Diagnostic Cytology
sheet arrangem ent, o fte n w ith slits between cells. E n d oth elial
cells fro m sm all b lo o d vessels m ay also be noted. T he y have
o vo id nuclei and ab und ant cytoplasm . T he y are also in sheet
arrangem ents lik e m esothelial cells, b u t the end o the lia l sheets
u su ally contain few er cells. U n lik e m esothelial cells, there are
no slits between cells.
Acute Pancreatitis
A cute pancreatitis occurs in adults betw een 40 and 70 years o f
age and o fte n fo llo w s a heavy m eal o r an a lc o h o lic debauch. It
is a d e b ilita tin g illness w ith an a b rup t onset. E a rly in th e dis-
ease, pancreatic enzym es, such as am ylase and lipase, are lib e r-
ated in to th e b lood stream . E ig hty percent o f acute pancreatitis
is associated w ith b ilia ry tract disease o r a lc oh olism . A lth o u g h
o n e -th ird to tw o -th ird s o f th e patients have gallstones, o n ly
5% o f th e p atients w ith gallstones develop pancreatitis. A lc o -
h o lis m is associated w ith tw o -th ird s o f a ll cases in the U n ite d
States. T he g allstone and b ilia ry sludge m ig rate fro m th e com -
m o n b ile duct v ia the c o m m o n channel to th e m a in pancreatic
duct fro m th e spasm o f sp hincter o f O ddi. In acute pancrea-
titis , th e pancreas appears edem atous. T he in ju ry to acinar
cells causes release and a c tivatio n o f th e digestive enzymes,
resu ltin g in necrosis and in fla m m a tio n o f th e pancreas and the
s u rro u n d in g tissues. T he pancreas contains patches o f coagu-
la tiv e necrosis rim m e d b y heavy n e u tro p h ilic in filtra te s. Foci
o f fa t necrosis in th e peripancreatic tissue, m esentery, and
o m e n tu m m ay appear as sm a ll o vo id y e llo w -w h ite nodules
and are due to th e fo rm a tio n o f calcium soaps th ro u g h the
m echanism o f sap o nifica tion . These fo ci m ay be detected b y
im ag ing techniques.
Fine-needle asp iration smears contain tig h tly packed clusters o f
necrotic acinar cells w ith p yknotic nuclei. O n the background,
fin e ly and coarsely g ranular necrotic debris is u su a lly present
and in te rm in g le d w ith num erous n eutrop hils. N ecrotic duc-
tal cells show ing karyorrhexis o r appearing as ghost cells are
som etim es noted. D egenerating fa t cells, lip id droplets, and
lip id -la d en macrophages w ith fo a m y o r vacuolated cytoplasm
are also noted .19,92 The vo n Kossa stain m ay dem onstrate som e
g ranular d ep osition o f calcium salts w ith in the necrotic debris.
T he fo rm a tio n o f calcium salts is an in d ic a tio n o f fa t necrosis.
Irritated m esothelial cells m ay be seen i f the m aterial is aspi-
rated fro m the b o d y o f the pancreas. These cells have slig h tly
enlarged, ovoid nuclei and sm all n u c le oli and occur in group-
ings w ith overlapping o f cells o r in d isord erly arrangements.
Occasional slits between cells are seen.
Chronic Pancreatitis
In a p p roxim ately o n e -th ird o f all patients w h o survive episodes
o f acute pancreatitis, the disease progresses to chronic pan-
creatitis. T he pancreas is firm and nod ular, w ith areas o f dense
fibrosis, loss o f acinar and islet com ponents, and in filtra tio n o f
lym phocytes and plasm a cells. P ro life ra tio n o f ducts and hyper-
plasia o f ductal e p ith elial cells w ith som e atypia are noted. Areas
o f calcification in the in te rs titia l tissue and pancreatic ducts are
present. D e struc tion o f the pancreatic parenchym a eventually
results in pancreatic insufficiency.
Autoimmune Pancreatitis
A d istinct fo rm o f chronic pancreatitis first reported in Japan in
199793 as "a u to im m u n e p ancreatitis" w ith a 1.86% incidence
is n o w recognized w orld w id e. C lin ic a lly, m ost patients present
w ith a mass at the head o f the pancreas, often w ith stricture o f
the distal ducts, causing obstructive jaundice m im ic k in g cancer
clinically. O n C T and m agnetic resonance im aging, there is a
capsule-like rim , corresponding to infla m e d peripancreatic tis-
sues,94 diffuse pancreas enlargem ent, m u ltifo c a l n arrow in g o f
the m a in pancreatic duct, narrow in g o f peripancreatic veins, and
tapered n arrow in g o f the distal c om m o n b ile duct w ith freq uent
contrast enhancem ent.95 T he m ean age o f th e patients is in the
late fifties w ith m ore m en th an w o m e n affected. H istolog ically,
a u to im m u n e pancreatitis is characterized b y dense in filtra te o f
T lym phocytes and IgG 4-positive plasm a cells around sm all and
large in te rlo b u la r ducts, accom panied b y fibrosis, a trop h y o f
acini (Fig. 2 8.6 5 ), and expansion o f periductal tissue b y p ro lif-
erating ductules (Fig. 2 8.6 6 ).96,97 A u to im m u n e pancreatitis can
be confirm ed b y elevated serum IgG4 and dram atic response to
steroid therapy. FN A find ing s was recently reported.98
I f the aspirate comes fro m periductal lym p hop lasm acytic in fil-
trate, th e aspirates w ill contain m an y lym phocytes and plasm a
cells and the diagnosis w ill be easy. I f the m aterial is aspirated
fro m areas o f dense fibrosis, the aspirates w ill be unsatisfactory
due to in su ffic ie n t cellularity. I f the sam ple is aspirated fro m a
region w ith p ro life ra tin g ductules, m an y sm all sheets o f ductal
e p ith e liu m w ill be present, m im ic k in g w e ll-d iffere ntia te d duc-
tal adenocarcinom a at lo w e r pow er e xa m in ation (Fig. 2 8.6 7 ).
However, on hig h-p ow er e xa m in ation the ductal e p ith e liu m
appears reactive rather th a n m alig nant, w ith p ro m in e n t nucle-
o li b u t w ith o u t anisonucleosis o r nuclear m em brane irre g ularity
(Fig. 28.6 8 ). In a d d itio n, sparse lym phocytes m ay be fo u n d in
the background, and lym p hop lasm acytic in filtra te m ay be fo u n d
in o the r passes. Synthesis o f the finding s fro m d iffe re n t passes
and a h ig h index o f suspicion o f a u to im m u n e pancreatitis b y the
gastroenterologist, rad iolog ist, and cytop atholog ist are essential
avoid pancreatoduodenectom y.
C ytolog ic d iffe re n tia tio n
Fig. 28.65 Autoimmune pancreatitis. Pancreatic parenchyma infiltrated
by lymphocytes and plasma cells, and lymphoid follicles, resulting in atrophy
of acini, fibrosis, and ductular proliferation. Histology (H&E x LP).
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