Transcript Allergic conjunctivitis1

Ocular allergy
Abdulrahman Al Muammar
Ocular allergy
Allergic eye diseases accounts for up to 3%
of all the medical consultations seen in
general practice.
The milder forms of allergic eye diseases
have fluctuating symptoms of itch, tearing,
and swelling.
Chronic form of the disease give rise, in
addition, to more severe symptoms including
pain, visual loss from corneal scarring,
cataract or glaucoma, and disfiguring skin
and lid changes.
Ocular allergy
Clinical classifications:
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1) Allergic conjunctivitis (AC):
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Acute allergic conjunctivitis:
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Seasonal or hay fever.
Toxic- induced (induced by acute contact with irritant,
drugs, preservatives, etc).
Chronic allergic conjunctivitis:
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Perennial.
Toxic-induced (long standing).
Ocular allergy
2) Contact dermatoblepharitis.
 3) Vernal keratoconjunctivitis (VKC
 4) Giant papillary conjunctivitis (GPC
 5) Atopic keratoconjunctivitis (AKC
 6) Atopic blepharoconjunctivitis (ABC).
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Sensitization
Acute and chronic diseases have in
common:
1) sensitization to environmental allergens.
 2)Ig E mast cells activation with
subsequent mediator cascade.
 3) conjunctival inflammation with
prevalence of eosinphils.
 4) the presence of lymphocytes with a Th2
profile of cytokines production .
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Sensitization
The conjunctiva is normally exposed to
pictogram quantities of environmental allergens
such as pollens, dust mite fecal particles,
animal dander and other proteins .
 When deposited on the mucosa, these antigens
are thought to be processed by lagerhans cells
and other antigen presenting cells (APC) in the
mucosal epithelium .
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Sensitization
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antigen is presented to native Th0 cells
expressing antigen – specific T cell receptors
recognize the antigenic peptide. Multiple
simultaneous contacts and cytokine exchange
between APC and T cells are necessary to
trigger antigen specific Th0 cells to differentiate
into Th2 lymphocyte .
Sensitization
. The cytokines released by Th2 cells (
IL3,IL4,IL5,IL6,IL13,GM-CSF) stimulate B cell
IgE production and inhibit development of Th1
mediated delayed type hypersensitivity
reactions .
 B cells which recognize the same allergen that
induce Th2 differentiation, in present of
appropriate signals such as IL4,IL6 and IL13
undergo heavy chain switching to produce IgE.
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Mast cells
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Mast cells particularly abundant in the conjunctival
stroma especially at the limbus.
The number of the mast cells in the conjunctiva has been
calculated to be 5000/mm3 .
conjunctival biopsies from symptomatic allergic patients
have shown an increase in subepithelial mast cells with
evidence of mast cells degranulation
Two different types of mast cells have sown in
conjunctiva, differentiated by their content of tryptase
alone ( mucosal mast cell or MCT) or both tryptase and
chymase ( connective tissue type mast cell or MCTC)
Mast cells
Proliferation of these cells in allergic disorders
is probably under influence of Th2 cytokins.
 Mast cells and basophils, bearing high affinity
surface receptors for Ig E are the most
important cells in IgE mediated reactions.
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Mast cells
Mast cells mediators:
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Histamine.
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Vasodilatation….smooth muscle constriction.
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Heparin.
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Prevent blood coagulation.
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Itching..redness.
Anti-inflammatory.
Tryptase.
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Potentiates histamine..activates eosinophils and mast
cells
Mast cells
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Prostaglandins and leukotrienes
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Capillary leakage..smooth muscle
contraction..increase granulocyte action..platelet
aggregation.
 Airway hyperresponsiveness…asthma.
Mast cells
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Eosinophil chemotactic factor-alpha (ECFalpha).
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Attract eosinophils.
Platelet activating factor (PAF).
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Platelet aggregation….neutrophil chemotaxis.
Bronchoconstriction…hypotension…hyperemia..
Chemosis.
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Eosinphils
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Influx of eosinphils is essential in allergic inflammation
and profound changes in conjuncatival mucosa.
Eosinophils are activated by interaction with other
inflammatory cells such as platelet activating factors.
Activated eosinophils release very basic highly charged
polypeptide including:
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Major basic protein (MBP).
Eosinophil cationic protein (ECP).
Eosinophil derived neurotoxin (EPX).
eosinophil peroxidase (EPO).
Eosinphils
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These proteins may bind to basement membrane
protoglycans and hyaluran to cause cellular
disaggregation and epithelial desquamation.
ECP and MBP are epithelial toxic and are involved in
corneal damage that may occur in sever chronic allergy.
Eosinphils are also important source of leukotriens,
prostaglandins and cytokines such as IL3, IL5, and GM
CSF, eotaxin and RANTES.
ECP and EPX tear level are correlated with clinical signs
and symptoms of allergic disease and maybe considered
local markers of eosinphil activation.
Neutrophils
Following allergen challenge, neutrophils are
the first cells to appear in tear fluid and the
predominant infiltrating cells in the conjunctive
during late phase.
 Although the role of neutrophils in allergic
disorders is not clear, they can release
inflammatory mediators including leukotriens
,PAF and cytokines.
 Tear level of myeloperoxidase (MPO). a
neautrophil activating marker are increased in
allergic conjunctivitis.
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Lymphocytes
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One of the most important process responsible for
orchestrating and regulating allergic inflammation is the
production of cytokines by T cells lymphocytes.
CD4-T cells are the predominant population in
conjunctival inflamed tissues.
T cells have been subdivided into two functionally distinct
subset on the basis of their cytokine profile:
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Th1 and Th2 .
Th1 is known to produce IL2 and interferon gamma(INFg).
Th2 is known to produce IL3,IL4,IL5.
Lymphocytes
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T cells in allergic inflamed tissues are mostly CD4 with
cytokine production profile of the Th2 type.
An increase in expression of Th2 type cytokine (IL4, IL5,
IL3) have been demonstrated in SAC, VKC and AKC.
Compared to SAC, VKC maybe considered a disease
with an over expression of these cytokines in addition to
other mechanism involved.
Conversely in AKC and GPC in addition to typical Th2
derived cytokines, increases of IL2 and INF-g has been
shown suggesting that in the most severe atopic
conditions a cell medicated hypersensitivity may also
occur.
Seasonal allergic
conjunctivitis
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Is the commonest and one of the mildest forms
of allergic conjunctivitis. It accounts for 25%50% of all cases of ocular allergy.
SAC is often associated by rhinitis and even
sinusitis.
70% of patients provide either a personal of
familial allergic history.
SAC can develop suddenly when patient comes
in contact with an appropriate antigen, such as
pollens, grasses, or trees.
SAC
Symptoms:
Itching.
 Watery discharge.
 Rhinitis.
 Sinusitis.
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SAC
Signs:
Not always present.
 Lid swelling.
 Ptosis.
 Conj hyperemia.
 Chemosis (=/- dellen).
 Papillary reaction.
 Follicular reaction.
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SAC
Diagnosis:
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Clinically.
Family history.
Conj scrapings for eosinophils.
Tear level of IgE, serum tear.
Radioallergosorbent test measures specific IgE
levels for a specific antigens.
Mast cells activity by measuring tryptase and
histamine levels in tear film.
SAC
Pathophysiology:
Type I hypersenstivity.
 Late phase reaction (LPR):
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Clinical, histological, or chemical response to
an antigen that occurs 3 to 12 hours after the
initial acute (early phase) mast cell-mediated
allergic reaction.
SAC
Treatment:
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Avoidance of allergen:
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Limit outdoor activities.
Use air conditioning or air filter system.
Drive car with windows closed.
Use protective eyegear when outdoor.
Washing allergen.
Antihistamines.
Mast cell stabilizers.
NSAIDs.
Steroids.
Immunotherapy.
Acute allergic toxic
induced conjunctivitis
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Usually triggered by external non- airborne
antigens such as drugs, contact lens solution,
irritants, and preservatives.
Type I medicated.
Symptoms are similar to SAC but no seasonal
component.
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Itching, tearing, eyelid erythema and swelling, and
conjunctival redness and chemosis. Typically occur
within minutes after application of an allergen.
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Bactriacin..cephalosporins..sulfacetamide..tetracycline
Atropine…homatropine.
Epinephrine..pilocarpine..apraclonidine.
Antiviral agents.
Thimerosal..chlorhexidine…bezalkonium chloride.
Acute allergic toxic
induced conjunctivitis
Diagnosis:
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Clinical presentation.
Offending agents.
Conj scrapings.
Treatment:
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Discontinue the offending agents.
Tears..
Cold compresses.
Antihistamines..
NSAIDs..
Steroid
Perennial allergic
conjunctivitis
PAC
Symptoms persist throughout the year,
with seasonal variation in up to 87% of
patients.
The clinical signs and symptoms are
similar to SAC, but more persistent.
Allergens could be house dust mites,
animals, etc..
Type I mediated.
PAC
Treatment:
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Avoidance of allergen:
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Cover for mattress and pillows.
Washing bedding regularly.
Reduce humidity.
Vaccum and damp dust.
Eliminate animals from house.
Washing allergen.
Antihistamines.
Mast cell stabilizers.
NSAIDs.
Steroids.
Immunotherapy
Contact
dermatoblepharitis
Reaction that may begin 24-72 hours
following instillation of topical medication.
Patients are often sensitized by previous
exposure to the offending drugs or
preservatives.
Acute eczema with erythema, leatherlike
thickening, and scaling of the eyelid.
Lower eyelid ectropion, and
hyperpigmentation.
Papillary conjunctivitis and mucoid discharge
may develop.
Contact
dermatoblepharitis
Medications commonly associated with
these symptoms:
Atropine..homatropine.
 Neomycine..gentamycine..tobramycine.
 Idoxuridine..trifluridine.
 Thimerosal.
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Type IV reaction.
Contact
dermatoblepharitis
Treatment:
Allergen withdrawal.
 In severe cases…brief course of topical
steroids applied to the eyelids and
periocular skin may speed resolution.
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VKC
Epidemiology:
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Rarely appear in patients younger than 3 or older than 25 years
of age.
M:F is 2:1.
The disease usually lasts 4 to 10 years and resolved after
puberty, but also can still be present and even worsened in
some adult patients.
Occurs more frequently in the Mediterranean area, central
Africa, India, and South America.
It also occur in cooler climates, such as Great Britain and other
northern European countries, which is possibly as a
consequences of migratory movements of the susceptible
population.
Association with atopy is 15 to 60%.
VKC
VKC is usually bilateral, although monocular forms
and asymmetric symptoms do occur.
Three clinical forms can be observed : tarsal, limbal
(more common in African and Asian patients), and
mixed tarsal/limbal.
In majority of the cases, the disease is seasonal,
lasting from the beginning of spring until fall.
Nevertheless, perennial cases have been observed,
especially in warm subtropical or desert climates.
VKC
Symptoms:
Itching.
 Tearing.
 Mucus secretion.
 Photophobia.
 Pain.
 Blepharospasm.
 Decreased visual acuity.
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VKC
Signs:
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Papillary reaction.
Conjunctival redness and edema
GPC.
Limbal gelatinous infiltrate.
Trantas dots.
Mucus discharge.
Pseudoptosis.
Tarsal conjunctival fibrosis.
VKC
Corneal involvement:
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SPK (Togby – Dusting of flour…uppper 1/3)
PEE.
Pannus.
Filamentary keratitis.
Shield ulcer.
Pseudogerontoxon.
Keratoconus.
VKC
Diagnostic approaches:
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Clinically.
Specific IgE maybe assayed in serum and tears.
CBC for eosinophilia.
Conj scraping and tear cytology:
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Eosinophils.
Basophils.
Neutrophils.
Tears tryptase level .
VKC
Pathogenesis:
Type I hypersensitivity.
 Type IV hypersensitivity.
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VKC
Histopathology:
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Proliferative and degenerative changes in the
epithelium:
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Prominent cellular infiltration in the substantia
propria:
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Occur early with marked acanthosis, and intraepithelial
pseudocysts.
Eosinophils, neutrophils, basophils, lymphocytes, and
plasma cells. Resident plasma cells and fibroblasts are
also increased.
Hyperplasia of the connective tissues:
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Mainly type III collagen, they run parallel to the surface
forming the fibrous structure for giant papillae.
Trantas dots.
Shield ulcer.
VKC
Therapy:
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Preventive measures:
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Mucolytic agents 10% Acetylcysteine
Tears/vasoconstrictors/ cold compresses.
Mast cells stabilizers:
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Change of climate.
Avoid exposure to nonspecific triggering factors such as
sun, wind, and salt water.
Should be used continuously throughout the season.
Antihistamines.
NSAIDS: either locally or systemically.
Steroids. Short pulses, topical/ tarsal injection.
Cyclosporine.
VKC
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Corneal ulcers….
Steroids-antibiotic/eye patching.
 Superficial keratectomy.
 PTK.
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GPC…..
Local steroid injection.
 papillae excision/cryotherapy/mucosal graft.
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AKC
Atopy is hereditary condition that manifests in
ocular diseases, skin abnormalities, and
respiratory tract dysfunction.
Atopy occurs in 5 to 20% of the general
population.
The term AKC is misleading, although ocular
surface disease is most prominent, the
disease usually involve the lid also.
AKC
Epidemiology:
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AKC occur in up to 25% of patients with atopic
dermatitis.
A review of family history frequently reveals the
presence of other diseases such as asthma, hay
fever, and urticaria.
AKC occurs more frequently in men.
Typically begin in the late teens or early twenties,
and they persist until the fourth or fifth decade of
life.
The peak incidence occurs between the ages of
30 and 50 years.
AKC
Clinical signs of the disease generally
improve with age and may totally regress.
 Patients with severe cases don't follow this
trend.
 AKC is often worse in the winter, but it
usually has a perennial pattern of
occurrence.
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AKC
Clinical features:
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Symptoms:
Bilateral itching
 Tearing
 Watery discharge
 Burning
 Photophobia
 Blurred vision.
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AKC
Signs:
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Lid:
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Thickening of the eyelid margins (tylosis)
Eyelid swelling.
Scaly, indurated, and wrinkled appearance of the periocular
skin
With profound swelling, a dennie-morgan folds or Dennie line is
seen.
Chronic inflammation can give upper lid ptosis.
Fissures can occur at the lateral canthus owing to excessive
skin rubbing.
An absence of lateral eyebrows, or Hertoghe’s sign can be
seen in severe form.
Marginal belpharitis caused by staphylococcal infection is
common.
AKC
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Conjunctiva:
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The conjunctive can be hyperemic to milky edematous.
Tarsal conjunctival papillary reaction is a common finding
usually in small to medium size, both upper and lower
conjunctive.
Limbal papillae.
Trantas dots.
Rarely GPC in lower conjunctive.
Conjunctival cicatrization and symblepharon most
commonly in the inferior fornix.
AKC
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Cornea:
PEE/PEK.
 Intraepithelial microcyst.
 Infecious and noninfecious corneal ulcer.
 Peripheral micropannus.
 Neovascularization extending to the central
cornea.
 Keratoconus in 16% of patients with AKC.
 Pellucidal marginal degeneration, and
keratoglobus.
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AKC
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Lens: ? In 5 to 25%
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Retina:
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Anterior subcapsular cataract (shield cataract).
Posterior subcapsular cataract ( related to steroid )
Retinal detachment.
Systemic disorders:
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Hay fever.
Asthma (? in 87%).
Atopic dermatitis ( ? In 95%)- chronic pruritic inflammation
of the skin mainly forehead, cheeks, and flexor surfaces of
the arms and legs, atopic dermatitis usually begin in
childhood.
VKC Vs AKC
VKC
AKC
Age of onset
Childhood, teens
age 20 to 50
Duration
Resolved in mid to late teens
Resolved by age 50
Seasonal variation
Markedly worse in spring
variable
Conjunctival papillae
GPC….upper lid
Small or medium size..upper
and lower
Conjunctival scarring
Uncommon
Can give symblepharon
skin
Uncommon
Often
Eosinophils
Numerous
Less munerous and less often
degranulated
Corenal vascularization and
scarring
Less extensive
More extensive
lens
No
ASCC/PSCC
AKC
Etiology and histopathology:
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Type I hypersenstivity reaction.
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Elevated levels of tear and serum IgE are charactristic of
exacerbated AKC.
Conj scraping showed approximately 50 million mast
cells, also an excess of eosinophils ( less than VKC)
Type IV hypersenstivity
Diminished cell medicated immunity is common.
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Staph aureus…..HSV……response to PPD.
AKC
Diagnosis:
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Family history.
Some level of disease activity is always present
with variable exacerbations.
Atopic dermatitis.
Papillary reaction more inferiorly than superiorly.
Rarely GPC inferiorly.
Usually begin in late teenage or more commonly
later.
Most severe type of ocular allergy.
AKC
In Vivo Tests:
Positive intradermal skin tests
Conjunctival challenge
Prausnitz-Kustner test
In Vitro Tests:
Basophil histamine release
Radioallergosorbent test (RAST)
AKC
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Conjunctival cytology - eosinophils
Tear histamine level – 10 ng/ml
normal
Tear IgE, Serum IgE
Eosinophilia > 500 cells/ml
AKC
Managemant:
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Tears.
Vasoconstrictors.
Cold compresses
Antihistamines
NSAID.
Mast cell stabilizers.
Steroid.
Cyclosporine.
Antibiotics.
Surgical: lid procedures/ PKP.
GPC
Characterized by the presence of
abnormally large papillae ( more than
0.3 mm in diameter) on the upper tarsal
conjunctiva, conjunctival hyperemia,
excess mucus secretion, foreign body
sensation, and itching.
First reported in 1970 in patients
wearing contact lenses.
GPC
Epidemiology:
Incidence among RCL user with average
period of 10 months is 10.5%.
 History of atopy plays a major role in
predisposition of GPC.
 Patients with GPC report higher incidence
of allergy to pollens as well as to
medications.
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GPC
Etiology:
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Contact lenses:
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Soft..any time between 3 weeks to 31/2 yrs after
wearing CL.
Rigid…may appear even after 11 ys.
Sutures..nylon/prolene.
Prosthesis.
Cyanoacrylate glue.
Scleral buckle.
Bleb/valve..
Vernal.
Atopy.
Epibulbar dermolipoma.
GPC
Symptoms:
Foreign body sensation.
 Intolerance to CLW.
 Itching.
 Irritation.
 Mucus secretion.
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GPC
Signs:
Enlarged papillae ( > 0.3 mm in diameter),
variable in numbers, and almost always in
the upper tarsal conjunctive.
 Mucus strands.
 Mild to severe hyperemia.
 Trantas dots and limbal inflammation..
 Ptosis.
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GPC
Stages:
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Stage I:
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Initial symptoms including mucus in the nasal corner
of the eye after sleep and mild itching after lens
removal. No papillae detected usually.
Stage II:
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Increased severity of mucus and itching and mild
blurring of the vision, which occur toward the end of
the usual lens wearing time.
Small, round papillae, conj is thickened, edematous
and hyperemic.
GPC
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Stage III:
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Increased severity of mucus and itching,
accompanied by excessive lens movement
associated with blinking.
CL surface become coated with mucus and debris.
GPC..increased in numbers and size.
Stage IV:
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Exacerbation of stage III.
CL intolerance.
CL are coated and cloudy soon after insertion.
GPC
Pathogenesis:
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Mechanical trauma…result in degranulation of mast cells
and disruption of the epithelial surface.
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Stimulate production of neutrophil chemotactic factors and
inflammatory mediators.
Immunological response consisting of both humoral and
cell mediated immunity.
Mediators in tear fluid:
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Increase tryptase.
increase Ig G,M,E.
Increase eosinophil ..MBP..ECP.
Increase histamine.
Decrease lactoferin.
GPC
treatment;
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Prevention:
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Lens design/hygiene.
Burying sutur knots.
Relieving the symptoms:
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Removal of the CL, prosthesis, suture.
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Symptoms usually dissipate within 48 hrs after d/c CL.
Change CL design..wearing times…hygiene.
Mast cell stabilizers…mainly in mild cases.
Steroid…..for moderate to severe cases.
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It may take months or even years for GPC to disappear, in some
patients, the papillae have not disappeared in more than 20 years,
yet these patients remain a symptomatic CLW.
Microbial Allergic
Conjunctivitis
Staphylococcal blepharoconjunctivitis.
• Phlyctenular keratoconjunctivitis.
• Splendore-Hoeppli phenomena
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Allergic granulomatous nodules
Ocular allergy treatment
approach
Elimination of allergen.
Eliminate eye rubbing.
Cool compresses/ tears/ vasoconstrictors.
Anithistamines for acute attack.
Mast cell stabilizer as prophylactic.
NSAIDs fro acute attack
Steroid mainly for AKC/ VKC / GPC in short
pulses..
Cyclosporine in VKC / AKC.
Immunotherapy.
Drug therapy
Antihistamines.
 Vasoconstrictors.
 Mast cell stabilizers.
 NSAIDs.
 Steroids.
 Cyclosporine.

Topical
antihistamine/vasoconstrictorw
Vascon-A.Naphcon-A.
AK-Con-A.Opcon-A.
Topical antihistamine
Livostin. Emadine.
Alocril Patanol.
Alamast Optivar Zaditor.
Systemic antihistamine
Claritin .Allegra. Benadryl .
Mast cell stabilizers
Opticrom
Alamast
Alomide
Zaditor
Antihistamine+Mast cell
stabilizer+ NSAID
Alamast
Optivar
NSAIDs
Acular
Ocufen
Steroids
FML
inflammase mild/forte
Pred mild/forte vexol
Alrex
Lotemax
Cyclosporine
Crolom
Alocril
Patanol
Optivar
Alocril
Zaditor
Voltaren
Aspirin
Antihistamines
H1 receptor
-Found throughout
the body.
-Vasodilation /
increase capillary
permeability.
-Smooth muscle
contraction.
-Selective H1
stimulation in
conj…..produce
itching without
vasodilation.
H2 receptor
-Predominantly
gut.
-Found on ocular
surface.
-Vasodilation.
-Smooth muscle
relaxation.
-Systemic H2
antagonist
produce decrease
in gastric acid
production
-Selective H2
stimulation in
conj…produce
vasodilation
(redness).
H3 receptor
-Responsible for negative
feedback regulation of
anaphylactic histamine
release.
-located on histaminergic
terminals of nerves.
-Not been identified on ocular
tissue.
-no selective therapeutic
agent yet.
Antihistamines
Topical antihistamine:


All H1 antagonist.
Antihistamine/vasoconstrictor.




Vascon-A (antazoline 0.5/naphazoline HCl 0.05). $10.99
Naphcon-A ( pheniramine maleate 0.3/ naphazoline
0.025). US $10.69
AK-Con-A ( pheniramine maleate 0.3/ naphazoline HCl
0.025).
Opcon-A (pheniramine maleate 0.315/ naphazoline HCl
0.027). US $14.49
Antihistamines


Livostin (CIBA Visio,n) (levocabastine HCl 0.05%).
$53.47
15000x more potent than pheniramine.


Emadine (Alcon), (emedastine difumarate 0.05%).
$53.84






4x/day.
Patanol (Alcon),(Olopatadine HCl 0.1%). $42.12


Onst approx 10 mins.last 4 hours.
Has dual action..antihistamine + mast cell stabilizer.
1 to 2 drops twice a day.
Alocril
Zaditor
Alamast
Optivar
Antihistamines
Systemic antihistamines:




Rarely prescribed by ophthalmologist.
Useful in patients with rhinitis.
Peak action within 1 to 2 hours.
Last 4 to 6 hours.




Claritin (loratadine) 10 mg daily.$26.99
Allegra (fexofentadine) 60 mg twice daily.$21.19
Benadryl (diphenhydramine).
Zytrec (cetirizine). $1/pill
Antihistamines
Side effect:

Topical:
Irritation.
 PEE due to preservatives.
 Dry eye symptoms.
 Vasoconstrictors should be used with caution in
patient with narrow angle/ HTN/ CVD/
arrhythmias.

Antihistamines

Systemic:
Sedation.
 Dizziness.
 Fatigue.
 Nausea.
 Vomiting.
 Diarrhea.
 Constipation.
 Dry eye.

Mast cell stabilizer


Opticrom (Akron) (Cromolyn sodium 4%).$15.79
Crolom (Bausch and Lomb) (cromolyn sodium 4%).US $59.59


Alomide (Alcon),(Lodoxamide 0.1%).$23.54







QID
QID.
Found to be superior to cromolyn in VKC.
Patanol
Alocril
Zaditor
Alamast
Optivar
H1 anatagonists+ mast
cell stabilizer+NSAID

Alocril (Allergan) ,(Nedocromil sodium 2%). $41.59


Zaditor (CIBA Vision), (ketotifen fumarate 0.025%).$36.70


TID to QID doses.
Alamast (Santen), (Pemirolast potassium 0.1%).US $65.59


BID.
BID
Optivar

BID
(azelastine HCI) US $61.59
NSAIDs
Topical:




Acular ( Allergan),(ketorolac tromethamine 0.5%).$50.15
Voltaren (CIBA),(diclofenac sodium 0.1%)
Ocufen (Allergan), ( flurbiprofen sodium 0.03%)
All act by:



Block the cyclo-oxygenase pathway, limiting production of
prostaglandins and thromboxanes.
Analgesic.
S/E:






PEE.
Persistent epithelial defect.
Stromal infiltration.
Ulceration.
Thinning.
Perforation.
NSAIDs
Systemic NSAIDs:

Aspirin:

1g /day for 6 weeks found to be useful in
treating VKC.
Steroids(topical)








FML (Allergan), (fluorometholone 0.1%).$ 35.74
FML-F (Allergan), (fluorometholone 0.25%).
Vexol (Alcon), (rimexolone 1%). $52.01
Pred Mild (Allergan),(prednisolone acetate 0.12%).$ 29
Pred Forte (Allergan), (prednisolone acetate 1%),$ 54
Ophtho-Tate (Kenral), (prednisone acetate 1%). $ 18
Inflamase Mild (CIBA), (prednisone phosphate1/8%).
$ 30
Inflamase Forte (CIBA), (prednisone phosphate 1%).
$ 28

Alrex (Bausch and Lomb), (loteprednol etabonate 0.2%). US
$38.09.

Lotemax (Bausch and Lomb) ,(loteprednol etabonate 0.5%). US
$33.69.

S/E:







Ocular descomfort.
Delayed epithelial healing.
HSV flare up.
Increase IOP.
PSCC.
Ptosis
Mydriasis.
Steroids
Local injection.
VKC.
 AKC.

Oral.

For severe cases as in AKC.
Cyclosporine
•
•
•
Cyclosporine (cyclosporine A, CsA) is a selective
immunosuppressant that inhibits IL2 and T-cell
activation. It also has an inhibitory effect on
eosinophils activation.
Topical CsA 2% was effective as steroid sparing
drug in severe VKC and AKC.
Its effect is usually transient.

S/E:
•
•
•
Intense stinging.
Keratitis.
Systemic CsA has been used in patients with
AKC.
Immunotherapy
Immunotherapy (also called Desensitization
or hyposensitization).
Long term administration of low but
progressively increasing doses of the
offending allergen until the evoked clinical
reaction is reduced or eliminated.
It has been attempted sublingually, nasally,
bronchially, ocularly, and subcutaneously
(usual route).
It takes 3 to 5 years.
Recent meta-analysis showed that it is useful
for allergic rhinitis and conjunctivitis.