Introduction
Since the invention of flexible fiber-optic endoscope in 1957, several modifications
and improved techniques have been developed to enhance the diagnostic yield of the
endoscopy procedure. The major drawback of conventional white light endoscopy (WLE)
is that it lacks accuracy in diagnosis and differentiation of various benign and premalignant
mucosal gastrointestinal lesions.[1] To overcome this, image-enhanced endoscopy techniques providing high-definition
images with good resolution and contrast enhancement have been developed. One such
technique is narrow-band imaging (NBI).[2]
NBI functions by filtering the illumination light. The red component of the standard
red, green, and blue filters is rejected and the selected bandwidth of the blue and
green lights is transmitted ([Fig. 1]). The mucosa is illuminated selectively with narrow-band wavelengths of blue (415
± 15 nm) and green (540 ± 15 nm).[3] The hemoglobin absorbs light at both these wavelengths and mucosa reflects it. The
blood vessels thereby appear dark brown against a light background providing the necessary
contrast between blood vessels and mucosa. While doing endoscopy procedure, real-time
change from white light to NBI is possible by using a “switch” whereby wavelength
of specific bandwidths 415 ± 15 nm and 540 ± 15 nm is only transmitted by a filter
that exists at the distal tip of the endoscope. This narrow band light illuminated
mucosa is reflected and the light reaches the couple charged device (CCD) which produces
electronic signals based on amount and wavelengths reflected. The signal from the
CCD gets processed by the video processor which resynthesizes the final output image.
Colors in final image are allocated by processor according to the human visual perception.
Fig. 1 Overview of NBI system and its principle. NBI, narrow-band imaging.
Normal Appearance of Stomach on NBI
On NBI, the normal gastric mucosa reflects different morphological architecture of
surface (S) and microvascular pattern (V) in the corpus and antrum referred to as
SV pattern.[4] Yao described the surface and vascularpattern of gastric mucosa using microanatomical
components of mucosa.[5] The major structural or surface components, that is, S pattern refers to the marginal
crypt epithelium, the crypt opening or pit, and the intervening portion between crypts.
In V, that is, vascular pattern, vessels are described as the subepithelial capillary
network and the collecting venule. When there is difficulty in categorizing a vessel
as capillary or venule, this is referred to microvessel.
In corpus, the marginal crypt epithelium is seen as whitish circle surrounding the
crypt opening.[5]
[6]
[7] The latter is seen as a round to oval brown dot in center of subepithelial capillary
network which appears as dark brown anastomosing capillaries giving a honeycomb appearance.
The intervening part appears light pink. The capillaries drain into deeper placed
collecting venules that are perceived as cyancolored spider-like/starfish-like thick
vessels interspersed regularly in mucosa[4]
[5]
[6]
[7]
[8] ([Fig. 2A]).
Fig. 2 (A) Normal corpus mucosa of stomach: (left) as seen by NBI without magnification, (right)
NBI with magnification: regular round to oval pits with honeycomb like SECN pattern
(blue arrow) and spider like collecting venules (green arrow). (B) Normal antral mucosa of stomach: (left) as seen by NBI without magnification, (right)
NBI with magnification: regular polygonal pits (red arrow) with coil or spring like
SECN pattern (blue arrow) and absence of collecting venules. NBI, narrow-band imaging;
SECN, subepithelial capillary network.
In the antrum, there are ridges that are separated by sulci. Each coil or wave-shaped
dark brown colored subepithelial capillary network is located at apical part of the
ridge and are separated by linear or reticular crypt opening[7]
[8]
[9] ([Fig. 2B]). The capillary vessels often anastomose to each other and appear as open loops.
The collecting venules are not normally seen in antrum as they are anatomically located
in the deeper plane compared with those in the corpus.
Body of the stomach is characterized by regular arrangement of connecting venules
and mucosa showing regular, small pits with dark areas encircling light areas. On
the other hand, antrum has well-defined ridge pattern without connecting venules and
regular circular areas in mucosa with light areas surrounding dark areas. These differences
are attributable to differences in vascular pattern and presence of connecting venules
at deeper level in antrum.[10]
NBI Appearances of Common Benign Gastric Lesions
Atrophic Gastritis/Gastric Atrophy
In atrophic gastritis, secondary to chronic inflammation of the gastric mucosa as
with Helicobacter pylori infection (85%), the rate of cell loss may exceed the ability of the stem cells to
replace lost cells of surface mucosa and glands resulting in thinning of the mucosa.
With white light endoscopy, atrophic gastritis is seen as atrophic mucosal folds that
are pale with a shiny surface; submucosal vessels are prominent. These appearances
are neither sensitive nor specific for atrophic gastritis.[11]
With NBI, there is loss of pits and subepithelial capillary network with irregular
arrangement of prominent collecting venules ([Fig. 3]). The sensitivity and specificity of these findings approaches up to 90 and 96%,
respectively.[12]
[13] Atrophic gastritis may vary from mild to severe. Complete loss of pits may be seen
in severe atrophy. There is not much data on role of NBI in detecting mild atrophy.
Fig. 3 Chronic atrophic gastritis (CAG): atrophied folds with pale mucosa in CAG. NBI showing
obscured surface and vessel pattern with irregular SECN and visible submucosal vessels.
NBI, narrow-band imaging; SECN, subepithelial capillary network.
Intestinal Metaplasia
White light endoscopy of the gastric mucosa correlates poorly with histological findings.[14]
[15]
[16]
[17] Intestinal metaplasia refers to replacement of foveolar and glandular epithelium
in oxyntic or antral mucosa by intestinal epithelium and is considered as the “break
point” in the gastric carcinogenesis cascade.
On WLE, intestinal metaplasia appears as shallow depressed and reddish area, slightly
raised or whitish flat area or flat lesion with color, similar to the background with
minimal morphological changes.[18]
[19] NBI has an additional benefit of differentiating intestinal metaplasia from normal
mucosa by outlining the color differences. A meta-analysis of four studies reported
sensitivity and specificity of 86 and 77%, respectively, for diagnoses of intestinal
metaplasia (IM) by NBI.[20]
Bansal et al observed that the presence of a ridge or villous pattern by NBI (pseudopylorization
of oxyntic mucosa) has a high specificity and sensitivity (80 and 100%, respectively)
for identifying intestinal metaplasia.[10] Uedo et al described a novel finding of fine blue–white lines at the crest of epithelial
surface described as the “light blue crests” on NBI–magnifying endoscopy (ME) with
a high sensitivity (89%), specificity (93%), and accuracy (91%) for the diagnosis
of IM.[21] In absence of magnification, the light blue crest is seen as white-blue (cyan color)
patches on NBI. It is defined as a fine blue–white line on the crest of the epithelial
surface/gyri ([Fig. 4]).
Fig. 4 Intestinal metaplasia (IM): (left) antrum showing slightly raised pale lesion (blue
arrow); (right) NBI-ME showing ridge pattern with LBC. ME, magnifying endoscopy; NBI,
narrow-band imaging.
A prospective blinded study showed that WLE with five random biopsies as per the Sydney
system was insufficient for detection of gastric intestinal metaplasia. This low yield
is likely because metaplastic lesions are often focal and are likely to be missed
on random biopsy sampling. Authors therefore recommend NBI-targeted biopsies plus
five mapping biopsies as per the updated Sydney system. Mapping biopsies alone without
NBI has a poor yield.[22]
Savarino et al reported that NBI detects gastric IM with an accuracy of 93%, a sensitivity
of 80%, a specificity of 96%, a positive predictive value of 84%, and a negative predictive
value of 95%.[23] A randomized crossover study by Dutta et al[24] showed superiority of NBI over WLE in diagnosing atrophic gastritis, as well as
IM. The authors noted that NBI identified additional lesions not detected on WLE.
Pimentel-Nunes et al,[25] in 2012, proposed a simple and reproducible classification system for the diagnosis
of IM and dysplasia. The authors noted that regular vessels with circular mucosa was
associated with normal histology (accuracy 85%) and tubulovillous mucosa was associated
with IM (accuracy = 84%, 95% confidence interval [CI]: 77–91%). Light blue crest had
moderate reliability (k = 0.62) and high specificity (87%) for IM.
Apart from light blue crest, other findings have been described in IM. White opaque
substance (WOS) was first reported by Yao et al. It is a substance present in the
superficial part of gastric neoplasias that obscures the subepithelial microvascular
architecture. WOS is an optical phenomenon caused by accumulated lipid droplets.[26]
[27]
[28]
The marginal turbid band (MTB) is another finding noted in IM. It is defined as an
enclosing, white turbid band on the epithelial surface/gyri.[21] Recently, another finding, namely, white villiform type mucosa which suggests atrophy
and intestinal metaplasia in the gastric antrum has been described[29]
Helicobacter pylori Infection
NBI is a potential tool to diagnose H. pylori related gastritis ([Fig. 5]). In gastric corpus, nonvisualization of normal collecting venules irrespective
of central opening and subepithelial capillary changes suggests H. pylori–associated gastritis (100% sensitivity, 92% specificity, and positive predictive
value (PPV) of 100%).[30]
[31]
[32] Tahara et al using NBI of nonneoplastic mucosa of gastric corpus, classified four
types to predict H. pylori infection and also described histological severity of gastritis and gastric atrophy.[33] Normal pattern was defined by small, round pits surrounded by SECN. Type-1 pattern
showed slightly enlarged, round pits with unclear or irregular SECN. Type-2 pattern
showed obviously enlarged, oval or prolonged pits with increased density of irregular
vessels and type-3 pattern revealed well-demarcated, oval or tubulovillous pits with
clearly visible coiled or wavy SECN.[33]
Fig. 5
H. pylori related chronic non atrophic gastritis: (left) on WLE, changes are not well appreciated;
(right) NBI: showing variable vascular density, pit enlargement, and absence of CV.
H, helicobacter; NBI, narrow-band imaging; WLE, white light endoscopy.
Pimentel-Nunes et al documented that regular vascular and surface pattern with variable
vascular density favored the presence of H. pylori infection.[24] Bansal et al showed that the sensitivity and specificity of a regular mucosal and
vascular pattern for the diagnosis of normal mucosa/mild gastritis were 89 and 78%,
while the sensitivity and specificity of an irregular pattern with decreased density
of vessels for the diagnosis of H. pylori was 75 and 88%.[10] Banerjee et al prospectively compared NBI with WLE in 74 patients and showed that
NBI can be a potential tool for real time diagnosis of H. pylori infection based on the presence of obscure pit pattern.[34] Yagi et al compared the diagnostic value of conventional endoscopy and magnifying
NBI for prediction of H. pylori status in patients after endoscopic resection of gastric cancer. The inter observer
agreement was moderate (k = 0.56) for conventional endoscopy and substantial (k = 0.77) for magnifying NBI. The sensitivity and specificity were 79 and 52% for conventional
endoscopy and 91 and 83% for magnifying NBI endoscopy, respectively.[35]
NBI has been used to investigate the changes of gastric mucosal patterns before and
12 weeks after H. pylori eradication. Patients who were successfully treated (confirmed with 13C Urea breath test) showed a change back to small oval or pinhole-like round pits,
as well as a reduction in the density of fine irregular vessels. In absence of severe
atrophy and intestinal metaplasia, the sensitivity and specificity of NBI for predicting
the H. pylori eradication was 100%. However, H. pylori eradication did not change NBI pattern in those with preexisting severe gastric atrophy
and intestinal metaplasia.[36]
Despite the changes associated with H. pylori infection being commonly seen, tests for H. pylori infection like rapid urease test, and histopathology may still be required for detection
of active infection where clinically indicated. More evidence is required on the role
of NBI in distinguishing current ongoing infection from past infection especially
in the setting of atrophic gastritis and intestinal metaplasia.
NBI Appearance of Other Benign Gastric Lesions
Fundic gland polyps ([Fig. 6A]) are usually small (1–5 mm) and multiple and are most commonly located in fundus
and body of the stomach. On WLE, these polyps are sessile, shiny, and translucent
with normal background mucosa and on NBI, as regular round mucosal pit pattern and
regular honeycomb or dense vascular pattern on a background normal gastric body mucosa.[37]
[38]
Fig. 6(A) FGP-on WLE and NBI showing round pits with honeycomb SECN and CVs with demarcation
line. (B) Hyperplastic polyp showing pits were dilated with coil-like enlarged vessels and
absent CVs. DL was present. NBI, narrow-band imaging; WLE, white light endoscopy;
CV, collecting venule; FGP, fundic gland polyp; LBC, light blue crest; SECN, subepithelial
capillary network; DL, demarcation line.
Hyperplastic polyp ([Fig. 6B]) are usually <2 cm in size, solitary (66%), and commonly located in antrum. They
are often associated with chronic H. pylori infection against a background of atrophic mucosa. On NBI, these polyps may have
tubular mucosal pattern, of several shapes, with thick but regular vessels or dense
vascular pattern.[37]
[38]
Portal hypertensive gastropathy is commonly seen in fundus and body and rarely in
antrum of stomach. The changes are usually submucosal; superficial mucosal biopsies
are frequently false negative.[39] Characteristics WLE appearance is mosaic or snake skin like pattern or a diffuse,
erythematous, and reticular cobblestone pattern of gastric mucosa consisting of small
polygonal areas, with superimposed red punctate lesions, >2 mm in diameter and a depressed
white border.[40]
[41]
[42] On NBI, red mosaic-like mucosa of portal hypertensive gastropathy is seen as extended
and swollen gastric pits with varying degrees of dilated and convoluted capillaries
surrounding the gastric pits, collecting venules are obscured.[43]
Gastric antral vascular ectasia (GAVE) is common in elderly (>70 years) women (80%);
30% cases are associated with portal hypertension. On WLE, GAVE appears as tortuous
columns of ectatic vessels simulating a “watermelon” or is seen as a diffuse pattern.
These areas of erythema are commonly arranged in a linear manner along folds in the
antrum and less commonly arranged as diffuse erythema in the antrum.[40]
[41]
[44]
[45] Hayashi et al described NBI appearance of GAVE as partial and marked dilatation
of the capillaries surrounding the gastric pits and capillaries located below the
gastric pits.[43] Chen et al described GAVE on magnifying NBI as ring type of red spots, which has
dilated, tortuous telangiectatic capillaries at the intervening part, providing a
sensitivity and negative predictive value of 100 and 100%, respectively.[46]
