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26]

Original Article

PTERYGIUM: Recent Trends and Perspectives—A Review of

Pathogenesis and Current Management Options
Helen A. Ginger-Eke, Chimdia E. Ogbonnaya1, Chinyelu N. Ezisi2
Lecturer Ebonyi State University Abakaliki Ebonyi State, Consultant Ophthalmologist/Glaucoma specialist, 1Senior Lecturer Ebonyi State University Abakaliki Ebonyi
State, Consultant Ophthalmologist/Glaucoma specialist, 2Lecturer Ebonyi State University Abakaliki Ebonyi State, Consultant Ophthalmologist/Paediatric
Ophthalmologist, Department of Ophthalmology, Federal Teaching Hospital, Abakaliki, Nigeria

Abstract
Objectives: (1) To review literature on the current understanding of the nature and pathogenesis of pterygium. (2) To highlight the recent
advances in the treatment of pterygium. Materials and Methods: Relevant subheadings were entered into PubMed search engine and 165
articles addressing our objectives were retrieved and reviewed. Results: Pterygium may be proliferative rather than degenerative in nature.
There is a strong correlation with ultraviolet radiation. Genetic alterations occur, such as point mutations of proto-oncogenesis such as Kirsten-
Ras and alterations in the expression of tumor suppressor genes (TSGs) (p53 or p63), alteration of matrix metalloproteinase in limbal and
corneal tissues, ultraviolet radiation (UVR) genetically mediated expression of various cytokines, growth factors, and growth factor
receptors. Oxidative stress may play a role, evidenced by the expression of certain proteins in pterygium tissues presumed to have a protective
role against oxidative stress-induced apoptosis. High prevalence of human papilloma viruses (HPVs) in pterygium tissue samples suggests a
possible role for HPV. Several techniques of surgery have evolved over time including the modified bare-sclera techniques, sliding, “merest
sclera,” adjunctive therapies with mitomycin C, 5-fluorouracil, corticosteroids, conjunctival autograft, limbal autograft, amniotic
membrane graft, use of fibrin glue, and subconjuctival injection of bevacizumab. Conclusion: Advances in the understanding of pterygium
have led to emerging treatment options that may not only reduce recurrent rates, but may also enable the use of less invasive treatment
methods. Recommendation: Ophthalmologists working in hot climates should update their knowledge on the current concepts in the
pathogenesis and management of pterygium to obtain better results.

Keywords: Pathogenesis, pterygium, treatment

INTRODUCTION cancers, because active cell proliferation occurs with

[1] minimal apoptosis.[7,8] Pterygium also displays other
Pterygium is a wing-shaped fibrovascular growth. It can be
tumor-like properties, such as invasion of cornea and its
divided into three recognizable parts: apex (head), neck, and
high recurrence after surgical excision. It also exists with
body. The raised triangular portion of the pterygium with its
secondary premalignant lesions.[7,9,10] These tumor-like
base toward the canthus is the body, the neck that includes the
properties suggest that pterygium is possibly a
superficial limbus, whereas the head invades the cornea and
premalignant tissue.[10] Several studies also showed that
forms the apex of the triangle.[2] A subepithelial cap or “halo”
the pathogenesis of pterygium is closely linked to the p53
is present in front of the head of the pterygium[3] and is
usually the first sign of pterygium.[4,5] Pterygium threatens
vision through various mechanisms, such as blocking the
visual axis as well as inducing significant astigmatism.[6] Address for correspondence: Dr. Helen A. Ginger-Eke, Lecturer Ebonyi State
Pterygium is widely regarded to be a degenerative condition University Abakaliki Ebonyi State, Consultant Ophthalmologist/Glaucoma
arising from benign growth of the conjunctiva, characterized specialist, Department of Ophthalmology, Federal Teaching Hospital Abakaliki.
Tel.: 08035043949;
by fibrovascularization, conjunctival invasion, and elastic
e-mail: helenginger1@gmail.com
degeneration of collagen. However, some studies have
shown that pterygium shares some similarities with
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How to cite this article: Ginger-Eke HA, Ogbonnaya CE, Ezisi CN.
DOI: PTERYGIUM: Recent trends and perspectives—A review of
10.4103/njo.njo_5_18
pathogenesis and current management options. Niger J Ophthalmol
2018;26:89-98.

© 2019 Nigerian Journal of Ophthalmology | Published by Wolters Kluwer - Medknow 89

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Gingereke, et al.: PTERYGIUM: Recent Trends and Perspectives
gene mutation.[11-15] Thus, pterygium is considered the result
of uncontrolled cellular proliferation, like a tumor.
EPIDEMIOLOGY
Pterygium has a worldwide distribution and is common in areas
that lie withina geographical latitude of 40° north and 40° south of
the equator.[16] Prevalence can be as high as 22% in these
equatorial areas and less than 2% in latitudes above 40°.[16-18]
Findings from an Asian region,[18] as well as Nigeria,[19]
corroborate this trend. However, within the same regions,
prevalence rates vary widely.[18-30] Achigbu and Ezepue[19] in
Enugu, Nigeria, found a prevalence rate of 19.3%. Among
motorcycle riders, whereas Ogbonnaya[20] in Abakaliki,
Nigeria, found a lower prevalence rate of 7.6% among patients
visiting a hospital eye clinic, which compares with some other
studies from parts of Asia that reported lower prevalence rates
ranging from 4.4% to 10.1%.[21-24] Several other studies from
parts of Africa, Europe, and Australia reported a lowerprevalence
rate ranging from 0.8% to 11.7%.[25-30]
Various risk factors have been suggested, including race, age,
social status, occupation, and educational background.[29-40]
A large North American study has reported pterygium to be
2.5 to 3 times higher in blacks than among whites, almost
twice as frequent among persons who worked outdoors but
was only one-fifth as likely among those who always used
sunglasses outdoors.[31] This study also found a positive
association between pterygium and age and people of
lesser educational background. Racial differences in
pterygium has also been reported by many studies.[29,32]
Outdoor work as a risk for pterygium development has
also been reported by other studies.[32,33] Sunlight
exposures (on an average of 1 h or more daily) were
strongly associated with a higher risk of developing
pterygium in people working outdoors.[34-37] However, a
study did not find a strong association between sun
exposure and pterygium.[28] Ultraviolet (UV) light
exposure may not be the only factor associated with the
development of pterygium. Dust and sand may contribute
to the development of pterygium. This could be explained by
the fact that the normal flow of tears is from out inwards
carrying with them any dust particles or fine foreign bodies as
sandy dust is coarse than fine dust thereby exciting the
inflammatory response with consequent formation of
pterygium. Educational interventions to modify these
potential exposures may assist in preventing pterygium.
Older age, male sex, lower educational level, rural
habitation, and nonsmoking have been reported by other
studies as independent risk factors for pterygium.[21,23,30,32]
Some studies reported a preponderance of female
gender,[25,38] whereas some others reported no significant
difference in gender in development of pterygium.[39]
CLINICAL PRESENTATION
Pterygium arises in the interpalpebral fissure as an elevated,
fleshy mass on the bulbar conjunctiva near the limbus in its
90 Nigerian Journal of Ophthalmology ¦ Volume 26 ¦ Issue 2 ¦ July-December 2018
early stage. Engorged radial vessels may appear over the
pterygium and adjacent conjunctiva and usually signal a
period of rapid growth. The bulbar conjunctiva may
become increasingly taut as the pterygium enlarges toward
the limbus. Symptoms of burning, irritation, lacrimation, and
foreign body sensation may accompany the growth of a
pterygium onto the cornea. Significant astigmatism may be
induced either with or against the rule as sectoral corneal
steepening occurs.[41,42] The astigmatism is often irregular
and may lead to decreased vision. As the apex approaches the
visual axis, glare and decreased contrast sensitivity appear. In
severe cases, symblepharon formation may limit ocular
motility and result in diplopia. The lesion may remain
quiescent for the remainder of the patient’s life or resume
growth again at a later time. Older, static lesions are often
associated with an arcuate line of iron deposition in the
superficial cornea immediately central to the cap known as
Stocker’s line.
PATHOGENESIS
The knowledge regarding the pathogenesis of pterygium
has expanded vastly. Before now, early theories have
proposed that pterygium development was associated
with specific lifestyles such as outdoor working,
exposure to sunshine, or dust. This led to the idea that
chronic ocular surface irritation by such environmental
factors might be the cause of the condition.[43,44] It was
also proposed that pterygium arises from other sunshine-
related conditions, such as pingueculum. Pingueculum
has no growth potential per se but may become
inflamed and can evolve into a true pterygium.[45]
Conjunctival vascular congestion frequently seen at the
area of pterygium growth nasally was also believed to be
caused by medial rectus activity that led to disturbance of
the blood flow. This was suggested to be associated with
pterygium growth.[43,44] Other early reports such as
pooling of tears, lacrimal composition, and unspecified
local effects of lactic acid secreted by periocular sweat
glands have all been implicated in the pathogenesis of
pterygium.[46-48]
Pterygium is now accepted as a distorted wound-healing
response and dysregulated cell proliferation disease rather
than a degenerative lesion.[10] Antiapoptotic mechanisms,[49]
cytokines,[50] growth and angiogenic factors,[51] viral
infections,[52-54] and heredity[55-57] have been proposed as
current causative agents in its pathogenesis.
CURRENT CONCEPTS
Role of ultraviolet rays
The direct pathogenetic role of solar radiation in pterygium
development has been reported by many studies.[23,35-37] UV
rays are the shorter wavelengths of nonionizing radiation
(wavelength 100–400 nm) lying below the visible spectrum.
Ultraviolet radiation (UVR) has been subdivided into
three bands: UV-A (400–320 nm), UV-B (320–290 nm),
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and UV-C (290–100 nm).[37] UV-A, or near UVR,
produces tanning (the browning of the skin due to an
increase in the skin content of melanin) and
photosensitivity reactions. UV-B causes sunburn (painful
erythema and blistering), and increased exposure to UV-B is
associated with an increased rate of skin cancer. UV-C is
germicidal and may also cause skin cancer.[58-60] The eyes
are normally protected and shielded from UVR by a number
of factors, such as the normal horizontal alignment of the
eyes, the orbits, and eyebrows which significantly reduces
ocular exposure to whole-sky irradiation.[61] Further
anatomical protection is provided by the nose, and the
cheeks, as studies have shown that the cornea acts as a
side on lens, focusing light incident on the temporal cornea
unto the opposite side of the eye. The anatomy of the
nose and cheek prevents this effect from occurring in the
opposite direction, that is, light incident at the nasal limbus
is not of such a peripheral angle as to allow a focusing effect
unto the temporal limbus.[61] The eyelids provide protection
that is further enhanced by squinting, a common reflex in
bright sunlight.[62-65] The eyes are relatively unprotected
laterally (albedo),[16] although the transmission of UVR by
internal reflection in the cornea may lead to a concentration
of UV irradiation at the nasal limbus, hence the high
incidence of nasal pterygium, an indication of the
pathogenetic role of solar light. Scattered light might also
follow alternative (transcameral) optical paths when
entering the eye, thus hitting limbal stem cells from their
inner surface.[16] The theory of transcameral pathway
proposed that light scattered in the anterior chamber may
deviate from the transpupillary course and be directed
towards the limbus. The ab interno irradiation of limbal
stem cells may cause genetic destabilization, eventually
leading to development of pterygium. UV light is
believed to cause pterygium[66] by inducing chronic
inflammatory cells in the conjunctiva[67] or damage
limbal stem cells.[68] However, the study by Anguria
et al.[69] suggests that inflammation may not be crucial
for pterygium to be present or to be opaque (i.e., a late
stage of pterygium that appears clinically as a thick opaque
vascular growth extending to the visual axis). Findings from
the same report show chronic pterygium inflammation is not
important for pterygium to recur after surgery, which is
consistent with a previous report.[70] It looks as if the
severity of chronic inflammation is independent of the
degree of exposure to sunlight.[70,71] Some reports have
shown that damaged limbal stem cells are not a factor in
pterygium occurrence[69,72] unlike contrary report by Pelit
et al.[73] Excessive exposure to sunlight has also been
correlated with collagen degeneration. However, collagen
degeneration has been discredited as a mechanism of
pterygium pathogenesis.[74] Some primary pterygia may
not show collagen degeneration histologically.[75,76] This
degeneration is not manifested in recurrent pterygia,
suggesting short durations of exposure to UV light,[74,77]
supporting the belief that level of sunlight exposure may not
be important for pterygium to occur or to recur.
Nigerian Journal of Ophthalmology ¦ Volume 26 ¦ Issue 2 ¦ July-December 2018
The role of genetically altered limbal stem cells
Immunohistochemical studies have found conjunctival,
limbal, and corneal cells to immunostain primarily for
matrix metalloproteinase-I (MMP-I). Limbal basal
epithelial cells (pterygium cells) were found in
immunostain for multiple types of MMPs (MMP-1, MMP-
2, MMP-3, MMP-9, membrane type 1-MMP, and membrane
type 2-MMP).[78] MMPs have been detected in the fibroblasts
and stroma of pterygium samples[79]; this suggests that these
MMPs were remodeling the pterygium stroma,[80] but this
was attributed to damaged limbal basal epithelial cells.[79] It is
believed that the altered MMP expression of limbal basal
epithelial cells (pterygium cells) enables them to invade and
dissolute Bowman’s layer leading to firm adhesion of the
lesion on the corneal surface.[77,78] However, some studies
did not find MMP expression in the pterygium fibroblasts or
stroma yet the limbal basal epithelial cells were
damaged.[69,81] These suggest that matrix remodeling
observed in pterygia is unlikely to be due to MMPs.
Rather, sunlight damage has been implicated.[82,83]
Oxidative stress
Generation of reactive oxygen species (ROS) by UV radiation
has been suggested as initiating events in the development of
pterygia.[84] Stocker line, an area of excess iron deposition at
the advancing edge of a pterygium has provided further
evidence for the importance of ROS in pterygium
formation. Expression of certain proteins in pterygium
tissues that are presumed to have a protective role against
oxidative stress-induced apoptosis has been identified by a
recent study.[85] In this study, aldehyde dehydrogenase
dimeric nicotinimide adenosine dinucleotide phosphate
(NADP)-preferring (ALDH3A1), protein disulfide-
isomerase A3, and peroxiredoxin II were found to be
significantly upregulated in pterygium and further
increased in recurrent pterygium. A previous study also
found peroxiredoxin I and II both to be upregulated in
pterygium.[85] Immunohistochemistry and western blot
analysis were both used in these studies to confirm that
these proteins were mainly detected in the basal epithelial
layer, and their expression was significantly increased in the
pterygium compared to normal conjunctiva.
Hence, future study directions could include topical
antioxidant therapy as a first-line treatment for pterygium
lesions.
Molecular genetic alterations
TSGs and proto-oncogenes (POGs) have been implicated in
the pathogenesis of pterygium. Using proteomic approach, 77
proteins were upregulated in pterygia.[85] Mitotic proteins
were seen to be among the proteins significantly affected.[85]
Large TSGs (large tumor suppressor kinase 1 (LATS1) and
large tumor suppressor kinase 2 (LATS2)) are the common
TSGs in the UV-induced DNA damage response signaling
pathways. DNA methylation in the promoter regions are the
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main cause of TSG silencing and can result in tumor
development. A recent study confirmed the significant
relationship between reduced expression of the LATS1 and
LATS2 through methylation and the risk of pterygium
formation.[86] Other reports have showed aberrant DNA
methylation and decreased expression of P16, E-cadherin,
TGM 2, MMP2, and CD24 genes in pterygium damage.[87-
89]
LATS2 also interacts with a negative regulator of p53 and
may function in a positive feedback loop with p53 that responds
to the cytoskeleton damage. Levels of p53 have also been
reported to be increased in pterygia by some studies.[78,90,91]
The levels of p53 expression in pterygia have been found to
differ between epithelial layers being higher in basal cells,
compared to more superficial layers.[78,92,93] This finding could
reflect increased exposure to UVR according to the proposed
theory of transcameral exposure of limbal basal (stem) cells to
solar light.
POG sequences may also be affected by UVR.[94,95] LATS1
is activated by Ras-association domain family 1 isoform A
that stimulates response to DNA damage. Mutations in genes
of the ras family POGs, including Harvey-Ras, Kirsten-Ras
(K-ras), and Neuroblastoma-Ras, have been detected in
cultured cells of mouse skin tumors following exposure to
near-UVR.[94] Restriction fragment length polymorphism and
sequencing analysis of primary and recurrent pterygia have
revealed K-ras mutations at codon 12 in 10% of pterygia. The
above findings pave the road for discovering drugs with the
regulation of methylation characteristic that will lead to better
therapy in treatment of pterygium.
Role of growth factors and cytokines
The expression of various cytokines, growth factors, and
growth factor receptors may be triggered by UVR genetic
mediated trauma.[81] Immunohistochemical and Enzyme-
linked immunosorbent assay (ELISA) techniques have
revealed the presence or altered expression of this factors
in pterygium.[96] UVR-inducible cytokines include the
interleukin-1 (IL-1) system,[97,98] the IL-6,[99,100] and IL-
8.[101,102] Growth factors involved in pterygium according to
previous reports include the epidermal growth factor (EGF)
and heparin-binding EGF, vascular endothelial growth
factor (VEGF), basic fibroblast growth factor, platelet-
derived growth factor, transforming growth factor-ß, and
insulin-like growth factor binding proteins.[81] However,
some growth factors were expressed in controls as in
cases, which suggests that overexpression of angiogenic
growth factors is not the reason for vibrant fibroblast
mitosis or for pterygium to occur,[103,104] rather the
upregulation of fibrogenic growth factors is most likely to
be the reason for pterygium to occur.[103-105] VEGF
has also been detected in increased amounts in pterygium
epithelium, compared with normal conjunctiva using
immunohistochemistry.[106] However, Bevacizumab
(Avastin®; Genentech Inc., South San Francisco,
California, USA), which is anti-VEGF, did not abolish
pterygium recurrence after surgery.[107]
92 Nigerian Journal of Ophthalmology ¦ Volume 26 ¦ Issue 2 ¦ July-December 2018
Role of viruses
Studies have revealed a high prevalence of oncogenic
human papilloma viruses (HPVs) in tissue samples,
suggesting a possible role for HPV in the pathogenesis
of pterygia. Type 18 was the most prevalent genotype,
followed by type 16, whereas less common genotypes were
types 58 and 59.[108]
Role of heredity
Although existing reports indicate that sunlight exposure is
the main factor in pterygium occurrence, studies on factors in
pterygium occurrence and recurrence have identified heredity
to be a crucial factor for pterygium development, and that
sunlight is only a triggering factor.[109]
TREATMENT OF PTERYGIUM
The treatment of pterygium can be conservative, medical, or
surgical.
Conservative treatment is indicated when symptoms are mild
and usually involves avoidance of smoke and dust-filled
environment. Use of ultraviolent blocking glasses has been
advocated by some authors in preventing progression.[110]
Medical treatment is used to relieve symptoms and involves
use of topical, preservative-free lubricants, vasoconstrictors,
and mild corticosteroids.
Surgical treatment is indicated when there is disturbance of
visual function, significant discomfort, and for cosmetic
reasons. The first report of a surgical treatment of
pterygium is more than 3000 years old.[111] Many
variations of this procedure since that time have been
published.[112,113] Only the current surgical techniques,
with adjunctive therapies, are discussed in this review.
CURRENT SURGICAL TECHNIQUES
Bare sclera technique: This is the most popular method for the
removal of primary pterygium and was first described by
D’Ombrain.[112] This technique involved the complete
excision of the pterygium head and removal of some of
the adjacent normal nasal bulbar conjunctiva along with
excision of the underlying Tenon’s capsule tissue, which
then resulted in a bare sclera. The remaining conjunctival
rim was then sutured onto the bare sclera surface at a variable
distance from sclerocorneal limbus. This technique was
associated with a high recurrence rate (30%–80%),[112] and
there is a higher risk of recurrence after re-excision of a
recurrent pterygium compared to a primary pterygium.[114]
Therefore, this technique has been modified to reduce the
recurrence rate.
Modified bare sclera technique: This technique was based on
the understanding of the important role of normal conjunctiva
in blocking pterygium regrowth on the corneal surface. These
techniques include
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Sliding conjunctival flaps: Sliding conjuctival flaps from both
inferior and superior limbus is used for primary closure of a
pterygium excision. A 1-year recurrence rate of only 5% has
been reported using this technique.[115]
“Merest sclera” technique: In this technique, the head and
midbody of the pterygium are excised and a tenonectomy is
extended beneath the conjunctiva to the adjacent rectus
muscle, particularly in young patients or large lesions.
Relaxing conjunctival incisions are made both superiorly
and inferiorly along the limbus, and the conjunctiva is
closed primarily and meticulously. A recurrences of only
2.1% is reported.[116]
Bare sclera technique with partial sclerectomy: In this
technique, the head of the pterygium was shaved off the
cornea, and its body was dissected from conjunctiva above by
blunt dissection until orbital fat was exposed. The pterygium
was bluntly dissected from underlying sclera and muscle and
then excised. A third partial thickness sclera flap 5 mm
vertically by 3 mm horizontally was raised from the sclera
bed measuring from limbus, this sclera was excised and
cautery applied minimally. The conjunctiva was then
anchored to the edge of the sclera using 8/0 silk suture
while leaving the sclerectomy bare. A recurrence rate of
9.1% is reported.[117] It is postulated that removal of the
superficial sclera with the episcleral tissue may remove with it
the factor responsible for recurrence of pterygium.
Conjunctival autograft
The transplantation of free autografts of superotemporal
bulbar conjunctiva from the same eye to close wounds
after the excision of advanced or recurrent pterygium was
described by Kenyon et al.[118,119] Cautery spots are used to
delineate the involved area of conjunctiva to be excised.
Sharp, superficial excision of the head of the pterygium
from the involved cornea to the limbus is performed. The
conjunctiva and Tenon’s capsule are bluntly and
meticulously dissected from the horizontal rectus muscle,
leaving behind the bare sclera and exposed rectus muscle.
Conjunctiva is secured to the sclera with absorbable suture
(e.g., 8-0 Vicryl) on a spatulated needle. Calipers are used to
determine the size of conjunctival graft required to resurface
exposed sclera and horizontal rectus muscle. The globe is
rotated inferomedially to expose an area of uninvolved
superior bulbar conjunctiva. Dimensions are marked with
several cautery spots, as large as 15 mm by 15 mm and
extending to the limbus. Free grafts are dissected as thinly as
possible, taking minimal subconjunctival tissue. The graft is
excised such that cautery marks remain with the graft tissue
margins, then the epithelial surface can be readily identified
when the graft is repositioned. The donor site does not
require suturing, but the conjunctival margins can be
advanced to the limbus with two interrupted sutures. The
free graft is transferred into the recipient bed and secured to
adjacent conjunctiva and episclera with interrupted sutures
of 8-0 Vicryl; 10-0 nylon is used for the limbal edge of the
graft.[118,119]
Nigerian Journal of Ophthalmology ¦ Volume 26 ¦ Issue 2 ¦ July-December 2018
A recurrence rate of 21% was reported.[120] Other authors
have reported a recurrence rate of 12.1%.[121]
Limbal autograft, a variation of free conjuctival autograft, has
been described. This was based on the understanding that
corneal epithelial stem cells are located at the limbus. Limbal
epithelial stem cells generate new corneal epithelial cells in
addition to inhibiting conjunctival epithelial invasion of the
cornea. However, there are little data supporting its efficacy.
Amniotic membrane grafts
Following a pterygium excision, the bare sclera area is
covered with either fresh or preserved amniotic membrane
tissue with basement membrane side up. However, there is
need to exclude infections such as human immunodeficiency
virus and hepatitis when using fresh amniotic membrane.[122]
The amniotic membrane is sutured through the episcleral
tissue to the adjacent healthy conjunctiva using 8 to 10 size
8.0 Vicryl sutures. A recurrence rate of 6%, 7.9%, 25%, and
28.1%,[123-126] respectively, has been reported by many
studies. Its efficacy in reducing recurrence of pterygium is
based on the understanding that amniotic membrane
promotes conjunctival epithelial wound healing, suppresses
fibroblasts, and reduces extracellular matrix production.[127]
Of recent, fibrin glue is now been used to replace or augment
sutures when attaching conjunctival grafts or amniotic
membrane. Fibrin glues has been useful in shortening
operating time and decreasing postoperative discomfort, as
well as decreasing recurrence rates.[122]
ADJUNCTIVE THERAPY
Various adjunctive therapies have been used with pterygium
surgery to decrease the risk of recurrence after its surgical
removal. However, these adjuctive therapies have their
drawbacks.
Cautery
Extensive use of intraoperative cautery with bare sclera,
particularly at the limbus, to augment the surgical removal
of the pterygium has been used by many surgeons. This was
based on the knowledge that blood vessel growth at the
operative site contributes to the recurrence of a
pterygium.[128] Some authors believe that cautery can lead
to the formation of hypertrophic scar tissue and discourage its
intraoperative use.[129]
Mitomycin C
Mitomycin C is an antineoplastic/antibiotic agent isolated
from the soil bacterium Streptomyces caespitosus. It inhibits
the synthesis of DNA, cellular RNA, and proteins in rapidly
growing cells.[130] Mitomycin C was first used topically at a
concentration of 0.04% (doses of 0.4 mg/ml) three times daily
for 1 to 2 weeks after pterygium surgery, with no recurrences
by Kunimoto and Mori.[131] Other reports have confirmed the
usefulness of mitomycin C in pterygium surgeries with a
recurrence rate ranging from 2% to 16%.[132-134]
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However, mitomycin C has been shown to be associated with
vision-threatening complications such as iritis, severe
secondary glaucoma, corneal edema, corectopia, sudden-
onset mature cataracts, scleral calcification, and corneal
perforation.[135]
Consequently, this motivated the use of a more dilute
concentrations (0.02%) of mitomycin C. Some reports have
described good results with no serious complications using
0.2 mg/ml of mitomycin C.[136-138] Presently, two approaches
have been developed for applying mitomycin C: postoperative
use of topical eye drops and intraoperative use of mitomycin C-
soaked sponges. Both have similar recurrence rates. A recent
report found pterygium surgery with intraoperative mitomycin
C to have similar recurrent rate when compared with
conjuctival autograft alone.[139] Hence, adjuvant role of
mitomycin C should be studied further.
5-Fluorouracil
5-Fluorouracil (5-FU) is a fluorinated pyrimidine that inhibits
the proliferation of fibroblasts. 5-FU is used intraoperatively
at a dose of 50 mg/ml for 3 to 5 min by most surgeons,
because 5-FU is cheaper than mitomycin C and is
associated with fewer side effects.[140] The recurrence rate
of 11.4% to 14% has been reported by Bekibele et al.[121] and
25% by Akarsu et al.,[140] respectively, has been reported. 5-
FU was also found to be marginally superior to conjunctiva
autograft in the prevention of pterygium.[121]
Corticosteroids
Several authors have advocated their use four times daily
for 2 weeks after the healing of the corneal epithelial
defect.[141,142] This is based on the understanding of the
direct antiangiogenic and their anti-inflammatory
effects.[143] Given the chronic nature of topical steroid
needs in pterygium management, a recent report has
advocated the use of loteprenol etabonate ointments in
the preoperative and postoperative management of
pterygium surgery based on its potency and safety
profile.[144]
Bevacizumab
Subconjunctival injections of Bevacizumab provide another
strategy to manage primary and recurrent pterygium. This is
based on the fact that vascular growth factors such as VEGF have
been detected in pterygium.[145,146] Subconjunctival injection of
0.2 ml (5 mg) of Bevacizumab (100 mg/4 ml Roche) following
the injection of 0.2-ml lidocain 2% in subconjunctival area of
pterygium body using a 1-ml syringe with 29-gauge needle,
showed marked reduction in the size of pterygium and regression
of blood vessels.[147-149] Subconjunctival injection of
bevacizumab has also been shown by studies to be
safe.[148,149] Subconjuctival bevacizumab benefit the complex
treatment of pterygium by reducing subjective complaints and
delaying surgical intervention. However, a preliminary
report[150] has found subconjuctival bevacizumab not useful
94 Nigerian Journal of Ophthalmology ¦ Volume 26 ¦ Issue 2 ¦ July-December 2018
in treating primary pterygium and also rather harmful. Further
studies are required in this area.
Topical bevacizumab therapy is also advocated.[151] One
study used it 1 month after surgical excision of recurrent
pterygium and found it to be well tolerated and effective in
preventing neovascularization.[152] There was no significant
difference in the recurrence rate in the study group; further
studies are required to support this result.
Laser therapy
The use of the argon laser in selected postoperative cases
has been described. In one report, argon laser was applied
at 50-mm spots to early neovascular fronds. The power
settings were limited to minimize conjunctival epithelial
damage[153]; the recurrence rate was unknown in this
report.
Beta irradiation
The most common use of beta radiation has been in the
management of pterygium, with local application of a
Strontium-90 source to prevent recurrence. Initially a
high dose of beta radiation was applied without surgical
excision, the aim being to induce regression of the lesion.
This was associated with a high recurrent rate that was
attributed to the high levels of UV. Recently,
administration after surgery, particularly for recurrent
pterygia, became widely adopted, with subsequent
reports, indicating a low recurrence rate ranging from
0% to 16%.[154-158]
A recent study[159] recommends a total combined dose of
2000 to 3000 cGy delivered in three fractions every other day
starting on the 6th day postsurgery. Adverse effects with beta
radiation for pterygium, such as lens opacity, scleral necrosis,
punched out ulcers have been widely reported.[160]
Consequently, use of beta radiation for pterygium has
diminished, with conjunctival autografting and topical
mitomycin C now being widely used. Conjunctival
autografting is reasonably effective and appears to be safe;
however, it is considerably more time consuming than other
methods.[161] Comparative data for beta radiation and mitomycin
C are conflicting: one study found mitomycin C to be more
effective[162]; another study suggested the converse,[163] a Dutch
study suggested equivalence[164]; and a randomized controlled
study suggested that beta radiation was more effective than either
conjunctival autografting or mitomycin C.[165]
CONCLUSION
Recently, there have been significant advances in the
understanding of nature of pterygium, the molecular and
biochemical events underlying pterygium pathogenesis,
and recent advances in its treatment. Recent advances in
the treatment have not only continued to reduce recurrent rate
but also may enable the use of less invasive treatment
methods other than surgery.
[Downloaded free from http://www.nigerianjournalofophthalmology.com on Sunday, August 16, 2020, IP: 202.67.32.26]
Gingereke, et al.: PTERYGIUM: Recent Trends and Perspectives
Recommendation
Pterygium is a very common eye disorder, particularly in the
tropics; thus, there is need for ophthalmologists, working in hot
climates to update their knowledge on the current concepts in
the understanding of the nature of pterygium as well as the
current treatment options to obtain better results.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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