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At least 1,423 records · Page 79Linked to original sources
PubMed2003

Motility and dysmotility of the biliary tract.

Muscle fibers in the biliary tree, and therefore the potential for dysmotility, are located in the gallbladder and the sphincter of Oddi. Dysmotility at either site is a potential cause of biliary pain in the absence of stones, although significant controversy persists. Diminished gallbladder emptying measured by biliary scintigraphy is an indication for cholecystectomy, although studies are contradictory regarding clinical benefit. It is likely that careful selection of patients for cholescintigraphic testing, many of whom have had missed stones or sludge, will identify patients who benefit from cholecystectomy. However, given the increased incidence of gallbladder stasis in functional gastrointestinal disorders, wide use of this study in patients with abdominal symptoms leads to a frequent failure to respond to cholecystectomy. Sphincter of Oddi dysfunction (SOD) has been best studied in patients with biliary type pain who have had prior cholecystectomy. Much less understood is the association of SOD with idiopathic recurrent acute pancreatitis and chronic pancreatitis. The least-studied clinical association for SOD is in patients with biliary pain and intact gallbladders. Elevated basal sphincter of Oddi pressure is predictive of clinical response to sphincterotomy in patients with postcholecystectomy pain in two randomized sham-controlled studies. However, patients with suspected SOD have the highest complication rate from endoscopic retrograde cholangiogram and sphincterotomy, and, therefore, careful patient selection is mandatory.

Adult↗
PubMed1991

Nonsteroidal anti-inflammatory drugs. Proposed guidelines for monitoring toxicity.

The most common toxicities of nonsteroidal anti-inflammatory drugs (NSAIDs) are gastropathy, renal dysfunction, and liver function abnormalities. We outline an approach to monitoring patients on long-term NSAID therapy, focusing on the early detection of complications. Gastropathy caused by NSAID use is more common in elderly patients or those with a history of dyspepsia, peptic ulcer disease, or alcohol abuse. Fecal occult blood testing and hemograms are less accurate in detecting gastropathy than direct visualization but are convenient and relatively inexpensive. We recommend the periodic use of these tests to detect NSAID-induced acute or chronic blood loss. Renal toxicity is seen in patients with preexisting renal disease or functional volume depletion and in the elderly. Complications include renal insufficiency, hyponatremia, hyperkalemia, and protein-uria. Renal function should be monitored during the first few weeks of NSAID therapy, especially in high-risk patients, with periodic testing thereafter. Hepatic toxicity is less common but warrants occasional determinations of alanine aminotransferase levels. Elderly patients and those with renal insufficiency or alcohol abuse have a higher risk of complications. Nonsteroidal anti-inflammatory drugs should be used cautiously in those patients at high risk for complications. Strategies can be used to limit toxicity. Patients taking these drugs long term should be monitored periodically for signs of blood loss, renal dysfunction, and hepatic dysfunction.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1993

Effect of citric acid and maltol on the accumulation of aluminum in rat brain and bone.

Deposition of aluminum in the body is responsible for the development of dialysis-related diseases in patients with renal dysfunction and may play a role in the development of certain neurodegenerative disorders. Although citric acid is known to be a strong enhancer of gastrointestinal absorption of aluminum, its effect on aluminum distribution and accumulation is not yet clear. Maltol has been shown to increase the neurotoxicity of aluminum, but little is known about its effect on aluminum deposition in the body. To elucidate the role of citric acid and maltol in aluminum accumulation and toxicity, rats were loaded intraperitoneally during a 7-day period with different amounts of aluminum chloride in absence or presence of citric acid or maltol before analysis of aluminum in serum, brain, bone, and urine. Coadministration of citric acid led to relatively reduced serum levels, as compared with aluminum and aluminum-maltol treatment. This is explained by both tissue elimination and enhanced renal elimination. Only at the highest aluminum dose (8 mg/kg body weight) was an enhancing effect of citric acid on accumulation of aluminum in brain observed; no effect on bone aluminum was seen. Furthermore, it was seen that citric acid alters the distribution pattern of aluminum. This may be explained by the postulation of a characteristic aluminum citrate species in serum. Administration of citric acid may increase this aluminum fraction in serum, thereby inducing an alteration of the distribution pattern. Maltol was shown to be a strong enhancer of aluminum accumulation in serum, brain, and bone. The rise of aluminum in these target tissues was dose dependent.(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum↗
PubMed1986

Carbohydrate antigen 19-9 (CA 19-9) and carcinoembryonic antigen (CEA) in pancreatic cancer. Role of age and liver dysfunction.

In order to ascertain the clinical usefulness of CA 19-9 in detecting pancreatic cancer in comparison with CEA, and to verify the influence of age and liver dysfunction on serum levels of these two antigens, serum CA 19-9 and CEA were assessed in 32 control subjects, 32 patients with pancreatic cancer, 26 with chronic pancreatitis and 43 with gastrointestinal extra-pancreatic diseases. Sensitivity, specificity and diagnostic accuracy of CA 19-9 and CEA in detecting pancreatic cancer were: 69% and 44%, 91% and 75%, 60% and 19% respectively. Linear correlations were observed between the age of the subjects on the one hand and CA 19-9 or CEA on the other. Significant relationships were also noticed between alanine-amino-transferase or bilirubin serum levels and CA 19-9 values. Serum CA 19-9 seems to be a better diagnostic tool than CEA in the assessment of pancreatic cancer; nevertheless the influence of liver dysfunction and age to some extent limits the diagnostic value of CA 19-9.

Adult↗
PubMed1992

Effects of peripheral hormones on memory and ingestive behaviors.

This article explores the mechanisms by which peripheral gastrointestinal hormones produce central nervous system effects on memory and feeding. Cholecystokinin produces its satiety effects and memory-enhancing effects by stimulating ascending vagal fibers. Hyperglycemia has been demonstrated to be a cause of memory dysfunction in persons with diabetes mellitus. A number of other hormones, such as amylin and bombesin, modulate both memory processing and feeding. The causes of the anorexia of aging are briefly reviewed.

Aging↗
PubMed2006

Gender, age, society, culture, and the patient's perspective in the functional gastrointestinal disorders.

Patients with functional gastrointestinal disorders (FGID) often experience emotional distress, a perceived lack of validation, and an unsatisfactory experience with health care providers. A health care provider can provide the patient with a framework in which to understand and legitimize their symptoms, remove self-doubt or blame, and identify factors that contribute to symptoms that the patient can influence or control. This framework can be strengthened with the consideration of various important factors that impact FGID but are often overlooked. These include gender, age, society, culture, and the patient's perspective. There is evidence for sex- and gender-related differences in FGID, particularly irritable bowel syndrome (IBS). Whereas the majority of FGID, including IBS, bloating, constipation, chronic functional abdominal pain, and pelvic floor dysfunction, are more prevalent in women than men, functional esophageal and gastroduodenal disorders do not appear to vary by gender. Limited studies suggest that sex differences in visceral perception, cardioautonomic responses, gastrointestinal motility, and brain activation patterns to visceral stimuli exist in IBS. Gender differences in social factors, psychological symptoms, and response to psychological treatments have not been adequately studied. However, there appears to be a greater clinical response to serotonergic agents developed for IBS in women compared to men. The impact of social and cultural factors on the meaning, expression, and course of FGID are important. The prevalence of IBS appears to be lower in non-Western than Western countries. Although further studies are needed, the existing literature suggests that they are important to consider from both research and clinical perspectives.

Age Factors↗
PubMed1994

Gastrointestinal aspergillosis and zygomycosis of cattle.

Gastrointestinal mycosis was diagnosed in 73 lesions of 32 cattle without a history of engorgement, and tissues of 29 animals were examined histopathologically. The omasum was the target organ for infection, followed by the rumen and reticulum. Acute necrohemorrhagic lesions dominated, with infiltration of neutrophils and thrombosis. The etiologic diagnosis was accomplished by indirect immunohistochemical staining of fungal elements with a panel of mono- and polyclonal antibodies raised against fungal antigens. Aspergillosis and zygomycosis were diagnosed in one or more organs of 11 (34.4%) and 20 (62.5%) cattle, respectively, and dual infections were found in three lesions of two animals. Candidosis was diagnosed in only one case. Hematogenous spread of fungi predominantly to the liver was seen in nine animals. Lymphogenic spread of aspergilli to mesenteric and omasal lymph nodes occurred in one and two animals, respectively. Factors that seemed to predispose to mycotic infection included presence of other diseases and intense antimicrobial therapy. These factors and post-partum status, which included 23 of 29 (79.3%) cows, predisposed to mycosis in several ways, e.g., reflux of acidic abomasal contents into the forestomachs, stasis of proventricular content, metabolic dysfunctions, and stress.

Animals↗
PubMed2000

[Clinical features of gastrointestinal diseases in patients with primary mitral prolapse].

Whether patients with mitral prolapse (MP) have specific features in the course of their gastrointestinal diseases (GD) was studied in 420 MP patients with various GD. Echocardiography and examination of the vegetative status were conducted in all the patients. On demand, esophagogastroduodenoscopy, ultrasonic investigation of the abdominal organs, multistage fraction duodenal intubation were made. The findings evidence of more severe course of GD in MP patients. This manifests in early onset, severe pain and dispeptic syndromes, marked mucosal inflammation and is explained by dysfunction of the vegetative nervous system and generalized dysplasia of the connective tissue.

Adult↗
PubMed2000

Carbonylation and disassembly of the F-actin cytoskeleton in oxidant induced barrier dysfunction and its prevention by epidermal growth factor and transforming growth factor alpha in a human colonic cell line.

BACKGROUND: Intestinal barrier dysfunction concomitant with high levels of reactive oxygen metabolites (ROM) in the inflamed mucosa have been observed in inflammatory bowel disease (IBD). The cytoskeletal network has been suggested to be involved in the regulation of barrier function. Growth factors (epidermal growth factor (EGF) and transforming growth factor alpha (TGF-alpha)) protect gastrointestinal barrier integrity against a variety of noxious agents. However, the underlying mechanisms of oxidant induced disruption and growth factor mediated protection remain elusive. AIMS: To determine: (1) if oxidation and disassembly of actin (a key cytoskeletal component) plays a major role in ROM induced epithelial monolayer barrier dysfunction; and (2) if growth factor mediated protection involves prevention of theses alterations. METHODS: Caco-2 monolayers were preincubated with EGF, TGF-alpha, or vehicle before incubation with ROM (H(2)O(2) or HOCl). Effects on cell integrity, barrier function, and G- and F-actin (oxidation, disassembly, and assembly) were determined. RESULTS: ROM dose dependently and significantly increased F- and G-actin oxidation (carbonylation), decreased the stable F-actin fraction (index of stability), and increased the monomeric G-actin fraction (index of disassembly). Concomitant with these changes were disruption of the actin cytoskeleton and loss of the monolayer barrier function. In contrast, growth factor pretreatment decreased actin oxidation and enhanced the stable F-actin, while in concert prevented actin disruption and restored normal barrier function of monolayers exposed to ROM. Cytochalasin-D, an inhibitor of actin assembly, not only caused actin disassembly and barrier dysfunction but also abolished the protective action of growth factors. Moreover, an actin stabilising agent, phalloidin, mimicked the protective actions of the growth factors. CONCLUSIONS: Oxidation, disassembly, and instability of the actin cytoskeleton appears to play a key role in the mechanism of oxidant induced loss of intestinal barrier integrity. In contrast, organisation and stabilisation of actin through promotion of its assembly plays a critical role in the mechanism of growth factor mediated protection.

Actins↗
PubMed2003

Role of enteric glial cells in inflammatory bowel disease.

Enteric glial cells (EGCs) represent an extensive but relatively poorly described cell population within the gastrointestinal tract. Accumulating data suggest that EGCs represent the morphological and functional equivalent of CNS astrocytes within the enteric nervous system (ENS). The EGC network has trophic and protective functions toward enteric neurons and is fully implicated in the integration and the modulation of neuronal activities. Moreover, EGCs seem to be active elements of the ENS during intestinal inflammatory and immune responses, sharing with astrocytes the ability to act as antigen-presenting cells and interacting with the mucosal immune system via the expression of cytokines and cytokine receptors. Transgenic mouse systems have demonstrated that specific ablation of EGC by chemical ablation or autoimmune T-cell targeting induces an intestinal pathology that shows similarities to the early intestinal immunopathology of Crohn's disease. EGCs may also share with astrocytes the ability to regulate tissue integrity, thereby postulating that similar interactions to those observed for the blood-brain barrier may also be partly responsible for regulating mucosal and vascular permeability in the gastrointestinal tract. Disruption of the EGC network in Crohn's disease patients may represent one possible cause for the enhanced mucosal permeability state and vascular dysfunction that are thought to favor mucosal inflammation.

Animals↗
PubMed1988

Intestinal permeability during chemotherapy for childhood tumours.

The intestinal permeability to mannitol and lactulose was measured in 29 children receiving treatment for solid tumours. At the time of study they had no gastrointestinal symptoms and appeared clinically well. However, there was a significant reduction in the absorption of mannitol when compared to normal children. This small bowel dysfunction may result in malabsorption of nutrients and drugs. There was a significant correlation between decreased mannitol absorption and low nutritional status.

Adolescent↗
PubMed2005

Angina pectoris with a normal coronary angiogram.

Angina in the setting of a normal angiogram (NOCAD) occurs in 20-30% of patients undergoing coronary angiography. The etiologies of NOCAD can be anatomically classified into three groups: epicardial disease, coronary microvascular dysfunction, and noncoronary disease. Epicardial disease resulting in NOCAD includes endothelial dysfunction, coronary artery spasm, and coronary artery bridging. Microvascular dysfunction may be secondary to hypertension, cardiomyopathy, infiltrative disease, valvular disease, or idiopathic. Noncoronary artery disease states involving other organs systems such as the pulmonary, gastrointestinal, or musculoskeletal systems can also result in NOCAD. This review focuses on the coronary etiologies of NOCAD. The pathophysiology of disease is discussed as well as a systematic diagnostic strategy. Potential therapeutic options and prognosis are also reviewed.

Clinical Trials as Topic↗
PubMed1976

Manifestations of systemic light chain deposition.

In two patients with terminal renal failure, manifestations of disease developed in multiple organ systems. One had a previous diagnosis of multiple myeloma with kappa light chain proteinemia and proteinuria. The other had idiopathic lobular glomerulonephritis. Hepatic and neurologic abnormalities developed in both; in the latter gastrointestinal, cardiac and endocrine disease developed as well. Clinical and pathologic correlations suggest that the retention and tissue deposition of light chains produced the organ dysfunction, inasmuch as free kappa light chain determinants were demonstrated histologically in the clinically affected organs. The deposition in these patients may be an extreme example of a common but previously unrecognized form of plasma cell dyscrasia.

Adult↗
PubMed2002

Dietary fat and salivary prostaglandin E2.

A study of the relation between dietary fat intake and salivary prostaglandin E2 was undertaken in Transkei, South Africa. Samples of saliva were obtained from (1) Transkeians on a very low fat diet, (2) Transkeians on a low fat diet, (3) Transkeians on a medium fat diet, (4) British patients. Salivary PGE2 means for the groups were (1) 2357 pg/ml, (2) 2020 pg/ml, (3) 733 pg/ml, (4) 312.5 pg/ml. Differences between groups 1 and 3, 1 and 4, and 2 and 4 were significant. Rural Transkeians on a low-fat diet have an elevated level of PGE2 in saliva. As fat increases in the diet, PGE2 in saliva tends towards the level found in those who eat a western diet. An increase in the level of PGE2 production in the upper gastrointestinal tract and in the tissues of the body may be a factor in promoting cancer of the esophagus and diseases favored by Th1 immune dysfunction.

Black People↗
PubMed2006

Efficacy and tolerance profile of agomelatine and practical use in depressed patients.

Agomelatine is a new agent with a unique pharmacological profile, as the first melatonergic antidepressant. Its antidepressant efficacy has been demonstrated in the treatment of major depressive disorder (MDD) at a dose of 25 mg/day. Expectations from antidepressant therapies now go beyond efficacy alone, to include advantages in tolerability and safety. Due to its pharmacological profile, agomelatine does not induce the side-effects typical of other therapies, such as selective serotonin reuptake inhibitors (i.e. gastrointestinal disorders, weight gain, serotonergic syndrome and insomnia). Moreover, a placebo-controlled trial in MDD comparing the effects of agomelatine and venlafaxine on sexual dysfunction (another significant side-effect with current antidepressant medications) indicated the very favourable profile of agomelatine; in the same study, there was similar antidepressant efficacy in the same two groups. A double-blind, placebo-controlled trial investigating the effect of abrupt cessation of treatment demonstrated the absence of discontinuation symptoms with agomelatine, which was in contrast with the results observed with paroxetine. The ability of an antidepressant to relieve sleep complaints with no sedative effects is a key advantage because sleep complaints are a major presenting feature of depression. Again due to its unique pharmacological profile, agomelatine has been shown to positively influence disturbed circadian rhythms in depressed patients by significantly improving all phases of disturbed sleep and the overall quality of sleep, with a favourable impact on daytime alertness. In conclusion, experience with agomelatine across a range of clinical studies suggests that this compound offers a novel approach to the treatment of depression combining efficacy, even in severe depression, with an extremely favourable side-effect profile and sleep regulation. These properties give agomelatine a definite clinical advantage in the treatment of depression.

Acetamides↗
PubMed2004

Alpha2-adrenergic regulation of NO production alters postoperative intestinal smooth muscle dysfunction in rodents.

Alpha2-adrenergic receptor activation plays an important role in the development of postoperative ileus. Alpha2-adrenergic receptors also regulate nitric oxide (NO) production by the mononuclear phagocyte system. We have previously shown that intestinal manipulation leads to a significant increase in NO production by infiltrating monocytes within the intestinal muscularis. The purpose of this study was to investigate whether alpha2-adrenergic blockade with yohimbine would alter postsurgical intestinal smooth muscle dysfunction and NO production by infiltrating monocytes and macrophages within the intestinal muscularis. Rats underwent small bowel intestinal manipulation with or without yohimbine. In vivo gastrointestinal transit and in vitro jejunal circular muscle contractility was measured 24 h postoperatively. RT-PCR was used to detect inducible NO synthase (iNOS) expression. NO levels in tissue culture supernatants were measured. Immunohistochemistry was used to localize alpha2-adrenergic receptor expression in the intestinal muscularis. Yohimbine significantly decreased manipulation-induced delay in gastrointestinal transit and reversed the postoperative decrease in intestinal muscle contractility. Intestinal manipulation resulted in significant iNOS mRNA induction in the intestinal muscularis, which was markedly attenuated after yohimbine treatment. Yohimbine also significantly decreased the postoperative increase in NO released into intestinal muscularis tissue culture supernatant. Immunohistochemistry identified alpha2-adrenergic receptors on monocytes recruited postoperatively into the intestinal muscularis. This study demonstrates that alpha2-adrenergic receptor stimulation of the inflamed postoperative intestinal muscularis plays a significant role in aggravating postoperative ileus through an enhanced induction of iNOS mRNA and increased release of NO from manipulated intestinal muscularis.

Adrenergic alpha-Antagonists↗