Evaluation of the use of botulinum toxin in children with achalasia.

BACKGROUND: Achalasia is rare in children. Recently, injection of botulinum toxin into the lower esophageal sphincter has been studied as an alternative to esophageal pneumatic dilatation or surgical myotomy as treatment for achalasia. In the current study, the effects of botulinum toxin were investigated in the largest known series of children with achalasia. METHODS: Treatment for achalasia was assessed in 23 pediatric patients who received botulinum toxin from June 1995 through November 1998. Those who continued to receive botulinum toxin and did not subsequently undergo pneumatic dilatation or surgery were considered repeat responders. Results were compared with those of published studies evaluating the use of botulinum toxin in adults with achalasia. RESULTS: Nineteen patients initially responded to botulinum toxin. Mean duration of effect was 4.2 months +/- 4.0 (SD). At the end of the study period, three were repeat responders, three experienced dysphagia but did not receive pneumatic dilatation or surgery, three underwent pneumatic dilatation, eight underwent surgery, three underwent pneumatic dilatation with subsequent surgery, and three awaited surgery. Meta-analysis shows that, in the current study group, the data point expressing time of follow-up evaluation versus percentage of patients needing one injection session without additional procedures (botulinum toxin injection, pneumatic dilatation, or surgery) falls within the curve for those in studies on adult patients receiving botulinum toxin for achalasia. CONCLUSIONS: Botulinum toxin effectively initiates the resolution of symptoms associated with achalasia in children. However, one half of patients are expected to need an additional procedure approximately 7 months after one injection session. The authors recommend that botulinum toxin be used only for children with achalasia who are poor candidates for either pneumatic dilatation or surgery.

Chewing gum bezoars of the gastrointestinal tract.

Children have chewed gum since the Stone Age. Black lumps of prehistoric tar with human tooth impressions have been found in Northern Europe dating from approximately 7000 BC (Middle Stone Age) to 2000 BC (Bronze Age). The bite impressions suggest that most chewers were between 6 and 15 years of age. The Greeks chewed resin from the mastic tree (mastic gum). North American Indians chewed spruce gum. The first manufacturing patent for chewing gum was issued in 1869 for a natural gum, chicle, derived from the Sopadilla tree, indigenous to Central America. Chewing gum sold today is a mixture of natural and synthetic gums and resins, with added color and flavor sweetened with corn syrup and sugar. Chewing gum is big business. A significant amount of the $21 billion US candy industry sales is from chewing gums, many of which appeal almost exclusively to children. Despite the history and prevalence of gum chewing, the medical literature contains very little information about the adverse effects of chewing gum. In the present report, we briefly review gum-chewing complications and describe three children who developed intestinal tract and esophageal obstruction as a consequence of swallowing gum.

Differential diagnosis of dysphagia in children.

Dysphagia in children often presents a difficult diagnostic challenge. A systematic approach in each individual can help with diagnosis and treatment. An overview of the differential diagnosis and the diagnostic and treatment options available is provided.

Changes in plasma glutathione concentrations, turnover, and disposal in developing rats.

We have previously shown that sinusoidal reduced glutathione (GSH) efflux declines during development because of a declining maximum transport rate [Am. J. Physiol. 261 (Gastrointest. Liver Physiol. 24): G648-G656, 1991]. Because rat liver serves as the principal source of plasma GSH, we studied the response of plasma GSH to this declining inflow from liver. In immature (28- to 42-day) and mature (90- to 151-day) rats we injected tracer boluses of [35S]GSH intravenously and collected arterial samples over a 0.75- to 8-min interval while plasma GSH pool remained at steady state. Concentrations and radioactivities of GSH, oxidized glutathione (GSSG), cysteine (CYSH), cystine (CYSS), and cysteine-glutathione disulfides (CYSSG) and the radio-activities of proteins were measured in plasma. Our results show the following changes in plasma concentrations (microM): decreases in unbound (free) GSH (26.0 +/- 2.1 to 12.4 +/- 0.98; P < 0.001), total unbound GSH equivalents GSH + 2GSSG (29.1 +/- 2.1 to 15.3 +/- 1.2; P < 0.001), total reducible (unbound + bound) GSH (39.3 +/- 2.2 to 28.9 +/- 2.6; P < 0.025), and free CYSH (57.6 +/- 8.5 to 29.9 +/- 4.0; P < 0.05); no changes in GSSG (1.57 +/- 0.27 vs. 1.47 +/- 0.41), CYSS (36.7 +/- 12 vs. 43.4 +/- 17), and total unbound CYSH equivalents CYSH + 2CYSS (131 +/- 15 vs. 117 +/- 18); increases in total reducible (unbound + bound) CYSH (158 +/- 8.1 to 203 +/- 24; P < 0.05) and CYSSG (1.80 +/- 0.42 to 4.94 +/- 1.4 in microM GSH equivalents; P < 0.05). A concurrent decline occurred in irreversible disposal rate (IDR) of plasma GSH from 38.5 +/- 4.9 to 16.4 +/- 1.4 nmol.min-1.ml-1 (P < 0.001) as determined by compartmental analysis of tracer data. This 57% decrease in IDR parallels a decrease of 53% in the inflow of GSH estimated by perfused livers (17.0 to 8.0 nmol.min-1.ml plasma-1). However, perfused liver estimates do not match > 44-49% of plasma IDR. Thus perfused liver appears to underestimate the true rate of sinusoidal GSH efflux taking place in vivo. Some earlier arteriovenous data and our present portal vein-to-hepatic vein difference measurements appear to corroborate this view.