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.
         806
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