Journal of the American Academy of Dermatology
930 Brief communications can be used for herpes zoster.14 This may help limit renal and central nervous system toxicities occasionally encountered with this medication. Patients with herpes zoster require respiratory and contact isolation whereas those with herpes simplex virus require only contact isolation. I 4 This has tremendous practical implications for medical personnel, young children, and pregnant women who are not immune to varicella, as well as for immunocompromised patients. It is important to realize the possibility of coexistent herpes simplex virus and herpes zoster infection. s The site of infection is not an accurate predictor of herpes simplex virus type. 15 Thus diagnosis of type 1 Or 2 is important for several reasons, including (1) prognosis, inasmuch as the recurrence rate of genital herpes simplex virus 1 is less than that of genital type 2,15 (2) therapy, because the antiviral activity of chemotherapeutic agents can differ between the two herpes simplex virus typeS,16 and (3) epidemiology, for assessing the association of herpes simplex virus with other disease processes (e.g., cervical carcinoma),17 The suggestion has been made that surgeons avoid manipulation of sacral nerve roots as much as possible. 10 One study found that the use of preoperative interferon reduced the time of viral shedding and decreased the severity of the herpetic lesions. 18 A prospective study concerning the use of preoperative acyclovir in patients with known recurrent herpes simplex virus may be useful. REFERENCES 1. Slavin BH, Ferguson JJ Jr. Zoster-like eruptions caused by the virus of herpes simplex. Am J Med 1950;8:456-67. 2. Heskel NS, Hanifin JM. "Recurrent herpes zoster": an unproved entity? J AM ACAD DERMATOL 1984;10:486-90. 3. Correy L, Spear PG. Infections with herpes simplex virus. N Engl J Med 1986;314:686-91. 4. Layzer RB, Conant MA. Neuralgia in recurrent herpes simplex. Arch NeuroI1974;31:233-7. 5. Wheeler CE Jr. Pathogenesis of recurrent herpes simplex infections. J Invest DermatoI1975;65:341-6. 6. Nowinski RC, Tam MR, Goldstein LC, et aL Monoclonal antibodies for diagnosis ofinfectious disease in humans. Science 1983;219:637-44. 7. Music SI, Fine EM, Togo Y. Zoster-like disease in the newborn due to herpes-simplex virus. N Eng! J Med 1971 ;284: 24-6. 8. Kahn G. Zoster and herpes simplex. Arch Dermatol 1967;95:298. 9. Forrest WM, Kaufman HE. Zosteriform herpes simplex. Am J OphthamoI1976;81:86-8. 10. Haverkow LW, Pazin GJ, Ho M, Nelson PB. Reactivation of type 2 herpes simplex by thoracolumbar neurosurgery. Ann Intern Med 1984;101:503-4. 11. Nabors MW, Francis CK, Kobrine, AI. Reactivation of herpesvirus in neurosurgical patients. Neurosurgery 1986;19:599-60l 12. Pazin GJ, Ho M, Jannetta PJ. Reactivation of herpes simplex virus·after decompression of the trigeminal nerve root. J Infect Dis 1978;138:405-9. 13. Baringer JR. Recovery ofherpes simplex virus from human sacral ganglions. N Engl J Med 1974;291:828-30. 14. Kalman CM, Laskin OL. Herpes zoster and zosteriform
15.
16. 17. 18.
herpes simplex virus infections in immunocompetent adults. Am J Med 1986;81:775-8. Reeves WC, Corey L, Adams HG, Vontver LA, Holmes KK. Risk of recurrence after first episode of genital herpes: relation to HSV type and antibody response. N Engl J Med 1981;305:315-9. DeClerq E, Descamps J, Verhelst G, et aL Comparative efficacy of antiherpes drugs against different strains of herpes simplex virus. J Infect Dis 1980;141:563-74. Rawls WE, Tomkins WA, Meinick JL. The association of herpesvirus type 2 and carcinoma of the uterine cervix. Am J EpidernioI1969;89:547-54. Pazin GJ, Armstrong JA, LamMT, TarrGC,JannettaPJ, Ho M. Prevention of reactivated herpes simplex infection by human leukocyte interferon after operation on the trigeminal root. N Engl J Med 1979;301:225-30.
Aluminum chloride hexahydrate and blistering in epidermolysis bullosa simplex 1. R. Younger, MBBS, G. C. Priestley, PhD, and
M. J. Tidman, MD,MRCP Edinburgh, Scotland
Anecdotal reports have attested to the efficacy of topical aluminum chloride hexahydrate in reducing blistering of the palms and soles in epidermolysis bullosa simplex 1,2 and pachyonychia congenita3 by virtue of its antiperspirant property. In both conditions blister formation tends to be more severe during the summer months, possibly as a result of an increase in the coefficient of friction of the skin caused by sweating and raised skin temperature. 4 We undertook a double-blind, placebo-controlled, crossover study of 20% aluminum chloride hexahydrate in 23 subjects, 4 to 63 years ofage (mean 23 ± 18 years), from six families, with unequivocal epidermolysis bullosa simplex (Weber-Cockayne syndrome). The trial was conducted between July and September 1989. A proprietary preparation of aluminum chloride hexahydrate (Drichlor) was used, and placebo, consisting ofthe diluent only, was provided by the manufacturer. Both preparations were analyzed for their aluminum content by an independent laboratory. Each subject was provided with both placebo and active medication in roll-on containers in a double-blind, randomized manner and were asked to apply one preparation to the right sole and the other to the left sole just before retiring to bed. New blisters on the treated areas were recorded daily by the patients, and they were objectively evaluated and photographed weekly. After 4 weeks of therapy and a "wash-out" period of 1 week the procedure was repeated for an additional 4 weeks with the From The University Department of Dermatology. Royal Infirmary of Edinburgh. Reprint requests: M. J. Tidman, MD, MRCP, Department of Dermatology, The Royal Infirmary, Edinburgh EH3 9YW, Scotland.
16/4/20322
Volume 23 Number 5, Part 1 November 1990
preparations on the contralateral side. Twenty subjects completed the first month of the trial, and 15 completed the second month. No unacceptable side effects of the antiperspirant were reported. No significant difference was observed in blister counts between the active preparation of aluminum chloride hexahydrate and the placebo in either phase of the study, although most subjects reported dryness on the sites treated with active drug. In the first month both active drug-treated and placebo-treated groups had an identical total blister count of 129, giving a mean per patient of 6.5 blisters on each foot. In the second month the totals were 81 (placebo) and 77 (activedrug), giving means of5.4 and _ 5.1 per foot, respectively (not significant by paired t test). We have been unable to confirm, therefore, that 20% aluminum chloride hexahydrate is an effective means of blister control in epidermolysis bullosa simplex. REFERENCES 1. Tkach JR. Treatment of recurrent bullous eruption of hands and feet (Weber-Cockayne disease) with topical aluminum chloride [Letter]. J AM ACAD DERMATOL 1982;6:1095-6. 2. Jennings JL. Aluminum chloride hexahydrate treatment of localized epidermolysis bullosa [Abstract]. Arch Dermatol 1984; 120:1382. 3. Tidman MJ, Wells RS. Control of plantar blisters in pachyonychia congenita with topical aluminum chloride [Letter]. Br J Dermato11988;118:451-2. 4. Naylor PFD. Experimental friction blisters. Br J Dermatol 1955;67:327-42.
Serum 8-methoxypsoralen (8-MOP) concentrations after bath water delivery of 8-MOP plus UVA Michael David, MD,a Nicholas J. Lowe, MD,a Rebat M. Halder, MD,b and Michael Borak, MDa Los Angeles, California, and Washington, D.C. The percutaneous absorption of 8-methoxypsoralen (8-MOP) in patients with psoriasis during bath water delivery of 8-MOP plus UVA was determined by a reverse high-performance liquid chromatographic method. Patients receiving oral PUVA served as a positive control group. Patients and methods. Twelve patients with psoriasis participated in the study after giving their informed consent. Eight From the Division of Dermatology, UCLA School of Medicine, University of California-Los Angeles,' and the Department of Dermatology, Howard University College of Medicine, Washington, D.C. b
Supported in part by The Skin Research Foundation of California, Los Angeles. Reprint requests: N. J. Lowe, MD, Southern California Dermatology and Psoriasis Center, 2001 Santa Monica Blvd., Suite 490W, Santa Monica, CA 90404. 16/4/20045
Briefcommunications 931 patients (seven men, one woman; age 18 to 79 years) received 30 minutes oftotal body 8-MOPbaths. Four patients who were taking ora18-MOP therapy served as a control group. Bath solutions were prepared by diluting 15 ml of 1%stock solution of 8-MOP in 80 L of body-temperature bath water (1.87 mg/L). At the end ofthe soak period, patients dried and immediately received UV radiation. Patients who were taking oraI8-MOP received a liquid-filled capsule formulation of 8-MOP (Oxsoralen-Ultra), 0.5 mg/kg weight 1V2 hours before UVAexposure. Blood samples were drawn from the patients before, immediately after, at 30 minutes, and at 60 minutes after the bath. In the oral PUVA group peripheral blood was obtained 1V2 and 24 hours after administration of the medication. A reverse-phase high-performance liquid chromatographic method was used to measure blood 8-MOP levels as described by Chakrabarti et a[,l Results obtained from patients' serum were plotted, and-peak heights were compared with theexternal calibration curve to determine the concentrations of8-MOP.
Results. Immediately after the bath, serum 8-MOP was detectable in five of eight patients, with mean value of 1.8 ng/ml; 30 minutes and 60 minutes after the bath the mean levels were 4.8 and 4 ng/mI, respectively. In the ora18-MOP patients, mean serum 8-MOPlevels was 108.87 n~/ml1 Jh hours after drug administr~tion. Twenty-four hours after oral ingestion serum, 8-MOP was nondetectable. Discussion. Fischer and Alsins 2 in 1976 reported the beneficial effect of trioxsalen baths and UV light for psoriasis. Their findings were subsequently confirmed by several authors. 3-5 In a more recent study no systemic side effects were observed with bath water delivery of 8-MOP plus UVA for psoriasis.6 These observations imply that systemic absorption of psoralen from PUVA bath is minimal. Aserum trioxsalen level of2ng/mI was found in two patients after trioxsalen bath treatment.? Our studies confirm extremely low 8-MOP levels result from 8-MOP bath water treatments and provide confirmation of the absence of systemic side effects in patients who are undergoing PUVA bath treatments. Risks of skin carcinogenicity from water-delivered 8-MOP are not known. In an 8-year follow-up of 149 patients treated with trioxsalen baths, no degenerative changes or carcinomas were found in treated skin.4 REFERENCES 1. Chakrabarti SG, Halder RM, Johnson BA, et al. 8-Methoxypsoralen levels in blood ofvitiligo patients and in the skin, ophthalmic fluids and ocular tissues of the guinea pig. J Invest DermatoI1986;87:276-9. 2. Fischer T, Alsins J. Treatment of psoriasis with trioxsalen baths and dysprosium lamps. Acta Derm Venereal (Stockh) 1976;56:383-90. 3. Salo OP, Lassus A, Taskinen J. Trioxsalen bath plus UVA treatment of psoriasis. Acta Derm Venereal (Stockh) 1981; 61:551-4. 4. Berne B, Fischer T, Michaelsson G, et al. An 8-year followup of 149 psoriasis patients. Photodermatology 1984;1 :1822. 5. Turjanma K, Salo H, Reunala T. Comparison of trioxsalen
930 Brief communications can be used for herpes zoster.14 This may help limit renal and central nervous system toxicities occasionally encountered with this medication. Patients with herpes zoster require respiratory and contact isolation whereas those with herpes simplex virus require only contact isolation. I 4 This has tremendous practical implications for medical personnel, young children, and pregnant women who are not immune to varicella, as well as for immunocompromised patients. It is important to realize the possibility of coexistent herpes simplex virus and herpes zoster infection. s The site of infection is not an accurate predictor of herpes simplex virus type. 15 Thus diagnosis of type 1 Or 2 is important for several reasons, including (1) prognosis, inasmuch as the recurrence rate of genital herpes simplex virus 1 is less than that of genital type 2,15 (2) therapy, because the antiviral activity of chemotherapeutic agents can differ between the two herpes simplex virus typeS,16 and (3) epidemiology, for assessing the association of herpes simplex virus with other disease processes (e.g., cervical carcinoma),17 The suggestion has been made that surgeons avoid manipulation of sacral nerve roots as much as possible. 10 One study found that the use of preoperative interferon reduced the time of viral shedding and decreased the severity of the herpetic lesions. 18 A prospective study concerning the use of preoperative acyclovir in patients with known recurrent herpes simplex virus may be useful. REFERENCES 1. Slavin BH, Ferguson JJ Jr. Zoster-like eruptions caused by the virus of herpes simplex. Am J Med 1950;8:456-67. 2. Heskel NS, Hanifin JM. "Recurrent herpes zoster": an unproved entity? J AM ACAD DERMATOL 1984;10:486-90. 3. Correy L, Spear PG. Infections with herpes simplex virus. N Engl J Med 1986;314:686-91. 4. Layzer RB, Conant MA. Neuralgia in recurrent herpes simplex. Arch NeuroI1974;31:233-7. 5. Wheeler CE Jr. Pathogenesis of recurrent herpes simplex infections. J Invest DermatoI1975;65:341-6. 6. Nowinski RC, Tam MR, Goldstein LC, et aL Monoclonal antibodies for diagnosis ofinfectious disease in humans. Science 1983;219:637-44. 7. Music SI, Fine EM, Togo Y. Zoster-like disease in the newborn due to herpes-simplex virus. N Eng! J Med 1971 ;284: 24-6. 8. Kahn G. Zoster and herpes simplex. Arch Dermatol 1967;95:298. 9. Forrest WM, Kaufman HE. Zosteriform herpes simplex. Am J OphthamoI1976;81:86-8. 10. Haverkow LW, Pazin GJ, Ho M, Nelson PB. Reactivation of type 2 herpes simplex by thoracolumbar neurosurgery. Ann Intern Med 1984;101:503-4. 11. Nabors MW, Francis CK, Kobrine, AI. Reactivation of herpesvirus in neurosurgical patients. Neurosurgery 1986;19:599-60l 12. Pazin GJ, Ho M, Jannetta PJ. Reactivation of herpes simplex virus·after decompression of the trigeminal nerve root. J Infect Dis 1978;138:405-9. 13. Baringer JR. Recovery ofherpes simplex virus from human sacral ganglions. N Engl J Med 1974;291:828-30. 14. Kalman CM, Laskin OL. Herpes zoster and zosteriform
15.
16. 17. 18.
herpes simplex virus infections in immunocompetent adults. Am J Med 1986;81:775-8. Reeves WC, Corey L, Adams HG, Vontver LA, Holmes KK. Risk of recurrence after first episode of genital herpes: relation to HSV type and antibody response. N Engl J Med 1981;305:315-9. DeClerq E, Descamps J, Verhelst G, et aL Comparative efficacy of antiherpes drugs against different strains of herpes simplex virus. J Infect Dis 1980;141:563-74. Rawls WE, Tomkins WA, Meinick JL. The association of herpesvirus type 2 and carcinoma of the uterine cervix. Am J EpidernioI1969;89:547-54. Pazin GJ, Armstrong JA, LamMT, TarrGC,JannettaPJ, Ho M. Prevention of reactivated herpes simplex infection by human leukocyte interferon after operation on the trigeminal root. N Engl J Med 1979;301:225-30.
Aluminum chloride hexahydrate and blistering in epidermolysis bullosa simplex 1. R. Younger, MBBS, G. C. Priestley, PhD, and
M. J. Tidman, MD,MRCP Edinburgh, Scotland
Anecdotal reports have attested to the efficacy of topical aluminum chloride hexahydrate in reducing blistering of the palms and soles in epidermolysis bullosa simplex 1,2 and pachyonychia congenita3 by virtue of its antiperspirant property. In both conditions blister formation tends to be more severe during the summer months, possibly as a result of an increase in the coefficient of friction of the skin caused by sweating and raised skin temperature. 4 We undertook a double-blind, placebo-controlled, crossover study of 20% aluminum chloride hexahydrate in 23 subjects, 4 to 63 years ofage (mean 23 ± 18 years), from six families, with unequivocal epidermolysis bullosa simplex (Weber-Cockayne syndrome). The trial was conducted between July and September 1989. A proprietary preparation of aluminum chloride hexahydrate (Drichlor) was used, and placebo, consisting ofthe diluent only, was provided by the manufacturer. Both preparations were analyzed for their aluminum content by an independent laboratory. Each subject was provided with both placebo and active medication in roll-on containers in a double-blind, randomized manner and were asked to apply one preparation to the right sole and the other to the left sole just before retiring to bed. New blisters on the treated areas were recorded daily by the patients, and they were objectively evaluated and photographed weekly. After 4 weeks of therapy and a "wash-out" period of 1 week the procedure was repeated for an additional 4 weeks with the From The University Department of Dermatology. Royal Infirmary of Edinburgh. Reprint requests: M. J. Tidman, MD, MRCP, Department of Dermatology, The Royal Infirmary, Edinburgh EH3 9YW, Scotland.
16/4/20322
Volume 23 Number 5, Part 1 November 1990
preparations on the contralateral side. Twenty subjects completed the first month of the trial, and 15 completed the second month. No unacceptable side effects of the antiperspirant were reported. No significant difference was observed in blister counts between the active preparation of aluminum chloride hexahydrate and the placebo in either phase of the study, although most subjects reported dryness on the sites treated with active drug. In the first month both active drug-treated and placebo-treated groups had an identical total blister count of 129, giving a mean per patient of 6.5 blisters on each foot. In the second month the totals were 81 (placebo) and 77 (activedrug), giving means of5.4 and _ 5.1 per foot, respectively (not significant by paired t test). We have been unable to confirm, therefore, that 20% aluminum chloride hexahydrate is an effective means of blister control in epidermolysis bullosa simplex. REFERENCES 1. Tkach JR. Treatment of recurrent bullous eruption of hands and feet (Weber-Cockayne disease) with topical aluminum chloride [Letter]. J AM ACAD DERMATOL 1982;6:1095-6. 2. Jennings JL. Aluminum chloride hexahydrate treatment of localized epidermolysis bullosa [Abstract]. Arch Dermatol 1984; 120:1382. 3. Tidman MJ, Wells RS. Control of plantar blisters in pachyonychia congenita with topical aluminum chloride [Letter]. Br J Dermato11988;118:451-2. 4. Naylor PFD. Experimental friction blisters. Br J Dermatol 1955;67:327-42.
Serum 8-methoxypsoralen (8-MOP) concentrations after bath water delivery of 8-MOP plus UVA Michael David, MD,a Nicholas J. Lowe, MD,a Rebat M. Halder, MD,b and Michael Borak, MDa Los Angeles, California, and Washington, D.C. The percutaneous absorption of 8-methoxypsoralen (8-MOP) in patients with psoriasis during bath water delivery of 8-MOP plus UVA was determined by a reverse high-performance liquid chromatographic method. Patients receiving oral PUVA served as a positive control group. Patients and methods. Twelve patients with psoriasis participated in the study after giving their informed consent. Eight From the Division of Dermatology, UCLA School of Medicine, University of California-Los Angeles,' and the Department of Dermatology, Howard University College of Medicine, Washington, D.C. b
Supported in part by The Skin Research Foundation of California, Los Angeles. Reprint requests: N. J. Lowe, MD, Southern California Dermatology and Psoriasis Center, 2001 Santa Monica Blvd., Suite 490W, Santa Monica, CA 90404. 16/4/20045
Briefcommunications 931 patients (seven men, one woman; age 18 to 79 years) received 30 minutes oftotal body 8-MOPbaths. Four patients who were taking ora18-MOP therapy served as a control group. Bath solutions were prepared by diluting 15 ml of 1%stock solution of 8-MOP in 80 L of body-temperature bath water (1.87 mg/L). At the end ofthe soak period, patients dried and immediately received UV radiation. Patients who were taking oraI8-MOP received a liquid-filled capsule formulation of 8-MOP (Oxsoralen-Ultra), 0.5 mg/kg weight 1V2 hours before UVAexposure. Blood samples were drawn from the patients before, immediately after, at 30 minutes, and at 60 minutes after the bath. In the oral PUVA group peripheral blood was obtained 1V2 and 24 hours after administration of the medication. A reverse-phase high-performance liquid chromatographic method was used to measure blood 8-MOP levels as described by Chakrabarti et a[,l Results obtained from patients' serum were plotted, and-peak heights were compared with theexternal calibration curve to determine the concentrations of8-MOP.
Results. Immediately after the bath, serum 8-MOP was detectable in five of eight patients, with mean value of 1.8 ng/ml; 30 minutes and 60 minutes after the bath the mean levels were 4.8 and 4 ng/mI, respectively. In the ora18-MOP patients, mean serum 8-MOPlevels was 108.87 n~/ml1 Jh hours after drug administr~tion. Twenty-four hours after oral ingestion serum, 8-MOP was nondetectable. Discussion. Fischer and Alsins 2 in 1976 reported the beneficial effect of trioxsalen baths and UV light for psoriasis. Their findings were subsequently confirmed by several authors. 3-5 In a more recent study no systemic side effects were observed with bath water delivery of 8-MOP plus UVA for psoriasis.6 These observations imply that systemic absorption of psoralen from PUVA bath is minimal. Aserum trioxsalen level of2ng/mI was found in two patients after trioxsalen bath treatment.? Our studies confirm extremely low 8-MOP levels result from 8-MOP bath water treatments and provide confirmation of the absence of systemic side effects in patients who are undergoing PUVA bath treatments. Risks of skin carcinogenicity from water-delivered 8-MOP are not known. In an 8-year follow-up of 149 patients treated with trioxsalen baths, no degenerative changes or carcinomas were found in treated skin.4 REFERENCES 1. Chakrabarti SG, Halder RM, Johnson BA, et al. 8-Methoxypsoralen levels in blood ofvitiligo patients and in the skin, ophthalmic fluids and ocular tissues of the guinea pig. J Invest DermatoI1986;87:276-9. 2. Fischer T, Alsins J. Treatment of psoriasis with trioxsalen baths and dysprosium lamps. Acta Derm Venereal (Stockh) 1976;56:383-90. 3. Salo OP, Lassus A, Taskinen J. Trioxsalen bath plus UVA treatment of psoriasis. Acta Derm Venereal (Stockh) 1981; 61:551-4. 4. Berne B, Fischer T, Michaelsson G, et al. An 8-year followup of 149 psoriasis patients. Photodermatology 1984;1 :1822. 5. Turjanma K, Salo H, Reunala T. Comparison of trioxsalen
![[Pathomorphogenesis of blistering in epidermolysis bullosa acquisita and epidermolysis bullosa dystrophica (author's transl)].](/assets/img/hold.png)
