Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1033_Библиотеки_им_академика_М_И_Перельмана
.pdf
444
https://t.me/medicina_free
F. Serrot
Endoscopic Features andClassication
ofEsophagitis
The endoscopic assessment of esophageal mucosal changes in
patients with reux symptoms is important to diagnose patients at
various degrees of severity. It is well known that the endoscopic
severity of esophagitis correlates with the likelihood of responding to certain treatments and with the risk of developing complications. Gastroesophageal reux disease with endoscopically
identiable lesions (erosions, stricture, and Barrett’s esophagus)
is dened as erosive gastroesophageal reux disease (GERD).
Fewer than 50% of patients with typical GERD symptoms have
endoscopically recognizable mucosal lesions [4]. On the other
hand, non-erosive reux disease (NERD) is characterized by the
presence of reux symptoms, abnormal pH monitoring, and
absence of endoscopically visible lesions, but with the histological changes consistent with microscopic esophagitis [5]. NERD
patients account for up to 60% of all patients with reux symptoms [6]. For this reason, an early diagnosis of GERD is crucial
because the chronic reux esophagitis is a key risk factor for the
development of Barrett’s esophagus, which is a precursor lesion
for esophageal adenocarcinoma.
A diagnosis of erosive reux esophagitis is established when
there are patchy, striated, or circular and conuent epithelial
defects (erosions) in the mucosa in the distal esophagus. Nearly
all of the guidelines on the diagnosis and treatment of reux disease recommend that reux esophagitis should be classied endoscopically. The European guidelines also recommend that ndings
such as stenosis, ulcer, Schatzki ring, metaplasia as well as the
presence of hiatal hernia should be documented [7].
Due to its ease of use and very minor interindividual variability
in the assessment, the Los Angeles (LA) classication should be
used. The LA classication system was published in its nal form
back in 1999 (Table32.1) [8].
It was developed by the International Working Group for the
Classication of Esophagitis, supported by the World Organization
of Gastroenterology, and was rst proposed in 1994. It was rst
32 Esophagitis
https://t.me/medicina_free
Table 32.1 Los Angeles classication of esophagitis (adapted from Lundell
etal. [8])
445
presented at the Los Angeles World Congress of Gastroenterology,
and hence the name of the classication. It is the most validated
classication system. Furthermore, it has been consistent at predicting the outcome of acid reux therapy, correlates well with
other tests of acid reux such as 24-h pH monitoring studies, and
when compared with other grading systems, it was the most
reproducible and practical [8].
Although the clinical signicance and accuracy of other ndings are not included in the LA classication, such as minimal
mucosal changes, it is needed to be validated rigorously before
446
ab
cd
https://t.me/medicina_free
F. Serrot
incorporating them into the classication system. Advances in
endoscopic imaging techniques have allowed the visualization of
these changes and could potentially in the future become relevant
at the time of evaluation of patients with GERD.
It is imperative to obtain an adequate mucosal visualization.
Meticulous washing with mucolytic and antifoaming agents as
well as the use of high-denition endoscope are an important
aspect of the technique.
Accurate endoscopic assessment of reux esophagitis presence and severity is vital in making accurate decisions about
patients' management and prognosis. Different types of therapy
will be indicated depending on the extent and severity of the
reux esophagitis seen on endoscopic evaluation as well as on the
extent of the symptoms.
Patients with mild cases of esophagitis, LA grade A/B
(Fig.32.1) should be treated with a PPI at the standard dosage for
Fig. 32.1 Los Angeles (LA) classication is the endoscopic scoring system
most commonly used to grade the severity of reux esophagitis. The LA system divides reux esophagitis into four categories (a–d) based on the extent
of esophageal mucosal breaks
32 Esophagitis
https://t.me/medicina_free
around 4 weeks. Most cases improve their symptoms as well as
endoscopic features. On the other hand, patients with severe
cases, LA grade C/D (Fig.32.1) should receive 8 weeks of PPI at
the standard dosage. These patients with more severe esophagitis
are at greater risk of local complications, cannot afford PPI step
down, and often require anti-reux surgery [9].
Once diagnosis of reux esophagitis has been made and treatment indicated, a decision has to be made regarding the need of
follow-up endoscopy. Evidence shows that repeat endoscopy is
not usually indicated for the control of healing of esophagitis. The
absence of symptoms is a relatively sensitive indication of adequate treatment. Symptom recurrence should be taken as an indication for the need of intensication of therapy rather than
endoscopy [10].
Lack of symptom improvement with PPI therapy, patients with
severe grades of esophagitis as well as the need to perform further
tissue sampling to clarify or conrm diagnosis of complications
such as Barrett’s metaplasia masked by erosive esophagitis are
some indications of follow-up endoscopy.
447
The Histopathology ofEsophagitis
The esophagus is lined by nonkeratinizing, stratied squamous
epithelium, and the stomach by columnar epithelium, respectively. The border between the stomach and the esophagus, that is
the GEJ, contains the lower esophageal sphincter, which is characterized as a variable zone of 2–4cm in length and a pressure of
approximately 10–26 mmHg, which is well above both intragastric and intra-esophageal pressures [11].
Upon endoscopy, the GEJ is the point where the tubular esophagus meets the gastric mucosal folds, also known as the “Z-line”.
In “normal” individuals, the GEJ is identical with the squamocolumnar junction (SCJ), the histological transition point between
esophageal squamous and gastric columnar epithelium (Fig.32.2).
In patients with GERD, the SCJ moves proximally as a result
of metaplastic changes. Thus, the histological SCJ is located
above the anatomical GEJ (Fig.32.3). Changes related to acute
448
https://t.me/medicina_free
Fig. 32.2 The anatomy of the gastroesophageal junction (GEJ) and the squamocolumnar junction (SCJ). In normal individuals, the SCJ is located directly
at the proximal margin of the gastric folds which corresponds to the anatomic
GEJ
F. Serrot
Fig. 32.3 In patients with GERD, the SCJ may become displaced proximally due to columnar metaplasia of the distal esophagus
and/or active GERD are diagnosed in squamous epithelium sampled from the distal esophagus, while the chronic consequences of
GERD, such us columnar metaplasia, are present in biopsies
sampled immediately below the SCJ.GERD is the major cause of
inammation and mucosal breaks of the squamous epithelium in
the distal esophagus. As a consequence, the reparative capacity of
the native squamous epithelium may be unable to tolerate the
acidic and/or proteolytic nature of persistent reux, and it adapts
to the damaging stimuli by converting into metaplastic columnar
epithelium.
32 Esophagitis
https://t.me/medicina_free
449
The histological diagnosis of GERD is generally believed to be
a tool of limited value [12]. The sensitivity and specicity of the
histological GERD diagnosis are generally believed to be low.
Several studies have, however, demonstrated that histology, if systematically applied, may render important diagnostic clues
(Fig. 32.4). This holds particularly true for individuals with
NERD, of whom approximately two-thirds have histological evidence of esophageal injury [13].
Fig. 32.4 Active reux esophagitis with basal cell layer hyperplasia and
elongation of stromal papillae
450
https://t.me/medicina_free
F. Serrot
In summary, GERD continues to be a burden to healthcare systems around the world. The diagnosis is mainly clinical. There are
specic indications for endoscopic evaluation of patients with
GERD such as failure of medical management with PPI. An accurate endoscopic assessment of reux esophagitis presence and
severity is vital in making accurate decisions about patients' management and prognosis. Los Angeles endoscopic classication is
the most validated, reproducible, and accurate in this setting, and
it should uniformly be used among endoscopists performing
upper gastrointestinal endoscopy procedures.
References
1. El-Serag HB, Sweet S, Winchester CC, Dent J.Update on the epidemiology of gastro-oesophageal reux disease: a systematic review. Gut.
2014;63:871–80. https://doi.org/10.1136/gutjnl- 2012- 304269.
2. Katz PO, Gerson LB, Vela MF.Guidelines for the diagnosis and management of gastroesophageal reux disease. Am J Gastroenterol.
2013;108:308–28.
3. Krugmann J, Neumann H, Vieth M, Armstrong D.What is the role of
endoscopy and oesophageal biopsies in the management of GERD? Best
Pract Res Clin Gastroenterol. 2013;27:373–85.
4. Fass R, Ofman JJ.Gastroesophageal reux disease–should we adopt a
new conceptual framework? Am J Gastroenterol. 2002;97(8):1901–9.
5. Vakil N, van Zanten SV, Kahrilas P, Dent J, Jones R, Global Consensus
Group. The Montreal denition and classication of gastroesophageal
reux disease: a global evidence-based consensus. Am J Gastroenterol.
2006;101:1900–20.
6. Modlin IM, Hunt RH, Malfertheiner P, Moayyedi P, Quigley EM, etal.
Diagnosis and management of non-erosive reux disease–the Vevey
NERD Consensus Group. Digestion. 2009;80:74–88.
7. Koop H, Fuchs KH, Labenz J, Lynen Jansen P, Messmann H, etal. S2k
guideline: gastroesophageal reux disease under the leadership of the
German Society for Gastroenterology, Digestive and Metabolic Diseases.
Z Gastroenterol. 2014;52(11):1299–346.
8. Lundell LR, Dent J, Bennett JR, Blum AL, Armstrong D, etal. Endoscopic
assessment of oesophagitis: clinical and functional correlates and further
validation of the Los Angeles classication. Gut. 1999;45(2):172–80.
https://doi.org/10.1136/gut.45.2.172.
9. Dent J.Management of reux disease. Gut. 2002;50(V):17–20.
32 Esophagitis
https://t.me/medicina_free
10. Richter JE, Peura D, Benjamin SB, Joelsson B, Whipple J.Efcacy of
omeprazole for the treatment of symptomatic acid reux disease without
esophagitis. Arch Intern Med. 2000;160:1810–6.
11. Odze RD. Unraveling the mystery of the gastroesophageal junction: a
pathologist’s perspective. Am J Gastroenterol. 2005;100:1853–67.
12. Takubo K, Honma N, Aryal G, Sawabe M, Arai T, etal. Is there a set of
histologic changes that are invariably reux associated? Arch Pathol Lab
Med. 2005;129:159–63.
13. Dent J.Microscopic esophageal mucosal injury in nonerosive reux disease. Clin Gastroenterol Hepatol. 2007;5:4–16.
451
Eosinophilic Esophagitis
https://t.me/medicina_free
33
TaylerJ.James
andNikolaiA.Bildzukewicz
Pathophysiology andEpidemiology
Eosinophilic esophagitis (EoE) is an allergic condition of the
esophagus caused by antigens that trigger an immune response in
susceptible individuals. As with other allergic conditions, a number of environmental and genetic factors are suspected to play a
role in a patient’s susceptibility to EoE [1].
The incidence of EoE in the United States is increasing, with
the current prevalence estimated between 0.5 and 1 case per 1000
[2]. EoE preferentially affects white males and young adults,
although all ages can be affected [3, 4].
Most patients diagnosed with EoE have a personal or family
history of atopic disorders such as atopic dermatitis, asthma, or
allergic conjunctivitis [5]. Seasonal variation patterns seen in EoE
suggest a role of aeroallergens in addition to food allergens as
potential triggers of the response [6, 7].
T. J. James · N. A. Bildzukewicz (*)
University of Southern California, Los Angeles, CA, USA
e-mail: Tayler.james@med.usc.edu; Nikolai.bildzukewicz@med.usc.edu
© Society of American Gastrointestinal and Endoscopic Surgeons
(SAGES) 2023
A. D. Patel et al. (eds.), The SAGES Manual of Physiologic
Evaluation of Foregut Diseases,
https://doi.org/10.1007/978-3-031-39199-6_33
453
454
https://t.me/medicina_free
T. J. James and N. A. Bildzukewicz
Presentation
EoE affects both children and adults, and symptoms vary with
age. Younger children can present with feeding difculties such as
gagging and refusal of solid food, whereas older children more
commonly present with abdominal pain, vomiting, and/or dysphagia [8, 9]. The most common symptom in adults is dysphagia
to solid foods [4]. Other symptoms in adults include food impaction, chest and/or abdominal pain, and GERD-like symptoms
such as heartburn and regurgitation [2, 4, 5].
The relationship between EoE and GERD is complex and differentiating between the two can be difcult. Historically, EoE
was thought to be solely a manifestation of GERD.However, not
all patients with suspected EoE were found to respond to antireux treatment, thus suggesting EoE as its own clinical entity
[10]. This led to a 2007 consensus denition to include “the
absence of pathological GERD” in the diagnostic criteria for EoE,
but this qualier was later eliminated due to a number of overlapping features between the two [11, 12].
Heartburn and dysphagia are symptoms common in both
GERD and EoE.Eosinophils can be present in biopsies of both,
although patients with GERD typically have <7 eosinophils per
high power eld compared to >15 that is diagnostic of EoE [3]. It
has been suggested that GERD can predispose at-risk patients to
EoE by increasing the permeability of the esophageal mucosa,
allowing food antigens to penetrate the esophageal wall and incite
the allergic response [13]. Additionally, EoE may contribute to
the development of GERD, as eosinophils produce substances
that can relax the lower esophageal sphincter and induce tissue
remodeling seen in GERD [14, 15]. In summary, while it appears
that EoE is a separate clinical entity from GERD, the pathophysiology and clinical presentations of the two are closely intertwined.
Diagnosis
The diagnosis of EoE, as determined by a 2018 expert panel,
requires the following: symptoms of esophageal dysfunction, at
least 15 eosinophils per high power eld on esophageal biopsy,
Соседние файлы в папке Библиотека им академика М.И. Перельмана