Document g2BXmjjYpw9G90XOrK94q8z33

FILE NAME: Philip Carey (PC) DATE: 1946 DOC#: PC004 DOCUMENT DESCRIPTION: Article from Medical Journal - The American Journal of Pathology J fT ". I me*##**##* THE AMERICAN JOURNAL 4 OF PATHOLOGY O f,d e l Publication of The American Associa/' ** o) Pat/iak f s l s and B e d er-l 1odists BOARD OF EDITORS CARL V. W EL LE R, Ec-nros-rN-Cmrr MALCOLM H. SOULE A ssistant C ditok j . HA RO LD AUSTIN* TRACY B. M \ W GPU" PAUL R. CANNON SHIELDS, WARREN HOWARD T. KARSNER H ARR Y M. ZI M >1I -A VOLUME XXII (January, March, and M ay; 1946 ANN AUhR 'uIUiliCAN ! . s. -> ' *>VV * COEXISTENT PULMONARY ASfcESTOsiS AND SA&C01D0 SIS * Jo^Kr H . Skavle?i , M .D ., and 'SuuEiiT J . F .ir fi.itn.<jrrT M.I>. <From the Percy Shields l^or.iicry f c; Di*t t.am PospHa*. Cincinnati s\ P u ira o n a iy .sbesinsL . rega rd e d as. a S n . I rr. d is e a s e "' b y C lo y n e a n d & Ir r e f'lL i rJ v -s first deserib u ! b y M t r r a y * u i :9 0 a . A lth o u g h F ah r 3 described r case in 1914. interest in this .disease was not re a w a k e n e d until th e c<u>e o f C o o k e a n d M c D o n a ld w a s des<-dbed in xQ 2f.4 Since that tunc. there have appeared in th e a v a ila b le jftefatiire report upon m:r>rexir?r.ie]y t eo necropsies or, ca se s o f pu lm on ary asb esto sjs:' *ir T h e p a u c ity o f p ro v e d ea ses, in c o m p a riso n "tn fh th o se o f silica -is if n ot d u e w h o lly 10 fa ilu r e to rep o rt su c h casus, io r in la rg e n ecrop sy series asbestor-is *s a p p a r e n tly o f in fre q u e n t occu r- rcu c e.3' ' 3 F u rth e r, d esp ite the w id e sp re a d u sa g e o i a sb e sto s p ro d ucts. th ere are com paratively few people engaged in the asbestos in d u stry . .As o f O cto b er, 1944. o n ly 0,700 p eo p le w ere em p lo yed in th is ind ustry' in the U n ited S ta tes 14 M u c h h as been w ritten about the ciin 'ca i. ruentsrer.ol >gk. i b io p sic a sp ects of sarco w o si- H ow ; rer. b e c a u se o f '*[ .- in :c and relatively' bem gn character o f this d i-case there are only ,v d detailed necropsy reports. From the available btc-atim - there have b een fo u n d o n ly - J r e p o u s o i r-eeropsle'-- o a c a se s o f sa rco id o sis.}i- M o st of these were sum m arized b y Pinner.'5 T h ese tw o diseases present m any cl! ic-l a u c roen tgen o gran u t sim ilarities, and, also, their m ore frequent fatal com plications alike: pulm onary tuberculosis and cardiopulm onary insufficiency. Bronchogenic carcinoma, a frequent com plication of puim onaiy asbestosis, ha? not, however, been described as associated w ith sar coidosis. Likew ise, mere has not been a previous description of asbe&,lusts w ith coexistent sarcoidosis. It is th e p u rp o se o f this report to present the findings in su c h .a unique case, the o n ly exam ple of eith er p u lm o n a ry asb estos's or sa .c o lu o sis 0 a series o f 1 8 7 ; n ecro p sies done at this ho-pitab jR.ru of C asf fbe ' - 0 v.; '... .. . . , , , 1,, _r, _q t!rri''inv*''jeui " v in iJetembcr, jo-ti- L- !nfi iL*. "ITK . ctM tv pjodaccd s;a;rT,f - - . bn ah. i-> did ROi expeniML. .-cunm . ,,r_. ; and he vas .Lie >0 Pc :<:< a V f Miiifc .>it r.'fp>!,itory difficultj; Ther \v:,s - hism".* of c< a.'h, him oa:,? s j Cuuliat ''raLairrO''t:meet. X, h .- udaij , jn .y.-e1, ] ,;<> e >'f e - ' ZLt-cew c' l|p; / J w ^ m p t'oms, there ws a weight losl ^ le<^ber;:'i943/ to I^ d C " 1944, a t which time he presented hiinsel'f lir m dical care. The patient had worked in an ^ h e p ^ p a n t fo r 25 years, the-last-. 10 years having been in a supervisory position^ Im p i^ fS h is entire time he had worked in one department in which asbestos pipe w as m ad e.T h ere was a slight but appreciable dust hazard associated with the sawing and splitting o f the dried asbestos pipe, despite precautionary exhaust ventilation.-The total time the patient had spent upon this final operation of sawing was unknown; nor was i t learned whether, he had been negligent in using the provided^respirators. T o the company's knowledge, this was their first case of asbestosis? Physical examination revealed the following findings : Temperature, 3 7 ' C .; respiration, 22 per minute ; arterial\'6 k)b4 : |eMure, 105/70 mm. H g;' heights 170 cm.; weight, 67 kg. The chest ^ras o f increased anteroposterior diameter. Respiratory excursions were equal but-decreased;' T h e percussion note was resonant and auscultation revealed fine rles over the bases o f the lungs, posteriorly. There were no evidences o f ,cardiac enlargement, in egidarity, or decompensation. Cyanosis and clubbing of the fingers were a b s e n t H e liv e r w as barely palpable. j? . Report on the roentgenogram of the chest (F ig. 1) was as follows: " The bony framework is normal. The trachea i s 'i n the midline. T h e hilum shadows are moderately enlarged, bilaterally. One small calcified area is present, in each hilum. 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 is present." Examination of the blood showed erythrocytes, 5.5 million; leukocytes, 6.6 thousand; 73 per cent neutrocytes; 21 per cent lym phocytes; 5 per cent monocytes; 1 per cent eosinophils; sedimentation rate, 26 mm. N o ' abnorm ality w as found in the urine. The vital capacf^, 2200 cc., was 51 per cent o f normal. Tuberculin tests were not done. The patient was seen at regular intervals and his only complaint was increasingly severe exertional dyspnea. A roentgenogram o f the chest 4 months, after the initial chest .film revealed no new findings. Although the patient greatly lim ited his. activities, dyspnea became progressively m ore severe so that eventually, everi at>.- bed rest, there was extreme air hunger. A t no tim e w ere there evidences o f cardiac failure. H e died approximately n months after the onset o f symptoms, apparently 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 clubbing 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. _ .w_Mxri r ___ _________ ,, ___ , ____ fim n - merable sK^Sy^elcvated/grajish green,'Srregidaxf ifan nodules, mm. itCdiamstfer, were present throughout the lung. Thin, radiating, ^ edand connected these nodules. Also, slightly thickened pletiral sepiaextended into the lung substance for variable depths. In lhe lung tissue about the bronchiof the second and third interspaces these noddies were somewhat confluent and ` ^ ^ * * '* * feK ^presjmtin of. dry emphysematop lung-tissue stud* djerdes.' I^s<SOT(m^lhe;* In Mung the same changes were observed as were present throughout* the left. However, the grayish green, irregular nOdules tended to be more numerous, larger; and more confluent. This was particularly true of the anterior portions of the lower and middle lobes;..A bo,n od ules were connected by thicker grayish black and bands,of fibrous tissue. Extending th^J^ ^^ P^^ diickeaed''pleural Septa cdapra flbrous^^Kti^^ aml about the dustersiof tubercles. __ ^ ^ and thinning of themucosa, the brondfei^ to those of-the left. on seetiOn cohsisted of dense, rubbery, anthracotic rims of, ydlowish white tissue. Calcification was nbt; The$^iEDud heart weighed 280 gm. and had the^fc measurements: tricuspid valve, 120 mm.; pulmonary valve, 80 mitral valve, 85p i;;, aortic valve, 65 mm.; rfi^t.ventricle waHfj to 8 mm.; left Ventricle wall, 15 mm. The greatest transvi ' ^ diameter was 13.5 cm. (The estimated normal heart weight on the basis of body length is 317 gm., plus or minus 40.22) T ^ 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 ;dpated and its columnae cameae 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 q by 6 cm. It was covered by a smooth capsule and the splenic 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 die walls of the respiratory bronchioles and the adjacent alveolar walls. Generally, these tubercles were of two types: sarcoidal and foreign body granulomas. The former predominated 'ey approximately ten to one. Tubercles of these types were intimately as sociated and, in addition, many intermediate types were presented. T he sarcoidal tubercles (Fig. 4) were free of caseation, contained no demonstrable organisms and were, for the most part, in the same stage of development; however, a minimal number presented some peripheral fibrosis and there was an occasional, coarse, collagenous ball. Generally, the tubercles were sharply demarcated, surrounded b y delicate reticulum, and did not present peripheral rims of lympho cytes. T hey consistefPof 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. T he giant cells appeared to be of two types: Langhans' cells and foreign body giant cells, with the former predominating. In many of the Langhans' cells .here were numerous 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 i in diameter (Fig. s). M ore frequently, the Langhans' cells contained uur.d, oval, or suggestively budding, intracytoplasmic bodies of Schaumann, * 25 to 50 fx. in diameter Rarely, these bodies appeared to lie outride of giant cells, and some enclosed irregular yellowish material ('Fig.->. 6 and 7). These bodies stained blue with hematoxylin and m ferrocyanide preparations were strongly positive for iron. Dr. Leroy U. Gardner,24 who also studied this case, stated that these bodies stained " red with acid fuensin of van Gieson-Weigert instead of black like elastic tissue" * Sfharimann, J. On ihr r.a.urC'. of n:rtin punki* e.;.ri.ri,-rks nD 'Cri* in . lym pb og tawik .rttosis k'nipn;:. U ia tn .J . Scandinuv... *, ; ;o .bVl y/ 'S*: :i=-?"** -v-;' -- -V C O EX ISTEN T ASBESTOSIS A N D SARCOIDOSIS 497 and that " von Kossa's calcium stain is n ega'tve." 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 K ossa's stain. An occasional giant cell contained one or more clefts suggestive oi cEolestero1 crystals. More frequently, however, doubly refractile, irregular spicules, plaques, and conchoid:;' masses were observed in giant cells. These doubly refractile 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 above the nodules ( Fig. 8). Asbestos bodies, singly or in clusiers and in mod erate numbers, were pre-ent J s o in the dense iibrotic areas <Fig. 9; and occasionally within alveoli (Fig. 10). Rare, laminated, calcified masses, enclosing apparent asbestos bodies ( Fig. 1 1) and other bodies which appeared to be of the Sc' .aumnnn variety, were present in the linear fibrotic bands. Asbestos bodies were also encountered in and about the sarcoidal tubercles and in the associated sarcoida! giant cells of both varieties, but more frequently in those of foreign body type. Tron 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 don e rv.m ix of collagen, masses of coarse elastic fibers, and fine reticulum. Tnc larger bronchi were remarkable only for sligbl chrome imla.-i- mation. T h e bronchioles and :..coiratory brouchioms. embedded in dense cemagen and surrounded by tubercles, were moderately dilated and presented conspicuous focal squamous metaplasia and moo ite chronic : ubmucosui inflammation, in the subpieuro! region, where the aslvstotic fibrosis and the grumulon...f us rerd ion nut-a in tense, he bronchiole, were irregularly diluted and lined by alien - ,` i: r -tr:| 0= tuli i iTuiVv-i v .d ,l;h 1 !' 498 SKAV1EM and KITTERHOFF many contained asbestos bodies and the associated granulomatous reaction. Within the peribronchial fibrous tissue there was a moderate amount of hemosiderin in. lirrarly disposed granules, and fine lipoid droplets. The small pulmonary arteries and arterioles presented slight intimal thickening, and those in the subpleurai one /ere surrounded by thick collars of elastic fibers. The intervening alveoli were m sderately dilated, the capillaries were 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 t leura 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 maciophages 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 bv and permeated by lymphocytes. " Asteroid bodies" and Schaumann bodies were not present in the .giant cells of these tubercles. No asbestos be lies were found. Those in the right ventricular myocardium were associated with considerable fibrosis. The results cf chemical and spectrographic analysis of lung tissue, performed under the ribecron of Dr. Leroy U. Gardner,24 are pre sented in Table I, fmu! (jiugnos,.s a w e . Alodeiate . tJctcnary usbestosis; cxleu .-as coidcs is oi pm. oo .0'/ and uoich'-h h i d bo. ;, ;- i.. d , ; marked d a o e s .:bn* ...y a n y o - a . - -W .;** - ...........- J........... -- s. v tfnn. fi*. .. . ' COEXISTEN X A5BEST0STS AND SAKCOIDQSl ? 499 arteries and arterioles in the lungs; m arked nodular obliterative pleural fibrosis; focal organising fibrinous, pleuritis; minimal sar coidosis if tfie heart, Ir-'er. spleen, and k idn eys; right ventricular cardiac dilatation and relative right ventricular hypertrophy; acute passive hyperem ia of the viscera, slight cirrhosis o f the liver; slight generalized arteriosclerosis; minimal fo cal chronic adrenalitis and nephritis; chronic posterior urethritis and interstitial prostatitis. T able 1 Chemical and Specfrographic Analysis of Ash [Dry T f sus, Approximately of Moist Tissue. Ask, 6.70% of Dry Tissue.) As oxides -`except Cl) ! As eiemeh. -- Chemical analysis Cu, Ag, Ilg] pu , b , c<n Mo J SiOi Fe,0 , AI2O3 BeO ZnO MnO CaO MgO BaO SrO TO2 V 2Os CrjOs NiO, C O N aiO UO ?2 Os a coi Total Per cent <0.15 2. 037 N o n e sound o-39 0.03 2.Q2 1,(8 N o n e found None found None found None found 0.07 <0.05 S`44 44.40 8.44 4.61 PlVSf.Ot -------------------- 88.?' .\'a : K 0: Ba Co. Al Mg P Si I'M Ma Ti Cu oSug Cr u lie P h Zri Hi Pt Cl ! Chemical saatys i- tr cent Spectrc'tfja-.-ic fibaly.*'.:; Arbitrary .caie o> v u anonnii 4 3'-'-7 Nono found None found 2 .j 0 2 0.7 &.o r.6 0.02 None found o.or None found OA 4.0 i : ' ' 3 -.G 75 Oo ;oo 75 3 s 2 3 -3 r 0 7 ~ 3 10 0 1- ....... ... __ D iscu ssio n C lin ically, in view of the significant history of exposure to asbestos, p je possibility of sarcoidosis w as never entertained. Tn rpfrorpcc!, the rapidly progressive, disabling dyspnea, unaccompanied by dences o f enlargem ent of the ligh t heart or cardiac failure, should ha v aroused suspicion that there was a -orcom ium t pulm onary lesion. \^bi`Stosis alone is nut usually accom panied ^y .such profound, rapidlv (jevi loping, respiratory embarrassment. In this avtc. however, thei VVi.: c no vollateral clinical *-, me;. -, 'v e 1 ;gi.:;.. ... ce-e- v .'7 e n e Soo *' A, ', >V,'V,^i*C' AMD' RITTERHOFF ' 'i ' .'" \ ^ strate sarcoid lesions and th e .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,18 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,22 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 25 was not usually accompanied by evidences of right ventricular failure. In view of the significant dilatation of the right side of the hS&rt 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 emphysen\a. This hypothesis, however, does not explain the severe dyspnea that is seen in occasional cases of diffuse miiiary 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 diffuse active inflammatory process throughout the lung? the Hering-Breuer reflex was exaggerated. Presumablv, there was either a tw re re 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. I t was difficult to determine how much of tire 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 Gumming0' 26 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 IJ. 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 simul taneously, but that probably the asbestosis was present to some degree before the sarcoid appeared. This opinion is based upon the occur rence of asbestos fibers and other iron-containing particles in the interior of the tubercle-like nodules and in some 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. Y et 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/7 who did not regard these inclusions as specific tor sarcoidosis. Rich,27 who was impressed by the frequency of Schaumann inclusions in sarcoidal lesions and b y their absence in unequivocal tuberculou lesions, noted that Metchnikoff reported the presence of calcified in clusions in the hyperplastic tuberculous lesions of experimentally in fected Algerian rat1-. Kraus s!> stated that the presence of calcified inclusion.- v,a- \ ''.''' ore not found in any krown pr:' "thlr-v -xcor r .w*5 s/- . ,? ,v^aag B ! ^ '. v > -.. ' sarcoidosis. Gardityar..?*pointed oat that, in his sarcoid material, bodies, regarded 1^ many to consist of calcium or .alcified remna of elastica, do not, by the von Eossa method, contain calcium, but^p? 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 refractile, nonlipoid sufc-^'f stance in giant cells and frequently in dose relation to Schaumanh bodies has not been emphasized in the literature On sarcoidosis. It | has been noted, however, that colorless and yellowish tinged refractile - material is often endosed by the Schaumann body. The fact these masses are frequently doubly refractile has not been stressed.}. It has been suggested that these endosed masses represent disintegrat- ' mg elastica; however, van Gieson-Weigert stains do not confirm this ,v suggestion. The origin of this refractile and doubly refractile material is not known. Being in and about many of the small, partially calcified ,- bodies, this doubly refractile material appears to be associated with n. the development of the Schaumann body. The larger and more densely ^ | L stained bodies*were not as frequently associated with visible douMrV ^ r:'' 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, w h i c h - blue with hematoxylin and red with acid fuchsin, is formed in responser a f to doubly refractile, nonlipoid substance and initially is impregnated vL,t by iroq and later, in amounts demonstrable by von Kossa's stain, by, calcium. - ` Wolbach,21 in 1911, Jadassohn, in 19x9,28 and Friedman,18 in 1944, have described a peculiar intracellular body in cases of sarcoidosis. * r This body, stellate in shape, varies in size up to 25 i, generally lies 4&1. in an intracytoplasmic 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 cyfonlasm. He w''S r.cv^r able V- ..lemon f .v teik'.-e in other - ... , f '' .*' i,t V|i" ' *' , ' '"' *'" y,) * COEXISTENT ASBESTOSIS AND SARCOIDOSIS 503 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 1 per cent of the giant ceils in the lungs and tracheobronchial lyinph nodes Definite transition stages of asteroid formation were suggest! by the presence of spicules on the pink, coccoid, intravacuolar, mtracytoplasmic bodies, particularly' jn 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, nonspecific biochemical cytopiasmic altentfitms In addition, such an asteroid is depicted in the giant cells of leprous lesions by Mallory28who called them "spiculated" bodies. No transition stage! between Wolbach's asteroids and Schaumann's inclusions were even remotely suggested. The pathogenetic relationships of asbestosis and sarcoidosis are dependent upon the chronologic development of die lesions and the nature of the causative agents. Historically and histologically, in this case, it is most likely that asbestosis preceded the development of sar coidosis. The predominant localization of the sarcoida! tubercles with in asbestotic zones of fibrosis with attendant morphologic modification of both lesions, as evidenced by asbestos bodies within sarcoidal 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 non caseating tuberculosis. `,r- '"'"':''m '`'.fip",' 1 ' ' M ^ S K A V L E M ''A N D R IT T E R H O F F REFERENCES 1. Gloyne, S. R., and Merewether, E. R. A. Asbestos. Occupation and Health Supplement International Labour Office, Geneva, 1938. (Cited by Sayers, R. R., and Dreessen, W. C. Asbestosis. Am. J. Pub. Health, 1939, 39, 205-214.) 2. Murray, M. Cited by Egbert.5 (Charing Cross Hosp. Gaz., 1900. Also: Departmental Committee on Compensation for Industrial Diseases. Minutes of Evidence, Appendices and Index, 1907. Cd. 3496, p. 127; Report,. 1907. Cd. 3495, p. 14.) 3. Fahr, T., and Feigel. Kristallbildung in der Lunge. Deutsche med. Wchnsckr., ,, 1914, 40, 1548-1549. (Cited by Egbert.5) 4. Cooke, W. E. Pulmonary asbestosis. Brit. M. J., 1927, 2, 1024-1025. Mc Donald,1S;.: Histology of pulmonary asbestosis. Ibid., 192;, 2, 1025-1026. (Cited by Egbert.5) m 5. Egbert, D: S. Pulmonary asbestosis. Report of a case with necropsy findings. Am. Rev. Tuberc., 1935, 31, 25-34. 6. Shull, J. R. Asbestosis. A roentgenological review of 71 cases. Radiology, 1936, 27, 279-292. 7. Lanza, A. J. Asbestosis. J. A. M. A., 1936, 106, 56S-369. 8. Lynch, K. M. Pulmonary asbestosis. IV. The asbestosis body and similar objects in the lung. J. A. M. A., 1937, 109, 1974-1978. 9. Williams, E. The presence of " curious bodies" in the lungs of South African goldminers. /. Path. & Bact., 1939, 48, 475-477. 10. Sutherland, C. L. Tuberculosis in the silica-risk industries. Lancet, 1940, 1, 8^-896. 11. Hannesson, H. A case of pulmonary asbestosis accompanied by pulmonary tuberculosis. Tubercle, 1941, 22, 40-44. 12. Hornburger, F. The co-incidence of primary carcinoma of the lungs and pulmonary asbestosis. Analysis of literature and report of three cases. Am. J. Path., 1943, 19, 797-807. 13. Auerbach, O. The pathology of the pneumoconiosis. Quart. Bull., Sea View Hosp., 1936-37 2, 3-27- 14. Monthly Labor Review, U.S. Department of Labor, Bureau of Labor Statistics, 1946, 62, p. 153, table 2. 15. Pinner, M. Noncaseating tuberculosis. An analysis of the literature. Am. Rev. Tuberc., 1938, 37, 690-728. 16. Horton, R., Lincoln, N. S., and Pinner, M. Noncaseating tuberculosis. Am. Rev. Tuberc., 1939, 39, 186-203. 17. Rubin, E. H., and Pinner, M. Sarcoidosis. One case report and literature review of autopsied cases. Am. Rev. Tuberc., 1944, 49, 147 -169. 18. Reisner, D. Boeck's sarcoid and systemic sarcoidosis (Bcsnier-Boeck-Scnau- mann disease): study of 35 cases. Am. Rev. Tuberc... 1944, 49, 289-307: 437-462. 19. Friedman, M. Sarcoidosis of the spleen. Report of a case with autopsy and a study of intracellular " asteroid bodies." Am. J. Path., 19+4, 20, 621-635. 20. Kraus, E. J. Sarcoidosis (Boeck-Besnier-Schaumann disease) as the cause of a pituitary syndrome. J. Lab. & Clin. Med., 194?, 28, 140-146. 21. Wolbach, S. B. A new type of cell inclusion, not parasitic, associated with disseminated granulomatous ' sions. /. 3/. Rcseardt, 1911, 24, 243-257. 22. Zeek, P. M. Heart weight. I. The weight of the normal human heart. Arch Path., T942, 34, 820-S32. 2'',. M.-Mnrv. F. II. iVhoIoLr:c;.! T. ; r.^ W v ' c1 ' 24. 25. 26. 27. 28. 29. Gardner, L. U. Persona] communication. Higgins, G. K. The effect of pulmonary tuberculosis upon the weight of the heart. Am. Rev. Tuherc., 1944, 49, 255-275. Gardner, L. U., and Cummings, D. E. Studies on experimental pneumono- koniosis. VI. Inhalation of asbestos dust: its effect upon primary tuberculous infection. J. Indust. Hyg. & Toxicol., 1951, 13, 65-81. Rich, A. R. The Pathogenesis of Tuberculosis. C. C. Thomas, Springfield & Baltimore, 1944, p. 722. Jadassohn. Zur Frage der "Sarcoide," des Lupus pernio und des Lupus miliaris in Kombination mit "Acnitis." Cor.-Bi. /. Schweiz. Aerzte, 1019, 49, 455- 4S8. Mallory, F. B. The Principles of Pathologie Histology. W. B. Saunders Co., Philadelphia & London, 1918, p. 207. [ Illustrations follow ] DESCRIPTION OF PLATES Plate 103 Fig. 1. Initial roentgenogram of the chest. Fig. 2. Photomicrograph of lung and adherent pleura showing subpleural, septal, peribronchiolar, and marked and focally nodular pleural fibrosis. X 4. %> P l \te 104 Fig. 3. Frontal section o left lun:. m um m m P late 105 t i c . 4. Lung, showing a du ster of sarcoidal tubercles, x 6c. Fl& a5n' iXntfXacytoTphlfasgmi3icntvaCceUuoXl'e'h. kXh n1c0a9r0!>.' fi!`s the fold contains an "asteroid" in Flate 106 Fig. 6. Lung. An inclusion of Schaumann encloses an oval yellow body. With polarized light, doubly retractile material surrounds this calcified mass. X 725. Fig. 7. A gilmt cell from the lung with inclusions of Schaumann. X 725. Mi m P late 107 Fig. 8. Lung with tubercles of foreign body type. The central tubercle has an asbestos body at its periphery. X 160. Fig. 9. Lung shovgiig asbestos bodies and dusters of hemosiderin-laden macro phages within an area of fibrosis. X 725.