GRAHAM-LITTLE-PICCARDI-LASSEUR SYNDROME IN A BULGARIAN PATIENT: CASE REPORT AND SHORT PATHOGENETIC UPDATE IN RELATION TO THE CONNECTION TO ANTIGEN/ MOLECULAR MIMICRY.
{"title":"GRAHAM-LITTLE-PICCARDI-LASSEUR SYNDROME IN A BULGARIAN PATIENT: CASE REPORT AND SHORT PATHOGENETIC UPDATE IN RELATION TO THE CONNECTION TO ANTIGEN/ MOLECULAR MIMICRY.","authors":"S Kordeva, V Broshtilova, G Tchernev","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Graham-Little-Piccardi-Lasseur syndrome (GLPLS) is a rare lichenoid dermatosis classified as a variant of follicular lichen planus, also known as classic lichen planopilaris. The condition is characterized by the triad of cicatricial scalp alopecia, noncicatricial alopecia in the axillary and groin regions, and numerous follicular papules distributed across the body. We present a 64-year-old female with clinically and histologically confirmed GLPLS. Two biopsies were conducted, resulting in lichen planopilaris/ pseudopelade Brocq and lichen planus hypertrophicus. Initial therapy included loratadine and topical clobetasol propionate. Due to the suspicion of possible drug-induced reaction, the antihypertensive therapy, which consisted of valsartan, bisoprolol, spironolactone, and chlorthalidone, was discontinued and replaced with moxonidine. Urinary infection caused by Escherichia coli and dental infection were noted. Prescribed outpatient treatment included acitretin, bilastine, and topical prednisolone for the scalp. Improvement was observed in the lesions located on the trunk and upper and lower extremities following betamethasone/salicylic acid ointment was prescribed, and methylprednisolone aceponate cream. Re-application or return of the old systemic medication on an outpatient basis resulted in a worsening/exacerbation of the clinical picture and a re-need to change medication. It is this fact that suggests that polymedication could also be considered as a trigger of lichen planus and its subforms such as GLPLS. The hypothesis surrounding alterations in tissue homeostasis as a potential trigger factor for autoimmunity is being discussed, with a specific focus on infectious and drug-induced forms of lichen planus, as well as Graham-Little-Lasseur syndrome.</p>","PeriodicalId":12610,"journal":{"name":"Georgian medical news","volume":" 357","pages":"61-67"},"PeriodicalIF":0.0000,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Georgian medical news","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Medicine","Score":null,"Total":0}
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Abstract
Graham-Little-Piccardi-Lasseur syndrome (GLPLS) is a rare lichenoid dermatosis classified as a variant of follicular lichen planus, also known as classic lichen planopilaris. The condition is characterized by the triad of cicatricial scalp alopecia, noncicatricial alopecia in the axillary and groin regions, and numerous follicular papules distributed across the body. We present a 64-year-old female with clinically and histologically confirmed GLPLS. Two biopsies were conducted, resulting in lichen planopilaris/ pseudopelade Brocq and lichen planus hypertrophicus. Initial therapy included loratadine and topical clobetasol propionate. Due to the suspicion of possible drug-induced reaction, the antihypertensive therapy, which consisted of valsartan, bisoprolol, spironolactone, and chlorthalidone, was discontinued and replaced with moxonidine. Urinary infection caused by Escherichia coli and dental infection were noted. Prescribed outpatient treatment included acitretin, bilastine, and topical prednisolone for the scalp. Improvement was observed in the lesions located on the trunk and upper and lower extremities following betamethasone/salicylic acid ointment was prescribed, and methylprednisolone aceponate cream. Re-application or return of the old systemic medication on an outpatient basis resulted in a worsening/exacerbation of the clinical picture and a re-need to change medication. It is this fact that suggests that polymedication could also be considered as a trigger of lichen planus and its subforms such as GLPLS. The hypothesis surrounding alterations in tissue homeostasis as a potential trigger factor for autoimmunity is being discussed, with a specific focus on infectious and drug-induced forms of lichen planus, as well as Graham-Little-Lasseur syndrome.