Leukemic infiltration of the esophagus.

BACKGROUND: Leukemic infiltrates of the esophagus have been described occasionally in autopsy series, but there are no reports of antemortem diagnosis. METHODS: Case reports are presented for three patients with acute myeloid leukemia in whom leukemic infiltration of the esophageal mucosa was diagnosed histologically and cytologically by endoscopic examination. Autopsies of patients with leukemia from 1976-1988 were reviewed. RESULTS: The autopsy review of 207 patients with leukemia showed evidence of leukemic infiltration in the esophagus in 7.2% of cases. The only clinical factor identified to be significantly associated with esophageal involvement by leukemic cells was a high initial leukocyte count. Esophageal involvement was associated with leukemic infiltration of other soft tissues and organs. CONCLUSIONS: Although the etiology of dysphagia in patients with acute leukemia is usually related to infection, reflux, chemotherapy toxicity, or benign strictures, the frequency of esophageal leukemic infiltration in this autopsy series suggests that this diagnosis must be considered. Esophageal leukemia is usually associated with widely disseminated soft tissue and visceral infiltrates.

Manometric aspects of Zenker's diverticulum.

Zenker's diverticulum is thought to result from disordered coordination between the pharynx and upper esophageal sphincter. Manometric studies of the upper esophagus have been helpful in testing the hypothesis of dysmotility in the formation and growth of a Zenker's diverticulum; however, the data have provided conflicting evidence. Manometric studies show that resting upper esophageal sphincter pressure is normal in some patients with Zenker's diverticulum and decreased in others. Abnormal premature relaxation and contraction of the upper esophageal sphincter seen in some patients with Zenker's diverticulum may be accompanied by pharnygeal contractions against a closed sphincter. This abnormality is thought by some investigators to be the cause of Zenker's diverticulum, but not by others who have found normal upper sphincter relaxation. Future manometric studies will very likely elucidate the pathogenesis of Zenker's diverticulum.

Aging-related alterations in human upper esophageal sphincter function.

Recent improvements in manometric catheters have made measurement of pharyngeal (P) and upper esophageal sphincter (UES) swallowing mechanics more reliable. Few studies have attempted to evaluate the effect of normal aging on P and UES mechanics. Pharyngeal and upper esophageal sphincter dynamics were studied in 10 healthy elderly adults (age greater than 60; range 62-79 yr) and 10 younger adults (age less than 60; range 24-59 yr). A solid-state intraluminal transducer system was used with a proximal unidirectional Konigsberg microtransducer and a circumferential (sphincter) transducer located 5 cm distally. Mean resting UES pressure was significantly (p less than 0.05) lower in the elderly than in the younger subjects (52 +/- 5 vs 72 +/- 6 (SE)) mm Hg. A significant inverse relation (R = -0.54; p less than 0.02) was found between age and resting UES pressure. Time from peak of pharyngeal contraction to UES nadir was significantly (p less than 0.05) shortened in the healthy elderly vs younger controls (10 +/- 30 vs 90 +/- 20 ms) during dry swallows. Our studies indicate that aging is associated with lower resting UES pressure and delayed UES relaxation, relative to the pharyngeal peak.

Scleroderma esophagus.

Scleroderma (systemic sclerosis) is a connective tissue disorder characterized by thickening and fibrosis of the skin and visceral involvement that may include the heart, lungs, kidneys, and gastrointestinal tract. At least 40-50% of patients with scleroderma experience esophageal symptoms such as heartburn and dysphagia, while up to 90% of patients have esophageal dysfunction on objective testing at some point in their disease. The disease results in smooth muscle dysfunction that causes esophageal aperistalsis and reduced lower esophageal sphincter pressures. Gastroesophageal reflux with poor acid clearance results with an increased incidence of complications such as peptic stricture and Barrett's esophagus. Aggressive medical therapy is necessary to prevent these and other complications of gastroesophageal reflux.

Esophageal chest pain.

Recurrent chest pain frequently results in significant disability and anxiety, even after cardiac disease has been excluded. A stepwise approach is recommended for the diagnosis of pulmonary conditions, musculoskeletal disorders and structural problems of the upper gastrointestinal tract that can produce chest pain. If a search for these disorders proves negative, an esophageal source of chest pain should be strongly suspected. Although gastroesophageal reflux disease is the most common and easily treated cause of esophageal chest pain, esophageal motility disorders should also be considered. Motility disorders include achalasia, diffuse esophageal spasm, nutcracker esophagus, hypertensive lower esophageal sphincter and nonspecific motility disorders.

Desensitization with human (recombinant DNA) insulin.

A 34-year-old woman developed gestational diabetes and was treated with insulin (beef-pork and beef) and oral therapy at various periods. She developed an insulin allergy; however, attempts at desensitization with the commercially available purified pork insulin desensitization kit (Eli Lilly Co.) were not successful. Reactivity to human (recombinant DNA) insulin as well as elevated IgE levels and eosinophilia were also demonstrated. A second desensitization attempt with human (recombinant DNA) insulin using a protocol developed by the authors was successful. This report discusses a desensitization procedure using human insulin in an insulin-allergic patient.