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 91 records · Page 5Linked to original sources
PubMed1992

[Gastrointestinal motility and autonomic nerve dysfunction].

Gastrointestinal motility is greatly influenced by both the autonomic nervous system (ANS) and the enteric nervous system (ENS). Dysfunction of ANS and/or ENS produces various kinds of dysmotility from the esophagus to the colon. Generalized autonomic dysfunction, often seen in diabetics, causes abnormal peristaltic waves in the esophagus, abnormal electrical activity of the stomach, delayed gastric emptying and delayed intestinal transit. Localized disorders of the enteric nervous system is seen in patients with achalasia and Hirschsprung's diseases. Functional disorders, without evidence of organic disorders, like non-cardiac chest pain, non-ulcer dyspepsia, irritable bowel syndrome, can be partly caused by abnormal function of autonomic nervous system.

Autonomic Nervous System↗
PubMed1975

Structure and function of the gastrointestinal tract in primary immunodeficiency syndromes (IDS) and in granulocyte dysfunction.

Gastrointestinal (GI) disease is frequently encountered in patients with defective defense mechanisms. The incidence of GI disease and the structure and function of the GI tract have been studied systematically in 41 patients with immunodeficiency syndromes (IDS) and in 9 patients with chronic granulomatous diesase (CGD). Giardia lamblia was a major cause of GI disease in patients with IDS. Eradication of the parasite resulted in disappearance of symptoms and malabsorption, and normalization of the villus architecture. Six of 9 patients with CGD had either GI symptoms or malabsorption or both. Typical histologic changes were found in the small intestinal and rectal mucosa of all patients biopsied.

Carotenoids↗
PubMed1988

Paraneoplastic visceral neuropathy as a cause of severe gastrointestinal motor dysfunction.

The purpose of this study was to define the cause of severe gastrointestinal motor dysfunction in 7 patients with lung cancer. Six patients had small cell carcinoma and 1 patient had pulmonary carcinoid. Their ages ranged from 58 to 74 yr. All had intestinal pseudoobstruction and obstipation/constipation; 6 of 7 patients had gastroparesis; 4 of 4 patients had esophageal peristaltic abnormalities; and 2 patients had neurogenic bladders, autonomic insufficiency, and peripheral neuropathy. Five of 7 patients had dilated small bowel with 4 of them showing slow transit of barium; 2 of 7 patients had dilated colons; and 3 of 7 patients had slow colonic transit. Five patients died 4-9 mo after onset of gastrointestinal symptoms, and 2 survived. Post-mortem or surgical samples of the esophagus, stomach, small bowel, and colon showed neuron and axon degeneration and dropout, lymphoplasmacytic infiltration, and glial cell proliferation within the myenteric plexus of 6 patients. The antrum from the seventh patient had inflammatory cells within the myenteric plexus but without neuron dropout. Neuron numbers were significantly less than normal in each area of the gastrointestinal tract. Thus, we conclude that lung cancer may be complicated by severe gastrointestinal motor dysfunction resulting from visceral neuropathy of the myenteric plexus, a paraneoplastic effect of the cancer.

Aged↗
PubMed1994

Gastrointestinal tract dysfunction in critical illness: pathophysiology and interaction with acute lung injury in adult respiratory distress syndrome/multiple organ dysfunction syndrome.

The adult respiratory distress syndrome (ARDS), a common complication of critical illness, is associated with a > 50% mortality rate. Refractory respiratory failure is, however, an uncommon cause of mortality in these patients. Most deaths are due to a syndrome of relentless organ dysfunction accompanied by abnormal organ system interactions, collectively referred to as the multiple organ dysfunction syndrome (MODS). MODS is associated with two chief pathophysiologic derangements: a) the unregulated activation of systemic inflammatory cascades; and b) alterations of oxygen uptake (VO2)-oxygen delivery (DO2) relationships. Current concepts regarding the pathophysiology of MODS, specifically its relationship to unregulated systemic inflammation and alterations in VO2-DO2 alterations, are discussed. Within this framework, current and future areas for investigation that may result in mechanism-specific innovations with the potential to interrupt events mediated by gastrointestinal dysfunction that lead to MODS are presented.

Animals↗
PubMed2002

Effects of Kampo medicine, keishi-ka shakuyaku-to (TJ-60) on alteration of diacylglycerol metabolism in gastrointestinal smooth muscle of diabetic rats.

AIM: To examine the effects of Kampo medicine, keishi-ka-shakuyaku-to (TJ-60) on the signal transduction in diabetic gastrointestinal dysfunction. METHODS: Experimental diabetic models were prepared using streptozotocin (STZ)-treated Wistar rats. Randomly selected STZ rats were treated with insulin (12 U/kg/d) or TJ-60 (1% of food intake). Diacylglycerol (DG) and DG kinase activities were quantified in isolated aortic smooth muscle tissue. RESULTS: One of the key element of the PI-turnover, DG kinase activity in resting state in gastric smooth muscle was significantly increased compared to the control value, and carbachol (CCh)-induced response was not detectable, but it was detected in the control rats. On the other hand resting activity in ileum did not differ from the control, but the CCh-induced responses were suppressed. Treatment with TJ-60 indicated resistant effects for the alteration of DG kinase activities in diabetic intestinal tissues. In order to reveal the mechanism of the effects, total content of DG was measured, because the DG plays important role in the PI-turnover and the DG converted from not only PI but also incorporated glucose under high glucose condition. Patterns of the change in DG levels were similar to those in DG kinase. These results indicate that the effect of TJ-60 occurs at the cellular level of DG. CONCLUSION: Dysfunction of gastrointestinal smooth muscle in diabetes is mediated by an alternation of DG and DG kinase. TJ-60 influences the alteration and relief the dysfunction.

Animals↗
PubMed1998

Identification of tryptophan hydroxylase as an intestinal autoantigen.

BACKGROUND: Autoimmune polyendocrine syndrome type 1 (APS1) is an autosomal recessive disorder with both endocrine and non-endocrine features. Periodic gastrointestinal dysfunction occurs in 25-30% of APS1 patients. We aimed to identify an intestinal autoantigen. METHODS: A human duodenal cDNA library was immunoscreened with serum samples from APS1 patients. A positive clone was identified and used for in-vitro transcription and translation, followed by immunoprecipitation with serum samples from 80 APS1 patients from Norway, Finland, and Sweden. Sections of normal and APS1-affected small intestine were immunostained with serum from APS1 patients and specific antibodies. An enzyme-inhibition assay was used to characterise the autoantibodies. FINDINGS: We isolated a cDNA clone coding for tryptophan hydroxylase. 48% (38/80) of APS1 patients had antibodies to tryptophan hydroxylase, whereas no reactivity to this antigen was detected in patients with other autoimmune diseases (n=372) or healthy blood donors (n=70). 89% (17/19) of APS1 patients with gastrointestinal dysfunction were positive for antibodies to tryptophan hydroxylase, compared with 34% (21/61) of patients with no gastrointestinal dysfunction (p<0.0001). Serum from antibody-positive APS1 patients specifically immunostained tryptophan-hydroxylase-containing enterochromaffin cells in normal duodenal mucosa. No serotonin-containing cells were seen in duodenal biopsy samples from APS1 patients. Serum from antibody-positive APS1 patients almost completely inhibited activity of tryptophan hydroxylase. INTERPRETATION: Tryptophan hydroxylase is an endogenous intestinal autoantigen in APS1, and there is an association between antibodies to the antigen and gastrointestinal dysfunction. Analysis of antibodies to tryptophan hydroxylase may be a valuable diagnostic tool to predict and monitor gastrointestinal dysfunction in APS1.

Adolescent↗
PubMed1993

Gastrointestinal regulatory peptides in systemic sclerosis.

OBJECTIVE: Gastrointestinal involvement commonly occurs in systemic sclerosis (SSc), but its pathogenesis is not well understood. Since there is evidence of a defect in neurotransmitter release, we were interested in examining the relationship between gastrointestinal dysfunction and plasma concentrations of gastrointestinal regulatory peptides in patients with SSc. We studied 43 consecutive patients, 18 with diffuse and 25 with limited cutaneous disease. METHODS: Levels of corticotropin-releasing hormone (CRH), gastrin, motilin, neuropeptide Y (NPY), and peptide YY (PYY) were determined by radioimmunoassay and high-performance liquid chromatography (HPLC). RESULTS: Plasma concentrations of CRH, motilin, NPY, and PYY were significantly increased among SSc patients compared with healthy control subjects, and HPLC-characterization of motilin, NPY, and PYY showed a different pattern of fragments. No correlation was found between esophageal hypomotility and the concentration of peptide. Acid output did not correlate with gastrin levels, but was more often increased in patients with increased CRH and NPY values. Fat malabsorption, assessed by the triolein breath test, was more common among patients with increased motilin and PYY. CONCLUSION: This study shows that elevated peptide concentrations commonly occur in patients with SSc. Since regulatory peptides are involved in gastrointestinal motility, secretion, and absorption, further characterization of this neuroendocrine system may help in understanding the complex regulation of gastrointestinal dysfunction in SSc.

Adult↗
PubMed2003

Overview of functional gastrointestinal disorders: dysfunction of the brain-gut axis.

Functional gastrointestinal disorders are common and incompletely understood. The gut is controlled by a complex interaction of sensory and motor neurons in the local enteric nervous system. Inputs from the central nervous system modify gut function, whereas inputs from the gut to the brain mediate symptoms. Dysfunction at one or more sites in the brain-gut axis is likely to produce the various functional gastrointestinal syndromes. Therapies likewise can be directed at one or more levels.

Autonomic Nervous System↗
PubMed2002

[Gastrointestinal tract dysfunction in critical illness].

Until relatively recently, the gastrointestinal (GI) tract was considered a dormant, metabolically and immunologically inactive organ in critically illnesses. However, the GI tract provides a number of crucial functions that, in fact, may influence morbidity and mortality of many critically ill patients. Its large absorptive area provides a site for nutrient digestion and utilization and serves as an important barrier preventing the systemic absorption of intraluminal microbes and its toxic products. Moreover, the GI tract is the largest reservoir of lymphocytes in the body, which significantly contribute to the immune response of the critically ill patients. The gut dysfunction occurs frequently and early in the intensive care patients. Abnormal colonization, impaired intestinal epithelial barrier function and bacterial translocation represent the key components of gut failure implicating in the pathogenesis of sepsis and multiorgan dysfunction. This review summarizes recent insights into the role of the gut in critically ill patients with particular focus on 1) the basis of "gut-origin hypothesis", 2) pathophysiology of gut dysfunction, 3) monitoring of intestinal function, and 4) protective measures and novel therapeutic strategies.

Bacterial Translocation↗
PubMed1995

Highly variable gastric emptying in patients with insulin dependent diabetes mellitus.

Some diabetic patients--particularly those with nausea and vomiting--frequently have evidence of delayed gastric emptying while other diabetic patients may in fact exhibit accelerated gastric emptying. Whether the presence or absence of symptoms of upper gastrointestinal dysfunction correlated with objective measures of gastric emptying in insulin dependent diabetic subjects was investigated. Twenty one insulin dependent diabetic patients underwent a solid phase gastric emptying scintiscan using in vivo labelled chicken liver. Thirteen patients had symptoms suggestive of gastrointestinal dysfunction (nausea, vomiting, early satiety, or constipation), while eight patients had no gastrointestinal symptoms. Eleven patients had orthostatic hypotension. All patients had been diabetic since childhood or adolescence. As a group, the diabetic patients showed a half time (T50) of gastric emptying (mean (SD) 150.0 min (163.7) that was not significantly different from that of 12 healthy control subjects (148.1 min (62.4)). Those diabetic patients without gastrointestinal symptoms and without orthostatic hypotension, however, showed a gastric emptying half time (70.1 min (41.6)) that was significantly faster than that of the control subjects. Conversely, those diabetic patients with nausea, vomiting, and early satiety (or early satiety alone) showed T50 values that were significantly greater than those of the diabetic patients without these symptoms. No correlation was found between the T50 value and the duration of diabetes, the fasting blood glucose at the time of study, or the respiratory variation in heart rate (E:I ratio). These observations indicate that highly variable rates of gastric emptying occur in insulin dependent diabetic patients, and that accelerated gastric emptying may occur in diabetic patients who have no symptoms of gastrointestinal dysfunction.

Adult↗
PubMed1993

Autonomic dysfunction in gastrointestinal motility disorders.

The records of 113 consecutive patients with a suspected gastrointestinal motility disorder referred between January 1988 and July 1991 were retrospectively reviewed. The aims were to identify the prevalence of autonomic dysfunction in those with or without associated neurological disease and to determine the diagnostic value of testing for autonomic dysfunction. All patients had gastrointestinal manometry (3 hours fasting, 2 hours fed), 94 of 113 underwent testing of sympathetic adrenergic and cholinergic function and cardiovagal cholinergic function. All tests were scored in a standard manner. There was a significant (p < 0.05) but modest (r = 0.28) rank correlation between autonomic and motility scores. This correlation was stronger (r = 0.67, p = 0.01) in diabetic patients. The number of patients in each group with autonomic dysfunction was as follows: irritable bowel syndrome nine of 33, idiopathic upper gastrointestinal dysmotility six of 21, diabetes mellitus nine of 13, identified non-diabetic neurological syndromes six of nine, postvagotomy or abdominal surgery three of 11, and myopathic pseudo-obstruction two of seven. Autonomic testing is useful in the assessment of autonomic involvement outside the gastrointestinal tract. Logistic discriminant analysis showed that autonomic function testing did not add to the diagnostic value of motility tests in distinguishing between patients with and without irritable bowel syndrome, although a slight improvement was indicated for identifying neuropathic dysmotilities. Thus, the aetiological role of general autonomic dysfunction in irritable bowel syndrome and idiopathic and postvagotomy dysmotilities deserves further study. The addition of autonomic function tests does not add substantially to the diagnostic accuracy of clinical, radiological, endoscopic, and manometric techniques in most patients referred for evaluation of a suspected motility disorder.

Autonomic Nervous System Diseases↗
PubMed2000

Diarrhea and abnormalities of gastrointestinal function in a cohort of men and women with HIV infection.

OBJECTIVE: The aim of this study was to determine the prevalence of gastrointestinal dysfunction in the era of improved treatment of HIV infection. METHODS: Gastrointestinal function was studied cross-sectionally in 671 persons with HIV. Absorptive function was measured by a 25-g D-xylose test, a Sudan-III stain for fecal fat on a 100-g fat diet, and serum levels of micronutrients. RESULTS: Eighty-eight percent had at least one abnormality of gastrointestinal function: 47.7% had low D-xylose absorption; 40.3% had a history of liver disease; 38.9% had diarrhea; 28.3% had chronic diarrhea; 22.5% had borderline or low serum vitamin B12 levels; 12.2% had stool pathogens; and 7.2% were hypoalbuminemic. Men were more likely to have low D-xylose absorption, diarrhea, and stool pathogens than women. Intravenous drug users (IVDUs) were more likely to have a history of liver disease and hypoalbuminemia. However, borderline or low vitamin B12 levels were less frequent in IVDUs; they tended to have less diarrhea and a lower prevalence of stool pathogens. Despite less history of liver disease, 14.1% of women were hypoalbuminemic. Differences in patterns of gastrointestinal dysfunction are unlikely to be due to severity of immunosuppression as abnormalities were seen in all risk groups with CD4 >200 cells/mm3. D-xylose absorption below 30 mg/dl, current diarrhea, and borderline levels of vitamin B12 were associated with advanced immunosuppression. CONCLUSIONS: Abnormalities of gastrointestinal function are common in the current era of HIV treatment, appear early in the course of HIV infection, and in the absence of diarrhea. Gender and IVDU are important determinants of the type and frequency of gastrointestinal abnormalities.

Adult↗
PubMed1996

Gastrointestinal symptoms and diabetes mellitus in children and adolescents.

Because it may be difficult to evaluate gastrointestinal diseases in children with insulin-dependent diabetes mellitus (IDDM), this report highlights several clinical features unique to diabetes and emphasizes the relationship between gastrointestinal pathology and glycemic control. Two children with IDDM are described whose hyperglycemia, ketosis, and abdominal pain were the presenting features of H. pylori-positive duodenal ulcer disease and acute appendicitis, respectively. A third nondiabetic child developed persistent postprandial hyperglycemia as the initial manifestation of dumping syndrome. These patients illustrate the relationship between glycemic control and gastrointestinal pathology in children with diabetes and the effects of gastrointestinal dysfunction on glucose regulation in nondiabetic children. In children with IDDM, gastrointestinal pathology can be confused with ketoacidosis and complicate diabetes control and management. Early recognition and treatment of the underlying gastrointestinal disease often improves glycemic control. Furthermore, severe gastrointestinal dysfunction in nondiabetic children may deleteriously influence glycemic regulation and may be confused with childhood diabetes.

Adolescent↗
PubMed1991

Gastrointestinal motor dysfunction in acquired selective cholinergic dysautonomia associated with infectious mononucleosis.

This report documents the disturbance in gastrointestinal motor function in a patient with selective cholinergic dysautonomia that occurred following acute infectious mononucleosis. Apart from the gut, other organs affected included the pupils, sweat glands, lacrimal and salivary glands, and urinary bladder. Autonomic function tests showed the preservation of sympathetic adrenergic functions in contrast to the generalized involvement of postganglionic parasympathetic and sympathetic cholinergic nerves, including denervation hypersensitivity of the pupil and urinary bladder to exogenous cholinergic agonists. Cardiac and abdominal vagal responses were abnormal. Colon myenteric plexus ganglion cells were normal by morphological and immunohistochemical studies, suggesting that the selective cholinergic dysautonomia was the most likely pathophysiologic process responsible for the observed motility disorder. This study documents the occurrence of selective cholinergic dysautonomia following a viral illness, the importance of the extrinsic neural control on the motor function of the gastrointestinal tract, and the usefulness of combined motility and autonomic function testing in the evaluation of patients with symptoms suggestive of gut dysmotility.

Adult↗
PubMed2004

Disruption of intestinal motility by a calcium channel-stimulating autoantibody in type 1 diabetes.

BACKGROUND & AIMS: Autonomic neuropathy, including gastrointestinal dysfunction, is a common complication of type 1 diabetes; however, its cause is uncertain. This study aimed to test whether functional autoantibodies cause the gastrointestinal dysfunction. METHODS: We used isolated mouse colon undergoing colonic migrating motor complex (MMC) activity to test for autoantibodies that disrupt colonic motility. Purified immunoglobulin G (IgG) from patients with type 1 diabetes or from controls was tested either in vitro or after passive transfer. Pharmacological studies of the interaction between the IgG and L-type calcium channel activator (Bay K8644) and inhibitors (nicardipine and verapamil) were performed. The effect of IgG on nerve-evoked contraction of the vas deferens longitudinal smooth muscle was also assessed. RESULTS: MMC activity was disrupted by IgG (0.2 mg/mL) from 8 of 16 patients with type 1 diabetes but not by control IgG. Passive transfer of diabetic IgG to mice also disrupted MMCs, showing access to the antigen in vivo. The acute effect of the autoantibody was mimicked by the dihydropyridine agonist, Bay K8644 (2-10 nmol/L), and both Bay K8644 and the autoantibody competitively inhibited the effect on MMC contraction of the dihydropyridine antagonist, nicardipine. Diabetic IgG, but not control IgG, altered the nerve-evoked contractile activity of vas deferens smooth muscle effects mimicked by Bay K8644. CONCLUSIONS: A novel functional autoantibody that activates smooth muscle L-type calcium channels at the dihydropyridine binding site is produced specifically by patients with type 1 diabetes and may mediate gastrointestinal and autonomic dysfunction in these patients.

Adult↗
PubMed1996

Neurologic dysfunction in gastrointestinal disease.

The various disease processes described in this review by no means exhaust the list of GI diseases in which neurologic dysfunction may occur, but merely serve as a representative sampling. Recognition is often a function of awareness, and the growing knowledge of the rich interaction between GI and neurologic systems on many levels suggests that additional associations will be uncovered in the future.

Acute Disease↗