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)

For the definition of histamine receptors the following prerequisites must be fulfilled: (1) Course of dose-response curves according to the mass-action law; (2) parallel displacement of these curves to the right in the presence of antagonists; (3) inhibition only by specific histamine antagonists; (4) slope of a Schild-plot not significantly different from unity. For H2-receptors these prerequisites could ideally be fulfilled, especially by the development of highly specific H2-receptor antagonists. However, this new class of compounds acts not only by mere competitive inhibition of histamine at its H2-receptor, but also by activating the metabolism of this secretagogue. A further explanation of the action of H2-receptor antagonists in the treatment of chronic duodenal ulcer may be given by studying the pathogenetic role played by histamine in the development of this disease: duodenal ulcer patients showed an increased liberation of histamine from mucosal mast cell stores as well as a decreased activity of histamine methyltransferase (i. e. longer action of histamine!). The rise in histamine content and histamine methyltransferase activity after vagotomy may be the basis for a biochemical explanation of the acid-reducing effect of this operation.
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PMID:[Histamine and its role in peptic gastric diseases: the discovery of histamine-H2-receptor antagonists]. 3 19

We describe a patient with fever and multiple osteolytic bone lesions accompanied by hypercalcemia, a duodenal ulcer, anemia, and thrombocytopenia. Bone marrow showed a dense infiltration by abnormal cells characterized by small basophil granula, erythrophagocytosis and nuclear atypia. These cells were positive for toluidine blue and partly for myeloperoxidase and chloroacetate esterase, expressed myeloid differentiation markers, and exhibited multiple numerical and structural chromosome aberrations. Molecular genetic analysis showed no breakpoint cluster region rearrangement. Electron microscopy demonstrated granula both of basophil and mast cell type. Concluding, in this patient an acute hematopoietic malignancy with many features of malignant mastocytosis but also with signs of a basophil differentiation. This is further support for a hematopoietic stem cell origin of human mast cells.
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PMID:Philadelphia chromosome-negative acute hematopoietic malignancy: ultrastructural, cytochemical and immunocytochemical evidence of mast cell and basophil differentiation. 210 68

The authors carried out a comparative examination of 68 patients with duodenal ulcer receiving monotherapy with cithemidine and a combination of cithemidine and dimedrol. Clinical data indicate that combined use of H1- and H2-histamine blockaders produce a reliable therapeutic effect. Morphological investigations of biopsies from the periulcerous region and morphometry of cellular and noncellular structures showed that the mechanism of this effect consists in strengthening of the mast cell apparatus adding the excess of tissue histamine.
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PMID:[A morphometric analysis of tissue homeostasis in peptic ulcer patients during treatment with antihistamine preparations]. 225 82

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

Patients undergoing surgery for pyloric stenosis secondary to duodenal ulcer were the subjects for the study. Two pieces of full thickness gastric wall (all coats) were obtained at laparotomy. The pieces were immediately split into two halves. One of these was used for histamine assay where as the other was used to study the mast cell population. Histamine content and mast cell population was found to be less in gastric mucosa of our patients as compared to values from normal human gastric mucosa. There was lack of correlation between mast cell population and histamine content which suggests that there could be some other storage sites for histamine.
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PMID:Histamine and mast cell study in the gastric tissue of south Indian patients suffering from duodenal ulcer with pyloric stenosis. 357 Apr 29

We describe a 65-year-old Japanese man with a 20-year history of telangiectasia macularis eruptiva perstans, who developed polycythemia rubra vera and duodenal ulcer 10 and 12 years respectively after the onset of mastocytosis. Involvement of mast cells was found in neither bone marrow nor gastrointestinal tract. Immunohistochemical staining revealed that the mast cell was positive for both tryptase and chymase, indicating the nature of cutaneous mast cells. Despite the coexistence of a hematologic disorder, our case is suggested to have cutaneous but not systemic mastocytosis presenting as telangiectasia macularis eruptiva perstans.
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PMID:Telangiectasia macularis eruptiva perstans in polycythemia rubra vera. 1187 25

The term mastocytosis denotes a heterogeneous group of rare hematological disorders characterized by abnormal accumulation of mast cells. While cutaneous mastocytosis is relatively frequent mast cell leukemia belongs to the rarest forms of human leukemia. In the following we present the case of an aleukemic mast cell leukemia and shall discuss the revised classification of mastocytosis based on the "Year 2000 Working Conference on Mastocytosis" held in Vienna, Austria. A 48 year-old caucasian man presented with a four-week history of diarrhea, obstipation, vomiting, rash, and mild fever. Clinical inspection revealed a disseminated itching rash and a mild hepatomegaly. Red and white blood cell counts were within the normal range. Levels of the alkaline phosphatase and serum histamine were significantly increased. There was no splenomegaly or lymphadenopathy. Cytologic and histologic investigation of the bone marrow revealed a marked increase in atypical mast cells. Since only a few circulating mast cells could be detected in a cytospin preparation of the blood, the diagnosis of an aleukemic mast cell leukemia was established. About four weeks after the diagnosis had been established, the patient died with signs of a hemorrhagic shock due to a massive gastrointestinal bleeding. Autopsy revealed widespread mast cell infiltration of bone marrow, spleen, liver and lungs, but also a small, deeply penetrating, non-specific duodenal ulcer. In conclusion, despite of presentation with signs of a primary gastrointestinal disorder, the patient was found to suffer from an exceedingly rare aleukemic mast cell leukemia ("malignant mastocytosis") and died after a total duration of the disease of only about three months.
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PMID:[Aleukemic mast cell leukemia (formerly: "malignant mastocytosis"): an extremely rare form of leukemia. A case report and simultaneously a contribution to revised classification of mastocytosis]. 1223 4

Peptic ulcer is a common disorder of gastrointestinal system and its pathogenesis is multifactorial, where smoking and nicotine have significant adverse effects. Smoking and chronic nicotine treatment stimulate basal acid output which is more pronounced in the smokers having duodenal ulcer. This increased gastric acid secretion is mediated through the stimulation of H2-receptor by histamine released after mast cell degranulation and due to the increase of the functional parietal cell volume or secretory capacity in smokers. Smoking and nicotine stimulate pepsinogen secretion also by increasing chief cell number or with an enhancement of their secretory capacity. Long-term nicotine treatment in rats also significantly decreases total mucus neck cell population and neck-cell mucus volume. Smoking also increases bile salt reflux rate and gastric bile salt concentration thereby increasing duodenogastric reflux that raises the risk of gastric ulcer in smokers. Smoking and nicotine not only induce ulceration, but they also potentiate ulceration caused by H. pylori, alcohol, nonsteroidal anti-inflammatory drugs or cold restrain stress. Polymorphonuclear neutrophils (PMN) play an important role in ulcerogenesis through oxidative damage of the mucosa by increasing the generation of reactive oxygen intermediates (ROI), which is potentiated by nicotine and smoking. Nicotine by a cAMP-protein kinase A signaling system elevates the endogenous vasopressin level, which plays an aggressive role in the development of gastroduodenal lesions. Smoking increases production of platelet activating factor (PAF) and endothelin, which are potent gastric ulcerogens. Cigarette smoking and nicotine reduce the level of circulating epidermal growth factor (EGF) and decrease the secretion of EGF from the salivary gland, which are necessary for gastric mucosal cell renewal. Nicotine also decreases prostaglandin generation in the gastric mucosa of smokers, thereby making the mucosa susceptible to ulceration. ROI generation and ROI-mediated gastric mucosal cell apoptosis are also considered to be important mechanism for aggravation of ulcer by cigarette smoke or nicotine. Both smoking and nicotine reduce angiogenesis in the gastric mucosa through inhibition of nitric oxide synthesis thereby arresting cell renewal process. Smoking or smoke extract impairs both spontaneous and drug-induced healing of ulcer. Smoke extract also inhibits gastric mucosal cell proliferation by reducing ornithine decarboxylase activity, which synthesises growth-promoting polyamines. It is concluded that gastric mucosal integrity is maintained by an interplay of some aggressive and defensive factors controlling apoptotic cell death and cell proliferation and smoking potentiates ulcer by disturbing this balance.
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PMID:Smoking and the pathogenesis of gastroduodenal ulcer--recent mechanistic update. 1461 84

A 21-year-old young girl presents with intense abdominal pain, nausea, diarrhea in the context of a cutaneous eruption formed by erythematous and papulous elements with brown violet aspect, very pruriginous, occasioned by the preparation of some fishmeal. Similar eruption debuted from childhood from the age of 4 year became rare with age. Since 3 years, the patient presents more intense digestive manifestation. The therapy with H2 antagonist (loratadine) and a mast cell stabilizer is beneficial over the digestive symptoms and in the same time cancel the pruritus and the erythema of the cutaneous lesions that remain hyperpigmented. The histopathological examination of a cutaneous lesion confirms the diagnosis of mastocytosis and the endoscopic examination discovers a duodenal ulcer and an erosive gastritis. The systemic mastocytosis is a rare disease, often associated with an urticaria pigmentosa, with difficult diagnosis in his absence. That's why, in patients with macular or nodular pigmented cutaneous lesions appeared in infancy and early childhood and which urticate in a characteristic manner when the skin is firmly rubbed, a cutaneous biopsy is necessary.
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PMID:Type Ib indolent mastocytosis with systemic involvement: cutaneous mastocytosis and gastrointestinal involvement at young girl. 1905 Aug 5

At upper gastrointestinal endoscopy to investigate unexplained diarrhea and iron deficiency anemia, duodenal biopsies are often taken to exclude a diagnosis of coeliac disease. While histology remains the gold standard for this diagnosis, recent developments in serological testing may overtake this as a first line test and biopsy restricted to confirming the diagnosis. Established coeliac disease on biopsy is straightforward, but early lesions may pose a challenge. Newer endoscopic procedures such as push-pull enteroscopy (balloon enteroscopy) with biopsy allow access to the small bowel beyond the second part of the duodenum. Controversy remains as to what constitutes the normal histology of the duodenum, and small bowel. Lymphocytic duodenosis (increased intraepithelial lymphocytes with normal villous architecture) in patients with negative coeliac serology can be associated with Helicobacter pylori, drugs, autoimmune and other diseases including food allergy. Full thickness small intestinal biopsies can aid in investigation of enteric neuropathies in severe dysmotility disorders. Biopsies are also taken to investigate malabsorption due to suspected infectious and metabolic disorders. Despite highly active anti-retroviral therapy (HAART), immunosuppressed patients may be affected by duodenal pathogens. The histology of duodenal mucosa in acid related disorders reflects the damage seen at endoscopy. Although the prevalence of duodenal ulcer disease is decreasing, drugs causing ulceration remain an important disease entity. Recent observations in functional bowel disorders suggest that the duodenum may be a key site for pathology. In functional dyspepsia, patients with early satiety may have excess eosinophil infiltration, and the mast cell is probably a key player in the irritable syndrome in the small intestine.
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PMID:Clinical value of duodenal biopsies--beyond the diagnosis of coeliac disease. 2232 33


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