Talley N J
Division of Gastroenterology, Mayo Medical School, Rochester, Minnesota 55902.
Aliment Pharmacol Ther. 1991;5 Suppl 1:145-62. doi: 10.1111/j.1365-2036.1991.tb00757.x.
Dyspepsia can be defined as the presence of upper abdominal pain or discomfort; other symptoms referable to the proximal gastrointestinal tract, such as nausea, early satiety, and bloating, may also be present. Symptoms may or may not be meal related. To be termed chronic, dyspepsia should have been present for three months or longer. Over half the patients who present with chronic dyspepsia have no evidence of peptic ulceration, other focal lesions, or systemic disease and are diagnosed as having non-ulcer (or functional) dyspepsia. Non-ulcer dyspepsia is a heterogeneous syndrome. It has been proposed that this entity can be subdivided into a number of symptomatic clusters or groupings that suggest possible underlying pathogenetic mechanisms. These groupings include ulcer-like dyspepsia (typical symptoms of peptic ulcer are present), dysmotility (stasis)-like dyspepsia (symptoms include nausea, early satiety, bloating, and belching that suggest gastric stasis or small intestinal dysmotility), and reflux-like dyspepsia (heartburn or acid regurgitation accompanies upper abdominal pain or discomfort). The aetiology of non-ulcer dyspepsia is not established, although it is likely a multifactorial disorder. Motility abnormalities may be important in a subset of dyspepsia patients but probably do not explain the symptoms in the majority. Epidemiological studies have not convincingly demonstrated an association between Helicobacter pylori and non-ulcer dyspepsia. Other potential aetiological mechanisms, such as increased gastric acid secretion, psychological factors, life-event stress, and dietary factors, have not been established as causes of non-ulcer dyspepsia. Management of non-ulcer dyspepsia is difficult because its pathogenesis is poorly understood and is confounded because of a high placebo response rate. Until more data are available, it seems reasonable that treatment regimens target the clinical groupings described above. Antacids are no more effective than placebo in non-ulcer dyspepsia, although a subgroup of non-ulcer dyspepsia patients with reflux-like or ulcer-like symptoms may respond to H2-receptor antagonists. However, there is no significant benefit of these agents over placebo in many cases. Bismuth has been shown to be superior to placebo in patients with H. pylori in a number of studies, but these trials had several shortcomings and others have reported conflicting findings. Sucralfate was demonstrated in one study to be superior to placebo, but this finding was not confirmed by another group of investigators. Prokinetic drugs appear to be efficacious, and may be most useful in patients with dysmotility-like and reflux-like dyspepsia.
消化不良可定义为上腹部疼痛或不适；也可能存在其他与近端胃肠道相关的症状，如恶心、早饱及腹胀。症状可能与进餐有关，也可能无关。若消化不良症状持续三个月或更长时间，则称为慢性消化不良。超过半数出现慢性消化不良的患者并无消化性溃疡、其他局灶性病变或全身性疾病的证据，被诊断为非溃疡性（或功能性）消化不良。非溃疡性消化不良是一种异质性综合征。有人提出，这一实体可细分为若干症状群或分组，提示可能的潜在发病机制。这些分组包括溃疡样消化不良（存在消化性溃疡的典型症状）、动力障碍（淤滞）样消化不良（症状包括恶心、早饱、腹胀和嗳气，提示胃潴留或小肠动力障碍）以及反流样消化不良（上腹部疼痛或不适伴有烧心或反酸）。非溃疡性消化不良的病因尚未明确，尽管它可能是一种多因素疾病。动力异常在一部分消化不良患者中可能很重要，但可能无法解释大多数患者的症状。流行病学研究并未令人信服地证明幽门螺杆菌与非溃疡性消化不良之间存在关联。其他潜在的病因机制，如胃酸分泌增加、心理因素、生活事件压力和饮食因素，尚未被确认为非溃疡性消化不良的病因。非溃疡性消化不良的治疗很困难，因为其发病机制了解甚少，且由于安慰剂反应率高而变得复杂。在获得更多数据之前，针对上述临床分组制定治疗方案似乎是合理的。在非溃疡性消化不良中，抗酸剂并不比安慰剂更有效，尽管一部分有反流样或溃疡样症状的非溃疡性消化不良患者可能对H2受体拮抗剂有反应。然而，在许多情况下，这些药物与安慰剂相比并无显著益处。在多项研究中，铋剂对幽门螺杆菌感染患者显示出优于安慰剂的效果，但这些试验存在若干缺陷，其他研究报告的结果相互矛盾。一项研究表明硫糖铝优于安慰剂，但另一组研究人员并未证实这一发现。促动力药物似乎有效，可能对动力障碍样和反流样消化不良患者最为有用。
