|Year : 1982 | Volume
| Issue : 4 | Page : 219-222
Advances in the treatment of allergic disorders of the eye
JN Rohatgi, HK Singh, AA Siddiqui
Department of Ophthalmology, Patna Medical College, Patna, India
J N Rohatgi
Department of Ophthalmology, Patna Medical College, Patna
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Rohatgi J N, Singh H K, Siddiqui A A. Advances in the treatment of allergic disorders of the eye. Indian J Ophthalmol 1982;30:219-22
|How to cite this URL:|
Rohatgi J N, Singh H K, Siddiqui A A. Advances in the treatment of allergic disorders of the eye. Indian J Ophthalmol [serial online] 1982 [cited 2020 Apr 7];30:219-22. Available from: http://www.ijo.in/text.asp?1982/30/4/219/29432
A good number of eye diseases or disorders are allergic in nature. These could be immediate or humoral type as well as delayed or cellmediated hypersensitive reactions. And the various allergens implicated are dust, pollens, cosmetics, feathers, drugs, chemicals, inhalents, food and bacteria. The bacterial ones are called micro-biallergic substances. The common organisms are bacterium tuberculosis, staphyaureus, streptococci, brucella and the treponema-pallidum.
To these may be added psychosomatic factors (which help in triggering the reactions) and emotional stress causing the allergic reactions to persist despite all treatment and thus, removal of emotional stress is an important factor in treatment.
Such allergic conditions of the eye and its adenexa could be divided into two broad groups (a) of the conjunctiva, cornea, lid and sclera and (b) of the inner layers of the eye the uvea and retina. A mention would be made of the clinically important ones only with their treatment indicating also the recent trends.
| Conjunctiva and lid|| |
(a) Phlyctenular kerato-conjunctivitis (conj.) attributed to endogenous tubercular allergy this being an example of microbiallergic reaction.
(b) Vernal or spring catarrah-exogenous allergen-pollen, dust or reaction to warmcliniate.
(c) Acute and chronic allergic conjunctivitis-from contact with pollens, animal dander, house-dust, or ingestion of certain food, drugs and inhalents.
(d) Blepharo-conj. from staphylococcal exotoxin as opposed to organism.
(e) Atopic dermatitis of the lid so far the treatment is concerned, both for acute and chronic allergic conjunctivitis as well for spring catarrah and phyctenular conj. the regimes (i) to avoid exposure to antigen-may not be so easy to follow (ii) Desensitisation with old tuberculin in some cases of Phlyctenular Kerato-conjunctivitis (iii) Palliative
(a) Vasoconstrictor Eye drops with or with out local anaesthetics.
(b) Antihistamines-Topical antihistamine eye-drop have little use. In severe cases systemic administration may be helpful.
(c) Presently the most useful therapy is topical steroids-drop or ointment as predenisolone Decadron etc.
Disodium-cromoglycate-drops have given relief in cases of vernal catarrah. This is worth noting for the principal effect of this drug is to prevent the release of histamine from mast cells.
2. For dermato-conjunctivitis and allergy of the eyelid-the treatment consist of- (i) a careful history to eliminate the responsible antigendrug spectacle- fran.e, cosmetics etc and (ii) Use of steroids in the form of drop, ointn ent and cream several times daily.
3. Blepharo-conjunctivitis is mostly due to staphylococcal exotoxin as opposed to the organism itself and in the treatment. (i) the first line is to get rid of infection by the use of sulphacetamide or chloromycetin drop or ointment and (ii) mechanical expression of the meibomian gland and thereafter, (iii) use of steroid locally as ointment and (iv) for stubborn cases, use of staphylococcal toxoid for desensitisation by intra-dermal injection of 0'01 cc. every 4 to 5 days and gradually increasing the dose to I c.c, subcutaneously.
In recurrent styes-staphylococcal allergy is said to be responsible for chronicity and recurrence.
2. Cornea 1. Rosacea Keratitis (not common in India). 2. Interstitial keratitis. 3. Contact keratitis. 4. Marginal keratitis. 5. Disciform keratitis.
Of these allergic manifestation in corneainterstitial keratitis is important. It is suggested that the cornea becomes allergic to the dead spirochaetal material remaining in it (cornea) from the intra-uterine infection. The subsequent entrance of any antigenic material (nature not clear) from the blood, produces a local allergic reaction in the form of deep parenchymatous keratitis.
Hence, in the treatment, mydriatic locally and cortico-steroids locally and systemically play a greater role than the specific anti-syphilitic treatment.
3. Uveal tract The common clinical condition is of uveitis both anterior and posterior. And in both, two types are reco;nised-(a) Non-granulomatous and (b) Granulomatous.
(a) The non-granulomatous uveitis-has an acute onset, is usually self-limiting and responds well to corticosteroid. Strepto-coccal allergy is thought to be the main etiological factor for the following reasons
(i) Ant. streptolysin (ASO) titre are found to be higher in patients with uveitis than in normal control.
(ii) Intra-dermal testing of sensitivity to alpha- Streptococci and sub-group A of Betastreptococci showed delayed positive reaction in patients with such an uveitis.
(iii) Desensitisation injections with specific streotococcal antigen has resulted in decreased frequency and severity of attacks.
But those who doubt, this argue as follows
(i) A large number of hospital patients have shown positive skin test to streptococcal material and this frequency seems to increase with age.
(ii) If streotococcal allergy is the case of non-granulomatous uveitis. One would expect frequency of uveitis in other conditions high also due to streptococcal allergy, such as acute rheu uatism and acute glomerulo-nephritis but this is not seen.
Besides streptococcal allergy-Other bacteria like staphylococcus, B. Coli, B. Pyocyaneous and Gonococci are reported also to act as antigens in allergic uveitis.
(b) Granulomatous uveitis-is mostly tubercular and thought to be caused by vascular invasion of the uveal tract by myobacteriumtuberculosis. And tuberculous allergy may contribute to its aggravation. It has been reported that during specific antituberculous treat ment with streptomycin. Isoniazed and PAS a few cases of granulomatous uveitis have got aggravated due to the release of tuberculous antigen following the death of tuberculusbacteria.
A granulomatous uveitis however, may not always be due to infection. It may sometimes be entirely allergic in nature. Thus, while sarcoid uveitis is granulomatous in its clinical and pathological manifestation, but sarcoid lesions have never been shown to contain an organism.
C. Sympathetic ophthalmic-Allergy to uveal pigment offers the best explanation as to how a perforating injury involving uveal-tissue and causing a granulomatous uveitis in the injured eye may be followed by a similar and more devastating uveitis in the other eye. The older theory of infection as the cause fails for no organism has ever been consistently discovered and inoculation experiments have failed to reproduce the disease.
The points in favour of its allergic origin to uveal pigment are :
(i) It has been shown that uveal pigment act as an antigen and give rise to a positive test in an intradermal test with uveal pigment in patients with sympathetic ophthalmic.
(ii) The time-interval of 3 to 8 weeks between the injury in one eye appearance of the disease in the sympathising eye, corresponds to the sensitisation-period in other immunological processes.
(iii) The histological picture is composed of a high concentration of eosinophils and plasma cells.
(iv) There is evidence of disturbance of pigment in areas other than the uveal tract as bleaching of the eye-lashes and leucodermic patches.
(v) A good response of the eye both injured and sympathising to local and systemic cortisone and if needed to ACTH-intravenously.
4. Endophthalmitis phaco-anaphylactica
While sympathetic ophthalmia is an allergic response to uveal pigment, allergy to lens protein in sensitised individual causes a violent uveitis which not only involves the uveal tract but spreads to vitreous and other inner layers of eye and may produce endophthalmitis.
This is a classical example in eye, of an allergic reaction to the innocuous lens protein. Lens protein is innocuous so long it is held within lens capsule but once it gets into the anterior chamber as a result of an extra-capsular lens surgery, discission operation for congenital cataract, trauma or hypermaturity, a severe inflammatory reaction occurs around the remnants of the lens matter. This is composed mostly of polymorphs and a higher proportion of eosinophils. Thereafter, granulation tissue forms containing epitheloid cells, plasma cells and lymphocyte in the anterior uvea-iris mostly. The cellular infiltration extends backwards into retina and vitreous.
The plasma shows a high tire of antilens antibody-Muller (1952-53) in his experimental work on rabbits had these rabbits sensitised to lens protein along with intramuscular injection of an adjuvent like staphylococci toxin. Thereafter, needling was done on these lens. The changes, that occurred after needling were same as those seen in endophthalmitis phacocymaphactica both clinically and histologically.
Endoophthalmitis-phacoanaphylactica thus, occurs in an individual who is sensitised to lensprotein and in the eye with operation or injury. It can also occur in the other eye and therefore, desensitization with lens protein has been practised to prevent its occurrence when surgery is contemplated in the second eye and an intracapsular lens extraction cannot be assured in such individuals who show a positive cuta neous sensitivity.
As the condition is allergic and as there, is a suggestion that staphylococcal infection may play a part in aggravating it-all avenues of infection in such individuals should be looked for in an individual who got violent post-operative uveitis following cataract surgery and he should receive systemic corticoid and specific antibiotics. It is, thus, suggested than in all severe or prolonged post-operative or post traumatic uveitis, skin test should be done for lens protein and uveal pigment.
A small percentage of patients suffering from atopic dermatitis tend to develop cataract in third decade.
Treatment-a world about treatment of these ocular allergies.
(i) Local and or systemic corticosteroids need no emphasis in allergic diseases of the eye.
(ii) Desensitisation :- the rationale is to reduce the degree of reactivity by the repeated systemic injection of suitable doses of the specific antigen which is assumed to combine with and neutralise the anti-bodies with the result that the tissues are restored to their primary non-reactive state. Some of the ocular infection described above-where the factor of allergy is suspected, have responded to desensitisation-particularly those due to tuberculosis, sterotococci and brucellosis.
Tuberculin is the best bacillary fraction for clinical use in tubercular allergy.
In streptococcal allergy :-This allergy is pro .sub bably an important etiological factor of ocular diseases since this is the most common organism present in focal infections. But desensitisation is rendered difficult by the multiplicity of antigenic types.
Time and again we see a Patient whose teeth has been extracted. Whose tonsils have been removed, whose sinuses have been opened up, whose appendix has been taken out, whose colon is being irrigated, whose prostage has been massaged (or whose endometrium has been scraped) all for the sake of uveitis which continues placidly in complete disregard of the multilation for which it has been responsible.
Hence, what is needed in a number of such cases is to reinforce the mechanism of immunity either passively or actively besides the treatment with corticosteroids both locally and systemically.