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K D Bardhan

Publications and source records attributed to K D Bardhan.

At least 37 records · Page 2Linked to original sources
PubMed2002

Mesenteric afferent nerves are sensitive to vascular perfusion in a novel preparation of rat ileum in vitro.

Using novel in vitro preparations of vascularly perfused rat ileum, we investigated mesenteric afferent sensitivity to vascular perfusion. Gut (GPP) and vascular (VPP) perfusion pressures were recorded simultaneously with afferent discharge (AD). After preconstriction (L-phenylephrine), capsaicin (100 microM, gut lumen) caused a transient increase in AD and a sustained fall in VPP, supporting afferent modulation of vascular tone. In turn, AD was affected by vascular perfusion rate (VPR). Increasing VPR step-wise (0.6 to 1.0, 1.4 and 1.8 ml/min) caused concomitant falls in AD, returning at 0.6 ml/min. Terminating flow (5 min) increased AD. Afferent responses were independent of changes in GPP, vascular O2, or the gut "tube" ("gut-off"). In gut-off studies, where capsaicin (100 nM ia) still reduced VPP, flow-associated falls in AD were abolished by the enzyme neuraminidase (0.2 U/ml ia or extravascularly over 20 min). In contrast, increased AD after stopped flow was unaffected. We propose that mesenteric afferents "sense" changes in vascular perfusion. The precise stimuli (pressure and/or flow) and the physiological relevance to control of local circulation remain to be determined.

Animals↗
PubMed2001

Efficacy of rabeprazole once daily for acid-related disorders.

Proton-pump inhibitors (PPIs) have revolutionized the treatment of gastroesophageal reflux disease (GERD) and peptic ulcer. To evaluate the efficacy of the new PPI rabeprazole, 12 controlled clinical trials were conducted worldwide-three for each indication (erosive or ulcerative GERD healing, long-term GERD healing maintenance, duodenal ulcer healing, and gastric ulcer healing). Rabeprazole was compared to placebo, the H2-receptor antagonist ranitidine, and the PPI omeprazole. Treatment duration ranged from < or =4 weeks for duodenal ulcer to < or =6 weeks for gastric ulcer, < or =8 weeks for GERD healing, and 1 year for maintenance of GERD healing. Rabeprazole was as effective as omeprazole for each indication and significantly more effective than ranitidine for healing of GERD (87% vs 66%) and duodenal ulcer (83% vs 73%). Rabeprazole was also superior to ranitidine in providing symptom relief, particularly in GERD.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2001

Ranitidine bismuth citrate with clarithromycin alone or with metronidazole for the eradication of Helicobacter pylori.

BACKGROUND: Both triple therapy with ranitidine bismuth citrate (RBC) plus two antibiotics for 7 days and dual therapy of RBC with clarithromycin for 14 days have been extensively studied; both regimens effectively eradicate Helicobacter pylori. However, few studies have assessed the efficacy of dual therapy given for 7 days. AIM: To compare the efficacy and safety of RBC 400 mg with clarithromycin 500 mg, alone or with metronidazole 400 mg, given twice daily for 7 days for the eradication of H. pylori. METHODS: This single centre, randomized, double-blind study involved 118 patients with dyspepsia or a history of peptic ulcer disease. H. pylori infection was detected initially by CLO test, and confirmed in 109 patients by urea breath test and/or microbiology culture. H. pylori eradication was assessed 4 and 12 weeks after the end of treatment by urea breath test. H. pylori antibiotic susceptibility was assessed pre-study in all patients, and post-treatment in patients with a positive post-treatment urea breath test. Adverse events were recorded throughout the study. RESULTS: H. pylori was eradicated in 93% of patients who received RBC with clarithromycin and metronidazole and in 84% of patients who received RBC with clarithromycin (intention-to-treat rates). Per protocol eradication rates were 98% and 90% for triple therapy and dual therapy, respectively. The eradication of metronidazole-resistant H. pylori was achieved in 100% and 88% of patients following dual therapy and triple therapy, respectively, and acquired resistance to clarithromycin occurred in only one patient following treatment failure. Both treatments were well-tolerated; only one patient (2%) was withdrawn from each treatment group due to adverse events. CONCLUSIONS: RBC with clarithromycin and metronidazole is a highly effective and well-tolerated triple therapy regimen for the eradication of H. pylori. RBC with clarithromycin dual therapy has a similar efficacy, and offers an alternative to triple therapy when there are concerns about treatment with metronidazole or the use of multiple antibiotics. Both regimens are effective against antibiotic-resistant strains of H. pylori.

Adult↗
PubMed2001

Comparable clinical efficacy and tolerability of 20 mg pantoprazole and 20 mg omeprazole in patients with grade I reflux oesophagitis.

BACKGROUND: Several clinical trials have shown that pantoprazole (40 mg) and omeprazole (40 or 20 mg) have similar efficacy and safety in the treatment of grade II-IV reflux oesophagitis (Savary-Miller classification). AIM: To compare the efficacy and safety of once-daily doses of pantoprazole (20 mg) and omeprazole (20 mg) with respect to symptom relief and healing of patients with grade I reflux oesophagitis. METHODS: Patients with endoscopically established grade I reflux oesophagitis (non-confluent, patchy red lesions with/without white fibrin coating) were enrolled into this randomized, open, parallel-group, multicentre study. A total of 328 patients (n=166 in the pantoprazole group, n=162 in the omeprazole group) were recruited in 23 centres. Patients received 4 weeks of treatment. If the reflux oesophagitis was not completely healed, the treatment was extended to 8 weeks. RESULTS: After 2 and 4 weeks of treatment with either pantoprazole or omeprazole, the rate of symptom relief was similar (70% vs. 79% and 77% vs. 84%, respectively). High healing rates were observed after 4 and 8 weeks (pantoprazole: 84% and 90%, respectively; omeprazole: 89% and 95%, respectively). Both treatments were well tolerated. The most frequently reported adverse events on pantoprazole and omeprazole, respectively, were nausea (8% vs. 7%), diarrhoea (5% vs. 6%) and headache (6% vs. 3%). CONCLUSIONS: After 4 and 8 weeks of treatment with pantoprazole (20 mg) or omeprazole (20 mg), patients with mild gastro-oesophageal reflux disease (grade I) showed comparably high rates of symptom relief and healing. Both treatments were safe and well tolerated.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2001

Tegaserod, a 5-HT(4) receptor partial agonist, relieves symptoms in irritable bowel syndrome patients with abdominal pain, bloating and constipation.

AIM: To investigate the efficacy and safety of tegaserod, a novel 5-HT(4) receptor partial agonist, in a randomized, double-blind, placebo-controlled, 12-week treatment, multicentre study. METHODS: Eight hundred and eighty-one patients with irritable bowel syndrome, characterized by abdominal pain, bloating and constipation, received tegaserod, 2 mg b.d. or 6 mg b.d., or placebo for 12 weeks. RESULTS: Tegaserod, 2 mg b.d. and 6 mg b.d., showed a statistically significant relief of overall irritable bowel syndrome symptoms, measured by a weekly, self-administered questionnaire. At end-point, treatment differences from placebo were 12.7% and 11.8% for 2 mg b.d. and 6 mg b.d., respectively. The effect of tegaserod was noted as early as week 1, and was sustained over the 12-week treatment period. Individual irritable bowel syndrome symptoms assessed daily also showed a statistically significant improvement of abdominal discomfort/pain, number of bowel movements and stool consistency, and a favourable trend for reducing days with significant bloating. Adverse events were similar in all groups, with transient diarrhoea being the only adverse event seen more frequently with tegaserod than placebo. CONCLUSIONS: Based upon the results of this study, tegaserod offers rapid and sustained relief of the abdominal pain and constipation associated with irritable bowel syndrome. Tegaserod is also well tolerated.

Abdominal Pain↗
PubMed2001

Tonsillar metastasis: A rare presentation of gastric carcinoma.

Metastatic carcinoma of the tonsil is uncommon. Tonsillar metastases rarely become apparent before the diagnosis of the primary neoplasm. We describe only the second reported case of tonsillar metastasis as a presenting feature of gastric carcinoma. A review of the literature is also discussed.

Aged↗
PubMed2001

Pseudomembranous esophagitis.

BACKGROUND: Little is known of pseudomembranous esophagitis, a condition of striking endoscopic appearance. Presented here is a description of its nature and outcome. METHOD: Information on all patients with upper GI disease seen in our unit are held in a computerized database that includes presentation, diagnosis (including pseudomembranous esophagitis), treatment, and outcome. RESULTS: Forty-eight patients (mean age 70 years) with pseudomembranous esophagitis were seen over 15 years; 42 were in-patients with various illnesses. At endoscopy, a thin, concentric membrane and/or thick slough covered the distal half and occasionally the entire esophagus. This layer, yellow or blackened, could be peeled away to reveal underlying friable esophageal submucosa. The membrane was composed of fibrinous exudate and inflammatory cells; there was no basement membrane, hence the term pseudomembrane. Patients were treated with histamine H2 receptor antagonists or proton pump inhibitors for about 3 months and followed by endoscopy or clinical observation. All became asymptomatic; the pseudomembrane had disappeared in 32 who underwent follow-up endoscopy. It recurred in 3 of 38 being followed (mean 3.2 years), again associated with another illness requiring hospitalization. The long-term outcome was poor, determined by age and general condition and independent of pseudomembranous esophagitis. Seven patients died within 3 months and 17 during follow-up (mean 42 months, range 5-140 months). CONCLUSION: Pseudomembranous esophagitis is an unusual condition of unknown cause, probably under-reported and associated with systemic illness. It heals rapidly and recurrence is uncommon.

Adolescent↗
PubMed2001

No clinical benefit of adding cisapride to pantoprazole for treatment of gastro-oesophageal reflux disease.

OBJECTIVE: Although a proton pump inhibitor (PPI) and a prokinetic drug are often combined for the medical treatment of gastro-oesophageal reflux disease (GORD), there are few well-conducted clinical studies on the efficacy and tolerability of this therapy. This study investigates whether pantoprazole plus cisapride leads to an additional benefit in comparison to pantoprazole alone. DESIGN AND SETTING: Randomized double-blind prospective multicentre study conducted in patients of 33 hospitals in Ireland, South Africa and the UK. PARTICIPANTS: A total of 350 intention-to-treat (ITT) patients aged 18 years or older with GORD of grade II and III were included in the study. The per-protocol (PP) population comprised 152 patients in the pantoprazole group and 136 in the pantoprazole plus cisapride group. INTERVENTIONS: Patients received either pantoprazole 40 mg once daily or pantoprazole 40 mg once daily plus cisapride 20 mg twice daily. Treatment outcome was assessed after 4 and 8 weeks. The primary criterion was endoscopically confirmed healing after 4 weeks. Additionally, relief of leading symptoms was studied. MAIN OUTCOME MEASURES: The prior null hypothesis was no difference in healing rates between both treatment groups. RESULTS: After 4 weeks of treatment 81% and 82%, and after 8 weeks 89% and 90%, of PP patients treated with pantoprazole or pantoprazole plus cisapride were healed, respectively. Thus, equivalence of the two treatment strategies could be proven. Additionally, improvement of symptom relief showed no significant difference between the two regimens. In contrast to disease grade at baseline, Helicobacter pylori status did not influence the healing rates in our study. Both study medications were tolerated well. CONCLUSION: Addition of cisapride to pantoprazole provides no further benefit in the treatment of GORD.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2001

Pantoprazole therapy in the long-term management of severe acid peptic disease: clinical efficacy, safety, serum gastrin, gastric histology, and endocrine cell studies.

OBJECTIVE: Pantoprazole is the third proton pump inhibitor to become available. When this study was started, there were few data on its long-term use. Our aim was to investigate this aspect and, because powerful inhibitors of acid secretion can cause hypergastrinemia and, in experimental animals, enterochromaffin-like cell hyperplasia, we also monitored serum gastrin and endocrine cell histology. METHODS: One hundred fifty patients refractory to H2-receptor antagonists, running an aggressive course or with complications, were entered into a 5-yr treatment program. We performed serial endoscopy, checked for adverse events, and laboratory values. We also monitored serum gastrin, gastric endocrine cell histology, and antral and corpus gastritis. RESULTS: This report presents results from up to 3 yr of treatment. Cumulative healing on 40-80 mg of pantoprazole was 82% at 4 wk and 92% by 12 wk. Most patients became asymptomatic within 4 wk. Remission on maintenance treatment with 40 mg (n = 111) was 85% at 12 months and 78% at 24 months. Treatment was safe; only four patients had adverse events definitely related to pantoprazole. Elevations in gastrin were modest and there were no significant changes in gastric endocrine cells. The number of enterochromaffin-like cells tended to decrease. CONCLUSION: Pantoprazole is effective, safe, and does not seem to be associated with large increases in serum gastrin or alterations in gastric endocrine cells.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2000

Assessing the conditions for in vivo electrical virtual biopsies in Barrett's oesophagus.

It has previously been shown that it is possible to differentiate between squamous and columnar epithelia in rat and resected human tissues using an impedance probe to make in vitro measurements. This probe can be passed down an endoscope allowing measurements to be made in patients. However, the probe emerges parallel to the oesophageal wall, with little room to manoeuvre. The conditions of control required to give reliable readings have been investigated. The importance of pressure applied and the angle of approach to the oesophagus was assessed. Pressures in the range 26.6 Pa to 46.3 kPa and angles in the range 15-90 degrees were considered. In in vitro studies it was observed that it was possible to obtain consistent readings with pressures greater than 2.9 kPa and with angles greater than 15 degrees between the probe and the oesophagus. These conditions can be achieved in vivo, and readings obtained from twelve patients are shown (45 readings on normal squamous, 34 on Barrett's oesophagus and 22 on stomach). At low frequencies (9.6-153.2 kHz), a Mann-Whitney test shows a significant difference (p < 0.001) when comparing the means from squamous and columnar, and also when readings from Barrett's and normal gastric epithelia are compared (p < 0.001).

Animals↗
PubMed2000

Mechanisms of Helicobacter pylori-induced rat gastric mucosal microcirculatory disturbances in vivo.

The exact mechanisms by which Helicobacter pylori infection results in gastric mucosal injury are unclear. However, it has been demonstrated that surface protein extracts of the bacterium can induce a number of disturbances within the rat gastric mucosal microcirculation, including platelet aggregation and macromolecular leakage (MML) of labeled albumin. This study aimed to determine the mechanisms involved in inducing these events using the technique of fluorescent in vivo microscopy. Male Wistar rats were pretreated with either ketotifen, a mast cell stabilizer (1 mg/kg), pyrilamine, an H1-receptor antagonist (30 mg/kg), hexanolamine-PAF, a PAF-receptor antagonist (10 microg/kg), L-arginine, the nitric oxide precursor (300 mg/kg) or vehicle, saline. Then 0.5 ml of H. pylori extract was administered to the exteriorized gastric mucosa of the anesthetized rat. Alterations in fluorescein-labeled albumin leak, vessel diameters, and acridine red-labeled leukocyte and platelet activity were determined over a 2-hr period. Saline pretreated animals demonstrated significant MML with a peak at 5 min (11%, P<0.02). This was prevented with ketotifen and pyrilamine, but not with hexanolamine-PAF (17.5%, P<0.05) and L-arginine (13%, P<0.05). Significant numbers of platelet emboli and thrombi were observed within mucosal capillaries and postcapillary venules with vehicle pretreatment; this was prevented with hexanolamine-PAF and L-arginine, but not with ketotifen and pyrilamine. In conclusion, these studies demonstrate that more than one mediator is involved in inducing the rat gastric mucosal microcirculatory disturbances associated with H. pylori administration. Mast cells and histamine are linked to MML, with PAF, probably not derived from mast cells, involved in platelet activation.

Animals↗
PubMed2000

Effects of chronic administration of Helicobacter pylori extracts on rat gastric mucosal microcirculation in vivo.

The mechanisms by which Helicobacter pylori contributes to gastroduodenal injury are unclear. We have previously described platelet aggregation within rat gastric mucosal microcirculation following acute administration of H. pylori extracts. However, leukocyte activation was not observed. This study aimed to determine whether chronic administration of H. pylori could induce leukocyte activation. Rats were gavaged with either H. pylori or E. coli extracts or with distilled water three times daily at three-day intervals. Acridine red was used to quantitate gastric mucosal leukocyte/platelet activity using fluorescent in vivo microscopy. Further animals received additional acute H. pylori after 1 hr and recordings were made for a further 1 hr. Significant numbers of "flyers," "rollers," and adherent leukocytes were observed throughout the study in H. pylori animals. Only adherent leukocytes were observed following E. coli. Acute H. pylori induced a further significant increase in adherent leukocytes. Significant platelet thrombi were also present in H. pylori-treated animals. In conclusion, earlier studies demonstrated platelet aggregation but no leukocyte activation, which is in contrast to the current chronic studies. Platelet activation may be the initial response to H. pylori and involved in recruitment of leukocytes. These activated cells may contribute to the development of gastric mucosal damage.

Animals↗
PubMed2000

Triple therapy for Helicobacter pylori eradication: a comparison of pantoprazole once versus twice daily.

BACKGROUND: Proton pump inhibitor-based triple therapy is recommended as treatment for Helicobacter pylori eradication. The proton pump inhibitor may be given once or twice daily. However, little information is available on how these two treatment strategies compare. METHODS: H. pylori-positive patients (two positive test results) with endoscopy-proven healed duodenal ulcer or non-ulcer dyspesia were randomly allocated to 1 week of double-blind treatment with pantoprazole 40 mg once or twice daily, plus clarithromycin 250 mg and metronidazole 400 mg twice daily. Eradication was defined as a negative 13C-urea breath test (13C-UBT) and histology, 4-5 weeks post-treatment. The follow-up phase comprised 12 months off therapy, with 13C-UBT at 6 and 12 months. RESULTS: Two hundred and four patients received treatment: pantoprazole once daily (x1), n=104; twice daily (x2), n=100. Eradication rates were 84% in both the pantoprazole x1 and pantoprazole x2 groups by modified intention-to-treat analysis and 89% and 87%, respectively, by per protocol analysis. Metronidazole resistance was found in 44% of pre-treatment cultures of H. pylori. Eradication rates were similar in susceptible (72%) and resistant (75%) strains. During follow-up, recrudescence of infection occurred in 3/118 patients. CONCLUSION: When using pantoprazole plus clarithromycin and metronidazole, the proton pump inhibitor can be used once daily without loss of efficacy.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2000

A double-blind, randomized, placebo-controlled dose-ranging study to evaluate the efficacy of alosetron in the treatment of irritable bowel syndrome.

BACKGROUND: Irritable bowel syndrome is a common gastrointestinal disorder characterized by abdominal pain and discomfort and altered bowel habit. Antagonism at the 5-HT3 receptor may be of benefit in the treatment of irritable bowel syndrome. AIMS: To evaluate the effect of 12 weeks of treatment with alosetron, a 5-HT3 receptor antagonist at doses of 0.1 mg b.d., 0.5 mg b.d. and 2 mg b.d. in irritable bowel syndrome patients. METHODS: A double-blind, placebo-controlled, parallel-group study with a 2-week screening and a 12-week treatment period was conducted. A total of 462 patients (335 female) recorded details of the severity of their abdominal pain, and bowel function daily on a diary card throughout the study. At monthly clinic visits patients recorded the severity of their abdominal pain/discomfort and diarrhoea on a visual analogue scale. RESULTS: In the total population and in the female subpopulation (but not in males) alosetron 2 mg b.d. significantly increased the proportion of pain-free days and decreased the visual analogue scale score for diarrhoea compared with placebo. Alosetron at doses of 0.5 mg b.d. and 2 mg b.d. led to a significant hardening of stool, and a reduction in stool frequency in the total population. CONCLUSION: Alosetron at a dose of 2 mg b.d. is an effective treatment for female patients with irritable bowel syndrome.

Adolescent↗
PubMed2000

Mast cell stabilization prevents ethanol-induced rat gastric mucosal injury: mechanisms of protection.

INTRODUCTION: We previously demonstrated that 60% ethanol increased macromolecular leakage and induced lesion formation in areas of permanent flow stasis within gastric mucosal vessels. Mast cells and their mediators have been implicated in acute mucosal injury. Fluorescent in vivo microscopy was used to assess the effects of ketotifen, a mast cell stabilizer, and pyrilamine, a histamine (H1)-receptor antagonist, on ethanol-induced rat gastric mucosal injury. METHODS: Experiments were carried out on anaesthetized rats pretreated orally with ketotifen (1 mg/kg) or pyrilamine (30 mg/kg). Fluorescein isothiocyanate-bovine serum albumin (FITC-BSA; 0.2 mL/100 g), a marker for quantitating macromolecular leakage was administered intra-arterially. Ethanol (60%) or distilled water was applied topically to the gastric mucosa. Macromolecular leakage of FITC-BSA, vessel diameters and leucocyte activity were quantified using image analysis. RESULTS: Pretreatment with ketotifen or pyrilamine, followed by ethanol, caused no change in macromolecular leakage compared with controls. Both compounds prevented blood flow stasis in all areas and no lesion formation was observed. However, increased leucocyte activity and increases in vessel diameter were observed following pretreatment with ketotifen and pyrilamine, respectively. CONCLUSIONS: The data suggest that vasoactive substances released from mast cells may be involved in the aetiology of ethanol-induced gastric mucosal damage. The prevention of these normal physiological responses to injury may lead to the employment of other microcirculatory mechanisms of defence.

Animals↗
PubMed2000

L-Arginine protects and exacerbates ethanol-induced rat gastric mucosal injury.

BACKGROUND AND AIMS: We have previously demonstrated that 60% ethanol (EtOH) increases macromolecular leakage and induces focal lesion formation in areas of permanent flow stasis within gastric mucosal vessels. Nitric oxide (NO) may prevent lesion formation by inhibiting leakage. This study used fluorescent in vivo microscopy to investigate (i) whether L-arginine (NO precursor) prevented EtOH induced injury and (ii) the mechanisms of protection. METHODS: Experiments were carried out on anaesthetized rats (hypnorm/diazepam) receiving either intra-arterial fluorescein isothiocyanate-bovine serum albumin (0.2 mL/100 g), a marker for quantitating leakage, or Acridine red (0.1 mL/100 g) which labels leukocytes. Animals then received 100, 300 or 500 mg/kg L-arginine (i.a.) followed by 60% EtOH or distilled water, topically applied to the gastric mucosa (n = 6 for each group). Vessel diameter, macromolecular leakage of labelled albumin from post capillary venules (PCV) and capillaries and leukocyte activity were quantitated using image analysis. RESULTS: L-Arginine (100 mg/kg) did not increase vessel diameter or prevent EtOH-induced lesion formation and leakage. Both 300 mg/kg and 500 mg/kg alone induced significant and sustained increases in PCV diameter after 15 (P< 0.01) and 5 min (P< 0.001), respectively. Lesion formation was only prevented by 300 mg/kg L-arginine, whereas 500 mg/kg exacerbated haemorrhagic lesion formation over the entire exposed mucosa. Neither 300 mg/kg nor 500 mg/kg L-arginine prevented leakage following EtOH. No leukocyte activity was observed following EtOH with or without L-arginine pretreatment. CONCLUSION: L-Arginine (300 mg/kg) prevented lesion formation. The mechanism of protection probably involved the increased blood flow in the dilated PCV and not the inhibition of leakage. The combined effects of EtOH and the possible high NO levels exacerbate gastric mucosal damage despite the increases observed in vessel diameter.

Animals↗
PubMed2000

Survival analysis in percutaneous endoscopic gastrostomy feeding: a worse outcome in patients with dementia.

OBJECTIVE: Percutaneous endoscopic gastrostomy (PEG) feeding has been validated in specific clinical situations such as acute stroke with dysphagia and oropharyngeal malignancy. The perception that gastrostomy insertion is safe and technically simple has led to an increase in the demands for PEG insertion, encompassing clinical applications such as in patients with dementia, in whom its role has not been justified. The purpose of this study was to compare the mortality of patients with dementia who were fed by PEG to that of other subgroups of patients requiring gastrostomy feeding. METHODS: The study focused on a cohort of 361 consecutive patients requiring PEG feeding between August 1992 and July 1997 from two District General Hospitals (Rotherham District General Hospital and Doncaster Royal Infirmary) in South Yorkshire. A retrospective cohort survival analysis was performed using the Kaplan-Meier survival method and Cox proportional hazards analysis. RESULTS: In all patients requiring gastrostomy feeding there is a high initial mortality of 28% at 30 days. However, patients with dementia have a worse prognosis compared to other subgroups, with 54% having died at 1 month and 90% at 1 yr (log rank test p < 0.0001). This difference remained significant (log rank p < 0.0001) after adjusting for age at the time of PEG insertion. CONCLUSIONS: This is the first demonstration in the United Kingdom that the mortality of patients with dementia who are fed by gastrostomy is considerable. Consequently, we may wish to advise against gastrostomy feeding in selected patients within this clinical setting.

Aged↗