A comparison of the patient and surgeon opinion on the long-term aesthetic outcome of reduction mammaplasty: have we improved over 15 years?

In 1996 we published a study evaluating the difference between patient and surgeon opinion on the aesthetic outcome of reduction mammaplasty (see Ref. 1). The patients rated the aesthetic outcome of their surgery as significantly higher than the consultant panel. The surgical panel suggested scope for improvement. Areas of dissatisfaction were poor scarring, high placement of the nipple areola complex and high rates of revision surgery. Fifteen years on, the same team has regrouped to repeat this assessment. In 1996 the consultants scored their own patient results. In 2011 they graded the results of their former trainee who has modified her operative technique to address aesthetic problems highlighted in the first study. Forty-four patients attended a review clinic at least one year post reduction mammaplasty. Patient scored their satisfaction using the original questionnaire employed in 1996. The cohort were photographed and their images graded blindly by the original surgical panel. Statistical analysis was performed by the original statistician. The patients graded aesthetic aspects of body harmony, breast mound appearance, nipple areolar complex appearance and post-operative scarring significantly more positively (p<0.01) than both the 1996 patient cohort and surgical panel. The consultant panel showed a trend for more positive grades for all aesthetic features assessed versus their previous views but this was only significant for breast mound symmetry. They expressed that there was a decrease in post-operative breast ptosis (p<0.04) and improvement in the nipple areolar complex position (p=0.02). The rate of revision surgery has decreased from 53% to 16% between the studies. In keeping with clinical audit, outcomes have been assessed and modifications implemented to address aesthetic concerns. Assessment of outcomes following the modifications demonstrates a trend for increased patient and surgeon satisfaction. Patient satisfaction however still exceeds that of the surgeons.

Effect of octreotide on gastric and small bowel motility in patients with gastroparesis.

BACKGROUND: Octreotide has been shown to have effects on gastric and small bowel motility with implications for its role in treating patients with upper gastrointestinal dysmotility syndromes. Our aim was to investigate the effect of octreotide on antral and small bowel motility in patients with gastroparesis. METHODS: Upper gastrointestinal manometry was carried out continuously for a period of 30 h in 11 patients with gastroparesis. The spontaneous migrating motor complex (MMC) in the fasting state and octreotide-induced MMCs were characterized and compared with regard to site of origin, duration of phase III, amplitude of phase III and propagation velocity of the MMC along the gut. The 2-h postprandial motility index was compared after a control meal as well as after a 100 microg octreotide administration. RESULTS: In all 11 gastroparetic patients, octreotide induced a phase III-like activity front within minutes after administration and this primarily originated in the small bowel (86% of activity fronts compared with 32% of fronts originating in the small bowel prior to octreotide administration (P < 0.004)). Gastric initiation of these activity fronts dramatically decreased after octreotide administration, occurring in 68% of activity fronts prior to octreotide administration and 14% of occasions after octreotide injection (P < 0.05). The postprandial antral motility index was markedly reduced after octreotide administration (11.33 +/- 0.39 vs. 7.96 +/- 0.76, P < 0.0003) and octreotide re-established a motility pattern during the postprandial period that was similar to that normally seen in the interdigestive state. The octreotide-induced phase III activity fronts appeared at a higher frequency and had a higher propagative velocity compared to the spontaneous phase III fronts in the fasting state (9.27 +/- 0.82 vs. 5.56 +/- 0.81 cm/min, P < 0.05). CONCLUSIONS: We conclude that octreotide's marked inhibitory effect on antral contractility may serve to worsen clinical symptoms in patients with gastroparesis and therefore this agent should not be given in the periprandial period. Those gastroparetic patients with associated small bowel dysmotility and diarrhoea from bacterial overgrowth may benefit from the nocturnal administration of octreotide because of its stimulatory effect of phase III MMC activity as well as its known inhibitory effect on small bowel secretions.

Effects of octreotide and erythromycin on gastric myoelectrical and motor activities in patients with gastroparesis.

Simultaneous recordings of gastric manometry and myoelectrical activity were made in 10 patients with gastroparesis. Intravenous erythromycin (100 mg) was administered in the fasting state for a period of 30 min. Subcutaneous injection of octreotide (100 microg) was administered before one of the four identical test meals. It was found that octreotide significantly decreased the antral motility index (30-min fasting: 4.51+/-1.04 vs 1.75+/-0.97, P < 0.02; 60-min fed: 5.16+/-1.44 vs 3.4+/-1.41, P < 0.05) and the dominant power of the EGG (fasting power: 35.19+/-1.54 vs 30.84+/-1.57 dB, P < 0.004; postprandial power increase: 5.52+/-1.06 vs -0.27+/-0.87, P < 0.001). Erythromycin significantly increased the antral motility index (3.16+/-0.96 vs 9.5+/-0.61, P < 0.001) and the dominant power of the EGG (28.86+/-1.57 dB vs 33.55+/-1.59 dB, P < 0.005) in the fasting state. An improvement in the regularity of the gastric slow wave was also noted with erythromycin. It was concluded that: (1) the inhibitory effect of octreotide on postprandial gastric motility and myoelectrical activity suggests that caution should be exercised when octreotide is used in patients with gastroparesis; and (2) the stimulatory effect of erythromycin on gastric myoelectrical activity may enhance gastric motility and gastric emptying in patients with gastroparesis.

Detrimental impact of acid and pepsin on the rate of luminal release of transforming growth factor alpha. Its potential pathogenetic role in the development of reflux esophagitis.

The impact of intraluminal acid and pepsin on the rate of esophageal luminal release of transforming growth factor alpha (TGF alpha), measured by RIA, in 21 asymptomatic volunteers and 26 patients with reflux esophagitis (RE) was investigated. Esophageal secretion was collected, using an esophageal perfusion catheter, during mucosal exposure to NaCl, HCl or HCl/Pepsin and final saline. The basal rate of luminal TGF alpha release in controls was steady throughout the entire four perfusion periods with saline. This rate declined by 71% during mucosal exposure to HCl (p = 0.002) and by 74% during esophageal perfusion with HCl/pepsin (p = 0.011). The basal rate of luminal TGF alpha release in patients with RE was 27% higher than the corresponding value in controls (1.076 +/- 0.140 vs. 0.850 +/- 0.180 ng/min, p = 0.050). Mucosal exposure to acid and acid/pepsin solutions in RE patients also resulted in a significant decline in the luminal release of TGF alpha by 43% (p < 0.001) and by 42% (p < 0.001) respectively. Despite this decline, TGF alpha in patients with RE was significantly higher (p < 0.001) than in controls. The decline in esophageal TGF alpha release during HCl and HCl/pepsin exposure may facilitate the development of mucosal damage. The increase in esophageal TGF alpha release in patients with RE may represent a compensatory mechanism developed by the mucosal inflammatory changes.

Declined human esophageal mucin secretion in patients with severe reflux esophagitis.

It has been recently demonstrated that human esophageal submucosal mucous glands exhibit the ability to secrete copious amounts of mucin, well known within the gastrointestinal tract for its protective quality against hydrogen ion and pepsin. Since mucin may also play a protective role within the esophageal compartment, we have studied the rate of secretion of esophageal mucin in patients with RE. Mucin was assessed by periodic acid-Schiff methodology in esophageal secretion collected during continuous perfusion with saline (period I) followed by HCl (period II), HCl/pepsin (period III), and final saline (period IV), mimicking the natural gastroesophageal scenario. The basal rate of the luminal release of mucin in patients with grade II RE was 18% lower as compared with controls. During exposure of the esophageal mucosa to an HCl/pepsin solution, esophageal mucin output in the RE group was 52% lower than in the control group (0.154 +/- 0.027 vs 0.320 +/- 0.049 mg/cm2/min; P = 0.025). Furthermore, the rates of esophageal mucin output in patients with grade III RE during esophageal perfusion with saline and HCl/pepsin were 62% (0.090 +/- 0.021 vs 0.239 +/- 0.036 mg/cm2/min; P = 0.016) and 86% (0.048 +/- 0.010 vs 0.320 +/- 0.049 mg/cm2/min; P = 0.001) lower when compared with corresponding values in controls. After endoscopic healing of RE, the overall impairment in the rate of esophageal mucin secretion in patients with grade II improved from 31% to 17% at the end of therapy, whereas in patients with grade III the impairment in mucin secretion improved only marginally from 71% to 69%.(ABSTRACT TRUNCATED AT 250 WORDS)

Diminished luminal release of esophageal epidermal growth factor in patients with reflux esophagitis.

OBJECTIVES: It has recently been demonstrated that human esophageal mucosa, containing numerous submucosal mucous glands, has the ability to elaborate significant amounts of esophageal epidermal growth factor (eEGF). Because of its role in the maintenance of the integrity of the esophageal mucosa, we elected to study the rate of secretion of eEGF in patients with reflux esophagitis (RE), compared with controls, using our newly developed esophageal perfusion model. METHODS: Fourteen healthy asymptomatic volunteers and 14 patients with endoscopically confirmed esophagitis underwent esophageal perfusion with saline, HCl (0.01 M, pH 2.1) HCl/pepsin (0.5 mg/ml of HCl), and ending NaCl solution during four consecutive 8-min perfusion periods. All perfusates were assayed for EGF by RIA (Amersham). Results are expressed as mean +/- SEM. Student's t test was used for statistical analysis. RESULTS: The basal rate of luminal EGF release in patients with RE was 3.78 +/- 0.29 ng/min. This value significantly declined (2.27 +/- 0.27 ng/min; p < 0.001) during mucosal exposure to HCl but was significantly enhanced when the HCl perfusing solution was supplemented with pepsin (4.20 +/- 0.29; p < 0.001 vs. HCl). Introduction of saline during the last perfusion period maintained a rate of luminal EGF release similar to that observed during the initial esophageal perfusion with saline. Luminal release of EGF in patients with RE was significantly lower, compared with corresponding values recorded in controls during perfusion with saline (3.78 +/- 0.29 vs. 14.1 +/- 1.25 ng/min; p < 0.00001), with HCl (2.27 +/- 0.27 vs. 5.95 ng/min; p < 0.0001), with HCl/pepsin solution (4.2 +/- 0.29 vs. 11.7 +/- 1.88 ng/min; p < 0.0001), and during the final perfusion period with saline (3.73 +/- 0.25 vs. 15.1 +/- 1.1 ng/min; p < 0.00001). Therefore, the rate of luminal EGF release in controls was 4-fold, 3-fold, 3-fold, and 4-fold higher than that of patients with RE during perfusion with initial saline, HCl, HCl/pepsin and final saline, respectively. CONCLUSIONS: 1) Decreased esophageal EGF in patients with RE may facilitate the development or delay the healing of mucosal injury. 2) Depletion of EGF from the mucus layer covering the epithelium under the impact of refluxed luminal acid/pepsin may be considered as one of the potential underlying mechanisms leading to damage of the esophageal mucosa during gastroesophageal reflux episodes.

Adenosine stimulates glycolytic flux in isolated perfused rat hearts by A1-adenosine receptors.

This study was designed to assess the role of adenosine in the regulation of exogenous glucose utilization by myocardium. Perfusion of isolated rat hearts with buffer containing D-[3-3H]glucose and analysis of the coronary effluent for 3H2O production was used as an indicator of glycolytic flux. Initially, glycolytic flux was determined during five different conditions: 1) normoxia; 2) normoxia plus 100 microM adenosine; 3) normoxia plus 100 microM adenosine and 10 microM 8-(sulfophenyl)-theophylline (SPT), an adenosine receptor antagonist; 4) hypoxia; and 5) hypoxia plus 10 microM SPT. Both adenosine and hypoxia produced an approximate threefold increase in glycolytic flux that was attenuated by adenosine receptor blockade with SPT. Next, hearts were perfused during normoxic conditions with various concentrations of either R-phenylisopropyladenosine (PIA), an A1-adenosine receptor agonist, or 5'-N-ethylcarboxamidoadenosine (NECA), an A2-adenosine receptor agonist. Significant increases in glycolytic flux occurred with PIA, whereas NECA treatment resulted in only a marginal stimulation of glycolytic flux. These data provide evidence that: 1) exogenous adenosine stimulated glycolytic flux in the normoxic myocardium; 2) endogenous adenosine stimulated glycolytic flux during hypoxia; and 3) the effect of adenosine on glycolytic flux was mediated by interaction with A1-adenosine receptors.