Potential oral or head and neck findings of bulimia and anorexia include dental erosion, xerostomia, increased rate of caries, and sialadenosis. Vomiting exposes teeth to acidic gastric contents, which leads to enamel erosion. The erosion pattern tends to involve the lingual surfaces of the maxillary anterior teeth ( Figure 12 ) and, in severe cases, the buccal surfaces of the posterior mandibular teeth. 39 Patients may have dental sensitivity to cold or sweet stimuli. Xerostomia may be caused by medications often used by patients with bulimia or anorexia (., antidepressants, diuretics, laxatives), as well as by vomiting and excessive exercise. 40 Because the buffering and cleansing properties of saliva are important for prevention of tooth decay, xerostomia leads to increased caries risk. Additionally, sialadenosis affects approximately 25 percent of patients with bulimia; bilateral parotid enlargement is the most common presentation. 41
The effects of glucocorticoids are mediated by cytosolic glucocorticoid receptors and result from both genomic and nongenomic mechanisms that also have a role in the therapeutic effects of these agents [ 1-3 ]. The AEs appear to result largely from transactivation that leads to increased expression of regulatory and antiinflammatory proteins [ 2 ]; by contrast, many of the clinically desirable effects appear to result primarily from transrepression, which results in the decreased production of proinflammatory proteins. Nongenomic effects of glucocorticoids include rapid, nonspecific interactions of glucocorticoids with cellular membranes, nongenomic effects medicated by cytosolic glucocorticoid receptors, and specific interactions with membrane-bound glucocorticoid receptors [ 2 ].
The frequency of neuropsychiatric symptoms appears to be increasing because of both better testing and increased clinician awareness [ 2 ]. The neuropsychiatric manifestations of SLE are varied and may be classified as primary neurologic and psychiatric disease (eg, related to direct involvement of the neuropsychiatric system) or secondary disease (eg, related to complications of the disease and its treatment) ( table 2 ). The latter are generally more common causes of neuropsychiatric symptoms and can be produced by a variety of mechanisms ( table 3 ).