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Gastric adenocarcinoma in a patient re-infected with H. pylori after regression of MALT lymphoma with successful anti-H. pylori therapy and gastric resection: a case report.

Ghoshal UC, Guha D, Bandyopadhyay S, Pal C, Chakraborty S, Ghoshal U, Ghosh TK, Pal BB, Banerjee PK - BMC Gastroenterol (2002)

Bottom Line: Helicobacter pylori (H. pylori) has been etiologically linked with primary gastric lymphoma (PGL) and gastric carcinoma (GC).However, he developed GC on follow up; this was temporally associated with recrudescence/re-infection of H. pylori.This case also documents a unique problem in management of PGL in tropical countries where re-infection with H. pylori is supposed to be high.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Gastroenterology, Seth Sukhlal Karnani Memorial Hospital & Institute of Postgraduate Medical Education and Research, 244, AJC Bose Road, Kolkata 700020, India. ghoshal@sgpgi.ac.in

ABSTRACT

Background: Helicobacter pylori (H. pylori) has been etiologically linked with primary gastric lymphoma (PGL) and gastric carcinoma (GC). There are a few reports of occurrence of both diseases in the same patients with H. pylori infection.

Case presentation: We report a patient with PGL in whom the tumor regressed after surgical resection combined with eradication of H. pylori infection. However, he developed GC on follow up; this was temporally associated with recrudescence/re-infection of H. pylori. This is perhaps first report of such occurrence.

Conclusions: Possible cause and effect relationship between H. pylori infection and both PGL and GC is discussed. This case also documents a unique problem in management of PGL in tropical countries where re-infection with H. pylori is supposed to be high.

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Related in: MedlinePlus

(A) Resected specimen of distal stomach showing diffuse infiltration by mononuclear cells without formation of lymphoid follicles with obvious cellular atypia and abnormal mitotic figures (H&E × 275). (B) The high power view of recurrent gastric tumor showing pleomorphic cells, abnormal mitotic figures, mucin secretion and formation of gland at places diagnostic of adenocarcinoma (H&E × 275).
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Figure 2: (A) Resected specimen of distal stomach showing diffuse infiltration by mononuclear cells without formation of lymphoid follicles with obvious cellular atypia and abnormal mitotic figures (H&E × 275). (B) The high power view of recurrent gastric tumor showing pleomorphic cells, abnormal mitotic figures, mucin secretion and formation of gland at places diagnostic of adenocarcinoma (H&E × 275).

Mentions: Hemoglobin=85g/L, TLC=6.7 × 109/L, ESR=78 mm/h. Chest radiograph was normal. Abdominal ultrasonogram did not reveal lymphadenopathy, hepatosplenomegaly or ascites. Upper gastrointestinal (UGI) endoscopy revealed hyperemic lower esophageal mucosa with multiple non-confluent erosions; there was excessive food residue inside the lumen and multiple hypertrophied gastric folds with erosions over these. Pyloric orifice was narrow and endoscope could not be negotiated into the duodenum. Six biopsies taken from the hypertrophied folds revealed only chronic inflammatory infiltrate and no specific pathology. H. pylori was not detected on histologic examination of gastric biopsies. In house rapid urease test (RUT) was positive within 15 minutes and scanning electron microscopy (SEM, Hitachi S530, Japan) from biopsies obtained from relatively normal looking areas revealed multiple round cells (might be lymphocytes, figure 1A) but no H. pylori. Serum titer for IgG antibody against H. pylori using ELISA based commercially available kit (Monobind Incorporation, California) was positive (21 IU/ml). Lansoprazole was started. With a diagnosis of gastric outlet obstruction, surgery was done after 2 weeks. After exploring the abdomen by midline incision thickening and nodularity of antrum were detected. There was no regional lymphadenopathy. Partial gastrectomy, removal of peri-gastric lymph nodes, closure of resected end of the duodenum in double layers and end-to-side ante-grade retro-colic gastrojejunostomy were done. Postoperative course was uneventful. Histological examination of resected specimen revealed transmural infiltration by mononuclear cells diffusely extending through muscularis mucosa into the submucosa without formation of lymphoid follicles, cellular atypia, abnormal mitotic figures (figure 2A) and lymphoepithelial lesions. On thorough histologic evaluation no evidence of synchronous GC was seen. Peri-gastric lymph nodes were not infiltrated by lymphoma. Bone marrow examination did not reveal any abnormality. On the basis of these morphological features a diagnosis of PGL (low-grade B cell lymphoma of MALT type by revised European-American classification) [12], stage I E: I1 (Musshoffs modification of Ann Arbor classification) [13] and H. pylori infection were made. Patient was treated with amoxycillin 1.5 g/d, omeprazole 40 mg/d and tinidazole 1 g/d for two weeks to eradicate the infection with H. pylori. UGI endoscopy repeated one month after completion of anti-H. pylori treatment revealed small sized stomach, no ulcer. RUT and Giemsa staining of biopsies obtained from proximal stomach were negative for H. pylori. However, a repeat UGI endoscopy done after six months revealed a benign-looking ulcer (1.5 cm in diameter) at gastrojejunostomy stoma. RUT and histology (Giemsa stain) on biopsies obtained from proximal stomach for H. pylori were still negative. Biopsy obtained by well technique from margin of the ulcer revealed chronic inflammatory infiltrate. Flow cytometry by standard technique [14] from these biopsies using anti-CD 19 (B cell marker) and anti-CD3 (T cell marker) monoclonal antibodies revealed polyclonal infiltrate with 6.6% CD 19 and 10.8% CD3 bearing cells (figure 3). With a possibility of benign stomal ulcer patient was treated with lansoprazole 30 mg/d for 3 months. After this period of treatment, healing of the ulcer and absence of H. pylori infection were documented by UGI endoscopy and negative RUT respectively (2 weeks after stopping lansoprazole). On follow up during the next six months, he remained well with improved appetite and weight gain (35 to 46 kg). He presented with recurrence of epigastric pain, anorexia and vomiting in August 1999. He had lost body weight (34 kg in August 1999). Examination revealed pallor, no peripheral lymphadenopathy and abdominal lump. UGI endoscopy: friable ulcerated growth involving most of stomach with reduced distensibility of the organ and patent gastrojejunostomy stoma. Since a possibility of recurrent PGL was considered, flow cytometry was done by standard technique [14] with biopsy from the tumor using anti-CD 19 (B cell marker) and anti-CD3 (T cell marker) antibodies; it revealed a polyclonal lymphocytic infiltrate consisting of 0.9% CD 19 and 3.9% CD3 bearing cells (figure 3). Biopsies obtained from relatively normal looking mucosa of stomach gave positive result to RUT. Histological examination revealed chronic gastritis but no intestinal metaplasia. SEM (Hitachi S530, Japan) with these biopsies revealed multiple bacilli suggestive of H. pylori (figure 1B). Histopathology of biopsy from margin of ulcers revealed multiple signet ring cells, cellular pleomorphism, mucin secretion, abnormal mitotic figures and gland formation at certain places (figure 2B). A diagnosis of GC and recrudescence / re-infection of H. pylori were made. Patient denied further treatment at this stage and left the hospital.


Gastric adenocarcinoma in a patient re-infected with H. pylori after regression of MALT lymphoma with successful anti-H. pylori therapy and gastric resection: a case report.

Ghoshal UC, Guha D, Bandyopadhyay S, Pal C, Chakraborty S, Ghoshal U, Ghosh TK, Pal BB, Banerjee PK - BMC Gastroenterol (2002)

(A) Resected specimen of distal stomach showing diffuse infiltration by mononuclear cells without formation of lymphoid follicles with obvious cellular atypia and abnormal mitotic figures (H&E × 275). (B) The high power view of recurrent gastric tumor showing pleomorphic cells, abnormal mitotic figures, mucin secretion and formation of gland at places diagnostic of adenocarcinoma (H&E × 275).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC102757&req=5

Figure 2: (A) Resected specimen of distal stomach showing diffuse infiltration by mononuclear cells without formation of lymphoid follicles with obvious cellular atypia and abnormal mitotic figures (H&E × 275). (B) The high power view of recurrent gastric tumor showing pleomorphic cells, abnormal mitotic figures, mucin secretion and formation of gland at places diagnostic of adenocarcinoma (H&E × 275).
Mentions: Hemoglobin=85g/L, TLC=6.7 × 109/L, ESR=78 mm/h. Chest radiograph was normal. Abdominal ultrasonogram did not reveal lymphadenopathy, hepatosplenomegaly or ascites. Upper gastrointestinal (UGI) endoscopy revealed hyperemic lower esophageal mucosa with multiple non-confluent erosions; there was excessive food residue inside the lumen and multiple hypertrophied gastric folds with erosions over these. Pyloric orifice was narrow and endoscope could not be negotiated into the duodenum. Six biopsies taken from the hypertrophied folds revealed only chronic inflammatory infiltrate and no specific pathology. H. pylori was not detected on histologic examination of gastric biopsies. In house rapid urease test (RUT) was positive within 15 minutes and scanning electron microscopy (SEM, Hitachi S530, Japan) from biopsies obtained from relatively normal looking areas revealed multiple round cells (might be lymphocytes, figure 1A) but no H. pylori. Serum titer for IgG antibody against H. pylori using ELISA based commercially available kit (Monobind Incorporation, California) was positive (21 IU/ml). Lansoprazole was started. With a diagnosis of gastric outlet obstruction, surgery was done after 2 weeks. After exploring the abdomen by midline incision thickening and nodularity of antrum were detected. There was no regional lymphadenopathy. Partial gastrectomy, removal of peri-gastric lymph nodes, closure of resected end of the duodenum in double layers and end-to-side ante-grade retro-colic gastrojejunostomy were done. Postoperative course was uneventful. Histological examination of resected specimen revealed transmural infiltration by mononuclear cells diffusely extending through muscularis mucosa into the submucosa without formation of lymphoid follicles, cellular atypia, abnormal mitotic figures (figure 2A) and lymphoepithelial lesions. On thorough histologic evaluation no evidence of synchronous GC was seen. Peri-gastric lymph nodes were not infiltrated by lymphoma. Bone marrow examination did not reveal any abnormality. On the basis of these morphological features a diagnosis of PGL (low-grade B cell lymphoma of MALT type by revised European-American classification) [12], stage I E: I1 (Musshoffs modification of Ann Arbor classification) [13] and H. pylori infection were made. Patient was treated with amoxycillin 1.5 g/d, omeprazole 40 mg/d and tinidazole 1 g/d for two weeks to eradicate the infection with H. pylori. UGI endoscopy repeated one month after completion of anti-H. pylori treatment revealed small sized stomach, no ulcer. RUT and Giemsa staining of biopsies obtained from proximal stomach were negative for H. pylori. However, a repeat UGI endoscopy done after six months revealed a benign-looking ulcer (1.5 cm in diameter) at gastrojejunostomy stoma. RUT and histology (Giemsa stain) on biopsies obtained from proximal stomach for H. pylori were still negative. Biopsy obtained by well technique from margin of the ulcer revealed chronic inflammatory infiltrate. Flow cytometry by standard technique [14] from these biopsies using anti-CD 19 (B cell marker) and anti-CD3 (T cell marker) monoclonal antibodies revealed polyclonal infiltrate with 6.6% CD 19 and 10.8% CD3 bearing cells (figure 3). With a possibility of benign stomal ulcer patient was treated with lansoprazole 30 mg/d for 3 months. After this period of treatment, healing of the ulcer and absence of H. pylori infection were documented by UGI endoscopy and negative RUT respectively (2 weeks after stopping lansoprazole). On follow up during the next six months, he remained well with improved appetite and weight gain (35 to 46 kg). He presented with recurrence of epigastric pain, anorexia and vomiting in August 1999. He had lost body weight (34 kg in August 1999). Examination revealed pallor, no peripheral lymphadenopathy and abdominal lump. UGI endoscopy: friable ulcerated growth involving most of stomach with reduced distensibility of the organ and patent gastrojejunostomy stoma. Since a possibility of recurrent PGL was considered, flow cytometry was done by standard technique [14] with biopsy from the tumor using anti-CD 19 (B cell marker) and anti-CD3 (T cell marker) antibodies; it revealed a polyclonal lymphocytic infiltrate consisting of 0.9% CD 19 and 3.9% CD3 bearing cells (figure 3). Biopsies obtained from relatively normal looking mucosa of stomach gave positive result to RUT. Histological examination revealed chronic gastritis but no intestinal metaplasia. SEM (Hitachi S530, Japan) with these biopsies revealed multiple bacilli suggestive of H. pylori (figure 1B). Histopathology of biopsy from margin of ulcers revealed multiple signet ring cells, cellular pleomorphism, mucin secretion, abnormal mitotic figures and gland formation at certain places (figure 2B). A diagnosis of GC and recrudescence / re-infection of H. pylori were made. Patient denied further treatment at this stage and left the hospital.

Bottom Line: Helicobacter pylori (H. pylori) has been etiologically linked with primary gastric lymphoma (PGL) and gastric carcinoma (GC).However, he developed GC on follow up; this was temporally associated with recrudescence/re-infection of H. pylori.This case also documents a unique problem in management of PGL in tropical countries where re-infection with H. pylori is supposed to be high.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Gastroenterology, Seth Sukhlal Karnani Memorial Hospital & Institute of Postgraduate Medical Education and Research, 244, AJC Bose Road, Kolkata 700020, India. ghoshal@sgpgi.ac.in

ABSTRACT

Background: Helicobacter pylori (H. pylori) has been etiologically linked with primary gastric lymphoma (PGL) and gastric carcinoma (GC). There are a few reports of occurrence of both diseases in the same patients with H. pylori infection.

Case presentation: We report a patient with PGL in whom the tumor regressed after surgical resection combined with eradication of H. pylori infection. However, he developed GC on follow up; this was temporally associated with recrudescence/re-infection of H. pylori. This is perhaps first report of such occurrence.

Conclusions: Possible cause and effect relationship between H. pylori infection and both PGL and GC is discussed. This case also documents a unique problem in management of PGL in tropical countries where re-infection with H. pylori is supposed to be high.

Show MeSH
Related in: MedlinePlus