284 Correspondence REFERENCES 1. Zackheim HS, Koh HK, Weinstock MA. Assessing clinical outcomes in cutaneous T-cell lymphoma. Hemato1 Oncol Clin NorthAm 1995;9:1021-9. 2. Anderson JR, Propert KJ, Harrington DP. Guidelines for reporting outcomes of lymphoma trials. J Clin Oncol 1988;6:559-60. 3. Kim YH, Jensen RA, Watanabe GL, Varghese A, Hoppe RT. Clinical stage IA (limited patch and plaque) mycosis fungoides: a long-term outcome analysis. Arch Dermatol 1996; 132: 1309-13.
Medical issues and emergencies in the dermatology office: Comments To the Editor: Drs. Fader and Johnson in their article entitled "Medical Issues and Emergencies in the Dermatology Office" (J Am Acad DermatoI1997;36:116) focus on the highly desirable goal of avoiding emergencies and disasters in the dermatology office. I offer the following comments on two of the issues they discussed. There is the vexing issue of the local anesthetic to be used in patients with possible or probable lidocaine sensitivity. The authors suggest: "Temporary anesthesia may also be achieved by the intradermal injection of 0.9% (normal) saline solution ... " (p. 6). This is not correct. Saline solution 0.9% does not have any anesthetic action; however, saline preserved with benzyl alcohol produces effective, albeit superficial and relatively brief, anesthesia. The effect can be prolonged by adding epinephrine in the concentration of 1:300,000. 1 Although benzyl alcohol is the preservative currently used in the United States in multiple-dose vials of injectable sodium chloride, this has not always been the case and may not be for other countries. The parabens, as well as phenol, have been used as preservatives for saline in the United States. (In the same issue of the Journal, the Surgical Pearl "Bacteriostatic Sodium Chloride Injection USP 0.9%" [Daniel CR III, Ellis GH. JAm Acad Dermatol 1997;36:92] failed to identify benzyl alcohol as the anesthetic agent in bacteriostatic sodium chloride.) Regarding the issue of electrosurgery and pacemakers, the authors do not mention hemostasis achieved by pinpoint electrocoagulation with a bipolar forceps. I have utilized this widely used technique for more than 15 years. The electric current passes only from one tip of the forceps to the other, producing intense localized heat. No current passes through the patient's body, and the bipolar forceps can be safely used in patients with implanted electrical devices. Bipolar forceps and the special two-line connecting cords required are available from many surgical suppliers. It should be noted that the bipolar forceps are only suitable for point electrocoagulation as is appropriate for hemostasis. Bipolar
Journal of the American Academy of Dermatology February 1998
forceps are not suitable for electrodesiccation or electrodestruction of lesions. Ernst Epstein, MD 100 S. Ellsworth Ave., Suite 707 San Mateo, CA 94401 REFERENCE 1. Holmes HS. Options for painless local anesthesia. Postgrad Med 1991;89:71-2.
Oral hairy leukoplakia in HIV-positive patients To the Editor: We read with interest the article by Husak et al. entitled "Oral Hairy Leukoplakia in 71 HIV-seropositive Patients: Clinical Symptoms, Relation to Immunologic Status, and Prognostic Significance" (J Am Acad Dermatol 1996;35:928-34). The authors state that they diagnosed oral hairy leukoplakia (OHL) in 71 of 456 patients (15.6%) with HIVassociated skin disorders, and they report the immunologic (median CD4 cell count, 235/111) and prognostic data (median survival time, 20 months) of these patients. Epstein-Barr virus (EBV) causes a wide spectrum of disease in HIV-positive patients and OHL is a prognostic marker in HIV infection. In addition, many nonHodgkin's lymphomas are Epstein-Barr virus-positive and OHL is proposed to be a risk factor for the development of an Epstein-Barr virus-associated lymphoma in patients with AIDS. 1 In a subsequent retrospective analysis of 406 patients with less than 350 CD4 cellS/ill, who were treated in our department between 1987 and 1995, OHL was diagnosed in 63 (15.5%). At the time of diagnosis moderate immunosuppression (median CD4 cell count, 256/111) was present in these patients. The median survival time was 26 months after diagnosis of OHL. These data confirm the results of Husak et al. However, the frequency of OHL and the prognosis of these patients depended on the therapeutic regimen. An analysis of our data shows that OHL was diagnosed in 16 of 62 patients (25.8%; median CD4 cell count, 251/111; median survival time, 17 months) who received no antiviral (acyclovir, ganciclovir, or foscamet) or antiretroviral (e.g., zidovudine, didanosine, zalcitabine) treatment, in 25 of 134 patients (18.6%; median CD4 cell count, 263/111; median survival time, 29 months) who received antiretroviral (nucleoside analogs, proteinase inhibitors) therapy, and in only 13 of 210 patients (6.2%; median CD4 cell count, 247/111; median survival time, 31 months) who received antiretroviral/antiviral combination therapy (e.g., acyclovirlzidovudine). Our results show that not only