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ARTICLE
Year : 1962  |  Volume : 10  |  Issue : 3  |  Page : 76-78

Primary localised amyloidosis of eyelid


G. R. Medical College, Gwalior, India

Date of Web Publication18-Mar-2008

Correspondence Address:
B S Darbari
G. R. Medical College, Gwalior
India
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Source of Support: None, Conflict of Interest: None


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How to cite this article:
Darbari B S, Sehgal V N. Primary localised amyloidosis of eyelid. Indian J Ophthalmol 1962;10:76-8

How to cite this URL:
Darbari B S, Sehgal V N. Primary localised amyloidosis of eyelid. Indian J Ophthalmol [serial online] 1962 [cited 2019 Nov 13];10:76-8. Available from: http://www.ijo.in/text.asp?1962/10/3/76/39565


  Case Report Top


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 Top


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.[13]

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 Top

1.
Agarwal, S., and Shrivastava, J. B. (1958), Brit J. Ophthal, 42, 433.  Back to cited text no. 1
    
2.
Boyd, W. (1960), A Textbook of Pathology, An Introduction to Medicine, Ed. 7, P. 93. Lea & Febiger, Philadephia.  Back to cited text no. 2
    
3.
Handousa., A., (1954), Brit, J. Ophthal., 38, 510.  Back to cited text no. 3
    
4.
Ishwarchandra and Sharma, K D., (1960), J. All-India Ophthal. Soc., 8, 72.  Back to cited text no. 4
    
5.
King, L. S., (1948), Amer. J. Path., 24, 1059.  Back to cited text no. 5
    
6.
Koletsky, S. and Stecher, R. M., (1939), Arch. Path. (Chicago), 27, 267.  Back to cited text no. 6
    
7.
Lubarsch, O., (1929), Virchows Arch. Path. Anat., 271, 867 quoted by No, I.  Back to cited text no. 7
    
8.
Oppel, O., (1956), Klin. Mbl. Augenheilk, 128, 145, quoted by No, I.  Back to cited text no. 8
    
9.
Redi, F., (1948), Cior. Ital. Optical 1, 227, 263 quoted in ophthalmic litera­ture.  Back to cited text no. 9
    
10.
Srinivasan, E. C. (1949), Proc. All ­India Ophthal. Soc., 10, 39.  Back to cited text no. 10
    
11.
Symmers. W. St., (1956), J. Clin. Path, 9, 187.  Back to cited text no. 11
    
12.
Virchow, R., (1955), Virchows Arch. Path. Anat., 6, 135, quoted by No. 11  Back to cited text no. 12
    
13.
Wahi, Pashupati, N., Wahi, P. N. and Mathur, K. N. (1954), J All-India Ophthal. Sox., 2, 45.  Back to cited text no. 13
    


    Figures

  [Figure - 1], [Figure - 2], [Figure - 3]



 

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