I
I
II
Eosinophilic pustular folliculitis Deborah L. Moritz, MD, and Craig A. Elmets, MD Cleveland, Ohio Eosinophilic pustular folliculitis is characterized by the spontaneous development of recurrent, sterile papules, pustules, and plaques on the face, think, arms, and occasionally the palms and soles. Although the large majority of the reported cases have occurred in Eastern Asians, most patients in the United States have been infants or men seropositive for human immunodefieiency virus. We describe a North American woman with eosinophilic pustular folliculitis who was neither seropositive for human immunodefieiencyvirus nor of Asiatic descent. (J AM ACADDERMATOL1991;24:903-7.) Eosinophilic pustular folliculitis was originally described in three Japanese men by Ofuji et al. 1 in 1970. The disease is characterized by recurrent clusters of pruritic, follicular, sterile papules and pustules that gradually extend peripherally and that have a tendency toward central clearing. Lesions in Asians resolve with slight hyperpigrnentation, but pigmentary changes may be absent in white persons. Sites of predilection include the face, back, and extensor surfaces of the upper extremities. Peripheral blood eosinophilia is present in approximately 50% of patients. 2 Histologically, the major distinguishing feature is abundant eosinophils that invade sebaceous glands and outer root sheaths of hair follicles. This is accompanied by nuclear fragments, a derrnal perivascular infiltrate composed predominantly of eosinophils, and eosinophilic spongiosis, which at times can lead to intraepidermal microabscess formation) More than 90% of reported cases of eosinophilic pustular folliculitis have been from Japan. In a review of the 72 cases reported before 1986, Takem a t s u et al. 4 noted that more than 80% of patients were men and that the peak incidence of the disease was in the third to fourth decade of life. In that population the disease had a chronic course with exacerbations and remissions. 4 The disease had been considered rare outside of Asia, but there have been
scattered reports of eosinophilic pustular foUiculitis in Europe 59 and in North America. 1~ In the United States 9 of the 13 cases in adults have been in homosexual men with an underlying human immunodeficiency virus (HIV) infection. Two thirds of these patients had Pneumocystis carinii pneumonia, and one third had Kaposi's sarcoma. 15,16 Of the four remaining patients, three were men and only one was a woman. 1~ s HIV testing was not reported in any of these persons. The course of eosinophilic pustular folliculitis in patients with acquired immunodeficiency syndrome (AIDS) differs from that originally described in Japanese patients. The disease is chronic and persistent rather than exacerbating and remitting. Moreover, the tendency for unusual clinical presentations is greater. Of the nine patients with AIDS reported, one had predominantly nonfollicular erythematous papules on the face, trunk, and thighs, with some tendency toward confluence into plaques; one had urticaria; and one had large, slightly elevated plaques restricted to the buttocks. The histologic features in each of these cases, however, were consistent with eosinophilie pustular folliculitis. 15,16 In this report we describe a woman with eosinophilic pustular folliculitis who was HIV negative, had no known risk factors for HIV infection, and was not of Asiatic descent.
CASE REPORT From the Immunodermatology Service, Department of Dermatology, Case Western Reserve University,UniversityHospitalsof Cleveland. Presented at The American Academy of Dermatology Gross and Microscopic Dermatology Symlmsium, Dec. 2, 1989. Reprint requests: Deborah Moritz, MD, Department of Dermatology, University Hospitals of Cleveland, 2074 Abington Rd., Cleveland, OH 44106. 16/4/22219
A 41-year-old white woman had a &month history of recurrent pruritic papules on the arms and face. The disease resolved spontaneously. Three months before her initial clinic visit, new erythematous, indurated papules, nodules, and pustules developed on the cheeks, temples, and forehead. The lesions were persistent and somewhat painful and gradually increased in number. Treatment with emollient creams worsened the disease, but exposure 9O3
904
Moritz and Elmets
Journal of the American Academy of Dermatology
Fig. 1. A and B, Indurated pustules, papules, and nodules on cheeks and forehead before therapy.
Fig. 2. A and B, Diffuse infiltration of hair follicles predominantly by eosinophils. (Hematoxylin-eosin stain; A, x40; B, X 100.) to sunlight had no appreciable effect. The patient denied fever or risk factors for HIV infection. She had no history of exposure to medications, toxins, or heavy metals. She had no Eastern Asian relatives and had not traveled outside the United States. Her medical and family histories were otherwise noncontributory. Examination revealed numerous, deep, indurated pus-
tules, papules, and nodules with oozing and crusting on the cheeks and forehead. The patient was initially treated with systemic erythromycin, topical clindamycin solution, and compresses. The crusting improved during 2 weeks, but the papulopustules became more confluent and remained erythematous and indurated (Fig. 1). A 2 mm punch biopsy specimen was obtained from the
Volume 24 Number 5, Part 2 May 1991
Eosinophilic pustular folliculitis
905
Fig. 3. A and B, Complete resolution with minimal postinflammatory changes after intralesional triamcinalone acetonide and topical hydrocortisone butyrate cream.
left cheek. Eosinophilic spongiosis of the epidermis and a diffuse infiltration of hair follicles composed predominantly of eosinophils were present. The underlying dermis had a mixed inflammatory infiltrate of lyrnphocytes, histiocytes, and abundant eosinophils (Fig. 2). Flame figures were not present nor were any abnormalities of endothelial cells detected. No fungal elements were present. These findings were considered diagnostic of eosinophilic pustular folliculitis. Bacterial, fungal, and acid-fast bacilli cultures of the skin obtained before antibiotic therapy were negative. A complete blood cell count showed 7100/ml leukocytes with 58% neutrophils, 27% lymphocytes, 8% monoeytes, 6% eosinophils, and 1% basophils. Serum for HIV antibody was negative both by enzyme-linked immunosorbent assay and by Western blot. The patient was treated with 0.1% hydrocortisone butyrate (Locoid) cream and two intralesional injections of triamcinolone acetonide (5 mg/ml), with gradual, complete resolution of her lesions (Fig. 3). DISCUSSION The spectrum of eosinophilic pustular folliculitis has expanded since its initial description in 1970. Involvement of the palms and soles has been reported and has been the initial site of presentation in approximately 25% of patients. 17 Because the palms and soles lack hair follicles, some authors have suggested that the disease be renamed "sterile eosinophilic pustulosis''~8 or "eosinophilic pustular der-
matosis."19 Recently, five infants with this condition were described by Lucky et al. 19 In contrast to the adult cases, the scalp was the primary area of involvement, with lesser involvement of the trunk. Finally, the disease is becoming increasingly recognized in association with HIV infections) 4t6 We believe that the clinical and histologic features of our patient fit within the spectrum of the Japanese form of eosinophilic pustular folliculitis. At one point the disease remitted spontaneously, consistent with the natural history of the disease as described by Ofuji. 2 The unusual feature is that our patient is only the second woman reported to have eosinophilic pustular folliculitis in the United States and was HIV seronegative. The etiology of eosinophilic pustular folliculitis remains obscure. The disease affects the pilosebaceous follicles above the entry of the sebaceous duct yet spares the lower part of the outer root sheath below the level of entry of the sebaceous duct. Because this is also a histopathologic feature of erythema toxicum neonatorum, a disease in which there are increased levels of skin surface lipids, sebaceous gland activity has been postulated by some to be an etiologic factor. 2, 4 Takematsu and Tagami 2~ have found lipid-soluble eosinophil chemotactic factors in skin surface lipids and in scale extracts of palmoplantar lesions of eosinophilic pustular folliculitis.
906
Journal of the American Academy of Dermatology
Moritz and Elmets
Table I. Classification of ecsinophilic folliculitis Ch~ieal (Japanese)
Sex
Age Clinical manifestations
Distribution of lesions Course Immunologic abnormalities Treatment
Males more than females Third to fourth decade Sterile follicular pustules and papules with peripheral extension and central clearing; resolution with slight hyperpigmentation Face, trunk, extensor surfaces of arms, palms and soles Recurrent excerbations and remissions None Systemic or intralesional corticosteroids, dapsone, indomethatin
Skin surface lipids have not been measured in patients with AIDS; however, there is a high prevalence of seborrheic dermatitis, which in certain circumstances has been associated with elevated sebum secretion rates. Thus increased levels of skin surface lipids m a y play a role in AIDS-associated eosinophilic pustular folliculitis as well. Although clarification of the nature of these lipid-soluble chemotactic factors awaits further studies, it is interesting that indomethacin has been used to successfully treat a patient with eosinophilic pustular folliculitis. 21 This suggests that a prostaglandin or one of its metabolites is the eosinophilic chemotactic factor responsible. Although eosinophilic pustular folliculitis has been associated with A I D S and A I D S is primarily a disease of deficient cell-mediated immunity, most studies of eosinophilic pustular folliculitis have focused on humoral alterations. A positive IgE radioallergosorbent test to the dust mite Dermatophagoides pteronyssimus, 6 a circulating autoantibody against the intercellular substance of the lower epidermis, 9 and high titers of circulating IgG and I g M directed against the cytoplasm of the basal cells of epidermis and the outer sheath of hair follicles 8
l-llV-rehated
Homosexual males Any Similar to Japanese variant; frequent atypical clinical presentations (nonfollicular erythematous papules, urticarial or large erythematous plaques Face, trunk, thighs, buttocks Chronic and persistent Deficient cell-mediated immunity UVB
Infantile
Males more than females First yr of life; may be congenital Sterile papules and pustules over the scalp with crusting; scattered clusters of pustules over the trunk or extremities Scalp, trunk; extremities less frequently Recurrent exacerbations and remissions Immunoglobulin deficiencies; WBC abnormalities High-potency topical steroids
have been identified in individual patients with eosinophilic pustular folliculitis. Of the five infants reported by Lucky et al., 19 one had low levels of IgG and IgA with high levels of I g M and another had a defect in white blood cell motility. Our patient improved after treatment with topical corticosteroids and intralesional injections of triamcinolone. Whether this represents a true response or a remission is uncertain, because lesions can spontaneously resolve. Trials with dapsone, systemic and/or topical corticosteroids, or a combination of the two have shown variable results. 1,2,7-14,16 Other treatment modalities reported as effective include indomethacin, zl oxyphenbutazone, sulfapuridine, aspirin, and colchicine. 2 Antibiotics are usually ineffective.2, 6-s, 10The treatment of eosinophilic pustular folliculitis in patients with AIDS has been difficult. 15,16 Buchness et al. 15 however, recently treated six patients with AIDS and eosinophilie pustular foUiculitis with UVB phototherapy. In all patients pruritus improved. Some patients also had resolution of their lesions, although the lesions recurred if phototherapy was discontinuedJ 5 On the basis of the clinical findings, course, and susceptible patient population, we propose that pa-
Volume 24 Number 5, Part 2 May 1991
tients with eosinophilic pustular foUiculitis be subclassified as either the classic (Japanese), HIVrelated, or infantile form of the disease (Table I). W h e t h e r each o f these forms of eosinophilic pustular foUiculitis represents a distinct clinical entity or different manifestations of the same disease awaits further elucidation of the pathogenesis. REFERENCES 1. OfujiS, Ogino A, Horio T, et al. Eosiaophiliepustular folliculitis. Acta Derm Venereol (Stockh) 1970;50:195-203. 2. Ofuji S. Eosinophilic pustular follieulitis. Dermatologica 1987;174:53-6. 3. Lever WF, Schaumburg-Lever G. Histopathology of the skin. 6th ed. Philadelphia: JB Lippincott Co, 1983:201. 4. Takematsu H, Nakamura K, Igarashi M, et al. Eosinophilic pustular folliculitis:report of two casesand reviewof the Japanese literature. Arch Dermatol 1985;121:917-20. 5. Camacho-Martinez F. Eosinophilic pustular folliculitis [Letter]. J AM ACADDEP,MATOL1987;17:686-8. 6. Cutler TP. Eosinophilicpustular folliculitis.Clin Exp Dermatol 1981;6:327-32. 7. Hoist R. Eosinophilic pustular folliculitis. Br J Dermatol 1976;95:661-4. 8. Nunzi E, Parodi A, Rebora A. Ofuji's disease: high circulating titers of IgG and IgM directed to basal cell cytoplasm. J AM ACADDERMATOL1985;12:268-73. 9. Vakilzadeh F, Suter L, Knop J, et al. Eosinophilicpustulosis with pemphigus-like antibody. Dermatologica 1981; 162:265-72.
Eosinophilic pustular folliculitis 907 10. Jaliman HD, Phelps RG, Fleischmajer R. Eosinophilie pustular folliculltis.J AM ACADDERMATOL1986;14:47982. 11. Dinehart SM, Noppakun N, Solomon AR. Eosinophilic pustular folliculitis.2 AM ACADDE~A:roL 1986;14:475-9. 12. Steffen C. Eosinophilicpustular.follieulitis (Ofuji's disease) with response to dapsone therapy. Arch Dermatol 1985; 121:921-3. 13. Colton AS, Schaclmer L, Kowalczyk AP. Eosinophilic pustular folliculitis.J AM ACADDEgMATOL1986;14:46974. 14. Jenkins D Jr, Fisher BK, Chalvardjian A, et al. Eosinophilic pustular folliculitisin a patient with AIDS. Int J Dermatol 1988;27:34-5. 15. Buchness MR, Lim HW, Hatcher VA, et al. Eosinophilie pustular foiliculitisin the acquired immunedefieiency syndrome. N Engl J Med 1988;318:1183-6. 16. Soeprono FF, Sehinella RA. Eosinophilie pustular follieulitis in patients with acquired immunodeficiencysyndrome. J AM ACADDERMATOL1986;14:1020-2. 17. Saruta T, Nakamizo Y. Eosinophilie pustular follieulitis: particularly with reference to lesions on the palm of the hand and sole of the foot. J Dermatol 1980;7:239-46. 18. Orfanos CE, Sterry W. Sterile eosinophile pustulose. Dermatologica 1978;157:193-205. 19. Lucky AW, Esterly NB, Heskel N, et al. Eesinophilir pustular folliculitisin infancy. Pediatr Dermatol 1984;1:202-6. 20. Takematsu H, Tagami H. Eosinophilicpustular folliculitis: studies on possible chemotactic factors involvedin the formation of pustules. Br J Dermatol 1986;114:209-15. 21. Miyauehi T, Fujigaki H, Uehara M, et al. Effect of indomethacin on eosinophilicpustular folliculitis.Acta Dermatol Kyoto 1985;80:9-14.
I
II
Eosinophilic pustular folliculitis Deborah L. Moritz, MD, and Craig A. Elmets, MD Cleveland, Ohio Eosinophilic pustular folliculitis is characterized by the spontaneous development of recurrent, sterile papules, pustules, and plaques on the face, think, arms, and occasionally the palms and soles. Although the large majority of the reported cases have occurred in Eastern Asians, most patients in the United States have been infants or men seropositive for human immunodefieiency virus. We describe a North American woman with eosinophilic pustular folliculitis who was neither seropositive for human immunodefieiencyvirus nor of Asiatic descent. (J AM ACADDERMATOL1991;24:903-7.) Eosinophilic pustular folliculitis was originally described in three Japanese men by Ofuji et al. 1 in 1970. The disease is characterized by recurrent clusters of pruritic, follicular, sterile papules and pustules that gradually extend peripherally and that have a tendency toward central clearing. Lesions in Asians resolve with slight hyperpigrnentation, but pigmentary changes may be absent in white persons. Sites of predilection include the face, back, and extensor surfaces of the upper extremities. Peripheral blood eosinophilia is present in approximately 50% of patients. 2 Histologically, the major distinguishing feature is abundant eosinophils that invade sebaceous glands and outer root sheaths of hair follicles. This is accompanied by nuclear fragments, a derrnal perivascular infiltrate composed predominantly of eosinophils, and eosinophilic spongiosis, which at times can lead to intraepidermal microabscess formation) More than 90% of reported cases of eosinophilic pustular folliculitis have been from Japan. In a review of the 72 cases reported before 1986, Takem a t s u et al. 4 noted that more than 80% of patients were men and that the peak incidence of the disease was in the third to fourth decade of life. In that population the disease had a chronic course with exacerbations and remissions. 4 The disease had been considered rare outside of Asia, but there have been
scattered reports of eosinophilic pustular foUiculitis in Europe 59 and in North America. 1~ In the United States 9 of the 13 cases in adults have been in homosexual men with an underlying human immunodeficiency virus (HIV) infection. Two thirds of these patients had Pneumocystis carinii pneumonia, and one third had Kaposi's sarcoma. 15,16 Of the four remaining patients, three were men and only one was a woman. 1~ s HIV testing was not reported in any of these persons. The course of eosinophilic pustular folliculitis in patients with acquired immunodeficiency syndrome (AIDS) differs from that originally described in Japanese patients. The disease is chronic and persistent rather than exacerbating and remitting. Moreover, the tendency for unusual clinical presentations is greater. Of the nine patients with AIDS reported, one had predominantly nonfollicular erythematous papules on the face, trunk, and thighs, with some tendency toward confluence into plaques; one had urticaria; and one had large, slightly elevated plaques restricted to the buttocks. The histologic features in each of these cases, however, were consistent with eosinophilie pustular folliculitis. 15,16 In this report we describe a woman with eosinophilic pustular folliculitis who was HIV negative, had no known risk factors for HIV infection, and was not of Asiatic descent.
CASE REPORT From the Immunodermatology Service, Department of Dermatology, Case Western Reserve University,UniversityHospitalsof Cleveland. Presented at The American Academy of Dermatology Gross and Microscopic Dermatology Symlmsium, Dec. 2, 1989. Reprint requests: Deborah Moritz, MD, Department of Dermatology, University Hospitals of Cleveland, 2074 Abington Rd., Cleveland, OH 44106. 16/4/22219
A 41-year-old white woman had a &month history of recurrent pruritic papules on the arms and face. The disease resolved spontaneously. Three months before her initial clinic visit, new erythematous, indurated papules, nodules, and pustules developed on the cheeks, temples, and forehead. The lesions were persistent and somewhat painful and gradually increased in number. Treatment with emollient creams worsened the disease, but exposure 9O3
904
Moritz and Elmets
Journal of the American Academy of Dermatology
Fig. 1. A and B, Indurated pustules, papules, and nodules on cheeks and forehead before therapy.
Fig. 2. A and B, Diffuse infiltration of hair follicles predominantly by eosinophils. (Hematoxylin-eosin stain; A, x40; B, X 100.) to sunlight had no appreciable effect. The patient denied fever or risk factors for HIV infection. She had no history of exposure to medications, toxins, or heavy metals. She had no Eastern Asian relatives and had not traveled outside the United States. Her medical and family histories were otherwise noncontributory. Examination revealed numerous, deep, indurated pus-
tules, papules, and nodules with oozing and crusting on the cheeks and forehead. The patient was initially treated with systemic erythromycin, topical clindamycin solution, and compresses. The crusting improved during 2 weeks, but the papulopustules became more confluent and remained erythematous and indurated (Fig. 1). A 2 mm punch biopsy specimen was obtained from the
Volume 24 Number 5, Part 2 May 1991
Eosinophilic pustular folliculitis
905
Fig. 3. A and B, Complete resolution with minimal postinflammatory changes after intralesional triamcinalone acetonide and topical hydrocortisone butyrate cream.
left cheek. Eosinophilic spongiosis of the epidermis and a diffuse infiltration of hair follicles composed predominantly of eosinophils were present. The underlying dermis had a mixed inflammatory infiltrate of lyrnphocytes, histiocytes, and abundant eosinophils (Fig. 2). Flame figures were not present nor were any abnormalities of endothelial cells detected. No fungal elements were present. These findings were considered diagnostic of eosinophilic pustular folliculitis. Bacterial, fungal, and acid-fast bacilli cultures of the skin obtained before antibiotic therapy were negative. A complete blood cell count showed 7100/ml leukocytes with 58% neutrophils, 27% lymphocytes, 8% monoeytes, 6% eosinophils, and 1% basophils. Serum for HIV antibody was negative both by enzyme-linked immunosorbent assay and by Western blot. The patient was treated with 0.1% hydrocortisone butyrate (Locoid) cream and two intralesional injections of triamcinolone acetonide (5 mg/ml), with gradual, complete resolution of her lesions (Fig. 3). DISCUSSION The spectrum of eosinophilic pustular folliculitis has expanded since its initial description in 1970. Involvement of the palms and soles has been reported and has been the initial site of presentation in approximately 25% of patients. 17 Because the palms and soles lack hair follicles, some authors have suggested that the disease be renamed "sterile eosinophilic pustulosis''~8 or "eosinophilic pustular der-
matosis."19 Recently, five infants with this condition were described by Lucky et al. 19 In contrast to the adult cases, the scalp was the primary area of involvement, with lesser involvement of the trunk. Finally, the disease is becoming increasingly recognized in association with HIV infections) 4t6 We believe that the clinical and histologic features of our patient fit within the spectrum of the Japanese form of eosinophilic pustular folliculitis. At one point the disease remitted spontaneously, consistent with the natural history of the disease as described by Ofuji. 2 The unusual feature is that our patient is only the second woman reported to have eosinophilic pustular folliculitis in the United States and was HIV seronegative. The etiology of eosinophilic pustular folliculitis remains obscure. The disease affects the pilosebaceous follicles above the entry of the sebaceous duct yet spares the lower part of the outer root sheath below the level of entry of the sebaceous duct. Because this is also a histopathologic feature of erythema toxicum neonatorum, a disease in which there are increased levels of skin surface lipids, sebaceous gland activity has been postulated by some to be an etiologic factor. 2, 4 Takematsu and Tagami 2~ have found lipid-soluble eosinophil chemotactic factors in skin surface lipids and in scale extracts of palmoplantar lesions of eosinophilic pustular folliculitis.
906
Journal of the American Academy of Dermatology
Moritz and Elmets
Table I. Classification of ecsinophilic folliculitis Ch~ieal (Japanese)
Sex
Age Clinical manifestations
Distribution of lesions Course Immunologic abnormalities Treatment
Males more than females Third to fourth decade Sterile follicular pustules and papules with peripheral extension and central clearing; resolution with slight hyperpigmentation Face, trunk, extensor surfaces of arms, palms and soles Recurrent excerbations and remissions None Systemic or intralesional corticosteroids, dapsone, indomethatin
Skin surface lipids have not been measured in patients with AIDS; however, there is a high prevalence of seborrheic dermatitis, which in certain circumstances has been associated with elevated sebum secretion rates. Thus increased levels of skin surface lipids m a y play a role in AIDS-associated eosinophilic pustular folliculitis as well. Although clarification of the nature of these lipid-soluble chemotactic factors awaits further studies, it is interesting that indomethacin has been used to successfully treat a patient with eosinophilic pustular folliculitis. 21 This suggests that a prostaglandin or one of its metabolites is the eosinophilic chemotactic factor responsible. Although eosinophilic pustular folliculitis has been associated with A I D S and A I D S is primarily a disease of deficient cell-mediated immunity, most studies of eosinophilic pustular folliculitis have focused on humoral alterations. A positive IgE radioallergosorbent test to the dust mite Dermatophagoides pteronyssimus, 6 a circulating autoantibody against the intercellular substance of the lower epidermis, 9 and high titers of circulating IgG and I g M directed against the cytoplasm of the basal cells of epidermis and the outer sheath of hair follicles 8
l-llV-rehated
Homosexual males Any Similar to Japanese variant; frequent atypical clinical presentations (nonfollicular erythematous papules, urticarial or large erythematous plaques Face, trunk, thighs, buttocks Chronic and persistent Deficient cell-mediated immunity UVB
Infantile
Males more than females First yr of life; may be congenital Sterile papules and pustules over the scalp with crusting; scattered clusters of pustules over the trunk or extremities Scalp, trunk; extremities less frequently Recurrent exacerbations and remissions Immunoglobulin deficiencies; WBC abnormalities High-potency topical steroids
have been identified in individual patients with eosinophilic pustular folliculitis. Of the five infants reported by Lucky et al., 19 one had low levels of IgG and IgA with high levels of I g M and another had a defect in white blood cell motility. Our patient improved after treatment with topical corticosteroids and intralesional injections of triamcinolone. Whether this represents a true response or a remission is uncertain, because lesions can spontaneously resolve. Trials with dapsone, systemic and/or topical corticosteroids, or a combination of the two have shown variable results. 1,2,7-14,16 Other treatment modalities reported as effective include indomethacin, zl oxyphenbutazone, sulfapuridine, aspirin, and colchicine. 2 Antibiotics are usually ineffective.2, 6-s, 10The treatment of eosinophilic pustular folliculitis in patients with AIDS has been difficult. 15,16 Buchness et al. 15 however, recently treated six patients with AIDS and eosinophilie pustular foUiculitis with UVB phototherapy. In all patients pruritus improved. Some patients also had resolution of their lesions, although the lesions recurred if phototherapy was discontinuedJ 5 On the basis of the clinical findings, course, and susceptible patient population, we propose that pa-
Volume 24 Number 5, Part 2 May 1991
tients with eosinophilic pustular foUiculitis be subclassified as either the classic (Japanese), HIVrelated, or infantile form of the disease (Table I). W h e t h e r each o f these forms of eosinophilic pustular foUiculitis represents a distinct clinical entity or different manifestations of the same disease awaits further elucidation of the pathogenesis. REFERENCES 1. OfujiS, Ogino A, Horio T, et al. Eosiaophiliepustular folliculitis. Acta Derm Venereol (Stockh) 1970;50:195-203. 2. Ofuji S. Eosinophilic pustular follieulitis. Dermatologica 1987;174:53-6. 3. Lever WF, Schaumburg-Lever G. Histopathology of the skin. 6th ed. Philadelphia: JB Lippincott Co, 1983:201. 4. Takematsu H, Nakamura K, Igarashi M, et al. Eosinophilic pustular folliculitis:report of two casesand reviewof the Japanese literature. Arch Dermatol 1985;121:917-20. 5. Camacho-Martinez F. Eosinophilic pustular folliculitis [Letter]. J AM ACADDEP,MATOL1987;17:686-8. 6. Cutler TP. Eosinophilicpustular folliculitis.Clin Exp Dermatol 1981;6:327-32. 7. Hoist R. Eosinophilic pustular folliculitis. Br J Dermatol 1976;95:661-4. 8. Nunzi E, Parodi A, Rebora A. Ofuji's disease: high circulating titers of IgG and IgM directed to basal cell cytoplasm. J AM ACADDERMATOL1985;12:268-73. 9. Vakilzadeh F, Suter L, Knop J, et al. Eosinophilicpustulosis with pemphigus-like antibody. Dermatologica 1981; 162:265-72.
Eosinophilic pustular folliculitis 907 10. Jaliman HD, Phelps RG, Fleischmajer R. Eosinophilie pustular folliculltis.J AM ACADDERMATOL1986;14:47982. 11. Dinehart SM, Noppakun N, Solomon AR. Eosinophilic pustular folliculitis.2 AM ACADDE~A:roL 1986;14:475-9. 12. Steffen C. Eosinophilicpustular.follieulitis (Ofuji's disease) with response to dapsone therapy. Arch Dermatol 1985; 121:921-3. 13. Colton AS, Schaclmer L, Kowalczyk AP. Eosinophilic pustular folliculitis.J AM ACADDEgMATOL1986;14:46974. 14. Jenkins D Jr, Fisher BK, Chalvardjian A, et al. Eosinophilic pustular folliculitisin a patient with AIDS. Int J Dermatol 1988;27:34-5. 15. Buchness MR, Lim HW, Hatcher VA, et al. Eosinophilie pustular foiliculitisin the acquired immunedefieiency syndrome. N Engl J Med 1988;318:1183-6. 16. Soeprono FF, Sehinella RA. Eosinophilie pustular follieulitis in patients with acquired immunodeficiencysyndrome. J AM ACADDERMATOL1986;14:1020-2. 17. Saruta T, Nakamizo Y. Eosinophilie pustular follieulitis: particularly with reference to lesions on the palm of the hand and sole of the foot. J Dermatol 1980;7:239-46. 18. Orfanos CE, Sterry W. Sterile eosinophile pustulose. Dermatologica 1978;157:193-205. 19. Lucky AW, Esterly NB, Heskel N, et al. Eesinophilir pustular folliculitisin infancy. Pediatr Dermatol 1984;1:202-6. 20. Takematsu H, Tagami H. Eosinophilicpustular folliculitis: studies on possible chemotactic factors involvedin the formation of pustules. Br J Dermatol 1986;114:209-15. 21. Miyauehi T, Fujigaki H, Uehara M, et al. Effect of indomethacin on eosinophilicpustular folliculitis.Acta Dermatol Kyoto 1985;80:9-14.
