[Clinical and pathogenetic features of esophageal spasm].

AIM: To comparatively analyze clinical manifestations in patients with primary esophageal spasm (ES) and its concurrence with gastroesophageal reflux disease (GERD) and the results of their instrumental examinations and psychodiagnostic tests. SUBJECTS AND METHODS: A total of 104 patients with the clinical and manometric signs of ES were examined and divided into two groups: 1) 42 patients with primary ES; 2) 62 patients with ES concurrent with GERD. The examination encompassed esophageal manometry, esophagogastroduodenoscopy, 24-hour pH metry, and an interview using a questionnaire to identify autonomic disorders, and the Mini-Mult test. RESULTS: The patients with primary ES compared to those with ES concurrent with GERD significantly more frequently showed severe pain syndrome (p = 0.009) and a paradoxical dysphagia pattern (p = 0.03); manometry revealed an incoordination in the motility of the entire esophagus (p = 0.001). Comparison of the statistical series of values for contraction amplitude and duration in the distal esophagus found no significant difference in the patients of both groups. Autonomic disturbances were detected in 76.0% of the patients with ES; but the intergroup differences were insignificant. Mental maladaptation was observed in 81.7% of the patients in the absence of intergroup differences. CONCLUSION: The etiopathogenetic factor of ES is a psychoautonomic response to chronic stress in both primary ES and its concurrence with GERD. The reflux of gastric contents into the esophagus does not appear to be one of the leading causes of ES. In primary ES, esophageal motor function is generally impaired to a much greater extent than that in ES concurrent with GERD. The degree of motor disorders is embodied in the specific clinical features of the disease.

Ambulatory oesophageal manometry and pH monitoring for investigation of chest pain: a New Zealand experience.

AIMS: Patients with chest pain of uncertain origin are often referred to gastroenterology to assess for possible oesophageal causes. Oesophageal spasm is difficult to ascertain with stationary manometry, as pain seldom occurs during this brief study. Twenty-four-hour ambulatory manometry and oesophageal pH recording (AMP) offers the opportunity to correlate pain symptoms with abnormal motility or acid reflux for more definitive diagnosis. AMP has been available at Christchurch Hospital since 2000 and we describe our experience. METHODS: Thirty-seven patients (23 female, 14 male) underwent AMP between January 2000 and January 2004. Tracings were analysed by automated software and manually by an experienced scientist and gastroenterologist. Case-notes were reviewed for history and drug data. RESULTS: Thirty-three patients (89%) experienced typical pain and/or dysphagia symptoms during AMP. Twenty-one had no correlation between symptoms and pH or manometric abnormalities, excluding reflux disease or an oesophageal hypercontractile disorder as a cause of symptoms. Only one patient had oesophageal spasm proven. One patient's pain correlated strongly with acid reflux. Seven others had reflux episodes during AMP with less consistent pain correlation. At least six patients required treatment for ischaemic heart disease after a negative AMP result. CONCLUSIONS: AMP has been a useful additional investigation for chest pain and was able to exclude oesophageal causes of pain in most patients studied. Oesophageal spasm appears to be a rare cause of chest pain in Christchurch. When a diagnosis was made on AMP, it was most often gastro-oesophageal reflux disease.

Diffuse esophageal spasm: a malfunction that involves nitric oxide?

OBJECTIVE: As recently suggested, nitric oxide (NO) may play an important role in the regulation of esophageal motility, being partly responsible for the latency period and latency gradient between the onset of a swallow and contractions of esophageal circular smooth muscles. Diffuse esophageal spasm appears to be a classical example in which the mechanisms normally responsible for the physiologic timing of the contractions occurring in the esophageal body after swallowing are disturbed. METHODS: Five patients (one male and four female; age, 18-48 years) with symptomatic esophageal spasm were give glyceryl trinitrate (GTN) intravenously in gradually increasing doses or L-arginine on two separate occasions and underwent manometric measurements of esophageal motility after wet swallows, using a multilumen perfused catheter system (Synetics Medical, Stockholm, Sweden). The amplitude, duration, and propagation of the contractions and the latency period were analyzed, using specially designed software. Additionally, during the GTN infusion period arterial blood pressure was measured every 5 min, RESULTS: GTN infusion given at a dose of 100 to 200 micrograms/kg-h intravenously caused the occurrence of and a dose-dependent elongation of the latency period after swallowing. The mean amplitude of the contractions did not show any significant alterations, whereas the mean duration of the contractions decreased significantly, from 11.2 +/- 4.8 sec to 5.4 +/- 0.8 sec. These effects were accompanied by significant alleviation of symptoms during swallowing. Interestingly, no adverse side effects such as headache or flush were observed at any dose of GTN. The blood pressure did not show any changes during the studies in any of the five patients. Administration of L-arginine (300 mg/kg-h intravenously) did not cause any significant alterations of motility pattern or alleviation of dysphagia. CONCLUSIONS: 1) NO may play an important role in the control of human esophageal motility, being involved in the mechanisms responsible for the timing of propulsive contractions in the body after swallowing; 2) GTN may to be of benefit in the treatment of diffuse esophageal spasm in symptomatic patients; and 3) patients with diffuse esophageal spasm may have a malfunction in endogenous NO synthesis and/or degradation.