Response to Beutner and Plunkett

Response to Beutner and Plunkett

728 Letters J AM ACAD DERMATOL OCTOBER 2007 adapted to a photographic camera or onto the camera of a digital video dermoscope. This simple method, p...

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728 Letters

J AM ACAD DERMATOL OCTOBER 2007

adapted to a photographic camera or onto the camera of a digital video dermoscope. This simple method, particularly useful for those who possess traditional contact dermoscopes, also permits a quick and reliable diagnosis and treatment monitoring of pediculosis, without the need of a microscope or other more sophisticated devices. Renato Marchiori Bakos, MD, MSc, and Lucio Bakos, MD, PhD Department of Dermatology, Hospital de Clı´nicas de Porto Alegre, Porto Alegre, Brazil Funding sources: None. Conflicts of interest: None declared. Reprint requests: Renato Marchiori Bakos, MD, MSc, Rua Coronel Bordini, 889, 90440-001 Porto Alegre, RS Brazil E-mail: [email protected]

Department of Dermatology,a University of Alabama at Birmingham School of Medicine; Wake Forest University School of Medicine,b Winston-Salem, North Carolina; and the Department of Dermatology, Eastern Virginia Medical School and Virginia Clinical Research, Inc, Norfolk c Drs Elewski, Fleischer, Jr, and Pariser have been investigators and consultants for Intendis. Correspondence to: Boni E. Elewski, MD, University of Alabama at Birmingham, Department of Dermatology, EFH 414, 1530 3rd Avenue South, Birmingham, AL 35294-0009. REFERENCES 1. Pelle MT, Crawford GH, James WD. Rosacea: II. Therapy. J Am Acad Dermatol 2004;51:499-512. 2. Elewski BE, Fleischer AB Jr, Pariser DM. A comparison of 15% azelaic acid gel and 0.75% metronidazole gel in the topical treatment of papulopustular rosacea: results of a randomized trial. Arch Dermatol 2003;139:1444-50. doi:10.1016/j.jaad.2006.11.026

REFERENCE 1. Di Stefani A, Hofmann-Wellenhof R, Zalaudek I. Dermoscopy for diagnosis and treatment monitoring of pediculosis capitis. J Am Acad Dermatol 2006;54:909-10. doi:10.1016/j.jaad.2006.11.011

Reply To the Editor: In reference to the October 2004 comprehensive overview of rosacea therapy,1 we would like to bring to your attention the results a major phase III trial comparing azelaic acid gel 15% with metronidazole gel 0.75%. These results were published in Archives of Dermatology in November 2003,2 after this continuing medical education article had been accepted and was in press. In this randomized, double-blind, parallel-group study of 251 patients, azelaic acid gel 15% demonstrated statistically significant superiority over metronidazole gel 0.75% in reducing inflammatory papules and pustules, improving erythema severity, and improving rosacea overall as assessed by two distinct investigator measures over a 15-week trial period. This study was sponsored by Berlex Laboratories (now Intendis, Berlin, Germany). As coauthors of this study, we believe the findings from a direct head-to-head comparison of a newer therapy (azelaic acid gel 15%) against a long-time standard therapy (metronidazole gel 0.75%) would be of great interest and value to clinicians charged with selecting the most appropriate treatment for their patients. Boni E. Elewski, MD,a Alan Fleischer, Jr, MD,b and David Pariser, MDc

Response to Beutner and Plunkett To the Editor: We thank Drs Beutner and Plunkett1 for their interest in our article.2 We would like to respond to their 4 points of clarification. First, Beutner and Plunkett1 called to attention that one of our 3 references citing cases of direct immunofluorescence (DIF)-negative dermatitis herpetiformis (DH) was incorrect.3 On reviewing this reference, we found that Peters and McEvoy3 reported a case in which ‘‘the possibility remains that the direct immunofluorescence results were false negative,’’ because the antiendomysial antibodies were positive and the patient improved with empiric use of dapsone. Similarly, it is possible that the two other patients in the control group (ie, those thought to not have DH) who had positive antiendomysial antibodies and negative DIF results also had a clinically more subtle presentation of DH. If this is true, then this study actually describes 27 patients with DH, 3 of whom had negative DIF findings. Hence, the number of patients who with DIF-negative results and DH may have been, depending on how one examines the data, as high as 3 of 27 (ie, ;10%) or as few as 0 of 24 (as Beutner and Plunkett1 suggest). This means that up to 10% (or as few as 0%) may have had DIFnegative DH. Second, although Beutner and Plunkett1 agree that enzyme-linked immunosorbent assay (ELISA) tissue transglutaminase antibody studies have a higher sensitivity than that of the immunofluorescence test for antiendomysial antibodies, they contend that

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tissue transglutaminase antibody studies have a lower specificity. Heil et al4 examined 204 serum samples in duplicates with commercial human ELISA kits and found the tissue transglutaminaseebased ELISA to be 100% specific. Third, Beutner and Plunkett1 suggest that our patient (who is actually one of us [S. H.]) could have the much more common celiac disease, without DH. They suggest that there should be ‘‘added checks to relate positive findings of tissue transglutaminase and/or antiendomysial antibody tests to DH. . . since other disorders that cause pruritic microvesicle formation do occur in celiac disease.’’1 These added checks might include a gluten challenge that ‘‘can lead to a flare in lesion formation in about 24 hours.’’1 Our patient did have several gluten challenges (purposely and accidentally). Each challenge led to the development of intensely pruritic vesicles localized to the elbows, face, or both within 24 hours. In addition, as Beutner and Plunkett1 suggested, our patient was evaluated by a gastroenterologist, who agreed with the diagnosis of DH/celiac disease. These parts of the history were not included in our original article because we had to shorten the ‘‘Case Report’’ section to conform to the stipulations of the ‘‘Medical Pearl’’ section. We agree that most patients with celiac disease do not have DH and that they could have other skin diseases that form microvesicles, such as allergic contact dermatitis. However, the diagnosis of DH, as Beutner and Plunkett1 mention, can be made without a DIF test if tissue transglutaminase tests yield positive findings and there are consistent clinical evaluations to rule out false-positive results, such as a regimen of glutenfree diet and gluten challenge. Our patient fulfilled both of these criteria. Fourth, Beutner and Plunkett1 recommend ordering the antiendomysial antibody test because it is $11 cheaper than the tissue transglutaminase ELISA when performed by Quest Diagnostics (Madison, NJ) and because it is ‘‘more specific.’’ Recently, two groups of investigators compared the sensitivity and specificity of tissue transglutaminase antibody testing and antiendomysial antibody immunofluorescent test.5,6 Reza et al5 concluded: ‘‘The best screening test for the detection of gluten-sensitive enteropathy in the general population is IgA tissue transglutaminaseeAb.’’ Hill et al6 concluded: ‘‘Tissue transglutaminase antibody [testing] is recommended as the first-line serological test for celiac disease.’’ Sylvia Hsu, MD, Anupam M. Desai, MD, and Ravi S. Krishnan, MD Department of Dermatology, Baylor College of Medicine, Houston

Funding sources: None. Conflicts of interest: None declared. Correspondence to: Sylvia Hsu, MD, Department of Dermatology, Baylor College of Medicine, 6620 Main St, Suite 1425, Houston, TX 77030 E-mail: [email protected] REFERENCES 1. Beutner EH, Plunkett RW. Methods for diagnosing dermatitis herpetiformis. J Am Acad Dermatol 2006;55:1112-3. 2. Desai AM, Krishnan RS, Hsu S. Medical pearl: using tissue transglutaminase antibodies to diagnose dermatitis herpetiformis. J Am Acad Dermatol 2005;53:867-8. 3. Peters MS, McEvoy MT. IgA antiendomysial antibodies in dermatitis herpetiformis. J Am Acad Dermatol 1989;21:1225-31. 4. Heil PM, Volc-Platzer B, Karlhofer F, Gebhart W, Huber WD, Benesch T, et al. Transglutaminases as diagnostically relevant autoantigens in patients with gluten sensitivity. J Dtsch Dermatol Ges 2005;3:974-8. 5. Reza AM, Mohammadkhani A, Fakheri H, Javad Zahedi M, Shahbazkhani B, Nouraie M, et al. Screening of the adult population in Iran for celiac disease: comparison of the tissue transglutaminase antibody and anti-endomysial antibody tests. Eur J Gastroenterol Hepatol 2006;18:1181-6. 6. Hill PG, Forsyth JM, Semeraro D, Homes GK. IgA antibodies to human tissue transglutaminase: audit of routine practice confirms high diagnostic accuracy. Scand J Gastroenterol 2004; 39:1078-82. doi:10.1016/j.jaad.2006.12.009

Reporting of number needed to treat and its difficulties To the Editor: We read with great interest the review article of Manriquez et al1 in the April issue of the Journal, which concentrated on importance of number needed to treat (NNT) in dermatologic trials. In this well-prepared review, the authors correctly explained different aspects of NNT. In our opinion, NNT is a controversial parameter when it is reported for chronic diseases. Imagine a trial comparing 1-cm with 3-cm excision margins for 1000 patients (500 for each treatment group) with melanoma in which the outcome is recurrence of tumor. At the end of 6 months, 50 patients in 1-cm group versus 25 in 3-cm group have recurrence. By 1 year, the numbers are 100 patients in the first group and 50 patients in the second group, and by 2 years, there are 200 and 100 patients with recurrence, respectively. The resultant NNTs would be 20, 10, and 5 for 6 months, 1 year, and 2 years, respectively (Table I). In this case, that NNT is based on absolute risk reduction; it decreases as a function of time and leads to the conclusion that the wider excision does prove, in fact, to have a greater absolute advantage over