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Correspondence |

Effects of Intravitreous Injection of Preserved and Nonpreserved Triamcinolone in Rabbit Retina

Petros E. Carvounis, BMBCh; Muhammad Abd El Barr, MS; Thomas A. Albini, MD; Eric R. Holz, MD
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Copyright 2006 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.

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Arch Ophthalmol. 2006;124(11):1666-1666. doi:10.1001/archopht.124.11.1666-a
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We read with interest the article by Dierks et al1 comparing the short-term effects of intravitreal injection of Kenalog-40 (Bristol-Myers Squibb, Princeton, NJ) with intravitreal injection of the vehicle and of triamcinolone acetonide in rabbit eyes. A 10% to 25% increase in a- and b-wave electroretinographic amplitudes of eyes with intravitreal injection of Kenalog-40 or triamcinolone compared with noninjected eyes was reported, although the probability of this being a chance finding (P value) was not stated.

Furthermore, the ratio of a- and b-wave amplitudes in the injected eyes to control eyes was compared across groups; there were no statistical differences except for an increase in the dark-adapted b-wave amplitude ratio only between the Kenalog-40 and vehicle groups at only 1 of 7 stimulating intensities (there was no statistical difference comparing intravitreal injection of the vehicle with intravitreal injection of triamcinolone). Details concerning the Bonferroni correction, which adjusts for multiple corrections (more than 80 in this article, increasing the likelihood of obtaining a P value of .02 by chance alone), were not provided. Consequently, it remains unclear whether the perceived elevation in amplitudes was real.

Dierks and colleagues concluded that triamcinolone may enhance rod pathway function and may be used in “inherited retinal degeneration . . . such as retinitis pigmentosa.”1 Unfortunately, increased b-wave amplitude has been described as a consequence of possible photoreceptor toxicity and as a drug-induced change.2 4

We commend Dierks and colleagues for urging further definition of the safety profile and mode of action of intravitreal triamcinolone. It is our view that despite widespread use of the latter, there is need for further clarification of the former.

AUTHOR INFORMATION

Correspondence: Dr Holz, Cullen Eye Institute, Baylor College of Medicine, 6565 Fannin St, NC 205, Houston, TX 77030 (eholz@bcm.tmc.edu).

Financial Disclosure: None reported.

REFERENCES

Dierks  D, Lei  B, Zhang  K, Hainsworth  DP. Electroretinographic effects of an intravitreal injection of triamcinolone in rabbit retina. Arch Ophthalmol 2005;1231563- 1569
PubMed
Tanimoto  N, Usui  T, Ichibe  M, Takagi  M, Hasegawa  S, Abe  H. PIII and derived PII analysis in a patient with retinal dysfunction with supernormal scotopic ERG. Doc Ophthalmol 2005;110219- 226
PubMed
Michaelides  M, Holder  GE, Webster  AR.  et al.  A detailed phenotypic study of cone dystrophy with supernormal rod ERG. Br J Ophthalmol 2005;89332- 339
PubMed
Brockway  LM, Benos  DJ, Keyser  KT, Kraft  TW. Blockade of amiloride-sensitive sodium channels alters multiple components of the mammalian electroretinogram. Vis Neurosci 2005;22143- 151
PubMed

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Dierks  D, Lei  B, Zhang  K, Hainsworth  DP. Electroretinographic effects of an intravitreal injection of triamcinolone in rabbit retina. Arch Ophthalmol 2005;1231563- 1569
PubMed
Tanimoto  N, Usui  T, Ichibe  M, Takagi  M, Hasegawa  S, Abe  H. PIII and derived PII analysis in a patient with retinal dysfunction with supernormal scotopic ERG. Doc Ophthalmol 2005;110219- 226
PubMed
Michaelides  M, Holder  GE, Webster  AR.  et al.  A detailed phenotypic study of cone dystrophy with supernormal rod ERG. Br J Ophthalmol 2005;89332- 339
PubMed
Brockway  LM, Benos  DJ, Keyser  KT, Kraft  TW. Blockade of amiloride-sensitive sodium channels alters multiple components of the mammalian electroretinogram. Vis Neurosci 2005;22143- 151
PubMed

Correspondence

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