Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe 4 children with seronegative inflammatory arthritis who had persistent, severe nausea and abdominal pain over several months, in spite of vigorous medical therapy, including antacids and histamine H2 receptor antagonists. Endoscopy and biopsy of gastric and duodenal mucosa showed antral gastritis and an increased number of mast cells in 3 of the 4 patients. In the fourth patient, urinary histamine levels were elevated. These findings suggest an association between inflammatory arthritis and localized mast cell disease in some individuals. Further studies are needed to determine whether this association represents an independent syndrome or whether mast cell-related disease is secondary to long-term treatment with nonsteroidal antiinflammatory drugs in children with mild arthritis.
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PMID:Seronegative juvenile rheumatoid arthritis and mast cell-associated gastritis. 167 Jun 19

The study of mast cells and nerve fibres in routine biopsies of human oxyntic mucosa was performed with the use of microscopic and ultrastructural methods. Simultaneous visualization of mast cells with Alcian blue and nerves with anti S-100 antibody allowed to study contacts between these two elements of lamina propria. Approximately 17% of mast cells appose nerves in gastric mucosa, which is less than the number of such contacts in the gut reported by other authors. We have found no differences between histologically normal mucosa and gastritis in the aspect of the total number of mast cells per 1 mm2 of lamina propria, number of their contacts with nerves and the ratio of mast cells apposing nerves to the total amount of mast cells. The ultrastructural study revealed significant polymorphism of mast cell-neuron contacts as well as the absence of any specialized structures at the site of adhesion between these two types of cells. The mode of degranulation of mast cells suggests that they are actively engaged in the reaction to noxious stimuli challenging the oxyntic mucosa.
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PMID:Close contacts between mast cells and nerve fibres in the human oxyntic mucosa. 184 85

The histological features that characterize alkaline reflux gastritis are typical of the histamine-mediated response to tissue injury. We have investigated this in nine patients with symptomatic reflux gastritis following partial gastrectomy for duodenal ulcer by determining the gastric mucosal mast cell count before and after Roux-en-Y biliary diversion. Following diversion, the histological picture changed from that of reflux gastritis to type B chronic gastritis in all cases. The mean mucosal mast cell count in all patients was 47.57/mm2 before diversion and 123.33/mm2 after diversion (P less than 0.05). Analysis of the paired data, in which eight out of nine patients showed a rise in mucosal mast cell numbers following bile diversion, also showed a significant difference before and after surgery (P less than 0.01). The gastric mucosal mast cell count is significantly less in reflux gastritis than in type B chronic gastritis. This is most likely to be due to increased degranulation, which would explain why striking vascular changes occur in the absence of inflammatory cell infiltration in reflux gastritis.
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PMID:Mucosal mast cells in reflux gastritis and chronic (type B) gastritis. 259 13

Effects of zinc in gastric ulcer have been reviewed through investigations carried out on zinc acexamate (ZAC). ZAC is an organic compound that has been shown to possess an experimental antiulcer effect and a wide therapeutic index, making it a useful drug in the treatment of peptic ulcer disease. ZAC protects from ulceration in several experimental models such as pylorus occlusion, reserpine-induced ulcer, necrotizing agents, PAF-induced ulcer and cold-restraint stress. ZAC first reduces the gastric acid output by inhibiting the mast cell degranulation, an action likely to be mediated through a membrane stabilizing action. Secondly, it enhances the mucosal protection factors by increasing mucus secretion, inhibiting the H+ retrodiffusion and improving microcirculation. ZAC is also effective in acetic acid-induced chronic ulcer, restoring the continuity of the damaged mucosa. Several clinical trials have shown the usefulness of ZAC in acute and maintenance treatment of both gastric and duodenal ulcers. Endoscopic studies showed that ZAC reduced the inflammatory processes (gastritis and duodenitis) associated with ulcer healing. This reduction was statistically significant and not observed with other comparative treatments (H2-antagonists). The observed side-effects were minimal and affected less than 2% of treated patients. The pharmacological profile, clinical effectiveness and good tolerance of ZAC suggest this compound as an interesting option in the treatment of peptic disease.
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PMID:Zinc compounds, a new treatment in peptic ulcer. 266 Nov 83

Thirty-five patients with fundic atrophic gastritis and achlorhydria were classified in two groups according to the presence or absence of fundic argyrophil, mostly enterochromaffinlike cell hyperplasia. Among the biologic and histologic parameters studied, the hyperplasic group differed only by a circulating hypergastrinemia and an antral G-cell hyperplasia. The histamine content, the histidine decarboxylase activity, and the mast cell number of fundic biopsies were determined in 10 controls, 16 of the preceding patients (11 with and 5 without fundic argyrophil-cell hyperplasia), and 5 patients with fundic atrophic gastritis and neither achlorhydria nor hyperplasia. Histamine content and histidine decarboxylase activity were increased only in the hyperplasic group despite an unchanged mast cell number. For all fundic biopsies the argyrophil-cell density was positively related to the histamine content. Finally, the argyrophil-cell hyperplasia occurring in fundic atrophic gastritis with achlorhydria is associated not with the gastritis intensity, as assessed by histologic and secretory criteria, but with a circulating hypergastrinemia and an increase of both fundic histamine content and histidine decarboxylase activity.
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PMID:Circulating gastrin, endocrine cells, histamine content, and histidine decarboxylase activity in atrophic gastritis. 275 21

Albino rats fed on 30% ethyl alcohol for 60 days demonstrated significant reduction in the histamine concentration of the gastric wall, estimated by bio-assay, as well as in the gastric mucosal mast cell population. It can, therefore be concluded that alcohol liberates histamine from the gastric mast cells even in the presence of alcohol-induced gastritis.
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PMID:Effect of alcohol-feeding on gastric mucosal mast cell population and gastric tissue histamine concentration in albino rats. 409 93

The histamine secreting enterochromaffin-like (ECL) cell is now recognized as the principal regulator of gastric acid secretion. Histamine is not only a primary modulator of acid secretion, but may be of relevance in gastritis and as a mitogen in gastric neoplasia. Study of the ECL cell has been limited since no pure preparation was available. We therefore developed a pure isolated ECL cell preparation with a purity of 90-95% as determined by total histamine content and chromogranin immunofluorescence. Trypan blue exclusion demonstrated > 95% viability. While gastrin and acetylcholine are known modulators of acid secretion, the role of adrenergic neurotransmitters has not been clearly delineated. The purpose of this study was to examine adrenergic modulation of ECL cell histamine release. To further define the inhibitory mechanisms of histamine secretion, we evaluated the mast cell histamine inhibitor sodium cromoglycate. Histamine secretion was determined by radioimmunoassay. Basal secretion was 0.6 +/- 0.2 nmol/10(3) cells. Gastrin stimulated histamine secretion with an EC50 of 3 x 10(-10) M. Octopamine (alpha-adrenergic agonist) (10(-11)-10(-4) M) failed to stimulate histamine secretion. Isoproterenol (beta-adrenergic agonist) stimulated histamine secretion (EC50, 6 x 10(-8) M) and was inhibited by propranolol (IC50 5 x 10(-10) M).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adrenergic and cromolyn sodium modulation of ECL cell histamine secretion. 753 Mar 10

There is an accumulation of evidence to suggest that mast cells may play a key role in gastrointestinal inflammation. We have investigated the numbers and heterogeneity in staining properties of mast cells in biopsies of the duodenum of normal subjects (n = 10), and of normal duodenum from patients with Crohn's disease of the ileum and/or colon (n = 7) or with Helicobacter-associated gastritis of the antrum/corpus (n = 6). In normal donors, two subsets of mast cells, one located in the duodenal mucosa and the other in the submucosa, were clearly distinguished by their morphology and dye-binding properties. Whereas submucosal mast cells stained metachromatically with Toluidine Blue after neutral formalin fixation and emitted a yellow fluorescence after staining with Berberine sulphate, those in the mucosa were invisible using these stains. In patients with gastritis or Crohn's disease, there were marked changes in the numbers of mucosal mast cells compared with control subjects even though the duodenal biopsies were from apparently uninvolved tissue. Gastritis was associated with increased mucosal mast cell numbers (controls: 187 +/- 23 cells mm-2; gastritis: 413 +/- 139 cells mm-2; p = 0.0004), but mean mucosal mast cell counts in the uninvolved duodenum of Crohn's patients were actually decreased (34 +/- 30 cells mm-2, p = 0.0147). The clear differentiation between mucosal and submucosal mast cells on the basis of metachromasia with Toluidine Blue was not seen in biopsies from the patients with gastritis or Crohn's disease. Previous studies which have suggested that there are no distinct mucosal and submucosal mast cell subsets in the human intestine may, therefore, have been affected by the use of tissue from diseased subjects. Heterogeneity in the expression of mast cell tryptase and chymase was seen by immunohistochemistry using specific antibodies, but the relative numbers of mast cell subsets were critically dependent on the methods used. Using a sensitive staining procedure, the majority of mucosal mast cells stained positively for chymase as well as for tryptase, an observation confirmed by immunoelectron microscopy and immunoabsorption studies. Our findings suggest that early stages in intestinal inflammation may be reflected in changes in mast cell numbers and in their staining properties, and call for a reappraisal of mast cell heterogeneity in the human intestinal tract.
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PMID:Number, fixation properties, dye-binding and protease expression of duodenal mast cells: comparisons between healthy subjects and patients with gastritis or Crohn's disease. 942 79

Urticaria pigmentosa (UP) is the most common form of cutaneous mastocytosis and may be associated with systemic involvement, most often of the bone marrow. The incidence of systemic involvement is not yet well established, however. To address this question, we subjected a group of 30 adults with histologically proved UP to a retrospective study that included history, physical examination, laboratory tests including cytokine measurements, radiologic examinations, and bone marrow biopsies. The most frequently associated clinical symptoms were recurrent flush episodes in 16 of 30 patients, alcohol intolerance in 13, pruritus in 10, and gastrointestinal problems in 11 (recurrent diarrhea, 8 patients; gastritis, 2 patients; and history of peptic ulcer, 1 patient). Of the 30 patients, 18 (60%) had mast cell infiltrates of the bone marrow (nodular type, 10 patients; diffuse interstitial type, 8 patients). Bone marrow involvement was not correlated with massive cutaneous mast cell infiltration, clinically or histologically, or with the incidence of clinical symptoms and associated hematologic disorders. None of the patients had experienced progression of clinical symptoms, skin or organ involvement, or development of hematologic malignant neoplasms since UP was first diagnosed (10 years on average). Urticaria pigmentosa was found associated with mast cell infiltration of the bone marrow in 18 patients (60%). However, bone marrow involvement does not seem to predict adverse clinical course.
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PMID:Urticaria pigmentosa: a clinical, hematopathologic, and serologic study of 30 adults. 949 99

Mast cell involvement in chronic gastritis in children was analyzed. 25 children with normal mucosa (controls), 20 children with chronic gastritis and 28 children with chronic gastritis and infected Helicobacter pylori were included to the study. Bioptic material from antrum and corpus of the stomach were stained with toluidine blue and anti-human mast cell tryptase to evaluate mast cell density. Changes in mast cells number were also estimated in 7 children before and after successful eradication of Helicobacter pylori infection. Mast cell density was significantly greater in children with chronic gastritis with or without Helicobacter pylori infection when compared to the controls. Mast cell degranulation was demonstrated by electron microscopy in children with chronic gastritis and infected Helicobacter pylori. Mast cell through it's numerous mediators may play a key role in chronic gastritis especially when Helicobacter pylori infection is present.
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PMID:[Mast cells in chronic gastritis of children]. 1139 16


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