Letters to the Editor
483
Anyhow, since the current knowledge on nail dermoscopy does not allow to establish whether a such finding is specific for ungual SK,1,4 surgical treatment and histological examination must be performed to exclude malignant lesions. G. Stinco,* E. Errichetti, P. Patrone Department of Experimental and Clinical Medicine, Institute of Dermatology, University of Udine, Udine, Italy *Correspondence: G. Stinco. E-mail: [email protected]
References 1 Bon-Mardion M, Poulalhon N, Balme B, Thomas L. Ungual seborrheic keratosis. J Eur Acad Dermatol Venereol 2010; 24: 1102–1104. 2 Baran R, Perrin C. Linear melanonychia due to subungual keratosis of the nail bed: a report of two cases. Br J Dermatol 1999; 140: 730–733. 3 Spaccarelli N, Wanat KA, Miller CJ, Rubin AI. Hypopigmented onychocytic matricoma as a clinical mimic of onychomatricoma: clinical, intraoperative and histopathologic correlations. J Cutan Pathol 2013; 40: 591–594. 4 Thomas L, Vaudaine M, Wortsman X, Jemec GBE, Drape JL. Imaging the Nail Unit. In Baran R, de Berker DAR, Holzberg M, Thomas L, eds. Baran and Dawber’s Diseases of the Nails and Their Management, 4th edn. Hoboken, NJ: Wiley-Blackwell, 2012: 101–182. 5 Dalle S, Depape L, Phan A, Balme B, Ronger-Savle S, Thomas L. Squamous cell carcinoma of the nail apparatus: clinicopathological study of 35 cases. Br J Dermatol 2007; 156: 871–874. 6 Cogrel O, Beylot-Barry M, Doutre MS. Subungual squamous cell carcinoma revealed by longitudinal erythronychia. Ann Dermatol Venereol 2008; 135: 883–885. DOI: 10.1111/jdv.12866
Crusted (Norwegian) scabies: an under-recognized infestation characterized by an atypical presentation and delayed diagnosis Editor Crusted scabies (CS) or Norwegian scabies is a rare, highly contagious infestation.1 CS generally affects patients with a weakened immune system, such as those with HIV, HTLV-1, malignancies, immunosuppressive or immunomodulator drugs or advanced age and those with sensitive impairment.1 Compared to conventional scabies, CS presents with hyperkeratotic plaques with yellowish crusts located on the limbs, trunk, ears and eyebrows.1 The presence of burrows or intense pruritus is rare.1,2 After not observing this disorder for many years, we have recently diagnosed several cases. Herein, we report the cases of CS seen in our department over the last 5 years. We identified 4 patients with CS (3 males, 1 female). The mean age was 73 years (range 52–78 years). All the patients had
JEADV 2016, 30, 446–556
multiple risk factors for CS (Table 1), and had received topical and oral corticosteroids before the diagnosis of CS was made. Two patients had also received acitretin + NB-UVB and one patient had received cyclosporine. Initially, all the patients showed pruritic erythematous papules on the trunk and legs. When the diagnosis of CS was made, 2 patients were erythrodermic with generalized thick scaly plaques (Fig. 1a,b). The other 2 patients had erythematous papules on the abdomen and showed localized scaly plaques on the buttocks (Fig. 1c) and around the umbilicus (Fig. 1d). The diagnosis was made after a median of 7.8 months (range 3–16 months) after the initial symptoms. All four cases showed mites, eggs or scyballa in skin scrapings from crusted plaques (Fig. 1e). In one case a skin biopsy revealed mites and eggs in the epidermis (Fig. 1f). All patients infested at least two other contacts (Table 1). All the patients were treated with repeated doses of full-body application of topical permetrin 5% and oral ivermectin 200 lg/kg, following different therapeutic approaches (Table 1). Complete resolution of the infestation was achieved in all cases. We identified a marked delay in the diagnosis of CS in our series. Although the pathogenesis of CS is poorly understood, a switch from a Th1 to a Th2 response would lead to a delayed hypersensitivity reaction.3 Animal studies have shown that symptoms start 4 weeks post-infestation, and crusted plaques appear 8–12 weeks later.4 However, this late onset may partially explain the delayed diagnosis in our patients. Another explanation is the presence of atypical forms of CS, such as psoriasiform, morbiliform, eczematous or bullous pemphigoid-like lesions,5–7 which often are erroneously treated with immunosuppressants. Therefore, errors in diagnosis and treatment lead to a delayed correct diagnosis and a greater risk of scabies outbreaks,8 sepsis and death.9,10 When CS is suspected or diagnosed, the clinician should identify the risk factors because they include severe diseases such as malignancy, HIV and other immunosuppressive conditions.1 In our series, the most common risk factors were immunosuppressive drugs and advanced age. Furthermore, if CS is suspected, skin scrapings should be repeated despite negative results, as we observed that in initial forms this test may have negative. To sum up, our results suggest that the delayed diagnosis is due to the lack of suspicion of CS, an atypical presentation, negative results of previous skin scrapings or poor knowledge of this condition. When patients present with atypical psoriasis, atypical morbiliform eruptions or erythroderma, CS should be considered so as to avoid full-fledged CS. A thorough, full-body examination and regular skin scrapings of suspicious lesions should be performed in these patients. Awareness of this rare form of scabies should be raised among dermatologists in view of the ageing population and the increasing use of immunosuppressants and immunomodulators.
© 2014 European Academy of Dermatology and Venereology
JEADV 2016, 30, 446–556
68
78
52
2
3
4
F
M
M
M
Sex
arthritis
Rheumatoid
use, hypertension
methotrexate
Deflazacort,
triflusal
bicarbonate,
materia, atopic dermatitis
papules
Pruritus sine
Drug eruption
erythematous
Pruritic
papules
HCTZ, potassium
erythematous
losartan,
Pruritic
psoriasis
Drug eruption,
psoriasis
papules
Pruritic
lichenoides,
papules
Heavy alcohol
Dx
condition
emolients
antihistamines,
Corticosteroids,
cyclosporine
prednisone,
antihistamines,
Corticosteroids,
acitretin
prednisone, NB-UVB,
antihistamines,
Corticosteroids,
acitretin
prednisone, NB-UVB,
antihistamines,
Corticosteroids,
dermatological
cutaneous
Pityriasis
previous
Treatment for
Dx for
Previous
erythematous
Pruritic
hypertension
Verapamil,
Initial presentation
erythematous
Enalapril
None
Previous ttx
syndrome,
Myelodisplastic
colon cancer
Prostate cancer,
Comorbidities
(umbilicus)
Localized
(buttocks)
Localized
Generalized
Generalized
presentation
scabies
Crusted
12
2.3
3.5
16.3
(months)
Dx
Delay in
N/A
Negative
N/A
Negative
scraping
skin
Initial
+++
+++
+++
+++
at Dx
scraping
Skin
IgE 950 UI/mL
Eos 1200/mm3,
IgE 2137 UI/mL
Eos 1100/mm3,
Eos 0/mm3
Eos 2900/mm3
Blood test
Bx, biopsy; Dx, diagnosis; Eos, eosinophils; F, female; HCTZ, hydrochlorothiazide; M, male; N/A, not available; NB-UVB, narrow band UVB.
78
(years)
Age
1
Case
Table 1 Clinical, microscopical and serological findings of patients with crusted scabies Treatment for
N/A
N/A
epidermis
parasites in the
15
200 l/day 1, 2, 8, 9,
daily + ivermectin
Permethrin 5%
15, 22, 29
200 l/day 1, 2, 8,9,
daily + ivermectin
Permethrin 5%
week 9 5 weeks
day 1/
acanthosis 2nd Bx:
ivermectin 200 l/ hyperkeratosis,
Permethrin 5% +
week9 2 weeks
200 l/day 1/ acanthosis
1st Bx:
5% + ivermectin
Permethrin
scabies
hyperkeratosis,
Initial Bx:
Histology
Resolved
Resolved
Resolved
Resolved
Outcome
Number
2
7
25
2
infested
of contacts
484
Letters to the Editor
© 2014 European Academy of Dermatology and Venereology
Letters to the Editor
485
(a)
(c)
(e)
(b)
(d)
(f)
Figure 1 Clinical presentation of crusted scabies and microscopic findings. Cases 1 and 2 presented with generalized forms, showing erythroderma and diffuse scaly plaques on the thorax and trunk (a), as well as fissures in the dorsum of the hands (b). Cases 3 and 4 presented with localized crusted plaques in the buttocks (c) and around the umbilicus (d). Direct observation of Sarcoptes scabiei adult mites, eggs and scyballa on skin scraping (e; original magnification 9100). Skin biopsy disclosing an adult mite and an egg in the epidermis (f; haematoxylin–eosin, original magnification 9200).
lamos,* J.F. Mir-Bonafe , A. Lo pez-Ferrer, O. Ye M.P. Garcia-Muret, M. Alegre, L. Puig Department of Dermatology, Hospital de la Santa Creu i Sant Pau, noma de Barcelona, Barcelona, Spain Universitat Auto lamos. E-mail: [email protected] *Correspondence: O. Ye
References 1 Hengge UR, Currie BJ, J€ager G, Lupi O, Schwartz RA. Scabies: a ubiquitous neglected skin disease. Lancet Infect Dis 2006; 6: 769–779. 2 Guldbakke K, Khachemoune A. Crusted scabies: a clinical review. J Drugs Dermatol 2006; 5: 221–227. 3 Walton SF, Beroukas D, Roberts-Thomson P, Currie BJ. New insights into disease pathogenesis in crusted (Norwegian) scabies: the skin immune response in crusted scabies. Br J Dermatol 2008; 158: 1247–1255. 4 Liu X, Walton SF, Murray HC et al. Crusted scabies is associated with increased IL-17 secretion by skin T cells. Parasite Immunol 2014; 36: 592–602. 5 Goyal NN, Wong GA. Psoriasis or crusted scabies. Clin Exp Dermatol 2008; 33: 211–212. 6 Almond D, Green C, Geurin D, Evans S. Lesson of the week: Norwegian scabies misdiagnosed as an adverse drug reaction. BMJ 2000; 320: 35–36. 7 Nakamura E, Taniguchi H, Ohtaki N. A case of crusted scabies with a bullous pemphigoid-like eruption and nail involvement. J Dermatol 2006; 33: 196–201. 8 Buehlmann M, Beltraminelli H, Strub C et al. Scabies outbreak in an intensive care unit with 1,659 exposed individuals–key factors for
JEADV 2016, 30, 446–556
controlling the outbreak. Infect Control Hosp Epidemiol 2009; 30: 354–360. 9 Glover A, Young L, Goltz A. Norwegian scabies in acquired immunodeficiency syndrome: report of a case resulting in death from associated sepsis. J Am Acad Dermatol 1987; 16: 396–399. 10 Roberts LJ, Huffam SE, Walton SF, Currie BJ. Crusted scabies: clinical and immunological findings in seventy-eight patients and a review of the literature. J Infect 2005; 50: 375–381. DOI: 10.1111/jdv.12867
Interest of high-definition optical coherent tomography (HD-OCT) for non-invasive imaging of dermatofibroma: a pilot study Editor Dermatofibroma (DF) is a common benign skin lesion characterized histologically by a fibrous proliferation in the dermis.1
© 2015 European Academy of Dermatology and Venereology
483
Anyhow, since the current knowledge on nail dermoscopy does not allow to establish whether a such finding is specific for ungual SK,1,4 surgical treatment and histological examination must be performed to exclude malignant lesions. G. Stinco,* E. Errichetti, P. Patrone Department of Experimental and Clinical Medicine, Institute of Dermatology, University of Udine, Udine, Italy *Correspondence: G. Stinco. E-mail: [email protected]
References 1 Bon-Mardion M, Poulalhon N, Balme B, Thomas L. Ungual seborrheic keratosis. J Eur Acad Dermatol Venereol 2010; 24: 1102–1104. 2 Baran R, Perrin C. Linear melanonychia due to subungual keratosis of the nail bed: a report of two cases. Br J Dermatol 1999; 140: 730–733. 3 Spaccarelli N, Wanat KA, Miller CJ, Rubin AI. Hypopigmented onychocytic matricoma as a clinical mimic of onychomatricoma: clinical, intraoperative and histopathologic correlations. J Cutan Pathol 2013; 40: 591–594. 4 Thomas L, Vaudaine M, Wortsman X, Jemec GBE, Drape JL. Imaging the Nail Unit. In Baran R, de Berker DAR, Holzberg M, Thomas L, eds. Baran and Dawber’s Diseases of the Nails and Their Management, 4th edn. Hoboken, NJ: Wiley-Blackwell, 2012: 101–182. 5 Dalle S, Depape L, Phan A, Balme B, Ronger-Savle S, Thomas L. Squamous cell carcinoma of the nail apparatus: clinicopathological study of 35 cases. Br J Dermatol 2007; 156: 871–874. 6 Cogrel O, Beylot-Barry M, Doutre MS. Subungual squamous cell carcinoma revealed by longitudinal erythronychia. Ann Dermatol Venereol 2008; 135: 883–885. DOI: 10.1111/jdv.12866
Crusted (Norwegian) scabies: an under-recognized infestation characterized by an atypical presentation and delayed diagnosis Editor Crusted scabies (CS) or Norwegian scabies is a rare, highly contagious infestation.1 CS generally affects patients with a weakened immune system, such as those with HIV, HTLV-1, malignancies, immunosuppressive or immunomodulator drugs or advanced age and those with sensitive impairment.1 Compared to conventional scabies, CS presents with hyperkeratotic plaques with yellowish crusts located on the limbs, trunk, ears and eyebrows.1 The presence of burrows or intense pruritus is rare.1,2 After not observing this disorder for many years, we have recently diagnosed several cases. Herein, we report the cases of CS seen in our department over the last 5 years. We identified 4 patients with CS (3 males, 1 female). The mean age was 73 years (range 52–78 years). All the patients had
JEADV 2016, 30, 446–556
multiple risk factors for CS (Table 1), and had received topical and oral corticosteroids before the diagnosis of CS was made. Two patients had also received acitretin + NB-UVB and one patient had received cyclosporine. Initially, all the patients showed pruritic erythematous papules on the trunk and legs. When the diagnosis of CS was made, 2 patients were erythrodermic with generalized thick scaly plaques (Fig. 1a,b). The other 2 patients had erythematous papules on the abdomen and showed localized scaly plaques on the buttocks (Fig. 1c) and around the umbilicus (Fig. 1d). The diagnosis was made after a median of 7.8 months (range 3–16 months) after the initial symptoms. All four cases showed mites, eggs or scyballa in skin scrapings from crusted plaques (Fig. 1e). In one case a skin biopsy revealed mites and eggs in the epidermis (Fig. 1f). All patients infested at least two other contacts (Table 1). All the patients were treated with repeated doses of full-body application of topical permetrin 5% and oral ivermectin 200 lg/kg, following different therapeutic approaches (Table 1). Complete resolution of the infestation was achieved in all cases. We identified a marked delay in the diagnosis of CS in our series. Although the pathogenesis of CS is poorly understood, a switch from a Th1 to a Th2 response would lead to a delayed hypersensitivity reaction.3 Animal studies have shown that symptoms start 4 weeks post-infestation, and crusted plaques appear 8–12 weeks later.4 However, this late onset may partially explain the delayed diagnosis in our patients. Another explanation is the presence of atypical forms of CS, such as psoriasiform, morbiliform, eczematous or bullous pemphigoid-like lesions,5–7 which often are erroneously treated with immunosuppressants. Therefore, errors in diagnosis and treatment lead to a delayed correct diagnosis and a greater risk of scabies outbreaks,8 sepsis and death.9,10 When CS is suspected or diagnosed, the clinician should identify the risk factors because they include severe diseases such as malignancy, HIV and other immunosuppressive conditions.1 In our series, the most common risk factors were immunosuppressive drugs and advanced age. Furthermore, if CS is suspected, skin scrapings should be repeated despite negative results, as we observed that in initial forms this test may have negative. To sum up, our results suggest that the delayed diagnosis is due to the lack of suspicion of CS, an atypical presentation, negative results of previous skin scrapings or poor knowledge of this condition. When patients present with atypical psoriasis, atypical morbiliform eruptions or erythroderma, CS should be considered so as to avoid full-fledged CS. A thorough, full-body examination and regular skin scrapings of suspicious lesions should be performed in these patients. Awareness of this rare form of scabies should be raised among dermatologists in view of the ageing population and the increasing use of immunosuppressants and immunomodulators.
© 2014 European Academy of Dermatology and Venereology
JEADV 2016, 30, 446–556
68
78
52
2
3
4
F
M
M
M
Sex
arthritis
Rheumatoid
use, hypertension
methotrexate
Deflazacort,
triflusal
bicarbonate,
materia, atopic dermatitis
papules
Pruritus sine
Drug eruption
erythematous
Pruritic
papules
HCTZ, potassium
erythematous
losartan,
Pruritic
psoriasis
Drug eruption,
psoriasis
papules
Pruritic
lichenoides,
papules
Heavy alcohol
Dx
condition
emolients
antihistamines,
Corticosteroids,
cyclosporine
prednisone,
antihistamines,
Corticosteroids,
acitretin
prednisone, NB-UVB,
antihistamines,
Corticosteroids,
acitretin
prednisone, NB-UVB,
antihistamines,
Corticosteroids,
dermatological
cutaneous
Pityriasis
previous
Treatment for
Dx for
Previous
erythematous
Pruritic
hypertension
Verapamil,
Initial presentation
erythematous
Enalapril
None
Previous ttx
syndrome,
Myelodisplastic
colon cancer
Prostate cancer,
Comorbidities
(umbilicus)
Localized
(buttocks)
Localized
Generalized
Generalized
presentation
scabies
Crusted
12
2.3
3.5
16.3
(months)
Dx
Delay in
N/A
Negative
N/A
Negative
scraping
skin
Initial
+++
+++
+++
+++
at Dx
scraping
Skin
IgE 950 UI/mL
Eos 1200/mm3,
IgE 2137 UI/mL
Eos 1100/mm3,
Eos 0/mm3
Eos 2900/mm3
Blood test
Bx, biopsy; Dx, diagnosis; Eos, eosinophils; F, female; HCTZ, hydrochlorothiazide; M, male; N/A, not available; NB-UVB, narrow band UVB.
78
(years)
Age
1
Case
Table 1 Clinical, microscopical and serological findings of patients with crusted scabies Treatment for
N/A
N/A
epidermis
parasites in the
15
200 l/day 1, 2, 8, 9,
daily + ivermectin
Permethrin 5%
15, 22, 29
200 l/day 1, 2, 8,9,
daily + ivermectin
Permethrin 5%
week 9 5 weeks
day 1/
acanthosis 2nd Bx:
ivermectin 200 l/ hyperkeratosis,
Permethrin 5% +
week9 2 weeks
200 l/day 1/ acanthosis
1st Bx:
5% + ivermectin
Permethrin
scabies
hyperkeratosis,
Initial Bx:
Histology
Resolved
Resolved
Resolved
Resolved
Outcome
Number
2
7
25
2
infested
of contacts
484
Letters to the Editor
© 2014 European Academy of Dermatology and Venereology
Letters to the Editor
485
(a)
(c)
(e)
(b)
(d)
(f)
Figure 1 Clinical presentation of crusted scabies and microscopic findings. Cases 1 and 2 presented with generalized forms, showing erythroderma and diffuse scaly plaques on the thorax and trunk (a), as well as fissures in the dorsum of the hands (b). Cases 3 and 4 presented with localized crusted plaques in the buttocks (c) and around the umbilicus (d). Direct observation of Sarcoptes scabiei adult mites, eggs and scyballa on skin scraping (e; original magnification 9100). Skin biopsy disclosing an adult mite and an egg in the epidermis (f; haematoxylin–eosin, original magnification 9200).
lamos,* J.F. Mir-Bonafe , A. Lo pez-Ferrer, O. Ye M.P. Garcia-Muret, M. Alegre, L. Puig Department of Dermatology, Hospital de la Santa Creu i Sant Pau, noma de Barcelona, Barcelona, Spain Universitat Auto lamos. E-mail: [email protected] *Correspondence: O. Ye
References 1 Hengge UR, Currie BJ, J€ager G, Lupi O, Schwartz RA. Scabies: a ubiquitous neglected skin disease. Lancet Infect Dis 2006; 6: 769–779. 2 Guldbakke K, Khachemoune A. Crusted scabies: a clinical review. J Drugs Dermatol 2006; 5: 221–227. 3 Walton SF, Beroukas D, Roberts-Thomson P, Currie BJ. New insights into disease pathogenesis in crusted (Norwegian) scabies: the skin immune response in crusted scabies. Br J Dermatol 2008; 158: 1247–1255. 4 Liu X, Walton SF, Murray HC et al. Crusted scabies is associated with increased IL-17 secretion by skin T cells. Parasite Immunol 2014; 36: 592–602. 5 Goyal NN, Wong GA. Psoriasis or crusted scabies. Clin Exp Dermatol 2008; 33: 211–212. 6 Almond D, Green C, Geurin D, Evans S. Lesson of the week: Norwegian scabies misdiagnosed as an adverse drug reaction. BMJ 2000; 320: 35–36. 7 Nakamura E, Taniguchi H, Ohtaki N. A case of crusted scabies with a bullous pemphigoid-like eruption and nail involvement. J Dermatol 2006; 33: 196–201. 8 Buehlmann M, Beltraminelli H, Strub C et al. Scabies outbreak in an intensive care unit with 1,659 exposed individuals–key factors for
JEADV 2016, 30, 446–556
controlling the outbreak. Infect Control Hosp Epidemiol 2009; 30: 354–360. 9 Glover A, Young L, Goltz A. Norwegian scabies in acquired immunodeficiency syndrome: report of a case resulting in death from associated sepsis. J Am Acad Dermatol 1987; 16: 396–399. 10 Roberts LJ, Huffam SE, Walton SF, Currie BJ. Crusted scabies: clinical and immunological findings in seventy-eight patients and a review of the literature. J Infect 2005; 50: 375–381. DOI: 10.1111/jdv.12867
Interest of high-definition optical coherent tomography (HD-OCT) for non-invasive imaging of dermatofibroma: a pilot study Editor Dermatofibroma (DF) is a common benign skin lesion characterized histologically by a fibrous proliferation in the dermis.1
© 2015 European Academy of Dermatology and Venereology
