幽門螺旋桿菌與十二指腸潰瘍因果相關的實證評估

Helicobacter Pylori and Duodenal Ulcers Assessment of the Evidence Suggesting Causation

10.6200/TCMJ.2006.3.3.02

王培東(Pair-Dong Wang)

柯霍準則 ； 幽門螺旋桿菌 ； 十二指腸潰瘍 ； 因果相關 ； Koch's postulates ； Helicobacter pylori ； Duodenal ulcer ； Causation

北市醫學雜誌

3卷3期（2006 / 03 / 01）

201 - 209

繁體中文

柯霍準則用來證實人類的某些疾病是由微生物所引起，是有其價值的。一位組織學上胃黏膜正常的自願者，吞服幽門螺旋桿菌，隨後發生一些輕微腸胃不適，症狀持續14天之久，在吞下細菌後的第10天，組織學上證實出現胃炎現象，但到第14天，這些症狀已大部份消失，推測這種急性幽門桿菌性胃炎可能會進展到一個慢性發炎狀態，再發展成消化性潰瘍。幽門螺旋桿菌感染和十二指腸潰瘍之間的相關性是非常強和一致性，時序性相關和生物學上的贊同性也存在，根除幽門桿菌後又有一個非常正面的效果；然而，正如大多數傳染病，單獨幽門桿菌並不是引起十二指腸潰瘍的充分因子，其他環境因子（例如吸菸、酗酒）和遺傳因子也很重要。長久以來一直認為十二指腸潰瘍是黏膜保護性和侵犯性因子的不平衡所造成，其實馬歇爾(Barry J. Marshall)和華倫(J. Robin Warren)兩人所發表的假說，與此觀念並不衝突，因為幽門桿菌感染過的黏膜是較柔弱而且容易受到胃酸的侵襲破壞；“無胃酸，無潰瘍”的觀念仍然是正確的，但必須藉“無幽門桿菌，無潰瘍”才是中肯的陳述。他們兩人的研究發現，成功地扭轉了醫界對消化性潰瘍的治療方式，因為現在可使用抗生素去中止十二指腸潰瘍疾病的自然史，正如“屋頂漏水”的觀念，最好的方法是去修補屋頂（黏膜），而不是中止下雨（胃酸）。

It has been accepted for many years that Koch's postulates are the reference standard to be used when linking an infective agent and a disease. A volunteer with histologically normal gastric mucosa received Helicobacter pylori by mouth. A mild gastroenteric upset developed and this lasted 14 days. Histologically proven gastritis was present on the tenth day after the ingestion of bacterial culture, but this had largely resolved by the fourteenth day. It is suggested that this disorder may under certain circumstances progress to a chronic infection, which predisposes the person infected to peptic ulceration. The association between H. pylori infection and duodenal ulcer is strong and consistent. A temporal relationship and biological plausibility has been shown to exist for H. pylori and ulcer formation and eradication of the bacterial infection has a very positive effect on the occurrence of ulcers. However, as in most infectious diseases, H. pylori alone is not sufficient to provoke the disease. Environmental factors such as smoking and drinking as well as possible genetic factors are also important. It has been recognized for many years that duodenal ulcers are a consequence of an imbalance between the protective and aggressive factors of the mucosa. This hypothesis is not contradictory to the relationship between H. pylori and ulcers described above. H. pylori infected mucosa is weakened and this would allow the main aggressive factor in the stomach, acid, to exert its detrimental effect. The concept of ”no acid, no ulcer” is still valid but should be counterbalanced by ”no H. pylori, no ulcer”. This theory has therapeutic implications since it is now possible to stop the natural history of the disease by administering antibiotics and this fits the ”leaking roof” concept. It is better to repair your roof (your mucosa) than to stop the rain (your acid).