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 1,747 records · Page 97Linked to original sources

Massive noninflammatory periportal liver necrosis following concentrated acetic acid ingestion.

In a fatal occurrence of massive liver necrosis following ingestion of concentrated (90%) acetic acid, the patient showed evidence of hemolysis, disseminated intravascular coagulation, and liver dysfunction at only 45 minutes after exposure. With refractory to vigorous supportive care, the patient s condition deteriorated until death occurred 39 hours after ingestion, despite some improvement of coagulopathy. Autopsy revealed corrosive injuries in the upper gastrointestinal tract and massive hepatic necrosis in a periportal distribution without significant inflammation. A direct effect of the noxious agent on hepatocytes involving the portal circulation is suggested.

Acetic Acid↗

Regional blood flow during continuous low-dose endotoxin infusion.

Escherichia coli endotoxin (ET) was administered to adult rats by continuous IV infusion from a subcutaneously implanted osmotic pump (Alzet). Cardiac output and regional blood flow were determined by the radiolabeled microsphere method after 6 and 30 hr of ET or saline infusion. Cardiac output (CO) of ET rats was not different from time-matched controls, whereas arterial pressure was 13% lower after 30 hr of infusion. After both 6 and 30 hr of ET, pancreatic blood flow and percentage of cardiac output were lower than in controls. Estimated portal venous flow was decreased at each time point, and an increased hepatic arterial flow (significant after 30 hr) resulted in an unchanged total hepatic blood flow. Blood flow to most other tissues, including epididymal fat, muscle, kidneys, adrenals, and gastrointestinal tract, was similar between treatments. Maintenance of blood flow to metabolically important tissues indicates that the previously reported alterations in in vitro cellular metabolism are not due to tissue hypoperfusion. Earlier observations of in vitro myocardial dysfunction, coexistent with the significant impairment in pancreatic flow, raise the possibility that release of a myocardial depressant factor occurs not only in profound shock but also under less severe conditions of sepsis and endotoxemia.

Animals↗

Carnitine in human immunodeficiency virus type 1 infection/acquired immune deficiency syndrome.

There is an increasing body of evidence that subgroups of patients infected with human immunodeficiency virus type 1 possess carnitine deficiency. Secondary carnitine deficiencies in these individuals may result from nutritional deficiencies, gastrointestinal disturbances, renal losses, or shifts in metabolic pathways. However, tissue depletion precipitated by drug toxicities, particularly zidovudine, is a major etiology and concern. Carnitine deficiency may impact on energy and lipid metabolism, causing mitochondrial and immune dysfunction. There are convincing laboratory data showing the in vitro ameliorative effects of L-carnitine supplementation of zidovudine-induced myopathies and lymphocyte function. Studies measuring the impact of L-carnitine supplementation on clinical characteristics are ongoing.

Carnitine↗

[A case of systemic AA amyloidosis complicating Crohn's disease].

Although systemic AA amyloidosis complicating Crohn's disease has been found in 0.5 to 6% in America and Europe, it is relatively rare in Japan. We report a case of systemic AA amyloidosis complicating Crohn's disease. In 1979, a 26-year-old Japanese man presented with diarrhea, melena and perianal abscesses, and was diagnosed as having Crohn's disease. He was treated with oral prednisolone, salazosulfapyridine and diet therapy. However, the gastrointestinal symptoms recurred and he was hospitalized several times. In 1991, his thyroid gland was found to be swollen, but with normal thyroid function, and his thyroid gland became larger subsequently. In October 1995, he showed renal dysfunction (blood urea nitrogen 33.2 mg/dl; serum creatinine 1.5 mg/dl) with proteinuria. His renal function had been deteriorating rapidly. On September 13, 1996, he was admitted to the Tsukuba University Hospital. At the time of admission, his renal function showed a blood urea nitrogen of 129.5 mg/dl with a creatinine of 5.4 mg/dl. The urine contained 0.8 g of protein per 24 hours. He presented with diarrhea for several days before admission and was treated with central venous hyperalimentation. Despite supportive care, he developed end-stage renal failure, then hemodialysis was initiated on October 7. His condition was complicated by a complete auriculoventricular block on October 18. He died of hemoperitoneum on October 25. On postmortem examination, extensive amyloid deposits were found in multiple organs including kidneys, intestine, heart, thyroid gland, lungs, liver, spleen, pancreas, gall bladder, adrenal glands, testis, prostate, bone marrow and parathyroid glands. Analysis of amyloid protein in the autopsy specimens showed type AA.

Adult↗

Corticosteroids for acute ischaemic stroke.

BACKGROUND: Much of the brain swelling in ischaemic stroke is due to cytotoxic oedema, which is related to cell membrane dysfunction. Early treatment with corticosteroids may help reduce the swelling and improve the outcomes after a stroke. OBJECTIVES: The objective of this review was to assess the effect of corticosteroids in acute presumed ischaemic stroke. SEARCH STRATEGY: We searched the Cochrane Stroke Group trials register and contacted investigators in the field. SELECTION CRITERIA: Published randomised trials comparing corticosteroids with placebo or control in people with acute (presumed or definite) ischaemic stroke. Trials were included if treatment began within 48 hours of stroke onset and if clinical outcome was assessed. DATA COLLECTION AND ANALYSIS: Two reviewers independently applied the inclusion criteria, assessed trial quality and extracted the data. MAIN RESULTS: Seven trials involving 453 people were included. Details of trial quality that may relate to bias were not available from most trials. No difference was shown in the odds of death within one year (odds ratio 1.08, 95% confidence interval 0.68 to 1.72). Treatment did not appear to improve functional outcome in survivors. Six trials reported neurological impairment but pooling the data was impossible because no common scale or time interval was used. The results were inconsistent between individual trials. The only adverse effects reported were small numbers of gastrointestinal bleeds, infections and deterioration of hyperglycaemia across both groups. REVIEWER'S CONCLUSIONS: There is not enough evidence to evaluate corticosteroid treatment for people with acute presumed ischaemic stroke.

Anti-Inflammatory Agents↗

The function of 5-HT3 receptors on colonic transit in rats.

The function of serotonin (5-HT)3 receptors on colonic transit was investigated in unanesthetized rats. The colonic transit was accelerated by 5-HT (10 mg/kg, s.c.), 2-methyl-5-HT (30 mg/kg, s.c.), neostigmine (0.03-0.1 mg/kg, s.c.), corticotropin releasing factor (CRF; 1 microgram intracerebroventricular administration) and restraint stress (for 45 minutes). A potent and selective 5-HT3 receptor antagonist, azasetron (+/-)-N-(1-azabicyclo[2.2.2]oct-3-yl)-6-chloro- 4-methyl-3-oxo-3,4-dihydro-2H-1,4-benzoxazine-8-carboxamide monohydrochloride ; 0.01-10 mg/kg, p.o. inhibited the 5-HT-, CRF- and stress-accelerated colonic transit in a dose-dependent manner. Ondansetron (10 mg/kg, p.o.) and granisetron (1 mg/kg, p.o) also inhibited the stress-accelerated colonic transit, but azasetron was more effective than these two drugs. Atropine methylbromide (0.1 mg/kg, s.c.) and tetrodotoxin (0.01 mg/kg, s.c.) inhibited the accelerated colonic transit under stress conditions, but methysergide (10 mg/kg, s.c.), SDZ205-557 (10 mg/kg, s.c.), domperidone (30 mg/kg, p.o.), trimebutine (300 mg/kg, p.o.), did not. Azasetron (10 micrograms) administered intracerebroventricularly did not inhibit the stress-induced acceleration. These results suggest that endogenous 5-HT which is released through stress accelerates the colonic transit via the 5-HT3 receptors and finally a cholinergic mechanism. It is considered that azasetron inhibits colonic transit particularly under stress conditions through the blockade of the peripheral 5-HT3 receptors. Azasetron may improve bowel function in stress-related colonic dysfunction like irritable bowel syndrome.

Animals↗

Disordered swallowing due to a syrinx: correction by shunting.

Disturbed deglutition is common in diseases of the brainstem and lower cranial nerves, but little is known about the mechanisms involved. We studied a 49-year-old man with symptoms of syringomyelia and syringobulbia lasting 7 years. Esophageal motility studies showed inability to initiate swallowing, esophageal hypomotility, and absence of the lower esophageal sphincter. After decompression of the syrinx by shunting, these abnormalities were corrected, and the patient could once again eat without aspiration. Medullary dysfunction caused by the syrinx was probably responsible for the swallowing difficulties.

Brain Diseases↗

[Relation between pyloric dysmotility and serum levels of gastrin, somatostatin and vasoactive intestinal polypeptide in patients with non-insulin dependent diabetes mellitus].

Serum levels of gastrin, somatostatin and vasoactive intestinal polypeptide were evaluated in 105 noninsulin dependent diabetics (25 of them had a pyloric dysfunction). The serum levels were determined by RIA and blood was taken before and after the test meal. The basal gastrin level was significantly higher in patients with the pyloric dysfunction (p < 0.001). 45 minutes later the serum levels of vasoactive intestinal polypeptide and somatostatin were significantly higher in diabetics with the pyloric dysfunction (p < 0.001). The serum levels of gastrin, somatostatin and vasoactive intestinal polypeptide were impaired in diabetics with the pyloric dysfunction and might be associated with its pathogenesis.

Diabetes Mellitus, Type 2↗

Feeding problems in cystinosis.

Nephropathic cystinosis, a rare autosomal recessive storage disease characterized by intracellular storage of free cystine due to a defect in lysosomal cystine transport, is the most common cause of Fanconi syndrome in childhood. Although manifestations of extrarenal organ involvement during the course of the disease are diverse, the spectrum of gastrointestinal (GI) problems has not yet been examined. In responses to a questionnaire from 70 (35%) of the 200 registered members of the Cystinosis Foundation, we found that GI symptoms are more common, more diverse, and occur at a younger age in patients with cystinosis than previously recognized. Ninety-three percent of interviewed subjects had GI symptoms at initial presentation, and the overall lifetime prevalence of GI problems in this group was 100%. Thirty percent have received gastric/jejunal tube feedings, and 7% required continuous or intermittent total parenteral nutrition. Fifty percent have been formally tested for GI abnormalities, and among these 77% have documented functional abnormalities (reflux/dysmotility, pseudo-obstruction, swallowing dysfunction). Early recognition and aggressive therapy of GI problems in cystinotic patients may ameliorate or prevent the development of disabling symptoms.

Adolescent↗

Haemostatic dysfunction and acute renal failure following envenoming by Merrem's hump-nosed viper (Hypnale hypnale) in Sri Lanka: first authenticated case.

A five years old boy was bitten by a Merrem's hump-nosed viper (Hypnale hypnale) in Central Province, Sri Lanka. He developed local swelling, incoagulable blood, thrombocytopenia, bleeding into the gastrointestinal tract, and acute renal failure. Treatment with Serum Institute of Indian polyspecific antivenom (specific for venoms of cobra, common krait, Russell's viper and saw-scaled viper) had no effect on the coagulopathy, which persisted for more than a week. The boy recovered after 27 d in hospital, during which he was treated with peritoneal dialysis for renal failure. Laboratory studies demonstrated that the venom of H. hypnale was procoagulant, fibrinolytic and aggregated platelets. This first authenticated case of life-threatening acute renal failure and haemostatic disturbances caused by H. hypnale, a species responsible for 27% of snake bites in Sri Lanka, demonstrates the need for a new antivenom with specific activity against the venom of this species.

Acute Kidney Injury↗

Status evaluation: sphincter of Oddi manometry. American Society for Gastrointestinal Endoscopy. Technology Assessment Committee.

SO manometry appears to be helpful in defining a group of patients with biliary pain or idiopathic recurrent pancreatitis who may benefit from endoscopic or surgical treatment. It is a procedure that requires considerable time and endoscopic expertise along with knowledge of the manometric interpretation of sphincter of Oddi dysfunction. The diagnostic accuracy of SO manometry and criteria for basing therapeutic decisions on manometric findings need further study and verification.

Biliary Tract Diseases↗

Concomitant manifestation of achalasia and sphincter of Oddi dysfunction.

We report the case of a 44-year-old woman who suffered from biliary-type pain after cholecystectomy, dysphagia, and weight loss. Examinations revealed sphincter of Oddi dysfunction (SOD) and achalasia. Complete relief of symptoms was achieved by endoscopic sphincterotomy and pneumatic dilation of the distal esophagus. This case report demonstrates for the first time the concomitant manifestation of two motility disorders of the upper gastrointestinal tract, i.e. achalasia and SOD. At present, any causal relationship seems speculative; however, both diseases were successfully treated using endoscopic procedures.

Adult↗

FAT10 plays a role in the regulation of chromosomal stability.

Aneuploidy is a key process in tumorigenesis. Dysfunction of the mitotic spindle checkpoint proteins has been implicated as a cause of aneuploidy in cells. We have previously reported that FAT10, a member of the ubiquitin-like modifier family of proteins, is overexpressed in several gastrointestinal and gynecological cancers. Here we show that FAT10 interacts with MAD2, a spindle checkpoint protein, during mitosis. Notably, we show that localization of MAD2 at the kinetochore during the prometaphase stage of the cell cycle was greatly reduced in FAT10-overexpressing cells. Furthermore, compared with parental HCT116 cells, fewer mitotic cells were observed after double thymidine-synchronized FAT10-overexpressing cells were released into nocodazole for more than 4 h. Nonetheless, when these double thymidine-treated cells were released into media, a similar number of G1 parental and FAT10-overexpressing HCT116 cells was observed throughout the 10-h time course. Additionally, more nocodazole-treated FAT10-overexpressing cells escape mitotic controls and are multinucleate compared with parental cells. Significantly, we observed a higher degree of variability in chromosome number in cells overexpressing FAT10. Hence, our data suggest that high levels of FAT10 protein in cells lead to increased mitotic nondisjunction and chromosome instability, and this effect is mediated by an abbreviated mitotic phase and the reduction in the kinetochore localization of MAD2 during the prometaphase stage of the cell cycle.

Aneuploidy↗

Wireless oesophageal pH monitoring: feasibility, safety and normal values in healthy subjects.

OBJECTIVE: A new wireless technique for oesophageal pH monitoring has recently been introduced (Bravo). To implement this technique in clinical practice, values of normal oesophageal acid exposure need to be defined in a large age- and gender-matched healthy population. The aims of this study were to investigate the feasibility and safety of the wireless technique and to establish normal values for oesophageal acid exposure. MATERIALS AND METHODS: Fifty-seven asymptomatic subjects underwent upper gastrointestinal endoscopy with transoral placement of a radio-transmitting capsule 6 cm above the squamocolumnar junction. Oesophageal acid exposure was monitored via a portable receiver during 48 h. RESULTS: Seven men were excluded from the study: capsule dysfunction in 1 and oesophagitis in 6. Fifty subjects (25 M, 25 F, median age 42 years) were included in the study. The radio-transmitting capsule was successfully attached to the oesophageal mucosa in all cases and there were no complications. During pH monitoring 2 capsules were prematurely detached after 32 and 36 h, respectively. The median percentage time with oesophageal pH of less than 4 was 0.7% on day 1 and 1.0% on day 2 (p = 0.033) and the 95th percentile for the 48-h recordings was 4.4%. CONCLUSIONS: Ambulatory pH monitoring using the Bravo system is feasible and appears to be safe. This is the first study to establish normal values for oesophageal acid exposure in a large age- and gender-matched healthy population and offers a basis for the use of the wireless technique in clinical practice.

Adult↗

Intestinal pseudo-obstruction followed by major clinical features of Kawasaki disease: report of one case.

Kawasaki Disease (KD) or atypical KD (AKD) rarely presents with intestinal obstruction or pseudo-obstruction. Others have reported gastrointestinal symptoms appearing with and up to 4 weeks after the occurrence of major clinical symptoms of KD. However, we presented a 1-year-old boy with prolonged fever who was found to have pyuria and liver dysfunction on the fourth day of fever. He developed a picture of intestinal pseudo-obstruction including bilious vomiting and abdominal distention on his fifth day of fever, four days before he developed the fissured lips. Because of the emergence of four major clinical criteria of KD, coronary artery dilatation, and aseptic meningitis, AKD was initially diagnosed and prompted the use of intravenous immunoglobulin on the tenth day of fever. Hydrops of the gallbladder, leukocytosis, increased ESR, and thrombocytosis were noted during hospitalization. These atypical features rarely develop all together in one patient with KD or AKD. Nevertheless, our patient had early intestinal pseudo-obstruction with almost all of the above unusual systemic manifestations and the late occurrence of clinical features of KD. We demonstrate that intestinal pseudo-obstruction in KD may develop earlier than other major clinical features and may improve under the conservative treatment. Surgery should be reserved for those who have complete intestinal obstruction presenting with significant peritoneal signs.

Humans↗

[Digestive involvement of scleroderma].

Digestive involvement in systemic sclerosis is frequent and serious, because it provides morbidity and fatality. From the pathophysiologic point of view, the first step could be Raynaud-associated neural dysfunction, followed by smooth muscle atrophy then irreversible muscle fibrosis. Oesophageal disorder is common with its main consequence: the occurrence of gastroesophageal reflux disease which could run into peptic erosive oesophagitis. Oesophageal manometry is the main diagnostic tool, gastrointestinal endoscopy helps to assess oesophageal mucosal inflammation and its possible sequels. Gastric involvement is rarely recognized but it is frequent in case of systematic investigation as well as small intestinal involvement which may provide a lot of complications: malabsorption, pseudoobstruction, bacterial overgrowth. At colonic level, anorectal involvement is frequent and leads to fecal incontinence and rectal prolapse. Reynold's syndrome is a special case which associates systemic sclerosis with primary biliary cirrhosis. The symptomatic treatments must be systematic and improve the disease's overall prognosis.

Diagnosis, Differential↗

Enteral nutrition and hepatosplanchnic region in critically ill patients - friends or foes?

Enteral nutrition (EN) is a preferred way of feeding in critically ill patients unless obvious contraindications such as ileus or active gastrointestinal bleeding are present. Early enteral nutrition as compared to delayed EN or total parenteral nutrition decreases morbidity in postsurgical and trauma patients. The hepatosplanchnic region plays a pivotal role in the pathophysiology of sepsis and multiple organ dysfunction syndrome. The beneficial effects of EN on splanchnic perfusion and energy metabolism have been documented both in healthy volunteers and animal models of sepsis, hemorrhagic shock and burns. By contrast, EN may increase splanchnic metabolic demands, which in turn may lead to oxygen and/or energy demand/supply mismatch, especially when hyperemic response to EN is not preserved. Therefore, the timing of initiation and the dose of EN in patients with circulatory failure requiring vasoactive drugs are a matter of controversy. Interestingly, the results of recent clinical studies suggest that early enteral nutrition may not be harmful even in patients with circulatory compromise. Nevertheless, possible onset of serious complications, the non-occlusive bowel necrosis in particular, have to be kept in mind. Unfortunately, there is only a limited number of clinically applicable monitoring tools for the effects of enteral nutrition in critically ill patients.

Animals↗

[Riley-Day syndrome (familial dysautonomia)].

Riley-Day syndrome (RDS, familial dysautonomia) is reviewed from a viewpoint of autonomic disturbance. RDS shows pandysautonomia, including alacrima, orthostatic hypotension, gastrointestinal paresis, and paroxysmal hyperautonomic state, such as hypertension, vomiting crisis, and blotchy erythema. Sensory disturbances, including absence of taste and pain sensation, are common. Fungiform papillae on the tongue are sparse. Tests of autonomic function reveal postganglionic dysfunction. Sural nerve biopsy reveals depletion of small myelinated fibers and unmyelinated fibers, which corresponds well with the sensory and autonomic disturbances. As to the pathogenesis of RDS, dysgenesis of neurons from the neural crest or abnormality of nerve growth factor has been suggested, but this remains undetermined.

Autonomic Nervous System↗