Document dQX8d86v6QaYjOyJBJknEBaR9

<i::i\ un1!^ i>f ti'tMlim'til. Stritiitl. fii> hH'-.ii liiMMiorajion d'\'cl(>;u'(l wiiiU* ho was wearing orthodontic appliances. After the literature was reviewed. only one situation was found wherein a single tooth, which had a metal bracket bonded to it, developed a greenback pigmentation on debonding.1' Pretreatment photo graphs showed the presence of a single white lesion at the site of the subsequent acquired pigmentation, representing decalcification, a com mon dental finding. It is unlikely that the pattern and type of tooth staining seen in all the teeth in patient 3 (which is similar to that observed in the other three cases) is related to wearing orthodontic appliances. Studies of minocycline-induced skin hyperpigmentation may elucidate its mechanism of action on teeth. Two patterns have been described in the skin. A generalized "muddy-brown" pigmentation, prominent in sunexposed areas, histologically shows increased pigment in the basal layer and dermal macrophages/"'" Histochemically this pigment is suggestive of meianin. The second pattern is a blue-black focal discoloration associ ated with areas of inflammation. Electron microscopy and histochemstry suggest a hemosiderinlike de posit, but it is not clear if this is in Case Reports fad hemosiderin, a minocycline deg radation product, or a drug-hemosi derin complex.'1' X-ray microanaly sis lias shown these pigment deposits to contain iron and, most recently, lesser amounts of calcium.'"' Tetracycline and minocycline may cause tooth discoloration by different mechanisms. Tetracycline's apparent ability to chelate calcium-orthophos phate may explain its specificity for staining developing deciduous and permanent teeth. Tetracycline's in ability to stain the teeth beyond the age of 7 years may be a function of the unavailability of free calcium for complexing. Minocycline, unlike tet racycline, complexes poorly with cal cium. Prior experience with tetracy cline restricted the use of minocycline in children; therefore, little informa tion is available about its effect on developing teeth. Minocycline's abili ty to chelate with iron and to form insoluble complexes may explain its role in causing pigmentation of the permanent teeth. The authors would like to thank William E. Wricht. DDS. Patient Care Section. National Institute of Denial Research, National Institutes of Health, for his assistance in evaluating our patients and reviewing the manuscript. References 1. Wallman IS, Hilton HB: Teeth pigmented by tetracycline. Lancet !9G2;l:S27-829. 'J ] ,\ Tin hc.'.u-Mi nail avd w*; It \ ti-rni Ueatnionl. /u l'/.o; 1 of U tr,jn 11- IT Clu-slaii II. krkkvn ]', Mjonul !'; 1 >ij.ofilorj,. lion of [MTiuanent front teeth in 3.1.`>7 Norivg. / gian children due to tetracyclines and n!hor | factors Son mi ,1 /). nl !,'< > 197?>,n'\1 -1 Tig. \ 4. i-Ynske NA, Millns JL: Cutaneous pig:t<,-n. ( tat ion due to minocycline hydrochloride. ./ J Acad Dermatol 19SO;2:;iOS-3H). 5. Harder RSW: Minoryclitie-n-lated hyperjiijr. ; mentation. Arch Dermatol IfthatlUldk'n-iiUt*. G. Wolfe I, Ueiehmister Jt Mitweyclinv hyper. pigmentation: Skin, tooth, nail and bone invoK-e. ment. Cutis 19M;33:45T-458. 7. Rook A. Wilkinson D. Ebling F. Textbook of Dennatuloyif. cd 3. London, Blackwell Scientific Publications. 1979. vol 2. p 1902- j 1 i ) : I j S. Goodman L, Giiman A: Goodman's and Gilman's The Pharmacolotiical Basts of Thera. peutics, ed 6. New York, Macmillan Publishing Co Inc. 1980. pp IUil-1191. - 9. Easier RSW, Kohncn PW: Localized hemo siderosis as a sequela of acne- Arch Dermatol 197$;114:1G95-2G97. 10. Simons JJ, Morales A: Minocycline and generalized cutaneous pigmentation. J /lm ,4carf Dermatol 1980:3:214-247. 11. Fenskc N, Millns JL, Greer KE; Minocy. cline induced pigmentation at sites of cutaneous inflammation. J.LV.-t ]9S0:21J: 1103-HOG. 12. McGrae JR. Zelickson AS: Skin pigmenta tion secondary to minocycline therapy. .4rcfi Dermatol 19?0:1 IG:12G2-12G5. 13. Sato S. Murphy G. Bcnhard JD. et ah fltrastructura! and x-ray microanalytical observations of minocycline related hyperpigmentation of the skin. J Incest Dermatol 19$1;77;2S4271. j 1 , 14. Gordon G, Sparano EM. latropoulos MJ: Hyin-rpigmentation of the skir. associated with minucvcline therapy. Arch Dermatol If*So; 121:GIS-G23. 15. Cven RF, Gwinnett AJ: Indelible iatrogen ic staining of enamel ft/.Wing thbonairg: A case report. Clin Orthodontics 19S0;11:713-715. Fig i -F coveting - eosin. on; rig 3. -- E tissue (on microcher Asbestos Bodies in Carcinoma of Colon in an Insulation Worker With Asbestosis Albert Ehriich. MO; Arthur N. Rohl. PhD; Edwin C. Holstein. MD CARCINOMAS involving the gastro intestinal tract, as a group, are the most common forms of cancer in the United States, with the colon and the rectum being the most frequently involved sites. Geographic pathology suggests that environmental factors play a strong role in the etiology of these From m Environmental Sciences Laboratory. Department of Community Medicine. Mount Sinai Medical Center, New York. RegtsM tesuev* to Environmental Sciences Lab oratory. Department of Community Medicine. Mount nai Medical Center, 1 Gustave L. Levy PI. New jrk. NY tOC29 (Dr Ehrlich). tumors. There is an increase in the number of deaths from colon cancer in asbestos workers. In a study of 17,800 asbestos insulation workers, instead of 38.1 expected deaths due to cancer of the colon and rectum, there were 59.' Other studies support the association between asbestos expo sure and colon-rectal cancer/ Report of a Case A 66-year-old asbestos insulator had worked for over 32 years putting asbestos around pipes and removing asbestos from old pipes. Dyspnea on exertion, without angina. started about 19G7. Clubbing of fingers and bilateral extensive rales were found on physical examination. The clinical diagnosis of advanced asbestosis was made by three physicians, based on the findings of severe parenchy mal and pleura] disease on roentgenogram as well as pulmonary restrictive ventila tory defects. On June 27, 19S3, a 20-cm segment of colon and a portion of mesentery were resected for a well-differentiated adeno carcinoma of the colon. A mild tissue reaction was found in the muscuia.-is of the normal bowel, consisting of foci of fibrosis. The serosa revealed a fibrotic replacement of fat. The peritone um covering the serosa was fibrotic (Fig 1). Asbestos bodies were not seen. Histoiogical sections of five patients with colon cancer who had no known asbestos exposure were examined micro scopically as controls. Fibrosis in the muscuiaris or serosa was not seen in these specimens. Five gr mal bow*, through a brane.'* E microscopi. tos bodies were found of digested Two hu and serost formaide'r men was asbestos fc iv (Fig 2 mesentery This was c per gram of asbestc been repo edge. A 2.0-$ digested i: rite. The r by trans Many am lied by e 2932 JAMA. Nov 22/29. 1985--Vol 254. No. 20 Asbestos Bodies--Ehrlich et al JAMA. No Mil-if. long c-At- &> J A i '-rP'K- Hyper- volve- * p,g i.--Fibrotic thickening of peritoneal layer, ! .(jeering serosa and mesentery (hematoxylm1 ggsin. original magnification X160). *>ok df entific s and "hera. ishing nemo* matat e and -lead inocy. neou$ sfltaArch ct al: <bser- ;enta7:264* i MJ: with 19SS; Fig 2. -- Some asbestos bodies found in digest of colon carcinoma and mesentery (original magnification X320). Fig 3.--Electron photomicrograph of amosite fibers found in colon carcinoma and mesentery tissue (original magnification X20.000). Fibers are identified by electron diffraction pattern and microchemical analysis (inset). gers )und need 'ans, chy- ram tila- ;t of .vere eno- :he ting ?d a oneFig entt own C'O* * Five grants of tumor and adjacent nor 1 mal bowel was digested and filtered through a polymer filter (Millipore) mem brane." Examination of the membrane microscopically revealed 54 typical asbes tos bodies (Fig 2). Thirty asbestos bodies were found in a second similar 3-g sample of digested bowel. Two hundred ten grams of mesentery | and serosal fat was in another container of I formaldehyde. Three grams of this speci men was digested." Twenty-eight typical asbestos bodies were found microscopical ly (Fig 2). A second digest of 2.8 g of mesentery revealed 34 asbestos bodies. This was an average of ten asbestos bodies per gram of wet tissue. Such quantitation of asbestos bodies in the colon has never been reported, to the best of our knowl edge. A 2.0-g portion of mesentery was digested in a solution of sodium hypochlo rite. The residue was prepared for analysis by transmission electron microscopy. Many amphibole asbestos fibers, identi. Red by electron diffraction of selected areas, were observed. Microchemical anal yses were obtained on fibers, using an energy-dispersive detector in conjunction with transmission electron microscopy. All fibers analyzed had the chemical com position of the asbestos amphibole mineral amosite (Fig 3). Amosite is one of the asbestos minerals most commonly used in insulation material. The concentration of amosite in the section of mesentery ana lyzed was 1.06X10* fibers per gram of dry tissue. Comment A substantial number of asbestos bodies was demonstrated in the tumor area and mesentery of an ade nocarcinoma of the colon in an asbes tos worker with asbestosis. This find ing is consistent with the conclusion of epidemiologic studies that asbestos exposure is associated with an ele vated risk of gastrointestinal cancer. This is especially so in view of a report' in which digestion technique'* was usvd U> study 21 specimens uf adenocarcinoma of the colon in the general population. Typical asbestos bodies were not found in any of the specimens. Asbestos fibers and bodies can be coughed up or swallowed and can be found on or in the bowel mucosa." * In this case, however, asbestos bodies were found in the mesentery.19 These asbestos fibers may have penetrated the lamina propria of the mucosa, followed by phagocytosis by neutro phils and macrophages, resulting in fibrosis and possible asbestos body formation, similar to the reaction that takes place in the lung.10 It is possible that the asbestos was biolog ically active, resulting in tissue injury in the colon, with foci of fibrosis in the muscularis and the serosa. There was also thickening of the peritoneal layer of the mesentery (Fig 1), resem bling the pleural fibrosis in pulmo nary asbestosis. An investigation is now in progress to search for asbestos bodies in digests of tissues of carcinoma of the colon in asbestos-exposed and appro priate control populations. The pur pose is to explore the possible causal relation between asbestos bodies in the bowel and colon carcinoma. The findings in this case report suggest the need for such a study. References 1. Seiikoff IJ, Hammond EC, Seidman H: Mortality experience of insulation workers in the U.S. and Canada: 1943-1976. 4nn XY Acad Sci 1979:330:91-116. 2. Miller AB: Asbestos fiber dust and gastro intestinal malignancies: Review of literature with regard to cause/effect relationship. J Chronic Dis 1978;31:23-33. 3. Smith J, Naylor B: A method for extracting ferruginous bodies from sputum and pulmonarytissue. An J Clin Pathol 1972:58:250-254. 4. Churg AM, Warnock ML Numbers of asbestos bodies in urban patients with iung cancer and gastrointestinal cancer and in matched controls. Chest 1979;76:143-149. 5. Rosen P. Savino A, Melamed M: Ferrugi nous (asbestos) bodies and primary cancer of the colon. Am J Clin Pathol 1974:61:135-138. 6. Cook PM: Review of published studies on gut penetration by ingested asbestos fibers. Environ Health Perspect 1983:53:121-130. 7. Meek ME: Transmigration of ingested asbestos. Environ Health Perspect 1983:53:149 152. 8. Lanper AM: Inorganic particles in human tissues and their association with neopiastic disease. Environ Health Perspect 1974;9:229233. 9. Auerbach O, Constas AS, Garfinkel L, et at: Presence of asbestos body in organs other than lung. Chest 1980;77:133-137. 10. Chrysta! RC, Gadek JE. Ferrans VJ, et al: Interstitial lung disease: Current concepts of pathogenesis, staging and therapv. An J Med 1981;70:542-567. t al JAMA, Nov 22/29, 1985--Vol 254, No. 20 Asbestos Bodies--Ehrlich et al 2933