Anomalies of peristalsis in idiopathic diffuse oesophageal spasm.

Oesophageal manometry revealed 'interrupted peristalsis'--proximal sequential contraction with simultaneous pressure increases in the mid-oesophagus and sequential contraction distally--and abnormally slow distal propagation of peristalsis in seven of a consecutive series of 12 patients with idiopathic diffuse oesophageal spasm (IDOS). These two abnormalities occurred together in six patients. It is proposed that 'interruption' of peristalsis and 'slow' distal propagation are apparent rather than real, and that they reflect failure of normal luminal obliteration during oesophageal contraction. This arguments is extended to the 'aperistalsis' of achalasia. It is also proposed that IDOS, achalasia, and related idiopathic motor disorders may share a common pathogenetic abnormality--namely, functional obstruction at the level of the lower oesophageal sphincter. According to this hypothesis, the presentation of the patient and the progression of his disease are determined by the degree and duration of that obstruction, and the functional reserve of the oesophageal body musculature.     

Secondary oesophageal peristalsis in patients with non-obstructive dysphagia.

Secondary peristalsis was investigated in 30 patients with non-obstructive dysphagia and 20 age matched controls. Oesophageal motility was recorded at 3 cm intervals along the oesophageal body. Primary peristalsis was tested with 5 ml water swallows. Secondary peristalsis was stimulated with 10 ml boluses of air and water injected in the mid-oesophagus and by distensions (5 seconds duration) with a 3 cm balloon at the same level. Primary peristalsis was normal in 19 of the 20 control subjects and in nine of the 30 patients with dysphagia; 11 patients had diffuse spasm and 10 had non-specific abnormalities of primary peristalsis. Secondary peristalsis was triggered significantly less frequently by air and water distension in dysphagia patients (median success rate of 10% for the air boluses and 0% for the water boluses) than in control subjects (50% and 30% respectively, p < 0.005), and was abnormal in six of nine patients with normal primary peristalsis, nine of 11 patients with diffuse spasm and eight of 10 patients with non-specific motor abnormalities. The median frequency of balloon induced secondary peristalsis, however, was not significantly different in the two groups (0% controls, 40% non-obstructive dysphagia, p = 0.22). For each stimulus, there were no significant differences in the response rate in the three subgroups of patients. The major pattern of failure of secondary peristalsis in response to the air and water boluses was the complete absence of any oesophageal response. The amplitude of complete secondary peristalsis triggered by the water boluses and the balloon was greater in the patients with dysphagia (p = 0.03) than in normal subjects, while the amplitude of the secondary peristaltic responses triggered by the air boluses was similar in the two groups. Secondary peristaltic velocity was also similar in normal subjects and patients with non-obstructive dysphagia. Patients with non-obstructive dysphagia show a noticeable defect in the triggering of secondary peristalsis which may make an important contribution to the delayed oesophageal bolus transit and dysphagia seen in this condition.     

Beta adrenergic influence on oesophageal peristalsis in man.

The effects of the beta-1 adrenergic agonist prenalterol and the beta-2 adrenergic agonist terbutaline on oesophageal peristalsis were studied in nine healthy volunteers with pressures recorded in the proximal, middle, and distal oesophagus. Two doses of the agonists were given after pretreatment with placebo, propranolol, or metoprolol in a double blind randomised fashion. Terbutaline 0.25 +/- 0.25 mg iv decreased peristaltic pressure in middle oesophagus from 8.1 +/- 1.1 to 5.1 +/- 0.8 kPa (p less than 0.01) and in the distal oesophagus from 9.5 +/- 1.0 to 4.7 +/- 0.6 kPa (p less than 0.001). Peristaltic velocity was decreased in the distal oesophagus after terbutaline from 3.3 +/- 0.2 cm/sec to 2.9 +/- 0.2 cm/sec (p less than 0.05). Prenalterol 1 mg iv was followed by a decrease of peristaltic pressure in the middle oesophagus from 10.2 +/- 1.3 to 7.7 +/- 1.1 kPa (p less than 0.01) and a decrease of peristaltic velocity in upper oesophagus from 3.6 +/- 0.2 to 3.3 +/- 0.1 cm/sec (p less than 0.05) while no significant changes were seen in the distal oesophagus. Pretreatment with the beta-1 blocker metoprolol 15 mg iv blocked the effects of prenalterol 1 mg iv but not the effects of terbutaline. Propranolol 10 mg iv blocked the effects of terbutaline on peristaltic pressure. After metoprolol infusion mean distal peristaltic amplitude was 11.9 +/- 0.8 kPa compared with 8.5 +/- 1.2 kPa after placebo (p less than 0.01). It is concluded that both beta-1 and beta-2 adrenoceptor stimulation significantly decrease oesophageal peristaltic pressure in man. The body of the oesophagus seems to be under beta adrenergic inhibitory influence under physiological conditions.     

Secondary oesophageal peristalsis in gastro-oesophageal reflux disease

BACKGROUND AND AIMS: To evaluate the status of secondary oesophageal peristalsis in gastro-oesophageal reflux disease (GORD) and the effect of healing of oesophagitis on these abnormalities. METHODS: Twenty-one patients diagnosed with GORD and 10 control subjects in the same age group were studied. Primary peristalsis was elicited by 10 5 mL water boluses and secondary peristalsis by 10 20 mL boluses of air injected 15 cm above the lower oesophageal sphincter. RESULTS: The pattern of primary peristalsis was normal in a significantly lower number of patients compared with control subjects, six patients (28.6%) versus seven controls (70%), (P<0.05). Similarly, the number of subjects with a normal pattern of secondary peristalsis was also lower in the patient group (zero vs three; P<0.05). A normal primary peristaltic response occurred with 71 (33.8%) of the 210 water boluses in the patients and 73 (73%) of the 100 water boluses in the control subjects, respectively (P<0.001). A normal secondary peristaltic response was seen with 15 (7.1%) of 210 air boluses in patients and 32 (32%) of 100 air boluses in the control subjects (P<0.001). The amplitude of secondary peristaltic waves and the duration of contraction (mean+/-SEM) were significantly lower in patients compared with the control subjects (43.5+/-4.7 vs 89.0+/-13.1 and 3.4+/-0.8 vs 3.9+/-0.3, respectively; P=<0.05). In the 13 patients in whom repeat evaluation was performed after healing of oesophagitis, there was no significant change in the number of patients with normal peristaltic response, number of normal responses to air and water boluses, or amplitude, duration and velocity of peristalsis. CONCLUSION: Significant abnormalities of secondary oesophageal peristalsis occur in patients with GORD and these are not reversed by healing of oesophagitis.     

Stimulation and characteristics of secondary oesophageal peristalsis in normal subjects.

The study evaluates the triggering and characteristics of secondary oesophageal peristalsis in 25 healthy volunteers. Secondary peristalsis was stimulated by rapid intraoesophageal injection of boluses of air and water, and by a five second oesophageal distension with a balloon. Air and water boluses triggered secondary peristalsis that started in the proximal oesophagus regardless of injection site. Response rates were volume dependent with 83% of the 20 ml air boluses triggering secondary peristalsis compared with 2% for the 2 ml water bolus (p < 0.0001). Response rates for air and water were similar for equal bolus volumes and were not influenced by the site of injection. In contrast, balloon distension usually induced a synchronous contraction above the balloon, with secondary peristalsis starting below the balloon after deflation. The peristaltic response rate to balloon distension was also volume dependent and the middle balloon was more effective in triggering secondary peristalsis than either the upper or lower balloons (p < 0.001). Secondary peristaltic amplitude was less than that of primary peristalsis (p < 0.001). Secondary peristaltic velocity with a water bolus was slower (p = 0.001) than that of primary peristalsis. Intravenous atropine significantly reduced secondary peristaltic responses to all stimuli. There was also a significant reduction in pressure wave amplitude for air stimulated secondary peristalsis while those for the water responses were similar. Secondary peristaltic velocity with air and water boluses was not changed by atropine. The reproducibility of testing secondary peristalsis was examined six volunteers and did not show any significant differences on separate test days in response rate and peristaltic amplitude or velocity. It is concluded that in normal subjects, secondary peristalsis can be more reliably triggered by intraoesophageal air or water infusion than balloon distension. Secondary peristaltic amplitude and velocity are stimulus but not site or volume dependent and propagation is partially mediated by cholinergic nerves.     

Intraluminal force transducer measurements of human oesophageal peristalsis

A force transducer has been developed to measure peristaltic propulsive force (`pull') in the oesophagus. Utilizing a mercury-in-Silastic strain gauge to which a sphere has been attached, this transducer can be calibrated to measure value for force, work, and power. Variability in force values were found between different peristaltic waves at the same site, between different sites in the same subject, and between different control subjects. Control subjects' patterns did not change when the subjects were studied on separate occasions. Patients complaining of dysphagia, who had normal radiographs and manometric tracings, revealed force values that were significantly different from control values. This device should prove useful in the quantitation of oesophageal muscle function.     

Oesophageal peristalsis. A simple system for the recording of oesophageal peristalsis, and the influence of bolus volume on peak peristaltic pressure amplitude

Peak oesophageal peristaltic pressure amplitude was recorded in 8 healthy subjects at points 5 and 15 cm proximal to the gastro-oesophageal sphincter, by using an in situ tip-transducer simultaneously with a continuous flush (Intraflo) perfused catheter system with external pressure transducer. Dry swallows and wet swallows of 2.5, 5 and 10ml, respectively, were made in random succession. In all cases the pressures recorded by either system correlated well. In all cases the peristaltic pressure amplitude was significantly higher after the wet swallows. The catheter and flow system used in this study is simple and makes recording of peristaltic pressures independent of the shape of the in situ transducer, and its therefore well suited for measuring the amplitude of oesophageal contractions.     

Effect of metoclopramide on oesophageal peristalsis and gastro-oesophageal sphincter pressure. A study in normal subjects

The aim of the present study was to measure the amplitude, the duration, and the velocity of the peristaltic pressure wave in the lower part of the oesophagus in the basal state and at different time intervals after oral intake of 10 and 20 mg metoclopramide. In addition, gastro-oesophageal sphincter pressure was measured in the basal state and 90 min after the intake of metoclopramide. The pressure studies were carried out in eight healthy subjects, using a pressure probe consisting of two open-tip polyethylene catheters that were fed by a capillary tubular system and connected to external pressure transducers. Sphincter pressure was measured (intermittent withdrawal), and the probe was positioned with the distal opening 5 cm orally to the sphincter. Dry and wet (bolus, 5 ml of water) swallows were made in randomized order in the basal state and at the time intervals after the intake of metoclopramide. Finally, the sphincter pressure measurement was repeated. No differences were seen with regard to the peristaltic activity: amplitude, duration, or velocity. Sphincter pressure rose from 12 to 19 mmHg after 10 mg (p less than 0.05) and from 13 to 20 mmHg after 20 mg metoclopramide (p less than 0.05). There were no significant differences between basal values and the response to 10 or 20 mg metoclopramide.     

Negative CLOtest pellet can be reused.

BACKGROUND: The CLOtest is based on the production of ammonia from urea in the presence of urease. In theory, substrate that has not been consumed in a negative test can be reused. METHODS: We collected negative CLOtest pellets after their first use and stored them at room temperature. Whenever a CLOtest was needed during endoscopy, two biopsy specimens were taken from the antrum. One specimen was tested with a new CLOtest and the other with one that had been used previously. Time to color change was observed in paired tests. RESULTS: We used 216 previously used CLOtest pellets with biopsy specimens obtained from 317 patients. Of the paired tests, 204 matched positive and 108 tested negative. Only 5 paired tests had discrepant results. Three had positive results only with a new CLOtest, and 2 were positive only with the reused test. In positive paired tests, there was significant linear correlation in log-transformed color change time between reused and new tests (p < 0.001). Ninety-two percent of previously used pellets were reused fewer than three times before they yielded a positive color change; the interval to this occurrence ranged from 2 to 15 days. Compared with the new CLOtest, the sensitivity of the reused CLOtest was 98. 6% and the specificity was 98.2%. CONCLUSIONS: A negative CLOtest kept at room temperature can be reused within a short period of time, in circumstances in which there are environmental and economic considerations to be taken into account.     

弦歌不辍，芳华待灼

2021,是中国共产党成立100周年。这一年有太多的记忆令我们感动！在中国共产党的带领下,我们伟大的祖国虽然经历了种种艰难险阻,依然取得了举世瞩目的伟大成就。脱贫攻坚、科技创新、航空航天、抗击疫情,无论是哪一项,都能成就荡气回肠的动人诗篇。在这样波澜壮阔的背景下,内分泌学界的广大同仁们休戚与共,一起书写了2021年度内...     

Bursts of non-deglutitive simultaneous contractions may be a normal oesophageal motility pattern.

The frequency and characteristics of non-deglutitive motor activity of the human oesophagus and its relation to motility patterns in the antrum and upper small intestine were studied in 25 fasted healthy subjects. Motility of the oesophagus, antrum, and upper small intestine was recorded by means of a manometric perfused catheter system. The most striking non-deglutitive motility pattern consisted of repetitive bursts of non-sequential pressure peaks occurring in the smooth muscle portion of the oesophagus. The mean number of pressure peaks per burst was 2.7 (SD 2) waves with a mean amplitude of 19.5 (SD 9.9) mm Hg and a duration of 3.09 (SD 0.22) seconds. The highest amplitude was 80 mm Hg and the longest burst consisted of 13 repetitive waves. The bursts were recorded up to a distance of 15-20 cm above the lower oesophageal sphincter. Ninety five per cent of the bursts occurred during a 15 minute period before the onset of phase 3 of the migrating motor complex in the antral or upper small intestinal area, or during the lower oesophageal sphincter component of the migrating motor complex. In conclusion, spontaneous bursts of non-sequential pressure peaks occurred in the smooth muscle part of the human oesophagus in relation to phase 3 of the migrating motor complex. They represent the oesophageal body component of phase 3 of the migrating motor complex and are not a sign of oesophageal motor abnormalities.     

Progression of liver fibrosis can be controlled by adequate chelation in transfusion-dependent thalassemia (TDT)

A substantial proportion of patients with transfusion-dependent beta-thalassemia major suffer from chronic liver disease. Iron overload resulting from repeated transfusions and HCV infection has been implicated in the development of liver fibrosis. Hepatic siderosis and fibrosis were assessed in 99 transfusion-dependent thalassemia (TDT) patients using transient elastography (TE) and liver iron concentration (LIC) assessed by T2*MRI at baseline and after 4 years. Data were analyzed retrospectively. At baseline, the overall mean liver stiffness measurement (LSM) was 7.4 ± 3.2 kPa and the mean LIC was 4.81 ± 3.82 mg/g dw (n = 99). Data available at 4 ± 1.5 years showed a significant reduction in LSM (6.6 ± 3.2 kPa, p 0.017) and hepatic siderosis measured by LIC (3.65 ± 3.45 mg/g dw, p 0.001). This result was confirmed when considering patients with iron overload at the time of the first measurement (n = 41) and subjects treated with a stable dose of deferasirox over the entire period of observation (n = 39). A reduction of LSM, yet not statistically significant, was achieved in patients on combined deferoxamine + deferiprone, while the group on deferoxamine (n = 11) remained stable over time. HCV-RNA positivity was found in 33 patients at T0, 20 of which were treated during the observation period. Patients who underwent anti-HCV therapy showed a more evident reduction in LSM (9 ± 3 vs 7 ± 3.1 kPa, p 0.016). Adequate chelation therapy is mandatory in order to prevent liver disease progression in TDT. Patients could benefit from regular non-invasive assessment of liver fibrosis by TE to indirectly monitor treatment adequacy and therapeutic compliance.