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Year : 1987  |  Volume : 35  |  Issue : 1  |  Page : 27-31

Graves' ophthalmopathy-role of radiation therapy

Department of Radiation Oncology, Institute Rotary Cancer Hospital, All India Institute of Medical Sciences, New Delhi - 29, India

Correspondence Address:
N R Datta
Department of Radiation Oncology, Institute Rotary Cancer Hospital, All India Institute of Medical Sciences, New Delhi - 29
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Source of Support: None, Conflict of Interest: None

PMID: 3450611

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A case of Graves' opthalmopathy treated with external radiotherapy has been reported. The role of radiation therapy in the management of this disease entity in context to the modern supervoltage era has ben discussed.

How to cite this article:
Datta N R, De S, Rath G K, Chander S. Graves' ophthalmopathy-role of radiation therapy. Indian J Ophthalmol 1987;35:27-31

How to cite this URL:
Datta N R, De S, Rath G K, Chander S. Graves' ophthalmopathy-role of radiation therapy. Indian J Ophthalmol [serial online] 1987 [cited 2022 Dec 7];35:27-31. Available from: https://www.ijo.in/text.asp?1987/35/1/27/26320

Graves' opthalmopathy is a distressing benign condition which may exist as a distinct clinical entity or may be associated with Graves' disease. Controversy still exists on whether ophthalmopathy should be regarded as an integral part of Graves' disease or a separate autoimmune condition [1]. However, the condition is of grave concern for the patient since this distressing, disabilitating and cosmetically unacceptable clinical condition if not treated adequately may result in optic neuropathy and blindness. Various therapeutic procedures have been adopted to control Graves' ophthalmopathy these being local symptomatic use of steroids to even orbital decompression [2].

The role of radiotherapy in the management of this ocular problem has been doubted by some, while others have obtained significant long term remission and control in the patients subjected to radiation therapy [2],[3],[4],[5].

This article presents a case of Graves' opthalmopathy in whom a good and stable response was achieved using orbital irradiation. The role of radiotherapy, its rationale and technique in the management of this clinical entity have , been analysed in this article.

  Case report Top

G.H. a 47 year old gentleman presented at the Institutes Rotary Cancer Hospital, All India Institute of Medical Sciences in February '85 with the features of proptosis of both eyes since 1979. He was diagnosed as a case of hyperthyroidism in 1978 and was initially treated with Neomeracazole. In 1981, he underwent partial Thyroidectomy following which in 1983 he developed acute corneal ulceration, proptosis and lagophthalmos and was managed conservatively.

General physical examination revealed a fairly well kept patient l with warm and dry extremities. His pulse and blood pressure was 82/mt. and 130/90 mm Hg. respectively. There were no other signs and symptoms of thyroid overactivity. Ocular examination" revealed bilateral proptosis, chemosis and lagopthalmos. Corneal sensations were intact and ocular movements were normal. Exophthalmometry was recorded to be 29 mm and 30 mm at a bar reading of 110 mm for right and left eye respectively. Fundoscopy was within normal limits. Examination of cardiovascular, abdominal and central nervous systems were also normal.

Heamogram and serum biochemistry did not reveal abnormality. Thyroid functions studies estimated normal TSH level while PBI was slightly raised (9.2 ug/100 ml.).

  Treatment Top

In view of the persisting and distressing proptosis the patient was taken up for orbital radiotherapy. Patient was treated in a linear accelerator (Clinac-20) with 15MV X-rays using parallel opposed lateral orbital fields with a 5 posterior tilt on both sides. The anterior border of the field was placed at the lateral orbital margin to spare the cornea and the lens. [Figure - 1]. The dose distribution was derived from a computerized treatment planning system (Nodecrest, RTP 80) with an aim to achieve a homogenous dose distribution in the retrobulbar tissue and sparing the pitutary and lens from any significant dose of ionization radiation. During radiation therapy a treatment shell was used to immobilize the patient. A total tumour dose of 20 Gray was delivered in 10 fractions over 2 weeks. Patient tolerated radiotherapy well. Following radiotherapy the proptosis and chemosis reduced quite markedly. Exophthalmometry revealed a corresponding figure of 18 mm and 20 mm for right and left eye respectively at a bar reading of 110 mm. The patient is doing well and is free of symptoms even during the 14 months of follow up.

  Discussion Top

The pathogenesis of Graves' opthalmopathy continues to be debated on whether is it an autoimmune disorder with a distinct clinical entity or a part of the symptom complex of Graves' disease. However, the pathological changes are well established and it demonstrates intraorbital and retrobulbar, inflammatory infiltrates comprising of lymphocytes, plasma cells and intersitial fluid which increases the soft tissue bulk. These impair the drainage of the conjunctiva and orbit leading to swelling of the lids, chemosis, proptosis, keratitis, corneal ulceration, loss of mobility of extraocular muscle are seen often in late stages of the disease and the presence of these indicates a bad prognosis regardless of the therapy [4].

The management of Graves' ophthalmopathy thus needs to be based on rationale which could help to prevent and treat this disease entity. Thus based on the above principle local measures using steroids have been used [6]. Correction of thyroid function by using thyroidectomy, antithyroid drugs and ablative radioiodine therapy have been also tried with dubious. Results [7]. Workers who believe the disease to be basically an autoimmune disease have tried to suppress the immune response cells or removal of immune complexes or antibodies using plasma exchange and Tcell suppressing drugs like cyclosporine [1],[8]. Results of all these approaches have been conflicting and inconclusive.

Use of radiotherapy in the treatment of Graves' ophthalmopathy is based on the theory of achieving local immunosuppression (2). It might be that radiotherapy interferes with a target other than inflammatory cells such as fibroblasts or muscle membrane components to prevent the development of infiltrative changes [9].

External radiotherapy has been reported to achieve a stable and good response in Graves' opthalmopathy. The use of orthovoltage units in the past [10] have lead to poor results due to probably lower dose, low energy and poor collimation of the beam.

Treatment with supervoltage radiation [4],[9] by Cobalt-60 unit or Linear accelerators has lead to encouraging results with a 55% - 97% response at a dose of 20 Gy/l0fr/2 weeks [2],[3],[5]. Careful maneuvering of the treatment portals using stimulators, CT Scan have greatly helped to minimize the radiation induced cataract to almost nil while achieving a homogenous dose distribution in the target tissues. The benefit is mainly seen in the soft tissue changes with relief of symptoms leading to the arrest of disease in majority of cases. However orbital radiotherapy has been found to be most effective when ophthalmopathy is at an early stage since there is lymphocyte infiltration in muscle and retroorbital tissue at this stage. Once the infiltrate has been replaced by fat or fibrous tissue the effectiveness of radiotherapy may not be very marked.

This patient had significant regression of the symptoms of proptosis and chemosis. Exophthalmometry also indicated a marked improvement compared to the pretreatment status. Careful treatment, planning and use of sharp edged photon beam enabled to reduce the dose to the lens thereby minimising the chance of radiation induced cataract.

Thus radiotherapy in this era of megavoltage treatment offers a major treatment modality for the rapidly progressive severe ophthalmopathy which are refractory to steroid to achieve a stable response. Orbital decompression should always be kept reserved for patients who fail to respond to radiotherapy.

  References Top

Taylor, P.R, 1985, Clinics in Endocrinal and metab., 14:331.  Back to cited text no. 1
Olivotto, I.A, Ludgata, C.m., Allen, L.H. and Rootman, J., 1985, Int. J Radiat,'Oncol. Biol. Phys., 11:2085.  Back to cited text no. 2
Bartjaena, L., Y1arcoeci, C., Chivato., L., Laddage., M, Lepri, G., Andreani, D., Cavallacci, G., Baschieri, L., and Pincherea, A., 1983, J., Clin. Endocrinol. Netab., 56:1139.  Back to cited text no. 3
Convington, E.E., Lobes.L. and Sudarsanam, A., 1977, Radiology, 122:797.  Back to cited text no. 4
Tang, C.S., Cromble, A.L., Hall, R. and Ross, W.M. 1980, Clin. Endocrinol, 13:545.  Back to cited text no. 5
Warner, S.C. 1966, Lancat i : 1004.  Back to cited text no. 6
Gwinup, G., Ellas, A.N and Asher, M.S., 1982. J. Of Artm. Med. Assoc., 247:2135.  Back to cited text no. 7
Weetman, A.P., IMcGregor, A.M., Ludgate, m. 1983, Lancet, ii:486. 31  Back to cited text no. 8
Oonaldson. S.S. Bagashaw, M.A. Kriss, J.P. 1973 J. Clin. Endocrinol. iletab. 37:276  Back to cited text no. 9
Beierwattes, W.H., 1953, J. Clin. Endocrinol. metab., 13:2090.  Back to cited text no. 10


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