LETTERS

Although ciprofloxacin may have been a factor in this patient's symptoms, the discrepancies between the earlier report (FDA 1639) and this one, as well as the failure of the authors to interpret correctly the cited references, casts doubts on the accuracy of the report.

Authors' reply

Dear Editor:

KEVIN HIGGINS, MD West Haven, Connecticut

Thank you for allowing us to respond to the comments of Dr. Higgins.

First, the patient's visual loss was caused by a toxic optic neuropathy as documented by careful neuro­ophthalmic evaluation and diagnostic testing. This con­clusion is the only logical diagnosis consistent with the clinical data.

Second, we would like to explain the discrepancies be­tween our article and the FDA 1639 report. The patient's age was 65 and not 56 as stated in the FDA 1639. The patient initially took Cipro for 2 months and continued to take this medication for an additional 2 months before seeking ophthalmologic evaluation. As stated in the article, he was a diabetic with osteomyelitis of the right foot, a recognized sequela of diabetic peripheral neuropathy. When speaking to his internist, after the FDA report, but before publication of our article, we learned that he was taking additional medication that he did not reveal to us during his first visit. It is crucial to note that he has con­tinued all these other medications, and his improvement in visual function has been associated with the discontin­uation of only Cipro.

In regard to the cited clinical studies, Arcieri et al re­ported on 25 uncontrolled clinical trials in which patients were administered a "usual dose" of Cipro ranging from 500 to 750 mg, twice a day, for a "mean duration" of 65 days of treatment. We were unable to determine from these data the cumulative dosage received by individual patients. Ophthalmologic side effects were reported in 8 of the 2829 enrolled in the study but only 800 of the 2829 patients were examined ophthalmologically.

After reviewing the data concerning the animal inves­tigations with Cipro, we appreciate Dr. Higgins' correction regarding the animal results, but these data in no way impact upon or detract from our patient's neuro­ophthalmic findings and the subsequent FDA 1639 report and publication in Ophthalmology.

We would like to remind ophthalmologists that the level of Cipro that we found to be associated with toxic optic neuropathy was substantially above the currently rec­ommended dosage. Our patient was fortunate that dis­continuation of the medication resulted in improved vi­sual function. Failure to recognize this syndrome might lead to irreversible visual loss, as commonly occurs with other toxic optic neuropathies.

In summary, the patient had a toxic optic neuropathy; he was taking more than usually recommended dosages

of Cipro (a drug with a structure similar to other com­pounds associated with toxic optic neuropathies); he im­proved after Cipro was discontinued; and minor differ­ences in this report, the FDA 1639, and the animal studies are not pertinent to this new observation about Cipro.

TAMARA R. VRABEC, MD ROBERT C. SERGOTT, MD EDWARD A. JAEGER, MD

PETER J. SAVINO, MD THOMAS M. BOSLEY, MD Philadelphia, Pennsylvania

Quenching of Anterior Segment Fluorescence

Dear Editor:

I read with interest the technique and ideas of Ormerod et al in the article "Anterior Segment Fluorescein Vi­deoangiography with a Scanning Angiographic Micro­scope."] Although not affecting their findings, I have con­cern with the statements in their article and Appendix in which they assert that given more molecules of fluorescein in the blood, more photons could be absorbed and more fluorescence could be obtained, and that optical fluores­cence in the eye is unobtainable unless arterial injections are used.

During my review of fluorescein,2 I found that the in­tensity of fluorescence of fluorescein in blood increases with increasing concentration of fluorescein up to a certain maximum (between 0.025% and 0.15%) and then falls off when this concentration is exceeded. This concentration quenching offl~orescence is important because it implies that attempts to increase the intensity of fluorescence of the retinal vessels by increasing the intravascular concen­tration of fluorescein (for example, by using more con­centrated solutions of fluorescein, rapid bolus injection, intra-arterial injection, etc.) will reach a point where flu­orescence will actually decrease with further increase in the intravascular concentration of fluorescein. The work of others is quoted in my review to show that when a bolus of fluorescein passes through a retinal arterial blood vessel and the concentration of fluorescein exceeds that at which concentration quenching occurs, a "double peak" in intensity of fluorescence is observed-fluorescence at first rises with increasing intravascular concentration, then falls when concentration quenching occurs, and then rises again as intravascular concentration falls with transit of dye through the vessel and concentration quenching di­minishes.

References

K. G. ROMANCHUK, MD, FRCSC Saskatoon, Saskatchewan, Canada

1. Ormerod LD, Fariza E, Hughes GW, Doane MG, Webb RH. Anterior segment fluorescein videoangiography with a scanning angiographic microscope. Ophthalmology 1990; 97:745-51.

2. Romanchuk KG. Fluorescein. Physicochemical factors affecting its fluorescence. Surv Ophthalmol1982; 26:269-83.

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