SARCOIDOSIS OF THE SPLEEN

REPORT OF A CASE WrIH AuTOPSY AN1D A STUDY OF INTRACELLULAR"ASTROID BODIES" *

MELVIN FRIFDMAN, M.D.(From the Hospitl of the University of Pexsylvai, P , Pa.)

Although Boeck's sarcoid of the spleen, as a more or less llizedform of the disease, is described under that title in no previously pub-lished autopsy report, it undoubtedly is of occasional occurrence andshould be induded in the differential diagnosis of splenomegalies ofobscure origin. In the literature there are several dinical case reportsof splenoinegaly caused by sarcoidosis, often unsuspected until dis-covered histologically, and it is probable that some autopsy reports ofthis disease have been published under another diagnosis, as I sindicate later.

T1IE SPLEN IN GENERAL SARCOIDOTIS

Involvement of the spleen in the course of generalized sarcoidosis isa fairly regular occurrence, as proved by both clinical and post-mortemdata. Thus, Palmer' stated in his review, "of the abdominal signs,splenomegaly is the most prominent," and he added that slight splenicinvolvement is quite common and that occasionally the enlargementmay be very great. Another example of this statement is found in therecent report of dinical data on five cases of Boeck's sarcoid, byBernstein and Oppenheimer.2 One spleen extended four fingersbreadthbelow the costal margin and had a palpable notch, a second spleenextended 2 cm. below the costal mar, a third extended I cm- belowthe costal margin, a fourth just reached the costal margn, and thefifth was not palpable. Of Nickerson's3 siX patients, four had spleno-megaly, with spleens weighing 200, 230, 640 and 89o gmi- respectively.He stated that splenomegly, with or without lymphadenopathy, wasthe most constant feature of his six cases.

Histologically, the spleen is the second most common site of involve-ment in generalized sarcoidosis, as shown in Table I. (The data havebeen collected from Pinner's4 review of all autopsied cases up to 1938and from twelve subsequent case reports,;I- induding my own. It isincomplete since in a few cases only partial autopsies were performed,while in others many tissues were not emined histologically. How-ever, it provides a fairly correct picture of the relative incidence in thevarious tissues. The case of Ronchese ' and the sixth case of Bern-

* Received for publication, July 6, I943.

621

FRn N

adOppenheimer 2ar tstein and are not included m this anatomical summarybecause they show too much evidence of ordinary tuberculosis.) Inview of the affinity of sarcoidosis for the reticulo-endothell system, itis not at all suprising to find-this high ience in the spleen; nor is itsurprising to observe that nearly all of the cases mined at autopsyshow a wi r ather th a loaiz distribution of the disease,even though most of the paiets had died of causes other than sar-coidosis itself.

Tmz Iladdenca of Tism exd Orgax InvoieiX 9wCam of Sroidos

Rz~ed ~by AstopsNumber of times

Thme at organ d

Lung 24Spl 21Lymph noces 21Liver 17Bone marrow 14Skin 12

7Gastroitestinaltract.Trachea and bronchi sTonsil 3

O tie repored to be ived x to 6 es are: heart, pituitary body, bri,cmd, prostate, tes thyroid, paceas, skeletal m=ore and nasl mc.

OCCURENCE oF LocA Iz= SARCcoIWSI OFo H SPLEENIn spite of this high incidence of spleniivolvement in the gen-

eralized form, sarcoidosis of the spleen as a disease in its ow right,with only in t or absent sarcoid lesions elsewhere, is but littleknown and therefore is usually unrecognized even when it does occur.The "pure" form, with no lesions outside of the spleen, is probablynonexistent, and the other cases with splenomegaly and vague symp-toms predominant in the dinical picture have usually been mis-diag-nosed. Thus, Palmer" referred to enlarged s s which were remoedfor "Banti's disease" and then found histdogically to show sarcoidosisinstead, and he therefore urged consideration of sarcoidosis in everycase of chronic sple ly. In Jadassohn's 4 third case, for example,the t prnted typical sarcoid lesions in skin and bones, re-sponded negatively to the Pirquet and Mantoux ( wxooo) tests fortuberculosis, and hid had spenetomy for Banti's disease 3 yearspreviously; the spleen showed sarcoidosis. In one of Longcope's9 casesof sarcoidosis, splenectomy was done for supposed Banti's disease andthe diagnosis of sarcoid made after histological examination of thespleen. In Engelbreth-Holm's I second case, in which splenectomy forsupposed Banti's disease was performed, the patient responded nega-

622

SARCODOSIS OF TE1 SPLEEN 623

tively to the Mantoux skin test for tuberculosis, showed no acid-fastbacilli in the spleen, and showed multiple, tiny, noncaseating tuberciesin the spleen. Although the case is reported as tuberculosis of the-spleen, this evidence is against tuberculosis and very strongly in favorof sarcoidosis, as will be discussed later.

Dressler's1 case of unepained splenomegaly was diagnosed assarcoidosis of the spleen on the basis of sarcoid lesions having beenfound in a sternal puncture, on roentgenological findings suggestive ofhila saroidosis, and on negative response to the Pirquet test and onlyweakly positive response to the Matoux test (usig I mg. of tuber-culin). Dressler conduded that many cases diagnosed as Banti's dis-ease or as tuberculous splenomegaly are actually sarcoidosis. That thepossibflity that sarcoidosis is a cause of splenomegaly of "obscureorign" is seeping into current dinical thought, is demonstrated by arecent dinicopathological discussion,17 involving a patient whose spleenreached nearly to his left iliac crest. His negative response to theMantoux test for tuberculosis, the elevation of total serum protein,and the hyperglobulinemia were the only signs of sarcoidosis. Thisdiagnoss was offered clinically, however, even before the pathologist'spresentation, to the group, of sarcoid lesions in specimens of liver andeyelid removed for biopsy. (The spleen was not removed and thepatient was living at the time of publication of that paper.)

TuBEicuLous SPLFNoMEGALY

"Primary" tuberculosis of the spleen, as opposed to the spleniclesions accompanymg active tuberculosis elsewhere in the body, is ac-companied by only minor tuberculous lesions elsewhere, usually in theabdominal lymph nodes, the liver and the lungs. As described byWimternitz,18 this is usually a severe and often fatal disease, and there-fore I believe that patients with mild symptoms or with no symptomsat all should be regarded with suspicion until the diagnosis definitelyhas been proved. Many of the more recently reported cases have hadsuch '"peuliarities" as negative skin tests for tuberculosis, absence oftubercle baclli in staied sections and even in inoculated guimea-pigs,absence of definite fever or of any severe symptoms, presence of onlynoncaseating tuberdes, and evidence of active or healed "miliarytuberculosis" of the spleen with only mild symptoms and with recovery.It hardly need be stated that each of these items is a point in favor ofsarcoidosis and against ordinary tuberculosis. In fact, a truly negativetuberculin skin test reaction in a patient with mild symptoms and non-caseating tubercles makes the diagnosis of sarcoidosis almost mandaltory; and such occurrences as "healed miliary tuberculosis," or the

FRIEEDAN

failure of tissue with active lesions to infect a guinea-pig, speak verystrogly against tuberculosis but are the customary findings m sar-coidosis. Let us now emie some individual cases.The earlier review by Winteritzl8 contributes thing definite to

our search for cases of sarcoidosis. T"ne majonty of his patienLtsdied as a direct result of splenc tusberculois or its generalized dis-semination, they had caion in the spl lons, and undoubtedlywere stright-forward cases of tuberculosis. Only a small number ofhis cases had mliary, noncaseous t ; a tubercun test wasreported in only one case (positive); and is t data are givento label any individual case even as '"posible" sarcoidosis. Most ofthe cases mentioned by Lubarsch" either had caseous tuberdes or hadinsifficient data, but one of his cases is very suggestive of sarcoidosis.This patient had a chronic course with splenomegaly and lymphadenop-athy, and the spleen was removed surgically and found to have small,miliary, pinhead-sized, noncaseating tuberdes with a definite reticulumframework in each one. (This reticulum framework differentiates sar-coidosis from tuberculosis, according to Nickerson,3 and others.) Aguinea-pig injected with spec tissue from this patient was alive 2 2months later. To exain this apparently beni miliary tuberculosis,Lubarsch postulated a very low virulence for the tubercle bacilli inthis case, which is one of the theories that have been offered for theexplanation of sarcoidosis itself. (This patient is stated to have diedof pulmonary tuberculosis some years later, after a healthy, asympto-matic interim; and although we might be tempted to consider thetuberculosis a separate disease in this case, perhaps even acquiredduring possible sanatorum treatment for his "tuberculous spleno-megaly," nevertheless the mode of death forces us to doubt the dassi-fication of this case as Boeck's sarcoid.)The report by Engelbreth-Holm"5 of 28 cases of tuberculous spleno-

megaly subSequent to Winternitz's18 review presents rather hopefulmaterial. His own second case (previously mentioned), with a negativeresponse to the Mantoux test, was diagnosed dinically as Banti'sdisease and showed noncaseating tuberdes and absence of tuberdebacilli in the surgically removed spleen; the potint was sti living andwell at the time of the report. His third case responded negatively tothe Pirquet test for tuberculosis, had miliary noncaseating tuberdes inthe spleen, and showed a connective tissue framework in the tuberdes.In his fourth case the spleen contained noncaseatig tbercles and noacid-fast bachilli. Of the 28 cases he reviewed (induding his own 4cases), 3 had Pirquet tests done, and all three were negative. (All

624

SARCOIDOSIS OF THE SPLEEN

were in cases with noncaseous tubercies.) Of the 9 cases reported asshowing add-fast bacilli in the tissue, 4 had miliary tuberdes and 5had larger caseous ones.

Since it would be unfair and inaccurate to use published statementsand photographs to re-diagnose cases of other writers, I can offer noconcise list of cases reported is tuberaclous splenomegaly which shouldbe labeled sarcoidosis; but I feel certain, for reasons already enum-erated, that many such cases exist. The case presented herein is be-lieved to be the first case of splenic sarcoidosis, with autopsy, to bereported under that diagnosis. The disease was asymptomatic, wasaccompanied by mild splenomegaly and with only a few, smal, scat-tered, sarcoid lesions in other tissues, and was a purely incidentalfinding in a woman who had died of min coccal meningitis. Thiscase has also provided an unusual opportunity to study certain ratherrare indusion bodies which have been previously described in cases ofsarcoidosis.

REPORT OF CASEM. E. S. was a white woman, 63 years old, who had visited the medical out-

patient department for sundry c aits duing the past 5 years.Past History. About 4 years previously her systolic blood pressure was reported

to be 270 m-. of Hg by her family physican. A fairly complete study in the clnic2 yes previously had revealed complete heart block with a very slow pulse rate,evidence of aortic stenosis and very sight cardiac enlargement. At that time therewas no enlar ent of her lymph nodes. The total serum protein level was 6.7 gm.per ioo cc., and other chemical studies, blood counts, urinalyses, and the spinalfluid colloidal gold curve revealed nothing abnormal. Wassermann tests on bloodand spinal fluid were negative. She had had weakness in the 6 months precedingher final entry, and had lost io pounds in weight in the past 2 months. Dyspneahad been gadully increasing during the past 2 years.

Present Iness. The patient was brought to the hospital in a semicomatose con-dition on January 4, I943, and the history was obtained from her brother. Shewas said to have developed malaise and epigastric pain and to have vomited black.material 2 days before entry. She improved on the following day, then suddenlybecame very ill, begn to "scream with pain," became confused and glassy-eyed,and showed "red marks" on her chest.

Pkysic i . The patient was completely confused, showed rigdity ofthe neck and positive Kenig and Brudzinsi signs, and had a macular petechialskin rash. Her -eyes were fixed in a glassy stare. The blood pressure was I5osystolic and 8o diastolic, the pulse rate was 6o per minute, and there were systolicmu rs at the mitral 'and aortic valve areas.

Laboratory Findigs. The white blood cell coumt was 24,000 per cmm. (aboutgo per cent polymorphonudear leukocytes), and the spinal fluid contained 2ooopolymorphonuclear leukocytes per amm., with intraceRlular and extraceUlular gram-negtive diplococai

Course. T'ne patient rapidly became stuporous and died within 5 hours of entry.Cinical Diagnoses. Meingococcal mingitis; chronic H aic endocarditis

with aortic stenosis.

625

626EDLAN

REPORT OF AUTOPSY

The autopsy was performed 14 hours after death.

Gross FindingsSkin. There were numerous ml petechiae on the skin of the ab-

domen, the thorax and most of the flexor surfaces.Heart. The heart weighed 500 gm. and showed thickened, fibrotic,

pally calcified aortic valve cusps, which were partially fused andhad caused marked stenosis of the valve. The mitral valve had thick-ened, fibrous, partly calcified leaflets and was slightly stenosed; thechordae tendinae were short and thick. The left ventricle was hyper-troph and masured I. cm in thicknes.

Lungs. The lungs were congested and mildly edematous.Spleen. The spleen weied 300 gm-, had a smooth red capsule, was

slightly softened and showed on its cut surface a myriad of tiny whitenodules 0.3 to I.o mm- in size, which were embedded in a soft red pulp.They could not always be distinguished grossly from malpighiancorpuscles, although they were thought to be a trifle smaler and werediscrete and ciumscribed. No aseation nor large nodules were seen.Lympk Nodes. No enlargement nor gross abnormality.Liver. The liver was moderately congested. The gaUblader ha a

thin, tough, white, fibrosed wall and was completely filled by a large,rough, brown calculus.

Brain. The brain weighed 1360 gm. and had a moderately thick,diffuse, subarachnoid purulent exudate which was most abundant onthe surface of the cerebral hemispheres.

Histological Findings

Spleen. The spleen was studded with discete, irc , tuber-cle-like lesions which were all of fairly uniform size (slightl llerthan a malpighian corpusle) and located iniimiely in thelymphoid tissue and siusoidal areas. Although they sometimes over-laped, the lesions tended to retain their individuality rather than tobecome confluent. The individual lesion was elliptical or spherical,and had a smooth and sharply outlined border and a reticulum andcollagenous connective tissue framework in which the fibers tended toradiate from center to periphery. There was a narrow zone of con-centrically arranged reticulum fibers at the edge of each sarcoidallesion. Endothelioid cells and multinucleated giant cells of varioussizes were embedded in the pale-staining colagenous connective tissue,and these were someimes oriented toward the center of the nodule.

626

SARCOIDOSIS OF THE SPLEEN

In the larger gnt cells there was a tendency for the nudei tobecome bunched together at one end, while the cytoplasm forming thebulk of the cell became the site of certain stiking processes. In mostgiant cels the ctoplasm showed a few or many punched-out dearareas, often with a tiny, pink-staining sphere or coccoid body in thecenter of each such vacuole. IThe larger vacuoles contained largerspberes, some of which had short, sharp pseudopodia or rays protrudingfrom their surfaces. In other cells these rays had become much longer,additional rays appeared, and the structure increased in size until itreached the maximum size observed (about 25 IL). At this stage therewas rarely more than one such structure in any single cell, althoughmany other "embryonic" vacuoles might be present, and the largeparent vacuole had become very irregular in order to adapt itself tothe shape of the full-sized body with its long rays. This fully devel-oped star-shaped body, to which I sa refer as an asteroid, wassomewhat more acidophilic and less granular than the cytoplasm of thegiant cell and often had a smal, bluish-pink-staining sphere exactly inits center. (The chemical properties are discussed later.) The asteroidswere found nowhere except within the cytoplasm of multinuleatedgiant cells. Only about 6 or 8 per cent of giant cells had fully devel-oped asteroids, although the majority of cells had sa vacuoles. Theaccompanying high-power photomicrographs of various giant cells havebeen arranged in order of development to ilustrate the hypothesis ofgrowth just descrbed.No acid-fast bacili were found in sections of spleen stained by the

Ziehl-Neelsen technic.Lymph Node. Sectioh of a sa abdominal lymph node near the

gallbladder showed numerous, sa, discrete collections of endothelioidand giant cells, with very little connective tissue and with no aseationin these lesions. These nodules were smaller and more youthful inappearance than those in the spleen, and their giant cells containedvacuoles and a few asteroids like those previously described.

Lungs. In several sections of lung tissue there was found an occa-sional, very tiny collection of endothelioid cells and perhaps a giantcell or two with an asteroid. There was some congestion.

Liver. In two large sections of liver there was found a tiny collectionof cells similar to those in the lung. There was moderate passive con-gestion.

Brain. There was some edema of the molecular layer of the cerebralcortex, adjacent to the thick layer of subarachnoid polymorphonudearexudate.

Other Tissues. Sections of myocardium, pancreas, gallbladder,

627

68FEDMAN

adrenal, kidney, ovary, pituitary gland, and abdominal skin showed noevidence of sarcoidosis, nor of any other lesion except chronic chole-cystitis. Other tissues were not sectioned.

Unfortunately all of the tissues were placed i iately in fixativeand nothing was available for culture or animal inoculation, as thepresence of sarcoidosis was not suspected until the slides were seen.

Anatomical Diagnoses

Meningococcal meningitis; rheumatic endocarditis, mitral and aortic,with aortic stenosis and left ventricular hypertrophy and with passivecongestion of lungs and liver; chronic cholelithiasis and cholecystitis;sarcoidosis of the spleen and lymph node, with isolated tiny sarcoidallesions in the lungs and liver.

STAINING AND C1MICAL REACTIONS OF ASTEROIDS

Since the asteroids were found only within giant cells of the specificlesions in spleen, lymph node and lung; since I have not seen them intuberculous or other material treated with the same formaldehydefixative; since they are present in frozen sections as well as in paraffinsections; and since they are seen with all stains and even in unstainedsections, they are presumed not to be artifacts and to be definitely partof the sarcoidal lesion. A resume of their properties, as thus far de-termined, is as follows:

I. Solubility. Asteroids fail to dissolve in water, alcohol, or xylol.2. Hydrogen ion concentration. The asteroids neither dissolve nor

show any morphological alteration when sections of spleen 5 u in thick-ness are immersed in either I per cent sodium hydroxide or IO per centformic acid for 15 minutes.

3. Fat stains. With scarlet red or Sudan III the asteroids remainunstained; some macrophages and a few giant cells contain smallglobules of neutral fat, but no fat is found in the specific vacuoles ofthe giant cells. With Nile blue sulfate asteroids are dark blue. WithFischler's fatty acid stain asteroids are very faintly salmon colored(negative).

4. Hematoxylin and eosin. Asteroids are pink.5. Phosphotungstic acid hematoxylin. Asteroids are vaguely bluish

or sometimes pale orange.6. Mllory's connective tissue stain. Asteroids are reddish violet

(about the same as cytoplasm of cells), negative for collagen.7. Masson's trichrome stain. Asteroids are gray (negative for col-

lagen).

628

SARCOIDOSIS OF THE SPLEEN

8. Hematoxylin and van Gieson's stain. Asteroids are yellow (nega-tive for collagen).

9. Wilder's reticulum and van Gieson's stains. Asteroids are palepinkish yelow (negative for reticulum).

Io. Weigert's elastic ssue stain. Asteroids contain no elastic tissue(nor does the rest of the sarcoidal lesion).

Conclusion. The asteroids are relatively stable chemically; theyresn neively to the more con stains for specific substances,and they bt lxmatey the sam staining reactions as thecL1NAs Of ; d or giant ce1Rs

DISCUJSSION

Such asteroids have been known for some time in connection withsarcoidosis, and Jadassohn,14 in I9I9, referred to "asteroid bodies" ofunkown microchemical identity in his first case. They are rarelymentioned in the more recent literature on sarcoidosis, however, prob-ably because they occur infrequently (judging by the other sarcoidmaterial in this laboratory).A type of indusion body which was not found in this case but which

is commonly described in sarcoidosis and which has been exhaustivelystudied by Schaumann is roughly spherical or oval-shaped, often hasconcentric laminations, may show yeast-like budding, is nearly alwayscalcified, and is usually large and often much larger than its parentgiant cell. Some of these bodies show rays or fascides, suggesting thatthey may be an older, more chronic, calcifying stage of the asteroid.Schaumann contended that these calcifying bodies may represent tissuereaction around nonbadllary, fungoid or mycotic forms of the tuberclebacillus, and that this nonbacillary form of the organism may be theetiological agent of sarcoidosis. Although the asteroid may possi'blybe a less mature form of the calcifying inclusion body, I can offer noevidence from this case to prove any relation between the asteroid andthe tubercle bacillus (nor any evidence against such relationship).

Wolbach,2" in I9II, described intracelular bodies exactly similar inmorphology and most staining reactions to these asteroids. These werefound in 5 cases in a series of900 autopsies. The patients had died ofsuch diverse diseases as malignant neoplasms and pernicious anemia,and following thyroidectomy. He therefore concluded that these bodieswere nonspecific. This study was completed before the general recopi-tion of Boeck's sarcoid as a disease entity, and Wolbach's descriptionof these bodies in noncaseating "tubercles" which tended to undergofibrosis is very strongly suggestive of sarcoidal lesions; his painstaking

629

630 N

care to rule out tuberculosis as the ase of the tubercles is furtherevidence of this point. The diversity of the as in theS patients detracts thing from the possibility of their having sar-coidosis, as most of the published auty reports of cases of sarcoi-dosis state that some other disease was the cause of death. An inter-eting point is the combined distribution of lesions in Wolbach's 5 cases(hmg, lymph nodes, liver, spleen), which is precsely the distributionin my single case.

Wolbach's 21 conclusions that the asteroid body is nonspecific, is nota parasiti organism and is a biochemical alterati of cytoplasm mightbe modified in the light of present knowledge to the following:

I. The asteroid may be nonspecific but ischarly found insarcoid lesions.

2. ThIe possi'bility of its being an extraneous organism cannot beexcluded, although it is doubtful.

3. Its causation and its ch ical or histological identity are stilunknown, specific tissue stains give negative results and it does notexhibit the features of a crystalline body.

SUMMARYI. Sarcoidosis of the spleen is an occasional cinica condition which

should be considerd in cases of obscure spl aly. In the past ithas been misd most often as Banti's disease or as tuberculous

2. In the case presented, sarcoidosis was found at autopsy to beprimarily splenic. In this instance sarcoidosis wasat andwas an i tal finding m a p nt who died of m ingococ

3. Itacellular asteroid bodies were present in the sarcoidal lesions.Investigation by histo mcal m s failed to give definite informa-tion as to their causation or histological identity.

REFERENCESI. Palmr, J. H. Boeck's diseas (sarcoid); its dinical groups and di

Cavad. M. A. J., I94o, 43, I-I8.2. Bernstein, S. S, and mer, B. S. Boeck's sarcoid; report of six cases

with omne crp y. J. Mt. S Hosp., 1942, 9, 329-343.3. N-ickrc, D. A. Boeck's sarid Report of six cases in which aotsiesWe

made. Arch. Path., I937, 24, 19-29.4. Pinner, M Nocaseating tuberculosis. An anlysis of the lit Am.

Rev. Txberc., 1938, 37, 690-728.S. Cotter, E. F. Boeck's sa Autosy in a case with viceral lesions. Arch.

Ixt. Mcd., 1939, 64, 286-295.

SARCOIDOSIS OF THE SPLE 631

6. Eric T. C., Odoin, G., and Stern, L Boeckes disa (sarcoid) of thecentral nrvom system; report of a case, with cmpete ciical and path-ologi study. Arch. Newol. & Psychit., 1942, 48, 6I3-621.

7. ofister, W. F., and Elrrei, G. T. G alized sarcoadosis of Boeck accom-pmnied with ftub ulosis and strlpococca bactermia. Arc. Path., 1941,31, 178-188.

8. Kraus, E. J. SarCods (Boek-Besnier-Shamann diseas) as the ause of apituitary syd e. J. Lab. & Cix. Med., 1942, A8, I40-46.

9. ogpe, W. T. Sacidosis, or Besier-Boe ann diseae. MA1941, 117, 1321-1327.

Io. Posner, L Sarc-dosRss J. Pediat., 1942, 20, 486-495.II. Spec, J-, and Waren, S. Boecs sarci Report of a case, with dinial

diagos cfied at autopsy. Arch. Ilt. Med., 1938, 62, 285-296.12. lice, F., and Sweaney, EL C. A fatal case of Bee-Be chau s

with autopsy findings. Ann. Jxt. Med., 1941, 15, 597-6o9.13. RoDchese, F. Sarcoid and tub sis; report of case with autopsy. Arch.

Dermat. & Syp., 1942,46, 860-871.14. J Zur Frage der "Sar e, des Lupus penio und des Lupus milia

Km mit "Acnitis." Cor.-Bi. f. schweis. Alet, 1919, 49, 455-458.IS. Hoi, J. A study of b o nomely and iccon-

of the cel emission from the bone manrow. Am. J. M. Sc., 1938,'95, 32-47-

x6. Dresske, M. Vber einen Fall von lie, durch ea ktio alsC Fcksch K-ankheit Verufizert. Kki. WchSckr., 1938, I7, 1467-1471.

17. Cabot case 28161. New E J. Med., 1942, 226, 657-659.i8. Winternitz, IC C. Tuberculosis of the sple Arch. iJt. Med.,. I92, 9,

680697.19 Lbs , 0. Pathologisce Anatomie der 1M,, In: Henk, F., and bsch,

0. Ha der p n tamnie ud Histo J.Sprn , Berin, 1927, I, Pt 2, 373-774.

2o. Sdc a, J. On the nature of certain lar c es present i tissueof y nulmatosis benigna. Acta sed. SCdiv., 194I, Io6, 239-253.

21. Wodbc, S. B. A new type of cell on, ted withdisseminaed los lesions J. M. Reseach, 1911, 24, 243-257.

[Iiusfion f oa]

DESCRIPTION OF PLATES

PIATE 125

FlcG I. Sarcoid nodules in spln, showing sooth, sharp bor Hematyn andeosin stain. X 30.

FIG. 2. Single nodule n splen, sowing oe giant cell and much fibrosis. Hema-toxyin and eosin stain. X go.

Fm- 3. Typical, but eatively in ificant, clection of a few gant and e elioidcei mn hlng. H a n and eon stain. X go.

FI. 4. Reticulum fram of sarcoid nodules in splee Wilders' retculumstain.X 9o.

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AiEuticA JouiiAL oY PATHOLOGY. VOL. XX

Friedman Sarcoidosis of the Spieen

633

PLATE 125

PLATE 1 26

(AU figures are from the spleen)Fic, 5. Giant cl with early vacuole formation. Hematoxylin and eosin stain.

X 795.

FIGs. 6 and 7. Several coccoid bodies have tiny irregular spicules. Hematoxylinand eosin stain. X 795.

FIGs. 8, 9 and Io. Asteroids of intermediate size; numerous coccoid bodies are pres-ent in small vacuoles in Figure io. Hematoxylin and eosin stain. X 795.

FIGS. II, I 2 and 13. "FUly developed" asteroid bodies in giant cells. Hematoxylinand eosm stain. X 795.

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