Anorexics and bulimics who vomit to compensate for real or perceived binges may develop perimolysis, a loss of the enamel and dentin on the lingual surface of the teeth caused by recurrent exposure of the teeth to gastric acids. Patients may complain of increased sensitivity to heat, cold, and acidic substances, as discussed in the chapter on oral medicine (see Chapter 7, "Oral Considerations in Patients with Gastrointestinal Disorders"). The large amounts of carbohydrates consumed by bulimic patients during binges may further exacerbate the problem, contributing to an elevated frequency of caries. Parotid gland enlargement is a common manifestation of bulimia (Cuellar and Van Thiel, 1986; Jacobs and Schneider, 1985). No treatment is required, and the parotid enlargement usually subsides over time with cessation of vomiting. Some individuals abuse syrup of ipecac to induce vomiting, placing themselves at risk for cardiotoxicity resulting from accumulation of emetine in cardiac muscle. There appears to be a dose-response curve, and ingestion of 3 to 4 bottles per day has been associated with cardiac arrest and severe cardiac arrhythmias (Sansone, 1984).
^Editor's Note: Because Crohn's Disease often presents in the same age group, an occasional psychologically complex young woman with Crohn's disease will be discovered in an eating disorder clinic.
as a result of recurrent self-induced vomiting. Higher rates of dysphagia, Barrett's esophagus, and esophageal stricture are reported in bulimic patients compared with controls. As with salivary gland swelling, alcohol abuse also increases the risk of esophageal pathology (Cuellar and Van Thiel, 1986).
Mallory-Weiss tear and even gastric rupture have occasionally been reported in patients with BN, presumably as the result of chronic vomiting (McGilley and Pryor, 1998). Data regarding gastric emptying are more mixed for BN than for AN, but at least one study revealed delayed gastric emptying in patients compared with controls. Treatment of the eating disorder improved gastric emptying time (Kamal et al, 1991).
GI complaints associated with the abuse of laxatives, particularly the stimulant laxatives, such as bisacodyl and phe-nolphthalein, and the anthracene derivatives (senna, cascara, danthron), include nonspecific complaints such as constipation, diarrhea, abdominal cramping or pain, nausea and vomiting, and distention and bloating. Other sequelae of laxative abuse include steatorrhea, protein-losing enteropathy, osteomalacia and melanosis coli. Rectal prolapse secondary to severe laxative abuse can also be seen in eating disorder patients.
Although hyperamylasemia is found in as many as 62% of patients with BN, it is usually salivary in origin. Nonetheless, Gavish and colleagues (1987) reported on 21 patients with recurrent hyperlipidemicpancreatitis, all of whom were subsequently diagnosed with BN, and one of whom died. it is important to reiterate the importance of assessing alcohol use in patients with eating disorders because of the overlap of GI pathology produced by these conditions.
Patients who abuse diuretics typically choose over-the-counter products, but may also use prescription medications (Roerig et al, 2003). Complications from diuretic abuse include toxicity from agents containing salicylates or acetaminophen, and hypokalemia from loop diuretics. Abrupt withdrawal from these agents may produce reflex fluid retention and edema, so diuretics should be tapered if abuse has been heavy.
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