Outcomes from chemoradiotherapy for patients with esophageal cancer.

Chemoradiotherapy is a widely used alternative treatment to surgical resection in certain patient groups with early esophageal cancer. The aim of this study was to retrospectively assess toxicity and outcome of patients treated with definitive chemoradiotherapy for early esophageal cancer at one institution. A retrospective analysis of all patients treated with chemoradiotherapy between February 2000 and December 2008 at a single tertiary center was performed with documentation of treatment given, toxicities recorded, and follow-up and outcome data. Sixty-two patients received chemoradiotherapy for esophageal cancer. There were 20 males and 42 female patients with an average age of 68 years. Histology revealed adenocarcinoma in 28 patients and squamous cell carcinoma in 34 patients. All patients were staged with a computerized tomography scan, endoscopic ultrasound and positron emission tomography scan. Selection criteria for chemoradiotherapy were unfit for surgery, upper esophageal squamous carcinoma, unresectable primary tumor, or patient choice. The majority of the patients received a combination of cisplatin and 5-fluorouracil chemotherapy with 55 Gy in 25 fractions of radiotherapy. Grade 3 toxicities were recorded in 11% of the patients. Eleven patients suffered from local recurrence and a stent was required in nine patients. Radiation strictures occurred in 10 patients requiring dilation in four. Five patients required a radiologically inserted feeding gastrostomy. The median overall survival was 21 months. Patients with adenocarcinomas and those with squamous cell carcinoma had a similar median survival. Overall survival was 70% at 1 year, 48% at 2 years, and 26% at 3 years. This case series of patients treated with chemoradiation for localized esophageal cancer suggest a generally well-tolerated treatment with survival rates after chemoradiotherapy comparable with those seen with surgery.

Gastro-oesophageal reflux and duodenogastric reflux before and after eradication in Helicobacter pylori gastritis.

OBJECTIVE: Helicobacter pylori and duodenogastric reflux (DGR) are both associated with chronic gastritis, peptic ulcer and gastric cancer. The nature of their interrelationship remains unclear. H. pylori eradication has also been reported to result in new or worsening acid gastro-oesophageal reflux (GOR). The aim of this study was to investigate the relationship between GOR, DGR and H. pylori infection. METHOD: 25 patients with H. pylori gastritis underwent ambulatory 24-hour oesophageal and gastric pHmetry and gastric bilirubin monitoring before and 12 weeks after H. pylori eradication, confirmed by 14C urea breath testing (UBT). Ten healthy subjects served as a control group. RESULTS: There were no differences between patient and control groups for gastric alkaline exposure or gastric bilirubin exposure (P> 0.25 in all categories). Oesophageal acid reflux was higher in the study group (P< 0.02). No differences were detected in oesophageal acid reflux, gastric alkaline exposure, or gastric bilirubin exposure (P = 0.35, 0.18 and 0.11, respectively) before and after eradication. CONCLUSIONS: Acid GOR is not increased by H. pylori eradication. DGR in patients with H. pylori gastritis is similar to that in healthy, non-infected subjects. H. pylori eradication produces no change in GOR or DGR. In patients with chronic gastritis, H. pylori infection and DGR appear to be independent of each other.

Reproducibility and intragastric variation of duodenogastric reflux using ambulatory gastric bilirubin monitoring.

Duodenogastric reflux has long been considered to be important in the pathogenesis of many gastric disorders that exhibit regional variation within the stomach. Ambulatory gastric bilirubin monitoring is a new technique and, although extensively validated, reproducibility and gastric regional variation have not been specifically addressed. Fourteen patients with symptoms of gastroesophageal reflux and 12 healthy subjects underwent 24-h ambulatory gastric bilirubin monitoring with the bilirubin sensor in the upper stomach. Gastric bilirubin monitoring with two simultaneous bilirubin probes, one in the upper stomach and the other in the antrum, was performed on a separate occasion. Gastric bilirubin exposure in the initial and repeat studies showed a good correlation (R = 0.60, P < 0.01). Gastric bilirubin exposure in the upper stomach and the antrum showed a high degree of correlation (R = 0.90, P < 0.01). In conclusion, reproducible results are obtained with ambulatory gastric bilirubin monitoring and duodenogastric reflux does not exhibit significant regional variation within the stomach.

The extent of duodenogastric reflux in gastro-oesophageal reflux disease.

BACKGROUND: It is known that duodenogastro-oesophageal reflux (DGOR) increases with worsening gastro-oesophageal reflux disease (GORD). It is unclear whether this is accompanied by increasing duodenogastric reflux (DGR). OBJECTIVE: To investigate the extent of DGR in a control group and 66 patients with GORD, using the technique of ambulatory gastric bilirubin monitoring. METHODS: Sixty-six patients with reflux symptoms (30 grade 0 or 1 oesophagitis (group 1), 16 grade 2 or 3 oesophagitis (group 2), 20 Barrett's oesophagus (group 3)) and 17 healthy controls were studied. All underwent oesophageal manometry followed by 24-h ambulatory oesophageal and gastric pH monitoring and gastric bilirubin monitoring. RESULTS: Median per cent total oesophageal acid exposure (pH < 4) was significantly less in the control group (0.6%) than in group 1 (2.8%, P< 0.05) and groups 2 and 3 (7.5% and 7.8% respectively, P< 0.001). There was no significant difference between any group in median per cent total time gastric pH was greater than 4. There was no significant difference in median per cent total gastric bilirubin exposure (absorbance > 0.14) between any group. However, in each group gastric bilirubin exposure was greater in the supine position than the upright position, being significantly greater in the control group (P< 0.05) and group 1 (P < 0.001). CONCLUSIONS: Gastric bilirubin exposure is similar across the spectrum of GORD severity. It is greater in the supine than in the upright position.

Effect of cholecystectomy on gastroesophageal and duodenogastric reflux.

OBJECTIVE: The majority of patients experience resolution of their symptoms after cholecystectomy, but a minority either find their symptoms unchanged or complain of new upper GI symptoms. It has been suggested that the effect of cholecystectomy on upper GI motility, sphincter function, or bile delivery may account for these postoperative symptoms. We aimed to determine whether cholecystectomy affects gastroesophageal reflux or duodenogastric reflux by using 24-h ambulatory pH and gastric bilirubin monitoring before and after surgery. METHODS: Seventeen symptomatic patients with gallstones underwent 24-h ambulatory esophageal and gastric pH-metry and gastric bilirubin monitoring. Helicobacter pylori status was ascertained in all patients by 14C urea breath test and serology. Combined pH and bilirubin monitoring was repeated 3 months after cholecystectomy. Eleven healthy subjects served as a control group. RESULTS: Three (17%) patients complained of persistent or new symptoms after surgery, whereas 14 (83%) patients were asymptomatic. Two patients (12%) underwent open cholecystectomy, and (88%) had the operation performed laparoscopically. No significant differences were detected in esophageal acid exposure (pH < 4), gastric alkaline shift (pH > 4), or gastric bilirubin exposure (absorbance > 0.14) after surgery. Three (17%) patients tested positive for Helicobacter pylori; the presence of infection did not appear to affect pre- or postoperative values. CONCLUSIONS: Cholecystectomy does not result in increased bile reflux into the stomach or increased gastroesophageal acid reflux. Those patients who had increased postoperative duodenogastric reflux were entirely asymptomatic. The symptoms of postcholecystectomy syndrome are unlikely to be related to increased duodenogastric reflux after surgery.

Effect of omeprazole on antral duodenogastric reflux in Barrett oesophagus.

BACKGROUND: The effect of long-term acid suppression therapy in Barrett oesophagus remains unknown, but the high intragastric pH generated has been shown to increase the cytotoxicity of duodenal refluxate on foregut mucosa. However, recent work suggests that duodenogastric reflux (DGR) may be reduced by omeprazole. AIM: To investigate the effect of omeprazole on the reflux of duodenal contents into the gastric antrum in Barrett patients and healthy subjects. METHOD: Fifteen patients with Barrett oesophagus and 14 healthy subjects underwent oesophageal manometry followed by 24-h ambulatory oesophageal and gastric pH and gastric bilirubin monitoring. The bilirubin sensor (modified by the addition of a weighted tip to facilitate manoeuvrability) was sited in the gastric antrum under fluoroscopic control. Combined ambulatory pH and bilirubin monitoring was repeated after 2 weeks on omeprazole 20 mg b.d. RESULTS: Changes in oesophageal acid reflux and gastric alkaline shift due to omeprazole were as expected (P < 0.001). There was no difference in total antral DGR between the Barrett and control groups (P = 0.56), and omeprazole had no significant effect on DGR in either group (P = 0.77 and 0.27, respectively). CONCLUSIONS: DGR into the antrum is of a similar level in Barrett patients and healthy controls. Omeprazole does not reduce the reflux of duodenal contents across the pylorus. Further work is required on the increased cytotoxic potential of continuing DGR in those on long-term acid suppression.

Effect of omeprazole 20 mg twice daily on duodenogastric and gastro-oesophageal bile reflux in Barrett's oesophagus.

BACKGROUND: Both acid and duodenal contents are thought to be responsible for the mucosal damage in Barrett's oesophagus, a condition often treated medically. However, little is known about the effect of omeprazole on duodenogastric reflux (DGR) and duodenogastro-oesophageal reflux (DGOR). AIMS: To study the effect of omeprazole 20 mg twice daily on DGR and DGOR, using the technique of ambulatory bilirubin monitoring. METHODS: Twenty three patients with Barrett's oesophagus underwent manometry followed by 24 hour oesophageal and gastric pH monitoring. In conjunction with pH monitoring, 11 patients (group 1) underwent oesophageal bilirubin monitoring and 12 patients (group 2) underwent gastric bilirubin monitoring, both before and during treatment with omeprazole 20 mg twice daily. RESULTS: In both groups there was a significant reduction in oesophageal acid (pH<4) reflux (p<0.005) and a significant increase in the time gastric pH was above 4 (p<0.005). In group 1, median total oesophageal bilirubin exposure was significantly reduced from 28.9% to 2.4% (p<0.005). In group 2, median total gastric bilirubin exposure was significantly reduced from 24.9% to 7.2% (p<0.005). CONCLUSIONS: Treatment of Barrett's oesophagus with omeprazole 20 mg twice daily results in a notable reduction in the exposure of the oesophagus to both acid and duodenal contents. In addition, delivery of duodenal contents to the upper gastric body is reduced.

Parotidectomy in childhood--with a review of the literature.

Parotid tumours in childhood are rare. Four patients under 16 years old having parotidectomy are described and the literature is reviewed. The presentation, pathology and prognosis of parotid tumours in childhood is different to that seen in adults. Half of the parotid tumours in childhood are malignant but most are of low grade. Rapid growth, if present, may be the only clue of malignancy and facial nerve palsy or cervical node metastasis have rarely been described. Adequate surgical excision with facial nerve preservation is the treatment of choice and radical neck dissection is rarely necessary. Radiotherapy should be avoided and the prognosis is very favourable. It is difficult to differentiate clinically between benign and low-grade malignant tumours and because of the high incidence of malignancy, all parotid tumours in childhood should be suspected of being malignant until proven otherwise.

Sternal wound dehiscence after internal mammary artery harvesting. Logical management.

There is clear evidence that the internal mammary artery is superior to other forms of vascular conduit in surgical coronary revascularisation. Its patency rate at 10 years is of the order of 2-3 times that of autologous saphenous vein. Unfortunately, harvesting of the internal mammary is associated with an increased incidence of sternal wound complications, probably due to temporary sternal devascularisation. The restoration of sternal blood supply has been shown to occur after several weeks. It is proposed by this group that delayed primary closure of dehisced wounds after 3-4 weeks is an effective way of dealing with this malignant and, fortunately, rare complication of arterial coronary artery revascularisation.

Examination and differential diagnosis of parotid swellings.

Uncommonly, the physical signs associated with a parotid swelling indicate the underlying pathology. More commonly, the physical signs permit only a differential diagnosis. A large variety of pathologies present as a discrete, mobile, painless mass in the parotid region.