Helicobacter pylori - Portal Neonatal

34
Infectious esophagitis
A definite diagnosis of HSV esophagitis requires
endoscopy and histology of the esophageal
mucosa, even though contrast radiographic
appearance of the esophagus may be suggestive by
showing multiple vesicles and ulcers as stellate or
volcano structures. Endoscopy usually reveals
small, well-circumscribed ulcers (Figure 3.3),
rarely vesicles, whereas deep ulcers, as seen with
CMV, are rare. 21,22 Brushing or biopsies should be
taken from the edge or periphery of ulcerations,
given that HSV infects squamous epithelial cells. 23
Histology reveals intranuclear Cowdry type A
inclusion bodies (eosinophilic material), ballooning
degeneration cells, multinucleated giant cells,
ground-glass-like nuclei and margination of chromatin.
24 Confirmation may require immunoperoxidase
staining or positive viral culture.
Although HSV esophagitis has a spontaneous resolution
in a normal host, antiviral therapy is
commonly used both in immunocompetent and
immunocompromised subjects. Several uncontrolled
trials and clinical experience indicate the
efficacy of acyclovir, a nucleoside analog, for the
treatment of HSV esophagitis. 25 Parenteral
acyclovir should be initiated until the patient can
be converted to oral therapy (when dysphagia or
odynophagia is resolved). Generally, patients are
treated with acyclovir for 7–10 days. Because resistance
to acyclovir has been reported, therapy with
foscarnet should be considered in case of clinical
failure with acyclovir. 25 Acyclovir is efficacious in
prophylaxis for patients undergoing transplantation
and those who are HSV-antibody-positive.
Table 3.4 lists the available antiviral agents for
treating viral esophagitis.
CMV is the most frequent infectious complication
of organ transplantation, occurring in 60–70% of
these patients. Esophagitis is one of the most
common manifestations in this setting. CMV is by
far the most frequent cause of esophageal ulcer in
patients with advanced HIV infection and a CD4
count lower than 100mm 3 (see reference 26). In
contrast to HSV esophagitis, CMV esophagitis has
rarely been detected in an immunocompetent
host; 27 however, CMV and HSV are equally
common organisms in transplant patients who do
not receive antiviral prophylaxis. 28 Odynophagia
is a constant feature and is typically severe; chest
pain of esophageal origin, mainly occurring upon
deglutition, is also described. Prior or co-existent
Figure 3.3 Herpes simplex virus esophagitis. Small, wellcircumscribed
ulcers (short arrows) and two small vesicles
(long arrows) in the lower third of the esophageal mucosa.
CMV infection in other regions (e.g. retinitis,
colitis) is not uncommonly found. 29
As with HSV, a definite diagnosis of CMV
esophagitis requires endoscopy and biopsy.
Contrast X-ray examination of the esophagus
reveals either focal or diffuse images of mucosal
ulcerations. Ulcers may be vertical or linear with
central umbilication, or may be diffuse and superficial;
30 they are usually deep and large in patients
with advanced HIV infection. Endoscopy remains
the definitive diagnostic tool for CMV esophagitis.
The endoscopic appearance is variable and may
include multiple shallow ulcers, solitary ulcers or
diffuse superficial esophagitis (Figure 3.4). In
contrast to Candida and HSV, brushing cytology
has a poor sensitivity and multiple biopsies should
be taken. Since the cytopathic effect of CMV
occurs at the level of endothelial and mesenchymal
cells in the granulation tissue, endoscopic
biopsies must be taken from the base of the ulcer. 31
Histology typically shows large cells with intranuclear
and intracytoplasmic inclusions having an
eosinophilic appearance. Immunohistochemical
stains can reveal more infected cells than routinely
appreciated with hematoxylin and eosin staining.
Mucosal biopsy is also more specific than viral
culture as with other esophageal infections. 32