Biomedical subjects

K Haruma

Publications and source records attributed to K Haruma.

At least 19 recordsLinked to original sources

PubMed2006

The usefulness of transabdominal ultrasound for the diagnosis of lower gastrointestinal bleeding.

BACKGROUND: Lower gastrointestinal bleeding is a frequent cause of hospitalization, but diagnostic methods for this condition are not fully established. Transabdominal ultrasound is a widely accepted diagnostic tool in bowel diseases. AIM: To evaluate the usefulness of transabdominal ultrasound for lower gastrointestinal bleeding. METHODS: We reviewed the medical records of consecutive patients who underwent transabdominal ultrasound as the first diagnostic procedure for acute haematochezia during the period June 1999 to June 2004. The study group comprised 111 patients and all underwent colonoscopy thereafter. Detection and diagnosis of lower gastrointestinal bleeding by ultrasonographic examination were evaluated by comparing the ultrasound diagnosis with the colonoscopic findings and final diagnosis. RESULTS: The bleeding site was localized by colonoscopy in 90 of the 111 patients (81%). The bleeding site was localized by ultrasound in 59 of the 90 patients (66%). When the bleeding site was in the rectum, ultrasonographic detectability was 30% (10/33); ultrasonographic detectability was 82-100% when the bleeding site was elsewhere. Rectal bleeding and diverticular bleeding were difficult to diagnose by ultrasound, but for the other diseases, diagnosis by ultrasonographic examination was possible in 91-100% of cases. CONCLUSIONS: Ultrasonographic examination may be an effective screening method for lower gastrointestinal bleeding.

Colon↗

PubMed2006

Anti-parietal cell antibody and serum pepsinogen assessment in screening for gastric carcinoma.

BACKGROUND: Anti-parietal cell antibody is found in patients with Helicobacter pylori-positive gastritis and is related to atrophic gastritis and gastric carcinoma. AIM: To identify the characteristics of patients at high-risk for gastric carcinoma in terms of anti-parietal cell antibody and serum pepsinogen. PATIENTS AND METHODS: Subjects were 92 H. pylori-positive patients (54 men, 38 women; mean age, 57.9 years; range, 15-88 years). The serum concentrations of pepsinogen I and II were determined by radioimmunoassay, and the presence of anti-parietal cell antibody was assessed by enzyme-linked immunosorbent assay. Degrees of inflammation and atrophy in the corpus of the stomach were evaluated histologically. RESULTS: Patients were classified into four groups according to anti-parietal cell antibody status and pepsinogen I/II ratio. Anti-parietal cell antibody-negative/pepsinogen I/II-low patients had the highest risk for gastric carcinoma (prevalence of gastric carcinoma: 7/13=53.8%, odds ratio=7.6, 95% confidence interval, 1.2-48.0). Anti-parietal cell antibody titre was high when inflammation in the corpus was severe (p=0.06) and significantly low when atrophy in the corpus was severe (p=0.01). CONCLUSION: Our results showed that patients with a negative anti-parietal cell antibody titre and low pepsinogen I/II ratio are at high-risk for gastric carcinoma.

Adolescent↗

PubMed2005

Clinical features of gastric cancer discovered after successful eradication of Helicobacter pylori: results from a 9-year prospective follow-up study in Japan.

BACKGROUND: Eradication of Helicobacter pylori is expected to prevent the development of gastric cancer. However, gastric cancer is sometimes discovered after successful eradication of H. pylori. AIM: To conduct a prospective study to determine the clinical features of patients who underwent successful eradication and were later diagnosed with gastric cancer. METHODS: A total of 1787 patients (1299 males and 488 females; mean age, 58.2 years; range: 15-84) who underwent successful eradication therapy between April 1994 and March 2001 were our study subjects. RESULTS: Gastric cancer occurred at a rate of 1.1% (20 of 1787) during the follow-up period. Gastric cancer comprises six of 105 (5.7%) with early gastric cancer after endoscopic resection, 12 of 575 (2.1%) with gastric ulcer and two of 453 (0.4%) with atrophic gastritis. Gastric cancer did not develop in any patient with duodenal ulcer. All patients with gastric cancer had baseline severe atrophic gastritis in the corpus. CONCLUSION: Careful endoscopic examination is necessary even after successful eradication of H. pylori in patients with early gastric cancer or gastric ulcer with severe mucosal atrophy in the corpus.

Adolescent↗

PubMed2005

Morphological changes in human gastric tumours after eradication therapy of Helicobacter pylori in a short-term follow-up.

BACKGROUND: It is controversial as to whether the development of gastric cancer is influenced by Helicobacter pylori eradication. If eradication itself influences the tumour morphology, this may affect the tumour discovery rate. AIM: To investigate the morphological changes in the gastric neoplasm after H. pylori eradication. METHODS: We studied 37 patients with eradication therapy. After a 1-month follow-up, endoscopic re-evaluation was performed and the appearance was compared with first image. All lesions were resected endoscopically, and were subjected to histological assessment and to immunohistochemistry. Serum gastrin levels were determined before and after eradication. RESULTS: Twenty-nine of 37 patients underwent successful eradication. The appearance of 11 lesions (33% of 33 lesions) became indistinct after successful eradication. All lesions were of the superficial-elevated type and the height of the lesions decreased. We detected normal columnar epithelium over the neoplasm in eight of the lesions. Higher expression of single-stranded deoxyribonucleic acid in the deep area was characteristic in tumours with an indistinct appearance. These changes did not correlate with the serum gastrin levels. CONCLUSIONS: The morphology of the gastric neoplasm change after eradication in the short-term. This may contribute to the decreased tumour discovery rate.

Adenocarcinoma↗

PubMed2005

Eradication of Helicobacter pylori increases the incidence of hyperlipidaemia and obesity in peptic ulcer patients.

BACKGROUND: Eradication of Helicobacter pylori improves clinical symptoms and quality of life in patients with peptic ulcer. AIM: To investigate the effect of eradication of H. pylori on body mass index and incidence of hyperlipidaemia in patients with peptic ulcer. PATIENTS AND METHODS: The study population comprised 50 patients (42 men, 8 women; mean age, 51 years; 28 gastric ulcer, 22 duodenal ulcer) who underwent physical and blood examination before and 1 year after undergoing eradication therapy and 100 sex- and age-matched control subjects. Body mass index, total cholesterol and triglyceride were measured before and 1 year after therapy. RESULTS: The eradication therapy group showed a significant increase in body mass index (22.7+/-2.5 kg/m2 before eradication versus 23.6+/-2.6 kg/m2 after eradication, p < 0.01), serum total cholesterol (204.1+/-33.2 mg/dL versus 221.2+/-38.8 mg/dL, p < 0.01), and triglyceride. Additionally, the eradication therapy group showed a significant increase in the incidence of hypercholesterolemia (30% versus 58%, p<0.01), hypertriglyceridaemia (28% versus 44%, p < 0.01) and obesity (12% versus 22%, p <0.05) 12 months after therapy. CONCLUSION: Our findings show that eradication of H. pylori significantly increases the incidence of hyperlipidaemia and obesity in patients with peptic ulcer.

Adult↗

PubMed2005

Famotidine prevents canine gastric blood flow reduction by NSAIDs.

AIM: To investigate the effect of famotidine on gastric blood flow reduction induced by diclofenac sodium, a common non-steroidal anti-inflammatory drug in Japan, using laser Doppler flowmetry in the canine stomach. METHODS: The gastric mucosal blood flow was measured by laser Doppler flowmetry in 15 healthy male beagles before and 60 min after the administration of diclofenac suppository (1.0 mg/kg) into the rectum. The examination was done in a crossover, single-blinded fashion. All dogs underwent both famotidine (0.5 mg/kg) and placebo (saline) injection simultaneously with the administration of diclofenac. In addition, the tissue concentration of prostaglandin E2 was measured. RESULTS: The blood flow decreased by 18.3 +/- 9.1% in the gastric body, by 26.3 +/- 8.1% in the antrum in the placebo group after the administration of diclofenac sodium, while the decreases seen were significantly smaller in the famotidine group: 3.2 +/- 12.6% in the gastric body and 7.9 +/- 16.5% in the antrum (P = 0.001 for the gastric body, P = 0.0034 for the antrum). Conversely, the percentage of mucosal prostaglandin E2 concentration decrease in each group did not show a significant difference. CONCLUSION: Famotidine alleviates the reduction of gastric blood flow induced by diclofenac sodium. Further, not only mucosal prostaglandins but also gastric acid may play an important role in non-steroidal anti-inflammatory drugs-induced gastric microcirculatory disturbance.

Animals↗

PubMed2005

Effect of famotidine on recurrent bleeding after successful endoscopic treatment of bleeding peptic ulcer.

AIM: We investigated the effect of acid suppression therapy on recurrent bleeding after successful endoscopic treatment of bleeding peptic ulcer. METHODS: A total of 400 patients with bleeding peptic ulcer received either intravenous infusion of famotidine (40 mg/day) (n = 207, 163 males, 44 females, mean age 61.5 years) or drip infusion of omeprazole (40 mg/day; n = 193, 134 males, 59 females, mean age 59.8 years) after successful endoscopic treatment. The fasting duration, hospital stay, volume of transfused blood, incidence of rebleeding and mortality were compared between the two groups. RESULTS: The incidence of rebleeding did not differ significantly between the famotidine group (9%) and the omeprazole group (8%). The mean hospital stay was significantly shorter in the omeprazole group (18.4 days) than in the famotidine group (21.5 days, P = 0.009). However, there was no statistically significant difference in fasting duration, volume of transfused blood or mortality. CONCLUSION: Our findings indicate that intravenous infusion of famotidine after successful endoscopic treatment is equivalent to drip infusion of omeprazole for prevention of recurrent bleeding.

Adolescent↗

PubMed2005

Effect of long-term half-dose famotidine therapy on corpus gastritis in peptic ulcer disease.

BACKGROUND: Recent studies showed that acid-suppressive therapy aggravates corpus gastritis in patients with Helicobacter pylori infection. AIM: The aim of this study was to evaluate the effect of famotidine, a histamine receptor antagonist on corpus gastritis in patients with peptic ulcer disease. METHODS: We enrolled 287 patients, 173 with duodenal ulcer and 114 with gastric ulcer and 100 patients with H. pylori-positive gastritis as control subjects. Patients with peptic ulcer were classified according to whether or not they received famotidine-maintenance therapy (20 mg/day) after primary treatment. At the time of endoscopy, biopsy specimens were obtained from the antrum and the corpus. The degrees of neutrophil and lymphocyte infiltration, atrophy and intestinal metaplasia were scored according to the updated Sydney System. RESULTS: The degrees of neutrophil infiltration and atrophy in the corpus were significantly less in patients with gastric ulcer or duodenal ulcer than in patients with H. pylori-positive gastritis (P < 0.01). Differences in the degrees of neutrophil infiltration and atrophy in the corpus between the non-maintenance group and the maintenance group were not significant. CONCLUSION: Long-term therapy with famotidine does not appear to lead to an increase in the incidence of corpus gastritis or corpus atrophy in patients with peptic ulcer disease.

Adolescent↗

PubMed2004

Chronic gastritis with expression of inducible nitric oxide synthase is associated with high expression of interleukin-6 and hypergastrinaemia.

BACKGROUND AND AIMS: High levels of inducible nitric oxide synthase and nitrotyrosine in Helicobacter pylori-infected gastric mucosa may contribute to development of gastric cancer. We investigated the relation between expression of inducible nitric oxide synthase and proinflammatory cytokines in gastric mucosa and serum markers of gastritis. METHODS: The study included 103 patients with H. pylori infection. We examined levels of interleukin-1beta, interleukin-6 and interleukin-8 by enzyme-linked immunosorbent assay and evaluated expression of inducible nitric oxide synthase and nitrotyrosine by immunohistochemical staining. Furthermore, we assessed serum levels of pepsinogens, gastrin, anti-parietal cell antibody, nitrite and nitrate, as markers of gastritis. RESULTS: Thirty-seven of 103 (35.6%) gastric mucosa specimens showed simultaneous expression of inducible nitric oxide synthase and nitrotyrosine. In these patients (inducible nitric oxide synthase-positive group), the serum level of gastrin was significantly higher than that of the inducible nitric oxide synthase-negative group (509.5 +/- 141.5 pg/mL vs. 210.0 +/- 227.2 pg/mL; P < 0.01), whereas there were no significant differences in serum levels of pepsinogen, anti-parietal cell antibody, and nitrate and nitrite or in scores of histological gastritis. Interleukin-6 levels were significantly higher in the inducible nitric oxide synthase-positive group than in the inducible nitric oxide synthase-negative group (25.9 +/- 7.0 pg/mg protein vs. 10.6 +/- 4.9 pg/mg protein; P < 0.05). CONCLUSIONS: Inducible nitric oxide synthase-producing gastritis was correlated with high levels of interleukin-6. Patients with hypergastrinaemia should be carefully followed on a long-term basis to ensure that the development of any malignancy is detected early.

Adult↗

PubMed2004

Sonographic detection of longitudinal ulcers in Crohn disease.

BACKGROUND: The purpose of this study was to investigate the characteristic sonographic features, such as focal disappearance of the wall stratification sign (FD sign), of longitudinal ulcers in patients with Crohn disease (CD). METHODS: A total of 545 sonographic examinations of patients with Crohn disease (n = 166), ulcerative colitis (n = 196), bacterial colitis (n = 78), ischemic colitis (n = 63), pseudomembranous colitis (n = 32), Behçet's disease (n = 7), and collagenous colitis (n = 3) were extracted. The sonographic findings were compared with those of a barium contrast study, colonoscopy, and resected specimens. In transverse views of the bowel segment, wall stratification was investigated. The FD sign was defined as the disappearance of the layered structure observed in a single portion of the bowel circumference. Prevalence of the FD sign was investigated for each disease. RESULTS: Eighty lesions (76 CD, 1 ulcerative colitis, 2 ischemic colitis, 1 Behçet's disease) with active single longitudinal ulcers were detected by barium contrast study and endoscopy. Among them, the FD sign was detected by ultrasonography (US) in 73 lesions (91.3%). No lesions with the FD sign were found by US without radiological or endoscopic findings of longitudinal ulcers. An in vitro study (water-immersion method) of resected specimens revealed that the FD sign reflected the focal destruction of wall stratification caused by the deep longitudinal ulceration. CONCLUSIONS: Ultrasonographic findings of FD sign are correlated with the existence of deep longitudinal ulcers, which are most frequently found in CD. US is a useful diagnostic modality for detecting longitudinal ulcers in patients with CD.

Adolescent↗

PubMed2004

Review article: influence of Helicobacter pylori on gastro-oesophageal reflux disease in Japan.

There is circumstantial evidence that infection with Helicobacter pylori is relatively protective for the occurrence of gastro-oesophageal reflux disease (GERD). It has been suggested that the Japanese population are protected against reflux oesophagitis by their high prevalence of H. pylori associated gastritis. Such gastritis, when becoming chronic, can lead to gastric atrophy, thereby reducing the likelihood of GERD. If this hypothesis is correct, the effects of H. pylori induced gastritis may be an important factor determining the earlier lower prevalence of oesophagitis in Japan, where this infection is especially common. In support of this idea a reduced prevalence of H. pylori infection in Japan, as is now being observed in young Japanese adults, may be, at least in part, responsible for the upsurge in the number of cases of reflux disease in Japan. Concomitantly, H. pylori eradication therapy in patients with gastritis or peptic ulcer disease, which is associated with an increase in gastric acid secretion, may also be at least partly responsible for the increased prevalence of reflux oesophagitis in the Japanese population.

Gastroesophageal Reflux↗

PubMed2004

Characteristics and trends of clarithromycin-resistant Helicobacter pylori isolates in Japan over a decade.

Clarithromycin has been administered to patients in Japan since 1991. Clarithromycin-resistant Helicobacter pylori strains have been on the rise in Japan. We obtained H. pylori isolates between 1989 and 2000 and examined mutations of the 23S rRNA gene, which are closely associated with clarithromycin resistance. Isolates were obtained from 356 patients with H. pylori infection treated at the Hiroshima University. Sixty-one of the patients received clarithromycin-based H. pylori eradication therapy. Mutations of the 23S rRNA gene were examined by polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) followed by sequencing analysis. Mutant strains were found in 42 of the 356 patients (11.8%). The prevalence of mutant strains increased from 0 to 20.4% during the 12-year study period. The prevalence increased to more than 10% by 1995 and then to more 20% after 1999. The H. pylori eradication rate was significantly higher in patients with wild-type strains than in patients with mutant strains (72.0 vs. 36.4%, p = 0.024). Our data indicate that clarithromycin-resistant H. pylori strains have increased rapidly since 1995 and that the effectiveness of clarithromycin-based H. pylori eradication therapies may soon be compromised. Other new therapies may be necessary as first-line treatments in Japan.

Adolescent↗

PubMed2003

The long-term effect of Helicobacter pylori eradication therapy on symptoms in dyspeptic patients with fundic atrophic gastritis.

AIM: To investigate whether curing Helicobacter pylori infection improves symptoms over the long-term in Japanese patients with nonulcer dyspepsia and fundic atrophic gastritis. METHODS: Ninety H. pylori-positive dyspeptic patients with fundic atrophic gastritis were enrolled in this study. We performed a randomized double-blind placebo-controlled trial comparing triple therapy (n=45) with that of placebo alone (n=45). Inflammation and mucosal atrophy were scored according to the Updated Sydney System. Symptoms were scored on a scale of 0 to 3 for six items. Fasting samples of gastric juice were taken before endoscopy, and gastric pH was determined. Serum gastrin and pepsinogen levels were measured, and body mass index was determined. These patients were followed up for 3 years, and all measures were evaluated both before and after therapy. RESULTS: Significant improvement in dyspeptic symptoms and gastritis scores, significant decrease in gastric pH, and significant increase in body mass index were found after 3 years eradication in nonulcer dyspepsia patients treated successfully for H. pylori infection. There were no significant changes in the placebo group. CONCLUSION: Our study shows that eradicating of H. pylori results in significant long-term reduction in symptoms of nonulcer dyspepsia with fundic atrophic gastritis.

Adult↗

PubMed2003

Long-term observation of reflux oesophagitis developing after Helicobacter pylori eradication therapy.

BACKGROUND: Development of reflux oesophagitis after Helicobacter pylori eradication therapy has been reported, but the prognosis is not well known. AIM: To evaluate the prognosis of patients with reflux oesophagitis that developed after eradication therapy by long-term observation. METHODS: Forty-five patients who developed reflux oesophagitis after successful H. pylori eradication therapy were followed up prospectively. All 45 patients were followed up by endoscopy more than 3 years after onset of reflux oesophagitis (3-year follow-up group) and nine were followed up more than 5 years after onset (5-year follow-up group). Endoscopic observations were performed yearly or when upper gastrointestinal symptoms recurred. Reflux oesophagitis was graded according to the Los Angeles Classification System. Presence of gastro-oesophageal reflux symptoms and medication of proton pump inhibitors, H2-blockers or prokinetics were investigated at final endoscopy. RESULTS: All patients were classified as grade A or B at initial endoscopy. At final observation, the grade of reflux oesophagitis improved in 35/45 (78.8%) patients from the 3-year follow-up group and 7/9 (78.8%) patients from the 5-year follow-up group. Reflux oesophagitis progressed from grade A to B in only four (8.9%) patients from the 3-year follow-up group and in no patients in the 5-year follow-up group. No patient progressed to grade C or D. Gastro-oesophageal reflux symptoms were seen in 12 patients (26.7%) from the 3-year follow-up group and four patients (44.4%) from the 5-year follow-up group. Among them, medication was needed continuously in only six (13.3%) and two (22.2%) patients, respectively. CONCLUSIONS: Reflux oesophagitis, which develops after H. pylori eradication therapy, rarely becomes a long-term clinical problem among patients who complete therapy successfully.

Amoxicillin↗

PubMed2003

The specific expression of hypoxia inducible factor-1alpha in human gastric mucosa induced by nonsteroidal anti-inflammatory drugs.

BACKGROUND: Hypoxia is a cause of gastric mucosal damage induced by nonsteroidal anti-inflammatory drugs (NSAIDs). The expression of hypoxia inducible factor-1alpha (HIF-1alpha) reflects the status of tissue ischaemia. AIM: To investigate the effect of NSAID administration on the expression of HIF-1alpha in human gastric mucosa. METHODS: We employed 71 patients including 14 with NSAID administration. The HIF-1alpha expression was estimated by immunohistochemistry using monoclonal antibody (H1alpha67) and raised antiserum (HI-3). Vascular endothelial growth factor expression was also examined by immunohistochemistry. HI-3 recognized hypoxia-induced protein in HeLa cells. RESULTS: In human gastric mucosa, HIF-1alpha was mainly expressed in the nuclei of the surface epithelial cells and in the neck zone both by use of HI-3 and of H1alpha67. The expression of vascular endothelial growth factor correlated well with that of HIF-1alpha. The level of HIF-1alpha in the surface epithelium was significantly higher in patients with administration of NSAIDs than those without NSAID use (P < 0.001) both in the gastric corpus and antrum. Helicobacter pylori infection did not affected the levels of HIF-1alpha. Long-term administration of rebamipide reduced the level of HIF-1alpha. CONCLUSION: HIF-1alpha expression is a new biological marker of ischaemia especially in NSAID-related gastric lesions.

Adolescent↗

PubMed2003

Review article: clinical significance of mucosal-protective agents: acid, inflammation, carcinogenesis and rebamipide.

While a great deal of clinical evidence has been found regarding anti-acids for the treatment of gastric disorders including peptic ulcers, not all disorders can be explained only by the hyperfunction of acid secretion. Especially in the Asian region, glandular atrophy is more prominent than in Western countries, therefore low acid output is often observed in these patients. Improvement of mucosal protection is rational therapy for these patients; this is the reason for use of these agents in Asian countries. Rebamipide has many biological activities for gastric mucosa such as increasing the blood flow and biosynthesis prostaglandins and the decrease of oxygen radicals. These suggest the possible efficacy of rebamipide in the prevention of both Helicobacter pylori-related and nonsteroidal anti-inflammatory drug (NSAID)-induced gastric injury, which has been proved by human studies. Rebamipide is the only mucosal-protective drug which can improve the histological gastritis in vivo, whereas anti-acids have a lesser effect in influencing gastritis. Improvement of gastritis is expressed not only in quantity but also in quality of gastritis, which is shown as the reduction of iNOS expression in the gastric mucosa. Clinically, it is suggested that rebamipide has the potential to prevent gastric carcinogenesis by improvement of histological gastritis.

Alanine↗

PubMed2003

Helicobacter pylori infection influences tumor growth of human gastric carcinomas.

BACKGROUND: Helicobacter pylori infection is considered a risk factor for gastric carcinoma. However, the effect of eradication therapy in gastric carcinoma patients is not well known. The aim of this study was to investigate the relationship between H. pylori infection and tumor growth of gastric carcinoma. METHODS: Fifty-one patients with gastric carcinoma participated in the study. Thirty-three were H. pylori-positive, 6 were H. pylori-negative, and 12 were diagnosed with gastric carcinoma after eradication of H. pylori. To investigate tumor growth of gastric carcinoma, cell proliferation and angiogenesis of the tumors were evaluated by immunohistochemical techniques using Ki-67 and CD34. RESULTS: The Ki-67 labeling index was 47.9 +/- 2.6 (mean +/- s) in the H. pylori-positive group, 38.1 +/- 3.6 in the H. pylori-eradicated group, and 22.2 +/- 5.5 in the H. pylori-negative group. It was significantly lower in the H. pylori-eradicated and H. pylori-negative groups than in the H. pylori-positive one, and a significant difference was also found between the H. pylori-positive and H. pylori-eradicated groups. The microvessel counts were 62.5 +/- 3.0, 50.2 +/- 4.0, and 66.0 +/- 9.8 in the positive, eradicated, and negative groups, respectively. A significant difference was found between the H. pylori-positive and H. pylori-eradicated groups. CONCLUSION: Our results suggest that H. pylori infection is associated with cell proliferation, and its eradication may influence tumor vascularity of gastric carcinoma. Therefore, H. pylori eradication therapy may contribute to the suppression of tumor growth.

Aged↗

PubMed2003

Autonomic nerve dysfunction is closely associated with the abnormalities of esophageal motility in reflux esophagitis.

BACKGROUND: While reflux esophagitis (RE) is often associated with esophageal motility dysfunction, the causes of this abnormal motility are not well understood. The aim of our study was to assess the relationship between esophageal motility and autonomic nerve dysfunction by comparing 14 healthy control subjects (11 M, 3 F; mean age, 56.4 years) with 26 patients with RE (19 M, 7 F; mean age, 60.4 years). METHODS: According to results of esophageal manometry, subjects with RE were assigned to group I (RE with esophageal motility dysfunction, n = 12) or group N (RE without motility dysfunction, n = 14). Autonomic neuropathy was assessed by measuring the heart rate coefficient of variation at rest (CVR-R), the Valsalva ratio for the R-R interval, the systolic blood pressure response to mental calculation, and the antral contractile response to modified sham feeding (MSF). RESULTS: CVR-R at rest was lower in group I (2.08 +/- 0.18) than in group N (3.80 +/- 0.44; P < 0.05). The frequency of antral contractile response to MSF per 3-min interval over 15 min was significantly lower in group I than in either group N or controls. The 15-min integrated antral contractile response, taken as the area under the contraction time curve, was much lower in group I (13.2 +/- 6.2) than in controls (55.6 +/- 9.2; P < 0.01). CONCLUSIONS: We conclude that esophageal motor dysfunction in some patients with RE may result from autonomic dysfunction.

Adult↗