Aralık 2011

95-97

İbrahim BIYIKOĞLU, Levent FİLİK

Department of Gastroenterology, Ankara Research Hospital, Ankara

Amaç: Portal gastropatili hastalarda Helikobakter pilori ve beta-2 mikroglobulin ilişkisi net olarak tanımlanamamıştır. Bu çalışmada, Helikobakter pilori infeksiyonu olan ve olmayan hastaların serum ve doku beta-2 mikroglobulin düzeyleri ve bu düzeylerin portal gastropati ile ilişkisi incelenmiştir. Gereç ve Yöntem: Portal gastropatili 25 hasta ve 22 sağlıklı birey çalışmaya dahil edilmiştir. Mide biyopsileri incelenmiş, serum ve doku beta-2 mikroglobulin düzeyleri bakılmıştır. Bulgular: Yirmibeş portal hipertansif gastropatili olgunun 15?inde Helikobakter pilori infeksiyonu bulunmuştur. Bu 15 hastanı n 8?inde (%53.3) subendotelial beta-2 mikroglobulin artışı görülmüştür. Helikobakter pilori olmayan 10 hastanın 3?ünde (%30) subendotelial beta-2 mikroglobulin bulunmuştur. Fark istatistiksel olarak anlamlıdır (p<0.01). Portal gastropatisi olan hastaların 5?inde gastropati orta derecede idi ve bu 5 olgunun hepsi de Helikobakter pilori pozitifti. Buna karşılık Helikobakter pilori olmayan hastaların hepsinde gastropati derecesi hafif derecede idi (p<0.001) Sonuç: Portal gastropatide Helikobakter pilori sıklığı değişmemektedir. Helikobakter pilori pozitif hastalarda gastrik mukozada beta-2 mikroglobulin depolanması daha yagındır.

Portal gastropati, Helikobakter pilori, beta-2 mikroglobulin

Beta-2 microglobulin (ß-2m) is a minor plasma protein, secreted from the plasma membranes as a result of the continuous regeneration of membrane proteins in the cell surface of all nucleated cells (1). The relationship between Helicobacter pylori (H. pylori) and ß-2m in patients with portal gastropathy has not been clearly defined yet. In this study, we aimed to compare the levels of serum and tissue ß-2m in patients with and without H. pylori infection and to examine the relationship between levels of serum and tissue ß-2m in patients with portal gastropathy.

Chronic liver disease was previously reported to be among the reasons for peptic ulcer disease (2). H. pylori is a very well-known etiologic agent of gastritis and peptic ulcer. On the other hand, the H. pylori and portal gastropathy relationship is still debatable. Foster et al.(3) showed a relatively low prevalence (17%) of H. pylori in patients with portal gastropathy and explained it by the unsuitable milieu of the gastric mucosa in portal gastropathy. However, in our study, 15 of 25 (60%) of our patients and 13 of 22 (59.1%) of the healthy controls had H. pylori infection. We attribute this to the high H. pylori prevalence in our country.

Portal gastropathy severity and the H. pylori relationship is unclear in the literature (4-6) (Table 4). H. pylori was shown to increase in mild portal gastropathy, but to decrease with severity of portal gastropathy. This was attributed to mucosal atrophy and mucus layer changes in severe portal gastropathy. Five of the study patients (20%) had moderate portal gastropathy, and all 5 patients had H. pylori infection. Hematoxylin-eosin (HE) and Warthin-Starry staining might not disclose H. pylori in some specimens. However, foveolar lymphoid follicular presentation in these samples with H. pylori serology is compatible with H. pylori infection. This could explain urease-positive patients whose biopsy samples did not disclose H. pylori.

ß-2m is a minor plasma protein, secreted from the plasma membranes as a result of the continuous regeneration of membrane proteins in the cell surface of all nucleated cells. Conz et al.(1) showed ß-2m accumulation in H. pylori-positive gastric mucosa but not in H. pylori-negative gastric mucosa biopsies in uremic study patients with high serum ß-2m. They also showed ß-2m accumulation in H. pylori-positive gastric biopsy samples in healthy controls. We found significantly higher ß-2m concentrations in our patient group (44%) than in healthy controls (22.7%) (p<0.01). On the other hand, we did not find a relationship between ß-2m and severity of portal gastropathy (p>0.05).

In conclusion, there is no change in H. pylori infection frequency in portal gastropathy. ß-2m deposition in gastric mucosa is more common in H. pylori-positive patients. There is an inverse relationship between portal gastropathy severity and ß-2m deposition.

Twenty-five patients with portal gastropathy and 22 healthy persons were enrolled in this study. Gastric biopsies were histologically analyzed, and tissue and serum ß-2m levels were measured. Urease test of gastric biopsy tissue samples was performed.

The demographic features and etiologic distribution are shown in Tables 1 and 2, respectively. H. pylori infection was detected in 15 of 25 portal gastropathy patients. Subendothelial ß-2m was detected in 8 of 15 (53.3%) portal hypertensive gastropathy patients with H. pylori. Table 3 shows the distribution of ß-2m levels of portal gastropathy patients with respect to the patients? features. Tissue ß-2m was detected in 3 of 10 (30%) portal hypertensive gastropathy patients without H. pylori. The difference between groups was statistically significant (p<0.01). Five of 13 healthy control cases with H. pylori but none of the healthy control cases without H. pylori were shown to have tissue ß-2m (p<0.001). Five of the patients in the patient group had moderate severity of portal gastropathy, and all 5 had H. pylori infection. However, all of the patients without H. pylori had mild portal gastropathy (p<0.001).

Chronic liver disease was previously reported to be among the reasons for peptic ulcer disease (2). H. pylori is a very well-known etiologic agent of gastritis and peptic ulcer. On the other hand, the H. pylori and portal gastropathy relationship is still debatable. Foster et al.(3) showed a relatively low prevalence (17%) of H. pylori in patients with portal gastropathy and explained it by the unsuitable milieu of the gastric mucosa in portal gastropathy. However, in our study, 15 of 25 (60%) of our patients and 13 of 22 (59.1%) of the healthy controls had H. pylori infection. We attribute this to the high H. pylori prevalence in our country.

Portal gastropathy severity and the H. pylori relationship is unclear in the literature (4-6) (Table 4). H. pylori was shown to increase in mild portal gastropathy, but to decrease with severity of portal gastropathy. This was attributed to mucosal atrophy and mucus layer changes in severe portal gastropathy. Five of the study patients (20%) had moderate portal gastropathy, and all 5 patients had H. pylori infection. Hematoxylin-eosin (HE) and Warthin-Starry staining might not disclose H. pylori in some specimens. However, foveolar lymphoid follicular presentation in these samples with H. pylori serology is compatible with H. pylori infection. This could explain urease-positive patients whose biopsy samples did not disclose H. pylori.

ß-2m is a minor plasma protein, secreted from the plasma membranes as a result of the continuous regeneration of membrane proteins in the cell surface of all nucleated cells. Conz et al.(1) showed ß-2m accumulation in H. pylori-positive gastric mucosa but not in H. pylori-negative gastric mucosa biopsies in uremic study patients with high serum ß-2m. They also showed ß-2m accumulation in H. pylori-positive gastric biopsy samples in healthy controls. We found significantly higher ß-2m concentrations in our patient group (44%) than in healthy controls (22.7%) (p<0.01). On the other hand, we did not find a relationship between ß-2m and severity of portal gastropathy (p>0.05).

In conclusion, there is no change in H. pylori infection frequency in portal gastropathy. ß-2m deposition in gastric mucosa is more common in H. pylori-positive patients. There is an inverse relationship between portal gastropathy severity and ß-2m deposition.

1. Conz PA, Dante S, Bernardini D, et al. Beta2 microglobulin and Helicobacter pylori infection in uremic dialysed patients. J Gastroenterol Hepatol 1992; 7: 191-3.

2. Iwao T, Toyanaga A, Sumino M, et al. Portal hypertensive gastropathy in patients with cirrhosis. Gastroenterology 1992; 102: 2060-5.

3. Foster PN, Wyatt JI, Bullimore DW, et al. Gastric mucosa in patients with portal hypertension. Prevalence of capillary dilation and Campylobacter pylori. J Clin Pathol 1989; 42: 919-21.

4. D?Amico G, Montalbano L, Traina M, et al. Natural history of congestive gastropathy in cirrhosis. Gastroenterology 1990; 99: 1558-64.

5. McCormick PA, Sankey A, Cardin F, et al. Congestive gastropathy and H. pylori: an endoscopic and morphometric study. Gut 1991; 32: 351- 4.

6. Özdemir S, fienturk H, Sezgiç N et al. The frequency of Helicobacter pylori infection in cirrhotic gastropathy. Gastroenteroloji Dergisi 1992; 1: 109-12.