title: Improvement of psoriasis during glucagon-like peptide-1 analogue therapy in type 2 diabetes is associated with decreasing dermal γδ T-cell number: a prospective case-series study.
abstract: BACKGROUND
  A few case reports suggest that incretin-based therapies could improve psoriasis in patients with type 2 diabetes, the mechanism(s) of which remain unclear.
  
  
  OBJECTIVE
  To determine the effects after 16-20 weeks of treatment with a glucagon-like peptide (GLP)-1 analogue on clinical severity and histopathological aspects of psoriasis in patients with type 2 diabetes, and to examine the presence of γδ T cells and the expression of interleukin (IL)-17 in psoriasis before and after treatment.
  
  
  METHODS
  Seven patients with type 2 diabetes and psoriasis were followed. Psoriasis Area and Severity Index (PASI) was measured at baseline (T0) and after 7 ± 1 (T1) and 18 ± 2 (T2) weeks' treatment with exenatide/liraglutide. The histopathological pattern of psoriasis, and flow cytometry and immunological data (γδ T-cell percentage and IL-17 expression) were obtained from psoriatic and control sites.
  
  
  RESULTS
  The mean PASI decreased from 12·0 ± 5·9 to 9·2 ± 6·4 (P = 0·04). Histological analysis showed a reduction in epidermal thickness after treatment. The dermal γδ T-cell percentage was higher in psoriatic lesions than in control specimens (P = 0·03), as was IL-17 expression (P = 0·018). A reduction of γδ T cells from 6·7 ± 4·5% to 2·7 ± 3·8% (P = 0·05) was demonstrated in the six patients with improved/unchanged PASI. A correlation between PASI and γδ T-cell percentage evolution during therapy (T2-T0) was noted (r = 0·894, P = 0·007). IL-17 was reduced in the four patients with the highest PASI reductions.
  
  
  CONCLUSIONS
  The administration of a GLP-1 analogue improved clinical psoriasis severity in patients with type 2 diabetes. This favourable outcome was associated with a decrease of dermal γδ T-cell number and IL-17 expression. Further studies are needed to establish long-term efficacy in (diabetic) patients with psoriasis.
authors: Department of Endocrinology and Nutrition, Avenue Hippocrate 10, B-1200, Brussels, Belgium.
authors: M
authors: M
authors: Buysschaert
authors: M
authors: M
authors: Baeck
authors: V
authors: V
authors: Preumont
authors: L
authors: L
authors: Marot
authors: E
authors: E
authors: Hendrickx
authors: A
authors: A
authors: Van Belle
authors: L
authors: L
authors: Dumoutier
mesh_terms: D000328:Adult; D002908:Chronic Disease; D003924:Diabetes Mellitus, Type 2 / Q000150:complications* / Q000188:drug therapy / Q000276:immunology; D000077270:Exenatide; D005260:Female; D052216:Glucagon-Like Peptide 1 / Q000031:analogs & derivatives* / Q000627:therapeutic use; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D054795:Incretins / Q000627:therapeutic use*; D020381:Interleukin-17 / Q000378:metabolism; D000069450:Liraglutide; D018655:Lymphocyte Count; D008297:Male; D008875:Middle Aged; D010455:Peptides / Q000627:therapeutic use*; D011446:Prospective Studies; D011565:Psoriasis / Q000150:complications / Q000188:drug therapy* / Q000276:immunology; D012720:Severity of Illness Index; D012867:Skin / Q000276:immunology; D013601:T-Lymphocytes / Q000378:metabolism; D016896:Treatment Outcome; D014688:Venoms / Q000627:therapeutic use*
chemical_list: D007004:Hypoglycemic Agents; D054795:Incretins; D020381:Interleukin-17; D010455:Peptides; D014688:Venoms; D000069450:Liraglutide; D052216:Glucagon-Like Peptide 1; D000077270:Exenatide