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Current Medical therapy for esophageal motility disorders

1992; Elsevier BV; Volume: 92; Issue: 5 Linguagem: Inglês

10.1016/0002-9343(92)80064-7

1555-7162

Sami R. Achem, Byron E. Kolts,

Fluorine in Organic Chemistry

Treatment of patients with an esophageal source of chest pain remains a challenging problem. Although a variety of measures—including nitrates, anticholinergics, sedatives, calcium channel antagonists, esophageal dilation, and psychological reassurance—are available for the management of esophageal chest pain, none has emerged as the treatment of choice. Studies of nitrate preparations for the treatment of painful motility disorders are limited by a small number of patients and the lack of randomized, placebo-controlled investigations. The efficacy of anticholinergic drugs in hypercontractile esophageal motility disorders has not been reported. In the only prospective placebo-controlled trial using an antidepressant, trazodone was superior to placebo in relieving symptoms in patients with a variety of esophageal motility disorders. Conflicting results have been described in placebocontrolled trials of the calcium channel antagonists nifedipine and diltiazem in patients with "nutcracker esophagus" or diffuse spasm. Information about the efficacy of verapamil and hydralazine is limited. Esophageal dilation has been useful in selected patients. For many patients, esophageal chest pain may be associated with gastroesophageal reflux. Treatment of these patients with nitrates, calcium channel antagonists, or anticholinergics may aggravate their reflux. The mechanisms of esophageal chest pain remain unknown. Recent studies have suggested that abnormal motility may not be the only factor associated with chest pain. An important number of patients have behavioral abnormalities, increased nociception, impaired coronary vasodilatory reserve, or a diffuse abnormality of smooth muscle. Research into rational therapy for chest pain patients should take into account the contribution of these other factors. Treatment of patients with an esophageal source of chest pain remains a challenging problem. Although a variety of measures—including nitrates, anticholinergics, sedatives, calcium channel antagonists, esophageal dilation, and psychological reassurance—are available for the management of esophageal chest pain, none has emerged as the treatment of choice. Studies of nitrate preparations for the treatment of painful motility disorders are limited by a small number of patients and the lack of randomized, placebo-controlled investigations. The efficacy of anticholinergic drugs in hypercontractile esophageal motility disorders has not been reported. In the only prospective placebo-controlled trial using an antidepressant, trazodone was superior to placebo in relieving symptoms in patients with a variety of esophageal motility disorders. Conflicting results have been described in placebocontrolled trials of the calcium channel antagonists nifedipine and diltiazem in patients with "nutcracker esophagus" or diffuse spasm. Information about the efficacy of verapamil and hydralazine is limited. Esophageal dilation has been useful in selected patients. For many patients, esophageal chest pain may be associated with gastroesophageal reflux. Treatment of these patients with nitrates, calcium channel antagonists, or anticholinergics may aggravate their reflux. The mechanisms of esophageal chest pain remain unknown. Recent studies have suggested that abnormal motility may not be the only factor associated with chest pain. An important number of patients have behavioral abnormalities, increased nociception, impaired coronary vasodilatory reserve, or a diffuse abnormality of smooth muscle. Research into rational therapy for chest pain patients should take into account the contribution of these other factors.