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Titre his teon concideratle noeresis and destruction of hepatie parenchyua,
lerving many ecllepred, enoty areas dsvold of livcr celle; these areas now consist
of condensed reticulum, newly formesd ductules, inflamaatory eclle, dilated caplle
l-ries and oven fresh hemorrhage.
The degres of neerosia veries from pleco to place,
rusviting in an irresilar nodularity of surviving peronchyra.
Epectal steins
fn2icate that the tanis which lie betean the irrogular nedules of parenct:ma consist
of condensad roticulua rather than tree collacen, sugpecting the appearance of
fostncorstic collapse which his not yet gore on to postneerotic scurring. The
surviving lobules are Glerupted and the liver cords broken up, HEsny liver cells
cr@ binuclcated or nultinuclested, There are mny inflermatory cells in the portal
crease Host of these are monomiclesr cclls ani cosincphilis levkocytes, although
esta nettrorphilie levrccytses cre also rresent. Svdl mmtcrs of the ssne inflamsatory
cells sre precent in the Icbules, There nre rany sm.ll intrecanaliculer bile
pluzs in the liver lobules, and larser bile ylucs in tho bile cucts of the portal
tractea,
This reflects tersinal hemtic failice,
A onsll amount of henosiderin
is econ in Kupffer celle, pirenchyxal colls and in rierophages within portel
twacte; this is probubly derived from the blood transfusions the patient received,
The yellow stellate crystals rcattercd throuch the ceetions may be hemteidin,
and probably sre artefectual,
On histolocic crowds alone, I veuld strongly suspect that this is a ese
of viral hepatitis with marked neerosts end collanca of tiscue. Vhen I bring
together the cliniesl end pithologic data, I conclude thit this case alnaxt
ecrtainly is eno of fatal horolosous cerun heptitis. The onsct of jJatmdice about
60 cive after the firet of a scriss of transfuniens ctroncly sugzests honolocous
serun hemtitie, and the lew weight of the liver (GO ec.) and ite gross and
rierezcopie appcarance indicate a necrotizing inflammatory hepatitis, such as
viral hepatitis, The patient survived thresa rnonths efter the onset of the liver
Giscaso. ‘ris is not at all unveval in viral hepatitis. Moreover, when paticnts
ath viral hepititis die 3 months after the oncet of the disease, the gross
ava nistolosle appesrance of the liver is idontical with that of the present cast.
I belicve it is hich wilikely that the hopatic lesion could heve teen caused
-*
D
Int of f.
t4
by ireadintiea alone or thit irrcdiatioa wss the rajor factor in the hopatie lesion.
% ciould tle noted that there are meny inflescutory calls in the liver, - as many
ag ara tevilly found in the averaze case of fatal viral hepatitis, Also note thet
seca
calls conslet of mononuclear cells as roll es eosinophilic and neutrophille
eviocytes.
I interpret this to reantthat the reticuleendothelial system vas in
pood condition to reesond by producing adeguate number of cells, which
-dea up in the liver. If the hepatic lecion vere ceused by irradiation alent,
“on that count of drvadistion that would produce euch a ecvore liver necrosis
vould heve
ny vircd cut the cuch more consitiva reticuleendothelial esystea end us sould
have escn no inflaccatory celle to epe2k of in the danaged livers
ck %
t
ffieiontly
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26453
usATOmeENERGY
COMMISSION
tasLORY
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ASIIED FORCES INSTITUTE OF PATHOLOGY
WALTER
REET
ATLAY
AOD
TAL
ce LER
6825 16.1 STLEZT, st. We
WASHINGTON 15, D.C.
Expaywe §
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15S
NON-CCRP
STATUS,VERIFIED ¢/1/é L
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