Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0007570 (celiac disease)
 13,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using immunohistochemical techniques we studied duodenal biopsies from 18 patients with coeliac disease and 24 patients with normal duodenal morphology. We had access to antisera against the following gastrointestinal peptides: cholecystokinin (CCK), gastric inhibitory peptide (GIP), gastrin-17, glucagon-enteroglucagon, motilin, neurotensin, pancreatic peptide (PP), secretin, somatostatin, substance P and vasoactive intestinal peptide (VIP). The somatostatin, GIP, CCK, and glucagon cells were increased in number in coeliac disease. The number of motilin cells was slightly increased, while secretin cells were reduced. Cells storing gastrin-17, substance P, or neurotensin were rare in all patients regardless of diagnosis. No PP immunoreactive cells were found and VIP was localised to neurons only. In biopsies from patients having a mucosa with ridging of villi the number of the various endocrine cell types did not differ from that in the control group.
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PMID:Duodenal endocrine cells in adult coeliac disease. 38 55

Coeliac disease in children is frequently associated with a slow growth rate. This observation may be linked to the malabsorption that occurs in these patients; however, the underlying mechanism remains unknown. To better understand this phenomenon, we have studied the growth patterns of 153 patients with coeliac disease for 2-9 years. Gastro-intestinal biopsies were performed before and after gluten exclusion. In a second group of 79 children, somatostatin levels and binding properties in the plasma and jejunal mucosa were measured. In a third group of 40 patients we measured insulin-like growth factor I (IGF-I) and IGF-binding protein 3 (IGF-BP3) levels. We found that in children diagnosed before 2 years of age weight was the most affected growth parameter. In children diagnosed after this age, height was more affected. Suppression of gluten intake induced an acceleration of growth velocity. Although plasma levels of somatostatin were not significantly altered, somatostatin concentrations in the jejunal mucosa of patients in the active phase of the disease were significantly elevated (p < 0.05). Children with coeliac disease exhibited significantly lower levels of IGF-BP3 when compared to patients with normal stature and growth velocities. In contrast, these patients showed an increase in IGF-BP3 levels after gluten exclusion from the diet.
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PMID:Growth in malnutrition related to gastrointestinal diseases: coeliac disease. 128 43

This study was undertaken to determine the effects of somatostatin 201-995 (SMS) on the maintenance dose of intravenous cyclosporine and on graft blood flow, exocrine secretion, and rejection after porcine pancreaticoduodenal allotransplantation (PDA). For seven days, 12 pigs (6 control, 6 SMS-treated) were studied to determine the effects of SMS on serum CsA concentrations. Twenty-six pigs (14 control, 12 SMS) with streptozocin-induced diabetes underwent PDA. Blood flow was measured through graft celiac and superior mesenteric arteries 15 and 60 min after reperfusion. SMS (75 micrograms s.c.) was given after the 15-min blood-flow measurement in the SMS group. Sixteen pigs (8 control, 8 SMS) were followed postoperatively with daily measurements of serum glucose and amylase concentrations, and urine amylase and trypsin activities. All pigs were immunosuppressed with azathioprine, prednisone, and i.v. CsA. SMS pigs also received SMS (75 micrograms s.c.) every 8 hr. SMS had no effect on maintenance dose of CsA or on serum amylase, urine amylase, or urine trypsin activities. Mean days to rejection were also not affected. Intraoperative graft blood flow was significantly decreased by SMS, but incidence of graft thrombosis was unchanged. These results suggest that in the porcine PDA model, SMS does not appear to inhibit exocrine secretion and potentially may adversely affect the early course of PDA by decreasing graft blood flow.
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PMID:The effect of somatostatin 201-995 on the early course of porcine pancreaticoduodenal allotransplantation. 167 Sep 73

The authors provide the data obtained during examination of 36 children with celiac disease and 18 children with lactase deficiency. The children's age ranged from 8 months to 15 years. All the children underwent spot biopsy of the gastric and duodenal mucosa followed by immunomorphological PAP-staining of the biopsy specimens and count of the number of gastrin- and somatostatin-producing cells. Gastrin in the blood serum was measured by radioimmunoassay. The children with celiac disease manifested an increase of the number of somatostatin-producing cells in the duodenum and decrease of their number in the pyloric part of the stomach, seen in the acute phase of the disease. The number of gastrin-producing cells remained unchanged. The level of gastrin declined in the acute phase and increased during a remission. The alterations described were found to be related to the atrophic processes in the small intestinal mucosa. In lactase deficiency, no significant alterations were established in the number of pyloric and duodenal endocrine cells or in blood gastrin level.
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PMID:[Disorders of humoral regulation of the digestive organ functions in children with malabsorption syndromes]. 167 86

Untreated celiac disease is characterized by gastrointestinal endocrine cell hyperplasia (ECH). This study investigated the constitutive nature of the ECH. Ten duodenal biopsies showing villous atrophy from adult celiacs were evaluated against ten sex- and age-matched controls. The mean number of endocrine cells per unit length of mucosa in the celiacs was compared with the control group using the Student t test. These values, respectively, were as follows: Churukian-Schenk method, 52.4 versus 29.6 (P = 0.001); Fontana-Masson, 32.5 versus 18.4 (P = 0.016); chromogranin, 33.4 versus 23.6 (P = 0.017); serotonin, 44.7 versus 26.7 (P = 0.006); somatostatin, 5.0 versus 5.4 (P = 0.631); and gastrin, 0.37 versus 0.37 (P = 1.000). There was thus ECH as shown by the first four stains with, in some areas, the endocrine cells continuously abutting against each other to form linear profiles. With respect to specific hormonal products, only serotonin showed ECH. These results suggest that the ECH in celiac disease is not a haphazard process but, instead, a selective proliferation of certain endocrine cell types.
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PMID:Gastrointestinal endocrine cell hyperplasia in celiac disease: a selective proliferative process of serotonergic cells. 168 34

We performed immunohistochemical analysis of specimens from three autopsied patients with Parkinson's disease, using antibodies to tyrosine hydroxylase (TH), vasoactive intestinal polypeptide (VIP), somatostatin, met-enkephalin, leu-enkephalin and substance P in an attempt to reveal the types of neurons that contain Lewy bodies (LBs) in the paravertebral and celiac sympathetic ganglia and in the enteric nervous system of the alimentary tract. In the sympathetic ganglia, almost all LB-containing neuronal cell bodies and processes were immunoreactive for TH. In the alimentary tract, however, most LBs were found in the VIP-immunoreactive (VIP-IR) neuronal cell bodies and processes. In spite of the significant presence of TH-IR neuronal cell bodies and processes in the alimentary tract, LB-containing TH-IR neuronal elements were rarely encountered. These findings indicate that in the alimentary tract, the VIP neuron system is mainly involved in the disease process of Parkinson's disease.
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PMID:Parkinson's disease: an immunohistochemical study of Lewy body-containing neurons in the enteric nervous system. 197 53

The intermediary pathways in the bombesin-induced somatostatin release were examined in isolated perfused rat stomach obtained from male rats that were fasted overnight. The stomachs were perfused by way of the celiac artery. On coinfusion of 1.0 mumol/L tetrodotoxin and 1 nmol/L bombesin, a significant depression in release of somatostatin was observed compared with that observed with bombesin alone. The 5-minute integrated somatostatin response after treatment with tetrodotoxin and bombesin was 173% +/- 14% of basal, which was significantly lower than that observed with bombesin alone (394% +/- 59% of basal, P less than 0.05) but significantly higher than that observed with medium-199 alone (95% +/- 7% of basal, P less than 0.05); this indicated that approximately 70% of the bombesin-stimulated somatostatin release was indirectly mediated through neural pathways, while a significant (approximately 30%) segment of it was mediated by nonneural mechanisms. To test if the 30% somatostatin release was secondary to gastrin release in response to bombesin, gastrin antiserum and bombesin (1 nmol/L) were coadministrated in the presence or absence of tetrodotoxin (1 mumol/L). Gastrin antiserum alone did not significantly affect basal release of somatostatin but caused a significant inhibition (approximately 23%) of bombesin-provoked somatostatin release. Coadministration of gastrin antiserum and tetrodotoxin attenuated bombesin-stimulated somatostatin release. Gastrin (1 mumol/L) alone significantly stimulated somatostatin release (150% +/- 10% of basal), which was completely attenuated in the presence of gastrin antiserum. Tetrodotoxin did not affect bombesin-elicited gastrin release, confirming that bombesin-stimulated gastrin release was directly mediated. To determine the nature of the neural pathways mediating the bombesin-induced somatostatin release, atropine (100 nmol/L) was used. Atropine inhibited bombesin-induced somatostatin release to the same extent as tetrodotoxin, indicating that cholinergic pathways mediated bombesin-induced somatostatin release. These results show that almost all the somatostatin response to bombesin is indirectly mediated, and is composed of a major neural (cholinergic) and a minor nonneural pathway. The nonneural mechanism appears to be contributed primarily by gastrin released in response to bombesin, which apparently has a short paracrine positive feedback effect on somatostatin release.
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PMID:Role of gastrin in bombesin-stimulated somatostatin release. 197 61

Changes in the somatostatin-like immunoreactivity (SLI) concentrations in gastric antral mucosa were detected by RIA following microinjections of synthetic somatostatin (SS) or cysteamine (CSH) into the ventromedial nucleus of the hypothalamus (VMH). SLI concentrations in the antral mucosa were increased by 60.8% (p less than 0.001) and 42.3% (p less than 0.05), respectively, one and four hours after microinjection of somatostatin (0.5 microgram/0.5 microliter) into the VMH, and decreased by 32.6% (p less than 0.05) four hours after microinjection of cysteamine (15 microgram/0.5 microliter) into the VMH. Moreover, microinjection of somatostatin (0.5 microgram/0.5 microliter) into the VMH could only elicit an increase of 16.0% (p less than 0.05) in the SLI concentration in the antral mucosa one hour after bilateral subdiaphragmatic vagotomies, but still produced an increase of 120.0% (p less than 0.05) following celiac ganglionectomies. In conclusion, somatostatin (exogenous and endogenous) in the VMH seems to affect the gastric somatostatin levels via the vagal nerves.
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PMID:Ventromedial hypothalamic somatostatin may affect gastric somatostatin concentration in rats. 197 57

Thirty duodenal and three upper-jejunal endocrine tumors are reported. Clinical manifestations included: a) the Zollinger-Ellison syndrome (10 cases); b) peptic ulcer disease in which hypergastrinemia was not documented (3 cases); c) cholestasis or cholelithiasis (4 cases); d) abdominal pain (4 cases); e) gastro-intestinal bleeding (1 case); f) celiac sprue (1 case). Ten further tumors were discovered incidentally, at autopsy or in pathological specimens after gastrectomy or duodenopan-createctomy. Histological pattern was trabecular in 19 cases, insular in 2 and mixed in ten cases. Two cases were typical ganglioneuromatous paragangliomas. All tumors were examined immunohistochemically. Twelve tumors contained gastrin, four somatostatin, six both of these peptides, one serotonin, two both gastrin and serotonin, and two tumors contained gastrin, serotonin and somatostatin. Ganglioneuromatous paragangliomas combined somatostatin and/or pancreatic polypeptide containing endocrine cells with protein-S100-positive Schwann cells. In four tumors no peptide or amine was demonstrated. Gastrin cell tumors (63.6% of our cases), both functionally active (gastrinomas) and clinically silent, predominated in the proximal duodenum, while somatostatin cell tumors (15.1%) and paragangliomas were mostly found in the periampullary region. Two tumors were classified as malignant on the basis of lymph node metastases, and both were jejunal gastrinomas associated with Zollinger-Ellison syndrome. Two somatostatin cell tumors had manifestations of von Recklinghausen's disease.
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PMID:Endocrine tumors of the duodenum and upper jejunum. A study of 33 cases with clinico-pathological characteristics and hormone content. 216 Apr 22

We review recent studies on the central neural control of esophageal motility, emphasizing the anatomy and chemical coding of esophageal pathways in the spinal cord and medulla. Sympathetic innervation of the proximal esophagus is derived primarily from cervical and upper thoracic paravertebral ganglia, whereas that of the lower esophageal sphincter and proximal stomach is derived from the celiac ganglion. In addition to noradrenaline, many sympathetic fibers in the esophagus contain neuropeptide Y (NPY), and both noradrenaline and NPY appear to decrease blood flow and motility. Preganglionic neurons innervating the cervical and upper thoracic ganglia are located at lower cervical and upper thoracic spinal levels. The preganglionic innervation of the celiac ganglion arises from lower thoracic spinal levels. Both acetylcholine (ACh) and enkephalin (ENK) have been localized in sympathetic preganglionic neurons, and it has been suggested that ENK acts to pre-synaptically inhibit ganglionic transmission. Spinal afferents from the esophagus are few, but have been described in lower cervical and thoracic dorsal root ganglia. A significant percentage contain calcitonin gene-related peptide (CGRP) and substance P (SP). The central distribution of spinal afferents, as well as their subsequent processing within the spinal cord, have not been addressed. Medullary afferents arise from the nodose ganglion and terminate peripherally both in myenteric ganglia, where they have been postulated to act as tension receptors, and, to a lesser extent, in more superficial layers. Centrally, these afferents appear to end in a discrete part of the nucleus of the solitary tract (NTS) termed the central subnucleus. The transmitter specificity of the majority of these afferents remains unknown. The central subnucleus, in turn, sends a dense and topographically discrete projection to esophageal motor neurons in the rostral portion of the nucleus ambiguous (NA). Both somatostatin-(SS) and ENK-related peptides have been localized in this pathway. Finally, motor neurons from the rostral NA innervate striated portions of the esophagus. In addition to ACh, these esophageal motor neurons contain CGRP, galanin (GAL), N-acetylaspartylglutamate (NAAG), and brain natriuretic peptide (BNP). The physiological effect of these peptides on esophageal motility remains unclear. Medullary control of smooth muscle portions of the esophagus have not been thoroughly investigated.
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PMID:Central neural control of esophageal motility: a review. 220 57


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