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Clinical
Mooren’s Ulcer
Dr. V.Rahul, DNB, Aravind Eye Hospital, Madurai
Epidemiology
Mooren's ulcer is a rare disorder, typically seen in
healthy adult men1 with no evidence of systemic
disease. It has been documented in a 3-year old
child2.
Wood and Kaufman having reported 9 cases
concluded that there were two clinical types of
Mooren's ulcer3. The first, limited type, is usually
unilateral, with mild to moderate symptoms,
generally responds well to medical and surgical
treatment. This type is believed to occur in older
patients and has become known as typical or
benign Mooren's ulcer. In contrast, the second
type is bilateral, with relatively more pain and
generally a poor response to therapy. The bilateral
variety, once believed to occur primarily in
younger patients, became known as atypical or
malignant Mooren's ulcer. The benign type is
quarter time bilateral and the malignant type 75%
time bilateral. Usually bilateral progressive form of
this disease occurs in older individuals.
Keitzman4 et al published a series of 37 cases
of progressive Mooren's ulcer in Nigeria affecting
primarily healthy men between the age of 20 and
30 years and the clinical course was very rapid, with
total involvement and destruction of the cornea
within 6 weeks. Perforation occurred in 36% of
the patients. A later report by Majekodunmi AA
et al5 confirmed that the malignant form was
the more common form occurring in the young
Nigerian men. As a result, the generalized belief
has developed that the progressive and relentless
atypical form of Mooren's ulcer has a predilection
for young, (black) men.
Lewallen and Courtright6, in their review of
the published series of Mooren's ulcer, suggest that
many of our current concepts of epidemiology of
Mooren's ulcer are not supported by available data.
They found that younger patients had bilateral
disease less frequently than older patients (1.5:1)
regardless of race and Caucasians were more than
twice as likely to have bilateral disease as blacks.
Although they found that men were 1.6 times
more likely to have Mooren's ulcer than are
women, it was pointed out that it could be due
to factors such as increased incidence of ocular
trauma in men (an association with Mooren's
ulcer is reported by some) or cultural patterns
that discourage female clinic attendance in certain
countries.
Clinical Features
Patients with Mooren's ulcer usually complain
of redness, tearing, and photophobia, but pain
is typically the outstanding feature. The pain
often is incapacitating and may well be out of
proportion to the inflammation. There may also
be a complaint of decreased visual acuity, which
may be secondary to associated iritis, central
corneal involvement, or irregular astigmatism due
to peripheral corneal thinning.
Mooren’s ulcer typically begins as a gray- white
infiltrate in the peripheral cornea. In most patients,
this process begins within the interpalpebral
fissure. It is followed by epithelial breakdown
and stromal melting. Eventually it develops into a
chronic, usually painful corneal ulcer. The corneal
ulceration spreads slowly involving the anterior
one third to one half of the corneal stroma. The
leading edge of the ulcer is undermined, infiltrated
and de-epithelialized. Because of the tissue
swelling, the exact depth of the undermining is
difficult to appreciate unless the overhanging edge
is removed. The ulcer progresses circumferentially
and centrally. As it progresses, it creates an
overhanging edge at its central border. Although
the ulcer may begin as a shallow furrow in the
peripheral cornea, over time it may involve the
2
limbus. The adjacent conjunctiva and sclera are
usually inflamed and hyperemic. The presence of
a peripheral corneal ulcer beginning at the limbus
with a gray, overhanging infiltrated edge at its
central border is characteristic of Mooren’s ulcer.
As the disease progresses, the ulcer can spread
both peripherally and centrally. Behind the
advancing edge of the ulcer, healing may take
place in the form of corneal reepithelializaton and
vascularization. Associated with this is scarring
and thinning. The healed areas remain clouded.
Sometimes the remaining residual cornea only
consists of descemet’s membrane with a small bit
of posterior corneal stroma covered by epithelium
known as contact lens cornea.
Generally, there is involvement of the limbus,
in contrast to some other forms of PUK,
such as that seen with rheumatoid arthritis or
staphylococcal marginal disease4. Vision may be
decreased because of irregular astigmatism caused
by peripheral corneal scarring. If the central cornea
is involved, vision is permanently impaired.
Classification of Mooren’s ulcer
Watson.P.G7 has classified the disease based on
the clinical presentation and the low dose anterior
segment fluorescein findings into
1) Unilateral Mooren’s ulcer
2) Bilateral aggressive Mooren’s ulcer
3) Bilateral indolent Mooren’s ulcer
Unilateral Mooren’s ulcer
It is a rare condition that primarily affects patients
aged above 60 years. Patients present with rapid
onset of redness and excessive pain in the affected
eye. Examination of the cornea will reveal the
typical features of Mooren’s ulcer, which may
progress slowly or extremely rapidly form a single
focal point.
Anterior segment angiography at this stage
reveals venular occlusion of all the local episcleral
and conjunctival vessels with the disruption of
limbal arcade and leakage from deep vessels at the
limbus and at the base of the ulcer.
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If left untreated or sometimes in spite of
treatment, the ulcer advances around the globe and
towards the centre. The epithelium at the base of
the ulcer and the remaining cornea remains intact.
Eventually the central corneal stroma is removed
entirely and all that remains is a thin layer of scar
tissue covering an intact endothelium and covered
by epithelium derived from conjunctiva.
Bilateral aggressive Mooren’s ulcer
Bilateral Mooren’s ulcer is commonly seen in
Indian subcontinent and in communities of
Indian origin and in parts of West Africa. It usually
affects patients between 14 and 40 years. They
may present with unilateral typical lesion in one
eye but soon may develop lesion in the other eye.
Angiography reveals changes in architecture of
episcleral vessels with some areas of closure. There
are no changes in conjunctiva but the angiogram
reveals a breakup of the limbal arcade, extension
of the vessels into the bed of the ulcer and leakage
from the tips of these vessels. The ulcers may
perforate spontaneously and if left untreated,
stromal tissue is eventually removed.
Bilateral indolent Mooren’s ulcer
It usually affects patients in their fifth decade or
older. It presents as bilateral indolent ulcers which
progress slowly. Some may heal spontaneously.
Angiography does not reveal any abnormality in
the vasculature of the episcleral or conjunctival
circulations. Abnormality of the limbal circulation
and changes at the bases of the ulcer are seen.
Pathology
The histopathology of Mooren's ulcer suggests an
immune process. Young and Watson8 studied the
corneas of three patients who underwent grafting.
They observed that the involved limbal cornea
consisted of three zones.
The superficial stroma was vascularized and
infiltrated with plasma cells and lymphocytes. In
this region, there was destruction of the collagen
matrix. Epithelium and Bowman's layer were
absent. The midstroma showed hyperactivity of
Vol. XIV, No.2, April - June 2014
fibroblasts with disorganization of the collagen
lamellae.
The deep stroma was essentially intact
but contained a heavy macrophage infiltrate.
Descemet's membrane and the endothelium were
spared. Heavy neutrophil infiltration, as well as
dissolution of the superficial stroma, was present
at the leading edge of the ulcer. These neutrophils
showed evidence of degranulation.
The adjacent conjunctiva shows epithelial
hyperplasia and a subconjunctival lymphocytic
and plasma cell infiltration.
Frank vasculitis is not present, and numerous
eosinophils may present in the nearby involved
conjunctiva during the course of healing.
Pathogenesis of Mooren's Ulceration
Gottsch 9 et al have shown that serum from
patients with Mooren’s ulcer contain antibodies
to a cornea associated antigen, COAg. This
antigen has now been found to be identical to
calgranulin C which only occurs in the corneal
stroma and in neutrophils. Recent studies have
identified calgranulin C as an important factor in
the pathogenesis of Mooren’s ulcer. Calgranulin C
is a neutrophil protein that binds to paramyosin,
a component of the thick filaments of parasite
muscle. Receptors for calgranulin C are also known
to occur on the surface of certain helminths.
Sensitisation to calgranulin C could occur either
acutely as a result of corneal infection or trauma,
in which corneal tissue breakdown occurs resulting
in the expression of normally cryptic tissue
specific corneal antigens, or gradually during the
normal slow turnover of tissue throughout the
years. In addition, sensitisation to calgranulin C
may occur subsequent to helminth infestation.
Antigen presenting cells (APC) normally present
at the limbus would present these “self ” or “cross
reactive” antigens in the form of short peptides
bound to HLA class II molecules. Sensitisation
would only occur in susceptible individuals with
the appropriate HLA genotypes as only a limited
repertoire of peptides can associate with each HLA
3
molecule. Under these circumstances antigen/
MHC specific T cells will be primed. At a later date
if one or both corneas are injured mechanically,
surgically, or as a result of infection there would
be macrophage infiltration of the cornea, and
IFNg induced upregulation of cellular HLA
expression. This would be particularly intense
if there is a high circulating level of calgranulin
C associated with a concomitant helminth
infestation and its accompanying neutrophilia.
An autoimmune response would then occur as a
result of the presentation to and the response from
previously primed effector T cells. Such a course
of events would explain the worldwide genetic
and geographic distribution, the rarity, and the
absolute corneal stromal tissue specificity of this
autoimmune condition.
Diagnosis
Mooren's ulcer is idiopathic and occurs in the
absence of any systemic process that may cause
PUK. It is a diagnosis of exclusion. Infectious
etiologies should be excluded by appropriate
cultures, because microbial keratitis can rapidly
progress and is usually amenable to antibiotic
therapy.
Mooren's ulcer is easily distinguished from
the noninflammatory corneal degenerations, such
as Terrien's or Pellucid marginal degeneration, in
which the epithelium remains intact and pain is
absent.
The presence of Mooren's-like ulcer requires
an extensive search for occult and potentially lethal
systemic diseases. A thorough medical history and
examination is mandatory, as is comprehensive
laboratory investigation. The investigation
may include a complete blood count with
evaluation of the differential count, platelet count,
erythrocyte sedimentation rate, rheumatoid factor,
complement fixation, antinuclear antibodies
(ANA), antineutrophil cytoplasmic antibody
(ANCA), circulating immune complexes,
liver function tests, VDRL and fluorescent
treponemal antibody absorption (FTA-ABS)
4
tests, blood urea nitrogen and creatinine, serum
protein electrophoresis, urinalysis, and a chest
roentgenogram. Additional testing is done as
indicated by the review of systems and physical
examination.
Differential Diagnosis
Rheumatoid arthritis
It is a frequent cause of peripheral ulcerative
keratitis10. The clinical appearance of the peripheral
ulceration is not unique in rheumatoid arthritis.
Frequently, there may be an associated scleritis, a
feature not characteristic of typical Mooren's ulcer.
Other associated ophthalmic findings include
keratoconjuctivitis sicca (the most common
ophthalmic finding), episcleritis, and sclerosing
keratitis. Advanced systemic involvement is usually
apparent at time of ocular involvement10. The
patient's clinical profile and positive serologic
studies, in particular rheumatoid factor, will help
establish the appropriate diagnosis.
Wegener’s Granulomatosis
Wegener's granulomatosis is a rare multisystem
granulomatous necrotizing vasculitis with upper
and lower respiratory tract and renal involvement.
Ocular involvement may be seen in upto 58%
of patients, including proptosis due to orbital
involvement, scleritis with or without PUK,
PUK alone, uveitis, and vasculitis11. A careful
review of systems may disclose a history of
upper or lower respiratory signs or symptoms
(epistaxis, sinusitis, rhinorrhea, hoarseness,
dysphagia, cough, or pleurisy), a history of
microscopic hematuria, arthralagias, or skin
lesions as the result of the underlying vasculitis
process. Prompt diagnosis is imperative because
the initiation of immunosuppressive therapy, such
as cyclophasphamide, can be both sight and life
saving11.
Polyarteritis nodosa
Classic polyarteritis nodosa (PAN) is a rare
multisystem disease characterized by necrotizing
vasculitis of small and medium-sized muscular
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arteries. The etiology is unknown, and the
diagnosis rests on the histopathologic identification
of typical vascular changes. Microaneurysms at the
bifurcation of the medium and small arteries are
highly characteristic of the disease, especially in the
kidney and mesentery. Choroidal vasculitis is the
most common ophthalmic manifestation. Other
ophthalmic findings include PUK, conjunctival
lesions, scleritis, choroiditis, retinal vasculitis,
optic atrophy, papilledema, exudative retinal
detachment, and central artery occlusion. Serologic
tests for hepatitis B surface antigen (HBsAg)
should be obtained because approximately 50%
of patients with PAN are seropositve.
Staphylococcal marginal keratitis
Staphylococcal marginal disease can present as
a peripheral corneal infiltrate with overlying
epithelial breakdown. There is a clear intervening
zone between the infiltrate and limbus, and the
keratitis is frequently accompanied by blepharitis.
Patients complain of photophobia and irritation,
but the severe and debilitating pain noted with
Mooren's ulcer is not described. Rapid clinical
improvement can usually be seen with mild topical
steroids. The ulcers are believed to represent
immune complex-mediated reactions to microbial
antigens12.
SLE
Relapsing polychondiritis
Systemic sclerosis
Inflammatory bowel disease
Gaint cell arteritis
Herpes simplex corneal ulcer
Terriens degeneration
It differs from Mooren's ulcer in that it is typically
painless, does not ulcerate and is usually non
inflammatory. It has been reported more frequently
in men and may occur at any age. The disease is
usually bilateral but may be asymmetrical13.
Terrien's degeneration usually begins in the
superior cornea, in contrast to Mooren's ulcer,
which typically begins in the interpalpebral region
Vol. XIV, No.2, April - June 2014
as a fine, punctate, stromal opacity. A clear zone
exists between the infiltrate and the limbus,
which becomes superficially vascularized. Slowly
progressive thinning follows. The thin area has
a sloping peripheral border and a sharp central
edge that is highlighted by a white lipid line. The
epithelium remains intact, although bulging of
thin stroma causes significant astigmatism. The
thinning slowly progresses circumferentially but
rarely centrally.
Pellucid degeneration
Pellucid degeneration causes bilateral, inferior
corneal thinning that leads to marked,
irregular, against-the-rule astigmatism. Pain and
inflammation are lacking and the epithelium is
intact, thus differentiating it from Mooren's ulcer.
Senile furrow degeneration
Thinning in the lucid interval between an arcus
and limbus may occur in the elderly. However,
the epithelium is intact and there is no infiltrate
or inflammation. The furrow is shallow and not
vascularized, with sloping central and peripheral
edges. Progression is extremely slow, and has no
risk of perforation.
- Ocular rosacea
- Leukemia
Treatment of Mooren's Ulcer
The overall goals of therapy are to arrest the
destructive process and to promote healing and
reepithelialization of the corneal surface.
Historically, the therapeutic agents tried
for Mooren's ulcer include subconjunctival
dichloride of mercury14, carbonic and nitric acid,
formalin15 and tincture of iodine16, trichloroacetic
acid16, subconjunctival heparin17, and cyanide of
mercury18.
In addition, a number of procedures, such
as irradiation19, galvanocautery20, paracentesis21,
vitamin B1 injections, tuberculin injections22, and
delimiting keratotomy23, have been attempted
with little success. Today, most experts agree
on a step-wise approach to the management of
5
Mooren's ulcer, which is outlined as follows:
1. Topical steroids
2. Conjunctival resection
3. Systemic immunosuppressives
4. Additional surgical procedure
5. Rehabilitation
Topical steroids
Initial therapy includes intensive topical steroids,
consisting of prednisolone acetate or prednisolone
phosphate 1%, hourly in association with topical
cycloplegics and prophylactic antibiotics 24. If
epithelial healing does not occur within 2 to 3
days, the frequency of topical steroid application
can be increased to every half hour. Once healing
occurs, the frequency can be reduced, and tapered
slowly over a period of several months.
Some authors have advocated oral pulse
therapy (60 to 100 mg daily of oral prednisone)
when topical therapy is ineffective after 7 to 10 days
or in cases where topical steroids may be dangerous
because of precariously deep ulcer or infiltrate.
Topical tetracycline or medroxyprogesterone may
be used for anticollagenolytic properties of each.
A therapeutic soft contact lens or patching
of the eye may be beneficial at this stage. Any
concomitant eye disease, such as acne rosacea,
meibomeitis, blepharitis, dry eye, or eyelid
abnormalities is addressed24.
Conjunctival Resection
Due to its luxurious vascular and lymphatic
endowment, the conjunctiva adjacent to the
peripheral corneal ulcer has been hypothesized to
serve as a major reservoir for various inflammatory
cells and cytokines, thereby playing a critical role in
the immuno-pathogenesis of peripheral ulcerative
keratitis. Moreover, the substantia propria of the
conjunctiva is filled with plasma cells25 which
are likely involved in the local production of
immunoglobulins found in the peripheral cornea.
Circulating antibodies against cornea, first found
in 1969 in patients with Mooren’s ulcer26, have
been postulated to be produced from these plasma
cells.
6
If the ulcer progresses despite the steroid
regimen, conjunctival resection is performed24. It is
usually performed under topical or subconjunctival
anesthesia. This consists of conjunctival excision to
bare sclera extending at least 2 clock hours to either
side of the peripheral ulcer, and approximately
4 mm posterior to the corneoscleral limbus and
parallel to the ulcer26. The overhanging lip of
ulcerating cornea may also be removed.
Cryotherapy of limbal conjunctiva has been
advocated by some authors and may have a similar
effect28.
In Mondino's series29, conjunctival resection
healed 3 of 4 unilateral ulcers and 3 of 3 bilateral
nonsimultaneous ulcers, but only 2 of 15 bilateral
simultaneous ulcers.
Brown reported that excision of the limbal
conjunctiva adjacent to the progressing ulcer
resulted in healing of the ulcers in 8 of 10 eyes
treated; however, it may be necessary to repeat this
procedure three times before a beneficial effect is
seen29.
Stilma studied 38 Mooren's corneal ulcers
and found that conjunctival excision with
thermocoagulation gave some relief at the site of
the ulcers, but recurrences at other places occurred
in at least 52% of cases31.
Kinoshita and colleagues32 reported success in
their series of 20 Mooren's patients treated with
keratoepithelioplasty. In this procedure, donor
corneal lenticles are sutured onto the scleral bed
after conjunctival excision. It is postulated that
the lenticles form a biological barrier between
host cornea and the reepithelializing conjunctiva
and the immune components it may carry. In
his study, 18 of 20 eyes (90%) showed prompt
remission after surgery.
Application of isobutyl cyanoacrylate, a tissue
adhesive, may work in the same way but perhaps
more simply and without the risk of epithelial
rejection, glaucoma secondary to the chronic
steroid use necessitated by keratoepithelioplasty
and development of neurotrophic keratitis32.
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Systemic immunosuppression
Those cases of bilateral or progressive Mooren's
ulcer that fail the preceding therapeutic attempts
will require systemic cytotoxic chemotherapy to
bring a halt to the progressive corneal destruction24.
The most commonly used agents are
Cyclophosphamide (2 mg/kg/day), Methotrexate
(7.5 to 15 mg once weekly) and Azathioprine
(2 mg/kg body weight/day).
Cyclophosphamide belongs to nitrogen
mustard group of alkylating agents. It has a
profound effect on lymphoid cells. It is given in a
dose of 2mg/kg body weight/day. The degree of fall
in white blood cell count is considered as the most
reliable indicator of immunosuppression produced
by cyclophosphamide. Common dose limiting
side effect includes bone marrow depression and
sterile hemorrhagic cystitis.
Azathioprine is a prodrug. It is metabolized
in the body and is converted into its active
metabolite, 6-mercaptopurine. It affects DNA
and RNA metabolism by being converted
into 6–thioinosine-5 phosphate by the enzyme
hypoxanthine guanine phosphoribosyl transferase
and is incorporated into nucleic acids leading to
false codes being generated. It is given at the dose
of 1 – 2.5 mg / kg body weight per day in divided
doses. Acute adverse effects of Azathioprine
therapy include leucopenia, thrombocytopenia
and gastrointestinal disturbances.
Methotrexate is a folate analogue which affects
the enzyme dihydrofolate recuctase. The enzyme
is imperative for production of tetrahydrofolate,
an important coenzyme in cell metabolism.
Methotrexate has antiproliferative effect on
endothelial cells, decreases leukotriene synthesis by
leukocytes and suppresses cell mediated immunity.
It is given in doses of 7.5 to 25 mg weekly. Folic
acid supplementation is recommended during
therapy with Methotrexate. Patients are advised to
abstain from alcohol. Side effects of Methotrexate
therapy include severe depression of white blood
cell count and thrombocytopenia. Hepatotoxicity
Vol. XIV, No.2, April - June 2014
is a common side effect. Liver enzyme levels twice
those of normals warrant withholding or stopping
of the medication. Other side effects include
acute pneumonitis, impairment of renal function,
alopecia. Methotrexate is teratogenic and is not
used during pregnancy and birth control is advised
for sometime after the medication is stopped.
Oral Cyclosporin A (5 - 10 mg/kg/day)
has been successfully used to treat a case of
bilateral Mooren's ulcer unresponsive to local
therapy with topical corticosteroids, silver
nitrate, and conjunctival resection, as well as
systemic immunosuppression with corticosteroids,
cyclophosphamide, and azathioprine33. It affects
release of interleukin. It works by suppression
of the helper T cell population and stimulation
of the depressed population of suppressor and
cytotoxic T cells present in patients with Mooren's
ulcer. Common side effects include hypertension,
renal impairment, parasthesias,hyperuricemia,
gingivitis, hypertrichorism.
Systemic immunosuppressive therapy is
best handled by close collaboration between an
ophthalmologist and oncologist. The potentially
serious side effects of systemic immunosuppressive
agents have led several groups to investigate the
efficacy of topical applied cyclosporin A in the
treatment of Mooren's ulcer34. In Holland's35 series
of a variety of anterior segment inflammatory
diseases; two patients had Mooren's ulcer. The
first, with bilateral disease, showed reduced
inflammation with minimal progression over 3
years, whereas the second, with unilateral disease,
showed resolution of the ulcer on this medication.
In Zhao and Jin's series, 15 of 18 eyes with
Mooren's ulcer improved, and 11 of these were
cured with topical cyclosporine A therapy (0.5%
solution). In both studies, local or systemic side
effects attributable to topical cyclosporine A were
not observed.
Foster reported arrest of the inflammatory
process and preservation of ocular anatomy
and function in 8 of 9 patients with bilateral
involvement treated with immunosuppressives
for 6 to 24 months36. Mondino has reported that
7
immunosuppressive drugs halted progression in 4
of 13 patients with Mooren's ulcer who did not
respond to topical corticosteroids or conjunctival
resection. In this series immunosuppressive drugs
were reserved for only the most severe, resistant
cases37.
Surgical Procedure
Superficial lamellar keratectomy involves resection
of overhanging lip of the ulcerating cornea and
application of tissue adhesive with bandage soft
contact lens application or amniotic membrane.
It has been shown to arrest the inflammatory
process and allow healing38. Superficial lamellar
keratectomy may aid the removal of corneal
antigenic stimulus of the autoimmune process
that causes stromal melting39. It may also act by
reducing activated keratocytes which may be a
source of collagenase40 and polymorphonuclear
neutrophils which have already invaded the
corneal stroma as part of the pathological process.
After refining the technique in previous series,
Nian and colleagues41 found 34 of 40 eyes to be
successfully healed after lamellar keratectomy.
Four of 6 eyes with recurrent ulcer healed with
retransplantation while the other patients refused
further intervention.
Some cases may progress to perforation
despite management. Small perforations may
be treated with application of tissue adhesive
and placement of a soft contact lens to provide
comfort and to prevent dislodging of the glue24.
When a perforation is too large for tissue adhesive
to seal the leak, some type of patch graft will be
necessary. This may range from a small tapered
plug of corneal tissue to a penetrating keratoplasty.
In case of larger peripheral perforations, a partial
penetrating keratoplasty can be performed. Rarely
conjunctival flaps or even penetrating keratoplasty
may be necessary. The prognosis of corneal graft
in the setting of acute inflammation in patients in
setting of Mooren’s ulcer is very poor.
Rehabilitation
Once the active ulceration has ceased and the
remaining cornea has been completely opacified,
8
it is possible to perform penetrating keratoplasty
on these patients, even in the face of a thinned
and vascularized cornea42. In these instances, a 13
mm tectonic corneal graft is first sutured in place
with interrupted 10-0 nylon or prolene sutures
with the recipient bite extending into the sclera so
that the suture will not pull through the thin host
cornea and then a 7.5 or 8.0 mm therapeutic graft
is placed. Surgical attempts at rehabilitation in
Mooren's ulceration is done only with concurrent
immunosuppression, even when the active disease
has been arrested, or is 'burned out,' because
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attempts at penetrating keratoplasty often are
associated with recurrence and graft failure. It
is believed that patients with treated Mooren's
ulcer should be immunosuppressed prior to
cataract surgery or corneal grafting procedure.
In absence of donor corneas Stilma31 et al have
suggested the usage of a free lamellar scleral auto
graft to restore the corneal defect, followed by
penetrating keratoplasty later. In his series of 38
eyes with corneal ulcer, six eyes with a progressive
iris prolapse and a flat anterior chamber were
reconstructed with the above technique.
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