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ACE and angiotensin II and nonarteritic anterior ischemic optic neuropathy
Letters to the Editor cellulitis involving the eye. Although the Hib vaccine has caused a dramatic decrease in many life-threatening pediatric diseases, it remains doubtful that it can be credited with a vast reduction of periorbital and orbital cellulitis, because Hib is not a significant cause of sinusitis.2 To bolster their argument that Hib bacteremia was common in periorbital cellulitis cases before the introduction of the Hib vaccine, the authors cite a 1978 article from Pediatrics.3 Unfortunately, this particular citation does not actually differentiate among the various H. influenza strains. Ambati et al seem to have assumed that any mention of this bacterium must refer to the B strain. Also, when the authors list the cultures found in their cellulitis patients, their results show only the type B strain as a causative factor. It is again likely that the authors took any outcome positive for H. influenza to be the type B strain. In fact, retrospective studies concerning H. influenza are often handicapped by the lack of strain-specific results by hospital laboratories in the past. Undoubtedly, the Hib vaccine has prevented that small subset of cellulitises actually caused by the type B. Because most sinusitises are due to nontypable H. influenza, however, we must keep this bacterium high in the differential of potential causes. CHANDAK GHOSH, MD, MPH New York, New York References 1. Haemophilus Influenzae Infections. In: Pickering LK, ed. Red Book 2000: Report of the Committee on Infectious Diseases, 25th ed. Elk Grove Village, IL: American Academy of Pediatrics, 2000;262–74. 2. Immergluck LC, Daum RC. Haemophilus Influenzae. In: Nelson WE, sr. ed. Behrman RE, Kliegman RM, Arvin AM, eds. Nelson Textbook of Pediatrics, 15th ed. Philadelphia: W.B. Saunders, 1996;762– 8. 3. Smith TF, O’Day D, Wright PF. Clinical implications of preseptal (periorbital) cellulitis in childhood. Pediatrics 1978;62: 1006 –9.
Although we do not disagree that the receptor polymorphisms likely do not play a role, we believe the proper statistical test must be used to support this conclusion. SEAN P. DONAHUE, MD, MPH Nashville, Tennessee Author reply Dear Editor: Dr. Donahue’s letter expresses concerns that in our article, “The Role of Angiotensin Converting Enzyme and Angiotensin II Type 1 Receptor Gene Polymorphisms in Patients with Nonarteritic Anterior Ischemic Optic Neuropathy (NAION),” further statistical analysis are required to support our conclusion that angiotensin-converting enzyme (ACE) and angiotensin II type 1 receptor (AT1R) have no role in the pathogenesis of the disease. The insignificant P values in our study could result from true lack of effect or from small sample sizes and, consequently, low power. We have carried out the power calculations requested by Dr. Donahue with respect to a 20% absolute difference in the allele frequencies of the presumed risks (D allele in the case of ACE and C allele in the case of AT1R). The calculations were based on the use of a two-sided 5% test. The power to detect a 20% difference in ACE and AT1R was 98.7% and 95.2%, respectively. More cogent is a computation of the 95% confidence intervals (CI) for the differences in the D and C allele frequencies (NAION patients minus controls). The 95% CI for the D allele of ACE was ⫺14.9, 6.5 and for the C allele of AT1R, was ⫺3.3, 16.4. For both polymorphisms, the 95% CI indicated small differences; and it ruled out a 20% increment among NAION patients over the controls. Thus, additional calculations support our conclusion that ACE and AT1R polymorphisms have no role in the pathogenesis of NAION. OPHIRA SALOMON, MD RIMA DARDIK, PHD RUTH HUNA-BARON, MD Tel-Hashomer, Israel DAVID M. STEINBERG, PHD Tel-Aviv, Israel
ACE and Angiotensin II and Nonarteritic Anterior Ischemic Optic Neuropathy Dear Editor: Salomon et al recently report (Ophthalmology 2000;107: 1717–20) on the frequency of polymorphisms for angiotensin-converting enzyme genes in patients with nonarteritic anterior ischemic optic neuropathy. They compared 74 patients with nonarteritic anterior ischemic optic neuropathy (NAION) to 71 control patients. They were unable to find any difference in the frequency of six different polymorphisms. They used a P value that was greater than 0.05 to support the conclusion that “The polymorphisms have no role in the pathogenesis of NAION.” Unfortunately, a P value cannot be used to support this conclusion. When two populations are compared using a statistical test and no difference is found between the groups, this does not mean that no difference exists. To determine this, the type II or beta error must be calculated. The authors did not do this. We would ask the authors to calculate the type II error to detect a 20% difference in polymorphism distribution for the two groups.
Active Ocular Syphilis Dear Editor: Dr. Browning’s excellent article on “Posterior Segment Manifestations of Active Ocular Syphilis: Their Response to a Neurosyphilis Regimen of Penicillin Therapy, and the Influence of Human Immunodeficiency Virus Status on Response” (Ophthalmology 107:2015–23), deserves special attention. We find his article to be profoundly useful in clinical practice. The author’s thoughtful review of his experience with 14 patients and specific statements in the Discussion provide clinically applicable recommendations. It has become all too commonplace for authors to provide politically correct and overly vague recommendations, which give the reader only clinically useless verbiage. The fact that his patients were drawn from a private practice setting makes the application of the information even much more useful.
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Although we do not disagree that the receptor polymorphisms likely do not play a role, we believe the proper statistical test must be used to support this conclusion. SEAN P. DONAHUE, MD, MPH Nashville, Tennessee Author reply Dear Editor: Dr. Donahue’s letter expresses concerns that in our article, “The Role of Angiotensin Converting Enzyme and Angiotensin II Type 1 Receptor Gene Polymorphisms in Patients with Nonarteritic Anterior Ischemic Optic Neuropathy (NAION),” further statistical analysis are required to support our conclusion that angiotensin-converting enzyme (ACE) and angiotensin II type 1 receptor (AT1R) have no role in the pathogenesis of the disease. The insignificant P values in our study could result from true lack of effect or from small sample sizes and, consequently, low power. We have carried out the power calculations requested by Dr. Donahue with respect to a 20% absolute difference in the allele frequencies of the presumed risks (D allele in the case of ACE and C allele in the case of AT1R). The calculations were based on the use of a two-sided 5% test. The power to detect a 20% difference in ACE and AT1R was 98.7% and 95.2%, respectively. More cogent is a computation of the 95% confidence intervals (CI) for the differences in the D and C allele frequencies (NAION patients minus controls). The 95% CI for the D allele of ACE was ⫺14.9, 6.5 and for the C allele of AT1R, was ⫺3.3, 16.4. For both polymorphisms, the 95% CI indicated small differences; and it ruled out a 20% increment among NAION patients over the controls. Thus, additional calculations support our conclusion that ACE and AT1R polymorphisms have no role in the pathogenesis of NAION. OPHIRA SALOMON, MD RIMA DARDIK, PHD RUTH HUNA-BARON, MD Tel-Hashomer, Israel DAVID M. STEINBERG, PHD Tel-Aviv, Israel
ACE and Angiotensin II and Nonarteritic Anterior Ischemic Optic Neuropathy Dear Editor: Salomon et al recently report (Ophthalmology 2000;107: 1717–20) on the frequency of polymorphisms for angiotensin-converting enzyme genes in patients with nonarteritic anterior ischemic optic neuropathy. They compared 74 patients with nonarteritic anterior ischemic optic neuropathy (NAION) to 71 control patients. They were unable to find any difference in the frequency of six different polymorphisms. They used a P value that was greater than 0.05 to support the conclusion that “The polymorphisms have no role in the pathogenesis of NAION.” Unfortunately, a P value cannot be used to support this conclusion. When two populations are compared using a statistical test and no difference is found between the groups, this does not mean that no difference exists. To determine this, the type II or beta error must be calculated. The authors did not do this. We would ask the authors to calculate the type II error to detect a 20% difference in polymorphism distribution for the two groups.
Active Ocular Syphilis Dear Editor: Dr. Browning’s excellent article on “Posterior Segment Manifestations of Active Ocular Syphilis: Their Response to a Neurosyphilis Regimen of Penicillin Therapy, and the Influence of Human Immunodeficiency Virus Status on Response” (Ophthalmology 107:2015–23), deserves special attention. We find his article to be profoundly useful in clinical practice. The author’s thoughtful review of his experience with 14 patients and specific statements in the Discussion provide clinically applicable recommendations. It has become all too commonplace for authors to provide politically correct and overly vague recommendations, which give the reader only clinically useless verbiage. The fact that his patients were drawn from a private practice setting makes the application of the information even much more useful.
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