Dysphagia is a manifestation of several clinical conditions of diverse origin. In spite of the variation in these disease entities in terms of their etiology, clinical presentation, natural history, and treatment, the mechanism of this clinical complaint is not always clear. We studied a group of patients with dysphagia for solids in whom no anatomic or motor abnormalities were encountered on standard studies. The group consisted of 37 patients, 25 women and 12 men, who were complaining of dysphagia of 6 months or longer duration and they did not demonstrate structural or motor abnormalities on barium esophagogram, esophagoscopy, and standard esophageal manometry. A group of 24 age-matched patients, 14 women and 10 men, with noncardiac chest pain served as the patient control. Esophageal contractile activities were studied after 10 wet swallows (5 ml of water) and 10 viscous swallows (5 cubic cm of marshmallow). Resting lower esophageal sphincter pressure and its relaxation response to swallows, amplitude of peristaltic activities, rate of dysphagia provoked during the study, and the frequency of abnormal esophageal contractions were evaluated. Six abnormal esophageal contractile activities-failed peristalsis, dropout, repetitive, simultaneous, spontaneous contractions, and aperistalsis-were utilized to generate an esophageal peristaltic dysfunction index. The mean LESP was 8.1 +/- 4.7 in the dysphagia group and 16.1 +/- 4.3 in the chest pain group. The mean amplitude of peristaltic contractions was 47.1 +/- 16.1 and 89.0 +/- 27.0 mmHg after wet swallows for dysphagia and chest pain groups, respectively. These values were 58.2 +/- 12.4 and 92.4 +/- 22.1 for viscous swallows. Swallowing provoked dysphagia in 89% of the dysphagia group after viscous swallows and 9% after wet swallows. In contrast, only 11% and 3% of control group complained of dysphagia during the study. This group of patients probably represent a cohort of patients with a nonspecific esophageal motor disorder in whom both clinical symptom and their esophageal motor counterpart can only be elicited in response to viscous swallows. We strongly believe in addition of viscous swallows in evaluating dysphagic patients in whom symptoms remain unexplained in light of standard studies.
To ascertain the effects of protein deprivation on hemopoietic parameters in otherwise healthy subjects, three volunteers were placed on diets containing 0.15 g protein/kg body weight for 8 days followed in 2 mo by another 8-day study period during which they ingested their usual diets containing more than 0.9 g protein/kg body weight. Complete blood counts, serum protein determinations, and tests of in vitro and in vivo leukocyte chemotaxis were performed prior to and at the conclusion of each study period. Subjects were phlebotomized of 500 ml on day 7 of each study period. Twenty-four-hour urinary erythropoietin excretion rates were assayed just prior to and again postphlebotomy. Reticulocyte counts were performed at intervals up to 1 wk postphlebotomy. Some of these determinations were replicated during a subsequent study. The hemoglobin and hematocrits decrased slightly but significantly after 8 days on low protein diets. Erythropoietin excretion rates and reticulocyte responses to phlebotomy were also less marked while subjects were on protein depleted diets. Leukocyte chemotaxis, measured both in vitro and in vivo, was also markedly reduced while subjects were on protein-depleted diets. We conclude that 8 days of moderately severe protein deprivation significantly impairs erythropoiesis and leukocyte function in otherwise healthy individuals.
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