The Role of GLP-1RAs in Treating Inflammatory Dermatologic Diseases

In recent years, glucagon-like peptide-1 receptor agonists (GLP-1RAs) have gained widespread use as treatment options primarily for obesity and type 2 diabetes due to their ability to induce weight loss and augment insulin and glucagon secretion. Endogenously, GLP-1 is a hormone produced primarily by the enteroendocrine cells of the intestinal wall in response to food intake. By binding the GLP-1 receptor, GLP-1 plays a vital role in the regulation of the following functions: 1) blood sugar, by increasing insulin and decreasing glucagon secretion;¹ 2) appetite, through action on the hypothalamus and gut to increase satiety;² 3) gastrointestinal motility, via slowing of gastric emptying;¹ 4) the gut-brain-pancreas axis, by impacting both digestion and food metabolism;³ and 5) blood pressure, by causing vasodilation and inhibiting the sympathetic nervous system.⁴ GLP-1RAs (eg, tirzepatide, semaglutide, and liraglutide) are synthetic peptides that mimic endogenous GLP-1, and use of these therapies has expanded beyond their metabolic functions in type 2 diabetes and weight loss into other diseases due to their anti-inflammatory properties and their ability to modulate immune function. GLP-1RAs have seen increased utilization in the management of dermatologic inflammatory diseases—in particular, psoriasis, hidradenitis suppurativa (HS), and atopic dermatitis (AD).

Herein, we review the benefits and risks of GLP-1RAs with a focus on these 3 chronic inflammatory conditions.

PSORIASIS

Psoriasis is a chronic skin condition affecting 2% to 3% of the population, and comprises both skin and systemic inflammation, the latter of which entails a higher risk of cardiovascular events such as heart attack and stroke. Patients with psoriasis also tend to have comorbid conditions like obesity, type 2 diabetes, or metabolic syndrome. Consequently, the potential metabolic advantages of GLP-1RAs in psoriasis seem logical. A recent 2025 study of more than 6,000 psoriasis patients with diabetes or obesity over a 2-year period, including 3,048 who were treated with GLP-1RAs and 3,048 who received other anti-diabetic or anti-obesity drug, found that psoriasis patients treated with GLP-1RAs had a 78% lower risk of death and a 44% lower risk of major cardiovascular events compared to those taking other diabetes or weight-loss medications.⁵ Furthermore, psoriasis patients have higher incidence of depression, anxiety, and increased alcohol or substance use. The same study observed that GLP-1RAs significantly reduced the risk of alcohol abuse by 65% and substance abuse by nearly 50%.⁵ These risk reductions were more pronounced in the cohorts with psoriasis compared to persons with obesity or diabetes without psoriasis, suggesting a direct causal benefit of GLP-1RAs.  

Other smaller studies have found benefits of GLP-1RAs in psoriasis as well. A meta-analysis of 4 trials involving 32 patients observed that patients treated by GLP-1RAs had a significantly lower psoriasis area and severity index (PASI) and lower fasting plasma glucose.⁶ A randomized controlled trial by Lin et al involving 25 psoriasis patients with type 2 diabetes treated with liraglutide for 12 weeks observed a mean dermatology life quality index (DLQI) decrease from 22 to 3.82 and histopathological analysis showed improvements in psoriasis skin lesions. Additionally, reductions in the expression of inflammatory cytokines IL-17, IL-23, and tumor necrosis factor-alpha (TNF-α) were observed.7  A similar study of 20 obese psoriasis patients treated with liraglutide 3 mg for 3 months showed a near 50% mean PASI decrease from 10 to 5.1 as well as significant reductions in body mass index (BMI), visual analogue scale (VAS) pain scores, and C-reactive protein (CRP), homocysteine, ferritin, and plasma cortisol levels.8 A prospective cohort study involving seven psoriasis patients with type 2 diabetes treated with liraglutide for 12 weeks observed a mean PASI decrease from 15.7 to 2.2 and a DLQI improvement from 21.8 to 4.1.9 Additionally, reductions in HbA1c, BMI, and waist circumference were observed.9 One randomized, placebo-controlled trial involving 20 obese, glucose-tolerant patients with plaque psoriasis, however, found no significant improvement in PASI after 8 weeks of liraglutide.¹⁰

While the metabolic advantages of GLP-1RAs likely explain some of these positive findings, other mechanistic possibilities include immunoregulative functions. For example, GLP-1RAs can target invariant natural killer T (iNKT) cells and consequently reduce the production of proinflammatory cytokines such as IFN-γ, IL-2, IL-4, IL-10, IL-17, TNF-α, and GM-CSF and possibly increase the production of anti-inflammatory cytokines such as IL-10.¹¹ GLP-1RAs also decrease dermal γδ T-cells, which are IL-23 stimulated cells that produce IL-17.¹¹ GLP-1RAs also reduce lymphocyte migration, inhibit the signaling pathways involved in the proliferation and migration of immune cells, and reduce transcription of pro‑inflammatory cytokines.¹¹ Finally, weight reduction reduces levels of TNF‑α, IL‑6, and other cytokines secreted by endocrinologic adipose cells and GLP‑1RAs may have effects on reward pathways and mood that exacerbate psoriasis or its comorbidities (ie, alcohol or substance abuse).⁵ 

HIDRADENITIS SUPPURATIVA

Hidradenitis suppurativa is a chronic inflammatory skin condition characterized by recurrent, painful, inflammatory nodules and deep-seated abscesses that, over time, result in irreversible anatomic changes including draining fistulae, sinus tracts, and hypertrophic scarring predominantly in intimate flexural areas like the axillae, breasts, groin, genitals, and buttocks. The prevalence of HS is challenging to esti­ mate but has been suggested to be as low as < 0.1% to > 4% of the population. ¹²

As with psoriasis, the direct benefit of weight loss from the GLP-1RAs might even be more logical, as obesity is both a predisposing and exacerbating risk factor for HS; increases skin friction, which can worsen symptoms and contribute to flares; inhibits wound healing; and leads to the co-occur­ rence of metabolic syndrome and type 2 diabetes in affected individuals. ¹³ BMI levels >30 kg/m² in HS patients have been shown to have elevated levels of irisin protein, peroxisome proliferator-activated receptor gamma (PPARγ), and insulinlike growth factor-1 receptor (IGF-1R), which are markers of metabolic disorders and obesity, ^14,15 and they also show increased expression of the IL-17 receptor, a notable proinflammatory cytokine involved in HS pathogenesis and an established target for treatment. ¹⁴ Several studies have dem­ onstrated that weight loss via bariatric surgery reduces both the prevalence and severity of HS lesions. ¹⁶

While the metabolic advantages of GLP-1RAs likely explain some of these positive findings, other mechanistic possibili­ ties include immunoregulative functions. For example, GLP1RAs can target invariant natural killer T (iNKT) cells and consequently reduce the production of proinflammatory cytokines such as IFN-γ, IL-2, IL-4, IL-10, IL-17, TNF-α, and GM-CSF and possibly increase the production of anti-inflam­ matory cytokines such as IL-10. ¹¹ GLP-1RAs also decrease dermal γδ T-cells, which are IL-23 stimulated cells that pro­ duce IL-17. ¹¹ GLP-1RAs also reduce lymphocyte migration, inhibit the signaling pathways involved in the proliferation and migration of immune cells, and reduce transcription of pro‑inflammatory cytokines. ¹¹ Finally, weight reduction reduces levels of TNF‑α, IL‑6, and other cytokines secreted by endocrinologic adipose cells and GLP‑1RAs may have effects on reward pathways and mood that exacerbate psoriasis or its comorbidities (ie, alcohol or substance abuse).⁵

GLP-1s in Your Practice

or obesity over a 2-year period, including 3,048 who were treated with GLP-1RAs and 3,048 who received other antidiabetic or anti-obesity drug, found that psoriasis patients treated with GLP-1RAs had a 78% lower risk of death and a 44% lower risk of major cardiovascular events compared to those taking other diabetes or weight-loss medications.⁵ Furthermore, psoriasis patients have higher incidence of depression, anxiety, and increased alcohol or substance use. The same study observed that GLP-1RAs significantly reduced the risk of alcohol abuse by 65% and substance abuse by nearly 50%.⁵ These risk reductions were more pro­ nounced in the cohorts with psoriasis compared to persons with obesity or diabetes without psoriasis, suggesting a direct causal benefit of GLP-1RAs.

Other smaller studies have found benefits of GLP-1RAs in psoriasis as well. A meta-analysis of 4 trials involving 32 patients observed that patients treated by GLP-1RAs had a significantly lower psoriasis area and severity index (PASI) and lower fasting plasma glucose.⁶ A randomized controlled trial by Lin et al involving 25 psoriasis patients with type 2 diabetes treated with liraglutide for 12 weeks observed a mean dermatology life quality index (DLQI) decrease from 22 to 3.82 and histopathological analysis showed improve­ ments in psoriasis skin lesions. Additionally, reductions in the expression of inflammatory cytokines IL-17, IL-23, and tumor necrosis factor-alpha (TNF-α) were observed.⁷ A similar study of 20 obese psoriasis patients treated with liraglutide 3 mg for 3 months showed a near 50% mean PASI decrease from 10 to 5.1 as well as significant reduc­ tions in body mass index (BMI), visual analogue scale (VAS) pain scores, and C-reactive protein (CRP), homocysteine, ferritin, and plasma cortisol levels.⁸ A prospective cohort study involving seven psoriasis patients with type 2 diabe­ tes treated with liraglutide for 12 weeks observed a mean PASI decrease from 15.7 to 2.2 and a DLQI improvement from 21.8 to 4.1.⁹ Additionally, reductions in HbA1c, BMI, and waist circumference were observed.⁹ One randomized, placebo-controlled trial involving 20 obese, glucose-tolerant patients with plaque psoriasis, however, found no significant improvement in PASI after 8 weeks of liraglutide.¹⁰

GLP-1s in Your Practice

Inflammatory and immunomodulating, just as in psoriasis. Krajewski et al performed a systematic review of GLP-1RAs in HS patients and demonstrated significant reductions in inflammatory nodules, abscess formation, and overall disease severity. ¹⁷ GLP-1RAs have been shown to inhibit TNF-α, which is another notable pro-inflammatory cytokine involved in HS pathogenesis and an established target for treatment. ¹⁸ GLP-1RAs also reduce invariant natural killer T-cell (iNKT) levels, which is significant as activation of these cells results in increased expression of pro-inflammatory cytokines such as IFN-γ, TNF-α, and IL-17. ¹⁹ In a study by Mei et al, liraglutide therapy was associated with reduced TNF-α levels, reduced activation of the nuclear factor κB (NF-κB) pathway, reduced secretion of monocyte chemo­tactic protein 1, as well as suppression of IL-17, IL-22, and IL-23. ²⁰

These anti-inflammatory benefits correlate to clinical and symptomatic improvements in patients with HS. For example, a small retrospective study of 30 obese HS patients treated with weekly semaglutide (~0.8 mg for ~8.2 months) resulted in a 5% weight loss, a reduction in flare frequency (every 8.5 weeks to every 12 weeks), modest reductions in inflammatory markers like HbA1c and CRP, and improvement in DLQI (13 to 9). ²¹ Similarly, a prospective case series of 14 patients with both HS and obesity treated with liraglutide 3 mg for 3 months demonstrated reductions in BMI, waist circumference, systemic inflammatory markers like CRP, homocysteine and plasma cortisol, and DLQI. ²² Gouvrion et al studied 66 patients with HS who were treated with a GLP-1RA for at least 3 months, with a median follow-up time of 18.5 months. They observed that 60% of patients reported a decrease in pain, 62% experienced a 1-point or higher reduction in their HS-PGA score, and 67% reported a reduction in the frequency of their flares. Additionally, these positive changes were observed in a subgroup of patients in which their other therapies remained unchanged, suggesting a direct effect of the GLP-1 RA. ²³ Not all patients experience benefit from GLP-1RAs, with some patients experiencing increased inflammation and more flares. ¹⁷

ATOPIC DERMATITIS

Atopic dermatitis (AD) is a chronic inflammatory skin condition affecting approximately 10% to 20% of children and 2% to 10% of adults. ^24,25 It is characterized by an impaired skin barrier and immune dysregulation. Unlike psoriasis and HS, patients with atopic dermatitis do not have the same tendency to be overweight or obese and are not prone to diabetes or metabolic syndrome, which makes the metabolic functions of GLP-1RAs less significant. Additionally, data on GLP-1 RA use in this population is sparse.

Perhaps the largest study was a 10-year analysis of 17,099 propensity score-matched patient pairs with type 2 diabetes, with or without AD, between 2015 and 2025, including pairs treated with GLP-1RAs. ²⁶ In this study, patients with AD vs those without AD showed higher risks for myocardial infarction (MI), heart failure, and ischemic stroke but not for MACE; patients with AD had a significantly lower risk for mortality than those without AD. Among type 2 diabetic patients with or without AD who were treated with GLP-1RAs, no differences were seen in the risks for mortality, new-onset MACE, MI, heart failure, or stroke. GLP-1RAs did, however, significantly reduce the risk for new-onset MACE, MI, heart failure, and ischemic stroke in patients with AD and type 2 diabetes, suggesting that the benefit of GLP-1RAs is in diabetes vs atopic dermatitis. Furthermore, this study only assessed systemic cardiovascular risk; it did not show that GLP-1RAs improve atopic dermatitis severity.

To the author’s best knowledge, no published randomized controlled trials or well‐documented case reports have shown that GLP-1RAs improve atopic dermatitis severity (eg, EASI, SCORAD, itch, flare frequency), and no in vivo or ex vivo studies have been performed showing that GLP-1RAs modulate the Th2 or barrier dysfunction pathways characteristic of AD. Despite the lack of published data for GLP-1RAs in AD, there still could be a theoretical benefit as GLP-1RAs have demonstrated anti-inflammatory properties in other diseases. One study by Daniel et al demonstrated that liraglutide impaired keratinocyte inflammatory signals by activating AMP-activated protein kinase (AMPK), leading to reduced production of pro-inflammatory cytokines such as TNF-α and IL-6. ²⁷ This mechanism suggests that GLP-1RAs could modulate immune responses in skin cells, potentially impacting inflammatory atopic dermatitis.

OTHER DISEASES

There have been two studies of GLP-1RAs in HAIR-AN syndrome (hyperandrogenism (HA), insulin resistance (IR), and acanthosis nigricans (AN)), both with liraglutide. The first study included 5 women, mean age of 29 ± 2.4 years, mean BMI of 31 ± 3.5kg/m², and no use of metformin within 3 months of the trial. ²⁸ Patients received liraglutide 1.8 mg per day subcutaneously (SC) for a mean duration of 14 ± 4 months. They found improvement of menstrual cycles, hirsutism and acanthosis nigricans. Mean BMI dropped minimally from 31 to 30, insulin dropped from 39.25 to 22.44, HOMA-IR (homeostatic model assessment of insulin resistance) dropped from 8.388 to 5.118, and testosterone dropped from 1.02 to 0.63. The second study was a case report of an 11-year-old female with polycystic ovary syndrome (PCOS), type 2 diabetes, acanthosis nigricans, hirsutism, poor glycemic control, and hyperinsulinemia.²⁹ She received liraglutide 0.3 mg SC once daily and metformin 0.5 g 4 times daily. After 13 months, the patient experienced normalized menstrual cycles and improvement of acanthosis nigricans. She lost 9.5 kg and had normalization of liver and lipid panels and decreased of insulin and C-peptide levels.

There are also some single case reports of GLP-1 RA use in other dermatologic conditions.

A 60-year-old women with a 40-year history of refractory Hailey-Hailey disease and type 2 diabetes received liraglutide 1.8 mg SC for 6 months, after which she had near complete resolution of lesions on her neck, axillae, and inguinal and abdominal folds as well as resolution of associated pain. ³⁰

A 57-year-old man with acne keloidalis nuchae, BMI 33.45 kg/m², androgenic alopecia, acanthosis nigricans, and insulin resistance received tirzepatide 2.5 mg SC every 7 days for 3 months, then 5 mg weekly for 6 months, and then 7.5 mg weekly for 3 more months. Afterward, he had marked improvement of hair loss at vertex scalp and bitemporal scalp with increased hair regrowth noted at 6 months as well as a 30-lbs weight loss and decreased HOMA-IR from 3.2 to 1.7. ³¹

A male patient in his 40s presented with a 30-year history of folliculitis decalvans and had failed multiple topical, oral, and intralesional steroids. He received tirzepatide 2.5 mg SC weekly titrated to 12.5 mg weekly over 9 months, after which he lost 50 pounds and experienced prominent hair regrowth as well as decreased pain, drainage, and flares. ³²

Finally, a 14-year-old female with childhood-onset congenital linear scleroderma previously managed with steroids, methotrexate, and mycophenolate mofetil presented with progressive erythema, atrophy, and subcutaneous fat loss. She received semaglutide for 7 months, after which she noted improved mobility and reduced skin hardness in her left arm. ³³

CONCLUSION

While these findings are encouraging, especially for diseases such as psoriasis and HS in which patients often are heavier and may have comorbidities like type 2 diabetes, insulin resistance, or metabolic syndrome, it’s important to recognize that most data to date come from small observational or retrospective studies with multiple possible confounders. Randomized controlled trials are absent and many patients in these small trials were treated with other therapies known to improve their underlying condition.

It is also important to recognize the complex pathogenesis of these diseases, which include genetic predispositions, immune system dysregulation, impact of environmental and behavioral factors, and the pleomorphic presentation across patients. Future studies that are prospective and controlled are required to add granularity to our understanding of how these potentially promising therapies might be optimally utilized in managing inflammatory disease in dermatology.

The author reports no relevant financial disclosures.

1. Zheng Z, Zong Y, Ma Y, et al. Glucagon-like peptide-1 receptor: mechanisms and advances in therapy. Signal Transduct Target Ther. 2024;9(234):1-29.

2. Park JS, Kim KS, Choi HJ. Glucagon-like peptide-1 and hypothalamic regulation of satiation: cognitive and neural insights from human and animal studies. Diabetes Metab J. 2025;49(3):333-347.

3. Bodnaruc AM, Prud’homme D, Blanchet R, et al. Nutritional modulation of endogenous glucagon-like peptide-1 secretion: a review. Nutr Metab. 2016;13(92):1-16.

4. Martins FL, Bailey MA, Girardi ACC. Endogenous activation of glucagon-like peptide-1 receptor contributes to blood pressure control: role of proximal tubule Na+/H+ exchanger isoform 3, renal angiotensin II, and insulin sensitivity. Hypertension. 2020;76(3):839-848.

5. Olbrich H, Kridin K, Zirpel H, et al. GLP-1RA and reduced mortality, cardiovascular and psychiatric risks in psoriasis: a large-scale cohort study. Br J Dermatol. 2025;Sep 3.

6. Chang G, Chen B, Zhang L. Efficacy of GLP-1 RA, liraglutide, in plaque psoriasis treatment with type 2 diabetes: a systematic review and meta-analysis of prospective cohort and before-after studies. J Dermatolog Treat. 2022;33(3):1299-1305.

7. Lin L, Xu X, Yu Y, et al. Glucagon-like peptide-1 receptor agonist liraglutide therapy for psoriasis patients with type 2 diabetes: a randomized-controlled trial. J Dermatolog Treat. 2022;33(3):1428-1434.

8. Nicolau J, Nadal A, Sanchís P, et al. Effects of liraglutide among patients living with psoriasis and obesity. Med Clin (Barc). 2023;161(7):293-296.

9. Xu X, Lin L, Chen P, et al. Treatment with liraglutide, a glucagon-like peptide-1 analogue, improves effectively the skin lesions of psoriasis patients with type 2 diabetes: a prospective cohort study. Diabetes Res Clin Pract. 2019;150:167-173.

10. Faurschou A, Gyldenløve M, Rohde U, et al. Lack of effect of the glucagon-like peptide-1 receptor agonist liraglutide on psoriasis in glucose-tolerant patients: a randomized placebo-controlled trial. J Eur Acad Dermatol Venereol. 2015;29(3):555-559.

11. Paschou IA, Sali E, Paschou SA, et al. GLP-1RAs in patients with psoriasis. Hormones (Athens). 2025;24:291-293.

12. Goldburg SR, Strober BE, Payette MJ. Hidradenitis suppurativa: epidemiology, clinical presentation, and pathogenesis (CME). J Am Acad Dermatol. 2020;82(5):1061-1082.

13. Phan K, Charlton O, Smith SD. Hidradenitis suppurativa and metabolic syndrome: systematic review and adjusted meta-analysis. Int J Dermatol. 2019;58:1112-1117.

14. Kaleta KP, Nikolakis G, Hossini AM, et al. Metabolic disorders/obesity is a primary risk factor in hidradenitis suppurativa: an immunohistochemical real-world approach. Dermatology. 2022;238:251-259.

15. Cacciapuoti S, Scala E, Luciano MA, et al. Irisin, a novel metabolic biomarker in hidradenitis suppurativa: correlation with clinical responsivity to anti-TNF-α therapy. Ital J Dermatol Venereol. 2023;158:124-127.

16. Kromann CB, Ibler KS, Kristiansen VB, et al. The influence of body weight on the prevalence and severity of hidradenitis suppurativa. Acta Derm Venereol. 2014;94:553-557.

17. Krajewski PK, Złotowska A, Szepietowski JC. The therapeutic potential of GLP-1 receptor agonists in the management of hidradenitis suppurativa: a systematic review of anti-inflammatory and metabolic effects. J Clin Med. 2024;13:6292.

18. Al-Badri MR, Azar ST. Effect of glucagon-like peptide-1 receptor agonists in patients with psoriasis. Ther Adv Endocrinol Metab. 2014;5:34-38.

19. Hogan AE, Tobin AM, Ahern T, et al. Glucagon-like peptide-1 and the regulation of human invariant natural killer T cells: lessons from obesity, diabetes and psoriasis. Diabetologia. 2011;54:2745-2754.

20. Mei J, Sun J, Wu J, Zheng X. Liraglutide suppresses TNF-α-induced degradation of extracellular matrix in human chondrocytes: a therapeutic implication in osteoarthritis. Am J Transl Res. 2019;11:4800-4808.

21. Lyons D, Louly NA, Pender E, et al. Semaglutide for weight loss in people with obesity as an adjunctive treatment for hidradenitis suppurativa: its impact on disease control and quality of life. Br J Dermatol. 2024;191:631-633.

22. Nicolau J, Nadal A, Sanchís P, et al. Liraglutide for the treatment of obesity among patients with hidradenitis suppurativa. Med Clin (Barc). 2024;162:118-122.

23. Gouvrion L, Delage M, Villani AP, et al. Glucagon-like peptide-1 receptor agonists in hidradenitis suppurativa. JAMA Dermatol. Published online August 13, 2025.

24. Laughter MR, Maymone MBC, Mashayekhi S, et al. The global burden of atopic dermatitis: lessons from the Global Burden of Disease Study 1990–2017. Br J Dermatol. 2021;184(2):304-309.

25. Choragudi S, Yosipovitch G. Trends in the prevalence of eczema among US children by age, sex, race, and ethnicity from 1997 to 2018. JAMA Dermatol. 2023;159(4):454-456.

26. Teotia V. GLP-1 receptor agonists reduce CV event risks in patients with T2D and atopic dermatitis. Medscape Medical News. 2025.

27. Daniel S, Waggett S, Lyles E, et al. A retrospective comparative analysis of cutaneous adverse reactions in GLP-1 agonist therapies. J Drugs Dermatol. 2025;24(4):413-415.

28. Livadas S, Androulakis I, Angelopoulos N, et al. Liraglutide administration improves hormonal/metabolic profile and reproductive features in women with HAIR-AN syndrome. Endocrinol Diabetes Metab Case Rep. 2020.

29. Li R, Li H, Yang Z, Zhang X. Combination of metformin with liraglutide in treating HAIR-AN syndrome in children: a case report and literature review. Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2023;48:1425-1431.

30. Barry R, Murray G, Hellen R, et al. Liraglutide, a GLP-1 agonist, as a new adjunct treatment in Hailey-Hailey disease: a case report. Clin Exp Dermatol. 2024;49:409-411.

31. Gordon ER, Musleh S, Bordone LA. Treatment of insulin resistance with tirzepatide leading to improvement of hair loss. JAAD Case Rep. 2024;50:123-125.

32. Morrissette K, Hansen S, Pavlis M, Murray JC: Improvement of recalcitrant folliculitis decalvans with tirzepatide: a case report. Cureus. 2024;16(12):e76267.

33. Chen H, Elhawi M, Tarbox M: The therapeutic effects of semaglutide in congenital linear scleroderma. Cureus. 2025. Doi:10.7759/cureus.88725