Pityriasis Amiantacea Following Bone Marrow Transplant

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Pityriasis Amiantacea Following Bone Marrow Transplant

Pityriasis amiantacea (PA) is characterized by adherence of hair shafts proximally.1 It has been associated with dermatologic conditions and rarely with medications. We describe a woman who developed PA following a bone marrow transplant with melphalan conditioning. We also review drug-induced PA and disorders that have been linked to this condition.

Case Report

A 67-year-old woman with a history of multiple myeloma was treated with 7 courses of chemotherapy (cyclophosphamide, bortezomib, prednisone). One month later, the patient underwent a bone marrow transplant with melphalan conditioning due to residual plasma cell myeloma. Following the transplant, she developed complete scalp alopecia. Prior to and following transplant, the patient’s hair care regimen included washing her hair and scalp every other day with over-the-counter “natural” shampoos. During drug-induced alopecia, the hair washing became less frequent.

The patient left the hospital 4 weeks posttransplant; her hair had started to regrow, but its appearance was altered. Posttransplant, the patient was maintained on bortezomib every other week and zoledronate once per month. She continued to develop multiple lesions in the scalp hairs during the following 4 months.

Eight months posttransplant she presented for evaluation of the scalp hair. Clinical examination showed hairs that were entwined together proximally, resulting in matting of the hair (Figure 1). A diagnosis of PA was established based on the clinical examination.

Treatment included mineral oil application to the scalp under occlusion each evening, followed by morning washing with coal tar 0.5%, salicylic acid 6%, or ketoconazole 2% shampoo in a repeating sequential manner. Within 1 month there was complete resolution of the scalp condition (Figure 2).

Figure 1. A, Distant view of the scalp of a 67-year-old woman showed pityriasis amiantacea presenting as proximal matting of hair with concretions around multiple hair follicles. B, Closer view showed the same.
Figure 2. A, Distant view of scalp after resolution of pityriasis amiantacea showed the hair without any matting. B, Closer view showed the same.

Comment

Clinical Presentation                                                                                                                                                                                                                                                                                                                                                             
Pityriasis amiantacea is characterized by thick excessive scale of the scalp1; it was initially described by Alibert2 in 1832. He described the gross appearance of the scales as resembling the feathers of young birds, which naturalists dub “amiante” or asbestoslike.1,2 In 1917, Gougerot3 explored infectious etiologies of this condition by describing cases of impetigo that transitioned into PA.1 Later, in 1929, Photinos4 described fungal origins of PA, giving credence to “tinea amiantacea.”1 However, more recent analyses failed to isolate fungus.5-7 As such, pityriasis (scaling) amiantacea is the more appropriate term, as emphasized by Brown8 in 1948. The cause of PA remains unclear; it is hypothesized that the condition is a reaction to underlying inflammatory dermatoses, though concurrent bacterial or fungal infection may be present.5,9

Prevalence                                                                                                                                                                                                                                                                                                                                                                             
Pityriasis amiantacea is considered to be most prevalent in pediatric patients and young adults; it is more common in females.1,9,10 In a review of 85 PA patients, more than 80% were women (n=69), and the mean age at presentation was 23.8 years. Approximately half of these patients had widespread scalp lesions (n=42); however, focal localized lesions were common.9 No hereditary patterns have been described, though 3 pairs of the 10 patients with PA in Ring and Kaplan’s7 review were siblings.

 

 


Clinical Findings                                                                                                                                                                                                                                                                                                                                                                   
Clinically, lesions of PA present as matted hairs.1 Thick scales encompass multiple hair shafts, binding down tufts of hair.1,6,11 Patients are asymptomatic, though the lesions may be accompanied by pruritus. The hairs enclosed by the scales in some cases may be easily pulled out.6 Notably, alopecia often accompanies PA; it often is reversible, but in some cases, it is permanent and can lead to scarring.9,12

Histopathology                                                                                                                                                                                                                                                                                                                                                                 
Submission of hair specimens to histopathology usually is not performed since the diagnosis often is established based on the clinical presentation.5 However, submitted specimens have demonstrated spongiosis and parakeratosis along with reduction in the size of the sebaceous glands.1,9 Additionally, follicular keratosis that surrounds the hair shafts with a sheath of horn is present.9 Acanthosis and migration of lymphocytes into the epidermis also have been found.1 Often, Staphylococcus aureus isolates are detected.9,13
 

Differential Diagnosis                                                                                                                                                                                                                                                                                                                                                                   
The clinical differential diagnosis of PA includes hair casts,11 pediculosis,14 and tinea capitis.12 In PA, thick scales surround hair shafts and thus bind down tufts of hair.9 In patients with pediculosis, nits are attached to the hair shaft at an angle and do not entirely envelop the hair shaft.14 In addition, PA may be complicated by impetiginization; bacteria often are found in the keratin surrounding the hair shaft and represent either normal flora or secondary infection.1,15 It has been speculated that microbial biofilms from S aureus and Staphylococcus epidermidis promote agglomeration of hair shafts and adherent scale.16 Bona fide dermatophyte infection of the scalp also may be concurrently present.12

Treatment                                                                                                                                                                                                                                                                                                                                                                                     
Our treatment included occlusion with mineral oil to loosen the scales from the scalp in tandem with shampoos traditionally used in patients with seborrheic dermatitis or psoriasis. Timely treatment is important to prevent scarring alopecia.13,17 Pityriasis amiantacea may be treatment resistant, and there are no specific therapeutic guidelines; rather, therapy should be targeted at the suspected underlying condition.17 Treatment generally includes keratolytic agents, such as salicylic acid.18 These agents allow enhanced penetration of other topical agents.19 Topical antifungal shampoos such as ketoconazole and ciclopirox are recommended,18 though other topical agents, such as coal tar and zinc pyrithione, also may benefit patients.13 Topical corticosteroids may be used if the condition is linked with psoriasis.13 Systemic antibiotics are added if S aureus superinfection is suspected.9

A single report described successful management of a patient with severe refractory PA who was treated with the tumor necrosis factor (TNF) α inhibitor infliximab.13 A 47-year-old woman presented with thick adherent scale on the scalp. She was treated with coal tar for 18 months but showed no improvement; the patient was subsequently prescribed salicylic acid 10%, clobetasol solution, and coal tar shampoo. After 3 months, when no improvement was observed, the patient was offered infliximab but declined. For 6 years the patient was treated with salicylic acid 20%, clobetasol (foam, lotion, shampoo, and solution), and coal tar shampoo without improvement. She then consented to infliximab therapy; after 3 infusions at weeks 0, 2, and 6, she demonstrated notable improvement. The patient was maintained on infliximab every 8 weeks.13

Pathogenesis                                                                                                                                                                                                                                                                                                                                                                                 
The pathogenesis of PA has yet to be definitively established, and the condition is usually idiopathic. In addition to bacterial or fungal etiologies,3,4 PA has been linked to medications (Table 1)16,20,21 and systemic conditions (Table 2).1,3,5,7-10,12,22-25

A PubMed search of articles indexed for MEDLINE using the search terms amiantacea, bone, drug, hair marrow, malignancy, melphalan, pityriasis, tinea, and transplant yielded 4 patients—2 men and 2 women (including our patient)—with possible drug-induced PA (Table 1)16,20,21; however, the onset after 2 years of medication (TNF-α inhibitors) or resolution while still receiving the agent (vemurafenib) makes the drug-induced linkage weak. The patients ranged in age from 21 to 67 years, with the median age being 37.5 years. Medications included melphalan, TNF-α inhibitors (adalimumab, infliximab),16,21 and vemurafenib20; it is interesting that infliximab was the medication associated with eliciting PA in 1 patient yet was an effective therapy in another patient with treatment-resistant PA. The onset of PA occurred between 1 month (melphalan) and 24 months (TNF-α inhibitors) after drug initiation. The patients’ associated diseases included Crohn disease,16,21 metastatic melanoma,20 and multiple myeloma.

Other conditions have been described in patients with PA (Table 2). Indeed, PA may be a manifestation of an underlying inflammatory skin disease.9 In addition to dermatologic conditions, procedures or malignancy may be associated with the disease, as demonstrated in our patient. Most commonly, PA is seen in association with psoriasis and seborrheic dermatitis; atopic dermatitis, bacterial infection, fungal infection, lichen planus, and neurodermatitis also have been associated with PA.1,3,5,7-10,12,18,22-25

Conclusion

Pityriasis amiantacea is a benign condition affecting the scalp hair. Albeit uncommon, it may appear in patients treated with medications such as melphalan, TNF-α inhibitors, and vemurafenib. In addition, it has been described in individuals with dermatologic conditions, systemic procedures, or underlying malignancy. Our patient developed PA following a bone marrow transplant after receiving conditioning with melphalan.

References
  1. Knight AG. Pityriasis amiantacea: a clinical and histopathological investigation. Clin Exp Dermatol. 1977;2:137-143.
  2. Alibert JL. De la porrigine amiantacée. In: Monographie des Dermatoses. Paris, France: Baillère; 1832:293-295.
  3. Gougerot H. La teigne amiantacee D’Alibert. Progres Medical. 1917;13:101-104.
  4. Photinos P. Recherches sur la fausse teigne amiantacée. Ann Dermatol Syphiligr. 1929;10:743-758.
  5. Verardino GC, Azulay-Abulafia L, Macedo PM, et al. Pityriasis amiantacea: clinical-dermatoscopic features and microscopy of hair tufts. An Bras Dermatol. 2012;87:142-145.
  6. Keipert JA. Greasy scaling pityriasis amiantacea and alopecia: a syndrome in search of a cause. Australas J Dermatol. 1985;26:41-44.
  7. Ring DS, Kaplan DL. Pityriasis amiantacea: a report of 10 cases. Arch Dermatol. 1993;129:913-914.
  8. Brown WH. Some observations on neurodermatitis of the scalp, with particular reference to tinea amiantacea. Br J Dermatol Syph. 1948;60:81-90.
  9. Abdel-Hamid IA, Agha SA, Moustafa YM, et al. Pityriasis amiantacea: a clinical and etiopathologic study of 85 patients. Int J Dermatol. 2003;42:260-264.
  10. Becker SW, Muir KB. Tinea amiantacea. Arch Dermatol Syphil. 1929;20:45-53.
  11. Dawber RP. Hair casts. Br J Dermatol. 1979;100:417-421.
  12. Ginarte M, Pereiro M, Fernández-Redondo V, et al. Case reports. pityriasis amiantacea as manifestation of tinea capitis due to Microsporum canis. Mycoses. 2000;43:93-96.
  13. Pham RK, Chan CS, Hsu S. Treatment of pityriasis amiantacea with infliximab. Dermatol Online J. 2009;15:13.
  14. Roberts RJ. Clinical practice. Head lice. N Engl J Med. 2002;346:1645-1650.
  15. Mcginley KJ, Leyden JJ, Marples RR, et al. Quantitative microbiology of the scalp in non-dandruff, dandruff, and seborrheic dermatitis. J Invest Dermatol. 1975;64:401-405.
  16. Ettler J, Wetter DA, Pittelkow MR. Pityriasis amiantacea: a distinctive presentation of psoriasis associated with tumour necrosis factor-α inhibitor therapy. Clin Exp Dermatol. 2012;37:639-641.
  17. Mannino G, McCaughey C, Vanness E. A case of pityriasis amiantacea with rapid response to treatment. WMJ. 2014;113:119-120.
  18. Jamil A, Muthupalaniappen L. Scales on the scalp. Malays Fam Physician. 2013;8:48-49.
  19. Gupta LK, Khare AK, Masatkar V, et al. Pityriasis amiantacea. Indian Dermatol Online J. 2014;5(suppl 1):S63-S64.
  20. Bilgiç Ö. Vemurafenib-induced pityriasis amiantacea: a case report. Cutan Ocul Toxicol. 2016;35:329-331.
  21. Zamperetti M, Zelger B, Höpfl R. Pityriasis amiantacea and folliculitis decalvans: an unusual manifestation associated with antitumor necrosis factor-α therapy. Hautarzt. 2017;68:1007-1010.
  22. Udayashankar C, Nath AK, Anuradha P. Extensive Darier’s disease with pityriasis amiantacea, alopecia and congenital facial nerve palsy. Dermatol Online J. 2013;19:18574.
  23. Hussain W, Coulson IH, Salman WD. Pityriasis amiantacea as the sole manifestation of Darier’s disease. Clin Exp Dermatol. 2009;34:554-556.
  24. Hansted B, Lindskov R. Pityriasis amiantacea and psoriasis. a follow-up study. Dermatologica. 1983;166:314-315.
  25. Hersle K, Lindholm A, Mobacken H, et al. Relationship of pityriasis amiantacea to psoriasis. a follow-up study. Dermatologica. 1979;159:245-250.
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Dr. Bari is from the Indiana University School of Medicine, Indianapolis. Dr. Cohen is from San Diego Family Dermatology, National City, California; Family Health Center of San Diego, California; Scripps Mercy Hospital Chula Vista, California; and the College of Osteopathic Medicine, Touro University California, Vallejo.

The authors report no conflict of interest.

Correspondence: Philip R. Cohen, MD, 10991 Twinleaf Ct, San Diego, CA 92131 ([email protected]).

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Dr. Bari is from the Indiana University School of Medicine, Indianapolis. Dr. Cohen is from San Diego Family Dermatology, National City, California; Family Health Center of San Diego, California; Scripps Mercy Hospital Chula Vista, California; and the College of Osteopathic Medicine, Touro University California, Vallejo.

The authors report no conflict of interest.

Correspondence: Philip R. Cohen, MD, 10991 Twinleaf Ct, San Diego, CA 92131 ([email protected]).

Author and Disclosure Information

Dr. Bari is from the Indiana University School of Medicine, Indianapolis. Dr. Cohen is from San Diego Family Dermatology, National City, California; Family Health Center of San Diego, California; Scripps Mercy Hospital Chula Vista, California; and the College of Osteopathic Medicine, Touro University California, Vallejo.

The authors report no conflict of interest.

Correspondence: Philip R. Cohen, MD, 10991 Twinleaf Ct, San Diego, CA 92131 ([email protected]).

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Pityriasis amiantacea (PA) is characterized by adherence of hair shafts proximally.1 It has been associated with dermatologic conditions and rarely with medications. We describe a woman who developed PA following a bone marrow transplant with melphalan conditioning. We also review drug-induced PA and disorders that have been linked to this condition.

Case Report

A 67-year-old woman with a history of multiple myeloma was treated with 7 courses of chemotherapy (cyclophosphamide, bortezomib, prednisone). One month later, the patient underwent a bone marrow transplant with melphalan conditioning due to residual plasma cell myeloma. Following the transplant, she developed complete scalp alopecia. Prior to and following transplant, the patient’s hair care regimen included washing her hair and scalp every other day with over-the-counter “natural” shampoos. During drug-induced alopecia, the hair washing became less frequent.

The patient left the hospital 4 weeks posttransplant; her hair had started to regrow, but its appearance was altered. Posttransplant, the patient was maintained on bortezomib every other week and zoledronate once per month. She continued to develop multiple lesions in the scalp hairs during the following 4 months.

Eight months posttransplant she presented for evaluation of the scalp hair. Clinical examination showed hairs that were entwined together proximally, resulting in matting of the hair (Figure 1). A diagnosis of PA was established based on the clinical examination.

Treatment included mineral oil application to the scalp under occlusion each evening, followed by morning washing with coal tar 0.5%, salicylic acid 6%, or ketoconazole 2% shampoo in a repeating sequential manner. Within 1 month there was complete resolution of the scalp condition (Figure 2).

Figure 1. A, Distant view of the scalp of a 67-year-old woman showed pityriasis amiantacea presenting as proximal matting of hair with concretions around multiple hair follicles. B, Closer view showed the same.
Figure 2. A, Distant view of scalp after resolution of pityriasis amiantacea showed the hair without any matting. B, Closer view showed the same.

Comment

Clinical Presentation                                                                                                                                                                                                                                                                                                                                                             
Pityriasis amiantacea is characterized by thick excessive scale of the scalp1; it was initially described by Alibert2 in 1832. He described the gross appearance of the scales as resembling the feathers of young birds, which naturalists dub “amiante” or asbestoslike.1,2 In 1917, Gougerot3 explored infectious etiologies of this condition by describing cases of impetigo that transitioned into PA.1 Later, in 1929, Photinos4 described fungal origins of PA, giving credence to “tinea amiantacea.”1 However, more recent analyses failed to isolate fungus.5-7 As such, pityriasis (scaling) amiantacea is the more appropriate term, as emphasized by Brown8 in 1948. The cause of PA remains unclear; it is hypothesized that the condition is a reaction to underlying inflammatory dermatoses, though concurrent bacterial or fungal infection may be present.5,9

Prevalence                                                                                                                                                                                                                                                                                                                                                                             
Pityriasis amiantacea is considered to be most prevalent in pediatric patients and young adults; it is more common in females.1,9,10 In a review of 85 PA patients, more than 80% were women (n=69), and the mean age at presentation was 23.8 years. Approximately half of these patients had widespread scalp lesions (n=42); however, focal localized lesions were common.9 No hereditary patterns have been described, though 3 pairs of the 10 patients with PA in Ring and Kaplan’s7 review were siblings.

 

 


Clinical Findings                                                                                                                                                                                                                                                                                                                                                                   
Clinically, lesions of PA present as matted hairs.1 Thick scales encompass multiple hair shafts, binding down tufts of hair.1,6,11 Patients are asymptomatic, though the lesions may be accompanied by pruritus. The hairs enclosed by the scales in some cases may be easily pulled out.6 Notably, alopecia often accompanies PA; it often is reversible, but in some cases, it is permanent and can lead to scarring.9,12

Histopathology                                                                                                                                                                                                                                                                                                                                                                 
Submission of hair specimens to histopathology usually is not performed since the diagnosis often is established based on the clinical presentation.5 However, submitted specimens have demonstrated spongiosis and parakeratosis along with reduction in the size of the sebaceous glands.1,9 Additionally, follicular keratosis that surrounds the hair shafts with a sheath of horn is present.9 Acanthosis and migration of lymphocytes into the epidermis also have been found.1 Often, Staphylococcus aureus isolates are detected.9,13
 

Differential Diagnosis                                                                                                                                                                                                                                                                                                                                                                   
The clinical differential diagnosis of PA includes hair casts,11 pediculosis,14 and tinea capitis.12 In PA, thick scales surround hair shafts and thus bind down tufts of hair.9 In patients with pediculosis, nits are attached to the hair shaft at an angle and do not entirely envelop the hair shaft.14 In addition, PA may be complicated by impetiginization; bacteria often are found in the keratin surrounding the hair shaft and represent either normal flora or secondary infection.1,15 It has been speculated that microbial biofilms from S aureus and Staphylococcus epidermidis promote agglomeration of hair shafts and adherent scale.16 Bona fide dermatophyte infection of the scalp also may be concurrently present.12

Treatment                                                                                                                                                                                                                                                                                                                                                                                     
Our treatment included occlusion with mineral oil to loosen the scales from the scalp in tandem with shampoos traditionally used in patients with seborrheic dermatitis or psoriasis. Timely treatment is important to prevent scarring alopecia.13,17 Pityriasis amiantacea may be treatment resistant, and there are no specific therapeutic guidelines; rather, therapy should be targeted at the suspected underlying condition.17 Treatment generally includes keratolytic agents, such as salicylic acid.18 These agents allow enhanced penetration of other topical agents.19 Topical antifungal shampoos such as ketoconazole and ciclopirox are recommended,18 though other topical agents, such as coal tar and zinc pyrithione, also may benefit patients.13 Topical corticosteroids may be used if the condition is linked with psoriasis.13 Systemic antibiotics are added if S aureus superinfection is suspected.9

A single report described successful management of a patient with severe refractory PA who was treated with the tumor necrosis factor (TNF) α inhibitor infliximab.13 A 47-year-old woman presented with thick adherent scale on the scalp. She was treated with coal tar for 18 months but showed no improvement; the patient was subsequently prescribed salicylic acid 10%, clobetasol solution, and coal tar shampoo. After 3 months, when no improvement was observed, the patient was offered infliximab but declined. For 6 years the patient was treated with salicylic acid 20%, clobetasol (foam, lotion, shampoo, and solution), and coal tar shampoo without improvement. She then consented to infliximab therapy; after 3 infusions at weeks 0, 2, and 6, she demonstrated notable improvement. The patient was maintained on infliximab every 8 weeks.13

Pathogenesis                                                                                                                                                                                                                                                                                                                                                                                 
The pathogenesis of PA has yet to be definitively established, and the condition is usually idiopathic. In addition to bacterial or fungal etiologies,3,4 PA has been linked to medications (Table 1)16,20,21 and systemic conditions (Table 2).1,3,5,7-10,12,22-25

A PubMed search of articles indexed for MEDLINE using the search terms amiantacea, bone, drug, hair marrow, malignancy, melphalan, pityriasis, tinea, and transplant yielded 4 patients—2 men and 2 women (including our patient)—with possible drug-induced PA (Table 1)16,20,21; however, the onset after 2 years of medication (TNF-α inhibitors) or resolution while still receiving the agent (vemurafenib) makes the drug-induced linkage weak. The patients ranged in age from 21 to 67 years, with the median age being 37.5 years. Medications included melphalan, TNF-α inhibitors (adalimumab, infliximab),16,21 and vemurafenib20; it is interesting that infliximab was the medication associated with eliciting PA in 1 patient yet was an effective therapy in another patient with treatment-resistant PA. The onset of PA occurred between 1 month (melphalan) and 24 months (TNF-α inhibitors) after drug initiation. The patients’ associated diseases included Crohn disease,16,21 metastatic melanoma,20 and multiple myeloma.

Other conditions have been described in patients with PA (Table 2). Indeed, PA may be a manifestation of an underlying inflammatory skin disease.9 In addition to dermatologic conditions, procedures or malignancy may be associated with the disease, as demonstrated in our patient. Most commonly, PA is seen in association with psoriasis and seborrheic dermatitis; atopic dermatitis, bacterial infection, fungal infection, lichen planus, and neurodermatitis also have been associated with PA.1,3,5,7-10,12,18,22-25

Conclusion

Pityriasis amiantacea is a benign condition affecting the scalp hair. Albeit uncommon, it may appear in patients treated with medications such as melphalan, TNF-α inhibitors, and vemurafenib. In addition, it has been described in individuals with dermatologic conditions, systemic procedures, or underlying malignancy. Our patient developed PA following a bone marrow transplant after receiving conditioning with melphalan.

Pityriasis amiantacea (PA) is characterized by adherence of hair shafts proximally.1 It has been associated with dermatologic conditions and rarely with medications. We describe a woman who developed PA following a bone marrow transplant with melphalan conditioning. We also review drug-induced PA and disorders that have been linked to this condition.

Case Report

A 67-year-old woman with a history of multiple myeloma was treated with 7 courses of chemotherapy (cyclophosphamide, bortezomib, prednisone). One month later, the patient underwent a bone marrow transplant with melphalan conditioning due to residual plasma cell myeloma. Following the transplant, she developed complete scalp alopecia. Prior to and following transplant, the patient’s hair care regimen included washing her hair and scalp every other day with over-the-counter “natural” shampoos. During drug-induced alopecia, the hair washing became less frequent.

The patient left the hospital 4 weeks posttransplant; her hair had started to regrow, but its appearance was altered. Posttransplant, the patient was maintained on bortezomib every other week and zoledronate once per month. She continued to develop multiple lesions in the scalp hairs during the following 4 months.

Eight months posttransplant she presented for evaluation of the scalp hair. Clinical examination showed hairs that were entwined together proximally, resulting in matting of the hair (Figure 1). A diagnosis of PA was established based on the clinical examination.

Treatment included mineral oil application to the scalp under occlusion each evening, followed by morning washing with coal tar 0.5%, salicylic acid 6%, or ketoconazole 2% shampoo in a repeating sequential manner. Within 1 month there was complete resolution of the scalp condition (Figure 2).

Figure 1. A, Distant view of the scalp of a 67-year-old woman showed pityriasis amiantacea presenting as proximal matting of hair with concretions around multiple hair follicles. B, Closer view showed the same.
Figure 2. A, Distant view of scalp after resolution of pityriasis amiantacea showed the hair without any matting. B, Closer view showed the same.

Comment

Clinical Presentation                                                                                                                                                                                                                                                                                                                                                             
Pityriasis amiantacea is characterized by thick excessive scale of the scalp1; it was initially described by Alibert2 in 1832. He described the gross appearance of the scales as resembling the feathers of young birds, which naturalists dub “amiante” or asbestoslike.1,2 In 1917, Gougerot3 explored infectious etiologies of this condition by describing cases of impetigo that transitioned into PA.1 Later, in 1929, Photinos4 described fungal origins of PA, giving credence to “tinea amiantacea.”1 However, more recent analyses failed to isolate fungus.5-7 As such, pityriasis (scaling) amiantacea is the more appropriate term, as emphasized by Brown8 in 1948. The cause of PA remains unclear; it is hypothesized that the condition is a reaction to underlying inflammatory dermatoses, though concurrent bacterial or fungal infection may be present.5,9

Prevalence                                                                                                                                                                                                                                                                                                                                                                             
Pityriasis amiantacea is considered to be most prevalent in pediatric patients and young adults; it is more common in females.1,9,10 In a review of 85 PA patients, more than 80% were women (n=69), and the mean age at presentation was 23.8 years. Approximately half of these patients had widespread scalp lesions (n=42); however, focal localized lesions were common.9 No hereditary patterns have been described, though 3 pairs of the 10 patients with PA in Ring and Kaplan’s7 review were siblings.

 

 


Clinical Findings                                                                                                                                                                                                                                                                                                                                                                   
Clinically, lesions of PA present as matted hairs.1 Thick scales encompass multiple hair shafts, binding down tufts of hair.1,6,11 Patients are asymptomatic, though the lesions may be accompanied by pruritus. The hairs enclosed by the scales in some cases may be easily pulled out.6 Notably, alopecia often accompanies PA; it often is reversible, but in some cases, it is permanent and can lead to scarring.9,12

Histopathology                                                                                                                                                                                                                                                                                                                                                                 
Submission of hair specimens to histopathology usually is not performed since the diagnosis often is established based on the clinical presentation.5 However, submitted specimens have demonstrated spongiosis and parakeratosis along with reduction in the size of the sebaceous glands.1,9 Additionally, follicular keratosis that surrounds the hair shafts with a sheath of horn is present.9 Acanthosis and migration of lymphocytes into the epidermis also have been found.1 Often, Staphylococcus aureus isolates are detected.9,13
 

Differential Diagnosis                                                                                                                                                                                                                                                                                                                                                                   
The clinical differential diagnosis of PA includes hair casts,11 pediculosis,14 and tinea capitis.12 In PA, thick scales surround hair shafts and thus bind down tufts of hair.9 In patients with pediculosis, nits are attached to the hair shaft at an angle and do not entirely envelop the hair shaft.14 In addition, PA may be complicated by impetiginization; bacteria often are found in the keratin surrounding the hair shaft and represent either normal flora or secondary infection.1,15 It has been speculated that microbial biofilms from S aureus and Staphylococcus epidermidis promote agglomeration of hair shafts and adherent scale.16 Bona fide dermatophyte infection of the scalp also may be concurrently present.12

Treatment                                                                                                                                                                                                                                                                                                                                                                                     
Our treatment included occlusion with mineral oil to loosen the scales from the scalp in tandem with shampoos traditionally used in patients with seborrheic dermatitis or psoriasis. Timely treatment is important to prevent scarring alopecia.13,17 Pityriasis amiantacea may be treatment resistant, and there are no specific therapeutic guidelines; rather, therapy should be targeted at the suspected underlying condition.17 Treatment generally includes keratolytic agents, such as salicylic acid.18 These agents allow enhanced penetration of other topical agents.19 Topical antifungal shampoos such as ketoconazole and ciclopirox are recommended,18 though other topical agents, such as coal tar and zinc pyrithione, also may benefit patients.13 Topical corticosteroids may be used if the condition is linked with psoriasis.13 Systemic antibiotics are added if S aureus superinfection is suspected.9

A single report described successful management of a patient with severe refractory PA who was treated with the tumor necrosis factor (TNF) α inhibitor infliximab.13 A 47-year-old woman presented with thick adherent scale on the scalp. She was treated with coal tar for 18 months but showed no improvement; the patient was subsequently prescribed salicylic acid 10%, clobetasol solution, and coal tar shampoo. After 3 months, when no improvement was observed, the patient was offered infliximab but declined. For 6 years the patient was treated with salicylic acid 20%, clobetasol (foam, lotion, shampoo, and solution), and coal tar shampoo without improvement. She then consented to infliximab therapy; after 3 infusions at weeks 0, 2, and 6, she demonstrated notable improvement. The patient was maintained on infliximab every 8 weeks.13

Pathogenesis                                                                                                                                                                                                                                                                                                                                                                                 
The pathogenesis of PA has yet to be definitively established, and the condition is usually idiopathic. In addition to bacterial or fungal etiologies,3,4 PA has been linked to medications (Table 1)16,20,21 and systemic conditions (Table 2).1,3,5,7-10,12,22-25

A PubMed search of articles indexed for MEDLINE using the search terms amiantacea, bone, drug, hair marrow, malignancy, melphalan, pityriasis, tinea, and transplant yielded 4 patients—2 men and 2 women (including our patient)—with possible drug-induced PA (Table 1)16,20,21; however, the onset after 2 years of medication (TNF-α inhibitors) or resolution while still receiving the agent (vemurafenib) makes the drug-induced linkage weak. The patients ranged in age from 21 to 67 years, with the median age being 37.5 years. Medications included melphalan, TNF-α inhibitors (adalimumab, infliximab),16,21 and vemurafenib20; it is interesting that infliximab was the medication associated with eliciting PA in 1 patient yet was an effective therapy in another patient with treatment-resistant PA. The onset of PA occurred between 1 month (melphalan) and 24 months (TNF-α inhibitors) after drug initiation. The patients’ associated diseases included Crohn disease,16,21 metastatic melanoma,20 and multiple myeloma.

Other conditions have been described in patients with PA (Table 2). Indeed, PA may be a manifestation of an underlying inflammatory skin disease.9 In addition to dermatologic conditions, procedures or malignancy may be associated with the disease, as demonstrated in our patient. Most commonly, PA is seen in association with psoriasis and seborrheic dermatitis; atopic dermatitis, bacterial infection, fungal infection, lichen planus, and neurodermatitis also have been associated with PA.1,3,5,7-10,12,18,22-25

Conclusion

Pityriasis amiantacea is a benign condition affecting the scalp hair. Albeit uncommon, it may appear in patients treated with medications such as melphalan, TNF-α inhibitors, and vemurafenib. In addition, it has been described in individuals with dermatologic conditions, systemic procedures, or underlying malignancy. Our patient developed PA following a bone marrow transplant after receiving conditioning with melphalan.

References
  1. Knight AG. Pityriasis amiantacea: a clinical and histopathological investigation. Clin Exp Dermatol. 1977;2:137-143.
  2. Alibert JL. De la porrigine amiantacée. In: Monographie des Dermatoses. Paris, France: Baillère; 1832:293-295.
  3. Gougerot H. La teigne amiantacee D’Alibert. Progres Medical. 1917;13:101-104.
  4. Photinos P. Recherches sur la fausse teigne amiantacée. Ann Dermatol Syphiligr. 1929;10:743-758.
  5. Verardino GC, Azulay-Abulafia L, Macedo PM, et al. Pityriasis amiantacea: clinical-dermatoscopic features and microscopy of hair tufts. An Bras Dermatol. 2012;87:142-145.
  6. Keipert JA. Greasy scaling pityriasis amiantacea and alopecia: a syndrome in search of a cause. Australas J Dermatol. 1985;26:41-44.
  7. Ring DS, Kaplan DL. Pityriasis amiantacea: a report of 10 cases. Arch Dermatol. 1993;129:913-914.
  8. Brown WH. Some observations on neurodermatitis of the scalp, with particular reference to tinea amiantacea. Br J Dermatol Syph. 1948;60:81-90.
  9. Abdel-Hamid IA, Agha SA, Moustafa YM, et al. Pityriasis amiantacea: a clinical and etiopathologic study of 85 patients. Int J Dermatol. 2003;42:260-264.
  10. Becker SW, Muir KB. Tinea amiantacea. Arch Dermatol Syphil. 1929;20:45-53.
  11. Dawber RP. Hair casts. Br J Dermatol. 1979;100:417-421.
  12. Ginarte M, Pereiro M, Fernández-Redondo V, et al. Case reports. pityriasis amiantacea as manifestation of tinea capitis due to Microsporum canis. Mycoses. 2000;43:93-96.
  13. Pham RK, Chan CS, Hsu S. Treatment of pityriasis amiantacea with infliximab. Dermatol Online J. 2009;15:13.
  14. Roberts RJ. Clinical practice. Head lice. N Engl J Med. 2002;346:1645-1650.
  15. Mcginley KJ, Leyden JJ, Marples RR, et al. Quantitative microbiology of the scalp in non-dandruff, dandruff, and seborrheic dermatitis. J Invest Dermatol. 1975;64:401-405.
  16. Ettler J, Wetter DA, Pittelkow MR. Pityriasis amiantacea: a distinctive presentation of psoriasis associated with tumour necrosis factor-α inhibitor therapy. Clin Exp Dermatol. 2012;37:639-641.
  17. Mannino G, McCaughey C, Vanness E. A case of pityriasis amiantacea with rapid response to treatment. WMJ. 2014;113:119-120.
  18. Jamil A, Muthupalaniappen L. Scales on the scalp. Malays Fam Physician. 2013;8:48-49.
  19. Gupta LK, Khare AK, Masatkar V, et al. Pityriasis amiantacea. Indian Dermatol Online J. 2014;5(suppl 1):S63-S64.
  20. Bilgiç Ö. Vemurafenib-induced pityriasis amiantacea: a case report. Cutan Ocul Toxicol. 2016;35:329-331.
  21. Zamperetti M, Zelger B, Höpfl R. Pityriasis amiantacea and folliculitis decalvans: an unusual manifestation associated with antitumor necrosis factor-α therapy. Hautarzt. 2017;68:1007-1010.
  22. Udayashankar C, Nath AK, Anuradha P. Extensive Darier’s disease with pityriasis amiantacea, alopecia and congenital facial nerve palsy. Dermatol Online J. 2013;19:18574.
  23. Hussain W, Coulson IH, Salman WD. Pityriasis amiantacea as the sole manifestation of Darier’s disease. Clin Exp Dermatol. 2009;34:554-556.
  24. Hansted B, Lindskov R. Pityriasis amiantacea and psoriasis. a follow-up study. Dermatologica. 1983;166:314-315.
  25. Hersle K, Lindholm A, Mobacken H, et al. Relationship of pityriasis amiantacea to psoriasis. a follow-up study. Dermatologica. 1979;159:245-250.
References
  1. Knight AG. Pityriasis amiantacea: a clinical and histopathological investigation. Clin Exp Dermatol. 1977;2:137-143.
  2. Alibert JL. De la porrigine amiantacée. In: Monographie des Dermatoses. Paris, France: Baillère; 1832:293-295.
  3. Gougerot H. La teigne amiantacee D’Alibert. Progres Medical. 1917;13:101-104.
  4. Photinos P. Recherches sur la fausse teigne amiantacée. Ann Dermatol Syphiligr. 1929;10:743-758.
  5. Verardino GC, Azulay-Abulafia L, Macedo PM, et al. Pityriasis amiantacea: clinical-dermatoscopic features and microscopy of hair tufts. An Bras Dermatol. 2012;87:142-145.
  6. Keipert JA. Greasy scaling pityriasis amiantacea and alopecia: a syndrome in search of a cause. Australas J Dermatol. 1985;26:41-44.
  7. Ring DS, Kaplan DL. Pityriasis amiantacea: a report of 10 cases. Arch Dermatol. 1993;129:913-914.
  8. Brown WH. Some observations on neurodermatitis of the scalp, with particular reference to tinea amiantacea. Br J Dermatol Syph. 1948;60:81-90.
  9. Abdel-Hamid IA, Agha SA, Moustafa YM, et al. Pityriasis amiantacea: a clinical and etiopathologic study of 85 patients. Int J Dermatol. 2003;42:260-264.
  10. Becker SW, Muir KB. Tinea amiantacea. Arch Dermatol Syphil. 1929;20:45-53.
  11. Dawber RP. Hair casts. Br J Dermatol. 1979;100:417-421.
  12. Ginarte M, Pereiro M, Fernández-Redondo V, et al. Case reports. pityriasis amiantacea as manifestation of tinea capitis due to Microsporum canis. Mycoses. 2000;43:93-96.
  13. Pham RK, Chan CS, Hsu S. Treatment of pityriasis amiantacea with infliximab. Dermatol Online J. 2009;15:13.
  14. Roberts RJ. Clinical practice. Head lice. N Engl J Med. 2002;346:1645-1650.
  15. Mcginley KJ, Leyden JJ, Marples RR, et al. Quantitative microbiology of the scalp in non-dandruff, dandruff, and seborrheic dermatitis. J Invest Dermatol. 1975;64:401-405.
  16. Ettler J, Wetter DA, Pittelkow MR. Pityriasis amiantacea: a distinctive presentation of psoriasis associated with tumour necrosis factor-α inhibitor therapy. Clin Exp Dermatol. 2012;37:639-641.
  17. Mannino G, McCaughey C, Vanness E. A case of pityriasis amiantacea with rapid response to treatment. WMJ. 2014;113:119-120.
  18. Jamil A, Muthupalaniappen L. Scales on the scalp. Malays Fam Physician. 2013;8:48-49.
  19. Gupta LK, Khare AK, Masatkar V, et al. Pityriasis amiantacea. Indian Dermatol Online J. 2014;5(suppl 1):S63-S64.
  20. Bilgiç Ö. Vemurafenib-induced pityriasis amiantacea: a case report. Cutan Ocul Toxicol. 2016;35:329-331.
  21. Zamperetti M, Zelger B, Höpfl R. Pityriasis amiantacea and folliculitis decalvans: an unusual manifestation associated with antitumor necrosis factor-α therapy. Hautarzt. 2017;68:1007-1010.
  22. Udayashankar C, Nath AK, Anuradha P. Extensive Darier’s disease with pityriasis amiantacea, alopecia and congenital facial nerve palsy. Dermatol Online J. 2013;19:18574.
  23. Hussain W, Coulson IH, Salman WD. Pityriasis amiantacea as the sole manifestation of Darier’s disease. Clin Exp Dermatol. 2009;34:554-556.
  24. Hansted B, Lindskov R. Pityriasis amiantacea and psoriasis. a follow-up study. Dermatologica. 1983;166:314-315.
  25. Hersle K, Lindholm A, Mobacken H, et al. Relationship of pityriasis amiantacea to psoriasis. a follow-up study. Dermatologica. 1979;159:245-250.
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Pityriasis Amiantacea Following Bone Marrow Transplant
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Practice Points

  • Pityriasis amiantacea (PA) is associated with several dermatologic conditions, including atopic dermatitis, bacterial and fungal infections, psoriasis, and seborrheic dermatitis.
  • Drug-induced PA is rare, but the condition has been reported in the context of treatment with tumor necrosis factor Symbol Stdα inhibitors and vemurafenib.
  • Our report suggests that PA may be associated with either melphalan conditioning, bone marrow transplant, or both.
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