Is psoriasis an autoimmune condition?

Psoriasis and Other Autoimmune Diseases: Are You at Risk?

Despite its very visible appearance on your skin, psoriasis is fundamentally an autoimmune condition, not a skin woe.

Autoimmune diseases share certain traits. With all autoimmune diseases, your body’s internal protection system misfires, and your body essentially begins attacking itself.

If you have psoriasis, you’re more likely to develop one or more other autoimmune diseases. A study published in November 2012 in the Journal of the American Academy of Dermatology concluded that people with psoriasis are nearly twice as likely as people without psoriasis to develop additional autoimmune diseases.

Of the 21 autoimmune diseases studied, 17 were found to be linked to psoriasis, including alopecia areata, celiac disease, scleroderma, lupus, and Sjogren’s syndrome. The autoimmune disease most strongly associated with psoriasis was rheumatoid arthritis (RA).

If you have psoriasis and psoriatic arthritis (PsA), your risk for an additional autoimmune disease increases even more. The study concluded that there may be a genetic or environmental cause that is shared across the spectrum of autoimmune diseases.

Psoriatic Arthritis or Rheumatoid Arthritis?

If you have psoriasis and consistently experience joint pains and aches, you should see your health care provider. PsA and RA are both very real possibilities for people with psoriasis.

Determining the type of arthritis you have can be challenging, but making the distinction is important, says Natalie E. Azar, MD, an assistant clinical professor of medicine and rheumatology at the New York University Langone Medical Center in New York City.

Although rheumatoid arthritis and psoriatic arthritis share many similar clinical features — for example, joint pain, stiffness, and swelling — it’s important to distinguish which condition you have in order to manage it well and know what to expect, Dr. Azar says.

In the last several years, Azar explains, physicians have come to understand more about PsA’s association with other health concerns already known to be linked to RA, such as uveitis, osteoporosis, metabolic syndrome, and increased cardiovascular risk, to name a few.

“Although treatment options can be strikingly similar,” Azar says, “significant advances have been made in the development and discovery of new biologic therapies very specific for PsA.”

Psoriatic arthritis occurs in as many as 30 percent of people who have psoriasis, but there is no single specific diagnostic test for the condition, says Azar. Your doctor may begin to suspect you have PsA if you’re experiencing changes to your skin and nails. Bring any such changes you notice to your doctor’s attention in case further testing is needed.

Your doctor may suspect rheumatoid arthritis from the presence of autoantibodies in your bloodstream known collectively as the rheumatoid factor. These antibodies are less typical in people with psoriatic arthritis.

Determining which kind of arthritis you have frequently depends on looking closely at how your joints are affected, Azar says. “RA involves the joints in a symmetrical fashion, and often, when rheumatoid factor is very high, there may be nodules under the skin. But PsA can present in a variety of different ways, from a large joint in asymmetric arthritis, to one, small finger joint of the hand.”

Another notable difference between the two diseases is the type of joint inflammation.

“RA is characterized by bone loss or erosion near the joint, while PsA is characterized by both erosion and new bone formation,” Azar says. RA affects mainly the joints, while PsA may also involve the entheses — the areas where muscles, ligaments, and tendons attach to the bone. People with PsA often experience recurrent bouts of tendinitis and plantar fasciitis. PsA can even involve the spine, resulting in spondylitis or sacroiliitis, painful conditions that tend to be absent in RA.

Signs and Symptoms to Watch For

There are more than 100 autoimmune diseases in all, and the list is growing, notes Amber L. Champion, MD, an endocrinologist who practices in North Platte, Nebraska.

“They are a diverse group of diseases and affect nearly every organ system of the body,” Dr. Champion says. She recommends talking with your doctor if you notice joint pain, patchy hair loss, skin tightening, frequent hives, or blood in your stool.

“Other symptoms might include unintended weight loss, abdominal pain, dry eyes and mouth, change in color inside the mouth, and headaches,” she adds. “Of course, these symptoms can be very nonspecific, so a thorough investigation is indicated if a symptom occurs.”

This will serve as part 2 of the 3-part First Report Managed Care Trends Report on autoimmune diseases. This second part will report the findings from survey participants on psoriasis and atopic dermatitis.

Data for this Trends Report was generated through a comprehensive survey of managed care professionals. Survey questions were developed by the editorial staff and vetted by 9 members of the Editorial Advisory Board. The types of questions asked in the survey focused on demographics, institutional practices, treatment guidelines, compliance and adherence measures, prior authorization criteria, and treatment decisions for some drug classes used in the management of autoimmune disease. The survey participants were also asked to provide comments on the challenges of treating the 5 autoimmune diseases covered in Trends Report from a managed care perspective.

The survey was distributed via a recognized survey platform and sent to the universe of managed care professionals from our email database. A total of 39 managed care professionals completed the survey with 11 partial completions. Data was then compiled based on all of the participants to generate this report.

For the survey participant demographic data, 93.9% said their organization has responsibility for commercial insurance plans. Nearly one-quarter of the survey participants (24.5%) said >5,000,000 lives are covered by their plan. Forty percent reported that their primary formulary is closed. In terms of generic dispensing rate, 32.7% said their generic dispensing rate is ≥85.0%. For complete demographic information, along with the survey findings on rheumatoid arthritis and psoriatic arthritis, please see the September issue.

The complete Trends Report will be available for download on Managed Health Care Connect at


Psoriasis is a chronic, genetic, immune-mediated inflammatory, multisystem skin disease affecting 7.5 million people in the United States.1,2 Five types of psoriasis exist and include plaque, guttate, inverse, pustular, and erythrodermic, of which 80% to 90% of people have plaque psoriasis. Psoriasis is generally characterized by patches of abnormal skin that are red, itchy, and scaly and most commonly manifests on the scalp, knees, elbows, hands, and feet.3 Psoriasis triggers are not universal. According to the National Psoriasis Foundation, stress, injury to skin, and reactions to medication are established psoriasis triggers.4 The economic burden of psoriasis is significant. In 2013, the direct costs associated with psoriasis ranged from $51.7 billion to $63.2 billion.5

Currently, there is no known cure for psoriasis. Treatments include traditional systemic and targeted oral agents and biologics. Several pharmacological therapies are in the drug pipeline to treat this often debilitating autoimmune disease.6,7

Survey Results

The survey participants were almost evenly divided in their response to whether their organization currently has treatment guidelines in place for the treatment of psoriasis, 48.8% said “yes” and 51.2% said “no.” In terms of the guidelines they have in place, 21.4% of the survey participants said these guidelines are based on a combination of internally- and national-developed guidelines, while 16.7% said they are based on national guidelines from professional organizations, and 7.1% said the guidelines are developed by their pharmacy benefit manager. See Figure 1.

When asked if their organization currently has prior authorization screening criteria for access to specialty pharmacy drugs to treat psoriasis, 69.0% of the survey participants said “yes.” The survey participants were next asked about their organization involvement in reporting adherence/compliance on the use of psoriasis medications obtained through a specialty pharmacy, 26.2% said “a moderate amount” and 23.8% said “a great deal.” Another 16.7% said “rarely.” See Figure 2.

Some specialty pharmaceuticals used in the treatment of psoriasis require in-office administration of the drug. Therefore, the survey participants were asked to select a percentage range that best represents their understanding of how many specialty pharmaceuticals require in-office administration to treat psoriasis, and 40.5% of the participants said 0% to 25%. Another 21.4% said 26% to 50%. However, nearly thirty percent (28.6%) of those who took the survey said they were not sure what percentage of specialty pharmaceuticals for psoriasis requires in-office administration. See Figure 3.

The majority of the survey participants (61.9%) said patients are “always” provided with safety information in addition to prescribing information with regards to the use of biologics in the treatment of psoriasis, while 21.4% said “sometimes.” See Figure 4.

Novel oral therapies, referred to as small molecule inhibitors, are emerging for the treatment of psoriasis.6 Apremilast (Otezla) is one example of a new oral small molecule therapy for psoriasis. It is a phosphodiesterase-4 inhibitor that received FDA approval8 in 2014. The survey participants were asked if they are seeing an increase in the utilization and prescribing of apremilast for psoriasis over the past 6 months, and the survey participants were split—35.7% said “yes” and 35.7% said “no.” Continuing with the topic of drug therapies, the survey participants were also split when asked if they have preferred biologic agents for the treatment of psoriasis—50.0% said “yes” and 50.0% said “no.”

Atopic Dermatitis

Atopic dermatitis is a common skin disease resulting from too many reactive inflammatory cells in the skin.9 While the disease is primarily found in children, it affects more than 30 million Americans.10 The disease is often referred to as eczema, dermatitis, atopic eczema, and atopic dermatitis. The condition presents as itchy, dry, red, scaly patches on the skin. These itchy patches generally appear on the face, forehead, and scalp, but can also be present anywhere on the body.11 Because atopic dermatitis is an uncomfortable chronic skin condition that can have a significant effect on quality of life, treatments are aimed at preventing atopic dermatitis from worsening, calming the skin, relieving the pain and itch, reducing emotional stress, and preventing infections.12,13 A treatment plan often includes emollients to keep the skin moisturized and topical steroids to bring flare ups under control, as well as lifestyle changes.

Survey Results

More than half of the survey participants (53.7%) said “yes” when asked if they consider atopic dermatitis to be an autoimmune disease based on the National Eczema Association’s statement14 that atopic dermatitis occurs at a molecular level.

When asked if their organization is actively promoting multidisciplinary management of atopic dermatitis, nearly sixty percent (58.5%) said “no,” while 19.5% said “yes.”

On the topic of treatment guidelines for atopic dermatitis, 36.6% of the survey respondents said their organization currently has treatment guidelines in place to treat this disease state. Among those survey participants who have treatment guidelines in place, 19.5% said they are based on a combination of internally- and national-developed guidelines, while 12.2% said they are based on national guidelines from professional organizations. See Figure 5.

Less than half of the survey respondents (46.3%) said “yes” when asked if their organization currently has prior authorization screening criteria for the treatment of atopic dermatitis.

A large majority of the survey respondents (82.9%) said they think more education is needed for physicians and other health care professionals about the serious nature of atopic dermatitis and its consequences when not treated adequately or appropriately. See Figure 6.

When asked if they are aware of pipeline agents for the treatment of atopic dermatitis, the majority of survey respondents (68.3%) said “no” compared with 31.7% who said “yes.”


The symptoms associated with psoriasis and atopic dermatitis can have a significant impact on quality of life for those living with these chronic skin diseases. Often individuals with these autoimmune diseases require lifelong management. Yet, the majority of survey respondents reported that their organizations do not have treatment guidelines in place to treat psoriasis and atopic dermatitis (51.2% and 63.4%, respectively). Because some specialty drugs are used in the management of psoriasis and atopic dermatitis, prior authorization screening criteria for access to these drugs has become a key issue among managed care stakeholders. The majority of the survey participants reported that their organization requires this step for psoriasis (69.0%). However, more than half of those surveyed said this process is not done for atopic dermatitis (53.7%).

Multidisciplinary management of atopic dermatitis is recommended, however, 58.5% of the survey respondents said their organization is not actively promoting it. Education is an important component is the management of atopic dermatitis. The majority of participants (82.9%) agreed that more education is needed for health care professionals about the serious nature of this disease state and the consequences when it is not treated adequately or appropriately. This was echoed by some of the survey respondents when they were asked to share their general thoughts and concerns for treating atopic dermatitis through an open-ended section of the survey (Box). Although medication adherence continues to be a challenge in managing psoriasis and atopic dermatitis, lack of treatment efficacy and drug cost play an important role.

1. Menter A, Gottlieb A, Feldman, SR, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: Section 1. Overview of psoriasis and guidelines of care for the treatment of psoriasis with biologics. J Am Acad Dermatol. 2008;58(5):826-850.

2. National Psoriasis Foundation. The Psoriasis and Psoriatic Arthritis Pocket Guide: Treatment Options and Patient Management. 3rd ed. Portland, OR; 2009.

3. About psoriasis. National Psoriasis Foundation website. Accessed September 9, 2016.

4. Psoriasis causes and triggers. National Psoriasis Foundation website. Accessed September 9, 2016.

6. Yiu ZZ, Warren RB. Novel oral therapies for psoriasis and psoriatic arthritis. Am J Clin Dermatol. 2016;17(3):191-200.

10. What is eczema? National Eczema Association website. Accessed September 9, 2016.

12. Drucker AM, Wang AR, Qureshi AA. Research gaps in quality of life and economic burden of atopic dermatitis: The National Eczema Association Burden of Disease Audit. JAMA Dermatol. 2016;152(8):873-874.

14. Atopic dermatitis found to be an autoimmune disease. National Eczema Association website. Accessed September 9, 2016.

Autoimmune Mechanisms of Psoriasis: Pathogenic Role of the IL-23/IL-17 Axis


Psoriasis is a chronic, recurrent, immuno-inflammatory disease of the skin and joints which in the most common form is manifested by erythematous, scaly plaques commonly occurring on the elbows, knees, scalp, and trunk . Psoriasis has a complex genetic background. A recent twin study showed that psoriasis represents a multifactorial disorder in which genetic factors account for about 70% of disease susceptibility, whereas environmental factors account for the remaining 30% . These findings indicate that the heritability is not the only cause of psoriasis, and other environmental factors such as skin microbiota may also contribute to the susceptibility to this immuno-inflammatory disease.

Histologically, psoriasis is characterized by inflammatory hyperproliferation and thickening of the epidermis, accompanied by altered differentiation of keratinocytes and their accumulation in the upper layers of the epidermis . Increased vascularization of psoriatic plaques follows keratinocyte hyperproliferation that results in a massive influx of innate and adaptive immune cells producing an array of inflammatory mediators which sustain the chronic inflammation .

Accumulation of inflammatory CD4+ Th1 cells, CD8+ cytotoxic T lymphocytes, and Th17 cells is accompanied by increased expression of IL-17A in psoriatic lesions . IL-17A, primarily produced by CD4+ Th17 cells and δγ T cells, operates at the interface of innate and adaptive immunity by activating keratinocytes to produce IL-17C that along with other keratinocyte-derived mediators serves to sustain the chronic inflammation in psoriatic plaques. Taken together, psoriasis is regarded as an IL-17-mediated inflammatory condition in which IL-17-producing CD4+ Th17 T cells, δγ T cells, and keratinocytes play a critical role.

The ability to stimulate acute and chronic inflammation has implicated IL-17 in the pathogenesis of various human systemic and organ-specific autoimmune disorders . In this regard, recent findings that implemented IL-17 in the pathogenesis of psoriasis also suggest an autoimmune nature of this immuno-inflammatory skin disease. The universal involvement of IL-17 in various autoimmune diseases has identified IL-17 as an ideal target for the development of immunotherapeutic approaches . Given the critical role of IL-23 in generating Th17 cells , multiple clinical trials targeting the IL-17/IL-23 axis in the pathogenic mechanisms of psoriasis are underway.

Role of microflora and molecular mimicry in psoriasis

Although the etiology of psoriasis is not fully elucidated, both hereditary and environmental factors contribute to the onset and periodic exacerbations of the disease. Skin plays a vital protective role as a physical barrier and habitat for resident microflora, a diverse community of microorganisms, generally comprised of harmless and beneficial species . Emerging evidence strongly suggests the existence of an intricate relationship between skin microflora and a complex network of keratinocytes, epithelial cells, and immune cells in the skin . In this regard, it has been long suspected that psoriasis may well be associated with alterations in the composition and representation of the cutaneous bacterial microflora, although classical cultivation-dependent microbiological methods did not permit a detailed identification of the cutaneous bacterial community. Recently, comparative high-throughput pyrosequencing analyses of microbiota in biopsies from psoriatic lesions and normal skin have demonstrated that Firmicutes species were significantly overexpressed, whereas Actinobacteria, the most prevalent and diverse phylum in normal skin, and Propionibacterium species, in particular, were significantly underrepresented in psoriatic lesions . The followed studies have confirmed the decreased presence of Propionibacteria and also revealed the decreased abundances of staphylococci in psoriatic lesions compared to healthy skin . Yet, it remains unclear whether the observed change in skin microbiota is the causative factor in the development of psoriasis.

Although the cause-effect relationship between dysbiosis of the skin microflora and auto-inflammatory mechanisms of psoriasis has yet to be fully elucidated, recent studies showed that tonsillar infections caused by Streptococcus pyogenes often precede the onset of psoriasis whereas periodic exacerbations are associated with skin colonization by Staphylococcus aureus, Malassezia, or Candida albicans . Different mechanisms have been proposed to describe how infections can trigger and/or exacerbate autoimmune diseases. Molecular mimicry is a mechanism in which a microbial antigen shares structural similarities with self-antigens and is typically characterized by the appearance of autoantibodies and self-reactive T cell clones. The concept of molecular mimicry has thus been proposed as a triggering mechanism of various autoimmune diseases including the onset and periodic exacerbations of psoriasis . In individuals susceptible to psoriasis, tonsillar infections with group-A hemolytic Streptococcus pyogenes may induce the rise of pathogen-specific T cell clones which may also cross-react with keratinocyte-derived autoantigens. Specifically, oligoclonal T cells were identified in the blood and psoriatic lesions which cross-reacted with determinants common to streptococcal M-protein and keratin . It appears that those psoriatic T cell clones selectively accumulated and persisted in the lesions but not in the healthy skin of patients with psoriasis .

Evidence for an autoimmune etiology

Autoimmunity is characterized by the breakdown of self-tolerance and abnormal antibody-mediated and/or T cell-mediated immune responses against self-antigens. Our understanding of the pathogenesis of psoriasis has evolved greatly over the years, and the question of autoimmunity is frequently debated. However, identification of genetic risk variants, the discovery of multiple autoantigens, and the role of Th17 cells commonly involved in various autoimmune diseases provide strong support for the concept of autoimmune pathogenic mechanisms of psoriasis.

Genetic variations have been identified for many common autoimmune diseases. Genome-wide association (GWA) studies have discovered numerous single nucleotide polymorphisms (SNPs) that confer the susceptibility to various autoimmune diseases . Like other autoimmune diseases, psoriasis has been shown to have a strong genetic component, with a concordance rate in identical twins of 40-70% . Over sixty psoriasis susceptibility loci have been identified among which the MHC Class I molecule HLA-Cw*0602 is the most significant since more than 60% of psoriasis patients are hetero- or homozygous for this allele . Other psoriasis susceptibility loci, to name a few, include ERAP1 encoding for an Endoplasmic Reticulum Aminopeptidase 1 and ERAP2 , which are both involved in antigen processing and presentation , IL23R , as well as TNFAIP3 (TNF-alpha induced protein 3), in which polymorphisms have also been implicated in rheumatoid arthritis, type 1 diabetes, celiac disease, and Crohn’s disease .

The discovery of autoantigens further supports the autoimmune concept in the pathogenesis of psoriasis. Molecular mimicry has been recognized as a triggering factor of many autoimmune diseases . Molecular mimicry has also been implicated in the pathogenesis of psoriasis . Streptococcal throat infection is a known trigger of acute guttate psoriasis, with an incidence of preceding infection ranging between 56-97% . Homology between the streptococcal M-protein and keratin 17 yields cross-reactive CD8+ T cells seen in patients with psoriasis, especially in patients with HLA-Cw*0602 . Another autoantigen that has been implicated in psoriasis is cathelicidin/LL-37, an antimicrobial peptide synthesized by keratinocytes and neutrophils in reaction to infection or trauma to the skin . Autoreactive T cells against cathelicidin were found in the peripheral blood of 75% of patients with moderate to severe psoriasis . It was recently found that ADAMTSL5 (ADAMTS-like protein 5) serves as a psoriasis autoantigen which overexpression by melanocytes is observed in HLA-Cw*0602 positive patients . TCRs of CD8+ T cells recognize ADAMTSL5 presented by melanocytes in psoriatic lesions and generate IL-17, a signature cytokine in psoriasis.

In addition to T cell-mediated immune responses, circulating auto-antibodies against calpastatin, a natural inhibitor of the protease calpain, have been identified in psoriasis patients but not healthy controls . Of importance, anti-calpastatin auto-antibodies were also found in various autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus, dermatomyositis, polymyositis, systemic sclerosis, Sjögren’s Syndrome, and overlap syndrome which further support the concept of psoriasis as an autoimmune disease . In addition, several autoantibodies such as anti-heat shock protein 65 antibodies , anti-stratum corneum antibodies and anti-squamous cell carcinoma antigen antibodies have been identified in psoriasis, although their clinical significance has yet to be determined.

Association between psoriasis and other autoimmune diseases has been the subject of ongoing investigation. A recent retrospective cohort study has demonstrated that patients with psoriasis are at higher risk of developing at least one other autoimmune disease with rheumatoid arthritis having the strongest association (3.6; 95% CI 3.4-3.9) . Another case-control study involving 12,506 psoriasis patients found that 0.29% of the patients had celiac disease compared with 0.11 % in the control group . Psoriasis patients were also found to have higher rates of Crohn’s disease and ulcerative colitis . Similarly, association of psoriasis with Hashimoto’s thyroiditis, Sjögren’s Syndrome and dermatomyositis has been recently reported . Taken together, the results of these association studies suggest a common aberrant mechanism(s) linking the development of classical autoimmune diseases and psoriasis, supporting the concept of psoriasis having an autoimmune nature.

The IL-23/TH17 axis in the pathogenic mechanisms of psoriasis

Since its discovery in the early nineties , IL-17 took the central stage in immuno-inflammatory mechanisms underlying the development of autoimmune diseases. Thus, IL-17 was implemented in pathogenic mechanisms of inflammatory bowel diseases, multiple sclerosis, and rheumatoid arthritis, in which both serum and tissue have elevated concentrations of IL-17 (reviewed in . In a similar manner, our understanding of the pathogenesis of psoriasis has evolved around the pathologic role of IL-17 since Th17 cells were identified in the dermis of psoriatic plaques . It was shown that IL-17 mainly produced by Th17 cells and dg T cells is responsible for downstream activation of an array of transcription factors leading to epidermal hyperplasia, leukocyte recruitment, and amplified skin inflammation .

In the skin, IL-17A and IL-17F are mainly produced by Th17 cells and dg T cells . Unequivocally, IL-17-producing CD4+ Th17 cells are culprits in the development of psoriatic plaques, as they have been isolated in the dermis of psoriatic lesions . In addition to production of IL-17, activated Th17 cells also secrete IL-21 and IL-22 . IL-22 is an IL-10 family cytokine that acts through STAT3 and has been shown to increase epidermal thickness through inhibition of keratinocyte differentiation . Treatment with neutralizing anti-IL-22 antibodies prevented development of psoriasiform disease in mice thereby identifying IL-22 as an important pathogenic factor in psoriasis and potential molecular target for disease therapy . Furthermore, cooperation between IL-17A and IL-22 leads to recruitment of leukocytes in the skin to further potentiate the inflammation. IL-17A and IL-17F also stimulate keratinocytes to synthesize various chemokines including CXCL2, CXCL3, CXCL5, and CXCL8 (IL-8) which mediate the chemotaxis of neutrophils and macrophages to the lesional skin leading to formation of Munro microabscesses, one of the characteristic histologic features of psoriasis .

IL-23 plays an important role in activation of Th17 cell-mediated immunity . Following some inciting event, whether it is infection or trauma, autoantigens are released in the epidermis and activate myeloid dendritic cells (mDCs) . Activated mDCs are the main source of IL-23 in psoriatic plaques . Although TGF-b1, IL-6, and IL-1b are required for Th17 cells differentiation from naïve CD4+ cells, IL-23 is the cornerstone cytokine in this process . In the absence of IL-23, the cytokines TGF-b1, IL-6, and IL-1b stimulate differentiation of T regulatory cells capable of potent suppression of inflammation .

Of particular importance, IL-23 has crucial roles in the pathogenesis of autoimmunity as it induces local tissue inflammation which is mainly mediated by IL-23-dependent production of IL-17 by Th17 cells . The transcription factor STAT3 is a key facilitator in the IL-23 signaling pathway, and upon activation, it induces transcription of inflammatory cytokines including IL-17A, IL-17F, IL-22, and IFN-g by Th17 cells . Emerging evidence unequivocally suggests that the IL-23/IL-17 axis represents the central immuno-inflammatory pathway in the pathogenesis of psoriasis and provides the rationale for the development of new anti-IL-17 and anti-IL-23 immuno-therapeutic approaches for treatment of patients with moderate-to-severe psoriasis plaques .

Targeting the IL-23/IL-17 axis

To date, the antibodies that specifically neutralize IL-23 or IL-17 have shown remarkable effectiveness for the treatment of psoriasis in clinical trials . As December 2018, a search of the database has revealed 25 either recruiting, active, or completed clinical trials using anti-IL-17 or anti-IL-17 receptor monoclonal antibodies for treatment of moderate-to-severe psoriasis. In early 2016, the US Food and Drug Administration (FDA) has approved the first anti-IL-17 monoclonal antibody (secukinumab, Novartis Pharmaceuticals) for the treatment of active psoriatic arthritis . Follow in the footsteps of Novartis, Eli Lilly has received the US FDA approval for anti-IL-17 monoclonal antibody for treatment of moderate-to-severe psoriasis. In February 2017, anti-IL-17 receptor antagonist (Brodalumab, Valeant Pharma) has received the US FDA approval to treat moderate-to-severe plaque psoriasis in people who have not improved with other treatments .

Similarly, our search of the database has revealed 11 clinical trials using anti-IL-23 monoclonal antibodies (as December 18, 2017). In October 2017, the U.S. Food and Drug Administration (FDA) has approved an expanded indication for anti-p40 subunit of IL-12/IL-23 monoclonal antibody (ustekinumab, Janssen Biotech, Inc.) for the treatment of adolescents (12 years of age or older) with moderate to severe plaque psoriasis .


Psoriasis has long been viewed as a chronic immune-mediated inflammatory disease of skin and small joints which is most commonly manifested by the formation of demarcated erythematous plaques. Although the etiology of psoriasis has been elusive, emerging evidence strongly implicates molecular mimicry as a triggering factor of psoriasis in genetically susceptible individuals. Autoreactive T cells and circulating autoantibodies were also found in psoriatic patients. Taken together, these findings support the concept that psoriasis is an autoimmune disease. Furthermore, accumulated evidence unequivocally shows that IL-17 and IL-23 cytokines are key players in the pathogenesis of psoriasis. In this regard, better understanding of the immunopathology of psoriasis has led to the development of new therapeutic modalities which selectively target IL-17 and IL-23. Biological agents, such as neutralizing anti-IL-17 and anti-IL-23 monoclonal antibodies, have been developed and tested in multiple clinical trials showing their effectiveness in the treatment of moderate to severe plaque psoriasis. Despite the efficacy of these biological agents anti-IL17 and IL-23 antibodies may potentially cause a systemic immunosuppression associated with an increased risk of infections and malignancies. Therefore, future clinical studies are needed to establish the safety record of these biological agents by showing that the benefits of anti-IL-17 and anti-IL-23 therapies overweight any potential adverse effects of these drugs in the treatment of moderate to severe plaque psoriasis.

  1. Schön MP, Boehncke WH (2005) Psoriasis. N Engl J Med 5: 1899-1912.
  2. Lønnberg AS, Skov L, Skytthe A, Kyvik KO, Pedersen OB, et al. (2013) Heritability of psoriasis in a large twin sample. Br J Dermatol 169: 412-416.
  3. Baliwag J, Barnes DH, Johnston A (2015) Cytokines in psoriasis. Cytokine 73: 342-350.
  4. Lowes MA, Kikuchi T, Fuentes Duculan J, Cardinale I, Zaba LC, et al. (2008) Psoriasis vulgaris lesions contain discrete populations of Th1 and Th17 T cells. J Invest Dermatol 128: 1207-1211.
  5. Kryczek I, Bruce AT, Gudjonsson JE, Johnston A, Aphale A, et al. (2008) Induction of IL-17+ T cell trafficking and development by IFN-gamma: mechanism and pathological relevance in psoriasis. J Immunol 1: 4733-4741.
  6. Res PC, Piskin G, De Boer OJ, Van der Loos CM, Teeling P, et al. (2010) Overrepresentation of IL-17A and IL-22 producing CD8 T cells in lesional skin suggests their involvement in the pathogenesis of psoriasis. PLoS One 24: e14108.
  7. Fouser LA, Wright JF, Dunussi Joannopoulos K, Collins M (2008) Th17 cytokines and their emerging roles in inflammation and autoimmunity. Immunol Rev 226: 87-102.
  8. Hofstetter HH, Ibrahim SM, Koczan D, Kruse N, Weishaupt A, et al. (2005) Therapeutic efficacy of IL-17 neutralization in murine experimental autoimmune encephalomyelitis. Cell Immunol 237: 123-130.
  9. Sonderegger, Michael O, Robert A, Bachmann, Kopf M, et al. (2006) Neutralization of IL-17 by active vaccination inhibits IL-23-dependent autoimmune myocarditis. Eur J Immunol 36: 2849–2856.
  10. Lubberts E (2008) IL-17/Th17 targeting: on the road to prevent chronic destructive arthritis? Cytokine 41: 84-91.
  11. Langrish CL, Chen Y, Blumenschein WM, Mattson J, Basham B, et al. (2005) Sedgwick JD, McClanahan T, Kastelein RA, Cua DJ. IL-23 drives a pathogenic T cell population that induces autoimmune inflammation. J Exp Med 17: 233-240.
  12. Grice EA, Segre JA (2011) The skin microbiome. Nat Rev Microbiol 9: 244-253.
  13. Findley K, Grice EA (2014) The Skin Microbiome: A Focus on Pathogens and Their Association with Skin Disease. PLoS Pathogens 10: e1004436.
  14. Gao Z, Tseng CH, Strober BE, Pei Z, Blaser MJ (2008) Substantial alterations of the cutaneous bacterial biota in psoriatic lesions. PLoS One 23: e2719.
  15. Fahlén A, Engstrand L, Baker BS, Powles A, Fry L (2012) Comparison of bacterial microbiota in skin biopsies from normal and psoriatic skin. Arch Dermatol Res 12: 15‑22.
  16. Paulino LC, Tseng CH, Strober BE, Blaser MJ (2006) Molecular analysis of fungal microbiota in samples from healthy human skin and psoriatic lesions. J Clin Microbiol 44: 2933-2941.
  17. Fry L, Baker BS (2007) Triggering psoriasis: The role of infections and medications. Clin Dermatol 25: 606‑615.
  18. Paulino LC, Tseng CH, Blaser MJ (2008) Analysis of Malassezia microbiota in healthy superficial human skin and in psoriatic lesions by multiplex real-time PCR. FEMS Yeast Res 8: 460-471.
  19. Rose NR (2017) Negative selection, epitope mimicry and autoimmunity. Curr Opin Immunol 49: 51-55.
  20. Diluvio L, Vollmer S, Besgen P, Ellwart JW, Chimenti S, et al. (2008) Identical TCR beta-chain rearrangements in streptococcal angina and skin lesions of patients with psoriasis vulgaris. J Immunol 176: 7104-7111.
  21. Sigmundsdottir H, Sigurgeirsson B, Troye Blomberg M, Good MF, Valdimarsson H, et al. (1997) Circulating T cells of patients with active psoriasis respond to streptococcal M-peptides sharing sequences with human epidermal keratins. Scand J Immunol 45: 688-697.
  22. Baker BS, Brown DW, Fischetti VA, Ovigne JM, Porter W, et al. (2001) Skin T cell proliferative response to M protein and other cell wall and membrane proteins of group A streptococci in chronic plaque psoriasis. Clin Exp Immunol 124: 516-521.
  23. Vollmer S, Menssen A, Prinz JC (2001) Dominant lesional T cell receptor rearrangements persist in relapsing psoriasis but are absent from nonlesional skin: evidence for a stable antigen-specific pathogenic T cell response in psoriasis vulgaris. J Invest Dermatol 117: 1296-301.
  24. Lucas CL, Lenardo MJ (2009) Identifying genetic determinants of autoimmunity and immune dysregulation. Curr Opin Immunol 37:28-33.
  25. Valdimarsson H, Thorleifsdottir RH, Sigurdardottir SL, Gudjonsson JE, Johnston A (2008) Psoriasis–as an autoimmune disease caused by molecular mimicry. Trends Immunol 30: 494-501.
  26. Hawkes JE, Chan TC, Krueger JG (2017) Psoriasis pathogenesis and the development of novel targeted immune therapies. J Allergy Clin Immunol 140: 645-653.
  27. Strange A, Capon F, Spencer CC (2010). Genome-wide association study identifies new psoriasis susceptibility loci and an interaction between HLA-C and ERAP1. Nature genetics 42: 985-990.
  28. Tsoi LC, Spain SL, Knight J (2012) Identification of fifteen new psoriasis susceptibility loci highlights the role of innate immunity. Nature genetics 44: 1341-1348.
  29. Liang Y, Sarkar MK, Tsoi LC, Gudjonsson JE (2017) Psoriasis: a mixed autoimmune and autoinflammatory disease. Curr Opin Immunol 49: 1-8.
  30. Filer C, Ho P, Smith RL, Griffiths C, Young HS, et al. (2008) Investigation of association of the IL12B and IL23R genes with psoriatic arthritis. Arthritis Rheum 58: 3705-3709.
  31. Bazsó A, Szodoray P, Szappanos Á, Korda J, Pálfi P, et al. (2015) Systemic Autoimmune, Rheumatic Diseases and Coinciding Psoriasis: Data from a Large Single-Centre Registry and Review of the Literature. Mediators Inflamm 2015: 657907.
  32. Cusick MF, Libbey JE, Fujinami RS (2012) Molecular mimicry as a mechanism of autoimmune disease. Clin Rev Allergy Immunol 42: 102-111.
  33. Lande R, Botti E, Jandus C, Dojcinovic D, Fanelli G, et al. (2014) The antimicrobial peptide LL37 is a T-cell autoantigen in psoriasis. Nat Commun 3: 5621.
  34. Arakawa A, Siewert K, Stöhr J (2015) Melanocyte antigen triggers autoimmunity in human psoriasis. J Exp Med 212: 2203-2212.
  35. Matsushita Y, Shimada Y, Kawara S, Takehara K, Sato S (2005) Autoantibodies directed against the protease inhibitor calpastatin in psoriasis. Clin Exp Immunol 139: 355-362.
  36. Jablonska S, Chorzelski TP, Beutner EH, Maciejowska EJarzabek C M, Rzesa G (1978) Autoimmunity in psoriasis. Relation of disease activity and forms of psoriasis to immunofluorescence findings. Arch Dermatol Res 261: 135-146.
  37. Rambukkana A, Das PK, Witkamp L, Yong S, Meinardi MM, et al. (1993) Antibodies to mycobacterial 65-kDa heat shock protein and other immunodominant antigens in patients with psoriasis. J Invest Dermatol 100: 87-92.
  38. El Rachkidy RG, Young HS, Griffiths CE, Camp RD (2008) Humoral autoimmune responses to the squamous cell carcinoma antigen protein family in psoriasis. J Invest Dermatol 128: 2219–2224.
  39. Wu JJ, Nguyen TU, Poon KYT, Herrinton LJ (2012) The association of psoriasis with autoimmune diseases. J Am Acad Dermatol 67: 924-930.
  40. Birkenfeld S, Dreiher J, Weitzman D, Cohen AD (2009) Celiac disease associated with psoriasis. Br J Dermatol 161: 1331-1334.
  41. Hsu LN, Armstrong AW (2012) Psoriasis and autoimmune disorders: A review of the literature. J Am Acad Dermatol 67: 1076-1079.
  42. Akiyama M, Ueno T, Kanzaki A, Kuwana M, Nagao M, et al. (2016) Association of psoriasis with Hashimoto’s thyroiditis, Sjögren’s Syndrome and dermatomyositis. J Dermatol 43: 711–712.
  43. Yao Z, Fanslow WC, Seldin MF, Rousseau AM, Painter SL, et al. (1995) Herpesvirus saimiri encodes a new cytokine, IL-17, which binds to a novel cytokine receptor. Immunity 3: 811-821.
  44. Iwakura Y, Ishigame H, Saijo S, Nakae S (2011) Functional specialization of interleukin‑17 family members. Immunity 1: 149-162.
  45. Goepfert A, Lehmann S, Wirth E, Rondeau JM (2017) The human IL-17A/F heterodimer: a two-faced cytokine with unique receptor recognition properties. Scientific Reports 7: 8906.
  46. McGeachy MJ, Cua DJ (2008) Th17 cell differentiation: The long and winding road. Immunity 28: 445-453.
  47. Di Cesare A, Di Meglio P, Nestle FO (2009) The IL-23/Th17 axis in the immunopathogenesis of psoriasis. J Invest Dermatol 129: 1339-1350.
  48. Ouyang W, Kolls JK, Zheng Y (2008) The Biological Functions of T Helper 17 Cell Effector Cytokines in Inflammation. Immunity 8: 454-467.
  49. Boniface K, Bernard FX, Garcia M, Gurney AL, Lecron JC, et al. (2005) IL-22 inhibits epidermal differentiation and induces proinflammatory gene expression and migration of human keratinocytes. J Immunol 15: 3695-3702.
  50. Ma HL, Liang S, Li J (2008) IL-22 is required for Th17 cell–mediated pathology in a mouse model of psoriasis-like skin inflammation. J Clin Invest 118: 597-607.
  51. Zaba LC, Fuentes Duculan J, Eungdamrong NJ, Abello MV, Novitskaya I, et al. (2009) Psoriasis is characterized by accumulation of immunostimulatory and Th1/Th17 cell-polarizing myeloid dendritic cells. J Invest Dermatol 129: 79-88.
  52. Tesmer LA, Lundy SK, Sarkar S, Fox DA (2008) Th17 cells in human disease. Immunol Rev 223: 87-113.
  53. Bettelli EY, Carrier W Gao, Korn T, Strom TB, Oukka M, et al. (2006) Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells. Nature 441: 235-238.
  54. Gaffen SL, Jain R, Garg AV, Cua DJ (2014) The IL-23–IL-17 immune axis: From mechanisms to therapeutic testing. Nat Rev Immunol 4: 585-600.
  55. Langley RG, Elewski BE, Lebwohl M (2014) Secukinumab in plaque psoriasis-results of two phase 3 trials. N Engl J Med 4: 326.
  56. Thaçi D, Blauvelt A, Reich K (2015) Secukinumab is superior to ustekinumab in clearing skin of subjects with moderate to severe plaque psoriasis: CLEAR, a randomized controlled trial. J Am Acad Dermatol 73: 400.
  57. Liu L, Lu J, Allan BW, Tang Y, Tetreault J, et al. (2016) Generation and characterization of ixekizumab, a humanized monoclonal antibody that neutralizes interleukin-17A. J Inflamm Res 9: 39-50.
  58. Gordon KB, Blauvelt A, Papp KA (2016) Phase 3 trials of ixekizumab in moderate-to-severe plaque psoriasis. N Engl J Med 375: 345-356.
  59. Farahnik B, Beroukhim K, Zhu TH (2016) Ixekizumab for the Treatment of Psoriasis: A Review of Phase III Trials. Dermatol Ther 6: 25-37.
  60. Gordon K, Kimball A, Chau D (2014) Impact of brodalumab treatment on psoriasis symptoms and health-related quality of life: use of a novel patient-reported outcome measure, the Psoriasis Symptom Inventory. Br J Dermatol 170: 705-715.
  61. Farahnik B, Beroukhim K, Abrouk M (2016) Brodalumab for the Treatment of Psoriasis: A Review of Phase III Trials. Dermatol Ther 6: 111-124.
  62. Ritchlin C, Rahman P, Kavanaugh A (2014) Efficacy and safety of the anti-IL-12/23 p40 monoclonal antibody, ustekinumab, in patients with active psoriatic arthritis despite conventional non-biological and biological anti-tumour necrosis factor therapy: 6-month and 1-year results of the phase 3, multicentre, double-blind, placebo-controlled, randomised PSUMMIT 2 trial. Ann Rheum Dis 73: 990-999.
  63. Kavanaugh A, Puig L, Gottlieb AB (2015) Maintenance of Clinical Efficacy and Radiographic Benefit Through Two Years of Ustekinumab Therapy in Patients With Active Psoriatic Arthritis: Results From a Randomized, Placebo‐Controlled Phase III Trial. Arthritis Care Res 67: 1739-1749.


Dear Editor:

The pathologic mechanisms of systemic lupus erythematosus (SLE) and psoriasis are different: psoriasis is caused by systemic inflammatory reaction from mainly Th1 cell activation, whereas SLE is caused by Th2 cell-related abnormalities. Cases of generalized psoriasis caused by the anti-CD20 monoclonal antibody rituximab and cases of aggravation of SLE after anti-tumor necrosis factor α biologics have been reported, suggesting the immunopathologic mechanisms of these two diseases are opposite1,2. However, we experienced a case of psoriasis accompanied by SLE. A 32-year-old woman had erythematous scaly macules and patches on the trunk, inguinal area, and forehead starting one year ago (Fig. 1A, B). Medical history included arthralgia progressing since one year ago, starting from the left third finger and spreading to all fingers, wrists, toes, ankles, knees, and hips (Fig. 2A). Serologic findings were as follows: anti-SSA/Ro Ab(+), anti-Smith Ab(+), fluorescent antinuclear antibody(+), and speckled pattern. She also presented with a malar rash starting 3 months ago. On the basis of clinical and serologic findings, she was diagnosed with SLE. She was prescribed methotrexate 15 mg weekly, hydroxychloroquine 400 mg, prednisolone 5 mg, and nonsteroidal anti-inflammatory drugs, and the pain seemed to abate. To evaluate skin lesions, the forehead lesion was subjected to biopsy. Histopathologic findings were consistent with psoriasis (Fig. 1C). The skin lesions responded to topical vitamin D3 analogue and topical steroid. Arthritis was evaluated by radiography; the findings of the left hip, bilateral middle fingers, and right index finger were suggestive of psoriatic arthritis, indicating that psoriasis preceded SLE (Fig. 2B). Th17 cells can be associated with the pathogenesis of various autoimmune and inflammatory diseases by producing several effector molecules. Interleukin (IL)-17 is a potent proinflammatory cytokine produced by highly activated Th17 cells and is well known to play a major role in maintaining chronic inflammation in psoriasis. Actually, skin biopsies from patients with psoriasis exhibit high IL-17, IL-22, and IL-23 expressions3. IL-22, one of the effector molecules produced by Th17 cells, induces antimicrobial agents and β-defensins in keratinocytes and promotes epidermal hyperplasia4. This cytokine is also known to be essential for the immune barrier function of epithelial cells. Recent evidence indicates IL-17 also plays a role in the pathogenesis of SLE. Patients with SLE have higher serum levels of IL-17 and IL-23 than healthy controls3,5. Interestingly, plasma IL-17 levels are correlated with SLE disease activity5. In animal models, IL-17 is related not only to T cell-mediated tissue injury, but also to the production of pathogenic autoantibodies. In the presence of IL-17, SLE-derived B cells increase anti-DNA production5. However, the exact function of IL-17 that leads to SLE remains unknown. Besides IL-17, IL-21 produced by Th17 cells causes CD8+ T cell proliferation and induces B cell differentiation4. In summary, we report a case of psoriasis accompanied by SLE. We propose the Th17 cell-mediated immune pathway is common to both diseases. This case suggests the potential utility of treating SLE with Th17 cell-targeting agents.

(A) Erythematous scaly patches on the forehead. (B) An erythematous scaly patch on the inguinal area. (C) Regular elongation of rete ridges, parakeratosis, and mononuclear cell infiltration in the epidermis (H&E, ×40; inset: ×100).(A) Swollen proximal interphalangeal joints on bilateral third fingers. (B) Radiograph showing marginal erosion at the right third proximal interphalangeal joint, small bony proliferation at the right index metacarpophalangeal joint, and suspicious erosion at the left middle proximal interphalangeal joint.


Medical Author: Frederick Hecht, M.D.
Medical Editor: Barbara Hecht, Ph.D.

Nov. 11, 2000 — Changes in one gene have been discovered that are shared by three common autoimmune diseases — the skin condition psoriasis as well as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). The genetic changes involve a gene called Runx-1.

What is Runx-1?
Runx-1 is a protein that acts as a transcription factor. It controls when genes are switched on or off. Runx-1 does so by binding to regulatory sequences — specific sequences of DNA — that are close to the genes they regulate. These DNA sequences, called Runx-1 binding sites, are scattered throughout the human genome, wherever there is a gene under the control of Runx-1.

Runx-1 stands for runt-related transcription factor 1. Runx-1 is also called AML1 because it is also altered in a form of acute myeloid leukemia, but that is a very different story, one to be told another time.

The Tie-in with Autoimmunity
Changes in Runx-1 appear to contribute to autoimmune diseases. A Runx-1 binding site on chromosome 2 is altered in many patients with systemic lupus erythematosus. Many psoriasis patients have a changed Runx-1 binding site on chromosome 17. And a Runx-1 binding site on chromosome 17 is changed in patients with rheumatoid arthritis. Thus, there are genetic connections, some involving Runx-1, between diverse autoimmune diseases.

The Tie-in with Lupus
The tie-in between Runx-1 and lupus is not new. It was reported back in 2002 by Ludmila Prokunina and her colleagues from Sweden. They found that a polymorphism (a normal variation) in the programmed cell death 1 gene dubbed PDCD1 was associated with susceptibility to systemic lupus erythematosus. They traced this down and found that it reflected an altered binding site for Runx-1.

The Tie-ins with Psoriasis and Rheumatoid Arthritis
The reports linking Runx-1 to psoriasis and to rheumatoid arthritis are very new. They were just published back-to-back online in the journal Nature Genetics on November 9. The work on psoriasis was from a multicenter American research effort while that on rheumatoid arthritis emanated from Japan.

The fact that Runx-1 is involved in at least three common autoimmune diseases is clearly remarkable and noteworthy. It is also clear that the changes in Runx-1 do not cause these diseases. Runx-1 is a susceptibility gene locus, or loci, since there are Runx-1 binding sites strewn about the genome. Changes in these different Runx-1 sites make a person vulnerable to these different autoimmune diseases.
Runx-1 appears to be one piece in the autoimmune disease puzzle.
Original Sources:

1. Prokunina, L. et al., A regulatory polymorphism in PDCD1 is associated with susceptibility to systemic lupus erythematosus in humans. Nature Genetics, Published online: October 28, 2002 doi:10.1038/ng1020.
2. Helms, C. et al., A putative RUNX1 binding site variant between SLC9A3R1 and NAT9 is associated with susceptibility to psoriasis. Nature Genetics. Published online: 9 November 2003, doi:10.1038/ng1268.
3. Tokuhiro, S. et al., An intronic SNP in a RUNX1 binding site of SLC22A4, encoding an organic cation transporter, is associated with rheumatoid arthritis. Nature Genetics. Published online: 9 November 2003, doi:10.1038/ng1267.
For additional information, please see the following areas:

Lupus and your skin: Diagnosis and treatment

When lupus affects your skin, a dermatologist may be part of your care team. This doctor specializes in diagnosing and treating conditions that affect the skin, hair, and nails.

How do dermatologists diagnose lupus on the skin?

When lupus affects the skin, a dermatologist will examine your skin. The doctor will look closely at the rash, patch, or other skin (or hair) problem. Your dermatologist may also ask if you have sores inside your mouth or nose. If you have these, be sure to tell your dermatologist.

Different types of lupus affect the skin. To learn which type affects your skin, your dermatologist may remove a bit of the diseased skin so that it can be examined under a microscope.

Removing the skin is a simple procedure, which your dermatologist can perform during an office visit. Called a skin biopsy, this procedure is often enough to determine whether the rash or other skin problem is cutaneous (medical term for skin) lupus.

Your dermatologist may also ask you about the medicines that you take. Some medicines can cause a type of lupus called drug-induced lupus. Be sure your dermatologist has a list of all the medicines you take.

How do dermatologists treat lupus on the skin?

To treat the lupus on your skin, your dermatologist will:

  • Tell you how to protect your skin from the sun

  • Prescribe medicine, if necessary

  • Recommend other lifestyle changes

Medicines that dermatologists prescribe to treat lupus on the skin include:

  • Corticosteroid that you apply to your skin or take as a pill: This helps to reduce the inflammation and clear the skin.

  • Corticosteroid that your dermatologist injects: This can help clear a thick patch on the skin or area of hair loss.

  • Antimalarial medicine: Developed to treat and prevent malaria, this medicine can also effectively treat lupus on the skin.

  • Steroid-sparing medicine that you apply to your skin: This works like a corticosteroid to reduce the inflammation and clear the skin.

  • Medicine that works on the immune system: These medicines include methotrexate, cyclosporine, and mycophenolate mofetil. They help calm the immune system.

Your treatment plan may include more than one medicine. This can increase how well the treatment plan works.

The goal is to clear the skin.

Preventing hair loss due to discoid lupus

If you have discoid lupus, clearing your skin can reduce your risk of scars, permanent hair loss, and discolored skin.

When discoid lupus forms on the scalp, you want to treat it early. Early treatment can prevent permanent hair loss.

To treat discoid lupus, your dermatologist may inject a thick patch with a corticosteroid to help it clear. An antimalarial medicine or a corticosteroid that you apply to your skin can help clear thinner patches.

If the patch turns into a scar, hair cannot regrow.

Drug-induced lupus requires different treatment

If your dermatologist thinks that a medicine you take is causing the lupus, you may need to stop taking the drug. You should work with your dermatologist or another doctor to find out.

Stopping some drugs like heart medicines can have serious consequences. You may need to start another drug or therapy immediately.

If you have drug-induced lupus, though, stopping the drug is the only way to find out. Testing cannot find out which drug is causing the lupus. If the lupus starts to clear a few months after you stop taking the drug, then the drug is likely the cause.

Drugs that most frequently cause drug-induced lupus are medicines used to treat high blood pressure like hydralazine and medicines used to treat heart disease like procainamide and quinidine.

Once the drug that causes the lupus is stopped and the symptoms clear, drug-induced lupus is considered cured.

When lupus on your skin clears

You may see unwanted side effects after a rash or other skin problem clears. Some people have dark or light spots on their skin. You may see a scar. If this happens, talk with your dermatologist. Your dermatologist may be able to treat these unwanted side effects.

Outcome: What can someone with cutaneous lupus expect?

Most people who have cutaneous lupus can lead active and productive lives. Treatment helps because it can clear the skin and reduce the effects that lupus has on your life. There is currently no cure for cutaneous lupus.

Costner MI, Sontheimer RD. “Lupus erythematosus” In: Wolff K, Goldsmith LA, et al. Fitzpatrick’s Dermatology in General Medicine (seventh edition). McGraw Hill Medical, New York, 2008:1515-35.

Vedove CD, Simon JC, et al. “Drug-induced lupus erythematosus with emphasis on skin manifestations and the role of anti-TNFα agents.” J Dtsch Dermatol Ges. 2012 Dec; 10(12): 889–97.

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