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S Sedghi

Publications and source records attributed to S Sedghi.

9 recordsLinked to original sources
PubMed2003

Comparative results of endoluminal gastroplasty and laparoscopic antireflux surgery for the treatment of GERD.

BACKGROUND: Transoral endoluminal gastroplasty (EG) by the Bard Endocinch device is available for the treatment of gastroesophageal reflux disease (GERD). This study assessed the early (<or=12 months) outcomes in patients undergoing EG performed by one gastroenterologist compared with another set of patients referred by the same gastroenterologist for laparoscopic antireflux surgery (LAS) at a foregut surgery center. METHODS: From June 2000 to July 2002, 87 consecutive patients cared for by a single gastroenterologist were diagnosed with refractory GERD and underwent either EG (n = 47) or referral for LAS (n = 40). Preoperative evaluation included symptom assessment, pH studies, and motility studies. Outcomes were assessed by symptomatic improvement and dependence on anti-acid medications. Data analyzed by chi-square or Mann-Whitney tests are reported as mean +/- SEM. RESULTS: Preoperative symptom duration, Johnson-DeMeester (JD) score, % time pH < 4, and reflux episodes were statistically similar in both treatment groups. The follow-up times for EG and LAS groups were 7.3 +/- 0.9 and 8 +/- 0.4 months, respectively. Of EG patients, 94% were available for follow-up, and all LAS patients had follow-up data. Overall, 66% of patients were satisfied with EG as compared to 93% after LAS (p = 0.1). Postoperative PPI/motility agent use was 32% for EG and 13% for LAS (p = 0.03). Identifiable causes of EG failure were premature procedure termination due to hypoxia or bleeding (three patients), intractable vomiting (two patients), and delayed gastric emptying (five patients). Three EG patients subsequently had LAS within 6 months of the procedure. CONCLUSIONS: LAS offers greater reduction in medication use than EG, as well as more durable patient satisfaction. Benefits of EG may include short-term symptomatic improvement while considering definitive surgical management.

Adult↗
PubMed1995

Modulation of neutrophil function by novel colonic factors: possible role in the pathophysiology of ulcerative colitis.

Tissue damage in acute ulcerative colitis (UC) may be triggered by neutrophils (PMNs) and their inflammatory mediators such as reactive oxygen species (ROS). Because circulating PMNs appeared normal in subjects with UC, we hypothesized that the critical abnormality that attracts and activates PMNs in UC is a local colonic factor. Accordingly, the colonic milieu was sampled by using in vivo rectal dialysis (mol wt < or = 12 kd). Normal PMNs were exposed in vitro to rectal dialysates (RD) from control subjects (cRD) or subjects with active UC (aRD) or inactive UC (IRD). PMN-derived ROS were measured by chemiluminescence. cRD did not increase ROS production by unstimulated PMNs; aRD significantly and concentration-dependently increased ROS; IRD gave intermediate results. cRD inhibited the PMN-stimulating effects of both the bacterial peptide formyl-methionyl-leucyl-phenylalanine (fMLP) and phorbol myristate acetate (PMA). aRD and IRD blunted the effect of fMLP and PMA significantly less than did cRD. Rectal dialysates from 44% of subjects with active UC exaggerated the fMLP effect, whereas potentiation occurred for only 13% of cRDs and 18% of iRDs. cRD preconditioned with either activated or nonactivated PMNs was not significantly different than unconditioned cRD. We thus infer the existence of colonic factors in UC that (1) can trigger PMNs to produce ROS and (2) have a proinflammatory modulatory effect on bacterial peptide-induced, PMN-mediated ROS production, thereby initiating or perpetuating inflammation and eventually causing tissue damage.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Elevated breath ethane levels in active ulcerative colitis: evidence for excessive lipid peroxidation.

OBJECTIVE: Reactive oxygen species (ROS) may be a major cause of tissue injury in ulcerative colitis (UC). One possible mechanism for ROS-mediated tissue injury is lipid peroxidation. Breath ethane and pentane excretion are noninvasive means for measuring peroxidation of omega-3 and omega-6 polyunsaturated fatty acid, respectively. Hence, we measured breath ethane in 17 subjects with active UC and correlated the results with disease severity. METHODS: Breath samples for ethane and pentane analysis were collected every 2 weeks, and rectal biopsies were obtained monthly to assess for chemiluminescence, a marker of ROS. Ethane and pentane concentrations (nmol/L) were measured by gas chromatography, and mucosal chemiluminescence was measured spectrophotometrically. Data were compared to control values (C) from healthy subjects. Disease activity was assessed both clinically and endoscopically. RESULTS: Ethane excretion was significantly elevated in patients (UC, 0.45 +/- 0.04; C, 0.33 +/- 0.06; p = 0.013). Ethane excretion was positively correlated with endoscopic score (r = 0.45; p < 0.05), symptom score (r = 0.34; p < 0.05), disease activity (r = 0.36, p < 0.05), and chemiluminescence (r = 0.65; p < 0.001). Pentane levels did not correlate with any of the clinical measurements. Chemiluminescence in the rectal tissue was positively correlated with endoscopic score (r = 0.71; p < 0.05) and disease activity (r = 0.61; p < 0.01). CONCLUSIONS: Tissue damage in UC may be ROS-induced lipid peroxidation. Disease activity can be assessed noninvasively by breath ethane excretion.

Acute Disease↗
PubMed1993

Increased production of luminol enhanced chemiluminescence by the inflamed colonic mucosa in patients with ulcerative colitis.

Reactive oxygen species have been implicated as mediators of inflammation in ulcerative colitis. Chemiluminescence is a reliable means of estimating reactive oxygen species in biological media. Increased reactive oxygen species values in the inflamed colonic mucosa in rats were seen by chemiluminescence. The aims of the study were to find out if chemiluminescence is raised in the colonic mucosa of patients with ulcerative colitis and correlates with disease activity, and to elucidate the sources of the chemiluminescence. It was found that reactive oxygen species, as measured by the chemiluminescence technique, are raised in inflamed colonic mucosa and correlates with symptom score, sigmoidoscopic score, disease activity, and activity of the neutrophil enzyme myeloperoxidase. Chemiluminescence was inhibited by a myeloperoxidase inhibitor (azide) and an H2O2 scavenger (catalase) but not by allopurinol, an inhibitor of the enzyme xanthine oxidase. Chemiluminescence was also inhibited by indomethacin, but this did not seem to be related to inhibition of cyclo-oxygenase. These findings suggest that a likely cellular source of reactive oxygen species in the inflamed colon of patients with ulcerative colitis is the neutrophil and that myeloperoxidase conversion of H2O2 to hypochlorous acid, contributes to the chemiluminescence signal and possibly, to the tissue injury. Neither cyclo-oxygenase nor lipoxygenase seem to play a part as sources for the chemiluminescence.

Adult↗
PubMed1992

Excessive production of reactive oxygen metabolites by inflamed colon: analysis by chemiluminescence probe.

Reactive oxygen metabolites (ROMs) are involved in inflammatory diseases and are postulated to contribute to tissue injury in colitis. To determine whether excessive ROMs are generated by inflamed colonic mucosa and to identify possible sources and type of ROMs, mucosal ROMs were estimated in rats and humans using a chemiluminescence probe. Colitis was induced in rats by intracolonic injection of acetic acid or intraperitoneal injection of mitomycin C. Intact, inflamed colon in rats produced more ultraweak chemiluminescence than normal colon. Inflamed mucosal scrapings from both rat models produced significantly more luminol-enhanced chemiluminescence. Addition of catalase, an H2O2 scavenger, or azide, a myeloperoxidase inhibitor, into the media significantly decreased chemiluminescence from inflamed mucosal scrapings. Indomethacin, an antioxidant cyclo-oxygenase inhibitor, also decreased chemiluminescence, but MK-866, a 5-lipoxygenase inhibitor, had no effect. Colonic biopsy specimens obtained during colonoscopy from patients with ulcerative colitis also produced more catalase-inhibitable chemiluminescence than normal colonic mucosa. These data indicate that excessive ROMs are produced by inflamed colonic mucosa in both humans and rats, which may contribute to tissue injury.

Adult↗
PubMed1992

Mitomycin C-induced colitis in rats: a new animal model of acute colonic inflammation implicating reactive oxygen species.

The mechanism of the tissue damage induced by colonic inflammation in ulcerative colitis is not established. We therefore developed and characterized a simple new rat model of acute colonic inflammation induced by a single systemic injection of mitomycin C. After an intraperitoneal injection of mitomycin-C, colon histologic examination revealed transient (3 to 14 days) diffuse, colonic inflammation and injury that, like human ulcerative colitis, was limited to the mucosal layer. The rest of the gastrointestinal tract was spared. Gut permeability, as measured by urinary excretion of orally administered lactulose and mannitol, was unchanged 3 days after injection, when inflammation was already present; permeability was increased at 7 days, when inflammation was maximal. Mitomycin C did not produce inflammation in experimentally bypassed segments of small bowel despite the presence of colonic-type bacteria, suggesting that lack of intraluminal bacteria was not responsible for the absence of inflammation in the small intestine. Chemiluminescence, a means of estimating levels of reactive oxygen species, was greater in the intact, inflamed colon of mitomycin C-treated rats than in bypassed segments. Moreover, inflamed mucosal scrapings produced more in vitro luminol-enhanced chemiluminescence. Furthermore, the reactive oxygen species scavengers allopurinol, catalase, and WR-2721 decreased inflammation severity. We therefore conclude: (1) the mitomycin C-treated rat is a novel, easy to prepare animal model of acute inflammation of colonic mucosa, with morphologic similarities to the acute phase of ulcerative colitis in human beings; (2) increased gut permeability in mitomycin C-treated rats is the result, not the cause, of the inflammation; and (3) reactive oxygen species play an important role in colonic inflammation and tissue injury in this model, and possibly in human ulcerative colitis.

Animals↗
PubMed1991

Effect of acute ethanol on esophageal motility in cat.

In man, acute ethanol administration decreases lower esophageal sphincter pressure (LESP), prolongs the duration, and lowers the amplitude of esophageal contractions. These changes may contribute to gastroesophageal reflux and esophagitis. To evaluate the underlying mechanisms of these changes an animal model is needed. Hence, we studied the effect of various doses of ethanol on esophageal motility in cats, an animal with an esophagus similar to man's. Similar to man, intravenous administration of ethanol significantly decreased LESP and amplitude of lower (smooth muscle portion) esophageal contractions. It also prolonged the duration of lower esophageal contractions, even through it had no effect on contraction velocity. The effect of ethanol on upper (striated muscle portion) esophagus was different. Ethanol had no effect on the amplitude of contractions, whereas it prolonged their duration and decreased their velocity. The effect of acute ethanol on LESP in four withdrawing alcoholic cats was similar to controls. However, the acute effect of ethanol on the esophageal contractions was less marked in alcoholics. Bilateral cervical vagotomy and intravenous injection of the neurotoxin tetrodotoxin before the administration of ethanol did not prevent the effect of ethanol on LESP. This data suggests that cat esophagus is a good model for studying the underlying mechanisms of the effects of acute ethanol because its response is similar to the esophagus of man, and the acute effect of ethanol on LESP is not neurally mediated but is the result of its direct effect on muscle.

Alcohol Drinking↗
PubMed1990

Role of reactive oxygen metabolites in experimental colitis.

Reactive oxygen metabolites are potent inflammatory mediators that may be involved in tissue injury in inflammatory bowel disease. To evaluate their role in inflammatory bowel disease, we investigated the effects of lowering the activities of reactive oxygen metabolites in experimental colitis induced by intracolonic administration of acetic acid in rats. Intracolonic administration of 5% acetic acid caused severe inflammation (mean (SEM) inflammatory score was 24.3 (0.7) of a maximum score of 32). Acetic acid at 2.5% produced moderate inflammation (score = 17 (1.4) v 4.0 (0.5) in control rats). This lower dose was used for subsequent experiments. Specific superoxide anion scavenger methoxypolyethylene glycol:superoxide dismutase, and reactive oxygen metabolites scavenger, sulfasalazine, significantly decreased the severity of inflammation (scores: 8 (4.4) and 9.8 (2.2) respectively). The xanthine oxidase inhibitors, tungsten and pterin aldehyde, failed to improve inflammation but another xanthine oxidase inhibitor, allopurinol, a compound with known superoxide anion scavenging effect, did limit the inflammation (10(2)). Inhibition of hydroxyl radical production by deferoxamine or lowering hydroxyl radical values by a scavenger, dimethyl sulfoxide, did not affect the severity of inflammation. These data suggest: (1) that reactive oxygen metabolites play an important role in experimental colitis, (2) that the xanthine oxidase pathway is not a major source of reactive oxygen metabolites in colitis, and (3) that tissue injury in experimental colitis is not caused by generation of hydroxyl radicals.

Animals↗