PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “gastrointestinal dysfunction”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,351 records · Page 75Linked to original sources
PubMed1995

Pathophysiology of alcoholic brain damage: synergistic effects of ethanol, thiamine deficiency and alcoholic liver disease.

Chronic alcoholism results in brain damage and dysfunction leading to a constellation of neuropsychiatric symptoms including cognitive dysfunction, the Wernicke-Korsakoff Syndrome, alcoholic cerebellar degeneration and alcoholic dementia. That these clinically-defined entities result from independent pathophysiologic mechanisms is unlikely. Alcohol and its metabolite acetaldehyde are directly neurotoxic. Alcoholics are thiamine deficient as a result of poor diet, gastrointestinal disorders and liver disease. In addition, both alcohol and acetaldehyde have direct toxic effects on thiamine-related enzymes in liver and brain. Alcoholics frequently develop severe liver disease and liver disease per se results in altered thiamine homeostasis, in cognitive dysfunction and in neuropathologic damage to astrocytes. The latter may result in the loss of neuron-astrocytic trafficking of neuroactive amino acids and thiamine esters, essential to CNS function. The present review article proposes mechanisms whereby the effects of alcohol, thiamine deficiency and liver disease combine synergistically to contribute to the phenomena of cognitive dysfunction and "alcoholic brain damage".

Alcoholism↗
PubMedDate not supplied

Adverse effects of nonsteroidal anti-inflammatory drugs on the gastrointestinal system.

Two enzymes, cyclo-oxygenase (COX) and 5-lipoxygenase, act upon arachidonic acids to produce prostaglandins and leukotrienes. Inhibition of COX-2 by non-steroidal anti-inflammatory drugs (NSAIDs) lowers synthesis of proinflammatory prostaglandins and produces analgesia. COX-2 is highly inducible by endotoxin, IL-1, hypoxia, epidermal growth factor (EGF), benzo[a]pyrene, and transforming growth factor beta 1(TGF-beta 1). COX-1 in constitutively expressed. Conventional NSAIDs also inhibit the synthesis of cytoprotective prostaglandins by COX-1 in the gastrointestinal tract. Surplus arachidonic acids accumulate and enhance the generation of leukotrienes via the lipoxygenase pathway inducing neutrophil adhesion to endothelium and vasoconstriction. The NSAIDs harboring a carboxyl group also inhibit oxidative phosphorylation (OXPHOS) lowering adenosine-triphosphate (ATP) generation leading to loss of mucosal cell tight junctions and increased mucosal permeability. Administration of NSAIDs that do not interfere with OXPHOS, and concomitant use of prostaglandin analogues to restore cytoprotection reduces complications of NSAID use. However, no NSAID that lacks potential for serious gastrointestinal toxicity is currently available. Selective inhibitors of COX-2 and 5-lipoxygenase are newer, promising drugs. Surprisingly, COX-2 null mice are able to mount an inflammatory response, suffering however, from kidney dysfunction and a shortened life span. Results of clinical studies on the long-term use of NSAID drugs such as selective inhibitors are still pending.

Aging↗
PubMed1995

Absorption of [7,8-14C]rac-a-lipoic acid from in situ ligated segments of the gastrointestinal tract of the rat.

rac-a-Lipoic acid (CAS 62-46-4, thioctic acid) is used in human therapy besides the parenteral route also orally in gastric juice soluble galenic formulations in patients suffering from diabetic polyneuropathy which also involves the gastrointestinal tract (GI) tract in about 20% of the diabetic population. In those patients the most common manifestation of the disease due to small intestine dysfunction is diarrhoea as a consequence of which malabsorption of orally administered drugs may result. Due to the importance of the knowledge on absorption characteristics, in preclinical studies on pharmacokinetics the extent of [14C]absorption from a solution of [7,8-14C]rac-a-lipoic acid was investigated in the rat after oral administration by means of comparison of the AUCs from the [14C]plasma concentrations vs those from the intravenous route, yielding 66%. An alternative evaluation by comparison of [14C]material excreted into the urine yielded 93% [14C]absorption. Despite this high and nearly complete absorption, due to the gastroenteral disturbances mentioned above, the question was investigated if the absorption is restricted to only a small area of the GI tract or is extended over a wider area. The latter is expected to make the absorption less sensitive against variations caused by gastrointestinal disturbances due to longer residence times in the GI tract. In order to approach most closely the physiological situation--as compared with different in vitro incubation techniques using isolated GI tract sacs--the in situ technique on 5 ligated areas of the GI tract of the aneasthetized rat (stomach, duodenum, jejunum, ileum, and colon with caecum) was established.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1981

Hyperalimentation-induced cholestasis. Increased incidence and severity in premature infants.

Two hundren sixty-seven neonates who received parenteral nutrition were monitored for signs of liver dysfunction. Cholestatic jaundice occurred in we infants, with a higher incidence in the more immature infants. There was an inverse correlation between severity of jaundice and the degree of prematurity. Infants with cholestasis remained without gastrointestinal feedings and received parenteral nutrition for periods of time significantly higher than infants without cholestasis. The incidence of this complication did not seem to correlate with the amount of protein infusate (amino acid solution). A higher incidence of sepsis was noted in infants who were affected by cholestasis. Close monitoring for signs of liver dysfunction in all neonates receiving parenteral nutrition is strongly recommended.

Bilirubin↗
PubMed1983

Gastric secretory and mucosal injury response to severe head trauma.

The problem of gastric secretory and mucosal injury response was evaluated in 19 patients who had suffered a severe head injury. Fifteen of 19 patients had some evidence of gastrointestinal hemorrhage. In 7 cases, this was marked. The mean volume of gastric secretions ranged from 36.4 ml/hour on Day 1 to 47.6 ml/hour on Day 6. The mean value of titratable acidity ranged from 3.4 meq/hour on Day 1 to 3.9 meq/hour on Day 6. Possible risk factors were analyzed as a means of predicting specific subgroups of severely injured patients who would be more prone to have gastrointestinal complications. During the first 6 days after injury, there was no significant association (correlation coefficient not significant at the 0.05 level of significance) of the presence of an intracranial mass lesion, elevated intracranial pressure, brain stem dysfunction or prior episodes of hypotension or hypoxia, sepsis, shock, or the requirement for pressor agents with elevated gastric acid output, mucosal erosion, or hemorrhage. Because no specific risk factor or factors could be identified, all severely brain-injured patients should be on some form of therapy for the prevention of gastrointestinal complications.

Adult↗
PubMed2005

[Extrahepatic cholestasia during therapy with Zolmitriptan (AscoTop)].

Because of recurrent abdominal pain, jaundice and elevated liver function tests, a sixty-two-year old man had been referred to hospital several times within the preceding six months. By means of ultrasonography, endoscopic retrograde cholangiopancreatography (ERCP) and magnetic resonant cholangiopancreatography, dilated extrahepatic bile ducts were diagnosed. Stones and a tumorous process were excluded. ERCP showed hypermotility of the upper gastrointestinal tract. Quantitative hepatobiliary scintigraphy demonstrated retention of activity in the intra- and extrahepatic bile ducts and delayed transit of activity to the duodenum as signs of papillary dysfunction. Drug anamnesis revealed that the patient had started migraine treatment with Zolmitiptan, a 5-HT (1B/1D)-receptor agonist of the second generation, six months before the beginning of the cholestasia syndrome. Because of the known increase in amplitudes of oesophageal motor waves and of lower oesophageal sphincter tone by Sumatriptan, a 5-HT (1B/1D)-receptor agonist of the first generation, Zolmitriptan treatment was stopped. Thereupon, laboratory findings normalised and the patient has been feeling well for more than one year. Serotonin is an important monamine neurotransmitter that acts both in the CNS and in the gastrointestinal tract on identical receptors and is transported by the same systems. Thus it is not surprising that therapeutic measures which influence the serotoninergic system in the CNS are also effective in the enteric nervous.

Bile Ducts, Extrahepatic↗
PubMed1987

Cord blood serum creatine kinase isoenzymes with placental dysfunction.

It has been suggested that perinatal asphyxia is not generally followed by neurological impairment unless there is preexisting chronic fetal distress. In cases of brain damage one can observe elevated levels of CK-BB. The purpose of our study was to evaluate CK isoenzymes in umbilical cord blood sera of newborns affected by chronic fetal distress. Fetal distress reflected by placental dysfunction was characterized by a diminished HPL level and decreased activity of CAP. We estimated CK isoenzymes with the use of DEAE-sepharose CL-6B column chromatography. Total CK activity was measured using kits supplied by Boehringer-Mannheim (Monotest CK-NAC aktiviert). The clinical state of examined newborns was estimated. Investigations were carried out in the group of 57 infants delivered after 37 weeks of gestation. Total CK activity in cord sera ranged from 40 to 400 U/l. Our results showed a significant rise of CK-BB activity in cord sera of newborns delivered from pregnancies with placental dysfunction (figure 2) as well as in cases of asphyxiated infants (figure 3). We were unable to demonstrate differences in total CK, CK-MM and CK-MB activities in all examined groups of newborns. Other authors have confirmed that severe asphyxia results in increase in CK-BB activity in cord blood. Infants with ominous fetal heart rate patterns have higher CK-BB activity. There are several possible sources for CK-BB activity in umbilical cord blood sera, i.e. fetal brain, lung, gastrointestinal tract, placenta and uterus. It appears that the brain is most likely the source of elevated CK-BB activity found in cord blood in cases of placental dysfunction.

Asphyxia Neonatorum↗
PubMed2000

Gastrointestinal and segmental colonic transit times in patients with acute and chronic spinal cord lesions.

STUDY DESIGN: Longitudinal study among patients with acute and chronic spinal cord injuries (SCI). OBJECTIVES: To compare total gastrointestinal transit times (GITT) and segmental colorectal transit times (CTT) in SCI patients with acute and chronic lesions to those of healthy volunteers. Furthermore, to examine the impact of time elapsed since injury on GITT and CTT, and finally to compare the pattern of colorectal dysfunction in patients with supraconal versus conal/cauda equina lesions. SETTING: Surgical Research Unit and Department of Neurosurgery, University Hospital of Aarhus, Denmark. METHODS: Patients took 10 radioopaque markers on six consecutive days and an abdominal X-ray was taken on day 7. GITT and CTTs were computed from the number of markers in the entire colorectum and in each colorectal segment respectively. We studied 26 patients with acute spinal cord lesions (15 supraconal and 11 conal/cauda equina lesions; time since injury=11 - 24 days) and 18 patients were available for follow-up 6 - 14 months later. Results were compared to 24 healthy volunteers. RESULTS: In patients with acute supraconal or conal/cauda equina lesions GITT and CTTs of the ascending, transverse, and descending colon were significantly prolonged, but rectosigmoid transit time was only significantly prolonged in patients with conal/cauda equina lesions. In patients with chronic supraconal lesions GITT and CTTs of the transverse colon and the descending colon were significantly prolonged. In patients with chronic conal/cauda equina lesions GITT and CTT of the transverse, the descending colon and the rectosigmoid were significantly prolonged. Thus, supraconal SCI resulted in generalized colonic dysfunction whereas chronic conal/cauda equina lesions resulted in severe rectosigmoid dysfunction. CONCLUSION: SCI results in severely prolonged colonic transit times both in the acute and chronic phase. However, the type of colorectal dysfunction depends on the level of SCI.

Acute Disease↗
PubMed2002

Neuronal control in gastrointestinal disease.

This short review is based on only a small selected sample of research to illustrate the wide variety of cellular mechanisms that underlie the neural basis of digestive diseases. The enteric nervous system and its effector cells are involved in the control of most gastrointestinal activities. The review summarises the neural mechanisms involved in normal and abnormal gastrointestinal functions. The gastrointestinal tract is exposed to a tremendous variety of foreign substances including those ingested with food and those produced by the extensive commensal and pathological bacterial flora. Normal functions controlled by the enteric neural circuits are well adapted to distinguish nutrients from harmful stimuli. The main enteric neural circuits have been identified in experimental animals and are being investigated in humans. The enormous variety of motor patterns observed in normal gastrointestinal tract is the result of interplay of a few fundamental mechanisms, including myogenic mechanisms; neurogenic accommodation, neurogenic propulsive mechanisms and migrating neurogenic motor activity. Motor dysfunctions of the gut are likely to be caused by abnormalities of one or more of these mechanisms. Disturbances of enteric neural functions can arise from physiological defence reactions to harmful insults, from abnormal activation of physiological circuits, or from pathological alterations of the enteric circuits. Vomit and expulsive propulsion and inflammation or bacteria neurally induced changes in motility are physiological defence mechanisms. Pathological alterations include toxic, autoimmune, genetic lesions also secondary to systemic diseases and can be partial and graded.

Adaptation, Physiological↗
PubMed1985

Treatment of bleeding esophageal varices by portoazygos disconnection and esophageal transection with the button of Boerema and EEA stapler: ten years' experience.

We present 64 patients with bleeding esophageal varices who have been treated with portoazygos disconnection, devascularization of the esophagogastric junction, and esophageal transection with the button of Boerema (32 patients) and EEA stapler (32 patients). The patients were treated between 1973 and 1983. Their ages ranged from 50 to 70 years. Based on Child's classification, 26 (37.5%) of the patients fell into class A, 35 (54.6%) in class B, and five (7.8%) in class C. These patients were also divided into three subgroups: group I--21 patients (32.8%) underwent emergency operations; group II--40 patients (62.5%) underwent semiemergency operations; and group III--three patients (4.7%) underwent elective operations. The perioperative mortality rate was 10.8%. With the Fischer exact test, we found the combined death rate of Child's classes A and B to be significantly lower than that for class C patients. The duration of follow-up ranged from 6 months to 9 years (average 32.9 months) in the 80% of the patients that we were able to follow. There was a 6.5% incidence of recurrent gastrointestinal bleeding and a 28% incidence of late encephalopathy. The incidence of transitory dysphagia was 40% when the button of Boerema was used as compared with 9% when the EEA stapler was used. The surgical approach presented herein is an attractive alternative to portosystemic decompression for patients in whom hepatic dysfunction is complicated by uncontrolled variceal hemorrhage.

Aged↗
PubMed1985

Side effects and complications of amiodarone therapy.

To assess the incidence of adverse effects associated with long-term amiodarone therapy, we reviewed the records of 217 consecutive patients who were treated for refractory arrhythmia. After an average of 11.8 months of therapy, one or more side effects occurred in 113 patients (52%). These were considered clinically significant in 42 patients (19.3%), mandating discontinuation of amiodarone in 18 (8.3%). The untoward reactions requiring discontinuation of amiodarone included thyroid dysfunction, visual disturbances, pulmonary infiltrates, ataxia, cardiac conduction abnormalities, and drug interactions. The mild side effects included corneal microdeposits, skin rashes, and gastrointestinal symptoms. There was a weak correlation between blood levels of amiodarone, the daily dose, and the cumulative dose (r = 0.23, p = 0.015). Drug levels were higher in symptomatic patients (p less than 0.03), although they received lower doses of amiodarone. While amiodarone is associated with frequent side effects, they are generally mild and do not necessitate drug discontinuation. Careful monitoring of therapy is essential to detect the potentially serious adverse reactions which are encountered in nearly 20% of patients.

Amiodarone↗
PubMed2004

Microbial-gut interactions in health and disease. Irritable bowel syndrome.

The intestinal microbiota interacts with several aspects of gastrointestinal function that may affect the expression or progression of disease. For example, a role for bacterial metabolism of bile acids and food has been linked to colorectal cancer development. Studies have also shown a potential role of the intestinal microbiota in the modulation of inflammation in the intestine and joints. Normal gut physiology is molded by the interaction between the intestinal microbiota and the host's gastrointestinal tissues, including motility, absorption and secretion, and intestinal permeability. Early studies in axenic mice demonstrated gross morphological abnormalities and gut motor dysfunction related to the absence of a normal microflora, raising the possibility that shifts in commensal bacterial populations could play a role in the development of altered motility states including functional disorders of the gut. This chapter concentrates on the experimental evidence for a role of intestinal microbiota and the potential therapeutic value of probiotics in functional diseases such as irritable bowel syndrome.

Animals↗
PubMed1995

A prospective controlled evaluation of endoscopic detection of angiodysplasia and its association with aortic valve disease.

BACKGROUND: In view of controversy about the association of aortic stenosis and angiodysplasia of the gut, we performed a prospective, controlled study to evaluate the relationship between aortic valve disease and gastrointestinal angiodysplasia. METHODS: Forty patients who had endoscopy for clinical indications such as gastrointestinal bleeding, anemia, polyps, colon cancer, and dyspepsia, and who were found to have angiodysplasia of the gastrointestinal tract, underwent two-dimensional and Doppler echocardiography. Thirty-seven controls matched for age, sex, indication, and nature of endoscopic examination, but without angiodysplasia, underwent similar echocardiographic examination. RESULTS: None of the patients in either group had aortic stenosis. The prevalence of aortic sclerosis, aortic insufficiency, and low left ventricular ejection fraction was similar in patients with and without angiodysplasia. CONCLUSIONS: This study does not support the role of aortic valve disease as the cause of angiodysplasia of the gastrointestinal tract. A subgroup of patients with angiodysplasia with aortic sclerosis, with or without other valvular disease (but none with aortic stenosis), had increased prevalence of gastrointestinal bleeding when compared with controls. When aortic valve disease or decreased left ventricular ejection fraction were analyzed as independent predictors, none of them in and of itself appeared to be a factor in bleeding from these gastrointestinal lesions.

Aged↗