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Graham-Little-Piccardi-Lasseur Syndrome Medication

  • Author: Patricia T Ting, MD, MSc, FRCPC, LMCC(Canada); Chief Editor: Dirk M Elston, MD  more...
 
Updated: May 10, 2016
 

Medication Summary

Topical, intralesional, and systemic corticosteroids; retinoids; and PUVA have been used with limited success. In recent years, various case reports have documented successful treatment of Graham-Little-Piccardi-Lasseur syndrome (GLPLS) with cyclosporine A, thalidomide, and metronidazole (authors' observation). No definite treatments have been developed for GLPLS. Patients tend to be treated empirically for this condition.

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Immunosuppressant agents

Class Summary

Immunosuppressant agents interfere with the immune processes that promote inflammation.

Cyclosporine A (Sandimmune, Neoral)

 

Cyclosporine A is an 11-amino acid cyclic peptide and natural product of fungi. It acts on T-cell replication and activity. It is a specific modulator of T-cell function and an agent that depresses cell-mediated immune responses by inhibiting helper T-cell function. Preferential and reversible inhibition of T lymphocytes in the G0 or G1 phase of the cell cycle is suggested.

Cyclosporine A binds to cyclophilin, an intracellular protein, which, in turn, prevents the formation of IL-2 and subsequent recruitment of activated T cells.

Cyclosporine A has approximately 30% bioavailability, but marked interindividual variability is reported. It specifically inhibits T-lymphocyte function with minimal activity against B cells. Maximum suppression of T-lymphocyte proliferation requires that the drug be present during the first 24 hours of antigenic exposure.

Cyclosporine A suppresses some humoral immunity and, to a greater extent, cell-mediated immune reactions (eg, delayed hypersensitivity, allograft rejection, experimental allergic encephalomyelitis, graft vs host disease) for a variety of organs.

Thalidomide (Thalomid)

 

Thalidomide is an immunomodulatory agent that may suppress excessive production of TNF-alpha and may down-regulate selected cell-surface adhesion molecules involved in leukocyte migration.

Tacrolimus topical (Protopic)

 

Tacrolimus topical reduces itching and inflammation by suppressing the release of cytokines from T cells. It also inhibits the transcription of genes that encode IL-3, IL-4, IL-5, GM-CSF, and TNF-alpha, all of which are involved in the early stages of T-cell activation. Additionally, it may inhibit the release of preformed mediators from skin mast cells and basophils and may down-regulate the expression of FcERI on Langerhans cells. Tacrolimus topical can be used in patients as young as 2 years. Drugs of this class are more expensive than topical corticosteroids.

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Antibiotics

Class Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Metronidazole (Protostat, Flagyl)

 

Metronidazole is an imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. It is used in combination with other antimicrobial agents (except to treat Clostridium difficile enterocolitis).

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Corticosteroids

Class Summary

Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

Betamethasone dipropionate (Diprolene)

 

Betamethasone dipropionate is a class I superpotent topical steroid; it suppresses mitosis and increases the synthesis of proteins that decrease inflammation and cause vasoconstriction.

Clobetasol (foam, spray, cream, ointment)

 

Clobetasol is a class I superpotent topical steroid; it suppresses mitosis and increases the synthesis of proteins that decrease inflammation and cause vasoconstriction.

Prednisone (Orasone, Meticorten, Sterapred, Deltasone)

 

Prednisone may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

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Antimalarial

Hydroxychloroquine sulfate (Plaquenil)

 

Hydroxychloroquine inhibits chemotaxis of eosinophils and locomotion of neutrophils and impairs complement-dependent antigen-antibody reactions. Hydroxychloroquine sulfate 200 mg is equivalent to 155 mg hydroxychloroquine base and 250 mg chloroquine phosphate. Weight-based dose adjustment and monitoring help to mitigate the risk of retinal toxicity.

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Contributor Information and Disclosures
Author

Patricia T Ting, MD, MSc, FRCPC, LMCC(Canada) Clinical Assistant Professor, University of Calgary Faculty of Medicine, Canada

Patricia T Ting, MD, MSc, FRCPC, LMCC(Canada) is a member of the following medical societies: Alberta Medical Association, American Academy of Dermatology, American Society for Dermatologic Surgery, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Canadian Dermatology Association

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Galderma; Janssen Inc.<br/>Received income in an amount equal to or greater than $250 from: Galderma; Janssen Inc.

Specialty Editor Board

David F Butler, MD Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

David F Butler, MD is a member of the following medical societies: American Medical Association, Alpha Omega Alpha, Association of Military Dermatologists, American Academy of Dermatology, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Phi Beta Kappa

Disclosure: Nothing to disclose.

Jeffrey J Miller, MD Associate Professor of Dermatology, Pennsylvania State University College of Medicine; Staff Dermatologist, Pennsylvania State Milton S Hershey Medical Center

Jeffrey J Miller, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, Society for Investigative Dermatology, Association of Professors of Dermatology, North American Hair Research Society

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Franklin Flowers, MD Department of Dermatology, Professor Emeritus Affiliate Associate Professor of Pathology, University of Florida College of Medicine

Franklin Flowers, MD is a member of the following medical societies: American College of Mohs Surgery

Disclosure: Nothing to disclose.

Neil Shear, MD Professor and Chief of Dermatology, Professor of Medicine, Pediatrics and Pharmacology, University of Toronto Faculty of Medicine; Head of Dermatology, Sunnybrook Women's College Health Sciences Center and Women's College Hospital, Canada

Neil Shear, MD is a member of the following medical societies: Canadian Medical Association, Ontario Medical Association, Royal College of Physicians and Surgeons of Canada, Canadian Dermatology Association, American Academy of Dermatology, American Society for Clinical Pharmacology and Therapeutics

Disclosure: Nothing to disclose.

Scott Richard Albert Walsh, MD, PhD Assistant Professor, Program Director, Department of Dermatology, University of Toronto, Sunnybrook Health Sciences Centre

Scott Richard Albert Walsh, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, International Society of Dermatology, Society for Investigative Dermatology, Canadian Dermatology Association

Disclosure: Nothing to disclose.

References
  1. Graham-Little EG. Folliculitis decalvans et atrophicans. Br J Dermatol. 1915. 27:183-5.

  2. Pai VV, Kikkeri NN, Sori T, Dinesh U. Graham-little piccardi lassueur syndrome: an unusual variant of follicular lichen planus. Int J Trichology. 2011 Jan. 3(1):28-30. [Medline]. [Full Text].

  3. Vashi N, Newlove T, Chu J, Patel R, Stein J. Graham-Little-Piccardi-Lassueur syndrome. Dermatol Online J. 2011 Oct 15. 17(10):30. [Medline].

  4. Zegarska B, Kallas D, Schwartz RA, Czajkowski R, Uchanska G, Placek W. Graham-Little syndrome. Acta Dermatovenerol Alp Panonica Adriat. 2010 Oct. 19(3):39-42. [Medline].

  5. László FG. Graham-Little-Piccardi-Lasseur syndrome: case report and review of the syndrome in men. Int J Dermatol. 2014 Aug. 53(8):1019-22. [Medline].

  6. Viglizzo G, Verrini A, Rongioletti F. Familial Lassueur-Graham-Little-Piccardi syndrome. Dermatology. 2004. 208(2):142-4. [Medline].

  7. Ghislain PD, Van Eeckhout P, Ghislain E. Lassueur-Graham Little-Piccardi syndrome: a 20-year follow-up. Dermatology. 2003. 206(4):391-2. [Medline].

  8. Bardazzi F, Landi C, Orlandi C, Neri I, Varotti C. Graham Little-Piccardi-Lasseur syndrome following HBV vaccination. Acta Derm Venereol. 1999 Jan. 79(1):93. [Medline].

  9. Rodriguez-Bayona B, Ruchaud S, Rodriguez C, et al. Autoantibodies against the chromosomal passenger protein INCENP found in a patient with Graham Little-Piccardi-Lassueur syndrome. J Autoimmune Dis. 2007 Jan 12. 4:1. [Medline].

  10. Rebora A, Rongioletti F, Drago F, Parodi. Lichen planus as a side effect of HBV vaccination. Dermatology. 1999. 198(1):1-2. [Medline].

  11. Vega Gutierrez J, Miranda-Romero A, Perez Milan F, Martinez Garcia G. Graham Little-Piccardi-Lassueur syndrome associated with androgen insensitivity syndrome (testicular feminization). J Eur Acad Dermatol Venereol. 2004 Jul. 18(4):463-6. [Medline].

  12. Mobini N, Tam S, Kamino H. Possible role of the bulge region in the pathogenesis of inflammatory scarring alopecia: lichen planopilaris as the prototype. J Cutan Pathol. 2005 Nov. 32(10):675-9. [Medline].

  13. Moretti S, Amato L, Massi D, Bianchi B, Gallerani I, Fabbri P. Evaluation of inflammatory infiltrate and fibrogenic cytokines in pseudopelade of Brocq suggests the involvement of T-helper 2 and 3 cytokines. Br J Dermatol. 2004 Jul. 151(1):84-90. [Medline].

  14. Horn RT Jr, Goette DK, Odom RB, Olson EG, Guill MA. Immunofluorescent findings and clinical overlap in two cases of follicular lichen planus. J Am Acad Dermatol. 1982 Aug. 7(2):203-7. [Medline].

  15. Bottoni U, Innocenzi D, Carlesimo M. Treatment of Piccardi-Lassueur-Graham Little syndrome with cyclosporin A. Eur J Dermatol. 1995. 5:216-9.

  16. Mirmirani P, Willey A, Price VH. Short course of oral cyclosporine in lichen planopilaris. J Am Acad Dermatol. 2003 Oct. 49(4):667-71. [Medline].

  17. Boyd AS, King LE Jr. Thalidomide-induced remission of lichen planopilaris. J Am Acad Dermatol. 2002 Dec. 47(6):967-8. [Medline].

  18. George SJ, Hsu S. Lichen planopilaris treated with thalidomide. J Am Acad Dermatol. 2001 Dec. 45(6):965-6. [Medline].

  19. Jouanique C, Reygagne P, Bachelez H, Dubertret L. Thalidomide is ineffective in the treatment of lichen planopilaris. J Am Acad Dermatol. 2004 Sep. 51(3):480-1. [Medline].

  20. Büyük AY, Kavala M. Oral metronidazole treatment of lichen planus. J Am Acad Dermatol. 2000 Aug. 43(2 Pt 1):260-2. [Medline].

 
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Follicular lichen planus eruption.
Lichen planopilaris of the scalp resulting in cicatricial alopecia.
 
 
 
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