Psoriasis is a chronic, relapsing inflammatory disorder that affects around 0.1%–3% of the global population. Its multifactorial etiopathogenesis involves an interplay between genetic predisposition and environmental factors with the cascade of host immunological response. Known triggers of psoriasis include smoking, emotional stress, trauma, infections, withdrawal of systemic steroids, and certain drugs.
Psoriasis is known to be associated with systemic comorbid conditions such as metabolic syndrome for which the patient might be on multiple drugs. This makes it prudent to carefully analyze the drugs which might aggravate psoriasis. Drugs implicated in causation of psoriasis can act by two mechanisms. It can act as a trigger to unmask preexisting psoriasis. This is called drug triggered psoriasis in which the disease may progress even after discontinuation of the drug. Alternatively, few drugs are implicated in drug-induced psoriasis where discontinuation of the drug will stop disease progression.
Rheumatologists frequently deal with psoriatic arthritis and its associated comorbidities. Hydroxychloroquine is very frequently used in the management of autoimmune rheumatic diseases such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and dermatomyositis. Nonsteroidal anti-inflammatory drugs (NSAIDs) are used as anti-inflammatory analgesics. Anti-tumor necrosis factor (TNF) agents and other biologicals are frequently indicated for the management of rheumatological disorders. Antifungals are often coprescribed in rheumatic disorders for fungal infections, owing to an immunocompromised state. Antiepileptics are often needed in seizure disorders accompanying diseases such as SLE and vasculitis. Depression necessitating therapy is encountered as an accompaniment of chronic pain and disease or as a manifestation of the disease process itself.
We searched PubMed (including MEDLINE and PubMed Central) on October 9, 2019, using the search term “Drug Induced psoriasis” and retrieved 4607 results. We limited our search to articles published in the past 10 years. Our search resulted in 2232 articles. The titles and abstracts of these articles were manually screened to identify observational studies, case series, case reports, and review articles. Other articles of relevance to the study topic were included based on the authors' personal knowledge and cross-referencing.
Drugs implicated in psoriasis can be classified as those with definite causal relationship, those with considerable but insufficient data, and those with occasional case reports [Table 1].
Drugs With Definite Causal Relationship
Both cardioselective and nonselective beta blockers have been implicated in psoriasis. These are one of the most strongly implicated drugs in causation of psoriasis. The most reliable explanation for the pathogenesis is the cyclic adenosine monophosphate (cAMP) pathway. cAMP is the key messenger involved in cellular differentiation. Because of blockade of the intracellular beta 2 receptors, a subsequent decrease in cAMP leads to keratinocyte hyperproliferation. Further, beta blockers lead to excessive release of cytokines from macrophages and neutrophils, which leads to exacerbation of psoriasis. The lag time between intake of drug and onset of psoriasis may range from weeks to as long as 12 months. Practolol is a prototype cardioselective beta blocker, which was withdrawn due to severe cutaneous side effects such as psoriasiform eruptions. In psoriasiform eruptions, lesions cleared after several weeks of discontinuing the medication and re-exposure resulted in exacerbation. Reports of psoriasiform eruptions with beta blockers such as metoprolol, atenolol, and nadolol began to appear in the 1980s. Animal studies also showed psoriasiform changes on histopathology in guinea pigs exposed to propranolol and oxprenolol. Pindolol has been shown to transform plaque-type psoriasis to pustular psoriasis. Even topically used beta blockers for open-angle glaucoma was reported to aggravate psoriasis and to induce nail changes of psoriasis. In pediatric population also, a single report of an 18-month-old child developing psoriasiform diaper rash was linked to intake of oral propranolol for infantile hemangioma. In a prospective cohort study from US, it was seen that long-term regular beta blocker use for more than 6 years significantly increased the risk of psoriasis (hazard ratio: 1.39; 95% confidence interval [CI]: 1.11–1.73).
Lithium, a commonly prescribed agent for bipolar disorder, has been linked with both induction and exacerbation of psoriasis (more frequently exacerbations). Due to a very narrow therapeutic range (0.6–1.2 mEq/L), plasma concentrations of more than 1.5 mEq/L can lead to multiple adverse reactions including flare-up of psoriasis. The currently accepted mechanism for lithium-induced psoriasiform eruption is linked to phosphatidylinositol pathway. Inositol is a second messenger involved in cellular growth and differentiation. Lithium blocks the phosphatidylinositol pathway by blocking the enzyme inositol monophosphate resulting in decreased intracellular calcium which further leads to increased keratinocyte proliferation. Oral supplementation with inositol was found to be beneficial in lithium-induced flare-up of psoriasis. The lag time for exacerbation of psoriasis was found to be 20 weeks and for induction of psoriasis, it was found to be around 48 weeks.
Clinically, plaque psoriasis was the most commonly reported form, although pustular variants, erythroderma, nail psoriasis and psoriatic arthropathy have also been reported. In a UK-based case–control study, long-term use of lithium was seen to have increased risk for incident psoriasis (odds ratio: 1.68, 95% CI: 1.18–2.39). Linear psoriasis has also been reported after therapy with lithium. Lithium is a common component of the soil and some mineral water springs. Some authors have found elevated plasma levels of lithium in psoriasis patients who were never treated with lithium. Further, epidemiological studies are required to prove the causal relationship between psoriasis and naturally occurring lithium.
Chloroquine and hydroxychloroquine are the commonly used synthetic antimalarials for prophylaxis and treatment of malaria and various rheumatological and dermatological illnesses. Synthetic antimalarials are potent inhibitors of the enzyme transglutaminase. Transglutaminase is involved in the process of epidermal turnover and changes in the level of this enzyme are thought be responsible for induction of psoriasis. The exacerbation of psoriasis is far more common than de novo induction of psoriasis. The lag period ranges between 2 and 12 weeks for exacerbation of psoriasis. Latency period of longer duration (40.5 weeks) was seen in case of pustular eruption in preexisting psoriasis. Resolution of lesions was noted after 1 month of discontinuation of therapy. Strong evidence of antimalarial-associated psoriasis comes from a review by Slagel and James, in which 31% of patients on antimalarials had exacerbation of psoriasis. During the Vietnam War, 40 American soldiers were prescribed chloroquine for malaria prophylaxis, of which 42% developed exacerbation of treatment-refractory psoriatic lesions. Psoriatic erythroderma and pustular psoriasis have also been reported after intake of antimalarials. Cases of psoriasis vulgaris with lupus erythematosus have been reported, possibly attributed to administration of antimalarials.
Nonsteroidal anti-inflammatory drugs
NSAIDs are commonly available over-the-counter drugs which are frequently used by patients, especially with rheumatological disorders. Both topical and systemic NSAIDs have been reported to exacerbate psoriasis. NSAIDs block the cyclooxygenase pathway which further inhibits the arachidonic acid metabolism and eventually leads to accumulation of leukotrienes. This is thought to be responsible for exacerbation of psoriasis. The lag period was found to be very short (average 1.6 weeks) in case of NSAID-associated exacerbations. The most commonly reported morphological type is generalized pustular psoriasis (GPP). In a large study of 462 patients, exacerbation of psoriasis was seen in six patients. Naproxen was found to be the most common implicated drug. In another study, it was found that propionic acid derivatives (ibuprofen, naproxen, and ketoprofen) were the most common culprits. In a study by Ellis et al., it was found that topical 1% indomethacin cream led to exacerbation of psoriasis in 14 out of 20 patients. GPP has also been reported with phenylbutazone. It is especially important for clinicians to recognize this exacerbation as many patients with psoriasis who have concomitant arthropathies often use over-the-counter NSAIDs.
The association between antibiotic intake and exacerbation of psoriasis is controversial as intercurrent infections have also been postulated as one of the risk factors for flare-ups. The possible mechanisms proposed are reduction in intracellular cAMP levels and interaction with the arachidonic acid pathway. Tetracyclines have been found to preferentially accumulate in psoriatic skin lesions. Due to the photosensitizing effect of tetracyclines, a Koebner like phenomenon is thought to be responsible for worsening of the skin lesions. There is no definitive lag period established for tetracycline-associated psoriasis. In a study conducted by Tsankov et al., it was found that 19 (4.1%) out of 462 patients had exacerbation of psoriasis after treatment with tetracycline group of drugs. It has been recommended that tetracycline group of drugs be avoided in those with preexisting psoriasis or with genetic predisposition to psoriasis (positive for HLA B13, B27, and B17 genotypes), although these recommendations may not be very practical.
Drugs With Considerable but Insufficient Data
Angiotensin-converting enzyme inhibitors
Angiotensin-converting enzyme (ACE) inhibitors are one of the most commonly prescribed drugs for hypertension and heart failure. As psoriasis is known to have multiple systemic comorbidities including hypertension and cardiovascular diseases, it is common to find psoriasis patients on long-term ACE inhibitors. ACE inhibitors block the catabolism of kinins, thereby potentiating their hyperproliferative effect on the skin. In a case–control study, it was found that ACE inhibitors were associated with psoriasis in patients more than 50 years of age. Although a direct causal relationship is difficult to establish, few reports did mention the rapid resolution of lesions within weeks of withdrawal of the drug. Some studies also suggest that in patients with a family history of psoriasis, a particular ACE genotype which translates to low ACE enzyme activity might make the patient more susceptible to develop psoriasis.
Interferon-alpha used in the treatment of hepatitis C, melanoma, and Kaposi sarcoma has been reported to cause exacerbation of psoriasis. This was more frequently reported in cases of hepatitis C infection. Both cutaneous psoriasis and psoriatic arthritis have been linked with exposure to interferon-alpha. Interferon-beta is mainly used to treat multiple sclerosis. Reports of exacerbation and induction of psoriasis have been reported in patients with multiple sclerosis receiving interferon-beta. Cases of psoriasis induced at injection site with interferon-gamma have also been reported.
Terbinafine has also been linked to both exacerbation and induction of psoriasis. According to a recent study, terbinafine stimulates monocytes to release cytokines such as interleukin-8 and TNF-alpha, both of which have a key role in the pathogenesis of psoriasis. Both plaque psoriasis and GPP have been reported to occur after terbinafine therapy. With a generalized pustular eruption, it may be difficult to differentiate it from acute generalized exanthematous pustulosis (AGEP), which is also known to occur with terbinafine. In contrast to GPP, the pustules in AGEP occur within hours or days of drug intake and have a rapid resolution on discontinuation of the drug.
Azole group of antifungals notably itraconazole has also been associated with exacerbation of psoriasis. Azoles have an immunomodulatory effect which tips the balance toward a Th1 predominant response. In a population-based, case–control, comparative study among patients with onychomycosis, it was found that those with recent exposure to both terbinafine and itraconazole had increased risk of psoriasis. On comparing the two antifungals, the risk was seen to be higher with itraconazole.
Emerging Drugs With Psoriasiform Eruptions
Tumor necrosis factor-alpha inhibitor-associated psoriasis
TNF-alpha inhibitors are indicated in the treatment of moderate-to-severe psoriasis, psoriatic arthritis, Crohn's disease, ankylosing spondylitis and RA. Paradoxically, TNF-alpha inhibitors are known to be associated with psoriasiform eruptions. The proinflammatory cytokine interferon-alpha produced by plasmacytoid dendritic cells might be implicated in pathogenesis of this paradoxical reaction. Certain other genetic factors such as polymorphisms in TNF-alpha promoter region may be risk factors, which influence the adverse effects seen with this drug. This type of reaction is well known with the non-dermatological indications for TNF-alpha inhibitors. Morphological types reported are plaque psoriasis, pustular psoriasis and palmoplantar psoriasis. In a recent systematic review, 216 cases of TNF-alpha-induced psoriasis were found in patients with Crohn's disease (41%), RA (37%), and ankylosing spondylitis (14%). The average lag period was within 1 year of treatment initiation. Most cases were reported with infliximab, while occasional reports were with adalimumab, etanercept, and certolizumab. Most cases were managed with topical antipsoriatic agents. Other treatment options include switching to another biological agent, although recurrences are known to occur.
Other biological agents
There have been anecdotal reports of psoriasiform eruptions with vedolizumab (alpha-4-beta-7 integrin antagonist), rituximab (anti-CD20 mAb), and paradoxical reaction with secukinumab and ixekizumab (anti-IL-17 blocker).
Vascular endothelial growth factor blockers
Vascular endothelial growth factor (VEGF) is implicated in the pathogenesis of psoriasis, as it contributes to papillary dermal angiogenesis and epidermal hyperproliferation. VEGF blocker-induced psoriasiform dermatitis is another example of a paradoxical reaction, the exact mechanism of which is unclear. Sorafenib which blocks the enzyme RAF kinase, is an antigrowth and antiangiogenesis drug; is also known to cause palmoplantar keratoderma and keratosis pilaris like eruption, suggesting its role in altering keratinocyte proliferation. In a recent case series, it was found that sorafenib-associated exacerbation of preexisting psoriasis occurred within 2 months, whereas induction of psoriasis occurred after a lag period of 2–9 months.
Anti-programmed cell death protein 1 drugs
Nivolumab and pembrolizumab are anti-programmed cell death (PD 1) drugs which serve as immune checkpoint inhibitors. Both exacerbation and induction of psoriasis has been reported with these drugs. The morphological types reported are plaque psoriasis and inverse psoriasis.
Drugs With Occasional Reports
Imiquimod is TLR7 agonist, which is used topically for the treatment of premalignant skin lesions, basal cell carcinoma, verruca and molluscum contagiosum. Cases of psoriasiform eruptions in children has been reported with use in viral infections. Single report of erythroderma secondary to topical imiquimod given for actinic keratosis has also been reported.
Anecdotal reports of psoriasis exacerbation with many other drugs have been seen: gemfibrozil; beta-lactam antibiotics; granulocyte colony-stimulating factor; antiepileptics such as valproate, carbamazepine, and levetiracetam; anti-depressants such as fluoxetine and bupropion; clonidine; calcium channel blockers; gold salts; mercury; potassium iodide; morphine, etc.
Management of Drug-Associated Psoriasis
Findings in case of drug-induced psoriasis are not very different from psoriasis vulgaris and include parakeratosis, hypogranulosis, and regular acanthosis. Features such as suprapapillary thinning and dilated vessels are not commonly observed.
Careful assessment of risk must be done before attempting drug rechallenge. In case alternatives are available, rechallenge is best avoided.In vitro tests like macrophage inhibition test and lymphocyte transformation test have been used in occasional reports, but given the cost and specialized infrastructure required to perform these tests, they have not gained popularity.
The differentiation between drug-induced and drug-triggered psoriasis is based on clinical resolution on withdrawal of the drug in drug-induced psoriasis. Such patients have a better prognosis and usually require only topical antipsoriatic therapy and emollients. Drug-triggered psoriasis requires systemic antipsoriatic therapy in addition to withdrawal of the drug. Treatment options for moderate-to-severe psoriasis include systemic agents such as methotrexate, cyclosporine, acitretin, and hydroxyurea, which should be tailored keeping in mind other comorbidities the patient might have. When the patient is on multiple agents and drug interactions is a cause for concern, phototherapy can be an excellent alternative. In patients in whom immunosuppressants are contraindicated, apremilast has emerged as a safe and effective treatment option. For severe cases refractory to conventional therapy, biologics may need to be given for adequate disease control. Consultation with a cardiologist is necessary in managing a patient on beta blockers, as due to the long and variable lag time, the effect of beta blockers on the course of psoriasis is underestimated. Lithium-exacerbated psoriasis can be recalcitrant to treatment and discontinuation of lithium is necessary. The presence of preexisting psoriasis is not an absolute contraindication to starting therapy with lithium, but the patient must be closely monitored for any cutaneous adverse reactions. For antimalarials, the consensus is to avoid in patients with preexisting psoriasis who would require antimalarials for malaria prophylaxis or for lupus erythematosus.
Psoriatic eruptions associated with drugs are rare and it is often difficult to establish a definite causal relationship. Overall, exacerbation of preexisting psoriasis is more commonly observed than induction of de novo psoriasis. The most frequent morphological variant is the plaque type. Based on literature, the latency period can be classified as early, intermediate, and late [Table 2]. It is often very challenging to distinguish dug-induced pustular psoriasis from a pustular drug eruption like AGEP, especially in the early stages. The further course of the disease usually gives a clearer picture. With the advent of newer targeted therapies, paradoxical activation of alternate pathways has led to a wide variety of cutaneous eruptions including psoriasiform eruptions. Further studies at the molecular level might help characterize these adverse effects. There are no definite consensus guidelines regarding contraindication of certain drugs in preexisting psoriasis and decision must be made on a case-to-case basis, based on the requirement of the patient.
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