This is a type of gastritis once referred to as Type A gastritis.
Epidemiology Disease Associations Pathogenesis Laboratory/Radiologic/Other Diagnostic Testing Gross Appearance and Clinical Variants Histopathological Features and Variants Special Stains/Immunohistochemistry/Electron Microscopy Differential Diagnosis Prognosis and Treatment Commonly Used Terms Internet Links
EPIDEMIOLOGY CHARACTERIZATION SYNONYMS Type A gastritis INCIDENCE AGE RANGE-MEDIAN SEX (M:F) GEOGRAPHY
DISEASE ASSOCIATIONS CHARACTERIZATION ANEMIA
High prevalence of atrophic body gastritis in patients with unexplained microcytic and macrocytic anemia: a prospective screening study.
Marignani M, Delle Fave G, Mecarocci S, Bordi C, Angeletti S, D'Ambra G, Aprile MR, Corleto VD, Monarca B, Annibale B.
Gastroenterology Department, Universita degli Studi di Roma La Sapienza, Italy.
Am J Gastroenterol 1999 Mar;94(3):766-72 Abstract quote
OBJECTIVE: Atrophic body gastritis (ABG) is characterized by atrophy of the gastric body mucosa, hypergastrinemia, and hypo/achlorhydria. Its association with pernicious anemia is well recognized. Gastric hypo/achlorhydria is known to affect iron absorption but ABG is rarely considered as a possible cause of iron deficiency (microcytic) anemia. The aims of this study were to validate a screening methodology for the detection of ABG in a consecutive series of patients with microcytic and macrocytic anemia and to investigate the clinical and gastric morphofunctional characteristics of the two hematological presentations of ABG.
METHODS: A two-part prospective study was carried out. Part A aimed to validate the screening methodology to detect the presence of ABG in patients with macrocytic and microcytic anemia who have no specific GI symptoms, by measuring their gastrin levels and verified by performing gastroscopy with biopsy. Part B aimed to detect the presence of ABG in a larger sample of anemic patients by our validated method and, by pooling the data of ABG patients, to determine the clinical, gastric histological, and functional characteristics pertaining to the macrocytic and microcytic presentations of ABG.
RESULTS: In part A, ABG was detected in 37.5% of patients with macrocytic and in 19.5% of those with microcytic anemia. Pooling the data of the ABG patients from part A and part B, microcytic ABG patients were on average 20 yr younger than those with macrocytic anemia. The majority of microcytic ABG patients were female, most of whom were premenopausal. H. pylori infection was widely represented in the microcytic ABG group (61.1%). They also had a lesser grade of body mucosal atrophy and lower hypergastrinemia levels, suggesting a less severe oxyntic damage of shorter duration.
CONCLUSIONS: Macrocytic anemia is not the only hematological presentation of ABG. Physicians evaluating patients with unexplained iron deficiency anemia should consider ABG as a possible cause by determining fasting gastrin levels and performing gastroscopy with biopsies of the body mucosa.
High Prevalence of Manifestations of Gastric Autoimmunity in Parietal Cell Antibody- Positive Type 1 (Insulin-Dependent) Diabetic Patients1
Christophe E. M. De Block, Ivo H. De Leeuw, Luc F. Van Gaal and the Belgian Diabetes Registry
Department of Endocrinology-Diabetology, University of Antwerp, University Hospital Antwerp (C.E.M.D.B., I.H.D.L., L.F.V.G.), B-2650 Edegem; and the Belgian Diabetes Registry, B-1090 Brussels, Belgium
Journal of Clinical Endocrinology & Metabolism Vol. 84, No. 11 4062-4067 Abstract quote
Previous studies have shown a high prevalence of gastric parietal cell antibodies (PCA) in type 1 diabetes, which can be accompanied by (sub)clinical autoimmune gastric disease. This study aimed to determine the grade of associated autoimmunity and to assess the pattern of prevalence of PCA by gender, age, duration of disease, age at onset of diabetes, and human leukocyte antigen (HLA) type in an adult type 1 diabetic population. Furthermore, to examine the clinical significance of being PCA positive, manifestations of gastric autoimmune disease were studied in PCA-positive and PCA-negative patients.
The population studied consisted of 497 type 1 diabetics (men/women, 252/245; mean age, 40.8 ± 12.1 yr; mean duration of disease, 16.4 ± 10.4 yr; mean age at onset, 26.9 ± 13.5 yr; mean hemoglobin A1c, 8.1 ± 1.6%). Associated autoantibodies were present in 39% and PCA were present in 20.9% of the subjects, particularly in older patients. Gender, duration, and age at onset of diabetes did not influence the appearance of PCA. Antithyroid peroxidase antibodies (aTPO) were more frequent in PCA-positive patients than in those without PCA (33.6% vs. 22.4%; P = 0.025), suggesting an association between gastric and thyroid autoimmunity. We could demonstrate an association between PCA and the HLA DR5 haplotype (P = 0.001) as well, but not with HLA DR3 and/or DR4. In the PCA-positive group, iron deficiency anemia was detected in 15.4%, and pernicious anemia was found in 10.5% of subjects. These autoimmune gastric manifestations were significantly more prevalent in PCA-positive diabetics than in PCA-negative subjects, in whom the percentages were 6.9% and 0.5%, respectively (P = 0.01 and P < 0.0001). PCA were prevalent in 84.6% of patients with pernicious anemia. A gastroscopic and anatomopathoplogical examination performed in a subgroup of 30 patients with gastric symptoms revealed atrophic gastritis in 13 of 14 PCA-positive patients and in 9 of 16 PCA-negative subjects (P = 0.04). PCA were present in 59.1% of patients with atrophic gastritis.
In conclusion, a high prevalence of parietal cell antibodies and associated autoimmune gastric disease is present in PCA-positive type 1 diabetics, recommending its screening. Early detection of PCA and iron deficiency anemia, pernicious anemia, and atrophic gastritis and the subsequent care could reduce the morbidity of type 1 diabetes.
Atrophic body gastritis: distinct features associated with Helicobacter pylori infection.
Annibale B, Marignani M, Azzoni C, D'Ambra G, Caruana P, D'Adda T, Delle Fave G, Bordi C.
Gastroenterology Unit, University La Sapienza Rome, Italy.
Helicobacter 1997 Jun;2(2):57-64 Abstract quote
BACKGROUND: Usually, atrophic body gastritis has been considered an autoimmune disease characterized by the presence of parietal cell antibodies. Previous investigations into the role of Helicobacter pylori infection have obtained conflicting results. The aim of this study was to investigate the prevalence and role of H. pylori in a prospectively investigated population of patients with corpus-predominant atrophic gastritis.
PATIENTS AND METHODS: A consecutive series of 67 newly diagnosed cases of atrophic body gastritis was derived from a screening of 326 patients with unexplained anemia or dyspepsia. Criteria for diagnosis were fasting hypergastrinemia, pentagastrin-resistant achlorhydria, and histological confirmation of body atrophy. In all 67 patients, H. pylori infection was evaluated independently by histological assay and urease test. The gastritis status of both the fundic and antral mucosa were graded according to the Sydney system. Parietal cell and intrinsic factor antibodies also were determined.
RESULTS: Active H. pylori infection was present in 26.8% of our patients and allowed us to identify a patient's subpopulation with a significantly smaller degree of body mucosa damage as shown by functional parameters (gastrin, gastric acid secretion, pepsinogen I) and histological assessment. In this subpopulation, a higher prevalence of gastric cancer familial history was found. Presence of parietal cell antibodies showed a similar prevalence in H. pylori-positive and H. pylori-negative patients (61.1% vs. 69.4%) and was not associated with significant functional and histological differences. Cure of infection determined an evident improvement of corporal atrophy as well as a reduction of hypergastrinemia.
CONCLUSION: Active H. pylori infection, a potential cause of oxyntic gland atrophy, is found in one-fourth of patients with newly diagnosed atrophic body gastritis.
Healing of Active, Non-Atrophic Autoimmune Gastritis by H. pylori Eradication.
Muller H, Rappel S, Wundisch T, Bayerdorffer E, Stolte M.
Institute for Pathology, Klinikum Bayreuth, University Hospital Carl-Gustav-Carus, Technical University of Dresden, Germany.
Digestion 2001;64(1):30-9 Abstract quote
Background and Aims: The antigastric antibodies present in Helicobacter pylori infection act as a marker for an ongoing antigastric autoimmune process in the gastric mucosa, which can already be diagnosed in the non-atrophic stage. In a retrospective, uncontrolled study, therefore, we investigated the question as to whether this type of gastritis can be healed by the eradication of H. pylori.
Patients and Methods: In 80 patients with an active, not yet atrophic autoimmune gastritis, we analysed a maximum of four investigations per patient over a period of up to 39.5 months. The following parameters were graded in the antral and corpus mucosa prior to and after H. pylori eradication treatment: grade and activity of the gastritis, H. pylori colonization, atrophy, parietal cell hypertrophy, and incidence of intestinal metaplasia. In addition, the typical parameters for this type of gastritis, such as grade of the periglandular lymphocytic infiltration, grade of glandular destruction and incidence of nodular ECL cell proliferates in the corpus mucosa were determined.
Results: In 64 patients (80%), H. pylori eradication treatment was followed by healing of the active autoimmune corpus gastritis, that is, the activity of the gastritis disappeared, and lymphocytic infiltration of the glands, glandular destruction and parietal cell hypertrophy was found to be significantly reduced.
Conclusions: Our uncontrolled, retrospective study confirms the existence of an active, not yet atrophic autoimmune gastritis as a sequela of H. pylori infection.
A study of autoimmune gastritis in the postpartum period and at a 5-year follow-up.
Burman P, Kampe O, Kraaz W, Loof L, Smolka A, Karlsson A, Karlsson-Parra A.
Department of Internal Medicine, University Hospital, Uppsala, Sweden.
Gastroenterology 1992 Sep;103(3):934-42 Abstract quote
The presence of autoimmune gastritis was investigated in 54 women with postpartum thyroiditis. Parietal cell antibodies (PCA) specific against H+, K(+)-adenosine triphosphatase (EC 188.8.131.52) were found in 18 women during pregnancy; in 10 of them, a 2-9-fold increase in the PCA level was observed in the postpartum period.
At a 5-year follow-up, the initially PCA-positive women still had elevated antibody levels. Hypergastrinemia and low pepsinogen levels were noted in 4 women. In 2 of these women low serum vitamin B12 levels had developed. In 6 of 9 PCA-positive women examined by gastroscopy, biopsy specimens from the gastric body mucosa contained mononuclear cells, mainly T lymphocytes (CD3+) and macrophages (Leu-M3+) combined with an aberrant epithelial expression of HLA-DR. In four patients with chronic gastritis, all parietal cells, as defined by a specific monoclonal antibody, were found to have immunoglobulin G (IgG) deposits by a double-immunostaining method. Three of them had microscopic evidence of atrophy, whereas in 1 patient the body mucosa was intact. In 1 further patient with intact glands at histological examination, the basolateral membrane of some oxyntic glands was coated with IgG.
The selective in situ deposition of antibodies associated with histologically intact parietal cells may support the concept that specific autoantibodies participate in the early pathogenesis of parietal cell destruction.
CHARACTERIZATION RADIOLOGIC LABORATORY MARKERS
CHARACTERIZATION GENERAL VARIANTS
HISTOLOGICAL TYPES CHARACTERIZATION GENERAL
The histopathological spectrum of type A gastritis.
Eidt S, Oberhuber G, Schneider A, Stolte M.
Institute of Pathology, Klinikum Bayreuth, Germany.
Pathol Res Pract 1996 Feb;192(2):101-6 Abstract quote
It has been recently shown that type A gastritis can be histologically diagnosed in the preatrophic stage.
In order to evaluate whether parietal cell atrophy in AG might correlate with other histopathological findings in the antral and body mucosa, we retrospectively investigated 171 consecutive cases of histologically diagnosed preatrophic (active) or atrophic type A gastritis (H&E, Warthin-Starry).
The prevalences of intestinal metaplasia (75% vs 44.4%) and micronodular hyperplasia (86.1% vs 52.4%) of endocrine cells in the oxyntic mucosa were significantly higher of parietal cell atrophy was present (p < 0.001 and p < 0.0001, respectively), whereas the prevalence of nodular lymphoid aggregates (77.8% vs 48.1%) and of Helicobacter pylori (14.3% vs 1.9%) in the oxyntic mucosa was significantly higher if parietal cell atrophy could not be detected (p < 0.001 and p < 0.01, respectively). In the antral mucosa, altered patterns of the inflammatory reaction could be demonstrated independent of the parietal cell mass possibly caused by impaired gastric acid production.
Our data support the notion that the development of parietal cell atrophy in type A gastritis represents a stepwise process including initial pseudohypertrophy of these cells.
Endocrine cell growths in atrophic body gastritis. Critical evaluation of a histological classification.
Bordi C, Annibale B, Azzoni C, Marignani M, Ferraro G, Antonelli G, D'Adda T, D'Ambra G, Delle Fave G.
Department of Anatomic Pathology, University of Parma, Italy.
J Pathol 1997 Jul;182(3):339-46 Abstract quote
The aim of the present study was to evaluate the correspondence of the classification of non-antral endocrine cell growths proposed by Solcia and co-workers with clinical features and non-endocrine mucosal changes.
For this purpose, 94 cases of newly diagnosed atrophic body gastritis were investigated using endoscopic biopsies and compared with 18 control subjects. The patients were subdivided into the following four groups according to the most severe pattern of endocrine cell proliferation found in the body mucosa, as shown by chromogranin A immunostaining: group 1, normal pattern (7 cases, 7.5 per cent); group 2, simple hyperplasia (6 cases, 6.5 per cent); group 3, linear hyperplasia (24 cases, 25.8 per cent); group 4; micronodular hyperplasia (56 cases, 60.2 per cent). Adenomatoid hyperplasia was found in only one case, thus precluding further analysis. Patients in groups 1 and 2 had lower acid secretion, higher gastrin level, and higher mean scores in all histopathological variables of chronic gastritis considered by the Sydney system when compared with controls, but did not differ among them in any parameter investigated.
When compared with groups 1 and 2, patients of groups 3 and 4 showed higher values of circulating gastrin, higher scores of glandular atrophy, and lower values of acid secretion and of mononuclear and neutrophil inflammatory cell infiltration. Moreover, group 4 patients differed significantly from those of group 3 in their higher gastrin levels and atrophy scores, and lower scores of neutrophil cell infiltration.
On the basis of these results, it is proposed that for practical purposes the normal and the simple hyperplasia patterns may be incorporated into a single group. It is concluded that this classification in its simplified form, based on a qualitative histological approach, shows clinical relevance without the need to perform expensive, time-consuming morphometric evaluations.
Autoimmune Gastritis: Distinct Histological and Immunohistochemical Findings Before Complete Loss of Oxyntic Glands
Michael Torbenson, M.D., Susan C. Abraham, M.D., John Boitnott, M.D., John H. Yardley, M.D. and Tsung-Teh Wu, M.D., Ph.D.
Division of Gastrointestinal/Liver Pathology, Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland
Mod Pathol 2002;15:102-109 Abstract quote
Autoimmune gastritis (AG) can be easily recognized when the histological features are fully developed, but recognizing AG before the complete loss of the oxyntic mucosa is more challenging. One feature of fully developed AG is enterochromaffin cell-like (ECL) hyperplasia, but its presence or absence in earlier stages of AG has not been fully evaluated.
A retrospective study of biopsy specimens from 40 patients was performed; all of the patients were originally diagnosed with possible AG based on the presence of lymphocytic infiltration and damage to oxyntic glands and/or the presence of metaplastic epithelium that disproportionately involved the body mucosa. Nineteen cases had follow-up serological studies for antiparietal cells and/or antiintrinsic factor antibodies: 13 were positive and 6 negative. The remaining 21 cases were indeterminate because of incomplete testing.
The histological findings were similar in the patients who were serologically positive and those who were indeterminate for AG. In all of these cases, the oxyntic mucosa showed lymphoplasmacytic infiltrates within the lamina propria with focal gland infiltration and damage. Sixty-five percent (22/34) of the cases showed intestinal and/or pyloric metaplasia, and 85% (29/34) showed parietal cell pseudohypertrophy. Chromogranin stains were performed in 11 of 13 cases with positive serological markers for AG, and all showed at least linear ECL cell hyperplasia. In contrast, none of the six cases with negative serological studies had linear ECL cell hyperplasia, P < .001.
In conclusion, the following constellation of findings supports a diagnosis of AG before the complete loss of oxyntic mucosa: deep or diffuse lymphoplasmacytic infiltrates within the lamina propria with foci of gland infiltration and damage, epithelial metaplasia, parietal cell pseudohypertrophy, and ECL cell hyperplasia at the linear or greater level.
VARIANTS ATROPHY, LACKING
Active autoimmune gastritis without total atrophy of the glands.
Stolte M, Baumann K, Bethke B, Ritter M, Lauer E, Eidt H.
Institut fur Pathologie, Klinikum Bayreuth, Bundesrepublik Deutschland.
Z Gastroenterol 1992 Oct;30(10):729-35 Abstract quote
To date, autoimmune gastritis has been diagnosed for the most part only when total atrophy of the oxyntic glands is detected.
On the basis of 40 patients without total atrophy of the glands, and with parietal cell antibodies in the serum, we show that the diagnosis of type A gastritis is also possible in the pre-atrophic stage.
The histological criteria for the diagnosis of active autoimmune gastritis without total atrophy of the glands are 1. usually dense, diffuse locally emphasized lymphocytic infiltration of the lamina propria between the glands in the oxyntic mucosa, 2. focal destruction of individual glands in the corpus of the stomach by lymphocytes, and 3. reactive pseudohypertrophy of the parietal cells.
A comparison with a group of patients with autoimmune gastritis and total atrophy of the glands shows that in active autoimmune gastritis, too, women are more frequently affected than men (in both groups, the sex ratio is approximately 3:1). Patients without atrophy of the glands are, on average, about 12 years younger than those with "burnt out" type A gastritis (average age 69.98:57.80 years). While in the case of burnt out type A gastritis, no colonisation with Helicobacter pylori was to be found, such colonisation was demonstrated for the corpus mucosa in 22.5%, and for the antral mucosa in 15.0%. In 27.5% a minimal or low-grade inactive superficial gastritis, as may be seen after eradication of Helicobacter pylori, was additionally diagnosed in the antrum.
A knowledge of the histological appearance of the pre-atrophic stage of type A gastritis might be of importance for the possible prevention of pernicious anaemia.
CHARACTERIZATION SPECIAL STAINS IMMUNOPEROXIDASE
Fundic argyrophil cell hyperplasia in atrophic gastritis: a search for a sensitive diagnostic method.
Belaiche J, Delwaide J, Vivario M, Gast P, Louis E, Boniver J.
Department of Gastroenterology, University of Liege, CHU Sart Tilman, Belgium.
Acta Gastroenterol Belg 1993 Jan-Feb;56(1):11-7 Abstract quote.
Hypergastrinemia induces argyrophil cell hyperplasia in oxyntic mucosa (FACH) in patients with non-antral atrophic gastritis, with or without pernicious anemia. This proliferation favours the development of carcinoid tumours.
In order to determine the most usual appropriate method to document FACH, we have studied 29 consecutive fundic biopsies from 26 patients with fundic chronic gastritis. The study encompassed gastrinemia levels, standard histology permitting the classification of chronic gastritis, demonstration of FACH by Grimelius stain, immunohistochemical studies using NSE, chromogranin A and by electron microscopy. The FACH was classified for each stain as slight, moderate or severe. The study displayed a relationship between the grade of gastritis and the density of argyrophil endocrine cells in oxyntic mucosa assessed by Grimelius stain (p < 0.0001) and chromogranin A (P < 0.01). There was also a relationship between the serum gastrin level and the density of argyrophil endocrine cells detected by these two stains (p < 0.001). A highly significant correlation was observed between Grimelius stain and chromogranin A (p < 0.0001). On the other hand, no significant correlation was noted with either NSE or electron microscopy.
We conclude that Grimelius stain and immunohistochemical studies against chromogranin A were the best methods for the demonstration of FACH in atrophic gastritis. One of these two techniques is sufficient in current practice for defining the patients at risk for subsequent surveillance.
DIFFERENTIAL DIAGNOSIS KEY DIFFERENTIATING FEATURES CHRONIC SUPERFICIAL GASTRITIS
Long-term observation of subjects with normal mucosa and with superficial gastritis: results of 23--27 years' follow-up examinations.
Ihamaki T, Saukkonen M, Siurala M.
Scand J Gastroenterol 1978;13(7):771-5 Abstract quote
261 subjects with a normal body mucosa or with superficial gastritis used as controls for an atrophic gastritis series have been followed up for 23--27 years. Of them, 41 died during the earlier and 63 during the present follow-up period. In all, 141 subjects were reexamined in 1976--1977 and 16 answered a questionnaire. None of the subjects had gastric carcinoma or an adenomatous polyp. One patient diagnosed and reported earlier had died of gastric carcinoma during the present period of observation.
Of the subjects with normal body mucosa 58% had developed superficial and 14% atrophic gastritis. Of those with superficial body gastritis 42% had developed atrophic gastritis and 18% showed an improvement of the gastritic changes. It should be noted, however, that earlier examinations were performed with blind biopsy and the present with direct vision gastroscopic biopsy.
The state of the antral and body mucosa was similar in 53%, antral changes dominated in 33% and the changes in the body in 14%. Intestinal metaplasia was found in 36%, atypical epithelium in 6%, parietal cell antibodies in 0.5% and intrinsic factor antibodies in 0.5%. The fasting serum gastrin level was above 100 ng/ml in 10%. Only 2 cases fulfilled the morphological, functional and immunological criteria of type A gastritis.
The present controls differed from the atrophic gastritis series in that the topography of gastritis was different and in that the incidence of metaplasia, atypia, gastric antibodies and high serum gastrin levels was markedly lower.
PROGNOSIS AND TREATMENT CHARACTERIZATION PROGNOSTIC FACTORS CARCINOID TUMORS
Morphology and pathogenesis of endocrine hyperplasias, precarcinoid lesions, and carcinoids arising in chronic atrophic gastritis.
Solcia E, Fiocca R, Villani L, Gianatti A, Cornaggia M, Chiaravalli A, Curzio M, Capella C.
Dept. of Human Pathology, Ist Medical Faculty, University of Pavia, Italy.
Scand J Gastroenterol Suppl 1991;180:146-59 Abstract quote
The spectrum of endocrine cell changes occurring in 80 cases of body-fundus chronic atrophic gastritis (CAG), mostly type A or multifocal, including various types of hyperplasia, precarcinoid lesions (20 cases), and neoplasia (carcinoid, 24 cases) have been analyzed histologically, histochemically, and ultrastructurally.
Changes associated with gland atrophy, pyloric- or intestinal-type metaplasia, regenerative hyperplasia, and hypergastrinemia have been identified and their neoplastic potential evaluated in the light of their proliferative capacity (bromodeoxyuridine incorporation) and clinicopathologic behavior.
A close link between disseminated precarcinoid lesions of non-tumor mucosa and multiple carcinoids (carcinoidosis) arising in hypergastrinemic type-A CAG is suggested. Hyperplastic changes, including endocrine cell clusters, seem to have no or only minimal neoplastic potential.
TREATMENT HELICOBACTER TREATMENT
Cure of autoimmune gastritis by Helicobacter pylori eradication in a 21-year-old male.
Stolte M, Meier E, Meining A.
Institut fur Pathologie, Klinikum Bayreuth.
Z Gastroenterol 1998 Aug;36(8):641-3 Abstract quote
BACKGROUND: More recent investigations have shown that in some patients Helicobacter pylori (Hp) antibodies can act as antigastric antibodies and lead to atrophic autoimmune gastritis of the oxyntic mucosa. The question thus arises as to whether this form of autoimmune gastritis can be healed by eradicating Hp.
METHODS: Case history of a 21-year-old man with active autoimmune gastritis of the oxyntic mucosa with lymphocytic infiltration of the entire lamina propria, foci of lymphocytic destruction of a number of glands, and hypertrophy of the preserved parietal cells, but no signs of Hp in the Warthin Starry stain. The search for parietal cell antibodies and intrinsic factor antibodies proved negative, while the level of the gastrin in the serum was slightly elevated. Since the presence of Hp IgG antibodies (243 U/ml) was confirmed. Hp eradication therapy was carried out.
RESULTS: 15 months after Hp treatment the Hp IgG antibody titre had decreased to 11 U/ml. The autoimmune gastritis had healed, and autoaggressive inflammatory infiltrates with focal destruction of corpus glands and hypertrophy of the parietal cells were no longer detectable.
CONCLUSIONS: Autoimmune gastritis induced by Hp may possibly be cured with Hp eradication treatment; to confirm this, further controlled prospective studies are needed.
Henry JB. Clinical Diagnosis and Management by Laboratory Methods. Twentieth Edition. WB Saunders. 2001.
Rosai J. Ackerman's Surgical Pathology. Eight Edition. Mosby 1996.
Sternberg S. Diagnostic Surgical Pathology. Third Edition. Lipincott Williams and Wilkins 1999.
Robbins Pathologic Basis of Disease. Sixth Edition. WB Saunders 1999.
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