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Dermatology > DISEASES OF THE ADNEXA
Graham-Little-Piccardi-Lasseur Syndrome
Article Last Updated: May 8, 2007
AUTHOR AND EDITOR INFORMATION
Section 1 of 11  
Author: Scott Richard Albert Walsh, MD, PhD, Assistant Professor, Program Director, Department of Dermatology, University of Toronto, Sunnybrook Health Sciences Centre
Scott Richard Albert Walsh is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, Canadian Dermatology Association, International Society of Dermatology, and Society for Investigative Dermatology
Coauthor(s):
Patricia T Ting, MD, Staff Physician, Department of Medicine, University of Calgary;
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
Editors: Franklin Flowers, MD, Chief, Division of Dermatology, Professor, Department of Medicine and Otolaryngology, University of Florida College of Medicine; David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Director, Division of Dermatology, Scott and White Clinic; Director Dermatology Residency Training Program, Scott and White Clinic; Jeffrey J Miller, MD, Associate Professor, Department of Dermatology, Penn State University, Milton S Hershey Medical Center; Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University; Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Author and Editor Disclosure
Synonyms and related keywords:
Graham-Little-Feldman syndrome, Lassueur-Graham-Little-Piccardi syndrome, Piccardi-Lassueur-Graham-Little syndrome, Graham-Little-Piccardi-Lassueur syndrome, follicular lichen planus, LP, lichen spinulosus et folliculitis decalvans, lichen planopilaris, alopecia, cheratosi spinulosa, keratotic spinulosa, lichenoid dermatosis, hair loss, GLPLS, GLPL syndrome
Background
In 1914, Piccardi described the first case of progressive scalp cicatricial alopecia, noncicatricial alopecia in the axilla and groin, and follicular lichen planus (LP) on the trunk and extremities, to which he gave the name cheratosi spinulosa (keratotic spinulosa). In 1915, Graham-Little1 published a similar case of a 55-year-old woman, referred by Lassueur of Lausanne, Switzerland. Later, Feldman also reported another similar case, which he termed lichen planus et acuminatus atrophicans in 1936. Subsequently, several other cases were reported. Graham-Little-Piccardi-Lasseur syndrome (GLPLS) is a rare lichenoid dermatosis defined by the triad of multifocal cicatricial alopecia of the scalp; noncicatricial alopecia of the axilla and groin; and a follicular LP eruption on the body, scalp, or both.
Pathophysiology
Based on clinical and histological studies, GLPLS is considered a variant of LP consisting of follicular LP (of the body and/or scalp) and lichen planopilaris (LPP, of the scalp). Estimates show that at least 50% of patients with GLPLS experience at least one episode of typical oral and/or cutaneous LP. Similar to LP, GLPLS is likely the result of a T-cell–mediated immune response of unknown etiology, which involves destruction of keratinocytes expressing specific antigens.
Frequency
International
GLPLS is relatively rare. A Medline search from 1951-2007 (all languages included) produced fewer than 40 cases of GLPLS in the literature.
Mortality/Morbidity
- Progressive cicatricial alopecia of the scalp leading to permanent hair loss may elicit psychosocial distress in the patient.
- GLPLS has not been associated with underlying systemic diseases or increased mortality rates.
Race
- Most reported patients are middle-aged white women; however, no ethnic predisposition has been noted.
Sex
- Reports show females are affected more frequently than males, although limited numbers preclude meaningful interpretation from the case reports.
- Only a few case reports in the literature cite affected males, which may be secondary to fewer males demonstrating concern over the disease.
Age
- Reported patients are aged 30-60 years.
History
- Patients are usually otherwise healthy middle-aged women.
- GLPLS is typically sporadic and nonfamilial. In 2004, Viglizzo et al2 reported one case of GLPLS in a 47-year-old mother and her 19-year-old daughter.
- The course of disease is slowly progressive (months to years) and often chronic. In 2003, Ghislain et al3 reported a 50-year-old woman who initially presented with disseminated LP, which then progressed to the classic triad of GLPLS over a 20-year period.
- While the chronological course of GLPLS is variable, most patients usually present with clinical findings in the following order, called the triad of GLPLS:
- Cicatricial alopecia of the scalp
- Noncicatricial alopecia of the axilla and groin
- Follicular LP eruption of the body, scalp, or both
- In most patients, cicatricial scalp alopecia does not respond to medical interventions and results in progressive and permanent patchy hair loss. In contrast, follicular LP eruptions usually demonstrate a good response to medical treatments.
Physical
Symptoms from the triad of GLPLS need not be present simultaneously.
- Cicatricial scalp alopecia is chronic and progressive through several stages:
- Mild perifollicular erythema (with or without pruritus)
- Follicular hyperkeratosis (keratotic and/or spiny papules)
- Patches of cicatricial alopecia with occasional tufts of normal hair
- Loss of residual normal tufts and hair follicles
- Cicatricial alopecia with permanent hair loss, clinically identical to pseudopelade of Brocq, in end-stage GLPLS
- Noncicatrizing alopecia of axilla, groin, and occasionally eyebrows and follicular LP of the skin (trunk, proximal limbs), scalp, or both usually resolve without treatment.
- Patients have a history of typical cutaneous and/or oral LP.
- In 1999, Bardazzi et al4 reported one case of GLPLS associated with hepatitis B vaccination and further suggested that GLPLS may also be associated with liver disease (ie, hepatitis).
Causes
The etiology of GLPLS is unknown; however, several hypotheses have been proposed.
- Immunologic: HLA-DR is one of several HLA subtypes associated with LP and GLPLS. HLA antigens are hypothesized to enhance a T-cell–mediated immune response of unknown etiology.
- Genetic: With the exception of one 2004 report by Viglizzo et al2 that documented a familial pattern of GLPLS correlated with the presence of HLA-DR1 in a mother and daughter, reports of GLPLS are usually sporadic, without any indication of genetic predisposition.
- Viral (hepatitis B virus): Both GLPLS and LP have been reported to be rare events following hepatitis B virus vaccination. The hepatitis B virus vaccine is hypothesized to stimulate the immune system and trigger LP eruptions in a nonspecific manner. LP-like eruptions have not been reported with other vaccinations.
- Hormonal: In 2004, Vega-Gutiérrez et al5 reported a case of GLPLS in a 19-year-old phenotypically female (genetically XY) patient with androgen insensitivity syndrome (testicular feminization). While the significance of both these findings is unknown, the authors implied that a hormonal etiology may be associated with the noncicatricial alopecia of the axilla and groin observed in persons with GLPLS.
- Others: Neuropsychological stress, vitamin deficiency (specifically vitamin A), and altered hormone levels have been suggested because most GLPLS patients are perimenopausal or postmenopausal women.
Alopecia Mucinosa
Lichen Planus
Lupus Erythematosus, Discoid
Pityriasis Rubra Pilaris
Pseudopelade, Brocq
Sarcoidosis
Other Problems to be Considered
Folliculitis decalvans
Keratosis pilaris et atrophicans
Lab Studies
- Some epidemiological studies describe a loose association between mucocutaneous LP and hepatitis C. However, this association has not yet been described in case reports of GLPLS.
- Initial investigations may include antinuclear antibodies (ANA), antiextractable nuclear antigens (AENA), hepatitis B and C serology, and liver function tests to exclude other associated systemic causes of cicatricial alopecia.
Imaging Studies
- No imaging studies are required.
Procedures
- A punch biopsy of the scalp may confirm the presence of cicatricial alopecia. Histologically, the end-stage lesions in GLPLS are indistinguishable from those of pseudopelade of Brocq, discoid lupus erythematosus, folliculitis decalvans, frontal fibrosing alopecia, and other forms of cicatricial alopecia.
- A skin biopsy of associated follicular papules may reveal the presence of histologic findings that correlate with the triad of GLPLS.
- The presence of noncicatricial alopecia in the axilla and groin can usually be diagnosed clinically, and further skin biopsies are not necessary.
Histologic Findings
Histology of cicatricial alopecia of the scalp In the early stage, an inflammatory perifollicular lichenoid infiltrate can be observed and is often associated with the infundibuloisthmic (bulge) region of the follicle. This infundibuloisthmic region contains stem cells responsible for regenerating the lower two thirds of the hair follicle, which is nonpermanent. The bulb region is spared. In end-stage GLPLS, atrophic dermis and fibrosed and empty hair shafts can be seen. One additional histological finding is keratinous follicular plugs with loss of sebaceous glands. A lichenoid lymphocytic infiltrate composed of mostly CD8 and CD4 T cells may irreversibly damage stem cells and hair follicles. Profibrogenic cytokines such as interleukin (IL)–4 and IL-6, transforming growth factor (TGF)–beta, and interferon (IFN)–gamma have been reported in association with LPP of the scalp. Direct immunofluorescence studies have reported immunoglobulin M, immunoglobulin G, and, occasionally immunoglobulin A at the hair follicle infundibulum and isthmus, as well as linear fibrinogen deposition along the dermoepidermal junction. Histopathology of follicular papules Findings include (1) lichenoid lymphocytic infiltrate in the upper dermis, (2) hyperkeratosis and focal hypergranulosis, (3) acanthosis with occasional saw-toothed rete ridges, and (4) dyskeratotic keratinocytes (Civatte or colloid bodies).
Medical Care
Topical, intralesional, and systemic corticosteroids; retinoids; psoralen plus ultraviolet light A (PUVA); and antimalarials have been used with limited success. In recent years, various case reports have documented successful treatment of 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.
- Corticosteroids (topical, intralesional, systemic) have not been shown to be effective in the treatment of cicatricial alopecia associated with GLPLS, although they are moderately effective for follicular LP. High- and super high-potency topical corticosteroids are still the treatment of choice for mild cicatricial alopecia or in patients in whom systemic medications are contraindicated. Intralesional triamcinolone acetonide is often ineffective for the treatment of cicatricial scalp alopecia. The same results have been documented for treatment with systemic corticosteroids, for which many adverse effects are known (eg, immunosuppression, osteoporosis, avascular necrosis, Cushing syndrome, diabetes, cataracts).
- Cyclosporin A was effective for the treatment of 5 eligible patients with GLPLS. The dose ranges from 3-5 mg/kg/d for 3-5 months. This dose has been reported to be more effective in the first stage of cicatricial alopecia prior to dermal alteration. A significant decrease in follicular papules, attenuation of hair loss, and patchy hair regrowth have been documented. Patients remained free of symptoms for up to 20 months following treatment, with no adverse effects reported. This medication may also be used for alopecia areata, lupus erythematosus, LP, and LPP. In 3 patients with LPP resistant to treatment with oral hydroxychloroquine or topical and intralesional corticosteroids, cyclosporin A aborted further progression of cicatricial alopecia.
- Thalidomide at 50-150 mg/d for up to 2 months has been associated with significant hair regrowth of cicatricial scalp alopecia in 2 case reports. More recently, however, thalidomide titrated up to 200 mg/d (from an initial 1-mo dose of 100 mg/d) was reported to be ineffective in a case series of 6 patients (4 with LPP and 2 with pseudopelade of Brocq) during a 6-month open-label trial. Previously, thalidomide has been successful in attenuating and reversing immune-mediated alopecia associated with discoid lupus erythematosus and erosive mucosal LP.
- Oral metronidazole at 500 mg twice daily for 8 weeks was used successfully at the authors' center for a female patient with GLPLS, with notable resolution of follicular papules and attenuation of cicatricial alopecia. To the authors' knowledge, this is the first report of GLPLS treated with metronidazole. In a 2000 study by Büyük and Kavala6 of patients with generalized LP, 13 (68%) of 19 patients showed complete response to 500 mg of oral metronidazole administered twice daily.
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 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.
Drug Category: Immunosuppressant agents
Interfere with immune processes that promote inflammation.
| Drug Name | Cyclosporine A (Sandimmune, Neoral) |
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| Description | An 11-amino acid cyclic peptide and natural product of fungi.
Acts on T-cell replication and activity. 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 G0 or G1 phase of cell cycle suggested.
Binds to cyclophilin, an intracellular protein, which, in turn, prevents formation of IL-2 and subsequent recruitment of activated T cells.
Has approximately 30% bioavailability, but marked interindividual variability is reported. Specifically inhibits T-lymphocyte function with minimal activity against B cells. Maximum suppression of T-lymphocyte proliferation requires that drug be present during first 24 h of antigenic exposure.
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. |
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| Adult Dose | 2.5-5 mg/kg/d PO in divided doses |
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| Pediatric Dose | Administer as in adults |
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| Contraindications | Documented hypersensitivity; uncontrolled hypertension or malignancies; renal failure; concomitant administration with PUVA or UVB radiation for psoriasis because may increase risk of cancer |
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| Interactions | Carbamazepine, phenytoin, isoniazid, rifampin, and phenobarbital may decrease concentrations; azithromycin, itraconazole, nicardipine, ketoconazole, fluconazole, erythromycin, verapamil, grapefruit juice, diltiazem, aminoglycosides, acyclovir, amphotericin B, and clarithromycin may increase toxicity; acute renal failure, rhabdomyolysis, myositis, and myalgias increase when taken concurrently with lovastatin; methylprednisolone and cyclosporine mutually inhibit one another, resulting in increased plasma levels of both |
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| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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| Precautions | Monitor renal function often by measuring BUN and serum creatinine levels and performing urinalysis; monitor triglyceride, cholesterol, uric acid, and magnesium values periodically; may increase risk of infection and lymphoma; reserve IV use only for those who cannot take PO |
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| Drug Name | Thalidomide (Thalomid) |
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| Description | Immunomodulatory agent that may suppress excessive production of TNF-alpha and may down-regulate selected cell-surface adhesion molecules involved in leukocyte migration. |
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| Adult Dose | 100-300 mg/d PO with water, preferably qhs and at least 1 h pc
<50 kg (110 lb): Start at low end of dose regimen |
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| Pediatric Dose | Not established |
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| Contraindications | Documented hypersensitivity; preexisting unstable neuropathy |
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| Interactions | May increase sedation with alcohol, barbiturates, chlorpromazine, and reserpine; due to teratogenic effects, women must use 2 additional methods of contraception or abstain from intercourse |
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| Pregnancy | X - Contraindicated; benefit does not outweigh risk
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| Precautions | Perform pregnancy test within 24-h prior to initiating therapy (qwk during first month, followed by monthly tests in women with regular menstrual cycles or q2wk in those with irregular menstrual cycles); bradycardia may occur; use protective measures (eg, sunscreens, protective clothing) against exposure to sunlight or UV light (eg, tanning beds); sedative effect can be significant and patient should be warned not to operate a motor vehicle after taking medication; monitor monthly by clinical examination for potential neuropathy; monitor at baseline and q6mo with nerve conduction studies to identify potential subclinical neuropathy; prescribing physician must enter STEPS (System for Thalidomide Education and Prescribing Safety; Celgene Corporation, 1-800-4-CELGENE) program established by manufacturer |
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| Drug Name | Tacrolimus topical (Protopic) |
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| Description | Reduces itching and inflammation by suppressing release of cytokines from T cells. Also inhibits 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, may inhibit release of preformed mediators from skin mast cells and basophils and may down-regulate expression of FcERI on Langerhans cells. Can be used in patients as young as 2 y. Drugs of this class are more expensive than topical corticosteroids. |
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| Adult Dose | Apply thin layer to affected skin areas bid and rub in gently and completely; continue treatment for 1 wk after clearing of signs and symptoms |
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| Pediatric Dose | <2 years: Not established
>2 years: Apply as in adults |
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| Contraindications | Documented hypersensitivity |
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| Interactions | None reported |
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| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
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| Precautions | Patients may experience a burning sensation during first few days of application; skin can become photosensitive and patients should be cautioned about exposure to direct or artificial sunlight and to use sunscreen; safety and efficacy in infected atopic dermatitis is not known; application under occlusion, which may promote systemic exposure, has not been evaluated (do not use ointment with occlusive dressings); absorption following topical applications of ointment is minimal (relative to systemic administration), but tacrolimus is excreted in human milk, and, thus, a decision should be made whether to discontinue nursing or to discontinue drug, taking into account importance of drug to mother (potential for serious adverse reactions in nursing infants from tacrolimus should also be a concern); concomitant use of alcohol may induce a flushing reaction |
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Drug Category: Antibiotics
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.
| Drug Name | Metronidazole (Protostat, Flagyl) |
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| Description | Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. Used in combination with other antimicrobial agents (except to treat Clostridium difficile enterocolitis). |
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| Adult Dose | 500 mg PO bid for 8 wk |
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| Pediatric Dose | Not established |
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| Contraindications | Documented hypersensitivity |
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| Interactions | May increase toxicity of anticoagulants, lithium, and phenytoin; cimetidine may increase toxicity; disulfiram reaction may occur with orally ingested ethanol |
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| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
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| Precautions | Adjust dose in hepatic disease; monitor for seizures and development of peripheral neuropathy |
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Drug Category: Corticosteroids
Have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.
| Drug Name | Betamethasone dipropionate (Diprolene) |
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| Description | Class I superpotent topical steroid; suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction. |
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| Adult Dose | Apply topically qd/bid |
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| Pediatric Dose | <12 years: Not recommended
>12 years: Administer as in adults |
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| Contraindications | Documented hypersensitivity; paronychia, cellulitis, impetigo, angular cheilitis, erythrasma, erysipelas, rosacea, perioral dermatitis, acne, viral or fungal skin infections |
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| Interactions | None reported |
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| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
|
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| Precautions | Do not use on skin with decreased circulation; can cause atrophy of groin, face, and axillae; may cause striae distensae or rosacealike eruption; may increase skin fragility; rarely may suppress HPA axis; if infection develops and is not responsive to antibiotic treatment, discontinue until infection is under control; do not use monotherapy to treat widespread plaque psoriasis |
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| Drug Name | Prednisone (Orasone, Meticorten, Sterapred, Deltasone) |
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| Description | May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. |
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| Adult Dose | 5-60 mg/d PO qd or divided bid/qid; taper over 2-3 mo as symptoms resolve |
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| Pediatric Dose | 4-5 mg/m2/d PO; alternatively, 0.05-2 mg/kg PO divided bid/qid; taper over 2-3 mo as symptoms resolve |
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| Contraindications | Documented hypersensitivity; viral infection, peptic ulcer disease, hepatic dysfunction, connective-tissue infections, and fungal or tubercular skin infections; GI bleeding or ulceration |
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| Interactions | Coadministration with estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics |
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| Pregnancy | |
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| Precautions | Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, insulin resistance, hypertension, electrolyte abnormalities, hyperlipidemia, myopathy, peptic ulcer disease, osteoporosis, cataracts, glaucoma, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use |
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Further Outpatient Care
- Regular follow-up is recommended to assess the course of the disease and the effectiveness of prescribed treatments. Ask patients about any adverse effects to medications and manage accordingly.
- Conduct appropriate laboratory studies as indicated with the use of systemic medications (ie, cyclosporine, thalidomide).
- Take necessary steps to prevent permanent cicatricial alopecia.
Prognosis
- Cicatricial scalp alopecia has a poor prognosis. This type of hair loss is permanent.
- Noncicatricial alopecia of the axilla and groin often spontaneously resolves.
- Follicular LP eruption on the body usually responds well to treatment; however, recurrence is not uncommon.
Patient Education
- Educate patients on the psychosocial aspects of progressive cicatricial alopecia.
- If indicated, discuss options and sources for cosmetic hairpieces to disguise end-stage scarring scalp alopecia.
Medical/Legal Pitfalls
- Failure to perform a biopsy on scalp lesions to confirm the scarring nature of the condition
- Failure to offer medical intervention in an attempt to prevent further spread of scarring and irreversible alopecia
- Failure to provide a clear discussion of the risk-to-benefit ratio of treatment options for this condition
| Media file 2:
Lichen planopilaris of the scalp resulting in cicatricial alopecia. |
 |  View Full Size Image | |
Media type: Photo
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Graham-Little-Piccardi-Lasseur Syndrome excerpt Article Last Updated: May 8, 2007
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