Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatic porphyrias are characterized by neurological symptoms manifested by abdominal pain, neuropathies and mental aberrations. Porphyrins are ubiquitous and essential biochemical constituents of living beings acting as mediators of oxidation reaction in the metabolism of the steroid, drugs, environmental chemicals or as a mean of exchanging gases, such as oxygen and carbon dioxide between the environment and the tissue of the body using endogenous polypeptide properties. The different porphyrins arising from the arrangement of normal heme synthesis are characterized by an accumulation and excretion of specific intermediate porphyrins and/or of precursors exerting toxic effect, initiating cascades of generations of polypeptides, neurotransmitters and gut-brain axis peptide responsible for the symptoms of clinical status. We studied polypeptide levels in 27 patients (19 females, 8 males) presenting acute attack of hepatic porphyria: 2 with ALA dehydratase-deficient porphyria; 9 with acute intermittent porphyria; 12 with porphyria cutanea tarda and 4 with variegate porphyria. During acute attacks of porphyria, polypeptides were found to be constantly increased: vasoactive intestinal polypeptide (VIP); neurotensin (NT); substance P; pancreatic polypeptide; gastrin-releasing peptide; gastrin and motilin. Administration of the somatostatin (antagonizing polypeptide), which was undetectable or low before treatment, apparently alleviated the acute symptomatology. Elevated levels of polypeptides, at least partly, contribute to appearance of acute symptoms in porphyria patients.
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PMID:Polypeptide levels increase during acute onset of hepatic porphyrias. 907 85

The actions of trimebutine [3,4,5-trimethoxybenzoic acid 2-(dimethylamino)-2-phenylbutylester] on the gastrointestinal tract are mediated via (i) an agonist effect on peripheral mu, kappa and delta opiate receptors and (ii) release of gastrointestinal peptides such as motilin and modulation of the release of other peptides, including vasoactive intestinal peptide, gastrin and glucagon. Trimebutine accelerates gastric emptying, induces premature phase III of the migrating motor complex in the intestine and modulates the contractile activity of the colon. Recently, trimebutine has also been shown to decrease reflexes induced by distension of the gut lumen in animals and it may therefore modulate visceral sensitivity. Clinically, trimebutine has proved to be effective in the treatment of both acute and chronic abdominal pain in patients with functional bowel disorders, especially irritable bowel syndrome, at doses ranging from 300 to 600 mg/day. It is also effective in children presenting with abdominal pain.
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PMID:Trimebutine: mechanism of action, effects on gastrointestinal function and clinical results. 936 86

A case of intestinal ganglioneuromatosis is reported. The symptoms were watery diarrhoea and abdominal pain of several months duration. Endoscopic examination of the oesophagus, ventricle, duodenum, colon and rectum was normal. Mucosal biopsies from colon and rectum revealed ganglia cells and thin nerve fibres in the lamina mucosa, giving the diagnosis ganglioneuromatosis. As a consequence of the diagnosis thyroid scintigraphy, CT-scanning of the thyroid and adrenal glands and measurement of serum calcitonin and gastrin were performed. The tests revealed an intrathoracic nodular struma, and beyond this no abnormalities. The relation of intestinal ganglioneuromatosis to Multiple Endocrine Neoplasia type II b is discussed and the necessity of performing mucosal-biopsy from endoscopically normal colonic mucosa in cases of chronic diarrhoea is emphasised.
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PMID:[Intestinal ganglioneuromatosis--a rare cause of chronic diarrhea]. 985 Jun 21

Recurrent abdominal pain (RAP) is a significant problem in the pediatric population, and there has been much recent interest in the role that Helicobacter pylori (Hp) might play in this disorder. In this case control study, the authors aimed to determine whether Hp is an agent responsible for RAP, and to assess fasting gastrin concentrations in children with and without RAP in the Hp-positive and -negative groups. The study was conducted in 42 patients with RAP and 50 healthy children attending routine day-case surgery as a control group, aged 3 to 15 years, over a 12-month period. Of the 42 children with RAP, 30 were seropositive (71.4%) for Hp IgG, and of 50 children in the control group, 32 were seropositive (64%) for Hp IgG (P > 0.05). We found that Hp infection was as high in healthy children as in children with RAP. The mean fasting gastrin levels in 62 Hp-seropositive children (60.4 ng/l) were not different from those in 30 Hp-seronegative children (57.3 ng/l) and those in 42 children with RAP (58.2 ng/l) were also not significantly different from those in 50 healthy children (62.9 ng/l). Thus, no association between childhood Hp infection, hypergastrinemia, and RAP was found in our Turkish population.
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PMID:Helicobacter pylori and hypergastrinemia in children with recurrent abdominal pain. 988 Jun 93

Gastric carcinoid tumors arise from enterochromaffin-like (ECL) cells, these tumors represent 2-41% of all neuroendocrine tumors and 0.3% of malignant gastric neoplasias, being more common in men than in women, and commonly affecting people over 60 years old. These tumors arise from accelerated proliferation of the ECL cells as a consequence of the hypersecretion of gastrin, situation that can be present in atrophic gastritis and the Zollinger-Ellison syndrome. We report the case of a 51 year old hispanic female who presented with a 3 month history of abdominal pain, meteorism and constipation; she was treated with ranitidine and metoclopramide without clinical improvement, thus she underwent upper gastrointestinal endoscopy which showed an atrophic gastritis and gastric polyps. Histopathologic examination revealed a neuroendocrine gastric tumor which was positive to serotonine and gastrin stainings. Hormonal screening showed normal serum levels of LH, FSH, estradiol, ACTH, progesterone, calcitonin and cortisol. The serum level of gastrin was elevated with 500 pg/mL. Gammagraphic scanning with octreotide was negative for metastasis.
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PMID:[Gastric neuroendocrine tumor]. 1006 36

The ciliated hepatic foregut cyst is an unusual solitary cystic lesion of the liver. In a series of 7 cases of hepatic ciliated cysts, we performed a histological, histochemical, and immunohistochemical study to better define the histogenesis of this rare entity. The patients were 4 women and 3 men, aged 39 to 75 years. Four patients presented with abdominal pain. In 3 cases the cyst was discovered incidentally on ultrasonography. The cysts measured from 1 to 4 cm in diameter. Microscopically, the lining of the columnar epithelium was composed of ciliated cells and mucin secreting goblet cells. The wall was composed of bands of smooth-muscle fibers surrounded by an outer fibrous capsule. The goblet cells stained with PAS, alcian blue, and high-iron diamine. The immunohistochemical study showed that endocrine cells were present within the cyst epithelium, positive for chromogranin, synaptophysin, bombesin, and calcitonin, and negative for serotonin, somatostatin, glucagon, insulin, gastrin, and pancreatic polypeptide. In all the cases, immunoreactivity of some cells for CC10 strongly suggested the presence of Clara cells. Our study shows that the epithelium lining ciliated hepatic foregut cysts has histological, histochemical, and immunohistochemical features similar to those observed in the bronchiolar epithelium. This lesion is a developmental ventral foregut abnormality that could arise from a bronchiolar bud of the tracheobronchial diverticulum.
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PMID:The ciliated hepatic foregut cyst, an unusual bronchiolar foregut malformation: a histological, histochemical, and immunohistochemical study of 7 cases. 1068 41

The histopathology of Fibrocalculous Pancreatic Diabetes (FCPD) has been extensively studied, but there are no reports on alteration in patterns of hormone secreting cells using immunohistochemistry in islets of FCPD patients. In this study, we report on the histopathology and immunohistochemistry of islets of FCPD patients and its possible correlation with the clinical picture. Pancreatic biopsies were carried out in six patients with FCPD at the time of surgery for abdominal pain. Routine histopathology and immunohistochemistry studies were carried out with six primary antibodies namely insulin, glucagon, pancreatic polypeptide (PP), somatostatin, vasoactive intestinal peptide and gastrin. Histopathology of the pancreas showed a spectrum of changes ranging from moderate to severe atrophy, fibrosis of the parenchyma and degeneration of the ducts. Nesidioblastosis was present in three patients. Immunohistochemical studies showed a decrease in the number of islets but some patients showed evidence of hyperplasia. There was an overall decrease in the percent of insulin cells and the positivity in the islets correlated with plasma C-peptide levels and the duration of diabetes. There was no consistent relationship with glucagon with some patients showing increased and other decreased positivity. There was a marked decrease in PP and somatostatin positivity, the significance of which is not clear. The reduction, but partial preservation of insulin positivity is consistent with the ketosis resistance shown by patients with Fibrocalculous Pancreatic Diabetes.
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PMID:Histopathology and immunohistochemistry of pancreatic islets in fibrocalculous pancreatic diabetes. 1113 79

Numerous epidemiologic studies suggest a relationship between lung cancer and peptic ulcer disease. Furthermore, various lung cancers synthesize and release a number of peptides such as gastrin and gastrin-releasing peptide that could cause acid hypersecretion; however, Zollinger-Ellison syndrome (ZES), because of a lung tumor, has never been described. We report such a patient for the first time. A 60-year-old man with a non-small cell lung carcinoma (large cell type) presented with diarrhea, heartburn, abdominal pain, and duodenal ulcers. Evaluation showed ZES was present (fasting hypergastrinemia, hyperchlorhydria) and control of all symptoms by omeprazole. No abdominal or cardiac tumor, the other known locations of gastrinomas causing ZES, was found on detailed tumor imaging studies. Resection of the lung tumor resulted in a decrease in gastrin levels to normal values. Plasma radioimmunoassays showed elevated gastrin, chromogranin A and normal levels of gastrin-releasing peptide, and 9 other hormones. The tumor showed similar immunocytochemical results. The characteristics of this case are compared with 100 cases of sporadic abdominal gastrinomas, and the evidence reviewed suggests why ZES should be considered in patients with lung cancer with peptic symptoms.
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PMID:A new cause of Zollinger-Ellison syndrome: non-small cell lung cancer. 1126 90

The present study was designed to evaluate the usefulness of plasma gastrin determinations as a diagnostic aid and to review the clinical and haematological findings in cattle with bleeding abomasal ulcers. Twenty-nine cows with bleeding abomasal ulcers and six healthy cows were used. Clinical and laboratory examinations, including plasma gastrin levels, were performed. Anorexia, depression, dark-coloured to black faeces, pale mucous membranes, abdominal pain, moderate tachycardia and tachypnoca were the most pronounced clinical symptoms in the cattle with bleeding abomasal ulcers. Plasma gastrin concentration was significantly higher (P < 0.05) in the cattle with bleeding abomasal ulcers than in healthy cows. The mean plasma gastrin concentration in healthy cattle was 103.2 pg/ml, while the mean plasma gastrin concentrations in cattle with bleeding abomasal ulcers were found to be 213.6 pg/ml. Haemoglobin levels, packed cell volume, total white blood cell count and mean corpuscular volume were significantly lower (P < 0.05) in the cows with bleeding abomasal ulcer than in the healthy cattle. The results of this study show that measurement of plasma gastrin can be useful in the diagnosis of bleeding abomasal ulcers in cattle.
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PMID:Plasma gastrin activity and the diagnosis of bleeding abomasal ulcers in cattle. 1176 13

A large number of families with familial isolated hyperparathyroidism (FIHP) have been reported. We wanted to determine if some of these families represent early manifestations of full-blown syndromes such as multiple endocrine neoplasia type 1 (MEN-1), as early identification may alter surgical and medical management. Four small families with a family history of hyperparathyroidism without clear-cut MEN-1 features were screened for a MEN1 mutation. The 10 exons of the MEN1 gene were amplified and analyzed by single-strand conformation analysis (SSCA). Abnormal SSCA shifts were then sequenced using an automated sequencer. Two germline mutations were found: R527X and P277H. The former was detected in three members of a family consisting of two children and a mother. At the time of testing the youngest son was normocalcemic and clinically normal but subsequently developed hyperparathyroidism (HPT). Since the initial testing, the family has been confirmed to be a MEN-1 family as the mother has developed abdominal pain and an elevated serum pancreatic polypeptide and the younger brother an anterior pituitary tumor and recurrent HPT. The latter P277H mutation was identified in two of three members tested from another family. Manifestations of MEN-1 syndrome have also developed. The father now has developed diarrhea and elevated serum gastrin; and the daughter has developed recurrent HPT. Genetic screening of families who clinically have FIHP is important and may influence the type of medical and surgical treatment and follow-up, as some have MEN-1 syndrome. Long-term screening for MEN syndromes should be included in this set of patients. Positive screening may predict disease and allow early detection and appropriate treatment before initiation of symptoms.
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PMID:Genetic screening for MEN1 mutations in families presenting with familial primary hyperparathyroidism. 1201 70


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