위암 환자에서의 Helicobacter pylori IgG 항체 양성률과 혈청 Pepsinogen I,II 농도

Abstract

[한글]

H.pylori 감염은 만성 위전정부 위염과 소화성 궤양을 일으킨다는 사실 이외에도 최근에는 위암발생의 위험요인으로 주목을 받고 있다. 그러나 한국에서는 위암의 발생이 높고 H.pylori 유병률 또한 정상성인의 약 70%로 비교적 높으므로 위암과의 연관성을 밝히는

데 어려움이 있다. 위암, 위축성위염 그리고 장화생에서는 혈청 pepsinogen Ⅰ 농도가 감소하나 H.pylori 감염은 혈청 pepsinogen Ⅰ 및 Ⅱ 농도를 증가시키므로 H.pylori 감염이 위암환자에서 위암 전구병소인 위축성 위염이나 장화생을 유발하였다면 혈청 pepsinogen

Ⅰ 및 Ⅱ 농도가 이를 반영할 수 있을 것이다.

본 연구자는 H.pylori 감염과 위암과의 연관성을 밝히기 위해서 174명의 위암환자와 165명의 정상성인에서 H.pylori IgG 항체(효소 면역 측정법)와 혈청 pepsinogen Ⅰ 및 Ⅱ 농도(면역 방사계수 측정법)를 비교 분석하여 다음과 같은 결과를 얻었다.

1. H.pylori IgG 항체 양성률은 위암군이 58.6%이고 정상군이 70.9%로 양군간에 차이가 없었고 연령별로 비교할 때도 양군간에 통게적으로 유의한 차이가 없었다.

2. H.pylori IgG 항체 양성률은 위암의 조직학적 형태에 따라 분류하여 장형 위암 (66.3%)과 미만형 위암(60.0%)간에 차이가 없었고 위암위치에 따라 분류하여 비분문암(64.8%)이 분문부암(12,5%) 보다 유의하게 높았다 (P <0.05)

3. 연령별로 혈청 pepsinogen Ⅰ 및 Ⅱ 농도를 비교할 때, 40, 50, 60대에서 위암군이 대조군보다 혈청 pepsinogen Ⅰ 농도가 유의하게 낮았다(p < 0.05). 위암군에서는 H.pylori 감염군과 비감염군 사이에 혈청 pepsinogen Ⅰ 및 Ⅱ 농도에 차이가 없었으나 대조군에서는 H.pylori 감염군이 비감염군보다 혈청 pepsinogen Ⅰ 및 Ⅱ 농도가 유의하게 높았다 (p< 0.05).

이상의 결과를 종합할 때 위암군에서 종양의 진행도, 조직형, 병기에 따른 H.pylori IgG 항체 양성률은 차이가 없었으나 종양의 위치에 따라서는 분문부암보다 비분문부암에서 양성률이 의미있게 높았다. 또한 대조군과는 달리 위암군에서는 h.pylori 감염여부에 따

른 Pepsinogen Ⅰ 및 Ⅱ 농도에 차이가 없음을 알 수 있어 PG Ⅰ 및 Ⅱ 농도변화에 근거한 H.pylori 감염과 위암발생사이의 직접적 연관성은 입증할 수 없는 것으로 사료되었다.

Helicobacter pylori infection and serum pepsinogen level in gastric carcinoma.

IL Ran Hwang

Department of Medical Science The Graduate School, Yonsei University.

(Directed by Professor Sang In Lee)

Helicobacter pylori (H.pylori) infection, thought to be causally related to

peptic ulcer and chronic antral gastritis, may also be associated with gastric

cancer. A considerable number of normal subjects in Korea were infected with

H.pylori and there was shill controversy in the role of H.pylori infection in

gastric carcinogenesis. Serum pepsinogen Ⅰ and Ⅱ levels may be indicator of

precancerous lesions such as atrophic gastritis and intestinal metaplasia, which

were known to be associated with gastric cancer and may be induced by H.pylori

infection.

The levels of senum H.pylori IgG antibody were measured using enzyme linked

immunosorbent assay and the levels of serum pepsinogen Ⅰ and Ⅱ using

immunoradiometric assay in 174 gastric cancer patients and 165 controls. There was

no statistically significant difference between the positive incidence of H.pylori

infection in gastric cancer patient (60.3%) and in control group (70.9%).

Antibodies to H.pylori were detected in 64.8% of non-cardiac gastric cancer

patients but in only 12.5% of cardiac gastric cancer patients (p<0.05). The

positive incidences of H.pylori infection in intestinal and diffuse histologic type

of gastric cancer were similar. Serum pepsinogen Ⅰ and Ⅱ levels were higher in

H.pylori infected controls than in uninfected controls (p<0.05). Serum pepsinogen

Ⅰ level was lower in gastric cancer patients than control group (p<0.05). However,

there was no difference in serum pepsinogen Ⅰ and Ⅱ levels between

H.pylori-infected and uninfected gastric cancer patients.

In conclusion, the positive incidece of H.pylori infection in gastric cancer was

similar to that in controls and there was no evidence of the direct relationship

between H.pylori infection and gastric carcinogenesis.

[영문]

Helicobacter pylori (H.pylori) infection, thought to be causally related to peptic ulcer and chronic antral gastritis, may also be associated with gastric cancer. A considerable number of normal subjects in Korea were infected with H.pylori and there was shill controversy in the role of H.pylori infection in gastric carcinogenesis. Serum pepsinogen Ⅰ and Ⅱ levels may be indicator of precancerous lesions such as atrophic gastritis and intestinal metaplasia, which were known to be associated with gastric cancer and may be induced by H.pylori infection.

The levels of senum H.pylori IgG antibody were measured using enzyme linked immunosorbent assay and the levels of serum pepsinogen Ⅰ and Ⅱ using immunoradiometric assay in 174 gastric cancer patients and 165 controls. There was no statistically significant difference between the positive incidence of H.pylori

infection in gastric cancer patient (60.3%) and in control group (70.9%).

Antibodies to H.pylori were detected in 64.8% of non-cardiac gastric cancer patients but in only 12.5% of cardiac gastric cancer patients (p<0.05). The positive incidences of H.pylori infection in intestinal and diffuse histologic type of gastric cancer were similar. Serum pepsinogen Ⅰ and Ⅱ levels were higher in H.pylori infected controls than in uninfected controls (p<0.05). Serum pepsinogen Ⅰ level was lower in gastric cancer patients than control group (p<0.05). However, there was no difference in serum pepsinogen Ⅰ and Ⅱ levels between

H.pylori-infected and uninfected gastric cancer patients.

In conclusion, the positive incidece of H.pylori infection in gastric cancer was similar to that in controls and there was no evidence of the direct relationship between H.pylori infection and gastric carcinogenesis.