Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Research is asking how H. pylori causes diseases, and also why the same bacteria produces different conditions in different persons. The process involves bacterial factors and the host's response. Some bacterial factors such as urease are produced by all strains of H. pylori. This enzyme may damage the gastric epithelium by practically releasing ammonia. Other bacterial factors such as vacuolating toxin are only produced by some strains, and these strains are more likely to cause ulcers or cancer. The host's response has been studied by physiologists, immunologists, and histologists, but the separation of systems is artificial. For example, physiologists find that H. pylori stops gastric D-cells from expressing somatostatin normally, which impairs reflex inhibition of acid secretion, but the D-cell malfunction is probably due to inflammatory factors. In H. pylori gastritis, the gastric epithelial cells behave like immunocytes and express class II molecules and cytokines such as interleukin-8. The patient's histological response to H. pylori is quite closely related to the disease outcome. Patients who respond by developing gastric atrophy are more likely to get gastric ulcers or stomach cancer, but patients whose gastric corpus remains healthy tend to secrete more acid and develop duodenal ulcers, particularly if they have gastric metaplasia in their duodenum. Studies of disease mechanisms provide a valuable insight into the development of these common diseases, and may enable us to identify at-risk groups who particularly merit eradication therapy.
 ...
PMID:Pathogenic mechanisms. 856 49

The incidence of surgical treatment of peptic ulcer decreased in the last two decades. The majority of procedures for surgical management of peptic disease impairs the ability of the stomach to receive and to store food. The intake of high protein-caloric content diets can improve some nutritional deficits expressed by loss of body weight and anemia. The mechanism responsible for diarrhea is unknown, but truncal vagotomy has the highest incidence. It is usually episodic, lessens over the first year after operation and rarely remains a severe problem. The decreasing levels of colecistokinin response after meal in gastrectomy and the division of hepatic branch of anterior vagus can cause gallbladder sludge and stone formation. Alkaline reflux explains gastritis and esophagitis after partial gastric resection. Surgical duodenal diversion, like a Roux-en-Y limb, have been successful in its control. The mechanism that leads to the dumping syndrome are loss of gastric reservoir function and rapid emptying of hyperosmolar meals into small intestine. Somatostatin analogues improve the symptoms caused by abnormal release of neurohormonal agents responsible of the behaviour of the gastrointestinal tract after meals. Cancer of gastric remanent may be due to increased bacterial overgrowth and nitrosation formation. The endoscopic follow-up is essential for early diagnosis of the stump cancer. In spite of all complications, the surgeon cannot have hesitations by carrying out radical approach meanly during catastrophic emergencies of peptic disease i.e. in elderly aged patients. Nowadays, the control of chronic sequelas is easy with conservative therapeutic.
 ...
PMID:[Peptic ulcer: late complications of the surgical treatment]. 858 Apr 56

The aim of this study was to investigate the consequence of Helicobacter pylori eradication on gastric mucosa and antral G and D-cells. Forty children, aged 5-17 years with Helicobacter pylori infection were assessed. Helicobacter pylori was detected by a urease test and identified by serological and microbiological methods. Twenty children were again assessed after the therapy (the combination of colloid bismuth subcitrate, amoxycillin and metronidazole). Gastroscopic examination was performed and at least six bioptic specimens were taken from the antrum, body and fundus. Tissue samples, processed with the paraffin method and stained with hematoxyllin and eosin, were assessed. Monoclonal antiserum Gastrin PAP kit 516 and somatostatin PAP kit 512 (DAKO) in the peroxidase-antiperoxidase technique (PAP) have been used to detect G and D-cells. Helicobacter pylori in the gastric mucosa was demonstrated with the Giemsa method. The results show the coincidence of Helicobacter pylori infection and the count of antral G and D-cells and active chronic gastritis in children. After the treatment Helicobacter pylori was eradicated in 70% of children. In 34% of these cases the eradication was followed by a diminution of activity of gastric antral mucosa inflammation and in 20% of these children the resolution of the inflammatory infiltration in the gastric mucosa was seen. A decrease of the antral G and D-cells count and also a diminution of G/D index in these cases were observed.
 ...
PMID:Morphological and immunohistochemical examinations of the dynamic changes of gastric mucosa associated with the treatment of helicobacter pylori infection in children. 877 26

There is evidence that gastric Helicobacter pylori (Hp) infection promotes duodenal ulceration by releasing gastrin. We therefore asked how Hp releases gastrin. Tumour necrosis factor alpha (TNF-alpha) is up-regulated in Hp gastritis and stimulates hormone release from pituitary cells, so we tested its effect on primary cultures of canine antral G cells and human antral fragments. TNF-alpha pretreatment (100 ng mL-1) of canine G cells significantly increased both basal (by 89%: P < 0.01) and bombesin-stimulated (by 39% P < 0.05) gastrin release. A similar pattern of increase was seen following TNF-alpha (20 ng mL-1) pretreatment of human antral fragments: basal gastrin release was increased by 38% (P < 0.05) and bombesin-stimulated by 26% (P < 0.05). This effect persisted during immunoblockade with anti-somatostatin antibody S6. We propose that TNF-alpha provides the link between Hp infection and gastrin release and thus contributes to duodenal ulceration.
 ...
PMID:Tumour necrosis factor alpha stimulates gastrin release from canine and human antral G cells: possible mechanism of the Helicobacter pylori-gastrin link. 886 24

Changes in endocrine and secretory functions and in the morfology of gastric mucosa in the course of quadruple H. pylori eradication regimen in 50 H. pylori positive patients: 25 with duodenal ulcer (DU) and 25 with non ulcer dyspepsia (NUD) were studied and compared to 10 healthy controls. Therapy resulted in ulcer healing in all DU patients and in 92% eradication of H. pylori in both groups of patients-DU and NUD. In DU and NUD patients in the course of eradication significant decrease in plasma gastrin was observed. Somatostatin concentration in gastric juice increased significantly in DU patients after anti-H. pylori therapy. EGF in gastric content of DU and NUD patients has risen statistically significantly in the course of H. pylori eradication. Gastric acid output and volume flow decreased insignificantly in both groups. The elimination of H. pylori from gastric mucosa in both DU and NUD patients led to significant decrease in the density and activity of gastritis.
 ...
PMID:Hormonal, secretory and morphological alterations in gastric mucosa in the course of Helicobacter pylori eradication in patients with duodenal ulcer and non-ulcer dyspepsia. 928 34

Acromegaly was the first pituitary disease to be recognised as a clinical entity, although initially it was not clear whether the eosinophilic adenomas causing pituitary enlargement were causative or just a manifestation of the syndrome itself. Following the documented clinical improvement of patients with acromegaly after partial hypophysectomy, it was proven that the pituitary adenomas were aetiological. The treatment of acromegaly has changed during the last decades; the introduction of the somatostatin (SMS) analogue octreotide has had major implications. Octreotide was the first SMS analogue to become available for clinical use. It is generally well tolerated, but is associated with the development of gallstones in 15 to 20% of patients. Other adverse effects include transient injection-site pain, abdominal, diarrhoea, gastritis (long term therapy) and loss of scalp hair. No long haematological or biochemical adverse effects have been reported. Desensitisation to the beneficial effects of octreotide therapy is highly unusual. A long-acting formulation of octreotide is being studied, and should be available by the end of 1997.
 ...
PMID:A risk-benefit assessment of octreotide in the treatment of acromegaly. 939 75

Helicobacter pylori infection increases gastric acid secretion in patients with duodenal ulcers but diminishes acid output in patients with gastric cancer and their relatives. Investigation of the basic mechanisms may show how H. pylori causes different diseases in different persons. Infection of the gastric antrum increases gastrin release. Certain cytokines released in H. pylori gastritis, such as tumor necrosis factor alpha and specific products of H. pylori, such as ammonia, release gastrin from G cells and might be responsible. The infection also diminishes mucosal expression of somatostatin. Exposure of canine D cells to tumor necrosis factor alpha in vitro reproduces this effect. These changes in gastrin and somatostatin increase acid secretion and lead to duodenal ulceration. But the acid response depends on the state of the gastric corpus mucosa. The net effect of corpus gastritis is to decrease acid secretion. Specific products of H. pylori inhibit parietal cells. Also, interleukin 1 beta, which is overexpressed in H. pylori gastritis, inhibits both parietal cells and histamine release from enterochromaffin-like cells. H. pylori also promotes gastric atrophy, leading to loss of parietal cells. Factors such as a high-salt diet and a lack of dietary antioxidants, which also increase corpus gastritis and atrophy, may protect against duodenal ulcers by decreasing acid output. However, the resulting increase of intragastric pH may predispose to gastric cancer by allowing other bacteria to persist and produce carcinogens in the stomach.
 ...
PMID:How does Helicobacter pylori cause mucosal damage? Its effect on acid and gastrin physiology. 939 59

Microstructural, endo- and exocrine changes in gastric mucosa of Non-Ulcer Dyspepsia patients with H. pylori infection in the course of eradication has been studied. Before, during and after anti H. pylori therapy plasma gastrin and somatostatin levels, EGF and somatostatin concentration in gastric juice and basal and pentagastrin stimulated gastric acid secretion were measured. Moreover microstructure of gastric mucosa specimens has been studied. Maximal Acid Output initially higher in NUD patients than in healthy volunteers increased slightly in the course of eradication. Plasma gastrin decreased while EGF and somatostatin concentration in gastric juice increased. After treatment the ratio of patients with pronounced features (activity) of gastritis was significantly reduced.
 ...
PMID:[Endocrine and exocrine gastric mucosal secretion in the course of H. pylori eradication in patients with non-ulcer dyspepsia]. 942 1

It is unclear why Helicobacter pylori produces different diseases in different persons. High and low acid secretion rates probably contribute to duodenal ulceration and gastric carcinogenesis, respectively. Both of these changes seem to be corrected by eradicating Helicobacter pylori. We are therefore exploring the basic mechanisms and asking why patients react differently? Helicobacter pylori products and certain cytokines released in Helicobacter pylori gastritis release gastrin from G-cells but inhibit parietal cells. Also tumour necrosis factor alpha inhibits somatostatin-cells and interleukin 1 beta inhibits enterochromaffin-like cells. The net result is that antral gastritis tends to increase, whilst corpus gastritis tends to decrease acid secretion. Corpus atrophy further lowers acid through loss of parietal cells. Factors postulated to increase corpus gastritis include host genetics, early acquisition of Helicobacter pylori, more aggressive strains, poor general health and diets high in salt or lacking in antioxidant vitamins. Further research should address the interaction of bacterium, host and environment with a view to preventing the serious clinical outcomes.
 ...
PMID:Host mechanisms: are they the key to the various clinical outcomes of Helicobacter pylori infection? 947 95

Helicobacter pylori is the cause of chronic type B gastritis and occurs in almost all patients with duodenal ulcers. Infection with H. pylori is characterized by an increased production of several inflammatory cytokines. Increasing evidence suggests a central role of these cytokines in the pathogenesis of H. pylori-associated gastritis and peptic ulcer disease. Cytokines may be crucial in the recruitment and activation of inflammatory cells and in stimulation of gastrin release. In addition to their proinflammatory properties, cytokines may also inhibit the ulcer occurrence by stimulation of prostaglandins and somatostatin release and by direct impairment of acid secretion. The balance of these factors may determine the clinical outcome of H. pylori infection.
 ...
PMID:Hypotheses on the role of cytokines in peptic ulcer disease. 972 29


<< Previous 1 2 3 4 5 6 Next >>