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A CLINICOPATHOLOGICAL STUDY OF
GASTRIC CARCINOMA
By
Dr. ROMMEL. S,M.B.B.S
Dissertation Submitted to the
Rajiv Gandhi University of Health Sciences, Karnataka
In partial fulfillment
of the requirements for the degree of
MASTER OF SURGERYin
GENERAL SURGERYUnder the guidance of
Prof. B. JAGADISHM.S.Professor and Unit Chief
Department of Surgery
MYSORE MEDICAL COLLEGE AND RESEARCH INSTITUTE,
MYSORE
APRIL 2011
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RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES
DECLARATION BY THE CANDIDATE
I hereby declare that this dissertation entitled A CLINICOPATHOLOGICAL
STUDY OF GASTRIC CARCINOMA is a bonafide and genuine research work
carried out by me under the guidance of my Guide Prof. B. JAGADISH, MS.
Department of General Surgery, and with Prof. Mudassir Azeez Khan, Department of
Community Medicine and Prof. Nataraju G., Department of Pathology Mysore
Medical College and Research Institute, Mysore as Co-Guides
Date:
Place: Mysore
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CERTIFICATE BY THE GUIDE
This is to certify that the dissertation entitled A CLINICOPATHOLOGICAL
STUDY OF GASTRIC CARCINOMA is a bonafide research work done by
Dr. Rommel .S. in partial fulfillment of the requirement for the degree of Master of
Surgery in General Surgery.
Date:
Place: Mysore
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CERTIFICATE BY THE CO-GUIDES
This is to certify that the dissertation entitled A CLINICOPATHOLOGICAL
STUDY OF GASTRIC CARCINOMA is a bonafide research work done by
Dr. Rommel .S. in partial fulfillment of the requirement for the degree of Master of
Surgery, General Surgery.
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ENDORSEMENT BY THE HEAD OF THE DEPARTMENT AND
PRINCIPAL
This is to certify that the dissertation entitled A CLINICOPATHOLOGICAL
STUDY OF GASTRIC CARCINOMA is a bonafide research work done by Dr.
ROMMEL. S. under the guidance of Prof. B. JAGADISH, Professor of Surgery,
Department of General Surgery, at K.R. Hospital attached to Mysore Medical College
and Research Institute, Mysore.
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COPYRIGHT
Declaration of the candidate
I hereby declare that The Rajiv Gandhi University of Health
Sciences, Karnataka shall have the rights to preserve, use and
disseminate this dissertation/ thesis in print or electronic format
for academic/ research purpose.
Rajiv Gandhi University of Health Sciences, Karnataka
Date:
Place: MysoreDr. ROMMEL. S
Post Graduate in GeneralSurgery
Mysore Medical Collegeand Research Institute,
Mysore
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ACKNOWLEDGEMENT
It gives me great pleasure in preparing this dissertation and I take this opportunity to
thank everyone who has made this possible. It is most appropriate that I begin by
expressing my gratitude to the Almighty for his Blessings.
I express my deep sense of gratitude and indebtedness to my most respected guide and
treasured teacher Prof. B. Jagadish. M.S., Professor and Unit Chief, Department of
Surgery, Mysore Medical College and Research Institute, Mysore whose wisdom and
appropriate blend of science and art in the practice of surgery has been and will
always be a constant source of encouragement.
I express my deep sense of gratitude to my Co-guides, Prof. Mudassir Azeez Khan,
Head of thye Department of Community Medicine and Prof. Nataraju G., Department
of Pathology for their support and guidance throughout this study.
I express my sincere thanks to Dr. AVADHANI GEETA. K., Professor and HOD of
Surgery, MMC&RI Mysore for her valuable advice and support.
I am also thankful to Assistant Professor Dr. Balasubrahmanya and Senior Resident
Dr. B.G. Ponnappa for their constant support, encouragement and valuable
suggestions.
I thank all the staff of the Department of General Surgery for all the help rendered.
I owe a lot to my post graduate colleagues and interns for their encouragement and
enthusiastic co- operation.
I always remember my family especially my brother for his support and
encouragement.
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I would like to thank Dr. Swati Kaktikar without whose help this would not have been
possible.
Lastly I would like to thank all the patients and their attenders for their co-operation.
Date :
Place : MysoreDr.ROMMEL. S
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LIST OF ABBREVIATIONS USED
(in alphabetical order)
A-Ascites
B- Body
C- Cardia
D-Diffuse
DC- Decreased capacity
DS- Dilated Stomach
EL- Emergency Laparotomy
EP- Enlarged Prostate
F-Fundus
FJ- Feeding Jejunostomy
G- Growth
GEJ- Gastro-oesophageal junction
GC- Greater curvature
HPR- Histopathology report
I- Infiltrative
IO- Inoperable
JJ- Jejunojejunostomy
LC- Lesser curvature
LS- Liver secondaries
M- Moderate
MA Minimal Ascites
MRD- Medical Renal Disease
O- Operable
P- Poor
PA- Pyloric Antrum
PALN- Paraaortic Lymph nodes
PE- Pleural effusion
Per- Perforation
Po- Polypoidal
PO- Pyloric Obstruction
PG- Partial Gastrectomy
PGJ- Palliative GJ
PGLN- Perigastric Lymph Nodes
PHLN- Porta Hepatis Lymph Nodes
PR- Per rectal examination
S-Splenomegaly
SWT- Stomach wall thickening
U-Ulcerative
UGI- U er astrointestinal
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ABSTRACT
Background
Cancer is the second most common cause of cancer related deaths worldwide. Major
changes have been noted in the site of gastric cancer occurrence. The west has noted a
paradigm shift with a steady increase in cancers of the proximal stomach and a
decline in cancers of the distal stomach. Gastric cancer is well known to be associated
with risk factors
Objectives
This study was undertaken at K.R. Hospital, Mysore attached to Mysore Medical
College and Research Centre to study the trends regarding prevalence, clinical
features, association of risk factors, site of occurrence and histopathology.
Methods
All patients with histological confirmation of gastric carcinoma attending
K.R.Hospital from January 2009 to July 2010 were studied and details regarding the
clinical presentation, sub site, pathological features and treatment were collected.
Results
Thirty two patients with histological confirmation of carcinoma stomach were
studied. Gastric carcinoma was seen in the older age group with male preponderance.
The association of risk factors was studied. Majority of the patients presented in the
advanced stage and distal tumours were the predominant subtype.
Interpretation and Conclusion
Gastric cancer is a common malignancy in this part and is commonly seen in the older
age group predominantly in males. Patients usually present in the advanced stage,
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however with the increasing use of upper gastrointestinal endoscopy early gastric
cancers are also being detected.
The association of risk factors is well known and consistent and hints at the
primordial prevention of the disease.
Unlike in the west where there has been a shift in the site of the tumour, distal
tumours continue to be the major subtype in this study.
A multidisciplinary approach combining population screening with molecular
biological techniques that are being developed is required to detect the cancer early
and improve prognosis.
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TABLE OF CONTENTS
SINo.
Contents Pagenumber
1 Introduction 1
2 Objectives 9
3 Review of Literature 5
4 Methodology 56
5 Results 58
6 Discussion 79
7 Conclusion 85
8 Summary 87
9 Bibliography 88
10 Annexures 94
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LIST OF TABLES
Sl. No Tables Pages
1 Lauren Classification System 12
2 Genetic Abnormalities in Gastric Cancer 17
3 TNM staging of gastric cancer 34
4 Stage grouping gastric carcinoma 34
5Japanese Gastric Cancer Association Staging System for
Gastric Cancer
36
6Sex distribution among carcinoma stomach patients
38
7Age distribution among carcinoma stomach patients
60
8Income group among carcinoma stomach patients
61
9 Comparison of risk factors between males and females 62
10Blood group distribution in carcinoma stomach patients 64
11Symptom analysis in patients of carcinoma stomach 66
12Analysis of signs in gastric cancer patients 68
13Sub site specific trends in carcinoma stomach 70
14Comparison of the macroscopic type in both sexes 71
15Comparision of symptoms with the site of the tumour 72
16Comparision of symptoms with macroscopic appearance 73
17Analysis of the site of tumour with signs 74
18Comparison of macroscopy with clinical signs 75
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19Comparison of histopathology 76
20Comparision of histology with the site of the tumour 77
21 Sex distribution among carcinoma stomach patients 80
22 Age distribution among carcinoma stomach patients80
23Socioeconomic groups among gastric cancer patients 81
24Blood group distribution in carcinoma stomach patients 81
25 Comparison of risk factors between males and females82
26Symptom analysis in patients of carcinoma stomach 83
27Sub site specific trends in carcinoma stomach 83
28Comparison of histology according to Broders classification 84
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LIST OF FIGURES
Sl.No Figures Pages
1 Borrmann classification of gastric carcinoma 8
2 Photomicrographs of gastric adenocarcinoma. 12
3 Role of Helicobacter pylori 17
4 T Stage defined by depth of penetration into gastric wall 34
5 Lymph node station numbers as defined by Japanese Cancer
Association 37
6 Japanese classification system for early gastric cancer 41
7 Endoscopic photograph showing ulceroproliferative growth in
antrum98
8 Endoscopic photograph showing early gastric cancer 98
9 Photograph showing gastric cancer invading the posterior wall and
perforating it99
10 Photograph showing palliative anterior gastrojejunostomy 99
11 Photograph showing partial gastrectomy specimen 100
12 Photograph showing opened partial gastrectomy specimen 100
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1
INTRODUCTION
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INTRODUCTION
Adenocarcinoma of the stomach was the leading cause of cancer-related
death worldwide through most of the 20th century. It now ranks second only to
lung cancer, and an estimated 875,000 new cases are diagnosed annually
worldwide. In many parts of the world, however, the incidence of gastric cancer
has gradually decreased, principally because of changes in diet, food preparation,
and other environmental factors. The declining incidence has been dramatic in the
United States, where this disease ranks seventh as a cause of cancer-related deaths.
Stomach cancer incidence rates are much lower in India than elsewhere, but the
stomach remains one of the 10 leading sites of cancer in both sexes in most of the
metropolitan registries. Cancer rates in India are rising with increasing migration
of rural population to the cities, increase in life expectancy and changes in
lifestyles.
Change of diet is among the factors that may be responsible for the
changing disease rates. Diet in India encompasses diversity unknown to most other
countries, with many dietary patterns emanating from cultural and religious
teachings that have existed for thousands of years. Very little is known, however,
about the role of the Indian diet in causation of cancer or its role, if any, in
prevention of cancer, although more attention is being focused on certain aspects
of the Indian diet, such as vegetarianism, spices, and food additives.
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The prognosis for this disease remains poor except in a few countries. The
explanations for these poor results are multifactorial. The lack of defined risk
factors and specific symptoms and the relatively low incidence have contributed to
the late stage at diagnosis seen in most Western countries. In Japan, where gastric
cancer is endemic, more patients are diagnosed at an early stage, which is reflected
by higher overall survival rates.
Although the incidence of gastric cancer has decreased dramatically over
the past century, the decline has been limited to cancers below the esophagogastric
junction. The number of newly diagnosed cases of proximal gastric and
esophagogastric junction adenocarcinomas has increased markedly since the mid-
1980s. These tumors are thought to be biologically more aggressive than distal
tumors and more complex to treat.
The only proven, potentially curative treatment for gastric cancer is
surgical resection of all gross and microscopic disease. Even after what is felt to
be a curative gastrectomy, disease recurs in both regional and/or distant sites in the
majority of patients. Efforts to improve these poor results have focused on
developing effective pre- and postoperative systemic and regional adjuvant
therapies.
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AIMS AND OBJECTIVES OF THE STUDY
1. To study the prevalence of carcinoma stomach as occurring in K.R.Hospital ,
Mysore.
2. To study the clinical presentation including the anatomic site of occurrence and
Histological type
3. To study the association of risk factors
4. To study the surgical modalities of treatment
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REVIEW OF LITERATURE
The stomach is a remarkable organ with important digestive, nutritional,
and endocrine functions. The stomach stores and facilitates the digestion and
absorption of ingested food, and it helps regulate appetite1. Wallace P. Ritchie, Jr.
called the stomach an elegant organ, once thought to be the seat of the soul,
always handy to bring to the dinner table, and a recognized source of ecstasy and
grief2. Approximately 90% of all tumours of the stomach are malignant, the vast
majority of which are adenocarcinoma.3
EPIDEMIOLOGY
Worldwide, gastric cancer remains the second or third most common
malignancy (nearly 900,000 new cases annually) and the second most common
cause of death (approximately 650,000 deaths).3, 4The incidence of gastric cancer
has significant geographic variation, with the highest incidence (75 to 100 per
100,000 men) occurring in Japan, Korea and parts of South America and Eastern
Europe and the lowest incidence(as low as 5 per 100,000 men) occurring in the
United States and Western Europe.3,5
In India, the stomach was estimated to be the fifth leading site in males and
the seventh in females in 1991 with age-standardized rates (ASRs) of 5.0 and 2.8
per 100,000 in males and females, respectively.
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With the establishment of the National Cancer Registry Programme, cancer
incidence data are available for 5 metropolitan areas and 1 rural area in India since
1982. From 1988 through 1992, the stomach was the leading site of cancer in
males in Chennai (ASR = 15.9 per 100,000) and Bangalore (ASR = 10.3), fifth in
Mumbai (ASR = 7.7) and fourth in Trivandrum (ASR = 6.8); among females, it
was the fourth leading site in Chennai (ASR = 7.0), fifth in Bangalore (ASR = 5.1)
and sixth in both Mumbai (ASR = 3.8) and Trivandrum (ASR = 2.5).6
In contrast with the general decline in incidence, an increase has been
observed for cardia lesions in many regions. Comparatively high rates are evident
for the United Kingdom/Ireland, Northern Europe, Australia and New Zealand,
China, and North America. The increase in incidence of cardia lesions has been
associated with parallel increases for adenocarcinomas of the lower esophagus,
where hyperacidity, reflux esophagitis, Barretts esophagus, and obesity have been
proposed as likely risk factors. 7In a study conducted in Tamil Nadu, the sites of
gastric cancer in order of frequency were antrum (67.3%) followed by
body(23.3%), proximal stomach(5.6%) and OGJ(3.8%) .8 A recent study from the
southern state of Kerala showed that carcinoma of the distal stomach has remained
predominant although a trend towards a proximal shift has been noticed. 9
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PATHOLOGY AND TUMOR BIOLOGY
Approximately 95% of all malignant gastric neoplasms are
adenocarcinomas, and in general, the term gastric cancer refers to adenocarcinoma
of the stomach. Other malignant tumors are very rare and include squamous cell
carcinoma, adenoacanthoma, carcinoid tumors, and leiomyosarcoma. Although no
normal lymphoid tissue is found in the gastric mucosa, the stomach is the most
common site for lymphomas of the gastrointestinal tract. 10
Morphologic features and classification
In 1965, Lauren described two histologic types of gastric adenocarcinoma,
intestinal and diffuse, which provided a model to understand better the etiology
and epidemiology of the disease.
Several pathologic classifications have been proposed based on the
morphologic features of gastric tumors.
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8
The Borrmann classification divides gastric cancer into five types depending on
macroscopic appearance.
Type Irepresents polypoid or fungating cancers
Type IIencompasses ulcerating lesions surrounded by elevated borders
Type III represents ulcerated lesions infiltrating the gastric wall
Type IVare diffusely infiltrating tumors
Type Vare unclassifiable cancers10,11
Fig. 1 Borrmann classification of gastric carcinoma
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Gross Morphology
There is wide variation in the gross appearance of carcinoma of stomach.
Many intermediate stages exist between the two extremes represented by the
fungating tumour growing mainly into the lumen and the flat, ulcerated and deeply
invasive tumour growing through the wall of the stomach.
Carcinomas located in the fundic area are more likely to have invaded the
submucosa and beyond at the time of surgery than those located in the pyloric
area.
Depending upon the relative amounts of mucin secreted and desmoplastic
reaction elicited, the tumour may have a fleshy, fibrous or gelatinous gross
appearance. In terms of location, any area of the stomach can be affected: anterior
and posterior wall, lesser curvature, and greater curvature (in that order of
frequency). Multiple tumours are found in approximately 6% of cases.
The non neoplastic mucosa adjacent to the carcinoma is often thickened; a
feature that may result in false negative endoscopic biopsies and that has been
attributed to production of epidermal growth factor by the tumour.
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Microscopy
Nearly all gastric carcinomas are of the adenocarcinoma type and
composed of one or more of the following four major cell types- foveolar,
mucopeptic, intestinal columnar and goblet cell.
As, described by Lauren, two major categories exist, which have been designated
intestinal (53%) and diffuse (33%).
The intestinal type of sporadic gastric adenocarcinoma has a hallmark
progression from normal gastric epithelium to atrophic to chronic atrophic gastritis
(typically due to Helicobacter infection) to intestinal metaplasia to dysplasia to
cancer. This assumption supported by electron microscopic and
immunohistochemical studies.
Their degree of differentiation ranges widely and correlates inversely with
tumor size. In the better differentiated tumors, most of the cells are columnar and
mucin secreting. Poorly differentiated variants have a predominantly solid pattern.
Exceptionally the better differentiated tumors are ciliated. The amount of mucin
production is highly variable, when abundant; it is often accompanied by
calcification.
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11
Diffuse type adenocarcinoma are best represented by the tumour type
clinically known as linitus plastica and currently designated as signet ring (adeno)
carcinoma. The gross alteration usually begins in the prepyloric area. Pyloric
obstruction often develops, as the wall of the stomach becomes thickened and
rigid. Sections of the wall show marked submucosal fibrosis, with or without
mucosal ulceration. The muscle is hypertrophied and segmented by the presence
of the parallel, grayish white, longitudinal lines that give it a comb like
appearance. The lines are continuous with foci of subserosal thickening.
Microscopically a diffuse growth of malignant cells is seen, associated with
extensive fibrosis and inflammation. Often the entire wall is involved.
Although an intramural type of signet ring carcinoma occurs in many cases
of this entity the mucosa is less affected than the deeper layers. Glandular
formations are rare and most tumour cells grow individually. Most of the mucin
produced as intra-cytoplasmic, resulting in the typical signet ring appearance.
There are few malignant tumours in the body that are more likely to be missed on
microscopic examination than this type of gastric carcinoma. Over the years
specimens have been seen from the stomach wall, lymph nodes, mesentery, pelvic
peritoneum and ovary that were initially misinterpreted as a begin process because
of the inconspicuousness of the tumour cell and the marked degree of
inflammatory and desmoplastic reaction. The tumour may also simulate
lymphoma because of its diffuse pattern of growth and the round shape of the cells
and their nuclei. 11
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Figure 2 Photomicrographs of gastric adenocarcinoma. A,Gastric adenocarcinoma intestinal
type (H&E, 25). B,Gastric adenocarcinoma intestinal type (H&E, 400). C,Gastric
adenocarcinoma diffuse type (H&E, 25). D,Gastric adenocarcinoma diffuse type (H&E,
400).Arrowson signet ring cells.
Table 1-- Lauren Classification System
INTESTINAL DIFFUSE
Environmental Familial
Gastric Atrophy, metaplasia Blood group A
Men>Women Women>men
Increasing incidence with age Younger age group
Gland formation Poorly differentiated, signet ring cells
Hematogenous spread Transmural/lymphatic spreadMicrosatellite instability, APC gene
mutations
Decrease E-cadherin
p53, p16 inactivation P53, p16 inactivation
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Broder's classification of gastric cancer grades tumors histologically from 1
(well-differentiated) to 4 (anaplastic). Bearzi and Ranaldi have correlated the
degree of histologic differentiation with the gross appearance of 41 primary gastric
cancers seen on endoscopy. Ninety percent of protruding or superficial cancers
were well differentiated (Broder's grade 1), whereas almost half of all ulcerated
tumors were poorly differentiated or diffusely infiltrating (Broder's grades 3 and
4).8
The WHO classification, 2000 classifies gastric cancer into
Adenocarcinoma- intestinal and diffuse types,
Papillary adenocarcinoma,
Tubular adenocarcinoma,
Mucinous adenocarcinoma,
Signet ring cell adenocarcinoma,
Adenosquamous adenocarcinoma,
Squamous cell carcinoma,
Small cell carcinoma,
Undifferentiated carcinoma and Others.11,12
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Classification of Esophagogastric Junction Cancers
Siewert and Stein have developed a classification system for adenocarcinoma
of the esophagogastric junction. Now commonly referred to as the Siewert
classification, this system recognizes three distinct clinical entities that arise
within 5 cm of the junction of the tubular esophagus and the stomach:
Type 1: Adenocarcinoma of the distal esophagus, which usually arises
from an area with specialized intestinal metaplasia of the esophagus (i.e.,
Barrett's esophagus) and may infiltrate the esophagogastric junction from
above.
Type II: Adenocarcinoma of the cardia, which arises from the epithelium of
the cardia or from short segments with intestinal metaplasia at the
esophagogastric junction
Type III: Adenocarcinoma of the subcardial stomach, which may infiltrate
the esophagogastric junction or distal esophagus from below
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The assignment of tumors to one of these subtypes is based on morphology
and the anatomic location of the epicenter of the tumor. Classification can be
performed based on the results of contrast radiography, endoscopy, CT, and
operative findings. The Siewert classification has important therapeutic
implications.13,14
Histochemical, immunohistochemical and electron microscopic features
The secretory product of most gastric adenocarcinoma(esp those of the
intestinal type) is an acid mucosubstance, easily detected with Mayers
mucicarmine, Alcian blue or colloidal iron stains and having feature analogous to
the those of intestinal type mucins. Various alterations in the syalidation of the
mucins occur and can be detected histochemically or immunohistochemically.
At the immunohistochemical level, the main mucin types expressed are
MUC1 for the intestinal type, MUC5AC for the diffuse and MUC2 for mucinous
types. There is also an interesting relationship between mucin type and is
prevalent with carcinoma of the antrum whereas MUC2 is expressed in greater
amounts in carcinoma of the cardia.
In terms of immunomarkers reactivity of gastric adenocarcinoma for
keratin, epithelial membrane antigen and CEA is the rule.11
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RISK FACTORS
Inherited Susceptibility
Case-control studies have observed consistent, up to threefold, increases in
risk for gastric cancer among relatives of patients with gastric cancer. Studies of
monozygotic twins have even shown a slight trend toward increased concordance
of gastric cancers compared with dizygotic twins. Large families with an
autosomal dominant, highly penetrant inherited predisposition for the development
of gastric cancer are rare. However, early-onset diffuse gastric cancers have been
described and linked to the E-cadherin/CDH1 locus on 16q and associated with
mutations in this gene. This seminal finding has been confirmed in other studies
with gastric cancers at a relatively high (67% to 83%) penetrant rate. Thus, E-
cadherin mutation testing should be considered in the appropriate clinical setting.
In fact, prophylactic gastrectomy should be considered strongly in families with
germ line E-cadherin mutation even without gross mucosal abnormalities by
endoscopic examination of the stomach.
Hereditary nonpolyposis colon cancer (HNPCC) involves germ line
mutations of DNA mismatch repair genes. Gastric adenocarcinoma may be
observed in families with HNPCC. Gastric cancers have also been noted to occur
in patients with familial adenomatous polyposis and Peutz-Jeghers syndromes.14
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Table 2 - Genetic Abnormalities in Gastric Cancer
Abnormalities Gene Approximate Frequency %
Deletion/suppression p53 6070
FHIT 60
APC 50DCC 50
E-cadherin
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Role of helicobacter pylori
As a commensal organism, Helicobacter pylori infection is widely
prevalent throughout the world. Despite its classification by the World Health
Organization as a class I carcinogen, infection with H. pylori does not typically
lead to gastric cancer. This underscores the importance of other factors, such as
virulence, environmental, and host factors, as well as genetic polymorphisms (e.g.,
in interleukin-1, a potent inhibitor of acid secretion). The blood group A
phenotype has been reported to be associated with gastric cancers. Helicobacter
pylori may adhere to the Lewis Blood Group antigen, indicating a factor for
increased risk for gastric cancer. Small variant alleles of a mucin gene, Muc1,
were found to be associated with gastric cancer patients when compared with a
blood donor control population.
The risk of gastric cancer in patients with chronic H. pylori infection is
increased about threefold. When compared to uninfected patients, patients with a
history of gastric ulcer are more likely to develop gastric cancer , and patients with
a history of duodenal ulcer are at decreased risk for gastric cancer. This may be
due to the fact that some patients develop antral-predominant disease
(predisposing to duodenal ulcer and somehow protecting against gastric cancer),
while other patients develop corpus-predominant gastritis, resulting in
hypochlorhydria and somehow predisposing to gastric ulcer and gastric cancer.
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Recently, it has been demonstrated that bone marrowderived stem cells
play a key role in the pathogenesis of gastric adenocarcinoma in patients with
chronic H. pylori infection. However, it must be recognized that gastric
adenocarcinoma is a multifactorial disease. Not all patients with gastric cancer
have H. pylori, and there are some geographic areas with a high prevalence of
chronic H. pylori infection and a low prevalence of gastric cancer (the "African
enigma"). Finally,H. pyloriinfected patients seem to be at decreased risk for the
development of adenocarcinoma of the distal esophagus and cardia region.
Perhaps the corporeal gastritis decreases acid secretion, creating a less damaging
refluxate and thus reducing the risk for Barrett's esophagus, the precursor lesion
for these tumors.14
Epstein Barr Virus
Epstein-Barr virus (EBV) has been found to be associated with a type of
gastric carcinoma (EBVaGC). EBV may be a factor initiating EBVaGC. EBV may
infect the surface epithelium of the stomach through the reactivated EBV-carrying
lymphocytes. Using PCR and EBER1 in situ hybridization, EBVaGC (definitely
amplifiable EBV-DNA and positive EBER1-signal in the nuclei of carcinoma
cells) was found in 8 of 72 gastric carcinomas (11%). EBVaGC was found in the
cardia (4/8) or body (4/8) of the stomach, and consisted of 7 advanced and 1
intramucosal carcinoma.
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Patients with EBVaGC showed high titers of anti-VCA IgG (8/8), anti-
VCA IgA (2/8) and anti-EA IgG (7/8) antibodies just before surgery. Anti-EBV
antibodies or EBER1 in situ hybridization may help to identify patients at high
risk for EBVaGC stomach.15
Diet
Diet is generally accepted as the main factor in gastric cancer etiology.
There is, however, no general agreement on the specific components of the diet
supposedly responsible for gastric cancer. The geographic distribution of the
disease shows marked inter-country contrasts but there are many examples of
culturally-divergent populations inhabiting the same land but having contrasting
gastric cancer rates. Migrants from high-risk areas acquire the low rates of
adoptive countries. Culture, not race or geography, appears as the main
determinant of gastric-cancer risk. Diet is the cultural component which offers the
most logical explanation of inter-population contrasts.
The gastric-cancer diet has been characterized as follows
(a) Low in animal fat and animal proteins
(b) High in complex carbohydrates
(c) A substantial proportion of the protein obtained from vegetable sources,
mostly grains and tubers
(d) Low in salads and fresh, green, leafy vegetables
(e) Low in fresh fruits, especially citrus
(f)
High in salt.
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In addition, a controversial role of nitrates has been reported.16Nitrates are
converted to carcinogenic nitrites by bacteria. Such bacteria may be introduced
through consumption of partially decayed foods, a practice that is more common
in the lower social economic strata worldwide.2
Humans are exposed to a wide range of N-nitrosocompounds (NOCs) from
diet, tobacco smoking, work place and drinking water, which are the major source
of exposure in the general population. Preformed exogenous nitrosamines are
found mainly in cured meat products, smoked preserved foods, foods subjected to
drying by additives such as malt in the production of beer and whiskey, pickled
and salty preserved foods.
Available data suggest that nitrosamines are found more frequently and at
higher concentration in Asian foods than in Western foods. On the other hand,
nitrosamines are formed endogenously from nitrate and nitrite. Although the levels
have reduced during the last 20 years, sodium nitrites are still widely used as food
preservatives in cured meat products. Nitrite is also formed in the human body
from oral reduction of salivary nitrate. Vegetables and water are the main sources
of nitrate intake. Nitrites are transformed into nitric oxide by gastric acid-catalyzed
formation, which acts as nitrosating agent of amines and amides, as consequence
of NOC. Under chronic inflammatory conditions, such as precancerous conditions
of gastric cancer (GC) and esophageal cancer (OC), nitrosating agents are
overproduced.17
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Excessive salt intake as a factor has epidemiologic and experimental
support.16A recent case-control study in Mumbai found that consumption of dried
fish increased the risk while green tea consumption decreased the risk of having
stomach cancer. A prospective case-control study from Trivandrum evaluated
dietary risk factors for stomach cancer and found that high consumption of rice,
spicy food, chili , and high-temperature food increased the risk of developing
stomach cancer.
Fried foods are associated with higher rates of cancer due in part to the
production of carcinogenic or mutagenic heterocyclic amines (HA) during the
cooking process. Case-control and prospective studies have reported an increased
risk of stomach, colon, and bladder cancers with moderate to heavy consumption
of fried foods. The use of the spice turmeric is associated with a reduced risk of
stomach cancer, in part because of its protective effect against the carcinogenic
bacterium H. pylori, a major risk factor for stomach cancer.18
Conversely, the consumption of raw vegetables, citrus fruits, and high-fiber
breads is associated with a lower risk for gastric cancer. The ascorbic acid and -
carotene found in fruits and vegetables act as antioxidants, whereas ascorbic acid
can also prevent the conversion of nitrates to nitrites.2
In a carefully conducted case-control study at Chennai, the authors have
identified alcohol consumption as an independent risk factor.19
Studies of the
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relation between alcohol consumption and the risk of GCA have been largely
inconclusive, and case-control studies from India have not identified alcohol
intake as an independent risk factor for GCA in India.20Beer specimens obtained
from several Indian cities in South India have been shown to contain N-
nitrosodimethylamine in large amounts,21and this may be an important factor for
the high risk of GCA associated with alcohol consumption in our part of the
country. 19
PRECANCEROUS LESIONS
Atrophic gastritis
This is a histological diagnosis. The main features are a variable degree of
inflammation, atrophy of gastric glands, and often associated intestinal metaplasia,
which changes are more commonly found in the antrum than in the body or the
fundus of the stomach.
Patients with atrophic gastritis are statistically at increased risk from cancer
of the stomach but precise measurement of this risk is yet to be determined. There
is a significant geographical relationship between areas of high frequency for
gastric carcinoma and the incidence of atrophic gastritis and intestinal metaplasia.
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Within the histological spectrum of atrophic gastritis intestinal metaplasia
is the most sensitive risk indicator. Most gastric cancers develop on a basis of
atrophic gastritis, but the epithelial change which statistically most predisposes to
malignancy is intestinal metaplasia.
Gastric ulcer
The incidence of so-called 'ulcer-cancer', that is, carcinoma developing in a
pre-existing peptic ulcer, has been debated hotly for many years. There are two
essential criteria for the diagnosis: first, there must be definite evidence of a pre-
existing ulcer (complete destruction of a zone of muscle, dense fibrous tissue in
the floor of the lesion, endarteritis and thrombophlebitis in surrounding vessels,
fusion of muscle coats and muscularis mucosae at the edge of the lesion) and,
second, there must be definite evidence of malignant change at the edge of the
ulcer quite distinct from any attempt at epithelial regeneration.
In any assessment one must remember that chronic ulcer and cancer may
coexist in a stomach without necessarily being causally related; studies in Japan
suggest that gastric ulcer and gastric cancer also have a different geographic
distribution. Ulcer-cancers undoubtedly do occur, particularly when the ulcer is
chronic, but the incidence of cancer developing in a proven peptic ulcer and the
presence of unequivocal evidence of previous peptic ulcer at the site of a proven
carcinoma are both probably not more than 1 %.
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Pernicious anemia
There is statistical and histological evidence that patients with pernicious
anemia are at increased risk from cancer of the stomach. True adenomatous polyps
and carcinoma of the stomach have been reported to be three to four times more
common in patients with pernicious anemia than in the general population
although a recent study suggests that this may be an underestimate, since some
patients with carcinoma but without overt pernicious anemia are in a 'pre-
pernicious anemia stage'.
Moreover, it appears that the carcinomas are mostly found in the body or
the fundus of the stomach rather than in the pyloric antrum, which is where most
gastric cancers are seen. 22
Gastric stumps
Balfour first reported a correlation between prior gastric surgery for benign
disease and the subsequent development of gastric cancer in 1922. Subsequent
meta-analyses support the conclusion that there is an increased risk for gastric
remnant cancer in patients with prior partial gastrectomy.However, the risk is only
observed after a latency of 15 years and is increased in patients operated on for
gastric but not duodenal ulcers.
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The incidence of malignancy ranges from 2% to 6% in gastric remnants,
and a variety of causative factors have been proposed to include alkaline duodenal
gastric reflux as well as increased N-nitroso compounds secondary to bacterial
overgrowth. The development of atrophic gastritis along with gastritis cystica
profunda can be associated with dysplasia in 5% of patients, for which
surveillance endoscopy is indicated.2
Gastric stump carcinomas usually develop close to the anastomosis on the
gastric side. Polypoid lesions are common in the same area, but their significance
has not yet been established; many are hyperplastic or regenerative polyps, and
others may be pseudo polyps resulting from the construction of the anastomosis.22
Gastric polyps
Polypoid lesions of the stomach can be divided into those with and without
malignant potential. The common ones, hyperplastic or regenerative polyps, have
insignificant malignant potential. Polypoid lesions in which the epithelium shows
dysplasia (which are called adenomas or borderline lesions by some) have a
significant capacity for malignant change. It is exceptional for gastric adenomas to
have a stalk, particularly a long one, and most of them are sessile. They can be
very flat, slightly elevated tumours and are more often single than multiple.
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Most gastric adenomas are of the intestinal type, which suggests that they
have developed on a basis of atrophic gastritis and intestinal metaplasia. Gastric
adenomas are uncommon but have a very significant potential for malignant
change.
It is possible that only a small minority of gastric cancers arise from
previously benign adenomas. The diagnosis of benign adenoma must be made
with care, because multiple sections through the tumour may show signs of
intramucosal carcinoma.
Mentriers Disease
There is a growing list of case reports of carcinoma of the stomach
complicating Menetrier's disease. The statistical risk of cancer in this disease is not
known, and anyway the diagnosis of Menetrier's disease is difficult to define both
clinically and pathologically.
There are descriptions of both intestinal metaplasia and epithelial dysplasia
of gastric epithelium in some of the reports.22
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CLINICAL MANIFESTATIONS
Most patients who are diagnosed with gastric cancer in the United States
have advanced stage III or IV disease at the time of diagnosis. The most common
symptoms are weight loss and decreased food intake due to anorexia and early
satiety. Abdominal pain (usually not severe and often ignored) also is common.
Other symptoms include nausea, vomiting, and bloating. Acute GI bleeding is
somewhat unusual (5%), but chronic occult blood loss is common and manifests
as iron deficiency anemia and heme-positive stool. Dysphagia is common if the
tumor involves the cardia of the stomach. Paraneoplastic syndromes such as
Trousseau's syndrome (thrombophlebitis), acanthosis nigricans
(hyperpigmentation of the axilla and groin), or peripheral neuropathy are rarely
present.
Physical examination usually is normal. Other than signs of weight loss,
specific physical findings usually indicate incurability. A focused examination in a
patient in whom gastric cancer is a likely part of the differential diagnosis should
include an examination of the neck, chest, abdomen, rectum, and pelvis. Cervical,
supraclavicular (on the left referred to as Virchow's node), and axillary lymph
nodes may be enlarged, and today can be sampled in the office with fine-needle
aspiration cytology. There may be a metastatic pleural effusion, or aspiration
pneumonitis in a patient with vomiting and/or obstruction.
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An abdominal mass could indicate a large (usually T4 incurable) primary
tumor, liver metastases, or carcinomatosis (including Krukenberg's tumor of the
ovary). A palpable umbilical nodule (Sister Joseph's nodule) is pathognomonic of
advanced disease, or there may be evidence on exam of malignant ascites.1
Gastric carcinoma may also present as multiple cutaneous nodules.23
Rectal exam may reveal heme-positive stool and hard nodularity
extraluminally and anteriorly, indicating so-called drop metastases, or rectal shelf
of Blumer in the pouch of Douglas.1
Preoperative Evaluation
Radiologic examination of the stomach can identify advanced gastric
cancers; however it is less accurate than endoscopy for identification of early
gastric cancer. All ulcers identified by x-ray examination should be referred for
endoscopic biopsy.
Radiologic criteria that suggest a benign ulcer include radiating folds and a
normal-appearing mucosal surface around the crater. Linitus plastica is suggested
by radiologic studies that demonstrate a nondistensible stomach.
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Endoscopy
When gastric cancer is suspected based on history and physical
examination, flexible upper endoscopy is the diagnostic modality of choice.
Although double-contrast barium upper GI radiography is cost-effective with 90%
diagnostic accuracy, the inability to distinguish benign from malignant gastric
ulcers makes endoscopy preferable. During endoscopy, multiple biopsy samples
(seven or more) should be obtained around the ulcer crater to facilitate histologic
diagnosis. When multiple biopsy specimens are taken, the diagnostic accuracy of
the procedure approaches 98%.
The addition of direct brush cytology to multiple biopsy specimens may
increase the diagnostic accuracy of the study. Additionally, the size, location, and
morphology of the tumor should be noted and other mucosal abnormalities
carefully evaluated. In select patients with advanced disease,
esophagogastroduodenoscopy provides a means for palliation through the use of
laser ablation, dilation, or tumor stenting. Although not included in the National
Comprehensive Cancer Network guidelines for the evaluation of gastric
adenocarcinoma, some centers are using endoscopic Ultrasonography (EUS) to
assist in the staging of this disease. EUS can gauge the extent of gastric wall
invasion as well as evaluate local nodal status. However, EUS cannot reliably
distinguish tumor from fibrosis; therefore, it is not a good modality for evaluating
response to therapy.2
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CT scan
Computed tomography (CT) scans of the chest and abdomen are the
primary imaging modalities for preoperative staging of stomach. In stomachs that
are well distended with contrast, wall thickness of >2 cm indicates transmural
extension of the tumor. Evidence of direct invasion of perigastric fat, diaphragm,
pancreas, transverse colon, and left lobe of the liver should be sought. Metastases
to the liver, lung, and other organs can also be documented.
For gastric adenocarcinoma overall accuracy of preoperative CT scans
ranges from 61 to 72%. 23 In women, a pelvic CT scan or ultrasound is also
recommended. CT of the chest may be needed for proximal gastric cancers The
major limitations of CT are in the evaluation of early gastric primaries and in the
detection of small (
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Positron Emission Tomography
Whole-body PET scanning uses the principle that tumor cells preferentially
accumulate positron-emitting 18F-fluorodeoxyglucose. This modality is most
useful in the evaluation of distant metastasis in gastric cancer but can also be
useful in locoregional staging. PET scan is most useful when combined with spiral
CT (PET-CT) and should be considered before major surgery in patients with
particularly high-risk tumors or multiple medical comorbidities.23
Laparoscopy
Because of the inaccuracy of CT and other modalities for the detection of
macrometastases smaller than 5 mm on the peritoneal surface or liver, laparoscopy
is recommended as the next step in the evaluation of patients with locoregional
disease. Laparoscopy can detect metastatic disease in 23% to 37% of patients
judged to be eligible for potentially curative resection by current-generation CT
scanning.
Laparoscopy may therefore improve palliation by avoiding a
nontherapeutic laparotomy in patients presumed to have localized gastric cancer.
The addition of laparoscopic ultrasonography may increase the sensitivity of
laparoscopic staging in gastric cancer as it has in other abdominal malignancies.
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Cytologic analysis of peritoneal fluid or of fluid obtained by peritoneal
lavage may reveal the presence of free intraperitoneal gastric cancer cells,
identifying patients with otherwise occult carcinomatosis. More sensitive methods
of detecting free intraperitoneal gastric cancer cells, such as immunostaining and
reverse-transcriptase polymerase chain reaction for carcinoembryonic antigen
(CEA) messenger RNA, are under investigation.2
STAGING
Many staging systems have been proposed for gastric adenocarcinoma. A
basic understanding of the older systems is necessary to understand the literature.
The pathologic staging system currently in use worldwide is the AJCC TNM
staging system. The TNM system can adequately stratify patients into distinct
groups with different risks for tumor-related death. A major revision occurred in
the AJCC staging system for gastric cancer in 1997 when nodal status
stratification was changed from location of nodes to number of positive nodes. In
the current staging system, a minimum of 15 nodes must be evaluated for accurate
staging. Nodal staging is then determined by the number of positive nodes, with
pN1 reflecting 1 to 6 positive nodes, pN2 designating 7 to 15 positive nodes, and
pN3 more than 15 positive nodes. 2
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TNM STAGING OF GASTRIC CARCINOMA
Table 3TNM staging of gastric carcinoma
Table 4: Staging of gastric carcinoma Fig .4 T Stage defined by depthof penetration into gastric wall
T: Primary tumor
Tis Carcinoma in situ; intraepithelial tumor without invasion of lamina propriaT1 Tumor invades lamina propria or submucosaT2 Tumor invades muscularis propria or subserosaT3 Tumor penetrates serosa (visceral peritoneum) without invasion of adjacent
structuresT4 Tumor invades adjacent structures
N: Regional lymph node
N0 No regional lymph node metastasisN1 Metastasis in 1 to 6 regional lymph nodesN2 Metastasis in 7 to 15 lymph nodes
N3 Metastasis in more than 15 regional lymph nodesM: Distant metastasisM0 No distant metastasisM1 Distant metastasis
STAGE T N M
0 Tis N0 M0IA T1 N0 M0IB T1 N1 M0
T2 N0 M0II T1 N2 M0
T2 N1 M0T3 N0 M0
IIIA T2 N2 M0T3 N1 M0T4 N0 M0
IIIB T3 N2 M0
IV T4 N1-3 M0T1-3 N3 M0Any T Any N M1
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Resection classification
The termR statuswas first described by Hermanek in 1994 and is used to
describe the tumor status after resection. R0 describes a microscopically margin-
negative resection, in which no gross or microscopic tumor remains in the tumor
bed. R1 indicates removal of all macroscopic disease, but microscopic margins are
positive for tumor. R2 indicates gross residual disease. Because the extent of
resection can influence survival, some authors include this R designation to
complement the TNM system. Long-term survival can be expected only after an
R0 resection; therefore, a significant effort should be made to avoid R1 or R2
resections.
Knowledge of the older staging systems and the Japanese system is crucial
to the understanding of the debate regarding lymphadenectomies for gastric
cancer. The Japanese Classification for Gastric Carcinoma (JCGC) staging system
was designed to describe the anatomic locations of nodes removed during
gastrectomy. Sixteen distinct anatomic locations of lymph nodes are described ,
with the recommendation for nodal basin dissection dependent on the location of
the primary. The lymph node stations or echelons are numbered and then further
classified into groups of echelons that correspond to the location of the primary
and reflect the likelihood of harboring metastases . The presence of metastasis to
each lymph node group then determines the N classification. For example,
metastases to any of the group 1 lymph nodes in the absence of disease in more
distant lymph node groups is classified as N1. 2
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Table 5 Japanese Gastric Cancer Association Staging System for Gastric Cancer
TUMOR STAGET1 Tumor invasion of mucosa and/or muscularis mucosa (M) or submucosa (SM)T2 Tumor invasion of muscularis propria (MP) or subserosa (SS)
T3 Tumor penetration of serosal (SE)T4 Tumor invasion of adjacent structures (SI)TX UnknownNODAL STAGE
N0 No evidence of lymph node metastasisN1 Metastasis to group 1 lymph nodes, but no metastasis to groups 2 to 3 lymph
nodesN2 Metastasis to group 2 lymph nodes, but no metastasis to group 3 lymph nodesN3 Metastasis to group 3 lymph nodesNX Unknown
HEPATIC METASTASIS STAGE (H)H0 No liver metastasisH1 Liver metastasisHX UnknownPERITONEAL METASTASIS STAGE (P)P0 No peritoneal metastasisP1 Peritoneal metastasisPX UnknownPERITONEAL CYTOLOGY STAGE (CY)CY0 Benign/indeterminate cells on peritoneal cytologyaCY1 Cancer cells on peritoneal cytology
CYXPeritoneal cytology was not performedOTHER DISTANT METASTASIS (M)M0 No other distant metastases (although peritoneal, liver, or cytological metastases
may be present)M1 Distant metastases other than the peritoneal, liver, or cytological metastasesMX UnknownSTAGE GROUPING
N0 N1 N2 N3T1 IA IB IIT2 IB II IIIA
T3 II IIIA IIIB IVT4 IIIA IIIBH1, P1, CY1, M1aCytology felt to be suspicious for malignancy should be classified as CY0.
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Fig 5 Lymph node station numbers as defined by Japanese Cancer Association
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LOCATION OF PRIAMRY TUMOUR INTHE STOMACH
LYMPH NODE STATION(No) DESCRIPTION Upper third Middle third Lower third
1 Right paracardial 1 1 2
2 Left paracardial 1 3 M
3 Lesser curvature 1 1 1
4sa Short gastric 1 3 M
4sb Left gastroepiploic 1 1 3
4d Right gastroepiploic 2 1 1
5 Suprapyloric 3 1 1
6 Infrapyloric 3 1 1
7 Left gastric artery 2 2 2
8a Anterior comm. hepatic 2 2 2
8p Posterior comm. hepatic 3 3 3
9 Celiac artery 2 2 2
10 Splenic hilum 2 3 M
11p Proximal splenic 2 2 2
11d Distal splenic 2 3 M
12a Left hepatoduodenal 3 2 2
12b,p Posterior hepatoduodenal 3 3 3
13 Retropancreatic M 3 3
14v Superior mesenteric vein M 3 2
14a Superior mesenteric artery M M M
15 Middle colic M M M
16al Aortic hiatus 3 M M
16a2,b1 Para-aortic, middle M 3 3
16b2 Para-aortic, caudal M M M
M, lymph nodes regarded as distant metastasis
Table 6- Grouping of Regional Lymph Nodes (Groups 1-3) by Location of Primary
Tumor According to the Japanese Classification of Gastric Carcinoma
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Spread of carcinoma of the stomach
No better example of the various modes by which carcinoma spreads can
be given than the case of stomach cancer. It is important to note that this distant
spread is unusual before the disease spreads locally and distant metastases are
uncommon in the absence of lymph node metastases. The intestinal and diffuse
types of gastric cancer spread differently. The diffuse type spreads via the
submucosal and subserosal lymphatic plexus and it penetrates the gastric wall at
an early stage.
Direct spread
The tumour penetrates the muscularis, serosa and ultimately adjacent
organs such as the pancreas, colon and liver.
Lymphatic spread
This is both by permeation and emboli to the affected tiers (see below) of
nodes. This may be extensive, the tumour even appearing in the supraclavicular
nodes (Trosiers sign). Unlike malignancies such as breast cancer, nodal
involvement does not imply systemic dissemination.
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Blood-borne metastases
This occurs first to the liver and subsequently to other organs including
lung and bone. This is uncommon in the absence of extensive nodal disease.
Trans peritoneal spread
This is a common mode of spread once the tumour has reached the serosa
of the stomach and indicates incurability. Tumours can manifest anywhere in the
peritoneal cavity and commonly give rise to ascites. Advanced peritoneal disease
may be palpated either abdominally or rectally as a tumour shelf.
The ovaries may sometimes may be the sole site of transcoelomic spread
(Krukenbergs tumours). Tumour may spread via the abdominal cavity to the
umbilicus (Sister Josephs nodule). 25
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TREATMENT OF LOCALIZED DISEASE
STAGE I DISEASE (EARLY GASTRIC CANCER) Classification and Risk
for Nodal Metastases
The Japanese Research Society for Gastric Cancer has classified early
gastric cancers (EGC) based on endoscopic criteria first established by the
Japanese Endoscopy Society for the description of T1 tumors.
The current classification system is used for both in situ and invasive
tumors and categorizes tumors based on endoscopic findings as follows:
Figure 6 .Japanese classification system for early gastric cancer. In the combinedsuperficial types, the type occupying the largest area should be described first,followed by the next type (e.g., IIc + III). Type 0I and Type 0IIa are distinguished asfollows: Type 0I: The lesion has a thickness of more than twice that of the normalmucosa. Type 0IIa: The lesion has a thickness up to twice that of the normal mucosa.
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Considering the risk for lymph node metastasis is important when
evaluating treatment options for patients with EGC. The frequency and anatomic
distribution of nodal disease are related to the depth of tumor invasion. 10
Treatment options for patients with EGC include
- Endoscopic Mucosal Resection (EMR),
- Limited surgical resection,
- Gastrectomy.
Endoscopic Mucosal Resection
This approach involves the submucosal injection of fluid to elevate the
lesion and facilitate complete mucosal resection under endoscopic guidance. Only
patients with tumors that have extremely low metastatic potential should be
offered EMR.
These are generally well-differentiated, superficial type IIa or IIc lesions
smaller than 3 cm in diameter and located in an easily manipulated area. Tumors
invading the submucosa are at increased risk for metastasizing to lymph nodes and
are not usually considered candidates for EMR.
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Limited Surgical Resection
Given the low rate of nodal involvement for patients with EGC, limited
resection may be a reasonable alternative to gastrectomy for some patients with
early EGC. There are no well-accepted pretreatment criteria for selection of
patients for limited resection. Based on the existing pathology data, patients with
small (less than 3 cm) intramucosal tumors and those with nonulcerated
intramucosal tumors of any size may be candidates for EMR or limited resection.
Surgical options for these patients may include gastrectomy with local excision.
Gastrectomy
Gastrectomy with lymph node dissection should be considered for patients
with EGC who cannot be treated with EMR or limited surgical resection and/or
patients who have intramucosal tumors with poor histologic differentiation or size
greater than 3 cm or who have tumor penetration into the submucosa or beyond.
Gastrectomy with lymph node dissection allows for adequate pathologic staging
and local therapy for these higher-risk patients.
There is no consensus on the extent of lymphadenectomy that should be
performed as part of gastrectomy for EGC. Dissection of level I lymph nodes is a
reasonable minimum standard at this time.
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STAGE II AND STAGE III DISEASE
Surgery
Surgical resection is the cornerstone of treatment for patients with localized
gastric cancer. However, for stages II and III disease, surgery is necessary but
often not sufficient for cure. The general therapeutic goal is to achieve a micro-
and macroscopically complete resection (R0). 10
Extent of Gastric Resection
There is no evidence that an extended gastric resection above and beyond
complete clearance of the primary tumor improves survival; i.e., total gastrectomy
does not improve survival over distal or proximal gastrectomy, provided that thetumor is removed completely with negative transection margins (R0 resection).
This has been confirmed in a number of randomized trials. The extent of
the gastrectomy therefore is site-dependent and focuses on complete removal of
the gastric carcinoma with preferably a 4- to 5-cm margin from the gross edge of
the tumor. Clearly, anatomic limitations influence this margin because in antral
lesions close to or involving the pylorus, only a limited portion of the duodenum
can be removed.
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In similar fashion, a lesser extent of uninvolved esophageal margin may be
acceptable provided complete histologic resection is possible.
In patients with a distal lesion, a distal subtotal gastrectomy is performed
essentially regardless of T stage. For proximal gastric cancers and true GE
junction cancers (Siewert types II and III), sub diaphragmatic proximal
gastrectomy with esophagogastrectomy, can be liberally used whereas some prefer
total gastrectomy for any lesion not in the antrum.
For midbody or more extensive lesions, total gastrectomy is required,
whereas for more distal lesions, a subtotal gastrectomy is the preferred approach.
It is important to emphasize that in most studies there is an increase in morbidity
and mortality when total gastrectomy is performed over distal subtotal
gastrectomy. Since long-term survival is not improved by the more extensive
resection, this is a further factor in favor of subtotal resection, provided that an R0
resection can be obtained.
Proximal resections, however, appear to have similar perioperative
morbidity and mortality to total gastrectomy.
Extended organ resection is reserved for patients with apparently node-
negative T4 lesions, in which complete resection requires resection of the invaded
portions of the diaphragm, pancreas, spleen, adrenal gland, or colon.27
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Extent of Lymphadenectomy
The dialogue surrounding lymphadenectomy involves at least two
important issues: (1) staging removal and histopathologic analysis of an adequate
number of lymph nodes, and (2) therapy determining if some forms of
lymphadenectomy are therapeutic for patients with gastric cancer.
The current AJCC staging system (sixth edition) requires analysis of 16 or more
lymph nodes to assign a pathologic N stage.
Adjuvant Therapy
The term adjuvant therapy is best used to describe additional treatment in
an attempt to increase cure rates in patients who have already undergone a
potentially curative resection. For gastric cancer, an R0 surgical procedure, in
which all gross disease has been removed, the margins of resection are
microscopically negative, and no distant metastases were found, is required before
adjuvant therapy is considered. Resections that leave microscopic or gross residual
disease are not adjuvant treatment, but rather therapy of known residual cancer.
The term perioperative chemotherapy (or neoadjuvant chemotherapy) involves the
use of systemic treatment before definitive, potentially curative surgery.
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Adjuvant Postoperative Systemic Therapy
Adjuvant postoperative systemic chemotherapy has not shown a significant
advantage over surgery alone.
Postoperative Adjuvant Intraperitoneal Chemotherapy
Peritoneal recurrence is a common component of the failure pattern for
patients with gastric cancer. The rationale for the use of intraperitoneal treatment
is based on the pharmacokinetic observation that drug concentrations within the
peritoneal cavity after intraperitoneal administration are much higher than those
achievable intravenously or orally.
For gastric cancer, an increasing number of reports have been published in
which immediate postoperative intraperitoneal therapy was given after potentially
curative resection. However, no definitive conclusions can yet be drawn regarding
the effectiveness of intraperitoneal postoperative chemotherapy in this setting.
Immunochemotherapy
The use of adjuvant immunostimulants (either protein-bound
polysaccharide (PSK) or a Streptococcus pyrogenes preparation, OK432) given in
association with cytotoxic chemotherapy has been studied, however larger studies
that are adequately powered would be necessary to definitively evaluate this
approach.
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Perioperative (Neoadjuvant) Chemotherapy
Perioperative (pre- and postoperative) chemotherapy, also known as
neoadjuvant chemotherapy, is an attractive concept in gastric cancer because many
patients, particularly Western patients, have locally advanced tumors at diagnosis
(T3 or T4, or obvious lymph node involvement).
Such patients are not only at substantial risk for distant metastasis, but local
extent of the tumor may make an R0 resection difficult.
There are two goals to perioperative treatment: reduce the stage of the
primary tumor to increase the likelihood that a R0 resection can be performed, and
begin at an early time to treat micrometastatic disease.
Adjuvant Radiation and Chemoradiation Therapy
Most of the studies that have evaluated radiation therapy as an adjuvant
have used concomitant 5-FU chemotherapy. There was a significant improvement
in survival with the combination of 5-FU and radiation compared with radiation
alone.
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Technical Treatment-Related Issues
Surgery
Beginning with laparoscopy allows for careful intraoperative staging of
disease. Inspection for the presence of ascites, hepatic metastases, peritoneal
seeding, disease in the pelvis (such as a metastasis), or ovarian involvement should
be performed. Once distant metastases have been ruled out, depending on the
location of the lesion, a bilateral subcostal incision or a midline abdominal
incision can be used to gain adequate exposure to the upper abdomen.
The stomach should be inspected to assess the location and extent of
tumor. The size and location of the primary tumor dictate the extent of gastric
resection. A D2 lymphadenectomy sparing the spleen and pancreas can be done
safely and provides an excellent specimen for surgical and pathologic staging, but
this procedure should only be performed by or with an experienced surgeon.
The D2 subtotal gastrectomy commences with mobilization of the greater
omentum from the transverse colon. After the omentum is mobilized, the anterior
peritoneal leaf of the transverse mesocolon is incised along the lower border of the
colon, and a plane is developed down to the head of the pancreas. The infrapyloric
lymph nodes are dissected and the origin of the right gastroepiploic artery and vein
are ligated.
With a combination of blunt and sharp dissection, the plane of dissection
continues on to the anterior surface of the pancreas, extending to the level of the
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common hepatic and splenic arteries. This maneuver can be tedious, but
theoretically it provides additional protection against serosal spread of tumor to
the local peritoneal surface.
The right gastric artery is ligated. At this point, the duodenum is divided
distal to the pylorus. The stomach and omentum are then reflected cephalad. The
gastro hepatic ligament is divided close to the liver up to the gastro esophageal
junction. Dissection is then continued on the hepatic artery toward the celiac axis.
Once near the celiac axis, the lymph node bearing tissue is dissected until
the left gastric artery is visualized and can be divided at its origin.
The proximal peritoneal attachments of the stomach and distal esophagus
can then be incised, and the proximal extent of resection is chosen. For tumors of
the mid- and proximal stomach, dissection of the lymph nodes along the splenic
artery and splenic hilum is important.
This technique is not indicated for antral tumors, given the low rate of
splenic hilar nodal metastases seen with these tumors. The stomach is then divided
5 cm proximal to the tumor, which dictates the extent of gastric resection.
Despite the fact that the entire blood supply of the stomach has been
interrupted, a cuff of proximal stomach invariably shows good vascularization
from the feeding distal esophageal arcade.
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When feasible, most surgeons prefer to anastomose jejunum to stomach
versus esophagus because of the technical ease and excellent healing.
Reconstruction using a variety of techniques has been described and is a matter of
personal choice.
TREATMENT OF ADVANCED DISEASE (STAGE IV)
Chemotherapy versus Best Supportive Care
Patients receiving chemotherapy as part of their treatment have a better
overall survival than those receiving best supportive care only, with an overall
hazard ratio of 0.39 (95% CI, 0.28 to 0.52). The median survival was improved
from 4.3 months for best supportive care to approximately 11 months for
chemotherapy.
Single-Agent Chemotherapy
For most drugs, a variety of doses and schedules have been studied. In the
absence of comparative trials using the same agent with different doses and
schedules, superiority of one regimen over the other cannot be assessed.
Combination Chemotherapy
Like other malignancies, multidrug regimens using agents that have a
single-agent activity have been extensively studied in gastric cancer.
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One of the most widely used combination chemotherapy regimens in upper
gastrointestinal tract malignancies, including gastric cancer, is the two-drug
combination of cisplatin and fluorouracil.
Other combination chemotherapy regimens include methotrexate,
fluorouracil, and doxorubicin (FAMTX); etoposide, leucovorin, and fluorouracil
combination; fluorouracil plus irinotecan; docetaxel added cisplatin fluorouracil;
epirubicin-cisplatin-fluorouracil; irinotecan-fluorouracil-leucovorin ; Cisplatin
Plus Irinotecan; Fluorouracil-Leucovorin-Oxaliplatin (FOLFOX)
Targeted Therapy
Bevacizumab
As with other solid tumors, including colorectal cancer, breast and lung
cancers, therapeutic agents with a specific tumor target are now entering study in
gastric and gastroesophageal junction tumors. One of the first compounds studied
was bevacizumab, a humanized monoclonal antibody that binds the vascular
endothelial growth factor ligand. Bevacizumab can safely be given with cytotoxic
chemotherapy, including in patients in whom the primary tumor was still in place.
Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors
Both erlotinib and gefitinib have been studied in gastroesophageal junction
and gastric cancers. The bulk of the data is currently available only an abstract
form. Cetuximab, an antibody to the epidermal growth factor receptor, is
undergoing study as a single agent and also in combination with systemic
cytotoxic chemotherapy.
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Radiation for Palliation
To date, no studies have evaluated the use of radiation therapy in patients
with locally recurrent or metastatic carcinoma of the stomach. Its use is likely to
be limited to palliation of symptoms such as bleeding or controlling pain
secondary to local tumor infiltration.
Although minimal data are available, radiation therapy seems to be fairly
effective (from anecdotal experience) in controlling bleeding, as is true in other
sites. This can often be accomplished at relatively low radiation doses. Pain from
local tumor invasion can also be palliated, although the dose required is higher (45
Gy).
Long-Term Side Effects of Therapy
Relatively little has been written in the oncology literature on the local
effects of therapy for gastric cancer and its long-term implications. The presence
of dumping syndrome is well known, with its resulting diarrhea and cramping, but
vasomotor effects such as palpitations and diarrhea also occur either very shortly
after a meal or 1 to 3 hours later. These symptoms probably result from rapid
transit of food from the stomach into the small bowel with the release of various
gastrointestinal hormones. These symptoms can be managed by adjusting the
volume of oral intake and other dietary manipulations. There is also a reactive
hypoglycemia that can result from the rapid insulin release after a meal with little
gastric reservoir.In addition to dumping, there are a number of malabsorption
issues that can be important. B12malabsorption is well known, and many patients
are placed on monthly supplements, even if it is not clearly needed.
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After partial gastrectomy one can often monitor B12 levels and replace
when needed. Iron and calcium absorption is improved by the gastric acid that is
eliminated or decreased by surgery or radiation therapy, and bypassing the
duodenum also decreases absorption. Low iron is discovered when patients
develop an iron deficient anemia, but calcium malabsorption may not be found for
many years when the patient develops osteopenia. Patients should be followed
with dual energy x-ray absorptiometry scans and/or placed on calcium
supplementation (calcium citrate is better absorbed than calcium carbonate).
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METHODOLOGY
The present study was undertaken at K.R. Hospital , Mysore from the period
January 2009 to July 2010 and included patients presenting to the out and in
patient departments at K.R.Hospital, Mysore. The tissue for diagnosis was
obtained by endoscopy or following surgical resection.
Source of Data
Patients presenting to K.R. Hospital, Mysore during the study period and those
found eligible were included in the study.
Sample size: Minimum of twenty five cases meeting criteria of the present study
Inclusion Criteria
Only patients with histological proven carcinoma stomach were included
Exclusion criteria
Patients with tumour recurrence
Investigations
Routine Blood investigations like Haemoglobin%, Total Count, Differential
Count, Bleeding Time, Clotting time.
Renal parameters like Blood Urea and Serum Creatinine
Liver Function Tests
Serum Electrolytes
Chest X-Ray
Blood Grouping
Special investigationslike Upper Gastointestinal Endoscopy, USG Abdomen and
CT Scan Abdomen
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The cases were studied with importance given to clinical history regarding nature
of presentation including diet history. The study of association of risk factors was
also undertaken. Thorough clinical examination, Ultrasonography, endoscopy, CT
in few cases and histopathologic diagnosis formed the basis of the study.
The anatomic site of occurrence, the macroscopic type and the histopathologic
type were studied in each case.
An earnest attempt was made to study all the cases in detail with serial follow-up,
the latter being incomplete due to non-responsive patients.
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RESULTS
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RESULTS
ANNUAL PREVALENCE: Graph-1
Gastric carcinoma is a common cancer with almost evenly distributed
annual prevalence.
The number of cases reported was greater in the first half of the year.
Graph-1
Annual distribution of cases from 2009 to July 2010
0
2
46
8
Jan Feb Mar Apr May Jun Jul Aug Sep Oct Nov Dec
No.ofcas
es
2010
2009
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SEX PREVALENCE: Table 7; Graph 2
Gastric cancer is more common in males with 75% of the cases being
males in this study. The Male: Female ratio was 3:1.
Table-7. Sex distribution among carcinoma stomach patients
SexPresent study
Cases %
Male 24 75
Female 8 25
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AGE PREVALENCE: Table 8; Graph 3
Carcinoma stomach is more common in the older age group with
increasing incidence after the age forty five. The maximum number of cases was
seen between the age groups 45 to 65. The youngest patient was aged 33 and the
oldest 79.
Table-8. Age distribution among carcinoma stomach patients
AgePresent study
Total % M F
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SOCIOECONOMIC STATUS: Table 9; Graph 4
In the present study majority of the patients(75%) belonged to the low
socioeconomic status. The prevalence among the high socioeconomic group could
not be studied as none of the patients belonged to this strata.
Table 9- Income group among carcinoma stomach patients
Income Group Present study
Cases %
Low 28 87.5
Middle 4 12.5
High 0 -
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RISK FACTORS: Table 10; Graph 5.0, 5.1
There are strong suggestions of the influence of environmental factors on
gastric cancer. The most common risk factors associated were spicy food and
mixed diet followed by tobacco and alcohol use.
In this study twenty seven(84.4%) patients consumed mixed diet and the
rest were vegetarians. The non vegetarians took meat/fish approx. thrice every
week.
All patients in the study group frequently and regularly consumed green
leafy vegetables.
Fruit consumption was frequent only in twenty two(68.7%) of the cases
with predominant of them being males(86.4%). Only three(13.6%) of the females
frequently consumed fruits.
High salt intake was not reported by any of the subjects in this study
although this value was not quantified and hence significance could not be
ascertained.
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Smoked foods though a common risk factor in many countries was
consumed only by Five (15.6%) of the patients and even in theses patients the
intake was not frequent. Majority of the patients, twenty seven(84.4%) reported to
the use of high spicy diet in everyday food.
Tobacco smoking in the form of cigarette and beedi smoking was seen in
nineteen (59.3%) patients, all being males. Five females and three males reported
to frequent use of betelnut which has been shown to a risk factor in the
development of gastric cancer.
Alcohol consumption was seen in sixteen(50%) of the patients, all males,
who consumed it regularly and for a period of more than ten years.
Table 10 - Comparision of risk factors between males and females, F- Frequent,O-Occasional
Risk factor Total Males(24) Females(8)
Cases % Cases % Cases %
Mixed diet 27 84.4 20 74.1 7 25.9
Veg diet 5 15.6 4 80 1 20
Green leafy F 32 100 24 75 8 25
O 0 0 - 0 -
Fruits F 22 68.7 19 86.4 3 13.6
O 10 31.3 5 50 5 50
High salt intake 0 - - - -
Smoked Foods 5 15.6 4 80 1 20
Spicy 27 84.4 21 77.7 6 22.2
Smoking 19 59.3 19 100 - -
Alcohol 16 50 16 100 - -
Betel nut 8 25 3 37.5 5 62.5
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BLOOD GROUP: Table 11; Graph 6
Blood group A showed the highest association with gastric cancer patients
with fourteen(43.7%) cases followed by blood group O and B.
Table 11 - Blood group distribution in carcinoma stomach patients
Study Blood Group (%)A + B+ AB+ O+
Present Study 14(43.7) 5(15.6) 1(3.1) 12(37.5)
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SYMPTOMS: Table 12, Graph 7
Anorexia was the most common symptom in patients and was reported in
twenty six (81.25%) of the patients. The next most common symptom was nausea
and vomiting reflecting the high prevalence of distal tumours. Twenty three
(71.8%) reported weight >10% of body weight.
Proximal tumours involving the gastooesophageal junction had dysphagia
as the predominant symptom. Only one patient in this study presented with
jaundice and none of the patients had supraclavicular lymphadenopathy at
presentation. One patient presented with features of peritonitis and was found to
have a growth in the body of the stomach which had perforated.
Early satiety was reported in sixteen (50%) of the patients which is
characteristic of tumours involving the stomach wall diffusely.
Symptom analysis among the two sexes revealed that nausea, vomiting and
weight loss were the most common symptoms followed by pain abdomen in
females. The most common symptoms in males were anorexia, abdominal pain
followed by nausea and vomiting.
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Table 12-Symptom analysis in patients of carcinoma stomach
Symptoms
Present study Males n=24 Females n=8
Cases % Cases % Cases %
Abdominal Pain 22 68.75 16 66.6 6 75
Nausea/vomiting 24 75 19 79.2 5 62.5
Weight loss 23 71.8 15 62.5 8 100
Anorexia 26 81.25 18 75 8 100
Early satiety 16 50 12 50 4 50
Jaundice 1 3.2 1 4.2 - -
Dysphagia 5 15.6 4 16.6 1 12.5
Malaena 7 21.8 5 20.8 2 24
Others 2 6.25 1 4.4 1 12.5
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SIGNS: Table 13, Graph 8
Overall, anemia was the most common sign in twenty one (65.6%) of the
cases followed by dehydration and ascites.
Visible gastric peristalsis the characteristic sign of gastric cancer was seen
only in four (12.5%) of the cases. Gastric cancer presented as mass abdomen in
six (18.75%) cases.
In females, anemia and ascites were the most common symptoms. None of
the females in this study had visible gastric peristalsis which was seen in three
(12.5%) of males.
Presentation with mass abdomen was commoner in females (37.5%) than
in males (12.5%).
Ascites at presentation suggesting the advanced stage of the disease was
more common in females (50%) compared to males (31.25%).
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Table 13 - Analysis of signs in gastric cancer patients
Signs Total
cases
% Male n=24 Female n=8
Cases % Cases %
Anemia 21 65.6 14 58.3 7 87.5
Icterus 1 3.12 1 4.2 - -
Dehydration 10 31.25 7 29.2 3 37.5
Ascites 10 31.25 6 25 4 50
VGP 4 12.5 4 16.6 - -
Mass abdomen 6 18.75 3 12.5 3 37.5
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SUBSITES: Table 14; Graph 9
The antrum was the most common site of affliction accounting for 75% of
all subsites. This was also similar in both the sexes with percentages of 70.8 in
males and 87.5 in females. Oesophagogastric tumours accounted for 9.37% of the
cases and were similar in both the sexes. None of the females in this study had
cancers of the body and proximal stomach.
Table 14- Sub site specific trends in carcinoma stomach
Sub site Total Male Female
Cases % Cases % Cases %
Oesophagogastric jn 3 9.37 2 8.3 1 12.5
Proximal stomach 2 6.25 2 8. 0 -
Body 3 9.37 3 12.5 0 -
Antrum 24 75 17 70.83 7 87.5
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MACROSCOPY: Table 15
The