UNIVERSITY OPHTHALMOLOGY CONSULTANTS

 

CASE OF THE MONTH

CASE #19

 

 
DISCUSSION

RETINAL VASCULAR OCCLUSIVE DISEASE: Potential causes of retinal vascular occlusive disease for this patient include

  • Purtscher-like retinopathy due to leukoembolization;
  • hypercoagulability;
  • noninfectious vasculitis with secondary retinal vessel occlusion;
  • hypertension during or due to the transplant surgery; and
  • infectious retinitis, ie, a viral retinitis.

ADVERSE EFFECTS OF MEDICATIONS: This patient used a number of medications with reported ocular side effects (see Adverse Effects).

CYLCLOSPORIN A: The pattern of retinal whitening observed is most consistent with a diagnosis of retinal arteriolar occlusion, and we suggest that cyclosporin A (CsA) may have played a role in the development of the patient’s condition. However, the observed retinal vascular changes might be due to an unrecognized side effect of one or more of the many other medications used by the patient (eg, Simulect, which is relatively new).

Cyclosporine is known to have a toxic effect on endothlial cells. As previously reported, Cs A-induced vascular damage may be directly linked to endothelial injury (1). Studies to date have indicated that ischemic fundus lesions develop only in patients receiving CsA, in association with total body irradiation (TBI), busulphan, and/or cyclophosphamide (CY) as conditioning therapy for transplantation.This condition can be reversed by reducing the dose of CsA or withdrawing the drug (2-5). The dose of CsA in these studies ranged from 4 to 12 mg/kg/day, whereas our patient received 4 to 8 mg/kg/day. Previous reports have shown that the combination of CsA and conditioning therapy has an additive effect on the development of microvasculopathy and capillary/arteriolar damage (3-5). Typical findings include multiple cotton-wool spots, retinal hemorrhages, lipid deposits, focal arteriolar narrowing, and optic disc edema (3-5).

We propose that Cs A alone may have caused retinal vascular disease in this patient; alternatively, the damaging effects of CsA may have been induced in the setting of an undiagnosed, underlying condition, either inherited or acquired.

CONCLUSION: It may be beneficial to include ophthalmic care in the management of patients receiving cyclosporin A, particularly for patients taking the drug to prevent transplant rejection. Both our findings and those of earlier studies (1-4) have shown that ocular complications of cyclosporine therapy may appear during the first 31 to 332 days after the start of therapy. Consequently, physicians should refer those patients receiving cyclosporine treatment for routine ophthalmologic evaluations, especially during the first year of therapy.


REFERENCES


 1. Zoja C, Furci L, Ghilardi F. et al. Cyclosporine-induced endothelial cell injury. Lab Invest
 1986; 55: 455-62.

 2. Lopez-Jimenez J, Sanchez A, Fernandez CS. et al. Cyclosporine-induced retinal toxic  blindness. Bone Marrow Transplant 1997; 20: 243-5.

 3. O'Riordan JM, FitzSimon S, O'Connor M, McCann SR. Retinal microvascular changes  following bone marrow transplantation: the role of cyclosporine. Bone Marrow Transplant   1994; 13: 101-4.

 4. Gloor B, Gratwohl A, Hahn H et al. Multiple cotton-wool spots following bone marrow  transplantation for treatment of acute lymphatic leukaemia. Br J Ophthalmol 1985; 69: 320-5.

 5. Bernauer W, Gratwohl A, Keller A, Daicker B. Microvasculopathy in the ocular fundus after  bone marrow transplantation. Ann Intern Med 1991; 115: 925-30.

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Dr. Yamani's e-mail address Please send comments to: Dr. Amir Yamani at yamani@pol.net
   
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