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Biomedical subjects

G Perdikis

Publications and source records attributed to G Perdikis.

At least 37 records · Page 2Linked to original sources
PubMed1996

Duodenogastric reflux causes growth stimulation of foregut mucosa potentiated by gastric acid blockade.

We investigated whether duodenogastric reflux (DGR) together with gastroesophageal reflux causes growth stimulation of the foregut mucosa and if additional gastric acid suppression enhances the effect of DGR. DGR was induced in rats using a split gastroenterostomy. A cardiomyotomy was performed across the gastroeophageal junction in order to enhance reflux into the esophagus. DGR rats were divided into six subgroups: DGR, DGR + truncal vagotomy, DGR + omeprazole, DGR + gastrin receptor blockade, DGR + omeprazole + gastrin receptor blockade, and DGR + gastrin. Two sham groups, one with and one without omeprazole treatment, served as controls. DGR significantly increased the weight and DNA content of the esophageal and gastric mucosa, which was further enhanced by vagotomy or omeprazole. Histology revealed foveolar hyperplasia in the stomach and esophageal mucosal hyperplasia in these groups. In addition, severe esophagitis was found in the DGR group receiving omeprazole. Omeprazole without DGR had no growth-stimulating effect on the foregut mucosa. DGR-induced growth stimulation was accompanied by hypergastrinemia. Increased growth in the stomach but not the esophagus was inhibited by gastrin receptor blockade. Gastrin administration did not result in enhancement of DGR-induced growth stimulation of the foregut mucosa. It is concluded that DGR, often present in severe reflux esophagitis, causes mucosal growth of the foregut of rats. This trophic response may explain why severe reflux esophagitis is associated with an increased risk of esophageal adenocarcinoma. DGR-induced growth stimulation of the foregut is potentiated by gastric acid suppression, suggesting that chronic antisecretory medication in gastroesophageal reflux may not always be advisable. Omeprazole + DGR caused severe esophageal damage, which may explain why antisecretory medication may fail to heal severe reflux esophagitis.

Animals↗
PubMed1996

Three-dimensional imaging of the lower esophageal sphincter in healthy subjects and gastroesophageal reflux.

The resting pressure and intraabdominal length are the most important factors which determine competence of the lower esophageal sphincter (LES). The intraabdominal sphincter vector volume (ISVV) is a single value which takes into account both of these measurements. Normal values of ISVV and of the total sphincter vector volume (TSVV) were established in 20 normal subjects. The sensitivity and the specificity of ISVV and TSVV were then evaluated in 81 patients with gastroesophageal reflux disease (GERD) and in 19 normal subjects and were compared with the usual stepwise pullback manometry (SPM) measuring the resting pressure of the LES at the respiratory inversion point. The motorized pullthrough technique was used to perform the vector volume procedure. Normal values of ISVV were 1870-10740 mm Hg2 x mm, and of TSVV 2200-13110 mm Hg2 x mm. The sensitivity of ISVV was 93.8% (p < 0.05), of TSVV 80.2%, and of SPM 81.5%. The specificity of ISVV and TSVV was 89.5% and of SPM 78.9% (not significant). Analysis of the intraabdominal sphincter vector volume is more sensitive than the total sphincter vector volume or standard stationary manometry in establishing a defective LES in patients with GERD. Intraabdominal sphincter vector volume analysis will allow surgeons better to identify patients with a defective LES who may be suitable for antireflux surgery.

Diagnosis, Computer-Assisted↗
PubMed1996

The hypertensive lower esophageal sphincter.

BACKGROUND: This study defines the entity of the hypertensive lower esophageal sphincter (HLES) and its treatment, including surgical implications. METHODS: Esophageal manometry was performed on 1,300 patients. Of these, 53 (4%) had HLES with resting pressure > 26.5 mm Hg, defined as the upper limit of normal resting LES pressure. Thirty-two of these patients had 24-hour esophageal pH studies. The response to treatment was assessed. RESULTS: Fourteen patients (26%) with HLES had achalasia. Of the remaining 39 (74%), 25 had an isolated HLES with normal esophageal body motility, 5 had a nonspecific esophageal motility disorders (NEMD), 4 were post-Nissen fundoplication, 3 had a nutcracker esophagus, and 2 had diffuse esophageal spasm (DES). Nineteen percent of HLES patients had gastroesophageal reflux on pH studies. Eighty-two percent of HLES patients responded well to symptom-directed medical therapy. Two patients with esophageal body dysmotility responded well to an esophageal myotomy with a partial fundoplication. CONCLUSIONS: Patients with the HLES form a heterogeneous group. Gastroesophageal reflux in HLES patients is not uncommon. Patients with HLES respond well to medical therapy. Carefully selected patients require surgery.

Adolescent↗
PubMed1995

An intraluminal surgical approach to the management of gastric bezoars.

Trichobezoars are difficult to remove endoscopically, often cause nausea and vomiting, and can result in small-bowel obstruction. A patient with a trichobezoar presented to our clinic with symptoms of partial small-bowel obstruction. Multiple attempts at flexible endoscopic removal were unsuccessful. Two large-diameter percutaneous gastrostomies with an inflatable balloon and distal foam-rubber stent to assure intragastric positioning were introduced under general anesthesia. Visualization was provided by a 0 degree panavision laparoscope placed through one of the gastrostomies. The bezoar was removed through the second gastrostomy using standard laparoscopic instruments. The patient made an uneventful recovery. This is the first reported case of percutaneous removal of a trichobezoar. We conclude large-diameter gastrostomies may serve as a port of access for numerous other intraluminal procedures.

Bezoars↗
PubMed1995

In vitro free radical production in rat esophageal mucosa induced by nicotine.

Oxidative stress induced by nicotine was investigated in the esophageal mucosa of rats. The homogenized mucosa was incubated for 30 min with 50, 100, 200, 400, and 800 ng/mg protein/ml nicotine or with 200 ng/mg protein/ml nicotine for 15, 30, 45, and 60 min. Esophageal mucosa was also incubated for 30 min with 200 ng/mg protein/ml nicotine with or without the scavengers superoxide dismutase (SOD), catalase, SOD+catalase, inactivated SOD, inactivated catalase, or albumin. Incubation with 0.9% NaCl served as control. There was a strong correlation between chemiluminescence and the nicotine dose (r = 0.75) or the nicotine incubation time (r = 0.77). Thirty-minute incubation of the esophageal mucosa with 200 ng/mg protein/ml nicotine increased chemiluminescence 5.5-fold and lipid peroxidation 3.3-fold. This response was dampened by SOD or catalase and abolished by SOD+catalase. Inactivated enzymes or albumin had no scavenging effect. These results demonstrate that nicotine causes oxidative stress to the esophageal mucosa.

Animals↗
PubMed1995

Free radical scavengers prevent reflux esophagitis in rats.

Free radical damage in reflux esophagitis of rats induced by 24-hr duodenojejunal ligation was studied. Oxygen free radicals were selectively blocked. Groups were: sham operation, reflux, reflux + superoxide dismutase (SOD), catalase, dimethylthiourea, allopurinol, and inactivated SOD or inactivated catalase alone or in the combination SOD + catalase or SOD + catalase + dimethylthiourea + allopurinol. Macroscopic esophagitis was inhibited only by SOD, alone or in combination with other agents. Esophageal mucosal lipid peroxidation was 10-fold increased in the reflux group compared to the sham group (P < 0.05). This response was damped by SOD > catalase (P < 0.05) but not by the inactivated enzymes, dimethylthiourea or allopurinol. SOD + catalase showed no significant improvement on SOD alone. Total inhibition of lipid peroxidation was achieved by combining all scavengers. Total glutathione (GSH) in the esophageal mucosa was stimulated by reflux. This response was inhibited by scavengers equivalent to their efficacy in preventing lipid peroxidation. It is concluded that reflux esophagitis is associated with free radical release with O2- being the main source. Free radicals appear to stimulate GSH production in this prolonged oxidative stress.

Animals↗
PubMed1995

Esophagitis in Sprague-Dawley rats is mediated by free radicals.

Free radical-mediated esophagitis was studied during duodenogastroesophageal reflux (mixed reflux) or acid reflux in rats. The influence of reflux on esophageal glutathione levels was also examined. Mixed reflux caused more gross mucosal injury than acid reflux. Gross mucosal injury occurred in the mid-esophagus. Total glutathione (GSH) in the esophageal mucosa of control rats was highest in the distal esophagus. The time course of esophageal GSH in rats treated by mixed reflux showed a significant decrease 4 hr after initiation of reflux, followed by a significant increase from the 12th hour on. Mucosal GSH was increased in both reflux groups after 24 hr but significantly more so in the mixed than in the acid reflux group. The free radical scavenger superoxide dismutase (SOD) prevented esophagitis and was associated with decreased GSH levels. GSH depletion by buthionine sulfoximine (BSO) prevented esophagitis and stimulated SOD production in the esophageal mucosa. It is concluded that gastroesophageal reflux is associated with oxidative stress in the esophageal mucosa. The lower GSH levels in the mid-esophagus may predispose to damage in this area. Duodenogastroesophageal reflux causes more damage than pure acid reflux. Oxidative stress leads to GSH depletion of the esophageal mucosa in the first few hours following damage but then stimulates GSH production. GSH depletion by BSO does not worsen esophagitis since it increases the esophageal SOD concentration.

Animals↗
PubMed1995

Free radical production in nicotine treated pancreatic tissue.

The ability of nicotine to induce oxidative stress in the pancreatic tissue of rats was investigated. Homogenized pancreatic tissue of Sprague-Dawley rats was incubated with nicotine in a dose of 200 ng/mg protein/ml for 15, 30, 45, and 60 min or was incubated for 30 min with nicotine in a dose of 50, 100, 200, 400, and 800 ng/mg protein/ml. Pancreatic tissue was also incubated with 200 ng/mg protein/ml nicotine with or without the scavengers superoxide dismutase (SOD), catalase, SOD+catalase, inactivated SOD, inactivated catalase, or albumin. Incubation with 0.9% NaCl served as control. There was a positive correlation between the duration of nicotine incubation and chemiluminescence (r = 0.6) or lipid peroxidation (r = 0.71) and also between the nicotine dose and chemiluminescence (r = 0.54) or lipid peroxidation (r = 0.66). Thirty minutes incubation of pancreatic tissue with nicotine in a dose of 200 ng/mg protein/ml increased chemiluminescence 5 fold and lipid peroxidation 2.5 fold. This response was dampened by SOD or catalase and abolished by SOD+catalase. Inactivated enzymes or albumin had no scavenging effect. These results demonstrate that nicotine causes oxidative stress to the pancreatic tissue of rats.

Animals↗
PubMed1995

Reflux esophagitis in humans is mediated by oxygen-derived free radicals.

BACKGROUND: Oxidative stress in reflux esophagitis was investigated before and after antireflux surgery. PATIENTS AND METHODS: Oxidative stress was studied in the distal and proximal esophagus of control patients (without esophagitis, but with other gastrointestinal disorders), of patients with various grades of esophagitis (including Barrett's esophagus), and in patients who had a Nissen fundoplication. Oxidative stress was assessed by chemiluminescence, lipid peroxidation (LP), and by measuring superoxide dismutase (SOD). RESULTS: Chemiluminescence and LP increased with the degree of esophagitis and was highest in patients with Barrett's esophagus; SOD decreased with damage, except in cases of Barrett's esophagus associated with mild esophagitis. Chemiluminescence and LP in reflux patients were higher in the distal than in the proximal esophagus, and SOD was lower, whereas no such difference was found in controls. Findings after Nissen fundoplication were similar to those of controls. CONCLUSIONS: Reflux esophagitis is mediated by free radicals depleting SOD. Barrett's esophagus is a severe form of oxidative damage; in some patients, high SOD levels may prevent severe esophagitis. Antireflux surgery prevents oxidative damage.

Barrett Esophagus↗
PubMed1995

Pathologic duodenogastric reflux associated with persistence of symptoms after cholecystectomy.

BACKGROUND: The aim of this study was to determine whether increased duodenogastric reflux contributes to postcholecystectomy symptoms. METHODS: Gastric pH monitoring, hepatobiliary scintigraphy, gastric emptying scans, and gastric acid analysis were performed in asymptomatic (n = 10) and in symptomatic (n = 27) patients after cholecystectomy. Normal subjects (n = 20), patients with dyspepsia related to gastric acid hypersecretion (n = 20), patients with reflux gastritis after gastric surgery (n = 10), and patients with confirmed primary pathologic duodenogastric reflux (n = 10) were studied as controls. Symptomatic patients also underwent upper gastrointestinal endoscopy. RESULTS: Symptomatic patients had significantly increased interprandial gastric exposure to pH < 3 compared with asymptomatic subjects, which correlated well with a high incidence of hepatobiliary scans positive for abnormal duodenogastric reflux and chronic gastritis on endoscopy. Gastric alkaline exposure in symptomatic patients was similar to that seen in patients with primary pathologic duodenogastric reflux and patients with duodenogastric reflux related to gastric surgery. Gastric acid secretion and gastric emptying were not altered. Five patients tested before and after laparoscopic cholecystectomy showed that nocturnal gastric alkalization was enhanced after operation. CONCLUSIONS: This study suggests that excessive duodenogastric reflux may be responsible for persistence of symptoms after cholecystectomy.

Adult↗
PubMed1994

Bone disorders following total gastrectomy.

Bone disorders following gastrectomy were studied by measuring absolute and relative bone mineral density of the Wards triangle, serum 1,25-(OH)2-D, alkaline phosphatase, and total serum calcium. The subjects were 20 males who had undergone total gastrectomy not more than three months previously (group A1). Seventeen of these patients were reviewed three years later (group A2). Absolute and relative bone density were significantly lower in group A2 than in A1 (0.52 +/- 0.011 g/cm2 versus 0.6 +/- 0.014 g/cm2, P < 0.01 and 85.5 +/- 1.4% age-matched control versus 95 +/- 1.3%, P < 0.01). 1,25-(OH)2-D was significantly lower in group A2 than in group A1 (14.3 +/- 0.97 pg/ml versus 20.6 +/- 1.02 pg/ml, P < 0.01). There was no difference in alkaline phosphatase and calcium serum concentration. The mean weight loss was 6.26 +/- 0.57% over the follow-up period, and weight loss correlated with absolute and relative bone density (r = -0.74, P < 0.01). There was a positive correlation between 1,25-(OH)2-D and absolute or relative bone density (r = 0.67, r = 0.62 and P < 0.01). These data suggest that bone density decrease has already occurred three years after total gastrectomy and is positively correlated to 1,25-(OH)2-D deficiency. As no differences in serum alkaline phosphatase and serum calcium concentration were found, these factors are of little value for the early detection of postgastrectomy bone disorders, whereas weight loss is a valuable screening parameter.

Aged↗
PubMed1994

Lymphangitis carcinomatosis of the lesser omentum: a prognostic factor in gastric cancer.

A series of 126 patients with gastric cancer who underwent radical gastrectomy with systemic lymph node dissection revealed 9 patients who survived for a median time of only 3 months. Of these 9 patients, 4 were classified by the UICC system as stage II and 5 as stage III, all of whom had lymphangitis carcinomatosis of the lesser omentum. These data suggest that although lymphangitis carcinomatosis of the lesser omentum is an uncommon finding, if it is present, curative surgery is impossible and an operation should therefore be limited to tumor palliation.

Adult↗
PubMed1994

Gastroesophageal reflux disease is associated with enteric hormone abnormalities.

Basal and postprandial levels of the foregut hormones gastrin, cholecystokinin (CCK), motilin, and pancreatic polypeptide, and the distal gut hormones neurotensin and peptide YY were measured in 20 patients with gastroesophageal reflux disease (GERD). GERD was defined by abnormal esophageal exposure to pH less than 4. Ten GERD patients had decreased lower esophageal sphincter (LES) pressure (mean: 4.5 mm Hg, range: 0.8 to 6.8 mm Hg), and 10 patients had normal LES pressures (mean: 14.1 mm Hg, range: 9.7 to 22.4 mm Hg). Eight age-matched healthy subjects were also studied. Basal levels of peptide YY were moderately decreased in GERD patients compared with controls irrespective of LES pressure. In patients with abnormal LES pressure, basal levels of motilin and the postprandial response of CCK were significantly decreased compared with controls; and basal levels of neurotensin and the postprandial response of gastrin were significantly increased compared with controls. Pancreatic polypeptide levels were similar in all groups. These gut hormone changes, which are more marked in patients with poor LES pressure, may reflect primary or secondary abnormalities in GERD.

Esophagogastric Junction↗
PubMed1994

Altered antroduodenal motility after cholecystectomy.

BACKGROUND: Persistent nonspecific symptoms such as epigastric pain, bloating, nausea, and bilious vomiting are common following cholecystectomy. The etiology of these symptoms is unknown, but abnormal antroduodenal motility associated with duodenogastric reflux (DGR) is a possible cause. PATIENTS AND METHODS: Sixteen postcholecystectomy patients and 19 healthy volunteers ("normals") were studied. Ten of the patients were asymptomatic and 6 were symptomatic. The study consisted of a 4-hour 99mTc-DISIDA (diisopropyl imidodiacetic acid) infusion and gastric aspiration, 24-hour intragastric pH monitoring, and 24-hour ambulatory antroduodenal manometry. RESULTS: The postcholecystectomy patients showed increased DGR of the infused 99mTc-DISIDA. The data are given as coulter counts x 10(6)/min. The increase was more marked in symptomatic postcholecystectomy patients (2.54 +/- 0.15) compared to asymptomatic patients (1.21 +/- 0.46) or normals (0.26 +/- 0.15). Postcholecystectomy patients had increased percentage of time with intragastric pH > 3. In the supine period in particular, the pH was > 3 in symptomatic patients 25.4% +/- 7.7% of the time versus 8.1% +/- 4.3% for asymptomatic patients (P < 0.01). The antral phase III frequency after cholecystectomy was 2.5 +/- 0.09 cycles/min compared to 3.2 +/- 0.08 cycles/min in normals (P < 0.0001). Furthermore, propagation of the phase III front in the duodenum was significantly slowed to 0.14 +/- 0.02 cm/s after cholecystectomy compared to 0.27 +/- 0.02 cm/s in normals (P < 0.001). The duration of phase III in the proximal duodenum after cholecystectomy was also decreased to 4.3 +/- 0.27 min compared to 5.9 +/- 0.35 min in normals (P < 0.005). CONCLUSIONS: Fasting antroduodenal motility is altered after cholecystectomy. The abnormality is associated with increased DGR, which is more marked in symptomatic patients.

Adult↗
PubMed1994

Comparative long-term results of laser-assisted balloon angioplasty and atherectomy in the treatment of peripheral vascular disease.

BACKGROUND: Early results of laser-assisted balloon angioplasty (LABA) and peripheral directional atherectomy (PDA) are encouraging. The true value of these procedures has remained in doubt, however, because of the absence of data on long-term objective patency rates. PATIENTS AND METHODS: From August 1988 through October 1993, LABA and PDA were performed on 151 limbs of 124 patients. Presenting symptoms were mild-to-severe claudication in 128 limbs (63 LABA, 65 PDA) and rest pain or necrosis in 23 (7 LABA, 16 PDA). Seventy-seven percent of the atherosclerotic lesions were localized in the iliofemoral tract (77% LABA, 76% PDA). Seventy limbs were treated with LABA and 81 with PDA. RESULTS: Initial hemodynamic and arteriographic success was achieved in 46 LABA limbs (66%) and 75 PDA limbs (93%) (P < 0.002). Mean follow-up was 16 +/- 2 months after LABA and 18 +/- 1 months after PDA. During this time, 32 failures were recorded in limbs treated with LABA, and 29 in limbs treated with PDA. The patency rate at 40 months was 23% in the LABA group and 45% in the PDA group (P < 0.005). Patency rates were not affected by the length or site of the arterial lesion or the runoff score. CONCLUSIONS: PDA had a better long-term patency rate than LABA, but long-term results were dismal with both techniques. PDA appears to have a limited role and LABA no role in the treatment of lower extremity occlusive disease.

Adult↗
PubMed1994

Laparoscopic Nissen fundoplication is an effective treatment for gastroesophageal reflux disease.

OBJECTIVE: The open Nissen fundoplication is effective therapy for gastroesophageal reflux disease. In this study, the outcomes in 198 patients treated with the laparoscopic Nissen fundoplication was evaluated for up to 32 months after surgery to ascertain whether similar positive results could be obtained. SUMMARY BACKGROUND DATA: To ensure surgical success, patients were required to have mechanically defective sphincters on manometry and increased esophageal acid exposure on 24-hour pH monitoring. The patients either had severe complications of gastroesophageal reflux disease or had failed medical therapy. These requirements have been found to be necessary to ensure a successful surgical outcome. METHODS: The disease was complicated by ulceration (46), stricture (25) and Barrett's esophagus (33). Patients underwent standard Nissen fundoplications identical in every detail to open procedures except that the procedures were carried out by the laparoscopic route. RESULTS: Perioperative complications included gastric or esophageal perforation (3), pneumothorax (2), bleeding (2), breakdown of crural repair (2) and periesophageal abscess (1). The only mortality occurred from a duodenal perforation. Six patients required conversion to the open procedure. The median hospital stay was 3 days. One hundred patients were observed for follow-up for 6 to 32 months (median 12 months), with outcomes similar to the open Nissen fundoplication. Further surgery was required for two patients who had recurrent gastroesophageal reflux and one who developed an esophageal stricture. Ninety-seven percent are satisfied with their decision to have the operation. CONCLUSIONS: The laparoscopic Nissen fundoplication can be carried out safely and effectively with similar positive results to the open procedure and with all of the advantages of the minimally invasive approach.

Anesthesia, General↗
PubMed1994

Prolonged ambulatory antroduodenal manometry in humans.

OBJECTIVES: To perform prolonged ambulatory recordings of antroduodenal motor activity in humans. METHODS: Antroduodenal manometric recordings were performed in 20 normal subjects (12 male, eight female, ages 19-41 years), using a 5-channel solid state catheter assembly (three antral, two duodenal transducers) positioned under fluoroscopy. A glass electrode simultaneously recorded pH in the antrum. RESULTS: Continuous, simultaneous recordings of antral and duodenal motor activity were obtained for 22.5 +/- 0.3 h. During fasting, 131 complete migrating motor complexes (MMCs) were recorded (6.6 +/- 0.9/subject). The average interval from onset of recording to completion of the first MMC cycle was 498 +/- 19.24 minutes. Significant diurnal variations were observed in MMC frequency (awake vs asleep: 0.25/subject/h vs 0.64/subject/h; p < 0.05), period (shorter during sleep), phase I duration (longer during sleep), and phase II duration (shorter during sleep). Among females, MMCs were more frequent and shorter. After meal administration, duodenal recording sites demonstrated a typical "fed" response; antral distension and/or retrograde catheter movement, on meal ingestion, however, precluded reliable antral "fed" recordings. CONCLUSIONS: Prolonged ambulatory antroduodenal manometry provides detailed and reliable information on fasting antral and duodenal motor activity, antral distension, and/or retrograde catheter migration on meal ingestion; there are limits, however, to the usefulness of this methodology for the evaluation of the fed motor response in the antrum.

Adult↗