Page 2 - 53-Peptic ulcer diseases (Loét dạ dày)
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53 Peptic Ulcer Disease
Francis K.L. Chan, James Y.W. Lau
CHAPTER OUTLINE EPIDEMIOLOGY
The epidemiology of PUD has undergone remarkable changes
EPIDEMIOLOGY � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � 806 in the past 2 centuries. The risk of developing PUD, and dying
ETIOLOGY AND PATHOGENESIS � � � � � � � � � � � � � � � � � � � � 806 from PUD, increased in successive cohorts born between 1840 and
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Hp Infection � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � 807 1890, and then declined thereafter. There was a peak in the inci-
Use of Aspirin and Other NSAIDs � � � � � � � � � � � � � � � � � � 807 dence of GU in the first half of the 19th century and a subsequent
Other Causes of Ulcers and Idiopathic Ulcers � � � � � � � � � 808 peak in the incidence of DU in the second half of the 19th century.
Sonnenberg proposed a birth-cohort effect to explain the peaks in
CLINICAL FEATURES AND DIAGNOSIS � � � � � � � � � � � � � � � 808 the incidence of, and mortality from, peptic ulcers. Hp infection
MEDICAL THERAPY OF ACTIVE PEPTIC ULCER acquired during childhood or adolescence became manifested as
DISEASE � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � 810 peptic diseases in later years. As Hp infection gradually declined in
Pharmaceutical Agents � � � � � � � � � � � � � � � � � � � � � � � � � 810 the population over time, the prevalence of infection also gradually
shifted from a younger toward older age groups. The incidence of
Hp-associated Ulcers � � � � � � � � � � � � � � � � � � � � � � � � � � 811 DU and GU has declined in parallel with the decline in the preva-
NSAID Ulcers � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � 812 lence of Hp infection, likely a result of improved sanitary condi-
Other Causes of Ulcers and Idiopathic Ulcers � � � � � � � � � 812 tions and a safer food and water supply.
REFRACTORY ULCERS � � � � � � � � � � � � � � � � � � � � � � � � � � � 812 Based on physicians’ diagnoses, the annual incidence of PUD
PREVENTION OF ULCER DISEASE � � � � � � � � � � � � � � � � � � 812 ranges from 0.14% to 0.19% in developed countries. Based on
hospital diagnoses, the incidence is lower: 0.03% to 0.17%. The
Antacids � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � 812 prevalence of PUD ranges from 0.12% to 4.7% for physician-
H2RAs � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � 813 diagnosed, and from 0.1% to 2.6% for hospital-diagnosed case
Misoprostol � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � 813 series. There is a wide geographic variation in the prevalence
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PPIs � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � 813 of PUD. In an endoscopic series involving 1022 volunteers from
COX-2 Inhibitors (In Place of NSAIDs) � � � � � � � � � � � � � � � 813 Shanghai, China (average age, 48 years), the prevalence of PUD
Assessing Risk and Choice of Agent(s) � � � � � � � � � � � � � � 814 was 17.2%, of whom 93% were infected with Hp. 5
The most frequent complication from PUD is bleeding; the
COMPLICATIONS AND THEIR TREATMENT � � � � � � � � � � � 815 reported annual incidence of bleeding among populations varies
Bleeding � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � 815 from 19 to 57 per 100,000 individuals (≈0.02% to 0.06%). Peptic
Perforation � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � 817 ulcer perforation (PULP), less frequent than bleeding, has reported
Obstruction � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � 818 incidences of 4 to 14 per 100,000 individuals (0.004% to 0.014%).
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STRESS ULCERS � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � � 819 Along with a decline in uncomplicated PUD cases, there is a similar
decline in incidence of ulcer complications in recent years. Laine and
colleagues used a national inpatient database to calculate the annual
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incidence of, and mortality from, GI complications during 2001 to
2009. During this time period, the incidence of peptic ulcer bleeding
An ulcer in the GI tract can be defined as a 5 mm or larger break in fell from 48.7 to 32.1 per 100,000. Over the same period, the age-
the lining of the mucosa, with appreciable depth at endoscopy or and sex-adjusted case fatality rates from UGI bleeding decreased
with histologic evidence of submucosal extension. An erosion is a from 3.8% to 2.7%. In 2009, the case fatality rate for UGI bleeding
break less than 5 mm. The distinction between an ulcer and an ero- (2.45%) was considerably lower than for UGI perforation (10.7%).
sion is somewhat arbitrary. The term PUD is used to include ulcer- In a nationwide population-based cohort study of 403,567 Taiwan-
ations and erosions in the stomach and duodenum from a number ese patients, hospitalizations for complicated peptic ulcers decreased
of causes. These lesions are called “peptic” because the enzyme significantly over a 10 year period ; thus the annual incidence of hos-
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pepsin, proteolytic at an acidic pH (see Chapter 51), plays a major pitalizations for bleeding DU or for perforated DU fell from 108 to
role in causing the mucosal breaks, regardless of the inciting agent. 40 and from 9.8 to 5.8 per 100,000, respectively. A similar decline
Decades of research focused on the role of gastric acid was evident for bleeding and perforated GUs (from 117 to 61 and
secretion and the effects of stress, personality type, and from 11 to 6 per 100,000, respectively).
genetics in the pathogenesis of PUD. The discovery of the
histamine-2 (H 2 ) receptor and development of H2RAs, and ETIOLOGY AND PATHOGENESIS
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subsequently PPIs, led to major changes in the management
of PUD. The discovery of Hp and its role in PUD (see Chap- The principal risk factors of PUD are Hp infection and NSAID
ter 52) transformed PUD from a chronic, recurrent disease use (Fig. 53.1) and as will be discussed, many patients with PUD
to a curable one. Hp infection remains an important cause have both of these risk factors. On the other hand, PUD patients
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of PUD in the world. In developed countries, frequent use of may have neither of these risk factors (Hp-negative, NSAID-
NSAIDs, including low-dose aspirin for cardiovascular indi- negative ulcers); some of these latter patients will have another
cations, has emerged as a leading cause of PUD, especially cause of ulcer such as gastrinoma (ZES; see Chapter 34), whereas
among the aging population. others will have ulcers that are idiopathic.
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