gastrins has been researched along with Pain* in 11 studies
3 trial(s) available for gastrins and Pain
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A phase I trial of the bombesin/gastrin-releasing peptide (BN/GRP) antagonist RC3095 in patients with advanced solid malignancies.
Bombesin/gastrin-releasing peptides (BN/GRP) were shown to bind selectively to cell surface receptors, stimulating the growth of various types of malignancies in murine and human models. The novel BN/GRP synthetic receptor antagonist, RC-3095, was able to produce long-lasting tumor regressions in murine and human tumor models in vitro and in vivo. Animal toxicology studies showed no detectable organ toxicity apart from local irritation at the injection site. The purpose of this study was to determine the safety and feasibility of the administration of RC-3095 by daily subcutaneous injections in patients with advanced and refractory solid malignancies. Twenty-five patients received RC-3095 once or twice-daily at doses ranging from 8 to 96 ug/kg. Dose was escalated in groups of 3-5 patients per dose level. The only toxicity observed was local discomfort in the injection site at the highest doses. A single dose administration of RC-3095 at the highest dose level (96 ug/kg) was tested in a clearly hypergastrinemic individual with the Zollingen-Ellison syndrome and produced a decrease in plasma gastrin down to 50% of basal levels in 6 h. There was no objective tumor responses in patients included in the study. A short-lasting minor tumor response was observed in a patient with a GRP-expressing progressive medullary carcinoma of the thyroid. Due to problems with the analytical method, plasma pharmacokinetic data was obtained only from two patients included at the highest dose level. In these patients, RC-3095 reached plasma concentrations >100 ng/mL for about 8 h, which were within therapeutic levels on the basis of prior data obtained in mice and rats. The plasma elimination half-life was between 8.6-10.9 h. Due to the occurrence of local toxicity at the injection site, the dose escalation procedure could not be fully evaluated up to a maximum tolerated dose. Thus, a recommended dose of RC-3095 for Phase II trials could not be clearly established. Considering the novelty of its mechanism of action and impressive preclinical anti-tumor activity, further studies exploiting new formulations of RC-3095 for human use, such as slow-release preparations, and analogues with a more favorable pharmacokinetics are warranted. Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Agents; Bombesin; Female; Gastrin-Releasing Peptide; Gastrins; Humans; Injections, Subcutaneous; Male; Middle Aged; Neoplasms; Pain; Peptide Fragments; Skin | 2006 |
Pantoprazole versus omeprazole in the treatment of acute gastric ulcers.
Pantoprazole is a new substituted benzimidazole which is a potent inhibitor of gastric acid secretion by its action upon H+,K(+)-ATPase.. The proton pump inhibitors pantoprazole and omeprazole were compared in a randomized, double-blind study in 219 patients with benign gastric ulcers. Patients received either pantoprazole 40 mg (n = 146) or omeprazole 20 mg (n = 73), once daily before breakfast for 4 weeks. Treatment was extended for a further 4 weeks if the ulcer had not healed.. After 4 weeks, complete ulcer healing was seen in 88% of protocol-correct patients given pantoprazole and in 77% given omeprazole (between-group difference P < 0.05). At 8 weeks, the corresponding values were 97% and 96% (not significant). In the comparative intention-to-treat analysis there were no statistical differences between the treatment groups. Among the patients who had ulcer pain prior to treatment, 79% of the pantoprazole group and 68% of the omeprazole group were pain-free after 2 weeks, and after 4 weeks 88% and 81%, respectively (not significant). Pronounced improvement in the other gastrointestinal symptoms was seen in both groups. Only 10% of patients in each group reported adverse events. There were moderate increases in fasting serum gastrin levels with both treatments at 4 and 8 weeks.. Pantoprazole, 40 mg once daily in the morning, is a highly effective, well tolerated treatment for acute, benign gastric ulcer. Pantoprazole and omeprazole were equally safe in the therapy of gastric ulcer. Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Acute Disease; Administration, Oral; Adult; Aged; Aged, 80 and over; Benzimidazoles; Double-Blind Method; Female; Gastrins; Humans; Male; Middle Aged; Omeprazole; Pain; Pantoprazole; Proton Pump Inhibitors; Stomach Ulcer; Sulfoxides | 1995 |
[Comparison of lansoprazole (30 mg) and omeprazole (20 mg) in the treatment of duodenal ulcer. A multicenter double-blind comparative trial].
The efficacy of lansoprazole (30 mg/d) and omeprazole (20 mg/d) has been assessed in active duodenal ulcer disease in 144 patients included in a multicentric, randomized, double-blind trial. After two weeks, the healing rates were 74% and 58% in the lansoprazole and omeprazole groups, respectively (P = 0.049). After 4 weeks, the healing rates were 94% in each group (NS). The delay to pain relief was 2 days for lansoprazole and 3 days for omeprazole (NS). Minor side effects occurred in 12% of the lansoprazole treated patients and in 13% of the omeprazole treated patients. No severe adverse events were reported. A slight increase in serum gastrin level was observed, similar in both groups (+35 UI/L and +19 UI/L for lansoprazole and omeprazole respectively). This study confirms previous results concerning the efficacy of both treatments in duodenal ulcer disease. The statistical difference observed for healing rates after 2 weeks could correspond to a faster efficacy for lansoprazole (30 mg) than for omeprazole (20 mg). Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Administration, Oral; Adult; Anti-Ulcer Agents; Double-Blind Method; Duodenal Ulcer; Female; Gastrins; Humans; Lansoprazole; Male; Middle Aged; Omeprazole; Pain | 1993 |
8 other study(ies) available for gastrins and Pain
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Acquisition of analgesic properties by the cholecystokinin (CCK)/CCK2 receptor system within the amygdala in a persistent inflammatory pain condition.
Pain is associated with negative emotions such as anxiety, but the underlying neurocircuitry and modulators of the association of pain and anxiety remain unclear. The neuropeptide cholecystokinin (CCK) has both pronociceptive and anxiogenic properties, so we explored the role of CCK in anxiety and nociception in the central amygdala (CeA), a key area in control of emotions and descending pain pathways. Local infusion of CCK into the CeA of control rats increased anxiety, as measured in the light-dark box test, but had no effect on mechanical sensitivity. By contrast, intra-CeA CCK infusion 4 days after Complete Freund's Adjuvant (CFA) injection into the hindpaw resulted in analgesia, but also in loss of its anxiogenic capacity. Inflammatory conditions induced changes in the CeA CCK signaling system with an increase of CCK immunoreactivity and a decrease in CCK1, but not CCK2, receptor mRNA. In CFA rats, patch-clamp experiments revealed that CCK infusion increased CeA neuron excitability. It also partially blocked the discharge of wide dynamic range neurons in the dorsal spinal cord. These effects of CCK on CeA and spinal neurons in CFA rats were mimicked by the specific CCK2 receptor agonist, gastrin. This analgesic effect was likely mediated by identified CeA neurons projecting to the periaqueductal gray matter that express CCK receptors. Together, our data demonstrate that intra-CeA CCK infusion activated a descending CCK2 receptor-dependent pathway that inhibited spinal neuron discharge. Thus, persistent pain induces a functional switch to a newly identified analgesic capacity of CCK in the amygdala, indicating central emotion-related circuit controls pain transmission in spinal cord. Topics: Amygdala; Animals; Cholecystokinin; Dark Adaptation; Disease Models, Animal; Exploratory Behavior; Freund's Adjuvant; Gastrins; Glutamate Decarboxylase; Inflammation; Male; Neurons; Nociception; Pain; Pain Threshold; Periaqueductal Gray; Rats; Rats, Sprague-Dawley; Receptor, Cholecystokinin B; Signal Transduction; Sincalide; Tetragastrin | 2019 |
A distressed woman with epigastric pain.
Topics: Carcinoid Tumor; Diagnostic Errors; Diarrhea; Female; Gastrins; Gastritis; Humans; Liver Neoplasms; Middle Aged; Pain; Stress, Psychological | 1996 |
Pharmacological profile of UP 5145-52, an original antiulcer and antisecretory agent.
The gastric and antiulcer effects of UP 5145-52, a new naphthyridinone derivative (1-phenyl-1,2-dihydro-2-oxo-1,8-naphthyridin-3-yl)-4-acetoxy butane, were studied in rats. UP 5145-52 dose dependently prevented the formation of gastric lesions induced by a necrotizing agent such as absolute ethanol, indomethacin or stress (ED50 values were 0.065, 1.26 and 0.72 mg/kg p.o., respectively). A beneficial action was also observed against indomethacin-induced intestinal lesions. UP 5145-52 inhibited total acid output in the pylorus-ligated rat (ED50 on total acid output was 0.16 mg/kg p.o.) and in the rat chronic gastric fistula model. The mechanism of antisecretory activity currently remains unknown as UP 5145-52 fails to bind to receptors involved in gastric secretion (H2 or muscarinic) and to inhibit H+/K+ adenosine triphosphatase. The ability of UP 5145-52 (1 mg/kg p.o.) to restore synthesis of gastric acid glycoproteins depressed by previous administration of absolute ethanol suggests that cytoprotection could play a role in the antiulcer efficacy of the drug. Topics: Adenosine Triphosphatases; Administration, Oral; Animals; Anti-Ulcer Agents; Dose-Response Relationship, Drug; Ethanol; Gastric Acid; Gastric Mucosa; Gastrins; Guinea Pigs; Indomethacin; Male; Naphthyridines; Pain; Rabbits; Rats; Rats, Inbred Strains; Receptors, Opioid; Stomach Ulcer | 1991 |
Antinociceptive action of cholecystokinin octapeptide (CCK 8) and related peptides in rats and mice: effects of naloxone and peptidase inhibitors.
Cholecystokinin octapeptide (CCK 8) produced significant antinociception in the tail immersion test in the rat, paw pressure test in the rat and acetylcholine-induced writhing test in the mouse after subcutaneous (s.c.) administration. In the hot plate test, CCK 8 (s.c.) showed antinociceptive activity if the latency to lick was used as the end point but if the latency to jump was recorded the antinociceptive effects were not evident. Cholecystokinin tetrapeptide (CCK 4) was shown to be antinociceptive in the writhing but not in the hot plate test after subcutaneous administration and appeared to be less potent than CCK 8 when tested under the same conditions. Antinociception induced by CCK 8 in the hot plate test (lick) could also be demonstrated after direct intracerebroventricular (i.c.v.) injection and this observation was also made with the CCK-related peptide FMRF amide. Antinociception induced by CCK 8 (which did not appear to be associated with reduced locomotor activity) was evident 5 min after intraventricular injection and was maximal at 10 min, the effect lasting over a 30-45 min period. The antinociceptive effect of CCK 8 was antagonised by naloxone and was potentiated by simultaneous administration of the peptidase inhibitors bestatin, thiorphan and captopril. Topics: Animals; Captopril; FMRFamide; Gastrins; Leucine; Male; Mice; Naloxone; Neuropeptides; Pain; Protease Inhibitors; Rats; Rats, Inbred Strains; Reaction Time; Sincalide; Tetragastrin; Thiorphan; Tiopronin | 1987 |
All that glisters is not gold.
Topics: Adolescent; Diagnosis, Differential; Duodenal Diseases; Duodenal Ulcer; False Positive Reactions; Female; Gastrins; Gastroesophageal Reflux; Humans; Pain; Stomach Diseases; Zollinger-Ellison Syndrome | 1985 |
American Association of Endocrine Surgeons. Presidential address: Coming of age.
Topics: Brain; Digestive System; Digestive System Physiological Phenomena; Endocrine Glands; Endocrinology; Europe; Gastrins; History, 19th Century; History, 20th Century; Humans; Nerve Tissue Proteins; Neurosecretory Systems; Neurotransmitter Agents; Pain; Pancreas; Parathyroid Glands; Peptides | 1984 |
Gastric acid secretion and serum gastrin levels in children with recurrent abdominal pain, gastric and duodenal ulcers.
Basal and histalog-stimulated gastric acid secretion and serum gastrin levels before and after a standard protein meal were compared in eight children with active duodenal ulcer (DU), four with active gastric ulcer (GU), and in seven children with recurrent abdominal pain (RAP) of undetermined etiology. There was no discernible difference in the pattern of abdominal pain in DU, GU, and RAP. Basal acid output, peak and maximal acid output, whether expressed as milliequivalents per hour or as milliequivalents per kilogram per hour, were comparable in children with DU, GU, and RAP. In contrast, serum gastrin levels, 1 and 2 hours after standard protein meal, were significantly higher in the DU children than in the GU or RAP group. These studies have suggested that hypersecretion of gastric acid may not be associated with duodenal ulcer or gastric ulcer disease in children, and that increased gastrin secretion and possible reduced acid responsiveness coexist in children with duodenal ulcers. Topics: Abdomen; Acute Disease; Adolescent; Child; Duodenal Ulcer; Female; Gastric Acid; Gastrins; Humans; Male; Pain; Recurrence; Stomach Ulcer | 1980 |
Nocturnal ulcer pain associated with slow-wave sleep.
It is suggested that the early-morning growth-hormone release associated with slow-wave sleep is due to inhibition of somatostatin secretion from the hypothalamus. It is also associated with inhibition of gastrointestinal somatostatin, causing a release of gastrin and insulin. Because the levels of glucocorticoid hormones are concurrently low, the insulin effect is unopposed and increases gut motility through augmented vagal tone. This results in an increased delivery of acid to the duodenum. In duodenal-ulcer patients, whose duodenal buffering capacity is reduced because of a relative deficiency of secretin response, this leads to pain. Topics: Animals; Cats; Circadian Rhythm; Duodenal Ulcer; Duodenum; Gastric Juice; Gastrins; Growth Hormone; Haplorhini; Humans; Insulin; Insulin Secretion; Pain; Pituitary Gland, Anterior; Sleep; Somatostatin | 1978 |