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 patients 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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