|Year : 1962 | Volume
| Issue : 3 | Page : 76-78
Primary localised amyloidosis of eyelid
BS Darbari, VN Sehgal
G. R. Medical College, Gwalior, India
|Date of Web Publication||18-Mar-2008|
B S Darbari
G. R. Medical College, Gwalior
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Darbari B S, Sehgal V N. Primary localised amyloidosis of eyelid. Indian J Ophthalmol 1962;10:76-8
| Case Report|| |
A man aged 35 years complained of heaviness and drooping of the left upper eyelid of 4 years duration. The onset was insidious and had been showing a gradual increase with the result that now for the past few months he had difficulty in opening the left eye. He had no history of trauma, itching or soreness of eyes. While talking, the patient had a tendency to lift up the face in order to see binocularly. The wrinkles on the left half of forehead were well marked due to over action of frontalis thereby raising the eyebrows. The palpebral aperture was narrow due to the ptosis of left upper lid which was covering the pupillary area almost completely. The lid was much thickened and drooping. The overlying skin was free. On evertion of the lid, a diffuse warty growth was seen extending all along the lid with palpebral conjunctiva inseparably adherent to it. It was almost of the size of almond with maximum central thickness of one centimeter. Fornices, bulbar conjunctive and lower lid were not involved. Movements of the eyeball were normal. Visual acquity was 6/6 in both eyes. All the ocular structure and fundi were normal. Systemic Examination revealed no abnormality.
The growth being friable, was excised piecemeal. Histologically the mass showed stratified squamous epithelium [Figure - 1]. At places the epithelium was thinned out. The underlying tissue showed areas of hyaline appearance which on staining with methyl violet showed classical metachromatic staining of amyloid [Figure - 2]. The amyloid deposition was predominently in relation with the muscle fibres. A few blood vessels, also showed thickening of their walls due to amyloid deposits. There were also areas of lymphocytic infiltration in relation with the amyloid deposits [Figure - 3]. Giant cells were absent. There was no calcification or cholesterol deposition.
| Comments|| |
The term 'Amyloid' which had been initially used by botanists for starch like substances was first used in Medical Science by Virchow (1955) who in his ingenious method of search for substances in animal tissue resembling the vegetable ones, concluded that what we now call amyloid, was probably isomeric with starch and cellulose, hence the name. Though the condition was known even earlier, its chemical composition and the nature of causative fundamental disturbance remained obscure. Now it is believed that amyloid is of variable composition and is a glycoprotein consisting mainly of protein, probably globulin combined with a sulphated polysaccharide, which is not chondroitin-sulphuric-acid as used to be thought (Symmers, 1956).
The old conception of amyloidosis as merely a complication of chronic syphilis, tuberculosis or septic disease of bones and joints is no longer adequate. Apart from its association with many other diseases like rheumatic and rheumatoid affections, myelomatosis, Hodgkins etc., and its occurrance in the absence of any recognised predisposing cause the so called 'generalised primary amyloidos', it has been observed to occur strictly localised to one site only.
It is interesting to note that amyloidosis of any kind is believed to be rare in our country and primary amyloidosis still rarer. Very few cases of localised ocular amyloidosis have been reported (Redi, 1948; Srinivasan, 1949; Wahi, Wahi and Mathur, 1954; Handousa, 1954; Agarwal and Shrivastava, 1958; Iswarchandra and Sharma, 1960).
The aetiology of localised amyloid deposits in the ocular tissues is obscure. Chronic conjunctivitis, other inflammatory conditions of the eye and trachoma have been suggested as etiological agents in majority' of cases (Oppel, 1956; Agarwal and Shrivastava 1958; Ishwarchandra and Sharma, 1960). However in our case no inflammatory condition, ocular or systemic could be detected. Histological features have been suggested to differentiate between primary and secondary amyloidosis (Lubarch, 1929) but often there is overlapping of these histological features (Kolestky, and Stecher, 1939; King, 1948; Agarwal and Shrivastava 1958). In our case also absence of antecedent or co-existant disease and involvement of the muscle tissue is in favour of primary amyloidosis while the classical metachromatic staining with methyl violet, association of chronic inflammatory cells and absence of gaint cell reaction are suggestive of secondary amyloidosis. Symmers (1956) however suggests that the description of 'primary and secondary' should not be interpreted as having definite aetiological significance and that no other criterion than the absence of a recognisable predisposing cause is needed in order to designate any case of amyloidosis as primary amyloidosis. Boyd (1960) thinks that all varieties of amyloidosis are probably related to one fundamental disturbance, the nature of which is still obscure. It is now increasingly believed that the condition may be a manifestation of a HYPERSENSITIVITY MECHANISM in which the antibody is precipitated with polysaccharides of the ground substance.
In primary amyloidosis there may be a reaction between some component of the serum globulin and tissue elements in the mesoblastic structures, a reaction which may have a basis of autosensitization with the production of autoimmune bodies. As is usual with localised amyloidosis the lesion was confined to mesodermal structures that is the muscle tissue and wall of the blood vessels.
| References|| |
Agarwal, S., and Shrivastava, J. B. (1958), Brit J. Ophthal, 42, 433.
Boyd, W. (1960), A Textbook of Pathology, An Introduction to Medicine, Ed. 7, P. 93. Lea & Febiger, Philadephia.
Handousa., A., (1954), Brit, J. Ophthal., 38, 510.
Ishwarchandra and Sharma, K D., (1960), J. All-India Ophthal. Soc., 8, 72.
King, L. S., (1948), Amer. J. Path., 24, 1059.
Koletsky, S. and Stecher, R. M., (1939), Arch. Path. (Chicago), 27, 267.
Lubarsch, O., (1929), Virchows Arch. Path. Anat., 271, 867 quoted by No, I.
Oppel, O., (1956), Klin. Mbl. Augenheilk, 128, 145, quoted by No, I.
Redi, F., (1948), Cior. Ital. Optical 1, 227, 263 quoted in ophthalmic literature.
Srinivasan, E. C. (1949), Proc. All India Ophthal. Soc., 10, 39.
Symmers. W. St., (1956), J. Clin. Path, 9, 187.
Virchow, R., (1955), Virchows Arch. Path. Anat., 6, 135, quoted by No. 11
Wahi, Pashupati, N., Wahi, P. N. and Mathur, K. N. (1954), J All-India Ophthal. Sox., 2, 45.
[Figure - 1], [Figure - 2], [Figure - 3]