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Biomedical subjects

T Vila

Publications and source records attributed to T Vila.

At least 19 recordsLinked to original sources
PubMed1999

Basal and stimulated gastrin and pepsinogen levels after eradication of Helicobacter pylori: a 1-year follow-up study.

AIM: A decrease in gastrin and pepsinogen (PG) levels 1 month after Helicobacter pylori eradication has been described repeatedly, but the long-term progression of such a decrease has been scarcely studied. We therefore studied the effect of H. pylori eradication on basal and stimulated gastrin and PG levels for 1 year. Initially, the usefulness of measuring these parameters for the noninvasive diagnosis of H. pylori eradication was validated. Furthermore, an assessment was made of the association between H. pylori reinfection and a re-increase in gastrin and PG values. Finally, an evaluation was made of the variables influencing gastrin and PG concentration, with particular attention to H. pylori infection and histological lesions of gastric mucosa. METHODS: Two-hundred and twenty-two patients with duodenal ulcer were studied prospectively. Exclusion criteria were the administration of antibiotics, H2 antagonists, omeprazole or bismuth prior to endoscopy. In all patients serum basal levels of gastrin, PGI, and PGII were measured before and 1 month after completing eradication therapy. In the successfully eradicated patients, gastrin, PGI, and PGII were also measured at 6 and 12 months. In 80 patients stimulated measurements of gastrin (after ingestion of two beef cubes) and PGI (after injection of pentagastrin) were also performed. H. pylori-negative patients after therapy underwent a urea breath test at 6 and 12 months, and patients who had stimulated gastrin and PG concentration measured had also an endoscopy performed at 6 months. RESULTS: H. pylori was eradicated in 73% of patients. A histological improvement was observed 1 month after completing H. pylori eradication therapy, both at gastric antrum and body (P < 0.001), while a further improvement at antrum was demonstrated at 6 months (P < 0.01). With regard to the different cut-off points for decreased basal and stimulated measurements for diagnosing H. pylori eradication, the best results were obtained, respectively, with PGII (sensitivity of 90% and specificity of 76%) and PGI 30 min after stimulation (sensitivity and specificity of 82%), with an area under the ROC curve of 0.87 in both cases. In the multiple regressions analysis H. pylori status correlated with gastrin, PGI and PGII after therapy (P < 0.001), while histological lesions correlated only with gastrin levels (P < 0.05). A decrease in basal and stimulated serum parameters was demonstrated immediately after eradication (Wilcoxon test, P < 0.001), and an additional decrease (at 6 months) was observed just in PGI (Friedman test, P < 0.01). However, gastrin and PGII values remained unchanged after the first month post-eradication. Seven patients were reinfected with H. pylori during follow-up. Quantitation of basal and stimulated gastrin and PGI levels was not reliable as a reinfection marker. Regarding basal PGII, the parallelism was strong at 6 months (re-increase in all four reinfected patients), although only in one out of three with reinfection at 1 year did PGII rise at that stage. CONCLUSIONS: (1) Measurement of gastrin and PG levels (especially basal PGII values) is a useful non-invasive method to confirm H. pylori eradication after therapy. (2) H. pylori eradication is associated with a significant decrease in basal and stimulated gastrin levels and in basal PGII levels that is detected immediately (1 month) after finishing treatment, and remains unchanged for 1 year. However, the decrease in basal and stimulated PGI levels occurs progressively for 6 months, although such levels remain also unchanged afterwards. (3) Measurement of gastrin and PGI concentrations has a limited usefulness in the diagnosis of H. pylori reinfections after successful eradication, although PGII determination could be more useful in this situation.

Breath Tests↗
PubMed1996

[Helicobacter pylori infection and basal levels of serum gastrins in patients with duodenal ulcer and subjects with normal endoscopy].

BACKGROUND: To study basal gastrin levels in duodenal ulcer patients and in those with normal endoscopy, according to Helicobacter pylori infection. METHODS: Eighty-four duodenal ulcer patients and 164 with normal endoscopy were studied. Biopsy specimens were taken from gastric antrum and body, and investigated for microbiology (Gram stain and culture) and histology (hematoxilin-eosin stain). Basal gastrin levels were measured (RIA). RESULTS: In duodenal ulcer patients the percentage of chronic gastritis was higher (p < 0.001) than in patients with normal endoscopy without H. pylori infection, and similar to patients infected by H. pylori. In patients with normal endoscopy (n = 164), those infected with H. pylori (n = 115) had higher (p = 0.02) gastrin levels (mean +/- SD) than non-infected (64 +/- 34 vs 51 +/- 14 pg/ml) and similar to duodenal ulcer patients (62 +/- 20 pg/ml). In the multiple regression model analysis H. pylori infection was the only variable which correlated with gastrin levels (regression coefficient 9.48 [SE = 4.59]; multiple correlation coefficient 0.22 [p = 0.008]). Additional variables (age, sex, duodenal ulcer) were not correlated with gastrin levels. Patients with chronic gastritis had higher gastrin levels (p < 0.01) than those with normal histologic mucosa. CONCLUSIONS: In patients with normal endoscopy, those infected with H. pylori had significantly higher basal gastrin levels than non-infected individuals, and similar to duodenal ulcer patients. Therefore, hypergastrinaemia seems to be associated with H. pylori infection, and is not a distinctive feature of duodenal ulcer disease.

Adolescent↗
PubMed1996

A survey for Cryptosporidium spp. in mammals at the Barcelona Zoo.

Mammals housed at the Barcelona Zoo belonging to the orders Carnivora, Artiodactyla, Perissodactyla and Proboscidea were examined for Cryptosporidium infections. A total of 183 fecal samples from 17 carnivores and 34 herbivores revealed patent infections in only 6 herbivore species (5 artiodactyls of the families Bovidae and Giraffidae and 1 perissodactyl of the family Rhinocerotidae); all carnivores were negative. Intensity of infection was found to be generally low. Connochaetes taurinus taurinus, Gazella dorcas neglecta, Kobus ellipsiprymmus and Giraffa camelopardalis constitute new host species for the parasite.

Animals↗
PubMed1996

Basal and stimulated gastrin levels and gastric acid output five months after therapy for Helicobacter pylori eradication in duodenal ulcer patients.

The aim of our study was to demonstrate the effect of Helicobacter pylori eradication on basal and stimulated serum gastrin levels and gastric acid output 5 months after therapy of patients with duodenal ulcer. Thirty-two patients (24 men and eight women with a mean age of 45 years) who had had endoscopy and were diagnosed as having duodenal ulcer entered the study. In all patients three biopsy specimens were taken from the duodenal bulb, gastric antrum, body, and fundus. These specimens were then sent for microbiological and histological examination. Triple therapy consisting of bismuth, metronidazole, and tetracycline was administered. Endoscopy was repeated 1 and 5 months after therapy, and biopsy specimens were again taken from the gastric antrum and body. Before treatment, serum samples were taken to measure basal and stimulated (90 min) gastrin levels after ingestion of two beef cubes, and basal and stimulated acid outputs (after pentagastrin) were studied. Measurements of gastrin and gastric acid output were repeated 5 months after therapy. H. pylori was eradicated in 26 patients (81.3%). Basal gastrin levels (mean +/- SD) at diagnosis and after eradication were 44 +/- 12 and 35.8 +/- 2 pg/ml, respectively (p < 0.05). Similarly, stimulated gastrin levels (integrated values) decreased from 5,303 +/- 1,526 pg/ml/min before therapy to 3,779 +/- 1,204 pg/ml/min after eradication (p < 0.001). However, basal (4.9 +/- 4mEq/h) and stimulated (28.5 +/- 10mEq/h) acid output did not vary after eradication (3.9 +/- 4 mEq/h and 26.2 +/- 12 mEq/h, respectively). We conclude that basal and stimulated gastric acid output are not changed by H. pylori eradication in duodenal ulcer patients 5 months after therapy, in spite of its association with a significant decrease in basal and stimulated gastrin levels.

Adult↗
PubMed1996

Verification of decreased basal and stimulated serum pepsinogen-I levels is a useful non-invasive method for determining the success of eradication therapy for Helicobacter pylori.

BACKGROUND: We wanted to demonstrate the effect of Helicobacter pylori eradication on basal and stimulated pepsinogen-I levels in duodenal ulcer patients and to verify whether modification of such levels is a useful method for determining the success of eradication therapy. METHODS: Thirty-two patients (24 men; mean age, 45 years) with active duodenal ulcer were studied. In all patients three biopsy specimens were taken from the duodenal bulb, gastric antrum, body and fundus for microbiologic and histologic examination. Triple therapy consisting of bismuth, metronidazole, and tetracycline was administered. Endoscopy was repeated 1 month after completing therapy, and biopsy specimens were again taken from the gastric antrum and body. Serum samples were taken at initial and repeat endoscopies, to measure basal and stimulated (120 min) pepsinogen-I levels after injection of pentagastrin. RESULTS: H. pylori was eradicated in 26 patients (81%). Significant histologic improvement, in both the antrum and body, was observed (p < 0.001). Basal pepsinogen-I levels (mean and 95% confidence interval) at diagnosis and after eradication were 106 (92-119) and 87 (74-100) ng/ml, respectively (P < 0.001). Similarly, stimulated pepsinogen-I levels (integrated values) decreased from 4790 (4199-5381) before therapy to 3970 (3383-4557) ng/ml.min after eradication (P < 0.001). Pepsinogen I levels did not change in patients in whom H. pylori was not eradicated. The area under the receiver operating characteristic curve for decreased basal and stimulated pepsinogen-I levels was 0.77 (SE, 0.09) and 0.79 (SE, 0.1), respectively. CONCLUSION: H. pylori eradication in duodenal ulcer patients was associated with a significant decrease in basal and stimulated pepsinogen-I levels. Measurement of these levels could determine how successful response to therapy has been in both the eradication and resolution of associated gastritis. Other advantages of this procedure are that it has low cost and results are evident at an early stage.

Adult↗
PubMed1996

[Basal levels of blood pepsinogen I and Helicobacter pylori infection in patients with duodenal ulcer and normal endoscopy].

AIM: To study basal pepsinogen I levels in patients with duodenal ulcer and in subjects with normal endoscopy, depending on Helicobacter pylori status. METHODS: One-hundred and one patients with duodenal ulcer and 74 controls with normal endoscopy were studied. Mean age and gender distribution were: 46 vs 42 years, and 74% vs 43% males, respectively. At endoscopy biopsies from the gastric antrum and body were obtained for histologic (H&E) and microbiologic (Gram and culture) study. Basal levels of serum pepsinogen I were measured (RIA). RESULTS: Among the subjects with a normal endoscopy, those with H. pylori infection had higher pepsinogen I levels (m +/- SD) than non-infected patients (77 +/- 27 vs 62 +/- 28 ng/ml; p < 0.05). Basal levels in duodenal ulcer patients were 107 +/- 38 ng/ml, higher (p < 0.001) than in the group with normal endoscopy (both with and without H. pylori). In multivariate analysis pepsinogen I levels were correlated with H. pylori infection (regression coef.= 17; SE= 8.1), duodenal ulcer (regr. coef.= 22; SE= 5.8) and smoking habit (regr. coef.= 24; SE= 5.2). CONCLUSION: Basal pepsinogen I levels were significantly higher in duodenal ulcer patients than in H. pylori infected subjects with normal endoscopy. The lowest levels corresponded to non-infected patients. Therefore, an additional factor other than H. pylori infection is likely involved in the hyperpepsinogenemia classically reported in duodenal ulcer patients.

Adult↗
PubMed1995

[Is measurement of basal levels of serum pepsinogen II useful in proving the eradication of Helicobacter pylori by treatment?].

BACKGROUND: The aim of this study was to demonstrate the influence of the eradication of Helicobacter pylori on the basal concentrations of serum pepsinogen II in patients with duodenal ulcer. METHODS: Thirty-two patients with active duodenal ulcer were prospectively studied. A triple therapy was used consisting in bismuth, metronidazole and tetracycline. At the time of initial endoscopy and in those performed 5 months later on completion of the treatment, biopsies of the gastric mucosa were taken for histologic and microbiologic studies, and the basal concentrations of serum pepsinogen II are also determined. RESULTS: The eradication of H. pylori was accompanied by a significant pathologic improvement (p < 0.001) in both the antrum and the gastric body. On eradication of H. pylori, the basal pepsinogen II value (m +/- SD) decreased from 9.2 +/- 2.7 ng/ml to 6.4 +/- 1.7 ng/ml after treatment (p < 0.001). However, when eradication was not achieved, these values increased (11.8 ng/ml) with respect to the initial determination (9.3 ng/ml) (p < 0.05). The area under the ROC curve was 0.99 (SE 0.01) with a sensitivity of 92% and specificity of 100% with respect to the diagnosis of infection eradication (cut off point of the decrease of pepsinogen levels O). CONCLUSIONS: The eradication of Helicobacter pylori in patients with duodenal ulcer is associated with a significant decrease in the basal concentrations of serum pepsinogen II measured 5 months after completion of treatment. The verification of this decrease constitutes a useful, inexpensive non invasive method to prove the eradication of H. pylori with treatment.

Adult↗
PubMed1995

[A global study of gastric secretion in duodenal ulcers: gastrin, pepsinogen and acid secretion].

AIM: To examine gastric secretion in duodenal ulcer patients; simultaneous assessment of serum gastrin and pepsinogen I levels and acid secretion. METHODS: 32 patients with duodenal ulcer disease were studied (mean age: 44.7 +/- 14 years, 24 males (75%). At endoscopy, biopsy specimens from duodenal bulb, antrum, body and gastric fundus were taken. Basal levels of acid secretion, pepsinogen I and gastrin were measured, as well as stimulated levels (with pentagastrin and beef meal). RESULTS: Mean (+/- SD) BAO and MAO was 5.5 +/- 4 and 27.7 +/- 10 mEq/h, respectively. BAO in males were higher than in females (p < 0.05). A positive correlation (p < 0.01) was observed between MAO, and basal and stimulated pepsinogen I. Basal and stimulated (integrated-90 min) gastrin levels were 43.4 +/- 12 pg/ml and 5,260 pg/ml min, respectively. No correlation between such levels and acid secretion or pepsinogen I was observed. Mean basal and stimulated (integrated-120 min) pepsinogen levels were 109.3 +/- 35 ng/ml and 4,950 +/- 160 ng/ml min, respectively, and they were higher in males (p < 0.01), and in smokers (p < 0.05). CONCLUSION: It was confirmed, in a group of duodenal ulcer patients, that BAO is higher in males than in females. There is a positive correlation between MAO and pepsinogen I levels, although this correlation is not present between gastrin levels and acid secretion or pepsinogen I. Pepsinogen I levels are higher in males and smokers.

Adult↗
PubMed1995

[Decrease of basal levels of gastrin following H. pylori eradication].

UNLABELLED: Hypergastrinemia has long been considered an important factor in the pathophysiology of duodenal ulcer. Moreover, H. pylori infection has been reported in virtually all duodenal ulcers. AIM: To demonstrate the influence of H. pylori eradication on the basal levels of serum gastrin in patients with duodenal ulcer. METHODS: Seventy-six patients with endoscopically proved duodenal ulcer were prospectively studied. At endoscopy three biopsy samples each were taken from duodenal bulb, gastric antrum, corpus and fundus. Two samples from every location were submitted for conventional histological examination and the other for microbiological examination (Gram staining and culture). Endoscopy was repeated one month after the end of therapy, when endoscopy samples were again obtained from the gastric antrum and corpus. Basal levels of gastrin were measured both at initial and repeat endoscopies. Different therapeutic regimes were used: Amoxycillin/Clavulanate plus omeprazole or ranitidine, and triple therapy. RESULTS: H. pylori eradication was associated with a significant histological improvement (p < 0.001), both in antrum and corpus. In those patients with eradicated H. pylori the differences in basal gastrin levels both at diagnosis and after therapy were 45.4 +/- 11 pg/ml and 36.7 +/- 10 pg/ml, respectively; these differences were statistically significant (p < 0.001). When eradication was not achieved differences were not significant. The area under the ROC curve constructed from the different cutoff points for the gastrin decreases was 0.68 (EE 0.06). CONCLUSION: H. pylori eradication in patients with duodenal ulcer was associated with a significant decrease in basal levels of serum gastrin. Although the verification of such a decrease doesn't have an optimal relationship between sensitivity and specificity, it could be an aid as a useful non-invasive method to monitor the efficiency of therapy, both in H. pylori eradication and in the resolution of the associated gastritis. This procedure is also associated with early results and a low cost.

Adult↗
PubMed1995

[A decrease in the basal levels of serum pepsinogen I after H. pylori eradication].

Hyperpepsinogenaemia has long been considered an important factor in the pathophysiology of duodenal ulcer. Moreover, H. pylori infection has been reported in virtually all duodenal ulcers. OBJECTIVE. To demonstrate the influence of H. pylori eradication on basal pepsinogen I levels in patients with duodenal ulcer. METHODS. 86 patients with endoscopically proven duodenal ulcer were prospectively studied. Different therapeutic regimens were used: Amoxycillin/clavulanate plus omeprazole or ranitidine, triple therapy, omeprazole and ranitidine. At diagnostic endoscopy and after therapy, three biopsy samples were taken from different levels and analyzed by microbiological and histological methods; also, basal pepsinogen I levels were measured. RESULTS. H pylori eradication was associated with a significant histological improvement (p < 0.001), both in gastric antrum and corpus. In patients where H. pylori was eradicated pepsinogen I levels decreased from 107.6 +/- 31 ng/ml to 79.7 +/- 32 ng/ml after therapy (p < 0.001); however, when eradication was not achieved differences were not significant. CONCLUSION. H pylori eradication in patients with duodenal ulcer was associated with a significant decrease in basal pepsinogen I levels. The verification of such a decrease could represent a useful non-invasive method to monitor the efficiency of therapy, both in H. pylori eradication and in the resolution of the associated gastritis. This procedure is also associated with early results and a low cost.

Adult↗
PubMed1993

Normal calcitonin response to pentagastrin stimulation in patients with chronic renal failure.

High calcitonin levels have been reported in chronic renal failure. To study the C cell response in patients with chronic renal failure, an intravenous bolus of pentagastrin was administered to 11 patients and 11 healthy subjects. Samples were obtained at 0, 1, 2, 3, 5 and 10 min for calcitonin assay. In order to detect only the active monomeric calcitonin, an immunoradiometric assay method was used. The influence of calcium, phosphate, alkaline phosphatase and intact parathyroid hormone was also evaluated. Although basal calcitonin levels were higher (p < 0.01) in chronic renal failure (mean +/- SEM: 10.1 +/- 2.9 pmol/l) versus healthy subjects (1.1 +/- 0.3 pmol/l), the area under the curve showed there to be no differences between the two groups. The rising branch of the area under the curve, employed as an expression of the C cell response capacity, showed no differences either (chronic renal failure vs healthy subjects: 5.6 +/- 2 vs 2.6 +/- 0.7 pmol l-1 min-1, p = 0.28). In the chronic renal failure group, a positive correlation was found (r = 0.625, p < 0.05) between the rising branch of the area under the curve and parathyroid hormone. We conclude that monomeric calcitonin is increased in chronic renal failure, but C cells of the thyroid respond to pentagastrin, as they do in normal subjects. This finding is of great clinical importance when a patient with renal impairment is evaluated for medullary thyroid carcinoma. The calcitonin response to pentagastrin seems to be related directly to the degree of secondary hyperparathyroidism in chronic renal failure.

Adolescent↗
PubMed1989

Serum ferritin levels after renal transplantation: a prospective study.

A prospective study was made of the evolution of serum ferritin levels in 112 renal transplant recipients with good graft function. The rise in hemoglobin value is accompanied by a decrease in basal serum ferritin levels which are lowest at the sixth month: 54.9 (2-1,516) vs. 109.6 (21-4,420) micrograms/l, p less than 0.001 (Xg and range). After this time, ferritin values increase, although they do not reach basal levels. Evolution after transplantation is mainly determined by the previous state of iron stores at the time of transplantation. While in the patients with high basal serum ferritin values these gradually decreased during the follow-up period, patients with low basal serum ferritin levels tend to replenish their iron stores after renal transplantation. These differences disappear at the third year when serum ferritin values are similar in all groups. An association between persistence of posttransplant anemia and low serum ferritin levels is observed. This event is not clinically relevant as anemia disappears in almost all cases and dietary iron is enough to normalize serum ferritin levels.

Adolescent↗
PubMed1981

Free fatty acid inhibition of exercise-induced growth hormone secretion.

In order to investigate the effect of plasma free fatty acids (FFA) elevations on growth hormone (GH) secretion in humans, paired physical exercise (ph.e.) tests were performed in nine untrained healthy volunteers of both sexes. Ph.e. tests were accomplished on a bicycle ergometer under a moderate work load (450 kpm/min x 40 min). On one of two test days, subjects were given 60 gr of a soy bean oil emulsion (Intralipid) 3 hr before, followed by two 50 mg heparin bolus injection, administered 10 min before and 15 min after the start of the exercise. Ph.e. in the control group induced a clear-cut elevation of GH levels which peaks at 40 min. On the other hand Intralipid plus heparin induced FFA elevation, completely block GH secretion elicited by exercise (p less than 0.05 at 20 and 40 min). There also seems to be a threshold level of FFA (3 mEq/l) above which GH suppression was complete. On the contrary, below this level GH blockade was rather inconsistent. FFA elevation has been able to block all the GH stimuli tested so far, and this data support a role of plasma FFA in GH regulation.

Adolescent↗
PubMed1979

The role of growth hormone in the pathogenesis of postmenopausal osteoporosis.

The secretory response of somatotropic hormone (STH) to arginine hydrochloride stimulation (0.5 g/kg) was studied in 13 postmenopausal women. Eight showed evidence of osteoporosis, based on clinical and morphoradiological data and on metacarpal cortical thickness measurement, and five had normal bone mass. In addition, the response to levodopa (500 mg) was determined in four of the osteoporotic patients. Baseline STH concentrations in the osteoporotic subjects did not differ from those in the nonosteoporotic group, but the latter showed a significant increase over the former at 45, 60, 90, and 120 minutes after stimulation. Similar findings were obtained with levodopa stimulation. Without necessarily implying a cause-effect relationship, our data appear to support the hypothesis that the poor secretory response of STH may be to some degree responsible for the osteopenia observed during the climateric.

Adult↗