RESUMEN

OBJECTIVES: Hemispheric neurologic symptoms, amaurosis fugax, and Hollenhorst plaques at eye examination are standard indications for carotid imaging to identify carotid artery occlusive disease (CAOD). Previous reports have suggested that other ocular findings, such as retinal artery occlusion and anterior ischemic optic neuropathy, are associated with CAOD. However, the predictive value of ocular findings for the presence of CAOD is controversial. The purpose of this study was to define the predictive value of ocular symptoms and ophthalmologic examination in identifying significant CAOD. METHODS: Over 3 years 145 patients were referred for carotid imaging on the basis of ocular indications in 160 eyes. Forty patients were excluded because of concurrent non-ocular indications for carotid imaging, leaving 105 patients referred exclusively for ocular indications to evaluate. Ophthalmologic history and eye examination were correlated with carotid duplex ultrasound findings. RESULTS: Amaurosis fugax was associated with a positive scan in 20.0% of carotid arteries (P =.022). Hollenhorst plaques at fundoscopic examination were associated with a positive scan in 18.2% of carotid arteries (P =.02). Ocular findings exclusive of Hollenhorst plaques were particularly poor predictors of CAOD, inasmuch as only 1 of 64 arteries (1.6%) had significant ipsilateral internal carotid artery stenosis (P =.022). Venous stasis retinopathy was the only ocular finding other than Hollenhorst plaques with any predictive value (1 of 5 scans positive; positive predictive value, 20.0%). CONCLUSIONS: Ocular symptoms and findings are poor predictors of CAOD. Amaurosis fugax, Hollenhorst plaques, and venous stasis retinopathy demonstrated moderate predictive value, whereas all other ocular findings demonstrated no predictive value in identifying CAOD.

Asunto(s)

RESUMEN

The authors report here the results of endoscopic cystogastrostomy performed on 3 children aged 11, 3, and 2.5 years with nonresolving pancreatic pseudocyst (PP) of 12, 9.5, and 7 cm in diameter. The etiology of PP was abdominal trauma in 2 and idiopathic acute pancreatitis in 1 case. Ultrasound and computed tomography scans confirmed the diagnosis and suitability for gastric drainage. After the puncture of cyst, a double pig-tail stent was placed for the permanent drainage of cystogastrostomy. Complete regression was confirmed by follow-up ultrasonography at 8, 6, and 7 weeks, respectively. There were no procedure-related complications, nor was there a recurrence of cyst during the 2 years of follow-up. This report suggests that children with nonresolving PP, that are anatomically accessible, can be treated successfully and safely by endoscopic drainage.

Asunto(s)

RESUMEN

Ursodeoxycholic-acid (UDCA) was introduced to the clinical practice as an effective agent for the dissolution of gallstones. The efficacy of UDCA was proved recently in the treatment of patients with chronic cholestatic liver disease. We demonstrate the hepatoprotective effect of UDCA in a patient with chronic cholestatic liver disease. A sixty-nine years old male patient was admitted to our department with severe jaundice. The laboratory and radiologic examinations revealed significant cholestasis without any morphological alterations. Among the serological tests the anti-HCV antibody was positive. Based on these findings and anamnestic data (no blood transfusion and/or operation), sporadic chronic C virus hepatitis was assumed with dominant cholestasis. The corticosteroid therapy even in high doses was ineffective, the liver function parameters worsened. Later UDCA (Ursofalk, Falk Pharma) was given at a dose of 250 mg three times daily. Clinical improvement was seen after the first week of UDCA treatment. The patient's complaints relieved parallel with decrease of serum bilirubin, gamma-glutamyl transferase and transaminase levels. These parameters showed further decrease during the treatment.

Asunto(s)

RESUMEN

Biochemical and molecular pharmacological studies were carried out in the gastric fundic mucosa during the development of stress ulcer in rats. The aims of this study were: (1) to evaluate the changes in membrane-bound ATP-dependent energy systems during the development of stress ulcer; (2) to prove (or to exclude) the presence of tissue hypoxia in the rat gastric mucosa during the development of stress ulcer; (3) to obtain further evidence of the existence of a feedback mechanism between ATP-ADP, ATP-cAMP, and cAMP-AMP transformations during the development of stress ulcer; (4) to analyze the different biochemical changes in the gastric mucosa before and after the macroscopic appearance of stress-induced gastric mucosal lesions (ulcers). The observations were carried out on both sexes of CFY-strain rats of 180 to 210 g body weight. The animals were deprived of food for 24 hours before the experiments. The animals were forced to swim in water (at 24 degrees C) for five hours. They were sacrificed at 0, 1, 2, 3, 4, and 5 hours after the introduction of stress. The tissue levels of ATP, ADP, AMP/ADP, and lactate were enzymatically measured; the cAMP was measured by radioimmunoassay. The adenylate pool (ATP + ADP + AMP), ratio of ATP/ADP, and "energy charge" [(ATP + 0.5 ADP)/(ATP + ADP + AMP)] were calculated. The membrane (Mg2(+)-Na(+)-K(+)-dependent) ATPase was prepared from the rat gastric fundic mucosa. Dose-response curves for epinephrine, cAMP, and AMP were determined on Na(+)-K(+)-dependent ATPase; also, the affinity, intrinsic activity curves, pD2, pA2 and alpha were calculated for all components. It was found that: (1) gastric mucosal lesions appeared and increased gradually from three hours after introduction of stress; (2) the extent of ATP-cAMP and cAMP-AMP transformations was increased considerably during the development of stress ulcer; (3) the extent of ATP-ADP transformation was completely inhibited; (4) the activity of Na(+)-K(+)-dependent ATPase from rat gastric fundic mucosa could be inhibited by epinephrine, cAMP, and AMP; (5) the ratio of ATP/ADP was unchanged in the first time period (from 0 to 3 hours), after which its value increased; (6) the value of "energy charge" (e.g., the extent of phosphorylation and/or dephosphorylation) of cells was decreased at two and three hours, after which its value returned to a normal level; (7) there was no increase in the tissue level of lactate; (8) several biochemical changes (decrease of ATP, ADP, "energy charge," increase of cAMP, AMP) preceded the macroscopic appearance of stress ulcer.(ABSTRACT TRUNCATED AT 400 WORDS)

Asunto(s)

Asunto(s)

Asunto(s)

RESUMEN

TISACID (a new, modern Hungarian Al-containing antacid) with a high acid-neutralizing capacity (greater than 26.8 mmol/g) also enhances gastric mucosal defense mechanisms (prostaglandin-dependent gastroprotection). A simple-blind, prospective, randomized, parallel multicentre clinical trial has been performed on both the clinical efficacy and possible side effects of TISACID monotherapy (Al-Mg-hydroxy-carbonate) on informed patients suffering from active duodenal ulcers. The study groups were as follows: Group "A": 3 g/day of TISACID (acid-neutralizing capacity = 78 mmol, n = 85), Group "B": 6 g/day of TISACID (acid-neutralizing capacity = 156 mmol, n = 88), Group "C": 12 g/day of TISACID (acid-neutralizing capacity = 312 mmol, n = 68), Group "D": (as control): (1.0 g/day cimetidine (HISTODIL, RGH, Budapest, n = 91). The total number of patients: 332. It was found that: 1. The new Hungarian antacid compound (both tablet and suspension) can essentially accelerate the healing rate of duodenal ulcers. 2. The cumulative healing rate of ulcers and the decrease of complaints can be achieved equally by relatively low doses of TISACID monotherapy and cimetidine alone. 3. There were no differences between the clinical potency and side-effects of TISACID tablet and suspension.

Asunto(s)

RESUMEN

Tisacid (a new, modern Hungarian AI-containing antacid) with a high acid-neutralizing capacity (greater than 26.8 mmol/g) also enhances gastric mucosal defense mechanisms (prostaglandin-dependent gastroprotection). A simple-blind, prospective, randomized, parallel multicentre clinical trial has been performed on both the clinical efficacy and possible side-effects of Tisacid monotherapy (AI-Mg-hydroxy-carbonate) on informed patients suffering from active duodenal ulcers. The four study groups were as follows: Group A: 3 g/day of Tisacid (acid-neutralizing capacity = 78 mmol, n = 85), Group B: 6 g/day of Tisacid (acid-neutralizing capacity = 156 mmol, n = 88), Group C: 12 g/day of Tisacid (acid-neutralizing capacity = 312 mmol, n = 68), Group D (as control): 1.0 g/day cimetidine (n = 91). The total number of patients was 332. It was found that the new Hungarian antacid compound (both tablet and suspension) can essentially accelerate the healing rate of duodenal ulcers; the cumulative healing rate of ulcers and the decrease of complaints can be achieved equally by relatively low doses of Tisacid monotherapy and cimetidine alone; and there were no essential differences between the clinical potency and side-effects of Tisacid tablets or the suspension.

Asunto(s)

Asunto(s)

RESUMEN

The efficacy of a 4-week cimetidine treatment was examined by a double-blind randomized study in 37 outpatients with endoscopically verified chronic gastric ulcer. The patients received a daily dose of 3 times 1 tablet and, at night before going to bed 2 more tablet, thus a total amount of 1 g cimetidine, or cimetidine-placebo, but in case of complaints they could take in addition a mixed alkaline powder. Patients not recovering in response to a 4-week treatment, were then administered daily 5 tablets of cimetidine up to their complete recovery. Endoscopic, laboratory and clinical examinations were carried out every other week. As a result of a 4-week treatment, 56% of the cimetidine group recovered. The difference was not significant (P less than 0.2). The size of the ulcer and the intensity of the complaints were reduced significantly in both groups. The decrease in the size of the ulcer was significantly greater in the first two weeks of cimetidine treatment than in the cimetidine-placebo group (P less than 0.05). This favourable dynamics of ulcer healing was not felt in the second two weeks of treatment, and after four weeks there was no difference in the size of the residual ulcer to between the two groups. Cimetidine seemed to be a suitable drug for treating chronic gastric ulcer, since its healing rate proved to be better than that of placebo, the gain in weight also was favourable and there were no side-effects.

Asunto(s)

Asunto(s)

RESUMEN

The membrane-bound ATP-dependent energy systems (ATP-membrane ATPase-ADP and ATP-adenylate cyclase-cAMP) play an essential role in the physiological regulation of the gastrointestinal mucosa and its damage in rat and man. A good, physiologically, hormonally and pharmacologically well controlled and regulated feedback system exists between the two energy systems. The significant increase of ATP transformation into ADP or cAMP represents a causative metabolic background of the development of gastric, duodenal and jejunal ulcer (damage) in man and rat. The ulcer preventive effects of vitamin A, beta-carotene, atropine, cimetidine, prostacyclin I2, and surgical vagotomy were studied in connection with their effects on the membrane-bound ATP-dependent energy systems of the gastric, duodenal and jejunal mucosa in man and rat. Atropine and cimetidine were applied in cytoprotective and antisecretory doses, and the tissue levels of ATP, ADP, AMP, cAMP and lactate were measured. The results indicated that the disturbed equilibrium between the two energy supply systems can be modified (normalized) by drugs and surgical vagotomy; the drug effect depends on the actual biochemism of the gastroduodenal mucosa; the values of affinities (pD2) and intrinsic activities (alpha) of the different drugs differ in relation to membrane-bound ATP-splitting enzymes; the changes in the membrane-bound ATP-dependent energy systems of the damaged rat gastric mucosa, produced by vitamin A and beta-carotene, depend on their cytoprotective doses which are connected with their cytoprotective effects; the biochemical changes induced by drugs (given in cytoprotective and anti-secretory doses) differ only quantitatively but not qualitatively; the drug effects on the membrane-located ATP-splitting enzymes (membrane ATPase and adenylate cyclase) in human gastric, duodenal and jejunal mucosa are similar to those in rats, but their affinities (pD2) and also their intrinsic activities (alpha) differ to the enzyme systems.

Asunto(s)

RESUMEN

Gastric mucosal damage was produced in rats after pyloric ligation by intragastric administration of 200 mg/kg aspirin diluted in 2 ml 150 mmol/l HCl. The animals in the control group received 2 ml saline solution, or submitted to pyloric ligation only. The animals were killed 4 h after the pyloric ligation, when the number and severity of gastric lesions (ulcers), and the gastric fundic mucosal level of adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), cyclic adenosine monophosphate (cAMP) and lactate, were noted and measured. The adenylate pool (ATP + ADP + AMP) and the energy charge (ATP + 0.5ADP). (ATP + ADP + AMP)-1 were calculated. It was found that: the gastric H+ output decreased significantly in the pylorus-ligated plus aspirin-treated animals; the number and severity of gastric lesions increased significantly in the pylorus-ligated aspirin-treated animals; the extent of ATP transformation into the ADP decreased significantly in the pylorus-ligated aspirin-treated animals; the extent of ATP transformation into the cAMP decreased significantly during the aspirin treatment; the values of adenylate pool and of "energy charge" remained unchanged in the different groups of animals. It is concluded that: the decreased H+ output in the pylorus-ligated plus aspirin-treated group can be obtained by the decreased extent of ATP transformation into the ADP by membrane ATPase, and the biochemical changes in the gastric mucosa indicate a decreased energy turnover.

Asunto(s)

RESUMEN

Gastric mucosal damage of pylorus-ligated rats was induced by the intragastric administration of aspirin at 200 mg/kg at the time of ligation. The animals were sacrificed at 0, 1, 2, 3, and 4 h after the treatment. The gastric lesions (ulcers) were counted and their severities were calculated, and the volume of gastric secretion and the H+ output were measured. The extent of lipid peroxidation was assessed by measuring the malondialdehyde (MDA) in the gastric mucosa, simultaneously with measurement of the activity of superoxide dismutase (SOD). It was found in these pylorus-ligated rats that: the number of visible gastric lesions was significantly higher 1 h after aspirin administration than at other times; the severity of gastric lesions increased significantly at the 3rd and 4th hour after administration of aspirin; the volume of gastric secretory responses increased gradually after administration of aspirin and to a higher extent than the H+ output; the H+ output was significantly less after aspirin administration than that after pylorus ligation only; the gastric mucosal SOD activity significantly increased 1 h after administration of aspirin, decreasing significantly and gradually thereafter; the tissue level of MDA remained unchanged 1 h after aspirin administration, decreasing significantly thereafter.(ABSTRACT TRUNCATED AT 250 WORDS)

Asunto(s)

Asunto(s)

RESUMEN

The disease peptic ulcer in patients does not present a uniform clinical entity. Hence, the therapeutic approaches to peptic ulcers are significantly different. Independently from the therapeutically given drugs, some common problems can be found in the methods of critical evaluation of the peptic ulcer therapy in patients. This paper deals with goals, the possible ways to evaluate critically the efficacy of peptic ulcer therapy and the problems in patients in relation to both evaluation of clinical pharmacology and as well as to everyday medical practice.

Asunto(s)

RESUMEN

The gastric cytoprotective effects of vitamin A, De-Nol and sucralfate were compared with the effectiveness of pirenzepine in healing ulcer in patients with chronic gastric ulcer. A total of 100 patients was randomized into different groups: the patients were treated with antacids, vitamin A (3 X 50.000 IU), De-Nol liquid (4 X 5 ml), sucralfate (4 X 1 g) or pirenzepine (3 X 50 mg). The treatment was continued for 4 weeks. At the beginning, 2 and 4 weeks after starting treatment the patients were subjected to endoscopy and the size of the ulcer was measured planimetrically. The ulcer-healing effect of De-Nol liquid was significantly better than that of the antacids (p less than 0.01). Ulcer size was reduced significantly in all groups (p less than 0.01), however, at the end of the study the gastric ulcers were smallest in the De-Nol treated group (p less than 0.001). The dynamics of ulcer healing in the second week was most favourable in the patients receiving vitamin A (p less than 0.01). The present data point to the cytoprotective effects of De-Nol liquid, vitamin A and sucralfate and to their ability of healing chronic gastric ulcers.

Asunto(s)

RESUMEN

The effects of cimetidine (12.5 mg i.m.) and atropine (0.125 mg i.m.) were studied on the basal (BAO) and pentagastrin (6 micrograms X kg-1 s.c.)-stimulated (MAO) gastric acid secretion; the gastric mucosal microbleeding provoked by one-day treatment with indomethacin (4 X 25 mg orally) in patients with chronic disorders of the joints. The extent of the gastric microbleeding was measured by spectrophotometric determination of haemoglobin in gastric lavage fluid. The aims of this study were to determine the doses of cimetidine and atropine in humans without any significant inhibitory effects either on the basal or on the maximal gastric acid output to evaluate the cytoprotective action of these doses of cimetidine and atropine on the indomethacin-induced gastric microbleeding in the man. It was found that cimetidine (12.5 mg i.m.) and atropine (0.125 mg i.m.) did not cause any significant inhibition either of the BAO or of the MAO; indomethacin (4 X 25 mg orally) significantly increased gastric microbleeding in the patients; cimetidine and atropine, in the above doses, were able to prevent significantly indomethacin-induced gastric microbleeding in the patients. These results provide evidence for the existence of gastric cytoprotective effects of cimetidine and atropine in humans.

Asunto(s)

RESUMEN

The effects of different doses (0.01-0.1-1.0-10.0/mg/kg-1) of beta-carotene were studied on gastric secretory responses of 4 hr pylorus-ligated rats: development of gastric mucosal damage (as assessed by number and severity of lesions) produced by intragastric administration of 0.6 M HCl; tissue level of adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), adenylate pool (ATP + ADP + AMP), ratio of ATP X ADP-1, "energy charge" (ATP + 0.5 ADP X X (ATP + ADP + AMP)-1) (during the development of gastric mucosal damage by 0.6 M HCl and of gastric cytoprotection by beta-carotene. It was found that beta-carotene did not decrease the gastric secretory responses of 4 hr pylorus-ligated rats; The development of gastric mucosal damage could be decreased dose-dependently by the administration of beta-carotene; the ATP transformation could be decreased by beta-carotene; the tissue levels of cAMP and AMP could be increased significantly and dose-dependently by beta-carotene; the ratio of ATP X ADP-1 could be increased significantly and dose-dependently by beta-carotene; the values of adenylate pool and "energy charge" remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Asunto(s)