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At least 811 records · Page 45Linked to original sources
PubMed1999

A 24-week randomized trial of controlled-release physostigmine in patients with Alzheimer's disease.

OBJECTIVE: To evaluate the safety and efficacy of controlled-release physostigmine, an acetylcholinesterase inhibitor, in patients with probable AD of mild to moderate severity. METHODS: A prospective, 24-week, randomized, multicenter, double-blind, parallel group study of patients was conducted. The study enrolled 475 patients at 24 sites. Patients met criteria for probable AD and were randomized to one of three arms: placebo, controlled-release (CR) physostigmine 30 mg daily, or CR physostigmine 36 mg daily. Dosage was escalated by a forced upward titration during the first 6 to 9 weeks of the trial, then maintained at a constant dose to 24 weeks. Primary outcome measures were the Alzheimer's Disease Assessment Scale-Cognitive subscale (ADAS-Cog) and the Clinician's Interview-Based Impression of Change-Plus with caregiver input (CIBIC+). Secondary outcome measures included the Clinical Global Impression of Change (CGIC), the Geriatric Evaluation by Relatives Rating Instrument, and an Instrumental Activities of Daily Living Scale. RESULTS: In an intent-to-treat population, the last observation carried forward analysis revealed a 2.9-point ADAS-Cog (p = 0.002) difference between physostigmine and placebo-treated patients for both dosages, and a 0.26 to 0.31-point difference on the CIBIC+ (p = 0.048). There were no significant differences on the secondary outcome measures except for a difference on the CGIC when analyzed by use of the Cochran-Mantel-Haenszel statistic (p = 0.014). There were significant increases in gastrointestinal side effects including nausea, vomiting, diarrhea, anorexia, dyspepsia, and abdominal pain for patients on either dose of physostigmine, resulting in a high dropout rate. Agitation was decreased significantly. There was no evidence of cardiac rhythm disturbance or liver function abnormalities. CONCLUSION: CR physostigmine enhanced cognitive and global function. It is relatively safe for the treatment of cognitive dysfunction secondary to AD. However, in light of the gastrointestinal side effects, a lower starting dose and a flexible titration schedule might lead to a more favorable adverse event profile in the clinical arena.

Aged↗
PubMed2005

Regional differences in gastrointestinal motility disturbances during acute necrotising pancreatitis.

Patients with acute pancreatitis often suffer from intestinal motility disturbances but the mechanism of this dysfunction is largely unknown. We studied the effect of acute necrotising pancreatitis (ANP) on in vivo gastrointestinal motility and in vitro intestinal contractility in mice. ANP was induced non-invasively by feeding young female mice a choline-deficient ethionine-supplemented (CDE) diet during 72 h. Gastric emptying and intestinal transit were measured in vivo 15 min after intragastric gavage of a semiliquid Evans blue bolus. Gastric and intestinal neuromuscular function was determined in vitro on isolated muscle strips. ANP significantly decreased gastric emptying from 61.2 +/- 9.8 to 34.9 +/- 7.1% and intestinal transit from 63.4 +/- 5.6 to 32.5 +/- 5.4%. ANP did not affect receptor-dependent and receptor-independent gastric muscle contractions except the contractions to substance P, which were slightly inhibited. In intestinal muscle strips, ANP significantly decreased contractions to EFS, carbachol, PGF(2alpha), substance P and KCl. Our results show that ANP delays gastric emptying in vivo, associated with a specific reduction in substance P contractility in vitro. ANP also impairs intestinal transit in vivo, associated with a non-specific reduction of intestinal contractility in vitro. We conclude that ANP impairs gastrointestinal motility in mice with underlying regional differences in the pathogenic mechanisms.

Acute Disease↗
PubMed2002

Botulinum neurotoxin and other treatments for fissure-in-ano and pelvic floor disorders.

BACKGROUND: The management of disorders of the lower gastrointestinal tract, such as chronic anal fissure and pelvic floor dysfunction, has undergone re-evaluation recently. To a large extent this is due to the advent of neurochemical treatments, such as botulinum neurotoxin injections and topical nitrate ointment. METHODS AND RESULTS: This review presents, inter alia, current data on the use of botulinum neurotoxin to treat lower gastrointestinal tract diseases, such as chronic anal fissure for which it promotes healing and symptom relief in up to 70 per cent of cases. This agent has also been used selectively to weaken the external anal sphincter and puborectalis muscle in constipation and in Parkinson's disease. Symptomatic improvement can also be induced in anterior rectocele by botulinum neurotoxin injections. CONCLUSION: Botulinum neurotoxin appears to be a safe therapy for anal fissure. It is more efficacious than nitrate application and does not require patient compliance to complete treatment. While it may also be a promising approach for the treatment of chronic constipation due to pelvic floor dysfunction, further investigation of its efficacy and safety in this role is needed before general usage can be advocated.

Anti-Dyskinesia Agents↗
PubMed2006

Inlet patch of gastric mucosa in upper esophagus causing chronic cough and vocal cord dysfunction.

BACKGROUND: An inlet patch of gastric mucosa in the upper esophagus is usually an incidental, congenital finding found during upper gastrointestinal tract endoscopy. Although it has been reported to cause dysphagia, strictures, adenocarcinoma, and webs, it has never been associated with cough and vocal cord dysfunction. OBJECTIVE: To report the first case of a patient with an inlet patch of gastric mucosa in the upper esophagus as the cause of a particularly troublesome, chronic cough that was initially missed on 2 upper endoscopies. METHODS: The patient is a 50-year-old man with a 7-year history of chronic cough associated with hoarseness, shortness of breath, and globus sensation. For diagnostic evaluation, pulmonary function tests, chest computed tomography, rhinolaryngoscopy, upper gastrointestinal tract endoscopy, and histologic examinations were performed. RESULTS: A multidisciplinary approach revealed several possible causes for the chronic cough, including vocal cord dysfunction, postnasal drip syndrome, allergic rhinitis, and mild gastroesophageal reflux disease that was only partially responsive to therapy. The results of 2 initial upper gastrointestinal tract endoscopies were interpreted as normal. A third endoscopy detected an inlet patch of gastric mucosa in the upper esophagus. Treatment with a high-dose histamine type 2 receptor antagonist and a proton pump inhibitor alleviated the patient's symptoms. CONCLUSIONS: An inlet patch of gastric mucosa in the upper esophagus is not uncommon, but it is often overlooked or believed to be an incidental, congenital finding. This is the first report, to our knowledge, of an inlet patch resulting in a troublesome, chronic cough.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2001

The gut as a neurological organ.

We refer to the gut as a neurological organ to emphasize the particular importance of the nervous system in the regulation of digestive functions, given that the gastrointestinal tract is innervated by five different classes of neurons: intrinsic enteric neurons, vagal afferents, spinal afferents, parasympathetic efferents and sympathetic efferents. Virtually each aspect of digestive activity is under the regulatory influence of neurons, among which the enteric nervous system (ENS) plays the most important part. The ENS acts like a brain in the gut that functions independently of the central nervous system, contains programmes for a variety of gastrointestinal behaviours and governs the activity of all gastrointestinal effector systems according to need. Intrinsic sensory neurons supply the ENS with the kind of information that this system requires for its autonomic control of digestion, whereas extrinsic afferents notify the brain about any data that are relevant to energy and fluid homeostasis and the sensation of discomfort and pain. Many diseases of the gut, particularly the functional bowel disorders, seem to be related to dysfunction of the ENS and other components of the gastrointestinal innervation. The ENS and extrinsic afferents are hence prime targets for the therapeutic management of gut diseases and for the relief of the pain and discomfort associated with these disorders.

Abdominal Pain↗
PubMed2005

Ischemic preconditioning protects against gut dysfunction and mucosal injury after ischemia/reperfusion injury.

Mesenteric ischemia/reperfusion (IR) damages the gastrointestinal epithelia and impairs gut function. Ischemic preconditioning (IPC) has been shown to protect organs against IR injury. We hypothesized that IPC protects the gut from IR injury. Rats were randomized to a sham group, a sham early IPC + IR group (sham IPC + SMA occlusion for 30 min and 6 h of reperfusion), an early IPC + IR group (IPC, three cycles of SMA occlusion for 4 min and reperfusion for 10 min) followed immediately by SMA occlusion for 30 min and 6 h of reperfusion), a sham 24-h group, a sham late IPC + IR group (sham IPC followed by additional reperfusion for 24 h + SMA occlusion for 30 min and 6 h of reperfusion), and a late IPC + IR group (IPC protocol followed by additional reperfusion for 24 h, and then SMA occlusion for 30 min followed by 6 h of reperfusion). At 6 h, transit was determined and expressed as the mean geometric center. Ileum was harvested for assessment of mucosal injury and myeloperoxidase (MPO) activity. Tissue water was determined using the wet-to-dry weight ratio to assess gut edema. Early IPC + IR significantly improved transit (3.9 +/- 0.2), decreased MPO levels (3 +/- 2), and lessened mucosal injury (1.2 +/- 0.3) compared with animals subjected to sham early IPC + IR (transit, 2.9 +/- 0.2; MPO levels, 9 +/- 1; mucosal injury, 3.0 +/- 0.6). Late IPC + IR also improved transit (6.0 +/- 0.4) and decreased MPO levels (1 +/- 1) compared with sham late IPC + IR (transit, 4.4 +/- 0.2; MPO levels, 8 +/- 1), however, there was no difference in the mucosal protection between late IPC + IR (1 +/- 0.3) and sham late IPC + IR (1 +/- 1). Our results suggest that early and late IPC improves intestinal dysfunction, decreases inflammation, and provides mucosal protection in the intestine after IR. Our results show that IR-induced gut dysfunction can be improved by IPC. Both phases of IPC can potentially be useful in the clinical setting of surgical patient care.

Animals↗
PubMed2001

Targeting the abnormalities of gastroduodenal functions in functional dyspepsia.

The current definition of functional dyspepsia changes the previous concept of absence of organic disease to the presence of a functional alteration of the upper gastrointestinal tract. From a theoretical point of view, the alteration of any major gastrointestinal function may induce dyspeptic symptoms. However, both asymptomatic subjects with some gastrointestinal functional alteration and dyspeptic patients without a demonstrable dysfunction are not unusual. This may be explained at least in part by the more recent concept of visceral sensitivity. The potential role of acid secretion in the pathogenesis of functional dyspepsia as well as the positive effect of antisecretory drugs in a proportion of patients may be based on an increased gastric acid secretion and duodenal acid overload, a hypersensitivity to acid and/or the development of acid-mediated gastrointestinal motor abnormalities. Helicobacter pylori infection may play a role in this context. Both interdigestive and postprandial gastrointestinal motility, mainly a delayed gastric emptying and an altered intragastric distribution of nutrients, have been described to be disturbed in up to half of the patients with functional dyspepsia. This may also be an explanation for the high frequency of intestinal bacterial overgrowth in these patients. Most probably, visceral hypersensitivity should be present for motor alterations to induce symptoms. This is the basis for future development of new drugs in the management of this functional syndrome. The role of H. pylori in the pathogenesis of functional dyspepsia is a matter of discussion, but a proportion of patients benefit from eradication therapy and, therefore this therapeutic approach should be taken into account.

Duodenum↗
PubMed1998

[Autonomic disorders in polyneuropathies].

BACKGROUND: Many polyneuropathies manifest autonomic disturbances. Diabetic neuropathy, the most frequent neuropathy in the western world, serves as model of the symptomatology of autonomic disturbances. DIABETIC NEUROPATHY: Clinical symptoms comprise pupillary and cardiovascular dysfunction such as orthostatic hypotonia and syncopes, thermoregulatory, gastrointestinal symptoms, disturbances in urogenital and respiratory function and unawareness of hypoglycemia. OTHER NEUROPATHIES: This article also describes autonomic symptoms in alcoholic neuropathy, in Guillain-Barré syndrome, in paraneoplastic polyneuropathies, in toxic neuropathies, in acute and subacute autonomic neuropathy, in amyloidosis, in porphyria, in familiar dysautonomia, in HIV infection and in botulism.

Autonomic Nervous System Diseases↗
PubMed1988

Mechanisms of nonsteroidal anti-inflammatory drug-induced gastric damage. Actions of therapeutic agents.

All nonsteroidal anti-inflammatory drugs (NSAIDs) used in the treatment of rheumatic diseases may cause gastric mucosal damage. Although the best-studied agent is aspirin, the mechanisms by which it damages the gastric mucosa are not fully understood. However, it is thought that the drug impairs mucosal defenses by penetrating the protective mucous and bicarbonate layers and damaging the epithelial lining cells. In turn, gastric acid is permitted to pour through the breached defenses. This "back-diffusion" of acid further injures cells and destroys capillaries and venules. This local damaging effect is pH dependent and is contributed to by the acid secretion of the stomach. Other mechanisms by which aspirin may induce or contribute to mucosal injury include inhibition of mucosal prostaglandin synthesis, reduction and alteration of mucus secretion, reduction of bicarbonate secretion, interference with cell turnover, as well as systemic effects such as platelet dysfunction. The mechanism by which nonaspirin NSAIDs cause gastrointestinal damage is uncertain. All are known to inhibit prostaglandin synthesis, which could contribute to their toxicity since prostaglandins found in the stomach both inhibit acid secretion and have mucosal defensive effects. Partial protections against aspirin-induced or other NSAID-induced gastric mucosal damage has been demonstrated, at least in some studies, by sucralfate, prostaglandins, omeprazole and histamine (H2)-receptor antagonists. Sucralfate appears to act primarily on local defensive mechanisms; its antisecretory effects are minimal. Prostaglandins exert a protective effect at both antisecretory and nonantisecretory (cytoprotective) doses, indicating that either or both mechanisms may be involved. The most recently studied agent, omeprazole, is the most potent of all acid inhibitors; it may also be cytoprotective, possibly as a result of its effects on sulfhydryl groups. Prostaglandins and omeprazole are not available in the United States and their potential side effects may limit their use in patients with chronic rheumatic diseases. Protection by H2-receptor antagonists is mostly related to reduction of acid secretion, though a cytoprotective effect may occur.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1982

A randomized, double-blind study of two combined and two progestogen-only oral contraceptives.

A randomized double-blind study of two combined oral contraceptives and two progestogen-only oral contraceptives was conducted using the same protocol at WHO Collaborating Centres for Clinical Research in Human Reproduction in Bombay and Ljubljana of the 518 women admitted to the trial, 123 received mestranol 50 micrograms + norethisterone 1mg (MES 50 + NET 1); 137 received ethinyl estradiol 30 micrograms + levonorgestrel 150 micrograms (EE 30 + LNG 150); 130 received norethisterone 350 micrograms/NET 350); and 128 received levonorgestrel 30 micrograms (LNG 30). At one year, between 52.6 and 61.0 percent of those recruited had discontinued oral contraceptive use for all reasons, and by two years, between 70.5 and 76.5 percent had discontinued the treatment. These rates did not differ between the four treatment groups. However, discontinuation rates for all medical reasons at one and two years, and at two years pregnancy rates and discontinuation rates for bleeding disturbances, were significantly lower in the EE/LNG preparation. The groups receiving the MES/NET, LNG and NET had similar pregnancy rates, discontinuation rates for all medical reasons and all bleeding disturbances. There were two ectopic pregnancies among the 22 pregnancies in the progestogen-only groups. Discontinuation because of headache, dizziness and other central nervous system symptoms were significantly more common in those receiving MES/NET compared to EE/LNG. In contrast, discontinuation for gastro-intestinal disturbances were significantly higher in the EE/LNG combined preparation. Bleeding disturbances in the first few cycles tended to be higher in NET than in the LNG group. The data suggest that greater consideration be given to the benefits and risks of including progestogen-only oral contraceptives in the family planning programmes of some countries.

Adolescent↗
PubMed2006

Hyperbaric oxygen therapy might improve certain pathophysiological findings in autism.

Autism is a neurodevelopmental disorder currently affecting as many as 1 out of 166 children in the United States. Numerous studies of autistic individuals have revealed evidence of cerebral hypoperfusion, neuroinflammation and gastrointestinal inflammation, immune dysregulation, oxidative stress, relative mitochondrial dysfunction, neurotransmitter abnormalities, impaired detoxification of toxins, dysbiosis, and impaired production of porphyrins. Many of these findings have been correlated with core autistic symptoms. For example, cerebral hypoperfusion in autistic children has been correlated with repetitive, self-stimulatory and stereotypical behaviors, and impairments in communication, sensory perception, and social interaction. Hyperbaric oxygen therapy (HBOT) might be able to improve each of these problems in autistic individuals. Specifically, HBOT has been used with clinical success in several cerebral hypoperfusion conditions and can compensate for decreased blood flow by increasing the oxygen content of plasma and body tissues. HBOT has been reported to possess strong anti-inflammatory properties and has been shown to improve immune function. There is evidence that oxidative stress can be reduced with HBOT through the upregulation of antioxidant enzymes. HBOT can also increase the function and production of mitochondria and improve neurotransmitter abnormalities. In addition, HBOT upregulates enzymes that can help with detoxification problems specifically found in autistic children. Dysbiosis is common in autistic children and HBOT can improve this. Impaired production of porphyrins in autistic children might affect the production of heme, and HBOT might help overcome the effects of this problem. Finally, HBOT has been shown to mobilize stem cells from the bone marrow to the systemic circulation. Recent studies in humans have shown that stem cells can enter the brain and form new neurons, astrocytes, and microglia. It is expected that amelioration of these underlying pathophysiological problems through the use of HBOT will lead to improvements in autistic symptoms. Several studies on the use of HBOT in autistic children are currently underway and early results are promising.

Autistic Disorder↗
PubMed1996

Motility of Oddi's sphincter: recent developments and clinical applications.

BACKGROUND: In recent years, applications of electromyographic, cineradiographic, scintilographic, and endoscopic manometric techniques have improved our knowledge of normal and abnormal motility of Oddi's sphincter. This sphincter coordinates the time and rate of secretion of about 3 liters of bile and pancreatic juice into the duodenum daily. METHODS: Oddi's sphincter may be evaluated by endoscopic manometry, ultrasound, dynamic hepatobiliary scintigraphy, and laboratory tests. Endoscopic manometry is the best method for evaluating the function Oddi's sphincter. RESULTS: The basal pressure of Oddi's sphincter is usually 5 to 15 mm Hg greater than the bile and pancreatic duct pressures. Phasic contractions of 50 to 150 mm Hg in amplitude and 3 to 8 contractions per minute in frequency are superimposed on the basal pressure. A small percentage of patients with gastrointestinal symptoms after cholecystectomy has sphincter of Oddi dysfunction, which may have structural abnormality (papillary stenosis) or functional abnormality (Oddi's sphincter dyskinesia). CONCLUSIONS: Elevated basal pressure ( > 40 mm Hg) is the most important manometric finding of Oddi's sphincter dysfunction. Endoscopic sphincterotomy is the treatment of choice for patients with Oddi's sphincter dysfunction and elevated basal sphincter pressure.

Biliary Tract Diseases↗
PubMed1999

Comparative quality-of-life analysis after radical prostatectomy or external beam radiation for localized prostate cancer.

OBJECTIVES: To determine and compare quality-of-life (QOL) evaluations from patients who received external beam radiation therapy or radical prostatectomy for the treatment of localized prostate cancer, and to compare differences in QOL assessments for urinary and sexual function after radical prostatectomy as reported by patient and physician. METHODS: Two hundred three patients treated by radical prostatectomy and 257 patients treated by external beam irradiation, all beyond 12-month follow-up after therapy, responded to a QOL questionnaire. The difference in responses with regard to bladder, bowel, and sexual function, overall satisfaction with treatment, and choice of the same treatment were assessed. Satisfaction with and choice of the same treatment were also specifically assessed according to bowel and bladder function and current disease status. The medical records of patients treated by radical prostatectomy were reviewed by an independent data manager to record the physician's assessment of continence and sexual function for comparison with that patient's assessment as noted in the questionnaire. RESULTS: Problems with urinary continence were more frequent among patients treated by radical prostatectomy; problems with gastrointestinal function were more frequent after irradiation. Sexual dysfunction was similar in both groups, although surgical patients experienced a greater impact on sexual relationships. The physician estimates of urinary continence were more favorable than the patient-reported outcomes. However, the physician estimate of sexual function closely approximated that of the patient. Preservation of sexual function among patients who underwent nerve-sparing surgery was disappointingly low. Only for the response to the question dealing with difficulty in achieving an erection was there a statistically significant benefit for patients receiving nerve-sparing versus non-nerve-sparing procedures. Patient satisfaction with and choice of the same treatment varied according to function and current disease status. Patients who had incontinence or bowel dysfunction or had evidence of recurrent disease were statistically less likely to choose the same treatment again when compared with functional and disease-free counterparts. Because irradiated patients were on average 6 years older than surgical patients, responses were adjusted for age; adjustment for age did not alter results. CONCLUSIONS: QOL is determined by the treatment received, by the assessment source, and by the patient's function and disease status at the time of assessment. Prospective and longitudinal studies will more accurately quantify immediate and chronic alterations in QOL. Uniformity of evaluation through consolidation of QOL instruments will permit more accurate cross-series and cross-treatment comparisons.

Adult↗
PubMed2001

Treatment of acute promyelocytic leukemia with arsenic compounds: in vitro and in vivo studies.

Arsenic compounds, Including arsenic trioxide (As2O3) and arsenic sulfide (As4S4), have recently been shown to be effective in the treatment of acute promyelocytic leukemia (APL). In vitro, As2O3 exerts a dose-dependent dual effect: it triggers apoptosis at relatively high concentrations (0.5 to 2.0 micromol/L) and induces partial differentiation at low concentrations (0.1 to 0.5 micromol/L). The apoptosis-inducing effect is associated with the collapse of mitochondrial transmembrane potentials in a thiol-dependent manner, whereas the retinoic acid signaling is required for APL cell differentiation. As2O3 over a wide range of concentrations (0.1 to 2.0 micromol/L) Induces degradation of PML-RARalpha as well as the wild-type PML and enhances the acetylation of histone, a process important for the transcriptional activation of genes. In vivo, As2O3 induces a high complete remission (CR) rate in patients with both primary and relapsed APL (around 85% to 90%). Side effects, such as skin reaction, gastrointestinal symptoms, electrocardiographic (EKG) changes, neuropathy, and liver dysfunction, are mild to moderate in relapsed patients, and severe hepatic lesions have been found in some primary cases. After CR obtained in relapsed patients, chemotherapy in combination with As2O3 as postremission therapy has yielded better survival than treatment with As2O3 alone. This is in line with the observation that remission induction with As2O3 is not sufficient in most cases to obtain a molecular remission as Judged by reverse-transcriptase polymerase chain reaction for PML-RARalpha fusion transcripts. The in vivo effect of As2O3 seems to be related to the expression of APL-specific PML-RARalpha oncoprotein, and a synergistic effect between As2O3 and ATRA has been shown in the APL mouse model. Besides As2O3, other arsenic compounds such as As4S4 also show a therapeutic effect in APL. Because the toxic effects of arsenic treatment in primary APL need to be investigated further, we propose use of ATRA as a first-line drug for remission induction in primary APL, whereas As2O3 can be incorporated into multidrug postremission therapy or used as rescue for relapsed APL patients.

Animals↗
PubMed1998

Intestinal and extraintestinal symptoms in functional gastrointestinal disorders.

Functional gastrointestinal disorders such as irritable bowel syndrome or functional dyspepsia have traditionally been regarded as syndromes limited to the digestive system. However, both clinical experience and published evidence show that patients with such disorders also report a series of other symptoms of physical distress, such as fibromyalgia and irritable bladder and alterations in vital functions, such as sleep, libido, appetite and energy level. Some of these extraintestinal symptoms can be explained in the context of an evolving comprehensive disease model which views functional gastrointestinal disorders as manifestations of alterations in the interactions between the nervous system, the viscera and the musculoskeletal system. Alterations in central circuits concerned with arousal, attention and fear, cognitions about bodily symptoms and possible alterations in the hypothalamic pituitary adrenal (HPA) axis may all contribute to the wide range of symptoms reported by affected patients.

Colonic Diseases, Functional↗
PubMed1997

Helicobacter pylori infection in haemodialysis patients and renal transplant recipients.

BACKGROUND: It is known that Helicobacter pylori (Hp) plays an important role in gastritis and peptic ulcer disease in the general population. Although dyspeptic complaints are frequent in haemodialysis (HD) patients and renal transplant recipients, there are few reports regarding the prevalence of Hp and its possible effects on this group of patients. This study was performed to examine the prevalence of Hp infection in patients on regular HD treatment and to detect its role in the pathogenesis of dyspepsia in this group of patients. METHODS: Two hundred and one patients with dyspeptic complaints were included in the study. The groups consisted of 47 HD, 54 renal transplant recipients, and 100 non-renal disease patients. Upper gastro-intestinal endoscopies were performed and gastric antral biopsies were obtained for urease test in all patients. RESULTS: Twenty-eight (60%) of the 47 HD and 38 (70%) of the 54 RTR were positive for Hp. Sixty-four (64%) of the 100 patients with various gastrointestinal complaints and known to have no renal dysfunction were positive for Hp. The Hp prevalences among the three groups were not significantly different (P > 0.05). The prevalence of Hp infection did not correlate with the haemodialysis duration nor the post-transplantation duration (P > 0.05). There was no correlation between the prevalence of Hp infection and duration of haemodialysis therapy or time post-transplantation. CONCLUSION: These findings suggest that HD patients are not protected against Hp infection as the Hp prevalences are as high as that for the non-renal disease group. The increased dyspeptic complaints may be partly related to Hp infection.

Adult↗
PubMed1977

Diabetic visceral neuropathy: treatment with bethanechol chloride.

An 86-year-old diabetic man developed nausea, emesis, abdominal distention, and decreased gastrointestinal motility. A Hollander test confirmed incomplete vagal dysfunction. Treatment with bethanechol chloride resulted in marked improvement which was reproducible after withdrawal and reinstitution of therapy. We believe that treatment with bethanechol chloride deserves further investigation in selected patients with diabetic visceral neuropathy.

Aged↗