidations of glucose, butyrate, and acetate were progressively reduced by low concentrations of ethanol (5% and 10%). The results indicate that (a) low concentrations of ethanol and alcoholic beverages with low ethanol content are direct stimulants of acid secretion and (b) the secretory and metabolic effects of low concentrations of ethanol seem to be mediated via its oxidation.

[Peptic ulcer: a failure of the defense mechanisms of the gastroduodenal mucosa?]. / La úlcera péptica: es una falla de los mecanismos de defensa de la mucosa gastroduodenal?

Peptic ulcer is an heterogeneous and multifactorial disease. Secretion of acid/pepsin is a critical permissive factor in gastroduodenal peptic ulceration. Therapy of this disease has been based mostly on this principle. The sole presence of the aggressive factor, acid/pepsin, is not enough to explain peptic ulceration. Mucosal defense (resistance) is another critical factor involved in pathogenesis of this disease. Defects in some gastroduodenal defense mechanisms have been found in patients with peptic ulcer disease, such as: synthesis and release of prostaglandins, mucus and bicarbonate secretions, and the luminal hydrophobic layer. Both the dictum "no acid-no ulcer" and the coroliary "normal healing-no ulcer" seems to be valid. Correction of a possible deficiency in mucosal defense/resistance may be a useful and practical principle is management of patients with peptic ulcer disease.

Ca2+ requirement for metabolic effects of secretagogues in the amphibian gastric mucosa.

The role of extracellular Ca2+ in metabolic effects induced by theophylline and histamine was investigated in the isolated toad gastric mucosa. Primary and secondary effects on metabolism were differentiated by using K(+)-free solutions, which blocked the secretory responses but not the metabolic ones. The stimulation of respiration induced by theophylline and histamine was dose dependent and was significantly decreased by Ca2(+)-free solutions. In the presence of 1.8 mM Ca2+, the rate of glycogen breakdown was increased by theophylline in a dose-dependent manner and the dose-response curve was somewhat similar to that obtained with oxygen uptake. This effect was inhibited by incubation in Ca2(+)-free solutions. Ca2+ stimulated the rate of glycogen utilization in a concentration-dependent manner. The rates of oxidation of exogenous glucose and pyruvate were significantly inhibited by Ca2(+)-free solutions in theophylline- and histamine-stimulated mucosa, whereas the rates of oxidation of butyrate and acetate were not significantly affected. The Ca2+ ionophore A23187 significantly stimulated the rate of oxygen uptake and this response was not blocked by omeprazole and Sch 28080, two specific inhibitors of gastric H(+)-K(+)-ATPase. The results indicate that Ca2+ is required for optimal stimulation of carbohydrate catabolism in the toad gastric mucosa.

Effects of bile salts on energy metabolism and acid secretion by the isolated toad gastric mucosa.

The effects of bile salts on energy metabolism and acid secretion were investigated in the amphibian gastric mucosa in vitro. Serosal exposure to deoxycholate (0.2-2 mM), cholate (2-8 mM), or taurocholate (4-80 mM), at pH 7.4, decreased acid secretion depending on the concentration and time of exposure. Mucosal application of cholate and taurocholate at pH 5.6 caused a more pronounced reduction in the apparent rate of acid secretion. Oxygen uptake and substrate oxidations were significantly inhibited by bile salts in a dose-dependent manner. At pH 7.4, 1 mM deoxycholate inhibited the respiration by 49% and the rates of oxidation by 51%, 52%, 78%, 74%, and 54% of control values, for glucose, pyruvate, succinate, acetate, and butyrate, respectively. Cholate and taurocholate were found to be less potent than deoxycholate. Tissue adenosine triphosphate concentration was decreased by 13%, 57%, and 67% with 0.5, 1, and 2 mM deoxycholate, respectively. We believe the impairment of energy metabolism could be involved in the mechanism of bile salt injury to the gastric mucosa.

Role of calcium in secretory and metabolic effects of substrates in the gastric mucosa.

The role of extracellular Ca2+ in the effects and oxidation of metabolic substrates was investigated in the isolated toad gastric mucosa. In the presence of lipoate, the stimulating effect of 10 mM glucose on spontaneous acid secretion was significantly reduced by 76% in Ca2+-free solutions. The inhibition was overcome by addition of 5 mM Ca2+. The increment in respiration induced by glucose was also blocked in the absence of external Ca2+. The effect of 10 mM pyruvate on acid secretion was inhibited by 37% in Ca2+-free solutions. The secretory responses induced by 10 mM butyrate and 10 mM octanoate were not significantly affected by Ca2+-free solutions. The rates of oxidation of [14C]-glucose and [14C]pyruvate were significantly reduced by incubating in Ca2+-free solutions containing 0.1 mM of EGTA. When O2 uptake and glucose oxidation were measured simultaneously in the same preparation, the increment in the rate of glucose oxidation accounted for by 43% of the total increase of respiration observed in the presence of Ca2+. The rates of oxidation of [14C]butyrate and [14C]acetate were not significantly affected by Ca2+-free solutions. The rate of oxidation of [14C]glucose exhibited saturation kinetics versus concentration and was lower in the absence of external Ca2+ under a range of glucose concentrations. Similar results were observed when the experiments were performed in the absence of external potassium to block the acid secretory process. Ca2+ stimulated the rate of glucose oxidation in a dose-dependent manner. The kinetics of 45Ca2+ efflux and 45Ca2+ uptake were not significantly affected by glucose and butyrate.(ABSTRACT TRUNCATED AT 250 WORDS)

Substrate-level energy dependence of acid secretion in the isolated human gastric mucosa.

The substrate-level energy dependence of acid secretion was investigated in the human gastric mucosa in vitro using biopsy specimens obtained during fiberoptic gastroscopy in symptomatic patients. The oxygen consumption and the accumulation of aminopyrine were used as indexes of secretory activity. Basal and histamine-stimulated oxygen uptake by fundic biopsy specimens were not affected by medications (pethidine and diazepam) administered during gastroscopy. Under substrate-depleted conditions, the oxygen consumption and the aminopyrine accumulation of fundic mucosa were not significantly increased by histamine. Stimulation of functional activities by gastric secretagogues was observed only in the presence of exogenous substrates. The ability of various substrates to support acid formation in the presence of gastric secretagogues was evaluated. Carbohydrates were found to be effective substrates in supporting the functional responses of the tissue, with glucose being the most effective. Propionate, butyrate, beta-hydroxybutyrate, and octanoate were ineffective as substrates. Glucose by itself, but not butyrate, significantly increased oxygen uptake and aminopyrine accumulation. The results suggest that the human gastric mucosa, in vitro, has an absolute requirement for metabolic substrates to support secretory responses and that carbohydrates seem to be the preferential substrates.

Effects of gastric secretagogues on tissue glycerol in the isolated amphibian gastric mucosa.

Histamine and theophylline, two gastric secretagogues, significantly increased tissue glycerol content by 121 and 66%, respectively, in the isolated toad gastric mucosa. This is new evidence in favor of the hypothesis that gastric secretagogues may act via lipid mobilization.

Effects of phenothiazines on acid secretion in the toad gastric mucosa.

The effect of phenothiazine antipsychotic drugs on acid secretion was investigated in the isolated toad gastric mucosa. The acid secretory responses induced by maximal doses of histamine, carbachol and theophylline were all inhibited in a similar fashion by chlorpromazine. The ID50 was between 300 and 600 microM. Histamine-stimulated H+ secretion was also inhibited by trifluoperazine. Soluble cyclic AMP-dependent protein kinase activity was not significantly affected by 300 microM chlorpromazine. Microsomal (H+ + K+)-ATPase activity was significantly reduced by chlorpromazine. The results indicate that phenothiazines can inhibit acid secretion in the toad gastric mucosa and that inhibition of the gastric (H+ + K+)-ATPase may be involved in the mechanism of action.

Inhibition by cimetidine of the secretory and respiratory responses induced by theophylline and cyclic AMP in the amphibian gastric mucosa.

1. The effects of cimetidine, a histamine H2-receptor antagonist, on acid secretory and respiratory responses induced by histamine, theophylline and dibutyryl cyclic AMP were investigated in the in vitro toad gastric mucosa. 2. Histamine- and theophylline-stimulated acid secretion was competitively inhibited by cimetidine. A significant but lesser degree of inhibition was observed on oxygen uptake. 3. Cimetidine significantly inhibited acid secretion and oxygen uptake stimulated by dibutyryl cyclic AMP. 4. The results may suggest that cimetidine may have an additional action beyond the point of cyclic AMP in the oxyntic cells.

Stimulation of pyruvate carboxylation by gastric secretagogues.

Pyruvate carboxylation was stimulated by 2 gastric secretagogues, histamine and dibutyryl cyclic AMP, and by butyrate. Thiocyanate, an inhibitor of acid secretion, produced a slight decrease. Avidin significantly reduced acid secretion and this effect was overcome by biotin and oxalacetate. The results suggest that carboxylation of pyruvate is one of the reactions controlling oxidative metabolism and acid secretion in toad gastric mucosa.

Role of fatty acid oxidation in mechanism of action of gastric secretagogues.

The role of beta-oxidation in the mechanism of stimulation of acid secretion was examined in toad gastric mucosa in vitro. The incubation with 4-pentenoate selectively inhibited in a dose-dependent manner the rate of 14CO2 formation from [1-14C]octanoate. Pretreatment with 20 mM 4-pentenoate sharply reduced the respiratory and secretory responses to theophylline and histamine. Tracer studies showed a major utilization of exogenous octanoate over glucose and pyruvate by the in vitro toad gastric mucosa. Theophylline and histamine stimulated by 69% the rate of octanoate oxidation. Over 60% of the increments in oxygen uptake produced by theophylline and histamine accounted for the increments in octanoate oxidation, whereas glucose and pyruvate together accounted for less than 25%. Octanoate-dependent respiration was shown to correlate with octanoate oxidation under both inhibition with 4-pentenoate and stimulation with theophylline. Theophylline stimulated by 25% the rate of octanoate oxidation in Cl--free glucuronate-nutrient solutions. The present work provides further evidence for the primary role of fatty acid oxidation in the mechanism of acid secretion in amphibian.