Case report
Hyperimmunoglobulin E syndrome presenting as eosinophilic pustular folliculitis: a case report Chi-Shou Lo1,2, MD, Chin-Yi Yang2,3, MD, Jui-Hung Ko2,3, MD, Wen-Yi Lee2,4, MD, PhD, I-Hsin Shih2,3, MD, and Yi-Chen Lin2,5, DDS
1 Department of Dermatology, Chang Gung Memorial Hospital, Keelung, Taiwan, 2 Chang Gung University College of Medicine, Taoyuan, Taiwan, 3Department of Dermatology, Chang Gung Memorial Hospital, Taipei, Taiwan, 4Department of Pediatrics, Chang Gung Memorial Hospital, Taipei, Taiwan, and 5Department of Dentistry, Chang Gung Memorial Hospital, Taipei, Taiwan
Correspondence Chin-Yi Yang, MD Department of Dermatology Chang Gung Memorial Hospital No. 199, Dunhua N. Rd., Songshan District, Taipei City 105, Taiwan, Republic of China E-mail: [email protected] Conflicts of interest: None. doi: 10.1111/ijd.12005
Introduction Hyperimmunoglobulin E syndrome (HIES) is a rare primary immunodeficiency disorder characterized by high serum IgE levels, eosinophilia, eczema, and recurrent cutaneous and sino-pulmonary infections.1 It was first described as Job’s syndrome in 1966 in two girls with recurrent skin abscesses, pneumonia, and chronic eczema.2 In 1972, hyperimmunoglobulin E syndrome (HIES) was named after the associated feature of greatly elevated serum IgE.3 Three genetic mutations of HIES have been found successively since 2006: tyrosinase kinase 2 (TYK2), signal transducer and activator of transcription 3 (STAT3), and dedicator of cytokinesis 8 (DOCK8).4 Skin findings of HIES similar to atopic dermatitis or eczema were described in previous literatures.2,5–7 Herein is a case of STAT3-mutated HIES manifesting with eosinophilic pustular folliculitis (EPF)-like symptoms. The cutaneous manifestations of HIES have also been reviewed. Case report An 11-year-old boy had sought a consultation for on and off itchy skin rashes on the face since the neonatal period. ª 2014 The International Society of Dermatology
He had a history of atopic dermatitis, recurrent respiratory tract infection, and otitis media since childhood and had been hospitalized many times due to recurrent pneumonia and gastroenteritis. At the age of 20 months, he had perforated ileocolitis with necrotizing fasciitis of the abdominal wall and underwent ileostomy, debridement, and split thickness skin grafting. Physical examination demonstrated multiple erythematous papules and tiny pustules with an erythematous base on the forehead and both cheeks (Figs. 1a and 2). Retention of primary teeth, funnel chest, and abdominal surgical scar were also noted. Skin biopsy taken from the cheek lesions showed basket weave hyperkeratosis, mild acanthosis, and numerous eosinophils and lymphocytes in the dermis, with infiltration into the pilosebaceous structures (Fig. 3). Histopathologic findings were similar to EPF. Complete blood cell count showed normal white blood cell count but elevated absolute eosinophil count at 1164/ mm3. Serum IgE level was also elevated to 45,900 IU/mL. Chest x-rays showed bronchiectasis of the right lower lung while the lumbosacral x-ray showed no scoliosis. Echocardiography revealed no abnormal findings. International Journal of Dermatology 2015, 54, 211–214
211
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Case report
HIES as eosinophilic pustular folliculitis
(a)
Lo et al.
(b)
(c)
Figure 1 Clinical photographs of the patient. (a) Multiple erythematous papules and tiny pustules with an erythematous base on the forehead and both cheeks. (b) The erythema subsided after 1 week of indomethacin and cyproheptadine treatment. (c) The rash nearly resolved after an additional 10 d of treatment with methylprednisolone
Under a strong suspicion of HIES, the STAT3 gene was analyzed by reverse transcription–polymerase chain reaction and sequencing. An autosomal dominant splicing mutation at intron 10 ( 2) A changing to G, leading to in-frame mutation located at the DNA-binding domain, was confirmed. Under the initial impression of EPF, the patient was initially treated with oral indomethacin 25 mg twice daily and cyproheptadine 4 mg twice daily for one week. The erythema of both cheeks improved, but the papulopustular lesions persisted (Fig. 1b). After adding oral methylprednisolone 4 mg/d for about 10 days, the skin rash significantly resolved (Fig. 1c). Prophylactic antibiotics with trimethoprim–sulfamethoxazole and fluconazole were initiated but discontinued due to complications of drug rash and severe diarrhea. After the skin rash improved, the patient was maintained on oral antihistamine and topical steroid treatment. Discussion HIES is a rare primary immunodeficiency disorder characterized by the classic triad of elevated IgE and eosinophilia, eczema, and recurrent cutaneous and
Figure 2 Closer view of skin rash on both cheeks International Journal of Dermatology 2015, 54, 211–214
pulmonary infection.1 Other clinical manifestations include pneumatocele, retention of primary teeth, scoliosis, joint hypermobility, frequent fracture of the long bones, and characteristic facies with increased nasal width and deep-set eyes.7 Before the discovery of associated genetic mutations of HIES, clinical diagnosis was based on the National Institutes of Health (NIH) scoring system that includes twenty-one related clinical and laboratory findings.8 Diagnosis of HIES is based on an NIH score of 40 points or higher.9 The score of the present case is fifty-seven points. The pathogenesis of HIES is related to defective Th17 differentiation and function,10 but the detailed mechanisms of cutaneous, skeletal, and immunologic defects remain unclear. Three genetic mutations have been found successively since 2006: TYK2 (signal transducer), STAT3, and dedicator of DOCK8. Mutation in STAT3 is the autosomal dominant form of HIES (AD-HIES), and mutations in the other two are autosomal recessive forms (AR-HIES). Each of these three mutations has distinct clinical manifestations. STAT3 mutation is associated with skeletal, connective tissue, and vascular abnormalities. TYK2 mutation is characterized with susceptibility to viral and non-tuberculous infections. Patients with DOCK8 mutation suffer from cutaneous viral infections and increased risk of malignancy.4 The current case is a sporadic case of STAT3 mutation due to the lack of family history. Skeletal abnormalities with retention of primary teeth and funnel chest are noted, but no connective tissue or vascular abnormalities have been found after the physical examination and imaging study. Skin manifestations are described as eczematous or atopic dermatitis-like appearance in previous literatures.2,5–7 However, the management and prognosis of HIES is different from that of eczematous or atopic dermatitis. Thus, it is very important to differentiate these ª 2014 The International Society of Dermatology
Lo et al.
HIES as eosinophilic pustular folliculitis
(a)
Case report
(b)
Figure 3 Histopathologic picture of the papulopustules on the cheeks. (a) Massive infiltration of inflammatory cells in the dermis and pilosebaceous structures. (b) The hair follicle was infiltrated by numerous eosinophils and lymphocytes. Hematoxylin and eosin, original magnification (a) 940; (b) 9400
diseases in the early period despite the absence of other distinctive features. Few reports have described papulopustular or vesicular eruptions in infancy or childhood in patients with HIES.11,12 Shirafuji et al.13 reported a 3year-old boy with HIES who developed itchy vesiculopapules on the face and scalp from the age of six months. Skin biopsy of a vesiculopapule on the face revealed eosinophil-rich infiltration involving hair follicles, similar to EPF. Chamlin et al.14 described eight children with HIES who presented with papulopustular eruptions on the face and scalp in the first year of life. The most consistent histopathologic findings from skin biopsy were eosinophilic spongiotic dermatitis. Two of the eight were initially diagnosed as having EPF based on skin biopsy. However, no objective criteria or genetic studies of HIES are confirmed in these studies. Eberting et al.6 suggested that a papulopustular eruption beginning in the neonatal period and involving the face, scalp, and neck is characteristic of HIES rather than of atopic dermatitis. A recent French study15 recruited twenty-one patients with STAT3 mutated AD-HIES and indicated that neonatal papulopustular rash followed by an impetiginized eczematous dermatitis is highly suggestive of AD-HIES. The skin presentation of our patient is consistent with this study result. To our knowledge, the present case is the first of HIES proven by the NIH scoring system and genetic studies (STAT3 mutation) manifesting with EPF clinically and histopathologically. We recognize this case as a type of EPF because both the clinical and pathological findings are consistent with the diagnosis of EPF. This case could be categorized as immunosuppression-associated EPF (ISEPF), which is related to immune dysfunction.16 Though IS-EPF is most commonly seen in patients with human immunodeficiency virus infection, IS-EPF has also been reported in other immunocompromised states, such as in patients with hematological malignancy after peripheral ª 2014 The International Society of Dermatology
blood stem cell or bone marrow transplantation.16,17 Our patient had been misdiagnosed as atopic dermatitis since infancy. This report highlights the importance of recognizing papulopustular eruptions in infants and children, especially those having other symptoms or distinctive features of HIES. In conclusion, HIES is a rare, multisystem disorder with cutaneous, immunologic, connective tissue, and skeletal abnormalities. Skin manifestations with papulopustular rash occur in early infancy. Earlier diagnosis leads to appropriate management and prevention of complications. References 1 Freeman AF, Holland SM. Clinical manifestations, etiology, and pathogenesis of the hyper-IgE syndrome. Pediatr Res 2009; 65: 32–37. 2 Davis SD, Schaller J, Wedgwood RJ. Jobs syndrome: recurrent cold staphylococcal abscesses. Lancet 1955; 1: 1013–1015. 3 Buckley RH, Wray BB, Belmaker EZ. Extreme hyperimmunoglobulinemia E and undue susceptibility to infection. Pediatrics 1972; 49: 59–70. 4 Freeman AF, Holland SM. Clinical manifestations of hyper IgE syndromes. Dis Markers 2010; 29: 123–130. 5 Hill HR, Quie PG. Raised serum-IgE levels and defective neutrophil chemotaxis in three children with eczema and recurrent bacterial infections. Lancet 1974; 1: 183–187. 6 Eberting CL, Davis J, Puck JM, et al. Dermatitis and the newborn rash of hyper-IgE syndrome. Arch Dermatol 2004; 140: 1119–1125. 7 DeWitt CA, Bishop AB, Buescher LS, et al. Hyperimmunoglobulin E syndrome: two cases and a review of the literature. J Am Acad Dermatol 2006; 54: 855–865. 8 Grimbacher B, Schaffer AA, Holland SM, et al. Genetic linkage of hyper-IgE syndrome to chromosome 4. Am J Hum Genet 1999; 65: 735–744. International Journal of Dermatology 2015, 54, 211–214
213
214
Case report
HIES as eosinophilic pustular folliculitis
9 Renner ED, Rylaarsdam S, Anover-Sombke S, et al. Novel signal transducer and activator of transcription 3 (STAT3) mutations, reduced T(H)17 cell numbers, and variably defective STAT3 phosphorylation in hyper-IgE syndrome. J Allergy Clin Immunol 2008; 122: 181–187. 10 Milner JD, Brenchley JM, Laurence A, et al. Impaired T(H)17 cell differentiation in subjects with autosomal dominant hyper-IgE syndrome. Nature 2008; 452: 773– 776. 11 Kamei R, Honig PJ. Neonatal Jobs syndrome featuring a vesicular eruption. Pediatr Dermatol 1988; 5: 75–82. 12 Blum R, Geller G, Fish LA. Recurrent severe staphylococcal infections, eczematoid rash, extreme elevations of IgE, eosinophilia, and divergent chemotactic responses in two generations. J Pediatr 1977; 90: 607–609.
International Journal of Dermatology 2015, 54, 211–214
Lo et al.
13 Shirafuji Y, Matsuura H, Sato A, et al. Hyperimmunoglobulin E syndrome: a sign of TH1/TH2 imbalance? Eur J Dermatol 1999; 9: 129–131. 14 Chamlin SL, McCalmont TH, Cunningham BB, et al. Cutaneous manifestations of hyper-IgE syndrome in infants and children. J Pediatr 2002; 141: 572–575. 15 Olaiwan A, Chandesris MO, Fraitag S, et al. Cutaneous findings in sporadic and familial autosomal dominant hyper-IgE syndrome: a retrospective, single-center study of 21 patients diagnosed using molecular analysis. J Am Acad Dermatol 2011; 65: 1167–1172. 16 Nervi SJ, Schwartz RA, Dmochowski M. Eosinophilic pustular folliculitis: a 40 year retrospect. J Am Acad Dermatol 2006; 55: 285–299. 17 Fraser SJ, Benton EC, Roddie PH, et al. Eosinophilic folliculitis: an important differential diagnosis after allogeneic bone-marrow transplant. Clin Exp Dermatol 2009; 34: 369–371.
ª 2014 The International Society of Dermatology
Hyperimmunoglobulin E syndrome presenting as eosinophilic pustular folliculitis: a case report Chi-Shou Lo1,2, MD, Chin-Yi Yang2,3, MD, Jui-Hung Ko2,3, MD, Wen-Yi Lee2,4, MD, PhD, I-Hsin Shih2,3, MD, and Yi-Chen Lin2,5, DDS
1 Department of Dermatology, Chang Gung Memorial Hospital, Keelung, Taiwan, 2 Chang Gung University College of Medicine, Taoyuan, Taiwan, 3Department of Dermatology, Chang Gung Memorial Hospital, Taipei, Taiwan, 4Department of Pediatrics, Chang Gung Memorial Hospital, Taipei, Taiwan, and 5Department of Dentistry, Chang Gung Memorial Hospital, Taipei, Taiwan
Correspondence Chin-Yi Yang, MD Department of Dermatology Chang Gung Memorial Hospital No. 199, Dunhua N. Rd., Songshan District, Taipei City 105, Taiwan, Republic of China E-mail: [email protected] Conflicts of interest: None. doi: 10.1111/ijd.12005
Introduction Hyperimmunoglobulin E syndrome (HIES) is a rare primary immunodeficiency disorder characterized by high serum IgE levels, eosinophilia, eczema, and recurrent cutaneous and sino-pulmonary infections.1 It was first described as Job’s syndrome in 1966 in two girls with recurrent skin abscesses, pneumonia, and chronic eczema.2 In 1972, hyperimmunoglobulin E syndrome (HIES) was named after the associated feature of greatly elevated serum IgE.3 Three genetic mutations of HIES have been found successively since 2006: tyrosinase kinase 2 (TYK2), signal transducer and activator of transcription 3 (STAT3), and dedicator of cytokinesis 8 (DOCK8).4 Skin findings of HIES similar to atopic dermatitis or eczema were described in previous literatures.2,5–7 Herein is a case of STAT3-mutated HIES manifesting with eosinophilic pustular folliculitis (EPF)-like symptoms. The cutaneous manifestations of HIES have also been reviewed. Case report An 11-year-old boy had sought a consultation for on and off itchy skin rashes on the face since the neonatal period. ª 2014 The International Society of Dermatology
He had a history of atopic dermatitis, recurrent respiratory tract infection, and otitis media since childhood and had been hospitalized many times due to recurrent pneumonia and gastroenteritis. At the age of 20 months, he had perforated ileocolitis with necrotizing fasciitis of the abdominal wall and underwent ileostomy, debridement, and split thickness skin grafting. Physical examination demonstrated multiple erythematous papules and tiny pustules with an erythematous base on the forehead and both cheeks (Figs. 1a and 2). Retention of primary teeth, funnel chest, and abdominal surgical scar were also noted. Skin biopsy taken from the cheek lesions showed basket weave hyperkeratosis, mild acanthosis, and numerous eosinophils and lymphocytes in the dermis, with infiltration into the pilosebaceous structures (Fig. 3). Histopathologic findings were similar to EPF. Complete blood cell count showed normal white blood cell count but elevated absolute eosinophil count at 1164/ mm3. Serum IgE level was also elevated to 45,900 IU/mL. Chest x-rays showed bronchiectasis of the right lower lung while the lumbosacral x-ray showed no scoliosis. Echocardiography revealed no abnormal findings. International Journal of Dermatology 2015, 54, 211–214
211
212
Case report
HIES as eosinophilic pustular folliculitis
(a)
Lo et al.
(b)
(c)
Figure 1 Clinical photographs of the patient. (a) Multiple erythematous papules and tiny pustules with an erythematous base on the forehead and both cheeks. (b) The erythema subsided after 1 week of indomethacin and cyproheptadine treatment. (c) The rash nearly resolved after an additional 10 d of treatment with methylprednisolone
Under a strong suspicion of HIES, the STAT3 gene was analyzed by reverse transcription–polymerase chain reaction and sequencing. An autosomal dominant splicing mutation at intron 10 ( 2) A changing to G, leading to in-frame mutation located at the DNA-binding domain, was confirmed. Under the initial impression of EPF, the patient was initially treated with oral indomethacin 25 mg twice daily and cyproheptadine 4 mg twice daily for one week. The erythema of both cheeks improved, but the papulopustular lesions persisted (Fig. 1b). After adding oral methylprednisolone 4 mg/d for about 10 days, the skin rash significantly resolved (Fig. 1c). Prophylactic antibiotics with trimethoprim–sulfamethoxazole and fluconazole were initiated but discontinued due to complications of drug rash and severe diarrhea. After the skin rash improved, the patient was maintained on oral antihistamine and topical steroid treatment. Discussion HIES is a rare primary immunodeficiency disorder characterized by the classic triad of elevated IgE and eosinophilia, eczema, and recurrent cutaneous and
Figure 2 Closer view of skin rash on both cheeks International Journal of Dermatology 2015, 54, 211–214
pulmonary infection.1 Other clinical manifestations include pneumatocele, retention of primary teeth, scoliosis, joint hypermobility, frequent fracture of the long bones, and characteristic facies with increased nasal width and deep-set eyes.7 Before the discovery of associated genetic mutations of HIES, clinical diagnosis was based on the National Institutes of Health (NIH) scoring system that includes twenty-one related clinical and laboratory findings.8 Diagnosis of HIES is based on an NIH score of 40 points or higher.9 The score of the present case is fifty-seven points. The pathogenesis of HIES is related to defective Th17 differentiation and function,10 but the detailed mechanisms of cutaneous, skeletal, and immunologic defects remain unclear. Three genetic mutations have been found successively since 2006: TYK2 (signal transducer), STAT3, and dedicator of DOCK8. Mutation in STAT3 is the autosomal dominant form of HIES (AD-HIES), and mutations in the other two are autosomal recessive forms (AR-HIES). Each of these three mutations has distinct clinical manifestations. STAT3 mutation is associated with skeletal, connective tissue, and vascular abnormalities. TYK2 mutation is characterized with susceptibility to viral and non-tuberculous infections. Patients with DOCK8 mutation suffer from cutaneous viral infections and increased risk of malignancy.4 The current case is a sporadic case of STAT3 mutation due to the lack of family history. Skeletal abnormalities with retention of primary teeth and funnel chest are noted, but no connective tissue or vascular abnormalities have been found after the physical examination and imaging study. Skin manifestations are described as eczematous or atopic dermatitis-like appearance in previous literatures.2,5–7 However, the management and prognosis of HIES is different from that of eczematous or atopic dermatitis. Thus, it is very important to differentiate these ª 2014 The International Society of Dermatology
Lo et al.
HIES as eosinophilic pustular folliculitis
(a)
Case report
(b)
Figure 3 Histopathologic picture of the papulopustules on the cheeks. (a) Massive infiltration of inflammatory cells in the dermis and pilosebaceous structures. (b) The hair follicle was infiltrated by numerous eosinophils and lymphocytes. Hematoxylin and eosin, original magnification (a) 940; (b) 9400
diseases in the early period despite the absence of other distinctive features. Few reports have described papulopustular or vesicular eruptions in infancy or childhood in patients with HIES.11,12 Shirafuji et al.13 reported a 3year-old boy with HIES who developed itchy vesiculopapules on the face and scalp from the age of six months. Skin biopsy of a vesiculopapule on the face revealed eosinophil-rich infiltration involving hair follicles, similar to EPF. Chamlin et al.14 described eight children with HIES who presented with papulopustular eruptions on the face and scalp in the first year of life. The most consistent histopathologic findings from skin biopsy were eosinophilic spongiotic dermatitis. Two of the eight were initially diagnosed as having EPF based on skin biopsy. However, no objective criteria or genetic studies of HIES are confirmed in these studies. Eberting et al.6 suggested that a papulopustular eruption beginning in the neonatal period and involving the face, scalp, and neck is characteristic of HIES rather than of atopic dermatitis. A recent French study15 recruited twenty-one patients with STAT3 mutated AD-HIES and indicated that neonatal papulopustular rash followed by an impetiginized eczematous dermatitis is highly suggestive of AD-HIES. The skin presentation of our patient is consistent with this study result. To our knowledge, the present case is the first of HIES proven by the NIH scoring system and genetic studies (STAT3 mutation) manifesting with EPF clinically and histopathologically. We recognize this case as a type of EPF because both the clinical and pathological findings are consistent with the diagnosis of EPF. This case could be categorized as immunosuppression-associated EPF (ISEPF), which is related to immune dysfunction.16 Though IS-EPF is most commonly seen in patients with human immunodeficiency virus infection, IS-EPF has also been reported in other immunocompromised states, such as in patients with hematological malignancy after peripheral ª 2014 The International Society of Dermatology
blood stem cell or bone marrow transplantation.16,17 Our patient had been misdiagnosed as atopic dermatitis since infancy. This report highlights the importance of recognizing papulopustular eruptions in infants and children, especially those having other symptoms or distinctive features of HIES. In conclusion, HIES is a rare, multisystem disorder with cutaneous, immunologic, connective tissue, and skeletal abnormalities. Skin manifestations with papulopustular rash occur in early infancy. Earlier diagnosis leads to appropriate management and prevention of complications. References 1 Freeman AF, Holland SM. Clinical manifestations, etiology, and pathogenesis of the hyper-IgE syndrome. Pediatr Res 2009; 65: 32–37. 2 Davis SD, Schaller J, Wedgwood RJ. Jobs syndrome: recurrent cold staphylococcal abscesses. Lancet 1955; 1: 1013–1015. 3 Buckley RH, Wray BB, Belmaker EZ. Extreme hyperimmunoglobulinemia E and undue susceptibility to infection. Pediatrics 1972; 49: 59–70. 4 Freeman AF, Holland SM. Clinical manifestations of hyper IgE syndromes. Dis Markers 2010; 29: 123–130. 5 Hill HR, Quie PG. Raised serum-IgE levels and defective neutrophil chemotaxis in three children with eczema and recurrent bacterial infections. Lancet 1974; 1: 183–187. 6 Eberting CL, Davis J, Puck JM, et al. Dermatitis and the newborn rash of hyper-IgE syndrome. Arch Dermatol 2004; 140: 1119–1125. 7 DeWitt CA, Bishop AB, Buescher LS, et al. Hyperimmunoglobulin E syndrome: two cases and a review of the literature. J Am Acad Dermatol 2006; 54: 855–865. 8 Grimbacher B, Schaffer AA, Holland SM, et al. Genetic linkage of hyper-IgE syndrome to chromosome 4. Am J Hum Genet 1999; 65: 735–744. International Journal of Dermatology 2015, 54, 211–214
213
214
Case report
HIES as eosinophilic pustular folliculitis
9 Renner ED, Rylaarsdam S, Anover-Sombke S, et al. Novel signal transducer and activator of transcription 3 (STAT3) mutations, reduced T(H)17 cell numbers, and variably defective STAT3 phosphorylation in hyper-IgE syndrome. J Allergy Clin Immunol 2008; 122: 181–187. 10 Milner JD, Brenchley JM, Laurence A, et al. Impaired T(H)17 cell differentiation in subjects with autosomal dominant hyper-IgE syndrome. Nature 2008; 452: 773– 776. 11 Kamei R, Honig PJ. Neonatal Jobs syndrome featuring a vesicular eruption. Pediatr Dermatol 1988; 5: 75–82. 12 Blum R, Geller G, Fish LA. Recurrent severe staphylococcal infections, eczematoid rash, extreme elevations of IgE, eosinophilia, and divergent chemotactic responses in two generations. J Pediatr 1977; 90: 607–609.
International Journal of Dermatology 2015, 54, 211–214
Lo et al.
13 Shirafuji Y, Matsuura H, Sato A, et al. Hyperimmunoglobulin E syndrome: a sign of TH1/TH2 imbalance? Eur J Dermatol 1999; 9: 129–131. 14 Chamlin SL, McCalmont TH, Cunningham BB, et al. Cutaneous manifestations of hyper-IgE syndrome in infants and children. J Pediatr 2002; 141: 572–575. 15 Olaiwan A, Chandesris MO, Fraitag S, et al. Cutaneous findings in sporadic and familial autosomal dominant hyper-IgE syndrome: a retrospective, single-center study of 21 patients diagnosed using molecular analysis. J Am Acad Dermatol 2011; 65: 1167–1172. 16 Nervi SJ, Schwartz RA, Dmochowski M. Eosinophilic pustular folliculitis: a 40 year retrospect. J Am Acad Dermatol 2006; 55: 285–299. 17 Fraser SJ, Benton EC, Roddie PH, et al. Eosinophilic folliculitis: an important differential diagnosis after allogeneic bone-marrow transplant. Clin Exp Dermatol 2009; 34: 369–371.
ª 2014 The International Society of Dermatology
