Ocular allergy

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Ocular allergy

• Abdulrahman Al Muammar

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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.

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Ocular allergy

• Clinical classifications
• 1) Allergic conjunctivitis (AC)
• Acute allergic conjunctivitis
• Seasonal or hay fever.
• Toxic- induced (induced by acute contact with
  irritant, drugs, preservatives, etc).
• Chronic allergic conjunctivitis
• Perennial.
• Toxic-induced (long standing).

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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

• 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 .

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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

• 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)

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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
• Histamine.
• Vasodilatation.smooth muscle constriction.
• Itching..redness.
• Heparin.
• Prevent blood coagulation.
• Anti-inflammatory.
• Tryptase.
• Potentiates histamine..activates eosinophils and
  mast cells

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Mast cells

• Prostaglandins and leukotrienes
• Capillary leakage..smooth muscle
  contraction..increase granulocyte
  action..platelet aggregation.
• Airway hyperresponsivenessasthma.

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Mast cells

• Eosinophil chemotactic factor-alpha (ECF-alpha).
• Attract eosinophils.
• Platelet activating factor (PAF).
• Platelet aggregation.neutrophil chemotaxis.
• Bronchoconstrictionhypotensionhyperemia..
• Chemosis.

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Eosinphils

• 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
• Major basic protein (MBP).
• Eosinophil cationic protein (ECP).
• Eosinophil derived neurotoxin (EPX).
• eosinophil peroxidase (EPO).

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Eosinphils

• 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.
•  

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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

• 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
• Th1 and Th2 .
• Th1 is known to produce IL2 and interferon
  gamma(INF-g).
• Th2 is known to produce IL3,IL4,IL5.

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Lymphocytes

• 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.

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Seasonal allergic conjunctivitis

• 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.

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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
• 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.

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SAC

• Pathophysiology
• Type I hypersenstivity.
• Late phase reaction (LPR)
• 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.

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SAC

• Treatment
• Avoidance of allergen
• 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.

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Acute allergic toxic induced conjunctivitis

• 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.
• Itching, tearing, eyelid erythema and swelling,
  and conjunctival redness and chemosis. Typically
  occur within minutes after application of an
  allergen.
• Bactriacin..cephalosporins..sulfacetamide..tetracy
  cline
• Atropinehomatropine.
• Epinephrine..pilocarpine..apraclonidine.
• Antiviral agents.
• Thimerosal..chlorhexidinebezalkonium chloride.

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Acute allergic toxic induced conjunctivitis

• Diagnosis
• Clinical presentation.
• Offending agents.
• Conj scrapings.
• Treatment
• Discontinue the offending agents.
• Tears..
• Cold compresses.
• Antihistamines..
• NSAIDs..
• Steroid

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Perennial allergic conjunctivitisPAC

• 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.

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PAC

• Treatment
• Avoidance of allergen
• 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

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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.

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Contact dermatoblepharitis

• Medications commonly associated with these
  symptoms
• Atropine..homatropine.
• Neomycine..gentamycine..tobramycine.
• Idoxuridine..trifluridine.
• Thimerosal.
• Type IV reaction.

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Contact dermatoblepharitis

• Treatment
• Allergen withdrawal.
• In severe casesbrief course of topical steroids
  applied to the eyelids and periocular skin may
  speed resolution.

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VKC

• Epidemiology
• Rarely appear in patients younger than 3 or older
  than 25 years of age.
• MF is 21.
• 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.

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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.

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VKC

• Symptoms
• Itching.
• Tearing.
• Mucus secretion.
• Photophobia.
• Pain.
• Blepharospasm.
• Decreased visual acuity.

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VKC

• Signs
• Papillary reaction.
• Conjunctival redness and edema
• GPC.
• Limbal gelatinous infiltrate.
• Trantas dots.
• Mucus discharge.
• Pseudoptosis.
• Tarsal conjunctival fibrosis.

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VKC

• Corneal involvement
• SPK (Togby Dusting of flouruppper 1/3)
• PEE.
• Pannus.
• Filamentary keratitis.
• Shield ulcer.
• Pseudogerontoxon.
• Keratoconus.

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VKC

• Diagnostic approaches
• Clinically.
• Specific IgE maybe assayed in serum and tears.
• CBC for eosinophilia.
• Conj scraping and tear cytology
• Eosinophils.
• Basophils.
• Neutrophils.
• Tears tryptase level .

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VKC

• Pathogenesis
• Type I hypersensitivity.
• Type IV hypersensitivity.

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VKC

• Histopathology
• Proliferative and degenerative changes in the
  epithelium
• Occur early with marked acanthosis, and
  intraepithelial pseudocysts.
• Prominent cellular infiltration in the substantia
  propria
• Eosinophils, neutrophils, basophils, lymphocytes,
  and plasma cells. Resident plasma cells and
  fibroblasts are also increased.
• Hyperplasia of the connective tissues
• Mainly type III collagen, they run parallel to
  the surface forming the fibrous structure for
  giant papillae.
• Trantas dots.
• Shield ulcer.

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VKC

• Therapy
• Preventive measures
• Change of climate.
• Avoid exposure to nonspecific triggering factors
  such as sun, wind, and salt water.
• Mucolytic agents 10 Acetylcysteine
• Tears/vasoconstrictors/ cold compresses.
• Mast cells stabilizers
• Should be used continuously throughout the
  season.
• Antihistamines.
• NSAIDS either locally or systemically.
• Steroids. Short pulses, topical/ tarsal
  injection.
• Cyclosporine.

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VKC

• Corneal ulcers.
• Steroids-antibiotic/eye patching.
• Superficial keratectomy.
• PTK.
• 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.

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AKC

• Epidemiology
• 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.

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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
• Symptoms
• Bilateral itching
• Tearing
• Watery discharge
• Burning
• Photophobia
• Blurred vision.

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AKC

• Signs
• Lid
• 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 Hertoghes
  sign can be seen in severe form.
• Marginal belpharitis caused by staphylococcal
  infection is common.

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AKC

• Conjunctiva
• 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.

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AKC

• 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

• Lens ? In 5 to 25
• Anterior subcapsular cataract (shield cataract).
• Posterior subcapsular cataract ( related to
  steroid )
• Retina
• Retinal detachment.
• Systemic disorders
• 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.

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VKC Vs AKC
VKC AKC
Age of onset Age of onset Childhood, teens age 20 to 50
Duration Duration Resolved in mid to late teens Resolved by age 50
Seasonal variation Seasonal variation Markedly worse in spring variable
Conjunctival papillae Conjunctival papillae GPC.upper lid Small or medium size..upper and lower
Conjunctival scarring Conjunctival scarring Uncommon Can give symblepharon
skin skin Uncommon Often
Eosinophils Eosinophils Numerous Less munerous and less often degranulated
Corenal vascularization and scarring Corenal vascularization and scarring Less extensive More extensive
lens lens No ASCC/PSCC
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AKC

• Etiology and histopathology
• Type I hypersenstivity reaction.
• 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.
• Staph aureus..HSVresponse to PPD.

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AKC

• Diagnosis
• 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.

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AKC

• In Vivo Tests
• Positive intradermal skin
  tests
• Conjunctival challenge
• Prausnitz-Kustner test
• In Vitro Tests
• Basophil histamine release
• Radioallergosorbent test (RAST)

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AKC

• Conjunctival cytology - eosinophils
• Tear histamine level 10 ng/ml normal
• Tear IgE, Serum IgE
• Eosinophilia gt 500 cells/ml

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AKC

• Managemant
• Tears.
• Vasoconstrictors.
• Cold compresses
• Antihistamines
• NSAID.
• Mast cell stabilizers.
• Steroid.
• Cyclosporine.
• Antibiotics.
• Surgical lid procedures/ PKP.

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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.

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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
• Contact lenses
• Soft..any time between 3 weeks to 31/2 yrs after
  wearing CL.
• Rigidmay appear even after 11 ys.
• Sutures..nylon/prolene.
• Prosthesis.
• Cyanoacrylate glue.
• Scleral buckle.
• Bleb/valve..
• Vernal.
• Atopy.
• Epibulbar dermolipoma.

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GPC

• Symptoms
• Foreign body sensation.
• Intolerance to CLW.
• Itching.
• Irritation.
• Mucus secretion.

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GPC

• Signs
• Enlarged papillae ( gt 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
• Stage I
• 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
• 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.

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GPC

• Stage III
• 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
• Exacerbation of stage III.
• CL intolerance.
• CL are coated and cloudy soon after insertion.

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GPC

• Pathogenesis
• Mechanical traumaresult in degranulation of mast
  cells and disruption of the epithelial surface.
• Stimulate production of neutrophil chemotactic
  factors and inflammatory mediators.
• Immunological response consisting of both humoral
  and cell mediated immunity.
• Mediators in tear fluid
• Increase tryptase.
• increase Ig G,M,E.
• Increase eosinophil ..MBP..ECP.
• Increase histamine.
• Decrease lactoferin.

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GPC

• treatment
• Prevention
• Lens design/hygiene.
• Burying sutur knots.
• Relieving the symptoms
• Removal of the CL, prosthesis, suture.
• Symptoms usually dissipate within 48 hrs after
  d/c CL.
• Change CL design..wearing timeshygiene.
• Mast cell stabilizersmainly in mild cases.
• Steroid..for moderate to severe cases.
• 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.

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Microbial Allergic Conjunctivitis

• Staphylococcal blepharoconjunctivitis.
• Phlyctenular keratoconjunctivitis.
• Splendore-Hoeppli phenomena
• Allergic granulomatous nodules

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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.

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Drug therapy

• Antihistamines.
• Vasoconstrictors.
• Mast cell stabilizers.
• NSAIDs.
• Steroids.
• Cyclosporine.

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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 Crolom Alamast Alocril Alomide Patanol Zaditor Optivar
AntihistamineMast cell stabilizer NSAID Alamast Alocril Optivar Zaditor
NSAIDs Acular Voltaren Ocufen Aspirin
Steroids FML inflammase mild/forte Pred mild/forte vexol Alrex Lotemax
Cyclosporine
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Antihistamines
H1 receptor H2 receptor H3 receptor
-Found throughout the body. -Vasodilation / increase capillary permeability. -Smooth muscle contraction. -Selective H1 stimulation in conj..produce itching without vasodilation. -Predominantly gut. -Found on ocular surface. -Vasodilation. -Smooth muscle relaxation. -Systemic H2 antagonist produce decrease in gastric acid production -Selective H2 stimulation in conjproduce vasodilation (redness). -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.
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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

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Antihistamines

• Livostin (CIBA Visio,n) (levocabastine HCl
  0.05). 53.47
• 15000x more potent than pheniramine.
• Onst approx 10 mins.last 4 hours.
• Emadine (Alcon), (emedastine difumarate 0.05).
  53.84
• 4x/day.
• Patanol (Alcon),(Olopatadine HCl 0.1). 42.12
• Has dual action..antihistamine mast cell
  stabilizer.
• 1 to 2 drops twice a day.
• Alocril
• Zaditor
• Alamast
• Optivar

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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

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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.

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Antihistamines

• Systemic
• Sedation.
• Dizziness.
• Fatigue.
• Nausea.
• Vomiting.
• Diarrhea.
• Constipation.
• Dry eye.

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Mast cell stabilizer

• Opticrom (Akron) (Cromolyn sodium 4).15.79
• Crolom (Bausch and Lomb) (cromolyn sodium 4).US
  59.59
• QID
• Alomide (Alcon),(Lodoxamide 0.1).23.54
• QID.
• Found to be superior to cromolyn in VKC.
• Patanol
• Alocril
• Zaditor
• Alamast
• Optivar

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H1 anatagonists mast cell stabilizerNSAID

• Alocril (Allergan) ,(Nedocromil sodium 2).
  41.59
• BID.
• Zaditor (CIBA Vision), (ketotifen fumarate
  0.025).36.70
• TID to QID doses.
• Alamast (Santen), (Pemirolast potassium 0.1).US
  65.59
• BID
• Optivar (azelastine HCI) US 61.59
• BID

101
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.

102
NSAIDs

• Systemic NSAIDs
• Aspirin
• 1g /day for 6 weeks found to be useful in
  treating VKC.

103
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

104
Steroids

• Local injection.
• VKC.
• AKC.
• Oral.
• For severe cases as in AKC.

105
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.

106
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.