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H pylori are associated with chronic cholecystitis.World
J Gastroenterol. 2007 Feb 21;13(7):1119-22.
AIM: To study whether H pylori are associated with chronic
cholecystitis. METHODS: The subjects were divided into three groups: H
pylori-infected cholecystitis group, H pylori-negative cholecystitis
group and control group. Pathologic changes of the gallbladder were
observed by optic and electronic microscopes and the levels of
interleukin-1, 6 and 8 (IL-1, 6 and 8) were detected by
radioimmunoassay. RESULTS: Histological evidence of chronic
cholecystitis including degeneration, necrosis, inflammatory cell
infiltration, were found in the region where H pylori colonized.
Levels of IL-1, 6 and 8 in gallbladder mucosa homogenates were
significantly higher in H pylori-infected cholecystitis group than
those in H pylori-negative cholecystitis group and control group.
CONCLUSION: H pylori infection may be related to cholecystitis.
H pylori exist in the gallbladder mucosa of patients with chronic
cholecystitis.World
J Gastroenterol. 2007 Mar 14;13(10):1608-11.
AIM: To study whether H pylori locate in the
gallbladder mucosa of patients with chronic cholecystitis. METHODS:
Using Warthy-Starry (W-S) silver stain and immunohistochemistry stain
with anti-H pylori antibodies, we screened paraffin specimens in 524
cases of cholecystitis. H pylori urease gene A (HPUA) and H pylori
urease gene B (HPUB) were analyzed by polymerase chain reaction (PCR)
in the fresh tissue specimens from 81 cases of cholecystitis. RESULTS:
H pylori-like bacteria were found in 13.55% of the gallbladders of the
cholecystitis patients using W-S stain. Meanwhile, bacteria positive
for H pylori antibodies were also found in 7.1% of the gallbladders of
patients with cholecystitis by immunohistochemistry. Of 81
gallbladders, 11 were positive for both HPUA and HPUB, 4 were positive
for HPUA only and 7 were positive for HPUB only. CONCLUSION: H pylori
exist in the gallbladders of patients with chronic cholecystitis.
Hyperplasia, metaplasia, dysplasia and neoplasia lesions in chronic
cholecystitis - a morphologic study.Rom
J Morphol Embryol. 2007;48(4):335-42.
The aim of the study was to analyze the association between chronic
cholecystitis, premalignant lesions and gallbladder cancer. The group
consisted in 3901 cases of cholecystectomies, diagnosed as acute
cholecystitis (250 cases - 6.4%), chronic cholecystitis (3619 cases -
92.8%) and gallbladder carcinoma (32 cases - 0.8%). Chronic
cholecystitis associated premalignant lesions as follows: hyperplasia
in 124 cases (7.8%), metaplasia in 86 cases (5%) and dysplasia in 10
cases (0.4%). Only in nine cases, the diagnosis of gallbladder
carcinoma was formulated presumptively, before surgery; for the other
23 cases this diagnosis was established after the pathologic exam on
the cholecystectomy piece. In the areas adjacent to the neoplastic
proliferation, premalignant lesions (hyperplasia, metaplasia,
dysplasia) were identified in 34.4% cases. The identification of
premalignant modifications in the morphologic background of chronic
cholecystitis is an argument in favor of the
metaplasia-dysplasia-neoplasia sequence and justifies recent
recommendations for the performing of colecystectomy.
Study on carcinogenesis in chronic cholecystitis.Rocz
Akad Med Bialymst. 2004;49 Suppl 1:49-51.
Not only bile but also chronic cholecystitis may play a role in
gallbladder carcinogenesis. Numerous studies have revealed a close
correlation between chronic inflammation and neoplasia. The
experiments were conducted on paraffin sections, obtained from 377
surgically resected gallbladders with chronic cholecystitis.
Immunohistochemical reaction was conducted on deparaffinized sections,
using a monoclonal antibody against 8-hydroxydeoxyguanosine (8-OHdG),
a biomarker of oxidative DNA damage. An increase was found in the
expression of 8-hydroxydeoxyguanosine in chronic cholecystitis. The
level of 8-OhdG expression is associated with inflammation intensity
and disease duration. DNA damage, observed in chronic cholecystitis,
indicates a correlation between chronic inflammation and gallbladder
carcinogenesis.
Histologic analysis of chronic inflammatory patterns in the
gallbladder: diagnostic criteria for reporting cholecystitis.Ann
Diagn Pathol. 2003 Jun;7(3):147-53.
Cholecystectomy is one of the most common surgical procedures.
Inflammatory disease is by far the most common pathology of the
gallbladder. Terms for describing cholecystitis are numerous, thus
there is no uniform terminology. One hundred cholecystectomies and 10
gallbladders from autopsies were reviewed and inflammatory changes
were analyzed. Chronic cholecystitis was seen in 75% of cases with
epithelial metaplasia and 73% with regenerative epithelium, the latter
being associated with erosion but not with the presence of lithiasis.
Muscular thickening and adipose deposits were mostly mild.
Inflammation was mild in 28%, moderatein 57%, and severe in 15%.
Activity was found in 29% of cases. Fibrosis was present in all cases:
26% mild, 62% moderate, and 12% severe. Autopsy cases did not show
significant changes. A simple and reproducible scoring system of
inflammation and fibrosis of the gallbladder is proposed. Three
numbers refer to mild, moderate, or severe degrees of chronic
inflammation and activity, with a final score that results from adding
both values. The fibrosis is classified in three different stages. The
final report uses both values to classify the chronic cholecystitis. A
scoring system for chronic cholecystopathy to replace descriptive
terms would give an exact transduction of the observed changes in an
objective fashion that could not be misinterpreted by physicians or
other pathologists.
Diffuse lymphoplasmacytic chronic cholecystitis is highly specific
for extrahepatic biliary tract disease but does not distinguish
between primary and secondary sclerosing cholangiopathy. Am
J Surg Pathol. 2003 Oct;27(10):1313-20.
Previous studies of gallbladder pathology in
primary sclerosing cholangitis (PSC) have suggested that a distinctive
histologic triad ("diffuse lymphoplasmacytic acalculous cholecystitis,"
composed of diffuse, mucosal-based, dense lymphoplasmacytic
infiltrates) is commonly present in gallbladders of patients with PSC
and is relatively specific for that disease. However, prior control
populations have included only patients with cholecystitis/cholelithiasis
and hepatitis, and have not evaluated patients with non-PSC-associated
extrahepatic biliary tract disease. We recently observed cases of
diffuse lymphoplasmacytic chronic cholecystitis in a subset of
patients with biliary tract disease associated with lymphoplasmacytic
sclerosing pancreatitis and among patients undergoing Whipple
resection for pancreatic head malignancy, suggesting that diffuse
lymphoplasmacytic chronic cholecystitis is not specific for PSC. We
studied 20 gallbladders from patients with obstructive jaundice due to
malignancies of the pancreatic head, duodenum, or ampulla and 5
gallbladders from patients with choledocholithiasis, and compared them
with 20 gallbladders from patients with PSC and 20 gallbladders with
cholelithiasis. The following histologic features were evaluated:
degree of mucosal and deep inflammation, lymphoid nodules, epithelial
metaplasia, muscular hypertrophy, Rokitansky-Aschoff sinuses,
fibrosis, and cholesterolosis. Gallbladders in malignancy-associated
obstructive jaundice were nearly identical to gallbladders in PSC with
respect to scores for mucosal inflammation, lymphoid nodules, and
frequency of diffuse lymphoplasmacytic chronic cholecystitis (60% vs.
50%, respectively). PSC gallbladders, however, were significantly more
likely to contain focal or extensive epithelial metaplasia (P = 0.01).
The cholelithiasis control group was characterized by lack of
significant mucosal inflammation in the majority of cases (95%) and
frequent Rokitansky-Aschoff sinuses, fibrosis, and muscular
hypertrophy. Gallbladders in the choledocholithiasis group showed
overlapping histologic features with PSC/malignancy-associated
obstructive jaundice and cholelithiasis. These results suggest that a
pattern of diffuse lymphoplasmacytic chronic cholecystitis is highly
specific for extrahepatic biliary tract disease but does not
distinguish between primary and secondary cholangiopathies.
Lymphoplasmacytic Chronic Cholecystitis
and Biliary Tract Disease in Patients With Lymphoplasmacytic
Sclerosing Pancreatitis. American Journal of Surgical
Pathology. 27(4):441-451, April 2003.
Lymphoplasmacytic sclerosing pancreatitis (LPSP)
represents a distinctive form of chronic pancreatitis characterized by
diffuse fibroinflammatory infiltrates that can involve both the
pancreatic ducts and acinar parenchyma. Several cases of inflammatory
infiltrates within the gallbladder have been reported in association
with LPSP, but the spectrum of gallbladder pathology in patients with
LPSP has not been systematically reviewed. Many patients with LPSP
have distal CBD fibrosis, strictures, and inflammation, features that
overlap somewhat with primary sclerosing cholangitis (PSC). In PSC, a
pattern of gallbladder pathology termed "diffuse acalculous
lymphoplasmacytic chronic cholecystitis" has been previously described
as showing a triad of diffuse, mucosal-based, plasma cell-rich
inflammatory infiltrates. We studied 20 gallbladders from patients
with LPSP and compared them with 20 gallbladders in PSC, 20
gallbladders with chronic cholelithiasis, and 10 gallbladders from
patients with benign (non-LPSP) pancreatic disease. The following
features were evaluated: degree and composition of mucosal
inflammation and deep (mural) inflammation, lymphoid nodules,
metaplasia, dysplasia/neoplasia, fibrosis, muscular hypertrophy,
Rokitansky-Aschoff sinuses, and cholesterolosis. The majority (60%) of
gallbladders in LPSP contained moderate or marked inflammatory
infiltrates and lymphoid nodules, frequencies similar to PSC but
significantly higher than in chronic cholelithiasis and benign non-LPSP
pancreatic disease. LPSP gallbladders received the highest scores for
deep inflammation of all groups, and 35% of LPSP gallbladders showed
transmural chronic cholecystitis. Overall, "diffuse lymphoplasmacytic
chronic cholecystitis" was present in 50% of PSC cases and 25% of LPSP
cases, but in only 5% of chronic cholelithiasis and none of non-LPSP
benign pancreatic disease. Mucosal inflammation in LPSP gallbladders
correlated significantly with the presence of inflammation in the
extrapancreatic portion of the CBD. These findings suggest that
inflammatory pathology of the gallbladder is frequently associated
with LPSP and that it is part of the spectrum of biliary tract disease
in these patients, rather than a simple reflection of the pancreatitis
itself.
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