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The prevailing theory is that the phospholipidosis is primarily an adaptive response to CAD exposure rather than a toxic response. In this case, the cell adapts to the drug exposure by sequestering it in the lamellar bodies, thus reducing potential toxicity to intracellular structures. In the process of doing this, however, concentrations of the drug can reach millimolar levels in the lamellar bodies 50 ; . Studies have failed to definitively show that the presence of CAD-induced phospholipidosis is detrimental to the organism. Isolated cell studies have demonstrated that the presence of the condition may or may not result in changes in pulmonary cellular function, and where this occurs, the consequences to the intact organism are unknown. Additionally, studies involving whole animals have not demonstrated adverse effects attributable to the presence of CADphospholipidosis, at least for the lungs. These studies have been summarized previously 2, 17, 51 ; and will not be reviewed here. The following discussion will expand upon certain studies that highlight what the authors believe are illustrative of our state of knowledge in this field. Reasor et al. 51 ; administered amiodarone to rats, inducing phospholipidosis in alveolar macrophages. Using this model, a number of pulmonary host defense functions were evaluated. The pulmonary clearance of Listeria monocytogenes was not affected by the phospholipidotic condition. Using an ex vivo alveolar macrophage culture system, the presence of the phospholipidosis had no effect on the phagocytosis of heat-killed yeast cells, the induction of luminol-dependent chemiluminescence, the spontaneous release of interleukin-6 or tumor necrosis factor- , or spontaneous and LPS-stimulated release of interleukin-1. In contrast, the LPS-stimulated release of interleukin-6 and tumor necrosis factor- was enhanced compared with nonphospholipidotic cells. In the context of the functions studied, the induction of pulmonary phospholipidosis appeared not to impair pulmonary host defense processes in rats. A study by Ferin 52 ; demonstrated impaired pulmonary clearance of particles in rats treated with the CAD chlorphentermine, but the presence of phospholipidosis in the lungs was not verified. Sun et al. 53 ; examined the effects of the CAD amiodarone on rat and human hepatocytes, ex vivo. They reported that the induction of lamellar bodies preceded a decrease in cell function, which preceded cell death. The results could be interpreted that the induction of lamellar bodies is not directly associated with toxicity, but rather toxicity may result from higher drug concentration in the tissue tissue overdose effect ; . However, as the number of lamellar bodies within cells reached high levels, cytotoxicDRUG-INDUCED PHOSPHOLIPIDOSIS 827 and soma.
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REFERENCES 1. Stewart WF, Lipton RB, Celentano DD, Reed ML. Prevalence of migraine headache in the United States: relation to age, income, race, and other sociodemographic factors. JAMA. 1992; 267: 64-69. Lipton RB, Stewart WF. Migraine in the United States: a review of epidemiology and health care use. Neurology. 1993; 43 Suppl 3 ; : S6-S10. Lance JW. Current concepts of migraine pathogenesis. Neurology. 1993; 43 Suppl 3 ; : S11-S15. Capobianco DJ, Cheshire WP, Campbell JK. An overview of the diagnosis and pharmacologic treatment of migraine. Mayo Clin Proc. 1996; 71: 1055-1066 and zanaflex.
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Gordon CM, Radovick S, Emans J. Another positive pregnancy test. Adolescent Medicine: State of the Art Reviews 1996: 7 3 ; : 361-368. Rome ES, Vazquez I, Emans SJ. Nutritional Problems in Adolescence. In: Walker A and Watkins J, editors ; . Nutrition in Pediatrics. London: B.C Decker, London, 1996, pp. 691704. Forman S, Emans SJ editors ; . Adolescent medicine, editorial overview. Current Opinion in Pediatrics 1997; 9: 299. Emans SJ. Menarche and Beyond: Do eating and exercise make a difference? Pediatric Ann 1997; 26: Suppl 137-141. Forman SF and Emans SJ. Adolescent Health Care. Contemporary Internal Medicine in press ; . Chiou VM, Shrier LY, and Emans SJ. Emergency Postcoital Contraception. J Pediatr Adoles Gynecol 1998; 11: 61-72. Emans SJ and Biro F. Secondary Sexual Characteristics and Menses in Young Girls. Pediatrics, letter to the editor 1998; 101 5 ; : 949-950. Forman SF, Emans SJ. Editorial overview adolescent medicine. Current Opinion in Pediatrics 1998; 10: 337. Kahn JA, Emans, SJ. Gynecologic examination of the prepubertal girl. Contemporary Ob Gyn 1998; 7: 71-90 and in Patient Care 1999; 71-105 March and in Contemporary Pediatrics. 1999; 16: 148-158. Kahn JA, Mansfield J, Emans SJ, Laufer MR. Special Problems in the Adolescent: Adolescent Gynecology. In Burg FD, Wald ER, Ingelfinger JR, Polin RA. Gellis and Kagan's Current Pediatric Therapy 16. W.B. Saunders Company, Philadelphia, PA 1999 Perlman SE, Kahn JA, Emans SJ. Should pelvic examinations and Papanicolaou cervical screening be part of preventive health care for sexually active adolescent girls? J Adolesc Health 1998; 23: 62-67. Kahn JA, Emans SJ. Pap smears in adolescents: To screen or not to screen. Pediatrics 1999; 103: 673-674. Forman SF, Emans SJ. Editorial overview adolescent medicine. Current Opinion in Pediatrics 1999; 11: 281-282. Gordon CM, Radovick S, Emans SJ. Another positive pregnancy test. Adolesc Medicine: State of the art reviews. 1996; 7: 1-8. Bravender T, Emans SJ, Laufer MR. Use caution when determining "virginal" vs "nonvirginal" status [letter]. Arch Pediatr Adolesc Med 1999; 153: 773-4. Perlman S, Emans SJ. Human papillomavirus screening in pediatric victims of sexual abuse. In Stockman JA ed. ; The Year Book of Pediatrics. 1999, Mosby, Baltimore. Pp186-187. Emans SJ, Sulak PJ. Adolescence, sexuality, and contraception. Dialogues in Contraception 1999; 6 2 ; 4--6!
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