Search

The function of the oesophagus is relatively straightforward—to transport the swallowed food into the stomach. In order to meet this functional need, the design of the oesophagus is simple; a relatively straight muscular tube that is guarded at it two ends by the upper and lower oesophageal sphincters. Following a voluntary act of a swallow, the two sphincters relax and open and a contraction wave or peristalsis sweeps behind the bolus autonomously. The contraction wave sweeps through the entire length of the oesophagus followed by closure of the two sphincters. Neuromuscular control mechanisms that bring about normal functioning of the two sphincters and oesophageal peristalsis are complex and require fine coordination of the muscles and nerves at the level of the central and peripheral nervous system. Disturbance of sphincters and peristalsis causes symptoms of dysphagia and oesophageal pain. The latter may manifest either as chest pain (pressure-like sensation) or heartburn (retrosternal burning). The nature of dysfunction in oesophageal motor disorders has been the subject of intense investigation for several decades. In this paper, we will review briefly the physiology of oesophageal peristalsis and lower oesophageal sphincter and then attempt to understand what may be wrong in motor disorders of the oesophagus. Novel pharmacological approaches to treat oesophageal motor disorders are also discussed. The anatomy of the oesophagus is unique; it is made up of skeletal muscle in the upper one third, a mixture of skeletal and smooth muscle in the middle one third, and smooth muscle only in the distal one third in humans. The upper oesophageal sphincter is composed of all skeletal muscle and the lower oesophageal sphincter of all smooth muscle. The muscularis propria of the oesophagus, similar to the rest of the gastrointestinal tract, is made of two distinct muscle layers that are arranged in a circular …

The discovery that Helicobacter pylori infection is the main cause of most gastroduodenal diseases has been a major breakthrough in gastroenterology. It has dramatically changed the management of these diseases which are now considered as infectious diseases and are treated with antibiotics. Triple therapy, including two antibiotics, amoxicillin and clarithromycin, and a proton pump inhibitor given for a week has been recommended as the treatment of choice at several consensus conferences.1–6 However, this treatment may fail for several reasons, as reported elsewhere.7 In fact, the main reason for failure was found to be H pylori resistance to one of the antibiotics used (that is, clarithromycin). Other treatments have also been proposed, including metronidazole, a drug for which resistance is also a problem although to a lesser extent, as well as tetracycline, fluoroquinolones, and rifamycins for which resistance has become an emerging issue.8,9 Our aim was to review the prevalence of H pylori resistance to these various antibiotics, their clinical importance, and methods of testing, especially in light of the resistance mechanism which allows application of molecular methods. Numerous studies have been performed to determine the prevalence of H pylori resistance to antibiotics. However, many of them have drawbacks, in particular concerning the number and representativeness of the strains tested. Most of the studies were performed in specialised centres, with recruitment of special cases which are not always representative of patients as a whole and, because these studies are monocentric, the number of patients may be low, leading to wide confidence intervals of the prevalence rates obtained. Ideal studies involving patients who are representative of a given region are few. An alternative has been to analyse prevalence data obtained from clinical trials aiming to evaluate new regimens. As prevalence is in essence an evolving phenomenon, only …