- Email: [email protected]
Treatment of acquired perforating dermatosis with narrowband ultraviolet B
LETTERS CASE NOTES Treatment of acquired perforating dermatosis with narrowband ultraviolet B To the Editor: Ohe et al1 recently described the effective treatment of acquired perforating dermatosis (APD) with narrowband ultraviolet B (NB-UVB). They treated five patients with NB-UVB two to three times weekly and observed a complete clearance of lesions after 10 to 15 exposures. Patients were permitted to use topical corticosteroids, which had been given without satisfactory effects before starting NB-UVB. The authors attempted NB-UVB for the treatment of APD based on the fact that the disease appears to improve during summer months, and that photo(chemo)therapies are effective on uremic pruritus and prurigo nodularis as well. Unfortunately, Ohe et al1 did not mentioned in their paper that several patients with APD have previously been described in the literature who were treated either with conventional UVB2,3 or even NB-UVB.4,5 We would like to summarize these case observations and report an additional patient who was successfully treated with NB-UVB. In a previous review on APD it has been reported that conventional UVB caused complete clearance of skin lesions in two patients, and improvement in another two patients in whom one was additionally treated with topical retinoic acid.2 Achievement of a fair or a good response with conventional UVB in three patients in whom APD was associated with renal failure has also been reported.3 Bayramgu¨rler et al4 recently reported a female patient with APD associated with diabetes mellitus and chronic renal failure. Her condition significantly improved after 24 exposures of NB-UVB over a 13-week treatment period. Phototherapy was combined with oral hydroxyzine 50 mg daily. There was no relapse in the 3month follow-up period. Satchell et al5 described
two patients suffering from APD, diabetes mellitus, and hypercholesterolemia who were treated with combination therapies, including NB-UVB. One patient did not respond to potent topical corticosteroids and hydroxyzine 25 mg daily and required NB-UVB to control APD. The other patient, having failed to respond to topical corticosteroids, oral antihistamines, and NB-UVB, required systemic treatment with acitretin. We present a 47-year-old female patient suffering from severely itching papules with a central plug surrounded by erythema on the upper limbs and back (Fig 1, A). Clinical presentation and histopathologic findings of two biopsy specimens were well consistent with the diagnosis of APD. We could exclude internal diseases such as diabetes mellitus, renal and liver dysfunction, and lymphoma. However, we found evidence for hypercholesterolemia and atopic diathesis in our patient. On an inpatient basis, NB-UVB was initiated 5 times weekly for a fortnight. Then she continued as an outpatient a thrice weekly NB-UVB schedule for another 4 weeks (skin type I; initial dose: 0.1 J/cm2; maximum dose 0.6 J/cm2; cumulative dose: 12 J/cm2). Concomitant therapy was restricted to the use of 3% urea and 2% polidocanol containing moisturisers. After 6 weeks of treatment, the patient reported relief of pruritus accompanied by significant reduction of skin lesions (Fig 1, B). A 3-month follow-up period did not reveal recurrence of her skin disease. APD is an uncommon reactive skin condition usually associated with internal diseases such as diabetes mellitus and chronic renal failure. The disease is characterized by itchy keratotic umbilicated papules showing elimination of necrotic basophil collagen tissue in histologic examination. APD is difficult to treat. Nevertheless, spontaneous
Fig 1. APD on the upper back before (A) and after (B) NB-UVB phototherapy. J AM ACAD DERMATOL
FEBRUARY 2005 363
364 Letters
J AM ACAD DERMATOL FEBRUARY 2005
resolution is not infrequently observed.2 Apart from anti-proliferative and anti-inflammatory effects, NBUVB seems to be particularly effective in relief of pruritus, which may play the key role in the pathogenesis of APD.6 If the patient is protected from scratching and the underlying disorder is controlled, APD generally improves.2 Most APD patients treated with NB-UVB had concomitant active therapies such as potent topical corticosteroids and antihistamines.1,4,5 It is therefore impossible to draw definitive conclusions from the aforementioned case observations whether NB-UVB monotherapy of APD would be effective as well. Because APD is a relatively rare disease, one has to fall back upon therapeutic experiences obtained from well-described case reports and small trials. To exclude, however, a bias of results caused by concomitant topical therapies or spontaneous resolution, half-side comparison trials would be very useful in this condition. In conclusion, NB-UVB appears to be an effective adjuvant phototherapeutic regimen for patients with APD. There is no evidence, however, that NB-UVB should be preferred to conventional UVB in the management of APD. Thilo Gambichler, MDa,b Peter Altmeyer, MDa Alexander Kreuter, MDa Department of Dermatology Ruhr-University Bochum, Bochum, Germanya Department of Dermatology Oldchurch Hospital, Romford, London, UKb
REFERENCES 1. Ohe S, Danno K, Sasaki H, Isei T, Okamoto H, Horio T. Treatment of acquired perforating dermatosis with narrowband ultraviolet B. J Am Acad Dermatol 2004;50:892-4. 2. Faver IR, Daoud MS, Su WP. Aquired reactive perforating collagenosis. J Am Acad Dermatol 1994;30:575-80. 3. Hurwitz RM. The evolution of perforating folliculitis in patients with chronic renal failure. Am J Dermatopathol 1985;7:219-31. 4. Bayramgu¨rler D, Apaydin R, Cetiner D, Zinciri C. Narrow-band ultraviolet B phototherapy for acquired perforating dermatosis. Australas J Dermatol 2003;44:76-8. 5. Satchell AC, Crotty K, Lee S. Reactive perforating collagenosis: a condition that may be underdiagnosed. Australas J Dermatol 2001;42:284-7. 6. Gambichler T, Breuckmann F, Boms S, Altmeyer P, Kreuter A. Narrowband UVB (TL-01) phototherapy in skin conditions beyond psoriasis. J Am Acad Dermatol (in press). doi:10.1016/j.jaad.2004.08.018
Macular arteritis in Japanese patients To the Editor: Recently, Fein et al1 reported 3 cases of a novel form of cutaneous arteritis presenting with hyperpigmented macules, termed macular arteritis.
We describe here two similar Japanese cases of macular arteritis.
CASE 1 A 49-year-old Japanese man visited our hospital for evaluation of a 4-year history of asymptomatic macules on his lower extremities. These skin lesions gradually spread over his buttocks and upper extremities. He was a heavy smoker, smoking 40 cigarettes daily for more than 30 years. He had multiple, 1 to 2 cm in diameter, round and reticular erythematous-brownish pigmented macules scattered over the lower extremities and buttocks (Fig 1, A), and diascopic examination did not affect the color of the skin lesions. The pigmented macules were nontender, but slightly indurated. Histopathologic examination of a pigmented macule on his thigh demonstrated that the epidermis and papillary dermis were unremarkable, but a marked perivascular lymphocytic infiltration was noted around a small artery in the subcutaneous fat. Hypertrophy of the tunica intima with fibrinoid necrosis and infiltration of lymphocytes around the adventitia were noted. There was a marked narrowing of the vessel lumen; however, no destruction of the tunica intima was noted by elastic tissue stain (Fig 1, B and C). There was no evidence of melanin pigment incontinence, deposition of hemosiderin, or leukocytoclastic vasculitis in the entire specimen. Deposition of neither immunoglobulins nor complement was detected by direct immunofluorescence. All laboratory tests including C-reactive protein (CRP), hepatitis serology, antinuclear antigens (ANA), CH50, antineutrophilic cytoplasmic antibody (ANCA), cryoproteins, and renal function were within the reference range. A kidney biopsy was obtained that was unremarkable. Over 5 years of follow-up, the patient’s disease is stable, and medication has not been needed. The patient remains in good condition.
CASE 2 A 52-year-old Japanese woman presented with a 4-month history of asymptomatic and hyperpigmented macules on her lower extremities that gradually increased in number. The patient has smoked approximately 20 cigarettes a day for 32 years. Physical examination was otherwise unremarkable except for the presence of multiple, 1 cm in diameter, asymptomatic, erythematousbrownish hyperpigmented macules over her lower and upper extremities symmetrically (Fig 2, A).
two patients suffering from APD, diabetes mellitus, and hypercholesterolemia who were treated with combination therapies, including NB-UVB. One patient did not respond to potent topical corticosteroids and hydroxyzine 25 mg daily and required NB-UVB to control APD. The other patient, having failed to respond to topical corticosteroids, oral antihistamines, and NB-UVB, required systemic treatment with acitretin. We present a 47-year-old female patient suffering from severely itching papules with a central plug surrounded by erythema on the upper limbs and back (Fig 1, A). Clinical presentation and histopathologic findings of two biopsy specimens were well consistent with the diagnosis of APD. We could exclude internal diseases such as diabetes mellitus, renal and liver dysfunction, and lymphoma. However, we found evidence for hypercholesterolemia and atopic diathesis in our patient. On an inpatient basis, NB-UVB was initiated 5 times weekly for a fortnight. Then she continued as an outpatient a thrice weekly NB-UVB schedule for another 4 weeks (skin type I; initial dose: 0.1 J/cm2; maximum dose 0.6 J/cm2; cumulative dose: 12 J/cm2). Concomitant therapy was restricted to the use of 3% urea and 2% polidocanol containing moisturisers. After 6 weeks of treatment, the patient reported relief of pruritus accompanied by significant reduction of skin lesions (Fig 1, B). A 3-month follow-up period did not reveal recurrence of her skin disease. APD is an uncommon reactive skin condition usually associated with internal diseases such as diabetes mellitus and chronic renal failure. The disease is characterized by itchy keratotic umbilicated papules showing elimination of necrotic basophil collagen tissue in histologic examination. APD is difficult to treat. Nevertheless, spontaneous
Fig 1. APD on the upper back before (A) and after (B) NB-UVB phototherapy. J AM ACAD DERMATOL
FEBRUARY 2005 363
364 Letters
J AM ACAD DERMATOL FEBRUARY 2005
resolution is not infrequently observed.2 Apart from anti-proliferative and anti-inflammatory effects, NBUVB seems to be particularly effective in relief of pruritus, which may play the key role in the pathogenesis of APD.6 If the patient is protected from scratching and the underlying disorder is controlled, APD generally improves.2 Most APD patients treated with NB-UVB had concomitant active therapies such as potent topical corticosteroids and antihistamines.1,4,5 It is therefore impossible to draw definitive conclusions from the aforementioned case observations whether NB-UVB monotherapy of APD would be effective as well. Because APD is a relatively rare disease, one has to fall back upon therapeutic experiences obtained from well-described case reports and small trials. To exclude, however, a bias of results caused by concomitant topical therapies or spontaneous resolution, half-side comparison trials would be very useful in this condition. In conclusion, NB-UVB appears to be an effective adjuvant phototherapeutic regimen for patients with APD. There is no evidence, however, that NB-UVB should be preferred to conventional UVB in the management of APD. Thilo Gambichler, MDa,b Peter Altmeyer, MDa Alexander Kreuter, MDa Department of Dermatology Ruhr-University Bochum, Bochum, Germanya Department of Dermatology Oldchurch Hospital, Romford, London, UKb
REFERENCES 1. Ohe S, Danno K, Sasaki H, Isei T, Okamoto H, Horio T. Treatment of acquired perforating dermatosis with narrowband ultraviolet B. J Am Acad Dermatol 2004;50:892-4. 2. Faver IR, Daoud MS, Su WP. Aquired reactive perforating collagenosis. J Am Acad Dermatol 1994;30:575-80. 3. Hurwitz RM. The evolution of perforating folliculitis in patients with chronic renal failure. Am J Dermatopathol 1985;7:219-31. 4. Bayramgu¨rler D, Apaydin R, Cetiner D, Zinciri C. Narrow-band ultraviolet B phototherapy for acquired perforating dermatosis. Australas J Dermatol 2003;44:76-8. 5. Satchell AC, Crotty K, Lee S. Reactive perforating collagenosis: a condition that may be underdiagnosed. Australas J Dermatol 2001;42:284-7. 6. Gambichler T, Breuckmann F, Boms S, Altmeyer P, Kreuter A. Narrowband UVB (TL-01) phototherapy in skin conditions beyond psoriasis. J Am Acad Dermatol (in press). doi:10.1016/j.jaad.2004.08.018
Macular arteritis in Japanese patients To the Editor: Recently, Fein et al1 reported 3 cases of a novel form of cutaneous arteritis presenting with hyperpigmented macules, termed macular arteritis.
We describe here two similar Japanese cases of macular arteritis.
CASE 1 A 49-year-old Japanese man visited our hospital for evaluation of a 4-year history of asymptomatic macules on his lower extremities. These skin lesions gradually spread over his buttocks and upper extremities. He was a heavy smoker, smoking 40 cigarettes daily for more than 30 years. He had multiple, 1 to 2 cm in diameter, round and reticular erythematous-brownish pigmented macules scattered over the lower extremities and buttocks (Fig 1, A), and diascopic examination did not affect the color of the skin lesions. The pigmented macules were nontender, but slightly indurated. Histopathologic examination of a pigmented macule on his thigh demonstrated that the epidermis and papillary dermis were unremarkable, but a marked perivascular lymphocytic infiltration was noted around a small artery in the subcutaneous fat. Hypertrophy of the tunica intima with fibrinoid necrosis and infiltration of lymphocytes around the adventitia were noted. There was a marked narrowing of the vessel lumen; however, no destruction of the tunica intima was noted by elastic tissue stain (Fig 1, B and C). There was no evidence of melanin pigment incontinence, deposition of hemosiderin, or leukocytoclastic vasculitis in the entire specimen. Deposition of neither immunoglobulins nor complement was detected by direct immunofluorescence. All laboratory tests including C-reactive protein (CRP), hepatitis serology, antinuclear antigens (ANA), CH50, antineutrophilic cytoplasmic antibody (ANCA), cryoproteins, and renal function were within the reference range. A kidney biopsy was obtained that was unremarkable. Over 5 years of follow-up, the patient’s disease is stable, and medication has not been needed. The patient remains in good condition.
CASE 2 A 52-year-old Japanese woman presented with a 4-month history of asymptomatic and hyperpigmented macules on her lower extremities that gradually increased in number. The patient has smoked approximately 20 cigarettes a day for 32 years. Physical examination was otherwise unremarkable except for the presence of multiple, 1 cm in diameter, asymptomatic, erythematousbrownish hyperpigmented macules over her lower and upper extremities symmetrically (Fig 2, A).