|Year : 1983 | Volume
| Issue : 7 | Page : 869-871
Aetiopathogenesis of lepromatous ititis
SP Garg, VK Kalra, N Verma
Dr. Rajendra Prasad Centre for Ophthalmic Sciences A.I.I.MS. New Delhi, India
S P Garg
Dr. Rajendra Prasad Centre for Ophthalmic Sciences A.I.I.M.S., New Delhi-110 029
|How to cite this article:|
Garg S P, Kalra V K, Verma N. Aetiopathogenesis of lepromatous ititis. Indian J Ophthalmol 1983;31:869-71
| Introduction|| |
As per 1971 estimates there are 3.2 million patients of leprosy in India. One of the common disability in leprosy is blindness as complications due to leprosy frequently terminate to blindness. Ocular complications in leprosy mainly occur by involvement of anterior segment. A chronic iridocyclitis is a frequent complication of lepromatous leprosy. Different opinions have been presented in literature regarding the genesis of iritis in leprosy. Cameron 1961, Choyce 1969, Weekeroon 1969 are of the opinion that it is infective in origin. Asymptomatic nature, relative lack of signs and absence of organisms lead others to hypothesize a neuroparalytic basis to explain the iritis.
The present study was undertaken at Leprosy Home Shahdra, Delhi, by us to understand the genesis of uveitis in lepromatous leprosy.
| Material and methods|| |
A total of 982 inmates of Leprosy Home were surveyed. Detailed ophthalmic examination including slit lamp examination was done. The findings were recorded in a proforma. 48 intraocular operations were done (cataract extraction & optical iridectomy).
In each case aqueous tap was done before entering the anterior chamber. Aqueous was centrifuged and sediment stained by Gram's stain and Z.N. Stain. Complete iridectomy was performed as a routine. The iris tissue was fixed in formaldehyde and processed for histopathology by Haematoxylin and Eosin and special staining for acid fast bacilli.
| Observations|| |
Results: The incidence of uveitis and its varied manifestations are highlighted in [Table - 1][Table - 2][Table - 3][Table - 4].
None of the 15 samples of iris removed at complete iridectomy showed presence of A.F.B. None of the 15 samples of aqueous of lepromatous iritis was positive for A.F.B. when the smears were made from the sediment of centrifuged samples.
Histopathology showed presence of chronic inflammatory cells in majority of irides. In 3 cases no histopathological anomaly was seen. Diffuse atrophy of the muscle involving both the sphincter as well as dilator muscle was seen in 4 cases.
Discussion: The manifestations and later effects of acute iritis which occur as a part of lepra reactions is a well known entity and of granulomatous nature. By contrast chronic iritis of lepromatous leprosy offers a different nature as it lacks symptoms, has minimal ocular signs and is non responsive to topical steroids.
The absence of organisms in aqueous and iris in all the cases of lepromatous leprosy along with chronic, low grade uveitis noted in our study also goes in favour of a non organismal basis.
Evidences for neuroparalytic iritis are:
1) Organismal: (a) Preferential attachment of leprabacilli to nerves in various organs, a similar affliction might occur in iris.
(b) Preferential lodgement of organism to cooler parts of body (testes, nose, ear).
As iris temperature is 3.5°C less than that of body temperature (Schwartz 1962) it can be a preferential site.
2) Clinical: (a) Sluggishly reacting pupils with anisocoria without overt signs of uveitis goes in favour of neproparalytic basis.
(b) Corneal nerve involvement is a well known clinical entity in leprosy. A parallel situation might occur in iris.
3) Pharmacological: (a) Early autonomic denervation hypersensitivity has been described by Bauschard and Swift (1972) in which pupils of lepromatous patients responded positively to epinephrine in an abnormal way.
(b) Poor response to anticholinergic drugs like atropine as the basic fault lies in adrenergic nerve fibres.
4) Histopathological: Lack of organisms in aqueous or iris and functional changes much more marked as compared to organic iris changes.
The presumed pathogenesis -sub of chronic lepromatous iritis is that during primary bacteremia, bacilli lodge in. autonomic nerve fibres of iris and cause a'slow degeneration of nerves which causes a secondary muscular atrophy. Due to the atrophy of muscle, toxins are released which cause a low grade chronic uveitis with mild flare, KPs. and cells with eyes remaining essentially white and asymptomatic.
Further studies to demonstrate selective muscle atrophy, electron microscopic studies for demonstrating organisms in the autonomic nerves are needed along with pharmacological studies to come to a definite conclusion regarding the exact genesis.
| References|| |
|1.||Cameron, A.N. Leprosy and its ocular manifestations. Trans. Ophthalmol. Sec. U.K 1961, 81: 63747. |
|2.||Choyce, D.P. The diagnosis and management of ocular leprosy. |
|3.||Duke Elder, S. -System of Ophthalmology, (1977) Uveal diseases, Page 298. |
|4.||Ffytche, T.J, Role of iris changes as a cause of blindness in lepromatous leprosy. Brit. Jt. Ophthalmol. 1981, 65: 231-39. |
|5.||Swift, T.R and Bauschard, F.B. Pupillary reactions in lepromatous leprosy. In. J. Leprosy 1972, 40: 142-48. |
|6.||Weekeroon, L. Ocular leprosy in Ceylon. Brit. J Ophthal. 1969,53: 457-65. |
[Table - 1], [Table - 2], [Table - 3], [Table - 4]