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Biomedical subjects

P Layer

Publications and source records attributed to P Layer.

At least 73 records · Page 4Linked to original sources
PubMed1996

[Are proton pump inhibitors superior to H2 receptor antagonists within the scope of H. pylori eradication therapy? Meta analysis of current parallel group comparisons].

The combined treatment with acid lowering drugs and antibiotics is widely accepted for H. pylori-eradication therapy. There are, however, controversies regarding the influence of the acid lowering drug on H. pylori-eradication rates. Therefore, this meta-analysis aimed to assess the available parallel-group eradication studies with proton pump inhibitors and H2-receptor antagonists and to compare H. pylori-eradication rates for both classes of acid lowering drugs. METHODS. We performed a broad based medline search to retrieve all published treatment trails for H. pylori-infection. In addition, a manual search of the abstracts of major national and international meetings was conducted. In total seven publications of eight comparisons with a parallel group design comparing H2-receptor antagonists and proton pump inhibitors plus antibiotics with a total of 538 patients were identified. Non parametric tests were utilized to assess the influence of the acid lowering drug on eradication rates. Furthermore, logistic regression adjusting for duration of antibiotic treatment and the number of antibiotics was used to compare the different acid lowering drugs. RESULTS. All studies utilized omeprazole as the proton pump inhibitor with doses ranging from 20 mg/die to 2 x 20 mg/die. Ranitidine (with doses ranging from 2 x 150 mg/die to 2 x 300 mg/die) was used in six trials and nizatidine (2 x 300 mg/die) in one trial. H. pylori was successfully eradicated in 78.6% (95% 73.6-83.5) with the proton pump inhibitor and in 76.5% (95% Cl 71.4-81.5) in patients treated with the H2-receptor antagonists. Utilizing two antibiotics instead of one antibiotic significantly increased eradication rates by 16.1% (95% Cl 9.3-22.8, p < 0.001). However, neither in protocols with one nor in protocols with two antibiotics the eradication rates significantly differed for regimens using H2-receptor antagonists or proton pump inhibitors. CONCLUSION. H. pylori-eradication rates for treatment protocols with one or two antibiotics in combination with an acid lowering drug are not different for the proton pump inhibitors or h2-receptor antagonists. Therefore, the question whether H2-receptor antagonists or proton pump inhibitors should be used in combination with antibiotics for H. pylori eradication therapy is without clinical relevance.

Anti-Ulcer Agents↗
PubMed1996

Ileal inhibition and modulation of carbachol-stimulated proximal small intestinal motor functions in humans.

Carbohydrates within the distal small intestine inhibit endogenously stimulated proximal gastrointestinal motor activity and induced an interdigestive-like pattern in humans. In order to further investigate the intermediary mechanisms of the ileal inhibitory effects, we intubated eight healthy volunteers with an oroileal multilumen tube and stimulated small intestinal motility exogenously with a continuous intravenous infusion of the cholinergic agonist carbachol. Additionally, the ileum was perfused for 15-min intervals with either carbohydrates (total load: 18 g) or normal saline as volume control. Ileal carbohydrate perfusion inhibited the carbachol-stimulated motility pattern significantly (p < 0.001) and induced phase-III-like motor activity; ileal saline had no effect. These data suggest that a direct inhibition of cholinergic systems may be involved in the ileal inhibitory effects on proximal small intestinal motility.

Adult↗
PubMed1995

Ileal release of glucagon-like peptide-1 (GLP-1). Association with inhibition of gastric acid secretion in humans.

There is evidence that the distal intestine participates in the regulation of gastric motor and secretory function. It was the aim of this study to examine in greater detail the effects of ileal nutrient exposure on human gastric acid secretion and to investigate potential intermediary mechanisms. Twelve normal subjects were intubated with an oroileal multilumen tube assembly for gastric, duodenal, and ileal perfusion of marker and test solutions, aspiration, and intestinal manometry. We studied ileal effects on gastric acid output in the unstimulated, interdigestive state (during early phase II, N = 6), and during endogenous stimulation by intraduodenal essential amino acid perfusion, N = 6) and on release of candidate humoral mediators, peptide YY (PYY) and glucagonlike peptide-1 (GLP-1), both known inhibitors of human gastric acid secretion. Compared with ileal saline perfusion, ileal carbohydrate (total caloric load: 60 kcal) decreased interdigestive gastric acid output by 64% (P < 0.01), and endogenously stimulated output by 68%, respectively (P < 0.005). Under all experimental conditions, ileal carbohydrate increased plasma GLP-1 by 80-100% (all P < 0.005). Ileal lipid perfusion had similar inhibitory effects on gastric acid output and stimulatory effects on GLP-1 release as had ileal carbohydrate. By contrast, ileal perfusion with peptone had no or only weak effects on either acid output or plasma GLP-1. Plasma PYY concentrations and suppression of gastric secretion in response to ileal perfusions were not correlated. In humans, both interdigestive and endogenously stimulated gastric acid output are inhibited in response to intraileal carbohydrate or lipids, but not protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Peptide YY inhibits exocrine pancreatic secretion in isolated perfused rat pancreas by Y1 receptors.

Peptide YY (PYY) inhibits exocrine pancreatic secretion in several species. Two receptors, Y1 and Y2, are known to mediate PYY actions. While PYY 1-36 binds equally to both receptor subtypes, a second endogenous form of PYY, PYY 3-36, selectively activates Y2 receptors. The importance of Y receptor subtypes for inhibition of exocrine pancreatic secretion by PYY is unknown. We studied the effects of PYY 1-36 on cholecystokinin octapeptide (CCK-8)-stimulated amylase secretion in an isolated perfused rat pancreas model. To characterize functionally the receptors involved we determined the effects of a Y1-selective agonist, [Pro34]PYY; a Y2 selective agonist, PYY 3-36; and neuropeptide Y (NPY) in this model. PYY 1-36 significantly inhibited stimulated amylase secretion in the denervated rat pancreas. [Pro34]PYY and NPY both inhibited exocrine pancreatic secretion as potently as PYY 1-36. Contrary to that, the Y2 selective agonist, PYY 3-36, was inactive. We conclude that PYY inhibits exocrine pancreatic secretion in this extrinsically denervated rat pancreas model by Y1 receptors.

Amylases↗
PubMed1995

Exocrine pancreatic function in diabetes mellitus.

The exocrine pancreas and pancreatic islet system have a multitude of complex anatomical and functional interrelations. In insulin-dependent diabetes mellitus, both exocrine pancreatic function and morphology appear to be altered, although this phenomenon and its responsible mechanisms have not been elucidated in detail in humans. However, reduced pancreatic secretion in insulin-dependent diabetes is not likely to result in impaired intraluminal nutrient digestion. Whether, the changes in exocrine pancreatic function and morphology are a result of disturbed islet (beta-cell) function or are due to a common immunological pathogenesis, as suggested by recent studies, remains to be clarified.

Animals↗
PubMed1995

[Pathogenesis and pathophysiology of sigmoid diverticulitis].

The sigmoid colon is the part of the large intestine which is most commonly involved in diverticular disease due to its anatomical properties. True diverticula containing all layers of the colonic wall are rare. The majority of diverticula found are pseudodiverticula. They are herniations of mucosa and submucosa through clefts in the colonic muscle layers as a result of morphologic changes of the colonic wall and an imbalance between the intraluminal pressure and the pressure in the abdominal cavity. Microperforations of the tip of the diverticula are an important factor leading to inflammation and symptomatic disease.

Colonic Diseases↗
PubMed1994

[Irritable colon syndrome].

The irritable bowel syndrome (IBS) is a common chronic functional disorder. Although its cause is unclear, a multifactorial etiology has been hypothesized with several putative pathophysiological mechanisms which may interact. These include abnormal intestinal motor function, abnormal visceral perception, psychosocial factors and luminal factors that irritate the small bowel and colon. A positive diagnosis should be made from an accurate history and physical examination and requires confirmation by exclusion of structural, metabolic and infectious processes that may result in similar clinical presentations. The IBS can be classified on the basis of its broad clinical spectrum of severity and variable patterns of dominant symptoms. Such a classification permits an appropriately graduated treatment approach that includes patient education, dietary adjustment, psychotherapeutic and behavioral techniques, as well as a symptom-orientated pharmaco- and psychopharmacotherapy. The majority of patients has mild symptoms and requires no specific treatment besides careful education and reassurance and dietary adjustment. For moderate symptom severity, additional psychotherapy and behavior techniques are indicated, which should be combined with pharmacotherapy targeted at the presumed pathomechanism. For severe symptoms, physician-based behavior modification and psychopharmacological agents may be needed.

Behavior Therapy↗
PubMed1994

[Pro34]peptide YY is a Y1-selective agonist at peptide YY/neuropeptide Y receptors.

We have investigated binding and functional effects of a new peptide YY analogue, [Pro34]peptide YY, at Y1 and Y2-like subtypes of receptors for peptide YY and neuropeptide Y. In binding studies [Pro34]peptide YY had a similarly high affinity as peptide YY to human Y1-like receptors in SK-N-MC cells, a human neuroblastoma cell line of presumed neurogenic origin, and HEL cells, a human cell line derived from a patient with Hodgkin's disease. In functional studies [Pro34]peptide YY stimulated Ca2+ elevations in both Y1-like receptor cell lines with similar potency and efficacy as peptide YY. In contrast to peptide YY [Pro34]peptide YY was 1000-fold less potent in binding to Y2-like receptors in porcine splenic membranes and lacked agonistic effects in another Y2-like receptor-mediated model system, i.e. inhibition of [3H]serotonin release from rat cerebral cortical slices. Thus, [Pro34]peptide YY is a highly Y1-selective full agonist of peptide YY/neuropeptide Y receptors. [Pro34]peptide YY could be useful for studying the importance of Y receptor subtypes in mediating peptide YY physiological actions.

Amino Acid Sequence↗
PubMed1994

[Amebic liver abscess with hepatobronchial fistula].

Four weeks after a holiday in Kenya a 57-year-old woman developed a fever up to 40 degrees C, right upper abdominal pain, icteric sclerae, nausea and vomiting. Laboratory tests revealed leukocytosis (24,400/microliters), markedly accelerated erythrocyte sedimentation rate (123 mm/h) and moderately increased activity of liver enzymes in serum. The liver was unremarkable on ultrasound. Four days after hospitalization the patient complained of dyspnoea and pleuritic pain. Ultrasound examination and computed tomography showed an abscess in the right lobe of the liver. Amoebic abscess of the liver being the most likely diagnosis, although the relevant serological tests were unremarkable and a titre increase occurred only later, treatment was started with metronidazole (four times 500 mg daily intravenously) and paromomycin (three times 10 mg/kg daily). Her condition significantly improved within a day. Two weeks later, however, she developed chest pain, dyspnoea and cough productive of large amounts of white-yellow sputum, even though antibiotic treatment was continuing. A transdiaphragmatic rupture of the abscess with formation of a hepatobronchial fistula proved to be the cause of these symptoms. The patient was treated surgically by drainage and suturing-over of the extensive diaphragmatic defect and after 2 weeks she was discharged symptom-free on a maintenance dose of diloxanide furoate (three times 500 mg/d orally).

Bronchial Fistula↗
PubMed1994

Two molecular forms of peptide YY (PYY) are abundant in human blood: characterization of a radioimmunoassay recognizing PYY 1-36 and PYY 3-36.

Two endogenous forms of PYY are abundant in man and dog, PYY 1-36 (PYY-I) and PYY 3-36 (PYY-II). PYY-II is a major molecular form of PYY in human colon, but it is not known, whether PYY-II is also released into the circulating blood. Several radioimmunoassays for measuring PYY-I in plasma have been developed, but it has not been reported, whether they equally detect PYY-II. We characterize a radioimmunoassay for measuring PYY in human plasma which equally recognizes PYY-I and PYY-II. Using this radioimmunoassay and reversed phase HPLC we demonstrate the existence of two forms of PYY in human blood, coeluting with synthetic PYY-I and PYY-II.

Adult↗
PubMed1994

The different courses of early- and late-onset idiopathic and alcoholic chronic pancreatitis.

BACKGROUND/AIMS: Compared with alcoholic pancreatitis, little is known about the natural history of idiopathic pancreatitis. Two hundred forty-nine patients with alcoholic pancreatitis and 66 patients with idiopathic chronic pancreatitis seen at our institution between 1976 and 1982 were investigated. METHODS: Records were analyzed retrospectively from the onset of symptomatic disease, and patients were followed up prospectively until 1985. Patients with early-onset (n = 25) and late-onset (n = 41) idiopathic chronic pancreatitis had a median age at onset of symptoms of 19 and 56 years, respectively. RESULTS: The gender distribution was nearly equal in idiopathic chronic pancreatitis, but 72% of patients with alcoholic pancreatitis were men (P = 0.001 vs. idiopathic). In early-onset idiopathic pancreatitis, calcification and exocrine and endocrine insufficiency developed more slowly than in late-onset idiopathic and alcoholic pancreatitis (P = 0.03). However, in early idiopathic chronic pancreatitis, pain frequently occurred initially (P = 0.003 vs. late and alcoholic) and was more severe (P = 0.04 vs. late and alcoholic). In late-onset idiopathic pancreatitis, pain was absent in nearly 50% of patients. CONCLUSIONS: There are two distinct forms of idiopathic chronic pancreatitis. Patients with early-onset pancreatitis have initially and thereafter a long course of severe pain but slowly develop morphological and functional pancreatic damage, whereas patients with late-onset pancreatitis have a mild and often a painless course. Both forms differ from alcoholic pancreatitis in their equal gender distribution and a much slower rate of calcification.

Adolescent↗