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Show Journal of Neuro- Ophthalmology 16( 2): 134- 136, 1996. 1996 Lippincott- Raven Publishers, Philadelphia Optic Neuropathy Following Elcatonin Therapy Hideya Kimura, M. D., Hirokazu Masai, M. D., and Satoshi Kashii, M. D., Ph. D. A 34- year- old man, who had a 14- year history of hemodialysis, presented with a sudden onset of blurring of vision in both eyes after elcatonin therapy for hypercalcemia. Fundus examination showed well- colored discs without swelling and normal retina in both eyes. Gold-mann kinetic perimetry demonstrated central scotomas in both eyes. One month after discontinuance of elcatonin, his best visual acuity returned to 20/ 20 in both eyes. Although a cause- and- effect relationship between elcatonin and optic neuropathy is not definitive, optic neuropathy is presumably linked to elcatonin therapy. Key Words: Optic neuropathy- Elcatonin- Hypercalcemia- Uremia- Hemodialysis. Elcatonin, a synthetic analog of eel calcitonin, is considered useful in the treatment of osteoporosis ( 1), Paget's disease ( 2), and hypercalcemia ( 3,4) because of its remarkable suppressive action on bone resorption as well as its putative stimulative effect on bone formation. To our knowledge, ocular side effects associated with elcatonin have not been previously reported. We encountered a patient who developed optic neuropathy following elcatonin therapy for hypercalcemia. CASE REPORT Manuscript received March 14, 1995; accepted June 16, 1995. From the Department of Ophthalmology, Faculty of Medicine, Kyoto University, Kyoto, Japan. Address correspondence and reprint requests to Dr. Satoshi Kashii, Department of Ophthalmology, Faculty of Medicine, Kyoto University, Sakyo- ku, Kyoto 606, Japan. A 34- year- old man was referred to us by his ophthalmologist regarding a two- week history of blurred vision in both eyes. The patient had a history of glomerulonephritis and had been undergoing hemodialysis 3 times a week for 14 years. On May 10, 1993, the patient received 40 units of elcatonin i. v. during hemodialysis because of hypercalcemia. Subsequent injections were administered on May 12, 14, and 17. On May 17, the patient noted a central scotoma in the left eye after the fourth injection of elcatonin, and later a similar scotoma developed in the right eye. He complained of no pain upon eye movements. Thus, his physician discontinued the further administration of elcatonin. Laboratory data on May 17 included a serum hemoglobin level of 9.7 g/ dl, a hematocrit of 27.9%, a white blood count of 7,600 cells/ mm3, a blood urea nitrogen level of 84 mg/ ml, a creatinin level of 15.5 mg/ ml, and a serum calcium level of 10.7 mg/ dl. He had no history of diabetes mellitus, hypertension, or tobacco or alcohol consumption. Family history was noncontributory. He was referred by his ophthalmologist on June 1. On our initial examination, his best corrected visual acuity was 20/ 40 in the right eye and 20/ 50 in the left eye. Color discrimination was grossly deficient. Pupils reacted promptly to direct light 234 OPTIC NEUROPATHY AFTER ELCATONIN 135 without afferent pupillary defect. Slit- lamp examination revealed a clear cornea and lens and a deep, noninflamed anterior chamber in both eyes. Fundus examination showed well- colored discs without swelling and normal retina in both eyes. Goldmann kinetic perimetry obtained the same day demonstrated central scotomas in both eyes ( Fig. 1). There were no abnormal findings in either eye on fluorescein fundus angiography. The patient showed a rapid, marked improvement in visual acuity as well as resolution of the scotoma. Ten days later, his best corrected visual acuity had gradually improved to 20/ 20 in the right eye and 20/ 25 in the left eye. One month after discontinuance of elcatonin, his best corrected visual acuity returned to 20/ 20 in both eyes. There was no central scotoma on Goldmann perimetry obtained 5 months later. DISCUSSION The differential diagnosis of optic neuropathy associated with chronic renal insufficiency includes several disorders. Diseases such as inflammation ( vasculitis), infection ( tuberculosis and cryptococcus), and vasculopathic conditions ( anemia, hypertension, and diabetes mellitus) can affect both the kidney and the eye. Medications used for treating renal insufficiency can be toxic to the optic nerve or cause side effects [ deferoxamine ( 5), steroid- induced pseudotumor cerebri, and antibiotics]. Renal failure causes a variety of metabolic disorders including uremia, anemia, and hypercalcemia. Uremia- associated optic neuropathy is a well- described complication of renal failure ( 5- 8). Hypercalcemia has been reported to cause ischemic optic neuropathy ( 9). The combination of hypertension and anemia may also predispose to vascular ocular complications. Hypotension is also one of the most serious frequent complications of hemodialysis and may induce anterior ischemic optic neuropathy ( 8,10). Optic nerve changes are usually observed in these conditions. In addition, the differential diagnosis of bilateral central scotomas includes tobacco- alcohol and Leber's hereditary optic neuropathy. Thus, as optic neuropathy associated with chronic renal insufficiency is multifactorial, we have to deal with the patient carefully. This patient showed no optic nerve changes in either eye, which is less likely to occur in uremia-associated optic neuropathy or ischemic optic neuropathy. Acute onset of visual loss with negative funduscopic findings may indicate acute retrobulbar optic neuritis. However, bilateral involvement in adults is rare. The differential diagnosis of bilateral central scotoma in a young man includes toxic optic neuropathy and Leber's hereditary optic neuropathy. Negative findings of peripapillary telangiectatic microangiopathy with fluorescein fundus angiography as well as the negative family history 120 105 90 75 60 LEFT RIGHT FIG. 1. Goldmann kinetic perimetry on June 1 demonstrated bilateral central scotomas. J Neuro- Ophthalmol, Vol. 16, No. 2, 1996 236 H. KIMURA ET AL. in this patient made the diagnosis of Leber's hereditary optic neuropathy less likely. In addition, although spontaneous recovery is also observed in patients with Leber's hereditary optic neuropathy, it usually takes much longer than was the case in this patient. Marked improvement after the elcatonin withdrawal favored a toxic etiology. The side effects of synthetic calcitonins so far reported include gastrointestinal symptoms ( nausea, vomiting, abdominal pain, diarrhea) and vascular symptoms ( flushing, tingling of the hands) ( 11). Ocular side effects associated with elcatonin have not been previously reported to our knowledge. Forty units of elcatonin a day is a recommended dosage to treat hypercalcemia. A cause-and- effect relationship between elcatonin and optic neuropathy is not definitive. However, the temporal profile of visual loss and improvement in relation to the initiation and discontinuance of elcatonin are compatible with that of toxic optic neuropathy. REFERENCES 1. MacLennan WJ. Osteoporosis. Br Med Bull 1990; 46: 94- 112. 2. Hosking DJ. Paget's disease of bone: an update on management. Drugs 1985; 30: 156- 73. 3. Martin TJ. The therapeutic uses of calcitonin. Scott Med J 1978; 23: 161- 5. 4. Hosking DJ. Treatment of severe hypercalcemia with calcitonin. Metab Bone Dis Relat Res 1980; 2: 207- 12. 5. Hamed LM, Winward KE, Glaser JS, Schatz NJ. Optic neuropathy in uremia. Am } Ophthalmol 1989; 108: 30- 5. 6. Knox DL, Hanneken AM, Hollows FC, Miller NR, Schck HL Jr, Gonzales WL. Uremic optic neuropathy. Arch Ophthalmol 1988; 106: 50- 4. 7. Saini JS, Jain IS, Shar S, Mohan K. Uremic optic neuropathy. / Clin Neuro- ophthalmol 1989; 9: 131- 3. 8. Haider S, Astbury NJ, Hamilton DV. Optic neuropathy in uremic patients on dialysis. Eye 1993; 7: 148- 51. 9. Chappel D, Farrington K. Primary hyperparathyroidism presenting as unilateral visual loss. Postgrad Med J 1991; 67: 469- 70. 10. Servilla KS, Groggel GC. Anterior ischemic optic neuropathy as a complication of hemodialysis. Am J Kidney 1986; 8: 61- 3. 11. Gennari C, Passed M, Chierichetti SM, Piolini M. Side-effects of synthetic salmon and human calcitonin. Lancet 1983; 8324: 594- 5. / Neuro- Ophthalmol, Vol. 16, No. 2, 1996 |
