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Biomedical subjects

B Annibale

Publications and source records attributed to B Annibale.

At least 91 records · Page 5Linked to original sources
PubMed1991

Antral gastrin cell hyperfunction in children. A functional and immunocytochemical report.

Antral gastrin cell hyperfunction is a rare condition, often associated with severe duodenal ulcer disease. In children, clinical and functional characteristics of this syndrome are poorly known. Two cases are described here: one child had melena and the other had moderate abdominal pain, both without peptic ulceration. Basal and postprandial increase of gastrin levels showed a response over the upper normal range, indicating gastrin cell hyperfunction. Acid hypersecretion, both basal and after pentagastrin stimulation, was also found in the two children, confirming the biological effect of their sustained hypergastrinemia. Gastrin cell counts were within the normal range, while the number of somatostatin D cells was significantly reduced. This report stresses the importance of diagnosing antral gastrin cell hyperfunction in children because this unrecognized condition may manifest with serious complications (bleeding) or nonspecific abdominal symptoms.

Abdominal Pain↗
PubMed1991

Effects of somatostatin on human intestinal lamina propria lymphocytes. Modulation of lymphocyte activation.

We have investigated the effect of somatostatin (SOM) on the mitogen-induced activation of lamina propria mononuclear cells isolated from the human intestinal mucosa (LPMNC) and of the autologous peripheral blood lymphocytes (PBMNC). The occurrence of specific SOM receptors and their biological characteristics were also investigated. The counts of interleukin-2 receptor (IL-2R)-positive cells after mitogen stimulation were significantly lower in the presence of SOM. This effect of SOM appeared to be dose dependent, with SOM concentrations ranging between 1 pM and 1 microM. The amount of SOM required for the 50% inhibition of this expression was 1000 times lower in the LPMNC population than in the PBMNC. Binding studies showed that human LPMNC bear specific receptors for SOM and demonstrated that the affinity of these receptors was 1000 times higher than that of the SOM receptors present on the PBMNC (Kd 2.1 +/- 0.34 nM vs. 910 +/- 46 nM, respectively). The inhibitory effect of SOM on the proliferative response appeared to be restricted to PBMNC, with a maximal inhibition at 1 nM SOM, while LPMNC proliferative response was poorly affected. SOM inhibited the in vitro immunoglobulin production of both PBMNC and LPMNC over a wide range of concentrations, with a maximal inhibition at 1 nM. At this concentration the effect of SOM on IgA was more pronounced in the PBMNC than in the LPMNC. Our results lend support to the concept that in humans SOM plays a role in the modulation of the immune response at the level of the intestinal mucosa where cell-to-cell interactions between SOM releasing nerve fibers and cells and the immune system occur.

DNA↗
PubMed1991

Reversible sustained increase of gastrin and gastric acid secretion in a subgroup of duodenal ulcer patients on long-term treatment with H2 antagonists.

We assessed the effect of long-lasting inhibition of gastric acid secretion on basal and meal-stimulated serum gastrin and gastric acid secretion in 37 patients on long-term maintenance treatment with H2 antagonists for severe relapsing and/or complicated duodenal ulcer disease. After a mean of 142 weeks (range, 28-324 weeks) of continuous treatment, gastric acid secretion, basal plasma gastrin, and gastrin response to a test meal were evaluated. All tests were performed a week after drug discontinuation to exclude rapidly reversible hypergastrinemia. Gastrin levels were above the normal range in seven patients (18.9%). After H2 antagonist were stopped for 6 weeks, basal gastrin returned to normal levels in all cases [from a median of 180 (range, 130-350) pg/ml to 58 (25-90) pg/ml] and peak meal-stimulated gastrin significantly decreased from a median of 500 pg/ml to 245 pg/ml (p = 0.02). In patients with hypergastrinemia, the discontinuation of H2 antagonists for 6 weeks led to a significant decrease of gastric acid secretion. Patients who developed hypergastrinemia spent more weeks on full-dose treatment and had more recurrences during therapy. The results of the present investigation demonstrate that a long-lasting inhibition of gastric acid secretion can induce, in a small percentage of patients, a reversible sustained hypergastrinemia and a consequent increase of acid secretion, which conceivably could lead to more frequent relapses of duodenal ulcer disease.

Adolescent↗
PubMed1990

Neurohumoral control of gallbladder motility in healthy subjects and diabetic patients with or without autonomic neuropathy.

Patients affected by diabetes mellitus are reported to have an increased incidence of gallbladder abnormalities. The pathophysiologic mechanisms for this phenomenon are unclear. In the present study ultrasonography was used to determine gallbladder emptying in response to a meal or separate cephalic or hormonal stimulation in 21 diabetic patients and 10 healthy subjects. Gallbladder emptying and refilling after a meal were similar in diabetic patients and healthy subjects. When diabetics were divided according to the presence or absence of cardiac autonomic neuropathy (AN), a significant reduction of gallbladder emptying in response to cephalic stimulation was found in diabetics with AN (P less than 0.01 in comparison with diabetics without AN or healthy subjects). A dose-response curve of gallbladder emptying in response cerulein, a cholecystokinin analog, at concentrations of 0.25, 1, and 4 micrograms/kg/min was evaluated. No differences of gallbladder emptying were found in the three groups of subjects, indicating that gallbladder sensitivity to hormonal stimulation is not changed in diabetic patients with or without AN. Diabetic patients with AN have a significant reduction of gastric acid output and pancreatic polypeptide (PP) secretion in response to cephalic stimulation (P less than 0.05 in comparison with diabetic patients without AN or healthy subjects). Cerulein-induced PP secretion was similar in all three groups of subjects (P greater than 0.05). This study indicates that in diabetic patients with AN, gallbladder emptying as well as gastric acid and PP secretions induced by neural stimulation are markedly reduced in comparison to diabetics without AN.

Adult↗
PubMed1990

Effects of high in vivo levels of vasoactive intestinal polypeptide on function of circulating lymphocytes in humans.

To examine the possible in vivo significance of the immunomodulatory effects of vasoactive intestinal polypeptide described in vitro, several parameters of peripheral blood lymphocyte function were studied in a patient with a pancreatic endocrine tumor and high circulating levels of vasoactive intestinal polypeptide. There was no imbalance of the circulating lymphocyte subpopulations, and the in vitro responses of the patient's lymphocytes to mitogens were normal. However, there was an increased number (32%) of peripheral lymphocytes expressing interleukin 2 receptor. Serum immunoglobulin M levels were higher than in controls, and the patient's lymphocytes exhibited a spontaneous in vitro immunoglobulin M production higher than normal. Comparable increases in both interleukin 2 receptor expression and immunoglobulin M production were induced in vitro in normal peripheral lymphocyte cultures by the addition of vasoactive intestinal polypeptide concentrations similar to that detected in the patient's plasma. These findings indicate that a modulatory effect of vasoactive intestinal polypeptide on lymphocyte activation and immunoglobulin synthesis may be operating in vivo. They also suggest that vasoactive intestinal polypeptide does not mediate major defects in peripheral blood lymphocyte function in vivo.

Adenoma, Islet Cell↗
PubMed1990

Medical treatment of antral gastrin cell hyperfunction: role of nonantisecretory therapy.

Antral G cell hyperfunction (AGCH) is a rare condition, often associated with severe duodenal ulcer disease poorly responsive to medical therapy. Up to now, no studies have been designed to investigate a possible role of medical treatment in the management of this syndrome. In this study we treated 9 AGCH patients with duodenal ulcer, unhealed with the prolonging standard doses of H2 antagonists (300 mg/day ranitidine or 800 mg/day cimetidine), with a nonantacid therapy, tripotassium dicitrato bismuthate (TDB). 6 out of 9 patients showed a complete healing after 8 weeks of treatment. The healing was irrespective to eradication of Campylobacter pylori. After 9 weeks' suspension of H2 blockers basal gastrin levels decreased significantly by 31.5%, whereas peak meal-stimulated levels, although decreased in 6 out 9 patients, were not significantly affected by the withdrawal of the H2 antagonists. Nonantisecretory therapy seems to be an efficacious alternative in the management of AGCH patients.

Adolescent↗
PubMed1990

Gastrin pathophysiology: antisecretory drugs.

The management of maintenance therapy in peptic disease (oesophagus, stomach, duodenum) with antisecretory drugs should keep in consideration the aspect of developing hypergastrinemia: gastrin exerts a throphic effect on gastric ECL and parietal cells. After a long term maintenance therapy (3-5) years) with ranitidine 150mg/die in a group of 55 patients affected by duodenal ulcer, 20% of them developed hypergastrinemia and gastric hypersecretion (evaluated after one week of drug withdrawal). The same 20% of the subjects showed increased relapse rates with respect to those who did develop the same gastrin/gastric acid increase.

Gastric Acid↗
PubMed1989

Somatostatin infused during acute pancreatitis retains its biological activity.

Somatostatin (SST) is used in the treatment of acute pancreatitis (AP) to inhibit pancreatic exocrine secretion, which represents one of the goals of medical treatment in this disease. Its therapeutic efficacy, however, is poor. One hypothesis, which has not yet been investigated, is that i.v. SST might be broken down by blood proteolytic enzymes. In order to evaluate the structural integrity and biological activity of infused SST, somatostatin-like immunoreactivity (SLI) and levels of pancreatic enzymes were monitored in the blood stream during the infusion of SST-14 (3,5 micrograms/kg/h for 48 h) in eight patients with severe acute pancreatitis. SLI was measured by both radioimmunoassay (RIA) and high-pressure liquid chromatography (HPLC). The results indicate that SLI levels increase promptly after the beginning of infusion, with a slower increase between 6 and 36 h, and a rapid increase again at 48 h. HPLC analysis shows a single peak of SLI with the same retention time as standard SST-14. Total amylase, lipase, and trypsinogen significantly decreased compared with pretreatment values (48, 63.1, and 77.4%, respectively) after 24 h of SST infusion, while a decrease in elastase 1 (62.6%) was observed later at 48 h. These results indicate that in severe AP, somatostatin recovered in plasma retains its biological activity: it inhibits pancreatic circulating enzymes, an action not influenced by breakdown of the peptide, as demonstrated by HPLC of the SLI measured in plasma.

Acute Disease↗
PubMed1987

Dose-response effect of somatostatin-14 on human basal pancreatic hormones.

The effect of increased doses of Somatostatin-14 (3, 10, 30, 100, 300 micrograms/h) on basal release of insulin, pancreatic glucagon and pancreatic polypeptide (PP) was investigated on eight normal volunteers. Levels of Somatostatin-like immunoreactivity (SLI) was determined in order to correlate the increased SLI levels with the degree of islet hormone inhibition (r = 0.9947, p less than 0.01). By increasing the basal levels of SLI by one-third, a significant inhibition (p less than 0.01) of insulin, glucagon, and PP was noted (78.5, 78.6, 75.2%, respectively, on basal levels). The maximal effect was obtained with 300 micrograms/h for insulin, with 30 micrograms/h for glucagon and 100 micrograms/h for PP. In evaluating the relative inhibitory potency of somatostatin, expressed as ED50, the theoretic potency of somatostatin on each peptide had similar values, ranging from 30 to 10 micrograms/h. The present data show that a minimal peripheric increase in SLI is able to regulate basal islet pancreatic hormones.

Adult↗
PubMed1986

Pancreatic polypeptide response to a protein-rich meal in diabetic patients with and without neuropathy.

A protein-rich meal and insulin-induced hypoglycemia (ITT) are two of the most important stimuli on pancreatic polypeptide (PP) secretion in diabetic patients. Previous studies have shown a reduced PP response to ITT in diabetic patients with autonomic neuropathy (AN). Twelve patients without AN (mean age 44 +/- 10.8 yr, mean duration of diabetes 11 +/- 5.6 yr), 9 with AN (51.4 +/- 6 yr, 15.8 +/- 6.9 yr) and 9 controls (N) were studied. AN was assessed by the evaluation of the beat-to-beat variation of the heart rate during deep breathing. PP secretion was stimulated by a protein-rich meal (200 g meat, 150 g milk). All insulin-dependent diabetic (IDD) patients lacked circulating PP antibodies. All diabetic patients showed a significant reduction in the early vagal phase compared to controls. This behavior was more evident in diabetic patients with AN and the secondary phase of these two groups overlapped with the response of controls. These data may be explained by the initial alterations of vagal functions not detectable by current methods.

Adult↗
PubMed1985

Evidence that bombesin releases extragastric gastrin in man.

Bombesin-induced gastrin release from extragastric sources has been investigated in two groups of patients without gastric antrum: 11 patients with total gastrectomy and 11 patients with subtotal (Billroth II) gastrectomy. A 30-min bombesin infusion (5 ng . kg-1 . min-1) caused a prompt significant gastrin increase (P less than 0.05) in both groups of patients. The gastrin response to bombesin was significantly (P less than 0.005) lower in patients without antral tissue than in the control group (n = 7). The individual peak gastrin responses, in totally (TG) and subtotally (SG) gastrectomized patients, were significantly over basal levels (TG: peak 100.3 +/- 12 vs. basal 62.8 +/- 9.1, P less than 0.005; SG: peak 96.9 +/- 9.4 vs. basal 72.4 +/- 6.8, P less than 0.001; pg/ml, mean +/- S.E.M.). These data indicate that bombesin acts not only on antral G cells, but on all gastrin cells in the gastrointestinal tract.

Adult↗
PubMed1985

Bombesin effects on human GI functions.

In this article some of the actions of amphibian skin peptide Bombesin (BBS) on human gastrointestinal and pancreatic functions are reviewed. BBS causes increases of lower esophageal sphincter pressure, delay of gastric emptying, inhibition of mechanical activity of duodenum and jejunum and gallbladder emptying. BBS also releases in man gastrin and stimulates gastric acid secretion. BBS administration induces release of insulin, glucagon and pancreatic polypeptide from human Islet of Langerhans and causes secretion of pancreatic bicarbonates and enzymes in duodenal juice and release of pancreatic enzymes in blood stream.

Bombesin↗
PubMed1985

Peptides of the APUD system in amphibian skins.

Methanol extracted skins from 84 species of amphibia were screened, measuring by RIAs: gastrin-CCK, VIP, calcitonin, GIP, PP and motilin. G-CCK-like immunoreactivity was found in 97.6%; VIP-like immunoreactivity in 41%; CT-like immunoreactivity in 34%; GIP-like immunoreactivity in 10%; PP-like immunoreactivity in 40% and MT-like immunoreactivity in 60% of the samples. The use of a sequence-specific radioimmunoassay and of gel-chromatography confirmed the caerulein-CCK-8-like nature of the immunoreactive material. Detected amounts of the other peptides (VIP, CT, GIP, PP, MT) were too low for bioassay or chromatographic studies, thus leaving the question open if they are due to some kind of unspecific interferences or, most likely, to species-specificity differences of the used antisera.

APUD Cells↗
PubMed1985

Gastric acid and pancreatic polypeptide responses to modified sham feeding: indication of an increased basal vagal tone in a subgroup of duodenal ulcer patients.

The effect of sham feeding upon gastric acid secretion and pancreatic polypeptide release was investigated in 28 patients with duodenal ulcer in order to evaluate whether high basal vagal activity is the cause of basal acid hypersecretion in patients with duodenal ulcer and basal secretion higher than 30% of their peak acid output. The patients were divided into two groups based on the ratio of basal/pentagastrin stimulated peak acid output (BAO/PAO) was higher or lower than 0.30: group A n = 19 (BAO/PAO less than or equal to 0.30) and group B n = 9 (BAO/PAO greater than 0.30). Gastric acid response to sham feeding (SAO) was significantly higher than basal level in group A (SAO: 11.4 mEq/h (2.5-20.1) vs BAO: 5.2 mEq/h (0.8-22.9), p less than 0.01, median (range)) while in group B the acid secretion did not increase with sham feeding (SAO: 9.6 mEq/h (4.5-13.6) vs BAO: 8.8 mEq/h (6.3-13.8) ns, median (range)). A negative correlation (r= -0.6118226, p less than 0.01) was found between acid increase expressed as basal subtracted sham feeding response (SAO-BAO) and BAO/PAO ratio of the entire group of duodenal ulcer patients (n = 28) suggesting that the greater is basal acid secretory capacity the smaller is acid increase in response to residual vagal activation. Pancreatic polypeptide response to sham feeding was higher in group A than in group B but no correlation (r = 0.20, n = 28) nor individual covariation was found between acid and pancreatic polypeptide secretions during vagal stimulation. sham feeding did not change serum gastrin. It is concluded that an increased vagal stimulation seems to be the cause of basal hypersecretion in a subgroup of patients with duodenal ulcer. The lact of correlation between the pancreatic polypeptide and acid responses to vagal stimulation interferes with the reliability of pancreatic polypeptide as indicator of vagal tone on gastric parietal cells.

Adult↗
PubMed1983

Effects of bombesin on gastrin and gastric acid secretion in patients with duodenal ulcer.

The effect of bombesin, a possible neurotransmitter of gastrin release, upon gastrin and gastric acid secretion was investigated in 25 patients with duodenal ulcer and in 16 normal subjects. In patients with duodenal ulcer bombesin (10 ng/kg/min) produced an increase in plasma gastrin output (median 22.4 (range 7.5-75.8) pmol/l/min) similar to that obtained in normal subjects (median 24.4 (range 5.8-56.5) pmol/l/min), whereas gastrin stimulated by a meal was significantly higher in the group of patients with duodenal ulcer (median 20.7 (range 9.2-42.9) vs 16.2 (range 3.4-22.2) p<0.05). Peak acid output induced by bombesin was significantly higher in patients with duodenal ulcer than in normal subjects (median 24.4 (range 9.0-63.8) vs 14.0 (range 3.0-24.8) mmol/h, p<0.05) despite identical gastrin outputs. The ratio (%) obtained by dividing the acid secretory response to bombesin by the response to pentagastrin, however, was similar in both normal subjects and patients with duodenal ulcer (median 55 (range 20-116) vs 58 (range 31-95) respectively). The difference between the gastrin response to food and bombesin could be explained by the fact that bombesin releases gastrin directly, whereas a protein meal involves several mechanisms (neural, peptidergic, paracrine, endocrine), either stimulatory or inhibitory. The above results indicate that a higher concentration in antral and/or duodenal gastrin is unlikely to be present in patients with duodenal ulcer. An increased parietal cell mass could explain the higher gastric acid response after bombesin infusion in our group of patients with duodenal ulcer.

Adult↗
PubMed1983

Effect of bombesin on plasma insulin, pancreatic glucagon, and gut glucagon in man.

The effect of bombesin on insulin, pancreatic glucagon, and gut glucagon was investigated in eight healthy volunteers and two pancreatectomized patients. Bombesin, infused iv at the constant rate of 5 ng kg-1 min-1, produced a sharp and statistically significant rise in the plasma insulin concentration. The peak was reached at 5 min (26 +/- 2.17 microU/ml; P less than 0.005 vs. basal values), followed by a prolonged and statistically significant (P less than 0.05) decrease in blood glucose. Pancreatic glucagon rapidly rose to a maximal value of 80.5 +/- 7.6 pmol/liter (P less than 0.005 vs. basal values). In contrast with the prompt increase in insulin and glucagon plasma levels, the peak in gut glucagon concentration (55.8 +/- 4.6 pmol/liter; P less than 0.005 vs. basal values) was reached 30 min after bombesin infusion was discontinued. In the two pancreatectomized patients, bombesin induced an increase in gut glucagon concentrations only. The results presented indicate that bombesin acts directly on the A and B cells of the pancreas, influencing glucose homeostasis; however, more complex mechanisms seem to be involved in gut glucagon secretion.

Adult↗