Document YrbOGbnB9rjJDowzrBde5Jpv8

^A.Orr^ ' fy/$ n Pfin . 0c (1 ry^c, U- c CL'>L 2 o-Li-^inJc ^ oa L oj (/cct/ic^l^ <3.'~X ( l ^ Y&>) ~Dllsty*0r% W /HfeOB A^0 ' ** * ft. ; ' COEXISTENT PULMONARY ASBESTOS^ AND SARCOIDOSIS * John H. Skavtuc, MX)., and Robxkt J. Rittmhoit, UJ), (From the Percy Skidds Laboratory t of Dunham Hospital, Cincinnati j, Ohio) Pulmonary asbestosis, regarded as a "modem disease" by Gloyne and Merewether,1 was first described by Murray * in 1900. Although Fahr3 described a case in 1914, interest in this disease was not re awakened until the case of Cooke and McDonald was described in 192 7* Since that time, there have appeared in the available literature reports upon approximately 150 necropsies on cases of pulmonary asbestosis.-12 The paucity of proved cases, in comparison with those of silicosis, is not due wholly to failure to report such cases, for in large necropsy series asbestosis is apparently of infrequent occur rence.6-13 Further, despite the widespread usage of asbestos prod ucts, there are comparatively few people engaged in the asbestos industry. As of October, 1944, only 19,700 people were employed in this industry in the United States.14 Much has been written about the clinical, roentgenologic, and biopsic aspects of sarcoidosis. However, because of the infrequency and relatively benign character of this disease there are only isolated detailed necropsy reports. From the available literature there have been found only 58 reports of necropsies on cases of sarcoidosis.1*-" Most of these were summarised by Pinner.1* These two diseases present many dinfcal and roentgeoographk' similarities, and, also, their more frequent fatal complications are alike: pulmonary tuberculosis and cardiopulmonary insufficiency. Bronchogenic carcinoma, a frequent complication of pulmonary asbestosis, has not, however, been described as associated with sar coidosis. Likewise, there has not been a previous description of asbestosis with coexistent sarcoidosis. It is the purpose of this report to present the findings in such a unique case, the only example of either pulmonary asbestosis or sarcoidosis in a series of 1870 necrop sies done at this hospital. Report op Case The patient was a white male, 43 years of age. Subsequent to hemorrhoidectomy in December, 1943, he had noticed that slight activity produced shortness of breath. He did not experience nocturnal dyspnea and he was able to lie flat in bed without respiratory difficulty. There was no history of cough, hemoptysis, or cardiac embarrassment. Notwithstanding a good appetite and the absence of gastric * Received for publication, May 9, 1945. t A sub-department of the Department of Medicine, College of Medicine, University Cincinnati. 493 C3 Co = C M* 'Uj Q <r-. ev oo QZ ' co T': fAJ- tu O- ' ^ s?;-; I. | B8 0005440 ** mmm mnm* 494 SKAVLEM AND KITTERHOFF symptoms, there was a weight loss of 22 pounds from December, 1943, to M 1944, at which time he presented himself for medical care. The patient had worked in an asbestos plant for 15 years, the last 10 u.)r. having been in a supervisory position. During this entire time he had worked in one department in which asbestos pipe was made. There was a slight but appreciable dust hazard associated with the sawing and splitting of the dried asbestos pi|,t. despite precautionary exhaust ventilation. The total time the patient had s|mu upon this final operation of sawing was unknown; nor was it learned whether h<had been negligent in using the provided respirators. To the company's knowlcd^. this was their first case of asbestosis. Physical.examination revealed the following findings; Temperature, 37" r respiration, 22 per minute; arterial blood pressure, 105/70 mm. Hg; heieiu 170 cm.; weight, 67 kg. The chest was of increased anteroposterior diameter Respiratory excursions were equal but decreased. The percussion note was Tesonam and auscultation revealed fine riles over the bases of the lungs, posteriorly. Th,. fl. were no evidences of cardiac enlargement, irregularity, or decompensation. Cyanon. and clubbing of the fingers were absent. The liver was 'barely palpable. Report on the roentgenogram of the cheat (Fig. 1) was at follows; "The honv framework is normal. The trachea is in the midlinc. The hiium shadows ar|. moderately enlarged, bilaterally. One small calcified ana is present in each hiium. There are numerous small nodular densities scattered throughout both lung fields, especially throughout the lower lobes. There is some confluence of these densities in the left lower lobe. Emphysema present.** Krammation of the blood rhawed erythrocytes, 5.5 million; leukocytes. 61. thousand; 73 per cent aeutrocytes; tt per cent lymphocytes; 5 per cent monocyte: z per cent eosinophils; sedimentation rate, afi mm. No abnormality was found in the urine. The vital capacity, ssoo cc., was 51 per cent of normal. Tuberculin teats woe not done. The patient was seen at regular intervals and his only complaint was increasingly severe exertional dyspnea. A roentgenogram of the chest 4 months after the initial chest film revealed no new findings. Although the patient greatly limited In activities, dyspnea became progressively more severe so that eventually, even at bed rest, there was extreme air hunger. At no time were there evidences of cardiai failure. He died approximately 11 months after the onset of symptoms, apparent,y from respiratory failure. Autopsy Findings The necropsy was performed 5 hours after death. Superficially there was considerable decrease in the subcutaneous tissues and the body musculature. There was no dubbing of the nailbeds or dependent edema. The mediastinum was in the midline. Each lung completely filled its hemithorax and extended far into the anterior mediastinal space. The domes of the diaphragm, anteriorly, were at the level of the fourth interspace and fifth rib, right and left respectively. The lungs were encased in markedly thickened, tough, yellowish white, generally fused pleurae. The interlobar fissures were obliterated by easily broken adhesions. Lobation was normal. Hemorrhagic fi brinous material, present over the posterolateral aspect of the left lower lobe, loosely bound the thickened parietal pleura to the lung in this area. ;t o?d hi. FILESNOT Luiuz rKUiVi. u pbbT 002^5:1-^ ^ CG A- ' ' i COEXISTENT ASBESTOSIS AND SARCOIDOSIS 495 The frontal section of the left lung (Fig. 3) revealed coarse, lacy, tannish brown, hypercrepitant tissue throughout both lobes. Innu merable slightly elevated, grayish green, irregular, firm nodules, 1 to 2 mm. in diameter, were present throughout the lung. Thin, radiating, fibrous bands surrounded and connected these nodules. Also, slightly thickened pleural septa extended into the lung substance for variable depths. In the lung tissue about the bronchi of the second and third interspaces these nodules were somewhat confluent and a similar change was noted in the subpleural tissues for a depth of 3 to 5 mm. Generally, these nodules, present in moderate numbers, were sepa rated by wide zones of dry emphysematous lung tissue studded by. numerous minute, grayish tubercles. Dissection of the bronchi of the lower lobe disclosed that they were moderately dilated, cylindrically and saccularly, and lined by glistening white mucosa. In the right lung the same changes were observed as were present throughout the left. However, the grayish green, irregular nodules ^ ,,ui . tended to be more numerous, larger, and more confluent. This was ,, " xij > particularly true of the anterior portions of the lower and middle - V*- lobes. Also, the nodules were connected by thicker grayish black and - ~3 - grayish white interlacing bands of fibrous tissue. Extending deeply into the lung substance, thickened pleural septa communicated with the fibrous tissue in and about the clusters of tubercles. Except for ' ' ~ more pronounced dilatation and thinning of the mucosa, the bronchi of the right lung were similar to those of the left The tracheobronchial lymph nodes were moderately enlarged and on section consisted of dense, rubbery, arrthracotic centers and thin rims of yellowish white tissue. Calcification was not grossly de monstrable. The embalmed heart weighed 280 gm. and had the following measurements: tricuspid valve, 120 mm.; pulmonary valve, 80 mm.; mitral valve, 85 mm.; aortic valve, 65 mm.; right ventricle wall, 3 to 8 mm.; left ventricle wall, 15 mm. The greatest transverse cardiac diameter was 13.5 cm, (The estimated normal heart weight on the basis of body length is 317 gm., plus or minus 40.11) The tricus- pid/aortic valve and pulmonic/aortic valve ratios were 1.84 and 1.23, respectively. (These normally should be 1.68 and 1.05, respectively.28) The right ventricle was dilated and its columnae carneae and papillary muscles were more prominent than usual. No mural thrombi were demonstrable and the valvular endocardium was normal. The enlarged spleen was of normal configuration and measured 1S by 9 by 6 cm. It was covered by a smooth capsule and the splenic I QB 496 SKAVLEM AND KITTEBHOFF substance was firm and purplish red with normal markings. No tubercles were seen. The liver measured 22 by 16 by 10 cm. The remaining organs showed passive hyperemia and moderate generalized arteriosclerosis. Microscopic Findings Throughout the lung there was a conspicuous linear, interlacing, peribronchial and septal pulmonary fibrosis (Fig. 2). This was par ticularly prominent in the subpleural tissues. The intervening lung tissue was moderately emphysematous. Innumerable tubercles were present in the linear and peribronchial fibrotic areas and were present to a lesser extent in the walls of the respiratory bronchioles and tne adjacent alveolar walls. Generally, these tubercles were of two types: sarcoida! and foreign body granulomas. The former predominated by approximately ten to ooe. Tubercles of these types were intimately as sociated and, in addition, many intermediate types were presented. The sarcoids! tubercles (Fig. 4) were free of caseation, contained m demonstrable organisms and ware, for the most part, in the same stage of development; however, a minimal number presented some v peripheral fibrosis and there was an occasional, coarse, collagenous hall Generally, the tubercles were sharply demarcated, surrounded fay delicate reticulum, and did not present peripheral rims of lympho cytes. They consisted of peripherally arranged epithelioid cells sur rounding central, loosely arranged epithelioid and monocytic cells. Giant cells were, for the most part, centrally located and often com prised over half of the bulk of the nodule. The giant cells appearul to be of two types: Langhans' cells and foreign body giant cells, with the former predominating. In many of the Langhans' cells there wennumerous small vacuoles, each containing a pink, round body. Other Langhans' cells contained large, clear vacuoles; and, rarely, in those cells containing one large vacuole there was present an "asteroid" body, an intensely eosinophilic stellate mass, 15 to 20 fi in diameter (Fig. 5) More frequently, the Langhans' cells contained round, oval, or suggestively budding, intracytoplasmic bodies of Schaumann,* 25 to 50 ft. in diameter. Rarely, these bodies appeared to lie outside of giant cells, and some enclosed irregular yellowish material (Figs. 6 and 7) These bodies stained blue with hematoxylin and in ferrocyanid' preparations were strongly positive for iron. Dr. Leroy U. Gardner who also studied this case, stated that these bodies stained "red with add fuchsin of van Gieson-Weigert instead of black like elastic tissue" * Schaumann, J. On the nature of certain peculiar corpuscles present in tissue u lymphogranulomatosis benigna. Acta med. Scaadhwv^ 1941, 106, 239-253. Nfi' ij ` | BB 000541*3 | ! COEXISTENT ASBESTOSIS AND SARCOIDOSIS 497 and that "von Kossa's calcium stain is negative." Re-study of ap propriately stained sections revealed, as pointed out by Gardner, that the Schaumann bodies did stain red; however, a moderate number also contained calcium in variable degrees, as demonstrated by von Kossa's stain. An occasional giant cell contained one or more clefts suggestive of cholesterol crystals. More frequently, however, doubly retractile, irregular spicules, plaques, and conchoidal masses were observed in giant cells. These doubly retractile masses were often about, or in,, the Schaumann bodies, particularly the smaller and partially calcified forms. The foreign body tubercles were indefinitely demarcated and con sisted of rather closely packed, indefinitely arranged, large monocytes, and one or more foreign body giant cells. These tubercles, for the most part, were within the dense zones of fibrosis. Some, however, were present in alveoli and respiratory bronchioles. Golden yellow discoid, verruciform, and incompletely segmented asbestos bodies, many of which were in giant cells, were observed in and about-the nodules (Fig. 8). Asbestos bodies, singly or in clusters and in mod erate numbers, were present also in the dense hbrotic areas (Fig. 9) and occasionally within alveoli (Fig. to). Rare, laminated,'calcified masses, enclosing apparent asbestos bodies (Fig. is) and other bodies which appeared to be of the Schsumum variety, were present in tbs linear fibrotic bands. Asbestos bodies were aba encountered in and about the sarcoidal tubercles and in the associated sarcoldal giant cU of both varieties, but more frequently in those of foreign body type. Iron preparations clearly demonstrated the bizarre forms of the as bestos bodies. In many areas it was difficult to distinguish between the two types of lesions. This was particularly true throughout the subpleural re gion where both the lesions and asbestos bodies were more numerous, clustered, and embedded in a dense matrix of collagen, masses of coarse elastic fibers, and fine reticulum. The larger bronchi were remarkable only for slight chronic inflam mation. The bronchioles and respiratory bronchioles, embedded in dense collagen and surrounded by tubercles, were moderately dilated and presented conspicuous focal squamous metaplasia and moderate chronic submucosal inflammation. In the subpleural regions where the asbestotic fibrosis and the granulomatous reaction were most in tense, the bronchioles were irregularly dilated and lined by alternating strips of tall columnar and squamous epithelium. Only a few bron chioles contained neutrocytic exudate. The respiratory bronchioles were generally constricted, surrounded by masses of eiastica, and 498 SXAVLXM AND RITTSKHOTT many contained asbestos bodies and the associated granulomatous reaction. Within the peribronchial fibrous tissue there was a moderate amount of hemosiderin in linearly disposed granules, and fine lipoid droplets. The small pulmonary arteries and arterioles presented slight intimal thickening, and those in the subpleural zone were surrounded by thick collars of elastic fibers. The intervening alveoli were moderately dilated, the capillaries were arteries pleural coidosii cardiac passive gen ral nephrit congested, and there was a slight increase in collagen in the alveolar walls bordering the fibrous masses. Focally, clusters of alveoli con tained lipoid-laden macrophages. "Heart lesion cells'* were infrequent. Sections of the pleura revealed dense, laminated, and oval fenestrated bundles of collagen. Focally, there were indefinitely demarcated nodules which consisted of circularly, disposed lamellae of collagen. Superficially, the pleura presented slight fibroblastic activity and an occasional perivascular accumulation of lymphocytes and monocytes, some of the latter occasionally containing hemosiderin. No asbestos bodies were observed. The pleura over the left lower lobe, in addition, bore organizing fibrinous exudate on its visceral aspect. Sections of the tracheobronchial lymph nodes presented a repetitious pattern of sarcoidal tubercles with almost complete replacement of the lymphoid tissue. Throughout the nodes there were minimal diffuse fibrosis and several nodular masses of coarse collagen. The tubercles were similar to those in the lung as to structure and stage of develop ment. Inclusions of Schaumann were not observed and only a rare "asteroid" was present Asbestos bodies were not identified. A mod erate number of hemosiderin-containing macrophages were present in the remaining lymphoid tissue. Similar sarcoidal tubercles were present to a slight degree in the spleen and liver, and to a lesser extent in the kidneys, diaphragmatic muscle, and the right and left ventricular myocardium. These sarcoidal tubercles, however, were not as compactly arranged as those in the lung and tracheobronchial lymph nodes, and were surrounded by and permeated by lymphocytes. "Asteroid bodies" and Schaumann bodies were not present in the giant cells of these tubercles. No asbestos bodies were found. Those in the right ventricular myocardium were associated with considerable fibrosis. i t The results of chemical and spectrographic analysis of lung tissue, performed under the direction of Dr. Leroy U. Gardner,24 are pre sented in Table I. The final diagnoses were: Moderate pulmonary asbestosis; exten sive sarcoidosis of pulmonary and tracheobronchial lymph nodes; marked chronic pulmonary emphysema; slight sclerosis of the small f-*ffi1 J ' *i ;T Ui u NOT COME FROM PPG FILES I BB 00 ........ i',< ;.- * ' `i- f V. .3&i *r -'; .`*i?&**&**'* COEXISTENT ASBESTOSIS AND 8AECOIDOSI3 499 arteries and arterioleb in the lungs; marked nodular obliterative pleural fibrosis; focal organizing fibrinous pienritis; minimal sar coidosis of the heart, liver, spleen, and kidneys; right ventricular cardiac dilatation and relative right ventricular hypertrophy; acutepassive hyperemia of the viscera; slight cirrhosis of the liver; slight generalized arteriosclerosis; minimal focal chronic adrenalitis and nephritis; chronic posterior urethritis and interstitial prostatitis. Tabs I Chemical and Spectrograpkic Analysis of Ash (Dry Tissue, Approximately 144% of Moist Tissue. Ash, 6.70% of Dry Tissue.) Ai osUm (neept Cl) AiBkowat* Cfcemicil uuljiji Cu, Af, Hgl Pb, Bi, CcH Mo J SiO, Fe,0, AiiOg B*Q ZnO MbO co MgO M0 SK) vvo* 0,0, NiO, OO K>0 Cl CO, Tot*! Frr mm <O.IJ 9-7# a3 34 MJ t-49 I.I* NmIom4 Non* few* Nom femad NmwWd 0.07 <M| 144 44-# *-4 Pmm Mil ' N* K Sr B* Cft At P a p Mt Tl Ca Ac s Cr f% Zm m Tt a 1 I Ckwlaluiba fm mm 4 36.7 Noiwfoatt! Nona bud M tl a AM KmImM <4 +4 Spwtrofmphie u*f)r*a* Artitnry ttelt ef hMM tmiumlt 71 too f a s* 2 tern TJ S S ' i| ..... A ' 4 ' `V \ a s * ., *s *, t* a > - -v ` '-J?yV-r** Ajj ** *t Discussion Clinically, in view of the significant history of exposure to asbestos, the possibility of sarcoidosis was never entertained. In retrospect, the rapidly progressive, disabling dyspnea, unaccompanied by evi dences of enlargement of the right heart or cardiac failure, should have e, aroused suspicion that there was a concomitant pulmonary lesion. Asbestosis alone is not usually accompanied by such profound, rapidly developing, respiratory embarrassment. In this case, however, there were no collateral clinical evidences of sarcoidosis. It would seem that a clinical diagnosis of coexistent asbestosis and sarcoidosis would be justified only by biopsy of a lymph node or a skin lesion to demon- | 8B 0005446 | nr," A ' J; J w i: t? m' 1 Soo SKAVLEM AND BTCTEBHOFE strate sarcoid lesions and the discovery of asbestos fibers in the sputum, with a history of adequate exposure to asbestos fibers and roentgenographic evidences of diffuse pulmonary fibrosis. Asbestosis of the degree observed, alone should not have caused death, and sarcoidosis has generally been regarded as a benign process. Reisner,u however, on the basis of his observations on cases of pulmonary sar coidosis, stated "that one is not justified in assuming too confident an attitude regarding the ultimate outcome." This statement is particu larly true when, as in this case, sarcoidosis complicates pre-existing pulmonary disease. Pathologically, there were evidences of right heart strain in that there was marked dilatation of the right heart, evidenced by increased tricuspid and pulmonic/aortic valve ratios and slight passive hyperemia of the viscera. The total heart weight, however, on the basis of body length,23 was normal. As determined by the ratio of the left and right ventricular weights, it has been shown that there may be considerable relative right ventricular hypertrophy without an increase in the total heart weight. However, relative right ventricular cardiac hypertrophy in Higgins* series ** was not usually accompanied by evidences of right ventricular failure. In view of the significant dilatation of the right side of the heart and the slight sclerosis of the pulmonary arterioles, there was, in all probability, some degree of pulmonary hypertension in this case. However, in the absence of an increase in total heart weight and in the absence of evidences of chronic passive hyperemia of the viscera there was probably no, or insignificant, exaggeration of air hunger due to heart failure. It has been suggested that dyspnea in the pneumoconioses is due to capillary and arterial blockage by the fibrotic process. This, in all probability, is true to a variable degree in those persons with severe fibrosis of the conglomerate type with attendant extreme chronic emphysema. This hypothesis, however, does not explain the severe dyspnea that is seen in occasional cases of diffuse miliary studding of the framework of the lung by silicotic, tuberculous, sarcoidal. or neoplastic tubercles. It may be that the mechanism of dyspnea in such instances is due'to irritation of the vagus nerve endings with reflex stimulation of the respiratory center (Hering-Breuer reflex). In view of the equivocal evidences of hypertrophy of the right heart in this case, mechanical obstruction to the blood flow would not appear to be the responsible factor but, more likely, because of the difnwactive inflammatory process throughout the lungs, the Hering-Breuer reflex was exaggerated. Presumably, there was either a severe re- 1E' stfist,v' Mor Bprbest V men f: i^dica day r f i - stat t .. my His ; sarr FILES ) i Go i ':. j BB 0005447^^ COEXISTSNT ASBESTOSIS AND SARCOIDOSIS 501 spiratory alkalosis or acidosis. Tissue changes suggestive of alkalosis, such as calcification of the renal tubules, were not found. ` Microscopically, there was some difficulty in differentiating the two types of tubercles since there were many sarcoidal tubercles which contained asbestos fibers, and tubercles of indeterminate type, not containing fibers or inclusion bodies, were sometimes seen. It was difficult to determine how much of the fibrosis was due to asbestosis. Morphologically, since the majority, by far, of the sarcoidal tubercles were without evidences of fibrosis and apparently of the same age, it is suggested that this process was engrafted upon an established as bestosis. Further, on the basis of Gardner and Cummings'28 experi mental studies on asbestosis, the marked peribronchiolar fibrosis with sequestrated asbestos bodies, the marked pleural fibrosis and pleural septal fibrosis, and the metaplasia of the bronchiolar epithelium in dicate that the asbestosis was well established and over 700 to 800 days old. Dr. Leroy U. Gardner, who kindly examined the material,' stated: "In comparison with our other material the pigmented foci in your case seem to show more fibrosis and less localized emphysema. Histologically, this can probably be explained by the presence of sarcoid nodules within the asbestotic zones of reaction. I would infer that in your case the two conditions developed more or less standtaneously, but that probably the asbestosis was present to some degree bef re the sarcoid appeared. This opinion b based npon (he occurrence at asbestos fibers and other hoft-cootaining particles in the interior of the tubercle-like nodules and to same cases within the * giant cells themselves. The number of asbestos bodies is smaller than seen in many cases." Inclusions of the Schaumann variety, found only in the lung, oc curred in 4 per cent of the giant cells. Some of these enclosed goldenyellow, irregular bodies suggesting asbestos bodies, but similar to or ganic material previously described within such bodies. Yet there were definite asbestos bodies enclosed by similar dark blue material. Schaumann inclusions have been described in only 4 per cent of the reported necropsies on sarcoidosis as summarized by Rubin and Pin ner,17 who did not regard these inclusions as specific for sarcoidosis. Rich,27 who was impressed by the frequency of Schaumann inclusions in sarcoidal lesions and by their absence in unequivocal tuberculous lesions, noted that Metchnikoff reported the presence of calcified in clusions in the hyperplastic tuberculous lesions of experimentally in fected Algerian rats. Kraus 20 stated that the presence of calcified inclusions was a feature not found in any known granuloma except . 503 SKAVLEK AND BITTE&H077 sarcoidosis. Gardner 34 pointed out that, in his sarcoid material, these bodies, regarded by many to consist of calcium or calcified remnants of dastica, do not, by the von Kossa method, contain calcium, but, by the ferrocyanide method, give a strong reaction for iron. Only a moderate number of the Schaumann bodies observed in the present case were either wholly or partially calcified, yet all gave a strong reaction for iron. Studies on sarcoid lesions of lymph nodes and spleen from another case revealed only a few iron-staining noncalcified Schaumann bodies. The presence of doubly retractile, nonlipoid sub stance in giant cells and frequently in dose relation to Schaumann bodies has not beat emphasized in the literature on sarcoidosis. It has been noted, however, that colorless and yellowish tinged refractile material Is often enclosed by the Schaumann body. The fact that masses are frequently doubly refractile has not been stressed. It has been suggested that these endosed masses represent disintegrat ing elastica; however, van Gieson-Weigert stains do not confirm this yiggfstinn The origin of this refractile and doubly refractile material \is not known. Being in and about many f the small, partially calcified bodies, this doubly refractile material appears to be associated with the development of the Schmrmaaa body. The larger and more densely bodies were not aa frequently associated with visible doubly refractile substance. However, fractured and fragmented, apparently old, Schaumann bodies, as seen in control sarcoid material from lymph node and spleen, usually contained moderate amounts of doubly re fractile substance. Apparently then, the Schaumann body, which stains blue with hematoxylin and red with acid fuchsin, is formed in response to doubly refractile, nonlipoid substance and initially is impregnated by iron and later, in amounts demonstrable by von Kossa's stain, by calcium. Wolbach,31 in 1911, Jadassohn, in 1919,33 and Friedman,13 in 1944, have described a peculiar intracellular body in cases of sarcoidosis. This body, stellate in shape, varies in size up to 25 p, generally lies in an ihtracytoplasmic giant cell vacuole, and stains intensely with acidophilic stains except the central area which is basophilic. Wolbach described them as lying free in tissue spaces, in endothelial leukocytes, and in giant cells. Friedman found such bodies in only 6 to 8 per cent of the giant cells in his case. Both investigators attempted to determine the chemical structure of this stellate body by specific stains; however, they were unsuccessful. Both considered the pos sibility of its being an extraneous organism, although questionable. Wolbach regarded it as a nonspecific biochemical alteration of the cytoplasm. He was never able to demonstrate stellate bodies in other NOT COi.n \`ij in 1 i "1 nor\ j BB 0005449 1 COEXISTENT ASBBSTOSIS AND SAECOIDOSIS '50} material and decided that they were not similar to inclusions some times seen in cases of sarcoma. Friedman regarded these bodies as nonspecific but highly characteristic of sarcoid lesions. Friedman pro posed that these bodies be called "asteroids," but perhaps it would be better, eponymically, to call them Wolbach's asteroids. They have been described in 7 cases of sarcoidosis, and never in association with the Schaumann calcified inclusion body. In the present case asteroids were present in approximately T per cent of the giant cells in the lungs and tracheobronchial lymph nodes. Definite transition stages of asteroid formation were suggested by the presence of spicules on the pink, coccoid, intravacuolar, intracytoplasmic bodies, particularly in those giant cells in which the small vacuoles were clustered and dis integrating. In addition, an occasional Wolbach's asteroid, instead of lying in a large, clear vacuole, was surrounded by agminated ruptured vacuoles. In view of the presence of similar pink, coccoid, intra- ' vacuolar bodies, similar asteroids,'and the same suggestive stages of asteroid formation in the giant cells of talcum powder granuloma, as observed in one case in this laboratory, these giant cell cytoplasmic changes must be regarded as Wolbach originally suggested, nonspedfie biochemical cytoplasmic alterations. In addition, such an asteroid is depicted in the giant cells of leprous Mona by Mallory" who called them "spiculated" botBes. No transition, stages betowtn Wo&och*s asteroids and Schaumana** inchakms were even temotdy taggi' rtrd, The pathogenetic relationshipe of aabestoefs and sartoMnsie are dependent upon the chronologic development Of the lesios and the nature of the causative agents. Historically and Mstslogicafly, is this case, it is most likely that asbestosb preceded the development of sar coidosis. The predominant localisation of the sarcoids! tuberdea with** in asbestotic zones of fibrosis with attendant morphologic modification of both lesions, as evidenced by asbestos bodies within sarcoids! tubercles and lesions of indeterminate type, would suggest an analogy to the intimate relationship existent between tuberculosis and the pneumoconioses. It must be remembered, though, that even in. un complicated sarcoidosis the lesions occur in the framework of the lung, and therefore the morphologic relationships of the two may be' coincidental. This would be in agreement with those who believe that morphologically sarcoid is not reconcilable with tuberculosis. How ever, to those who regard sarcoidosis as a peculiar form of tuberculosis, this case then would be one of asbestosis with superimposed noncaseating tuberculosis. . The authors are indebted to Dr. Leroy U. Gardner who critically examined the (truss and microscopic material of this case and supplied the chemical analysis. 504 SKAVLEM AND BITTERHOFF REFERENCES 1. Gloyne, S. R_, and Merewether, E. R. A. Asbestos. Occupation and Hi- ,i , Supplement. International Labour Office, Geneva, 1938. (Cited by Saw, R. R., and Drcessen, W. C. Asbestosis. Am. J. Pub. Health, '939, 29, 305-214.) 2. Murray, M. Cited by Egbert. (Charing Cross Hasp. Got., 1900. Alv, Departmental Committee on Compensation for Industrial Diseases. Minim . of Evidence, Appendices and Index, 1907! Cd. 3496, p. 137; Report, jyo- Cd. 3495. P- U-) 3. Fahr, T., and FeigeL Kristallbildung in der Lunge. Deutsche med. Wcknschr ' 1914, 40, 1548-1549. (Cited by Egbert.#) 4. Cooke, W. E. Pulmonary asbestosis. Brit. if. 1927, a, 1024-1025-. m, . Donald, S. Histology of pulmonary asbestosis. Ibid., 1927, a, 1025-10-, (Cited by Egbert) 5. Egbert D. S. Pulmonary asbestosis. Report of a case with necropsy finding. Am. Rev. 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