J AM ACAD DERMATOL

NOVEMBER 20141016 Letters

Efficacy of oral retinoids in treatment-resistantlichen planopilarisTo the Editor: Lichen planopilaris (LPP) isclassified as a primary lymphocytic cicatricialalopecia.1 Topical and intralesional corticosteroids,oral tetracyclines, and oral hydroxychloroquine areconsidered by many as first-line agents in LPPfollowed by agents such as mycophenolate mofetiland cyclosporine1-3 Current literature suggests oralretinoids may benefit some patients with cutaneouslichen planus. However, the role of oral retinoids intreating LPP is unclear.

Ethics board approval was obtained to retrospec-tively evaluate the effectiveness of oral retinoids intreating patients with LPP who failed or had anincomplete response to 1 or more first-line agents.Patients were from the University of Toronto HairClinic over the years 2009 through 2013. Responserates to retinoids were determined; secondary endpoints included time to response, side-effect profiles,and concomitant treatments.

Of 189 patients evaluated with biopsy-proven LPP,21 patients (17 female, 4 male) were prescribedtreatment with oral retinoids after other treatmentsfailed to halt disease progression (ie, incompleteresponse). Of the 21 patients, the mean age of diseaseonset was 47.3 years, whereas the mean duration ofdisease at the time of assessmentwas 8.8 years. Duringthe course of therapy, 12 patients were treated withacitretin, 8 with isotretinoin, and 1 patient had a periodof treatmentwith each drug (Table I). The vastmajorityof patients previously received or was receivingtreatment with topical or injectable steroids, andother oral immunosuppressives/immunomodulators(Table I). Presence of 1 or more of the followingcriteria was used as an indicator of treatment response(clinical improvement): (1) improvement in erythema,scaling, or hyperkeratosis; or (2) cessation of hairshedding; or (3) conversion of individuals with apositive pull test result to a negative pull test result.Five of 21 (24%) of patients with treatment-resistantLPP were deemed to benefit from adjunctiveoral retinoid therapy with an approximate time of 2to 4months to clinical improvement. Other concurrenttreatments were maintained at the same dose ordecreased after the addition of retinoids, which madeit possible to attribute the clinical benefit to the retinoidtherapy. Of the responders, 3 received acitretin, and 2received isotretinoin. Notably, 4 of 5 responders hadlichen planus at other body sites (Table I).

The most common side effect of oral retinoidtherapy reported within the study was dryness ofthe skin and mucosae (43%). Other side effectsincluded hypercholesterolemia (14.2%), headaches(9.5%), and increased serum transaminases (4.7%).

Only 3 of 5 responders ultimately remained on oralretinoids with a 13- to 18-month follow-up interval.The remaining 2 patients had discontinued oralretinoid therapy because of relapse and further pro-gression of the disease.

Overall, we found oral retinoid therapy tobe a helpful adjunctive treatment in only a smallproportion of those with treatment-resistant LPP. Ourdata series of 21 patients represents one of the largestto date to evaluate the role of oral retinoids in thetreatment of LPP. A benefit of retinoid therapy wasfound in 2 of 3 patients reported by Spencer et al.4

In contrast, 6 patients reported by Assouly andReygagne2 did not show improvement.2

Our study is limited by its retrospective nature.Furthermore, given that retinoid therapy is not afirst-line treatment inour clinic setting, the studygroupis small despite the relatively large numbers of patientswe evaluated with LPP during the study period.Further study is required to determine what factorscontribute to the efficacy of retinoids in LPP.

Frank Spano, MD,a and Jeff C. Donovan, MD,PhDa,b,c,d

Division of Dermatology, Department of Medicine,Sunnybrook Health Sciences Centre, Toronto,a

Division of Dermatology, Department ofMedicine, Women’s College Hospital,b ClevelandClinic Canada,c and University of Toronto,d

Ontario, Canada

Funding sources: None.

Conflicts of interest: None declared.

Presented at the 88th Annual Meeting of theCanadian Dermatology Association Meeting,Quebec City, Quebec, Canada. June 27, 2013.

Correspondence to: Jeff C. Donovan, MD, PhD,University of Toronto Hair Loss Clinic, Women’sCollege Hospital, 76 Grenville St, Fifth Floor,Toronto, Ontario, Canada M5S 1B2

E-mail: jeffrey.donovan@utoronto.ca

REFERENCES

1. Kang H, Alzolibani AA, Otberg N, Shapiro J. Lichen planopilaris.

Dermatol Ther 2008;21:249-56.

2. Assouly P, Reygagne P. Lichen planopilaris: update on diagnosis

and treatment. Semin Cutan Med Surg 2009;28:3-10.

3. Baibergenova A, Donovan J. Lichen planopilaris: update on

pathogenesis and treatment. SkinMed 2013;11:161-5.

4. Spencer LA, Hawryluk EB, English JC III. Lichen planopilaris:

retrospective study and stepwise therapeutic approach. Arch

Dermatol 2009;145:333-4.

http://dx.doi.org/10.1016/j.jaad.2014.06.013

Table I. Summary of demographics, treatment regimen, and response

Patient

Age ( y),

sex Other sites LP

Previously

ineffective

treatments

(duration in

months)

Concurrent treatment

before addition of

retinoid (duration

in months)

Specific

retinoid

added Response to retinoid

1 43, M None HCQ (25)MMF (8)DOXY (7)CLOB (16)

PRED (5) ISO Clinical improvement at 2 mo;response maintained to 8 mofollowed by relapse

2 52, F R hand, R shoulder,L leg

None CLOB (18)HCQ (16)

ISO Clinical improvement at 3.5 mo;response maintained to 15-mofollow-up

3 50, F Nails PIO (7) CLOB (22)TAC (12)HCQ (19)

ACI Clinical improvement at 4 mo;response maintained to 18-mofollow-up

4 58, F Ears, nose, lip, nails HCQ (21)DOXY (6)CsA (7)

ILK (14)CLOB (25)Finasteride (54)

ACI Clinical improvement at 4 mo;response maintained to 6 mofollowed by relapse

5 67, F Axilla, legs, pubic None HCQ (19)CLOB (24)MINOX (13)ILK (16)

ACI Clinical improvement at 4 mo;response maintained to 13-mofollow-up

6 40, F None HCQ (17)DOXY (13)CLOB (19)

ILK (11)OCP (3 years)

ISO No response after 6 mo

7 43, F None DOXY (7)HCQ (24)CLOB (13)ILK (3)

OCP (3 years)TAC (8)

ISO No response after 8 mo

8 45, F None CLOB (13)ILK (3)DOXY (9)HCQ (22)MMF (4)TAC (7)

None ISO No response after 5 mo

9 49, M None DOXY (4)PRED (3)

HCQ (23)ILK (9)CLOB (18)

ISO No response after 9 mo

10 50, F Oral, nail, legs CLOB (22)ILK (13)DOXY (4)HCQ (15)MMF (7)

None ISO No response after 6 mo

11 68, F Oral ILK (11)HCQ (8)

CLOB (14) ISO No response after 5 mo

12 68, F None CLOB (22)ILK (15)DOXY (2)HCQ (16)MMF (3)CsA (4)

None ACI (3 mo)ISO (5 mo)

ACI not well tolerated andstopped at 3 mo

No response after 5 mo ISO

13 36, M None ILK (2)DOXY (6)HCQ (16)

CLOB (21) ACI No response after 7 mo

14 53, F Vulvar CLOB (4)TAC (13)ILK (14)DOXY (8)HCQ (17)MMF (3)

None ACI No response after 5 mo

Continued

J AM ACAD DERMATOL

VOLUME 71, NUMBER 5Letters 1017

Table I. Cont’d

Patient

Age ( y),

sex Other sites LP

Previously

ineffective

treatments

(duration in

months)

Concurrent treatment

before addition of

retinoid (duration

in months)

Specific

retinoid

added Response to retinoid

15 56, F Oral, nails CLOB (2)PRED (5)

ILK (18)HCQ (16)FLUO (22)

ACI No response after 10 mo

16 59, F None CLOB (3)ILK (15)DOXY (8)HCQ (22)CsA (4)

None ACI No response after 4 mo; stoppedbecause of increased lipids

17 61, F L buccal mucosa CLOB (13)DOXY (1)HCQ (6)

ILK (33)PIO (6)

ACI No response after 7 mo

18 62, F Arm, legs, oral DOXY (13)HCQ (17)

ILK (22)CLOB (12)

ACI No response after 6 mo

19 72, F None ILK (4)HCQ (16)MMF (7)

CLOB (26) ACI No response after 9 mo

20 73, F None HCQ (14) CLOB (17)ILK (9)

ACI No response after 5 mo

21 74, F None DOXY (8)CLOB (24)

ILK (31)HCQ (12)

ACI No response after 8 mo

ACI, Acitretin (25-50 mg orally daily); CLOB, topical clobetasol; CsA, cyclosporine (5 mg/kg); DOXY, doxycycline (100 mg orally twice a day);

F, female; FLUO, topical fluocinolone acetonide oil; HCQ, hydroxychloroquine (400 mg orally daily, to maximum 6.5 mg/kg); ILK, intralesional

triamcinolone acetonide (5 mg/mL) every 3-4 mo; ISO, isotretinoin (1 mg/kg); L, left; LP, lichen planus; M, male; MINOX, minoxidil 5% topical;

MMF, mycophenolate mofetil (1000 mg orally twice a day); OCP, oral contraceptive; PIO, pioglitazone (15-30 mg orally daily); PRED, oral

prednisone (0.5-1 mg/kg); R, right; TAC, topical tacrolimus.

J AM ACAD DERMATOL

NOVEMBER 20141018 Letters

Treatment of bullous pemphigoid withadjuvant immunoadsorption: A case series

To the Editor: Immunoadsorption (IA) has been usedas a rational, effective, and relatively safe treatmentin different case series of patients with pemphigus,but has only been reported in individual patientswith bullous pemphigoid (BP) so far.1 Because BPautoantibodies to the immunodominant domain ofBP180 (BP180 NC16A) are known to correlate withdisease severity, and pathogenicity of anti-BP180autoantibodies has been clearly shown in differentin vitro and in vivo models,2 autoantibody depletionby IA represents an attractive novel therapeuticprinciple for this disease.

In this investigator-initiated, open-label pilot study,7 patients (6 female, 1 male) with BP (based on bothdetection of linear deposits of IgG and/or C3 at thedermoepidermal junction along with circulating IgGautoantibodies against BP180 NC16A by direct immu-nofluorescence microscopy and enzyme-linkedimmunosorbent assay, respectively) aged between75 and 94 (mean 82) years were enrolled. All had skinblistering covering more than 30% of body surfacearea and disease duration of 1 to 24 (mean 6) months.

Before study enrollment, 4 patients had failed torespond to standard treatment with prednisolone(20-90mg/d) and topical clobetasol propionate partlyin combination with dapsone or mycophenolatemofetil for 1 to 24 (mean 6) months. IA was chosenas first-line therapy in the remaining 3 patients as theyshowed a particularly high disease activity (ie, morewidespread skin lesions).

Protein A IA (Immunosorba, Fresenius MedicalCare, Bad Homburg, Germany) was performed asdescribed previously.3 Following a previously pub-lished protocol for the treatment of pemphigus,1,3

patients were treated by 3 IA on consecutive days. Ineach therapy session, a mean plasma volume of 203mL/kg�1 body weight, representing 1.7 to 2.2 plasmavolumes, was processed over approximately 4 hours.In addition, all patients received prednisolone 0.25mg/kg/d, dapsone 1.0 to 1.5mg/kg/d, and clobetasolpropionate 0.05% ointment twice daily restricted toskin lesions, all of which was gradually tapereddepending on disease activity. Although IA slightlychanged plasma volume as a result of appliedanticoagulant solutions, it did not require substitutionof plasma components and therefore had no impacton dosages of any concomitant medication used.