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ORIGINAL ARTICLE
Year : 2017  |  Volume : 10  |  Issue : 6  |  Page : 562-567  

Histopathological study of portal hypertensive gastropathy using gastric biopsy


Department of Pathology, Dr DY Patil Medical College, Hospital and Research Center, Dr DY Patil Vidyapeeth, Pune, Maharashtra, India

Date of Submission20-Apr-2017
Date of Acceptance14-Aug-2017
Date of Web Publication17-Jan-2018

Correspondence Address:
Dr. Shirish S Chandanwale
Dr. D. Y. Patil Medical College, DPU, Pimpri, Pune - 411 018, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/MJDRDYPU.MJDRDYPU_82_17

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  Abstract 


Background and Objectives: Portal hypertensive gastropathy (PHG) refers to changes in the mucosa of the stomach in patients with portal hypertension. The diagnosis of PHG is usually made on endoscopy. It is clinically important because it may cause acute massive or insidious blood loss. We present a comprehensive study to ascertain the utility of gastric biopsy in identifying and assessing the presence and degree of pathological changes associated with PHG. Materials and Methods: Histological features of 30 gastric biopsies each from antrum and body of patients of portal hypertension with or without gastric symptoms were studied. They were grouped as Group A patients. Similarly, the histological features of 30 gastric biopsies each from antrum and body of patients of gastritis without portal hypertension were studied and were grouped as Group B patients. The biopsies were studied for mucosal changes such as edema in lamina propria, degree of inflammation, smooth muscle hyperplasia, collagen deposition, foveolar hyperplasia, intestinal metaplasia, presence of Helicobacter pylori, and fibrin thrombi. Results: Most common cause of portal hypertensive gastropathy was alcoholic liver cirrhosis. Histological features such as dilated congested capillaries, edema, extravasated red blood cell (RBC), and smooth muscle hyperplasia are more commonly seen in PHG (Group A) than gastritis (Group B) patients without portal hypertension. Conclusion: Alcoholic cirrhosis is a common cause of PHG. Dilated congested capillaries, edema, extravasated RBC, and smooth muscle hyperplasia are frequently seen in gastric biopsies of PHG patients than gastritis patients. These features are nonspecific.

Keywords: Biopsy, edema, endoscopy, gastropathy, inflammation, portal hypertension


How to cite this article:
Chandanwale SS, Gupta N, Sheth J, Naragude P, Gambhir AS, Pathak P, Nizam J. Histopathological study of portal hypertensive gastropathy using gastric biopsy. Med J DY Patil Univ 2017;10:562-7

How to cite this URL:
Chandanwale SS, Gupta N, Sheth J, Naragude P, Gambhir AS, Pathak P, Nizam J. Histopathological study of portal hypertensive gastropathy using gastric biopsy. Med J DY Patil Univ [serial online] 2017 [cited 2019 Dec 15];10:562-7. Available from: http://www.mjdrdypu.org/text.asp?2017/10/6/562/223373




  Introduction Top


Portal hypertensive gastropathy (PHG) refers to changes in the mucosa of the stomach in patients with portal hypertension. Cirrhosis of liver is considered to be the most common cause of portal hypertension.[1] Nearly half of the patients with portal hypertension are affected by PHG.[2],[3]

The diagnosis of PHG is usually made on endoscopy. The usual appearance of PHG on endoscopy is a mosaic-like or reticular pattern in the mucosa. Red spots may or may not be present.[4] PHG has been suggested as a marker of more severe liver disease in patients with cirrhosis.[5] Most of the patients with PHG will develop bleeding (acute or chronic) which is attributable to gastropathy.[5],[6],[7] Gastric biopsies in patients with PHG show ectatic blood vessels, evidence of the bleeding by the presence of extravagated red blood cells (RBCs) in the lamina propria, and edema in the mucosa and submucosa.[8],[9]

We present a comprehensive study to ascertain the utility of gastric biopsy in identifying and assessing the presence and degree of pathological changes associated with PHG.


  Materials and Methods Top


The prospective study was carried out in the Department of Pathology of medical teaching and research hospital from August 2012 to September 2014. We retrieved the diagnosis of these conditions from the medical records and the diagnosis was based on clinical history, laboratory parameters, and liver biopsy findings.

Inclusion criteria

The 30 gastric biopsies in patients of portal hypertension with or without gastric symptoms such as hematemesis, malena, and anemia were grouped as Group A. The 30 gastric biopsies in patients of gastritis without portal hypertension were grouped as control Group B.

Exclusion criteria

The gastric biopsies of neoplastic lesions were not included in the study. The diagnosis of these patients was based on clinical findings including endoscopic findings. Diagnosis of portal hypertension was based on the presence of clinical findings such as ascites or presence of dilated veins or varices and/or splenomegaly.

Thirty patients of portal hypertension were included in the study. Endoscopic biopsies each from antrum and body of the stomach of every patient were studied. Gastric biopsies from antrum and body of thirty patients who did not have portal hypertension were taken as control.

Institute ethics committee clearance was obtained before start of the study. Detailed clinical findings were undertaken into consideration.

The biopsy specimens were fixed in neutral formal saline. The tissues were paraffin processed and 3–5 μ thick sections were cut and stained with hematoxylin and eosin. Special stains such as Modified Giemsa and Masson's Trichrome stains were done on each biopsies to highlight Helicobacter pylori and connective tissue such as muscle and collagen, respectively. The histological findings were studied in detail and recorded.

Histological findings of Group A and Group B biopsies were compared for mucosal vascular changes, lamina propria edema, degree of inflammation, smooth muscle hyperplasia, collagen deposition, foveolar hyperplasia, intestinal metaplasia, presence of H. pylori and fibrin thrombi.

Smooth muscle hyperplasia was further graded into three grades, namely, Grade 0: smooth muscle confined to muscularis mucosa, Grade 1: smooth muscle presented in lamina propria, and Grade 2: smooth muscle fibers perpendicular to mucosa within the interfoveolar lamina propria.[10]

Collagen deposition was further graded into five grades, namely, Grade 0: No collagen deposition, Grade 1: few fine collagen strands in lamina propria, Grade 2: coarse collagen fibrils present in the lamina propria, Grade 3: fine or coarse fibrils present in the submucosa, and Grade 4: Thick scar-like collagen deposition in the submucosa.[11] A correlation was done using the software Epi info 7. Values of P < 0.05 were considered statistically significant.


  Results Top


Out of thirty patients of Group A, maximum (n = 14) patients were in the age group of 51–60 years. The age groups were comparable to Group B (n = 15). [Table 1] shows detailed age-wise distribution of thirty patients in Group A and Group B. Maximum patients were males, n = 28 and n = 25 in Group A and Group B, respectively. Out of 30 cases of PHG, maximum patients (n = 15) had alcoholic cirrhosis, followed by posthepatitis macronodular cirrhosis (n = 13) and remaining were primary biliary cirrhosis (n = 2).
Table 1: Age group distribution of patients with portal hypertensive gastropathy (Group A) and control Group B

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Mild lymphoplasmacytic infiltrate in mucosa was seen in eight patients of PHG as compared to all cases of chronic gastritis.

The mucosal capillary dilatation, congestion, and extravasation of RBCs were more pronounced in the gastric body than the antrum [Figure 1]. The difference between Group A and Group B was statistically insignificant (χ2 = 2.424, P > 0.05). [Table 2] shows detailed distribution of capillary dilatation, congestion, and extravasation of RBCs in both the groups.
Figure 1: Gastric biopsy mucosa show congested, dilated capillaries, and extravasated red blood cells (Hematoxylin and Eosin ×400)

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Table 2: Distribution of mucosal congestion, dilated capillaries, and extravasated red blood cell in gastric biopsies from antrum and body in Group A (patients with portal hypertensive gastropathy, total biopsy=60) and control Group B (total biopsy=60)

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In Group A patients, 30% patients had edema in the lamina propria in the antrum as compared to 20% patients of Group B. The 50% cases had edema in the lamina propria in the gastric body of patients with Group A as compared to 40% cases of Group B [Figure 2]. The 10% cases showed edema both in the lamina propria of antrum and the body in Group A patients as compared to 16.3% cases of Group B [Table 3]. The variability of lamina propria edema between the two groups was statistically insignificant (χ2 = 2.69, P > 0.05). [Table 4] shows detailed correlation between mucosal capillary dilatation and degree of inflammation. There were no significant differences between the degree of inflammation in gastric biopsies with capillary dilatation as compared with those absent capillary dilatation (χ2 = 0.632, P > 0.05).
Figure 2: Gastric biopsy mucosa show edema fluid (Hematoxylin and Eosin, ×400)

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Table 3: Distribution of edema in lamina propria of gastric biopsies from antrum and body in Group A (patients with portal hypertensive gastropathy, total biopsy=60) and control Group B (total biopsy=60)

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Table 4: Correlation between mucosal capillary dilatation and degree of inflammation gastric biopsies from antrum and body in Group A (patients with portal hypertensive gastropathy, total biopsy=60) and control Group B (total biopsy=60)

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Smooth muscle hyperplasia was more common in Group A patients as compared to Group B patients [Figure 3]. The Grade 1 smooth muscle hyperplasia was more common than Grade 2 hyperplasia in both Group A and Group B patients. [Table 5] shows distribution of smooth muscle hyperplasia in Group A and Group B patients. For the sake of statistical convenience, Grade 1 and 2 have been clubbed together. There was no significant difference in smooth muscle hyperplasia between Group A and Group B (χ2 = 1.423, P = 0.231, P > 0.05).
Figure 3: Gastric biopsy shows smooth muscle hyperplasia (Hematoxylin and Eosin, ×400)

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Table 5: Distribution of smooth muscle hyperplasia in gastric biopsies from antrum and body in Group A (patients with portal hypertensive gastropathy, total biopsy=60) and control Group B (total biopsy=60)

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[Table 6] shows distribution of collagen in Group A and Group B patients. Grade 1 and Grade 2 collagen deposition was more common in Group A [Figure 4] than Group B. None of the case showed Grade 3 collagen deposition. For the sake of statistical convenience, all the grades have been clubbed together. The difference in collagen deposition between Group A and Group B was statistically insignificant (χ2 = 1.080, P = 0.299, P > 0.05).
Figure 4: Gastric biopsy shows increased collagen (blue) in lamina propria (Masson's Trichome stain, ×400)

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Table 6: Distribution of collagen deposition in gastric biopsies from antrum and body in Group A (patients with portal hypertensive gastropathy, total biopsy=60) and control Group B (total biopsy=60)

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[Table 7] shows distribution of foveolar hyperplasia, intestinal metaplasia, presence of H. pylori, and fibrin thrombi in patients with Group A and Group B. The difference in foveolar hyperplasia, intenstinal metaplasia, presence of H. pylori [Figure 5], fibrin thrombi between the test and the control group was statistically insignificant, respectively (χ2 = 1.097, P > 0.05, χ2 = 0.873, P > 0.05, χ2 = 0.269, P > 0.05 and χ2 = 2.588, P > 0.05).
Figure 5: Gastric biopsy shows H. Pylori (arrow) (Giemsa stain, ×400)

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Table 7: Distribution of foveolar hyperplasia, intestinal metaplasia, presence of Helicobacter pylori, and fibrin thrombi in gastric biopsies from antrum and body in Group A (patients with portal hypertensive gastropathy, total biopsy=60) and control Group B (total biopsy=60)

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  Discussion Top


PHG is the term used to describe the endoscopic appearance of gastric mucosa in patients with cirrhotic or noncirrhotic portal hypertension with a characteristic mosaic-like pattern with or without red spots.[7] It is clinically important because it may cause acute massive or insidious blood loss.[12]

McCormack et al.[9] found maximum number of patients of PHG (52.2%) in the age group of 61–70 years; while in our study, maximum patients (46.6%) were in the age group of 51–60 years. McCormack et al.[9] and Sivanathan et al.[13] found viral hepatitis to be the most common cause of portal hypertension followed by liver cirrhosis. In our study, most common cause of portal hypertension was alcoholic liver cirrhosis followed by postviral hepatitis cirrhosis and primary biliary cirrhosis.

Corbishley et al.[14] in their study on PHG concluded that mucosal capillary congestion in the absence of inflammation is an important histological feature. Dixon et al.[15] made similar observations in their study. In contrast, Misra et al.[16] concluded that there was no correlation between the severity of mucosal vascular congestion and degree of inflammation in PGH. Similar observations were made in our study.

Lamina propria edema is attributed to the change in gastric blood flow.[17] Aydogan et al.[18] studied histological features of gastric mucosa in PHG due to intrahepatic and extrahepatic portal hypertension. They observed that lamina propria edema was a nonspecific parameter. In our study, the variability of lamina propria edema between Group A and Group B patients was statistically insignificant.

Nel observed smooth muscle hyperplasia in body and antrum as a consistent feature in reactive gastropathy than in PGH.[19] In contrast, we observed smooth muscle hyperplasia in body and antrum of 33.30% Group A cases as compared to 16.6% Group B patients. Li and Yang concluded in their study that submucosal fibrosis was as a result of intimal injury of visceral veins and destruction of contractile structure in visceral arterial wall.[20],[21] In our study, submucosal collagen deposition in body and antral mucosa was seen in only 23.30% cases as compared to 10% cases of control group.

We did not observe any significant difference in test and control group for foveolar hyperplasia [Table 7].

Ibrisim et al.[22] observed positive correlation between the prevalence of H. pylori-associated mucosal atrophy and intestinal metaplasia in stomach biopsies of patients with portal hypertension. While in our study, only 13.3% cases showed intestinal metaplasia; while in 40% biopsies, H. pylori were detected.

Gastric antral vascular ectasia (GAVE) needs to be differentiated from PHG. It is often done on endoscopic findings. On endoscopy, GAVE often shows antral involvement by diffuse or linear red patches. In PHG, lesions are often located in fundus of the stomach. Fibrin thrombi, gastric dilatation, increased spindle cell proliferation, and fibrohyalinosis can be seen in gastric biopsy.[23] In our study, six out of 30 cases showed fibrin thrombi compared to only one case in the control group.

Lam et al.[24] reported gastric polyp on endoscopy in 12 patients of portal hypertension. None of our patients had gastric polyp.

Corbishley et al.[14] suggested that histological changes seen in endoscopic biopsy of congestive gastropathy are not specific for the condition. Similar observations were made in our study.


  Conclusion Top


Gastric biopsy is very useful in the diagnosis of variety of gastric lesions. Diagnosis of PHG is done based on clinical findings and endoscopy. Gastric biopsy mucosal vascular changes such as dilated congested capillaries, edema, extravasated RBC, and smooth muscle hyperplasia are more commonly seen in PHG than gastritis patients without portal hypertension. However, these histopathology findings are nonspecific and were found to be statistically insignificant.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

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Ibrisim D, Cevikbas U, Akyüz F, Poturoglu S, Ahishali E, Güllüoglu M, et al. Intestinal metaplasia in portal hypertensive gastropathy: A frequent pathology. Eur J Gastroenterol Hepatol 2008;20:874-80.  Back to cited text no. 22
    
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]



 

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