Oral Treatments for Psoriasis and Psoriatic Arthritis: National Psoriasis Foundation

Oral systemic treatments are small molecule medicines that are taken by mouth. Systemic medications, aimed at those with moderate-to-severe psoriasis and psoriatic arthritis, are prescription drugs that work throughout the body. They are also used in those who are not responsive or are unable to take topical medications or UV light therapy.

Systemic psoriasis drugs have been around for more than 10 years and are taken by mouth in liquid or pill form or given by injection.

Newer oral systemic treatments selectively target molecules inside immune cells. By adjusting the complicated processes of inflammation within the cell, these treatments correct the overactive immune response that causes inflammation in those with psoriatic disease, leading to improvements in redness and a reduction in psoriasis scales, tenderness and swelling.

Some treatments, such as methotrexate, which is an oral systemic (see below), are also disease-modifying antirheumatic drugs (DMARDs). DMARDs may relieve more severe symptoms and attempt to slow or stop joint and tissue damage and the progression of psoriatic arthritis.

Soriatane is an oral retinoid, which is a synthetic form of vitamin A. Acitretin is the only oral retinoid approved by the U.S. Food and Drug Administration (FDA) specifically for treating psoriasis.

The exact way Soriatane works to control psoriasis is unknown. In general, retinoids help control the multiplication of cells, including the speed at which skin cells grow and shed. Learn more about Soriatane (acitretin).

Cyclosporine is an immunosuppressive drug that was first used to help prevent rejection in organ transplant patients. In 1997, the FDA approved Neoral (a trade name for cyclosporine) for adults with severe psoriasis and otherwise normal immune systems.

Cyclosporine suppresses the immune system and slows down the growth of certain immune cells. Learn more about Cyclosporine.

Methotrexate was initially used to treat cancer.  It was approved by the FDA in the 1970s for the treatment of severe psoriasis.

In a person with psoriasis, methotrexate binds to and inhibits an enzyme involved in the rapid growth of skin cells and slows their growth rate. Learn more about Methotrexate.

There are additional systemic medications that are not approved by the FDA for treating psoriasis and psoriatic arthritis. However, some doctors prescribe them “off-label” — a common and accepted medical practice. Learn more about Off-Label Systemics.

Nonsteroidal anti-inflammatory drugs (NSAIDs), including over-the-counter medications such as aspirin and ibuprofen as well as prescription products, help to decrease inflammation, joint pain and stiffness. Aspirin can help reduce pain, swelling and stiffness. Learn more about NSAIDs.

Otezla treats psoriasis and psoriatic arthritis by regulating inflammation within the cell.

Otezla inhibits an enzyme known as phosphodiesterase 4 (PDE4). This enzyme controls much of the inflammatory action within cells, which can affect the level of inflammation associated with psoriatic disease. Learn more about Otezla.

Aimed at reducing psoriatic arthritis inflammation, Xeljanz targets a specific part of the immune system (Janus kinase) to reduce the overactive response associated with psoriatic disease. The oral treatment also aids in reducing joint tenderness and swelling. Learn more about Xeljanz and Xeljanz XR.

Sotyktu selectively targets the immune system by inhibiting tyrosine kinase 2 (TYK2), a member of the Janus kinase (JAK) family. Sotyktu is approved for the treatment of adults with moderate-to-severe plaque psoriasis who are candidates for systemic therapy or phototherapy. Learn more about Sotyktu.

NPF Patient Navigatiors can answer your questions about oral treatments, including understanding their side effects and helping assess potential risks.

Contact the Patient Navigation Center

Last updated on 10/10/22 by the National Psoriasis Foundation.

Skin of Color Resource Center : National Psoriasis Foundation

[1] Armstrong AW, Mehta MD, Schupp CW, Gondo GC, Bell SJ, Griffiths CEM. Psoriasis Prevalence in Adults in the United States [published online ahead of print, 2021 Jun 30]. JAMA Dermatol. 2021;e212007. doi:10.1001/jamadermatol.2021.2007

[2] Kaufman BP, Alexis AF. Psoriasis in Skin of Color: Insights into the Epidemiology, Clinical Presentation, Genetics, Quality-of-Life Impact, and Treatment of Psoriasis in Non-White Racial/Ethnic Groups [published correction appears in Am J Clin Dermatol. 2018 Feb 16;:]. Am J Clin Dermatol. 2018;19(3):405-423. doi:10.1007/s40257-017-0332-7

[3] Can You Get Psoriasis if You Have Skin of Color? AAD.org. https://www.aad.org/public/diseases/psoriasis/treatment/could-have/skin-color. Accessed April 26, 2021

Additional Research

Rachakonda TD, Schupp CW, Armstrong AW. Psoriasis prevalence among adults in the United States. J Am Acad Dermatol. 2014;70(3):512-516. doi:10.1016/j.jaad.2013.11.013

Takeshita J, Eriksen WT, Raziano VT, et al. Racial Differences in Perceptions of Psoriasis Therapies: Implications for Racial Disparities in Psoriasis Treatment. J Invest Dermatol. 2019;139(8):1672-1679.e1. doi:10.1016/j.jid.2018.12.032

Takeshita J, Gelfand JM, Li P, et al. Psoriasis in the US Medicare Population: Prevalence, Treatment, and Factors Associated with Biologic Use. J Invest Dermatol. 2015;135(12):2955-2963. doi:10.1038/jid.2015.296

Holmes A, Williams C, Wang S, Barg FK, Takeshita J. Content analysis of psoriasis and eczema direct-to-consumer advertisements. Cutis. 2020;106(3):147-150. doi:10.12788/cutis.0070

Fischer AH, Shin DB, Gelfand JM, Takeshita J. Health care utilization for psoriasis in the United States differs by race: An analysis of the 2001-2013 Medical Expenditure Panel Surveys. J Am Acad Dermatol. 2018;78(1):200-203. doi:10.1016/j.jaad.2017.07.052

Sevagamoorthy A, Bazen A, Shin D, Barg FK, Takeshita J; Patient race affects dermatologists’ assessments and treatment of psoriasis. J Invest Dermatol. 2020;140(7S):S97.)

Alexis AF, Blackcloud P. Psoriasis in skin of color: epidemiology, genetics, clinical presentation, and treatment nuances. J Clin Aesthet Dermatol. 2014;7(11):16-24.

Eriksen WT, Raziano VT, Bazen A, Gelfand JM, Barg F, Takeshita J. Concerns About Psoriasis Differ by Race: Implications for Patient-Centered Goal-Setting and Counseling. J Invest Dermatol. 2019; 139(5S, Supplement 1):S37.

Shah SK, Arthur A, Yang YC, Stevens S, Alexis AF. A retrospective study to investigate racial and ethnic variations in the treatment of psoriasis with etanercept. J Drugs Dermatol. 2011;10(8):866-872.

Takeshita J, Augustin M, de Jong E, Lafferty K, Langholff W, Langley R, Leonardi C, Menter A, Alexis A. Psoriasis-Related Quality-of-Life Differs by Race/Ethnicity. J Invest Dermatol. 2019; 139(5S, Supplement 1):S148.

Gelfand JM, Stern RS. “The prevalence of psoriasis in African Americans: results from a population-based study.” J Am Acad Dermatol. 2005 Jan;52(1):23-6.

The role of infectious agents in the pathogenesis of psoriasis uMEDp

The etiology of psoriasis is still unclear. Meanwhile, the genetic predisposition to it is considered a proven fact. Often, infectious diseases become triggers that trigger the pathological process in patients with a genetic predisposition to psoriasis. The article presents the results of studies confirming a clear link between psoriasis and upper respiratory tract infection, as well as the risk of psoriasis in patients with chronic rhinosinusitis.

Psoriasis is a common chronic dermatosis of multifactorial origin. Clinically manifested as a monomorphic rash consisting of flat papules of various sizes, pink-red plaques. Small plaques merge into large ones and are quickly covered with loose silvery white scales. In addition to the skin, nails and joints are affected, and mucous membranes are extremely rare [1]. The prevalence of this disease is about 2% among the European population.

To date, the etiology of psoriasis remains unclear, but it is known about the genetic predisposition to it. It is believed that this is present in 2/3 of patients with clinical manifestations of psoriasis. Congenital predisposition is polygenic. 20 different gene localizations have been described that affect the risk of developing psoriasis [2]. The maximum risk is mediated by genes responsible for inflammation functions and immune responses. These include HLA-Cw6, which is most associated with psoriasis and determines clinical symptoms. In patients positive for this gene, the onset of the disease occurs at an earlier age, guttate psoriasis is more common in them, clinical manifestations are extensive, deterioration is associated with infections of the pharynx [3].

Various external factors act as triggers that trigger the pathological process in patients with a genetic predisposition to psoriasis. However, the nature of the antigen that activates T-lymphocytes in psoriasis is still unclear.

Often, the triggers of the external environment that activate the pathological process are infectious diseases. Thus, a clear relationship has been established between an upper respiratory tract infection caused by group A beta-hemolytic streptococcus and guttate psoriasis. For the first time, the relationship between psoriasis and streptococcal infection was established by Winfield [2] using the example of acute exanthemic psoriasis, which was preceded by an acute streptococcal infection of the pharynx [4]. Very often, such a relationship can be traced in the history of children and young people. Some researchers speculate about the role of streptococci in the initiation of psoriasis vulgaris based on reports of elevated antistreptolysin-O titers and/or positive oropharyngeal cultures for group A streptococci [5–7].

There are several ways for streptococci to enter epithelial cells. One of them is the binding of fibronectin to the surface molecules of streptococci, which allows the pathogen to penetrate the epithelial cells of the pharynx and tonsils. In tonsil tissue, streptococci can show resistance to antimicrobial factors of the body’s immune defense and antibiotics with an extracellular mechanism of action. As a result, the pathogen persists for a long time in the tissues of the tonsils and pharynx. This is confirmed by the results of the study of surgically removed tissues [2].

Further development of the pathological process involves the activation of T-cells by streptococcal superantigens. There is an induction of a specific skin homing receptor (from the English homing – returning home) on T cells, which explains their possible migration into the skin [4]. This assumption was also confirmed by S.L. Sigurdardottir et al.: in the study of tonsil tissue in patients with psoriasis, an increased content of T-cells with a specific skin homing receptor was revealed (in contrast to healthy individuals). Subsequently, identical oligoclonal T cells were identified in these patients in tonsil tissue and psoriatic plaques [8].

No less important is the ability of streptococci to molecular mimicry. Its classic example is rheumatic fever. Homologues between proteins of keratinocytes and streptococci have been identified – M-proteins and keratins (proteins of the cytoskeleton of keratinocytes) [4]. T cells of patients with psoriasis demonstrate an increased response not only to homologous peptides of streptococcal M-proteins [8–10], but also to human epidermal keratin [5, 8, 10, 11]. At the same time, streptococcal M-proteins were found in the papillae and epidermis of the affected skin. Using the polymerase chain reaction (PCR) method, specific streptococcal DNA was identified in patients with psoriasis in psoriatic rashes [2]. Apparently, streptococcal proteins penetrate the skin with the help of dendritic cells.

Presumably, exacerbations of the psoriatic process are initiated by a cross-reaction of T cells with epitopes of streptococcal M-proteins and human keratin [4, 8]. Thus, the immunological response by the principle of cross-reactivity against autologous proteins can persist after treatment of streptococcal infection.

A relationship has been established between ENT diseases and psoriasis [10, 12]. It is suggested that there is a possible risk of psoriasis in patients with chronic rhinosinusitis without nasal polyps. In the original study by I.J. Keller et al. for five years, patients with chronic rhinosinusitis without nasal polyps were followed up. Among 13,242 patients, the incidence of psoriasis was 1.41 cases per thousand people per year. This indicates an increased risk of developing psoriasis in such patients. In the comparison group, which included 39726 patients, 0.69 cases of psoriasis per thousand people per year were noted. The authors explain the comparison of two seemingly different diseases by the fact that chronic sinusitis without nasal polyps and psoriasis are considered Th ₁ -mediated pathology. One of the possible mechanisms for the development of psoriasis is the participation of S100 proteins, including psoriasin and calprotectin, which play a role in the formation and maintenance of antimicrobial protection. A decrease in the expression of these proteins in the epithelium of patients with chronic rhinosinusitis without nasal polyps was revealed, which can lead to a decrease in immune resistance and barrier function. The latter can initiate the development of psoriasis [13].

The important role of S100 proteins was also confirmed in the work of S.A. Ilina et al. Real-time PCR using oligonucleotide probes labeled with fluorescent agents was used to analyze the expression profiles of the S100A8 and S100A9 genes in psoriasis-affected skin and visually unaffected skin of the same patients before and after PUVA therapy. Experimentally, a significant increase in the expression of the S100A8 and S100A9 genes in the skin affected by psoriasis was shown compared to the unaffected skin of the same patients before treatment. After PUVA therapy, a decrease in the expression of S100A8 and S100A9 genes was observedin almost all patients. Thus, the obtained results suggest that the high level of expression of the S100A8 and S100A9 genes reflects the state of the pathological process in psoriasis, and the transcriptional activity of these genes is an indicator of the effectiveness of psoriasis treatment at the molecular level [14].

A number of studies on the effect of antibiotic therapy on the course of psoriasis also support the theory of the role of infectious agents in the pathogenesis of psoriasis.

Thus, positive dynamics was noted in the form of regression of rashes when rifampicin was prescribed in combination with penicillin or erythromycin [11]. One of the latest studies was based on the assumption that psoriasis vulgaris is the result of a chronic subclinical streptococcal infection of unclear localization. The study, which lasted two years, included 30 patients who suffered from the disease for more than five years and in whom previous therapy was ineffective. The titer of antibodies against streptolysin-O exceeded 200 IU/ml, in 7 patients a positive reaction to C-reactive protein was observed, group A streptococcus was detected in the culture of a throat swab in 2 patients, and Streptococcus viridans in 6 patients. For the first 24 weeks of benzathine therapy, benzylpenicillin (1. 2 million units) was administered intramuscularly every two weeks. For 25–48 weeks of benzathine, benzylpenicillin (1.2 million units) was administered once a month. Significant recovery was noted from the 12th week (the average value of the PASI index (Psoriasis Area and Severity Index) to the beginning – 32.7, after 12 weeks – 19.1, after 24 – 8.7, after 36 – 3.5, after 48 weeks – 1.5). During the two-year follow-up, the patients maintained remission. In 2010, the same group of researchers studied the effect of long-term use of azithromycin. Of 50 patients (with moderate to severe psoriasis), 30 received azithromycin for 24 courses (the first course was two weeks, for a total of 48 weeks): four days of oral administration of 500 mg once, then ten days off. The remaining 20 patients received a vitamin C tablet. Significant improvement in the PASI index was observed from week 12 in the majority of patients treated with azithromycin. At the end of the 48th week, 18 patients (60%) had excellent recovery, 6 (20%) patients had good recovery, and 4 (13%) patients had moderate recovery. PASI 75 (a decrease of at least 75% from baseline) was 80%, that is, it was observed in 24 patients. No significant changes were noted in the control group [15, 16].

S.L. Sigurdardottir et al., having analyzed the reports on the effectiveness of tonsillectomy in patients with psoriasis, came to the following conclusion. In some cases, this operation allows to achieve long-term remission, reduce the severity of skin rashes and doses of drugs, and, if possible, refuse to use expensive drugs, which is especially important due to the widespread introduction of biologics, or medical products of biological origin, into practice [8].

In addition, there is an assumption that a certain role in the pathogenesis of psoriasis belongs to the human papillomavirus (HPV, human papilloma virus) [17–19].

A connection between psoriasis and HPV carriage has been established. There are reports of the detection of various types of HPV DNA in epidermal scales of EV (epidermodysplasia verruciformis) as well as specific antibodies in the blood [20-22]. A model of psoriasis pathogenesis based only on epidermodysplasia verruciformis HPV influence has been proposed [23].

It is known that HPV carriage can be asymptomatic for a long time. Many types of HPV are dermal commensals. According to S.L. Sigurdardottir et al., beta-HPV virus was constantly detected in the skin of 23 (74%) healthy patients without any external manifestations for more than six months [24].

Commensal HPV carriage was confirmed after HPV was detected in skin samples from 38 (71%) psoriasis patients and only 36 (58%) control patients. In addition, it was shown that the level of HPVL in patients with psoriasis is significantly lower in the remission stage compared to the exacerbation stage. An increase in HPVL correlates with disturbances in the skin microflora and exacerbation of psoriasis (in particular, the amount of S. aureus increases) [25, 26].

With regard to the primary or secondary nature of elevated HPV carriage, it is believed that HPV carriage is primary in relation to the initiation of psoriasis. This assumption is based on the fact that the frequency of detection of EV-HPV in psoriatic scales in children coincides with the frequency of its detection in adults [27].

Based on the ideas about the initiating role of bacterial and viral agents in the pathogenesis of psoriasis, we conducted a study aimed at determining the presence or absence of a number of microorganisms in skin samples.

The material was skin samples obtained by puncture biopsy (punch length 5 mm), taken from skin areas affected by psoriatic rashes, as well as skin flakes obtained by scraping.

All participants in the study suffered from widespread psoriasis vulgaris (progressive stage). At the time of taking biopsies, patients had not received external therapy for at least a day. The duration of the disease ranged from several months to several years. In anamnesis, patients used various methods of therapy (external treatment, immunosuppressants, physiotherapy). In total, we examined 10 patients (6 men and 4 women). The age of the patients varied from 25 to 60 years. The study was approved by the Local Ethics Committee at the Institute of General Genetics of the Russian Academy of Sciences and complies with the principles set forth in the Declaration of the Helsinki Accord.

Biopsy specimens and skin flakes were examined by PCR for the qualitative detection of HPV (typing was not performed), S. pyogenes. For the first time, skin biopsy specimens were used to identify pathogen DNA, which makes it possible to exclude the assumption of transient contamination of the skin by bacterial and viral agents.

HPV was detected in four samples (both biopsy material and scales), and all of the obtained samples were taken from men. In one sample taken from a woman, S. pyogenes was found (in scales and biopsy).

Thus, out of ten samples of biopsy material and skin flakes received, five turned out to be positive (the presence of microorganisms), and the human papillomavirus prevailed (in four samples). The bacterial agent S. pyogenes was found in one sample.

The results obtained suggest that bacterial-viral agents play a key role in the pathogenesis of the psoriatic process and confirm the need for further detailed study of the role of the skin microbiota in this aspect.

News of the Pediatric University

Elena Semyonovna Bolshakova: « We find an individual approach to each patient »

psoriasis, why it is dangerous, as well as personalized methods of therapy that are used in the treatment of children with psoriasis at the Pediatric University, said Elena Semyonovna Bolshakova, head of the dermatovenerological department of the St. Petersburg State Pediatric Medical University.

Elena Semyonovna, please tell us what is psoriasis?

Psoriasis is a chronic disease with a genetic predisposition, provoked by a number of endo- and exogenous factors, characterized by hyperproliferation and impaired differentiation of epidermal cells. The maturation of such cells normally occurs in 28 days, in people with psoriasis in 4 days. Clinically, all of the above is manifested by the appearance of small papules with peeling, and then larger plaques.

Is psoriasis an incurable disease?

Psoriasis is an incurable disease with a chronic course, but with adequate and timely treatment, long-term remissions can be achieved.

How common is this condition?

According to statistics, this disease occurs in 2-4% of the world’s population.

Why does psoriasis occur?

There are a lot of theories about the origin of psoriasis. This issue is still being studied. As a rule, against the background of a genetic predisposition, under external or internal influence, a disease is triggered. External factors are different: stress, anxiety, vaccinations, taking various medications, eating disorders, alcohol, etc. Very often, the disease appears after bacterial or viral infections. Internal factors are chronic foci of infections (in the first place in children, the pathology of the ENT organs), concomitant diseases (pathology of the kidneys, pathology of the gastrointestinal tract, endocrine pathology, immune status disorders).

Is it hereditary?

The fact that psoriasis is inherited has long been assumed by various scientists. This was the basis for the development of the genetic theory of the occurrence of this disease. Until recently, confirmation consisted only in diagnosing the disease in a few blood relatives, regardless of the line of inheritance. Now, geneticists have discovered a certain gene defect that triggers the death of some cells in the human body under a certain set of circumstances. This in turn affects the occurrence of psoriatic rashes on the surface of the skin. But not every family traces the presence of the genetic heredity of psoriasis. Experts only confirm that about 63% of patients have blood relatives with such a dermatological skin lesion. Thus, geneticists define psoriasis as a hereditary disease, but having a multifactorial nature of its occurrence.

Is psoriasis contagious?

Psoriasis is absolutely not contagious.

At what age does the disease usually manifest itself?

Psoriasis can occur at any age, but in children it is most often school age.

Is there any difference in how the disease progresses in a child and in an adult?

The difference between the course of psoriasis in an adult and a child is revealed. In children, pruritus is very often expressed during the progression of the process, the exudative component of the rash is more pronounced, so for the first time it is not always easy to make this diagnosis right away. Often at first they put allergic dermatitis, atopic dermatitis. In addition, guttate psoriasis is more common in childhood. This type of psoriasis is associated, as a rule, with a bacterial infection, most often streptococcal – usually it is a sore throat or an exacerbation of chronic tonsillitis.

Please tell us about the personalized methods of therapy used in the department? What is their feature?

At our department, various forms of psoriasis are treated with the most personalized methods. We find an individual approach to each patient. We take into account heredity, history, comorbidities, identified foci of chronic infection, immunological and neuropsychiatric status in the selection of therapy.

For example, if we find that the main factor that triggered the onset or progression of psoriasis was an infectious process, then sometimes it is enough to conduct timely and adequate therapy for this infection so that the progression of the process passes into a stationary, and then into a remission stage. Sanitation of chronic foci of infection is being carried out. If the progression of the process is associated with stress, strong feelings, a consultation of clinical psychologists is carried out. If necessary, correct this condition. With psoriasis of moderate severity and severe forms, according to indications, systemic cytostatic therapy (methotrexate) is prescribed. These patients are under our control even after discharge, with subsequent adjustment of the dose and duration of therapy. According to indications, genetically engineered biological therapy is prescribed for children with moderate and severe psoriasis. We also approach this issue very individually. Taking into account the age of patients, medical history, the nature of the clinical picture, the presence of concomitant pathology, we select the most complementary drug for this child.

We have a wide range of possibilities for correcting the immunological status. The most effective in this matter is intravenous ultraviolet radiation and a blood laser. This procedure is carried out for children from school age, and for younger children – a transcutaneous blood laser.

The physiotherapy room in our department provides unique treatment methods for children suffering from psoriasis. Procedures are selected individually, taking into account the anatomical and physiological characteristics of each patient and the stage of the process.

We use multimodal methods for external therapy of children suffering from psoriasis. In external therapy, not only official ready-made external medicines are used, but also external therapy products made in the pharmacy of our University according to an individual recipe. These funds are selected for each child based on the characteristics of his skin, anamnesis, clinical picture.

Is psoriasis only an aesthetic problem?

Psoriasis is not only an aesthetic problem. With this disease, there is damage to the joints, internal organs can suffer – kidneys, liver, cardiovascular system.

Why is psoriasis dangerous?

Complications of psoriasis are dangerous. For example, psoriatic erythroderma, in which almost the entire skin is affected by confluent psoriatic plaques. Then all the functions of the skin are completely disrupted, in connection with which the work of internal organs is disrupted – the liver, kidneys, and the cardiovascular system. Psoriatic arthritis is a very serious disease, especially if several joints are involved in the process. Sometimes this process leads to disability of the patient.

What should I do to prevent the disease from getting worse?

So that the process does not escalate, we must try to exclude factors that can provoke the launch of this process – eliminate the stress factor, sanitize the foci of infection in time, treat comorbidities, lead a healthy lifestyle, and carry out rehabilitation measures. When we discharge our patients, we develop a plan of individual rehabilitation measures that will help them significantly prolong remission.

Are there any developments that could cure psoriasis?

Of course, developments are currently being carried out in the world, thanks to which it will probably be possible to cure psoriasis.