ABSTRACT
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.
Subject(s)
Bezoars/diagnosis , Chewing Gum , Esophagus , Rectum , Bezoars/therapy , Biopsy , Child, Preschool , Digestive System , Enema , Esophagoscopy , Female , Humans , Infant , Male , Physical Examination , Rectum/pathologySubject(s)
Anti-Inflammatory Agents, Non-Steroidal/adverse effects , Mesalamine/adverse effects , Pericardial Effusion/chemically induced , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Child , Dose-Response Relationship, Drug , Echocardiography , Female , Humans , Inflammatory Bowel Diseases/drug therapy , Mesalamine/therapeutic use , Pericardial Effusion/diagnosis , Pericardial Effusion/physiopathologySubject(s)
Abnormalities, Drug-Induced , Heroin/adverse effects , Methadone/adverse effects , Abdomen/abnormalities , Abnormalities, Drug-Induced/diagnostic imaging , Abnormalities, Drug-Induced/surgery , Biliary Atresia/chemically induced , Cleft Lip/chemically induced , Cleft Palate/chemically induced , Female , Humans , Infant, Newborn , Intestines/abnormalities , Male , Maternal-Fetal Exchange , Portoenterostomy, Hepatic , Pregnancy , UltrasonographyABSTRACT
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.
