Drug-induced Subacute Cutaneous Lupus Erythematosus Research Articles

Drug-induced subacute cutaneous lupus erythematosus secondary to Dupilumab: A case report

We present the case of a 63-year-old male with known rheumatoid arthritis, diabetes, hypertension, and peripheral neuropathy who developed drug-induced subacute cutaneous lupus erythematosus secondary to Dupilumab for his chronic hand dermatitis.

Subacute cutaneous lupus erythematosus following ribociclib therapy for metastatic breast cancer.

Drug-induced subacute cutaneous lupus erythematosus (DI-SCLE) has been associated with drugs with different mechanisms of action, including anti-hypertensives, tumour necrosis factor-α inhibitors and even some chemotherapy medicines. In the last years, a few reports have been described in patients treated with cyclin-dependent kinase (CDK) 4/6 inhibitors, palbociclib and abemaciclib. Here, we describe a case of DI-SCLE in association with ribociclib and exemestane in a woman diagnosed with metastatic breast cancer. Topical mometasone was prescribed for two weeks with complete resolution of lesions, also abemaciclib was substituted for ribociclib, and the patient had stable disease with no relapse of DI-SCLE. To our knowledge, this is the first report of ribociclib-induced SCLE but based on the DI-SCLE reported cases associated others CDK4/6 inhibitors, the role of this family of drugs in dermatopathology must be further investigated.

Subacute Cutaneous Lupus Erythematosus-Like Drug Eruption Related to Terbinafine in a Male

Patients with a history of or a predisposition to autoimmune or collagen vascular diseases are inclined to develop drug-induced subacute cutaneous lupus erythematosus (SCLE) due to terbinafine therapy. Here, we report a case of terbinafine-induced SCLE in a male patient, although classic SCLE most commonly affects females, and he did not have a diagnosis of or a history suggestive of a predisposition to autoimmune or collagen vascular diseases. Although the mechanism for terbinafine-induced SCLE has not been fully elucidated, we suggest that there may be distinctive mechanisms of terbinafine-induced SCLE of patients with and without a predisposition to or history of autoimmune or connective tissue diseases, which should be a focus of future research.

A Curious Case of Drug-induced Subacute Cutaneous Lupus Erythematosus.

Sir, Drugs causing drug-induced systemic lupus erythematosus (DI-SLE) are different from drugs causing drug-induced subacute cutaneous lupus erythematosus (DI-SCLE) except for tumor necrosis factor antagonists.[1] Isoniazid is known to cause DI-SLE. However, isoniazid causing DI-SCLE has been infrequently described in the literature. A 60-year-old female, a known case of tubercular osteomyelitis, presented with multiple erythematous scaly lesions over the body for the last 2 months. The patient was on antitubercular drugs HRZE (isoniazid, rifampicin, pyrazinamide, and ethambutol (HRZE) for 2 months and isoniazid, rifampicin, and ethambutol (HRE) for 2 months. The lesions developed after nearly 8 weeks of intake of HRZE. The cutaneous examination showed multiple annular erythematous scaly plaques over the face, trunk, and limbs with accentuation in the photo-exposed sites along with multiple targetoid lesions [Figure 1a and b]. The complete hemogram showed eosinophilia of 11%. The liver function test, renal function test, chest X-ray, 24-hour urine protein, and electrocardiogram (ECG) were within normal limits. Antinuclear antibody (ANA) was positive (1:90, homogenous pattern). The anti Ro/La, antihistone, anti dsDNA, antismith antibodies, and rheumatoid factor were negative.Skin biopsy revealed basal cell vacuolization, colloid bodies, pigment incontinence, infiltration of the vessel wall by inflammatory cells, and karyorrhectic debris [Figure 2a]. The patient was diagnosed as a case of SCLE and started on hydroxychloroquine 300 mg daily along with oral prednisolone 30 mg daily for 2 weeks, topical mometasone, and sunscreen; however, the lesions persisted. Because of the refractory nature of lesions, the drug was suspected as a possible trigger. As isoniazid is more commonly incriminated in systemic lupus erythematosus, isoniazid was stopped and replaced by oral levofloxacin. Rifampicin, ethambutol, and levofloxacin were continued along with levocetrizine and topical mometasone, and oral steroids were stopped. After 2 weeks of stopping isoniazid, there was a significant improvement in cutaneous lesions with complete subsidence of lesions at 4 weeks [Figure 2b]. The patient is on follow-up and has not reported any new lesions or systemic symptoms since then.Figure 1: Multiple erythematous annular scaly plaques over the gluteal area (a). Close-up photograph of the thigh showing annular scaly plaques and targetoid lesions (b)Figure 2: (a) Skin biopsy showing hyperkeratosis, parakeratoses, basal layer vacuolization, colloid bodies, and infiltration of the vessel wall by inflammatory cells. (H & E 10×). (b) Subsiding lesions over the thigh after 2 weeks of stopping isoniazidDI-LE has predominantly systemic symptoms such as fever, arthritis, and serositis, whereas LE-specific skin changes are relatively uncommon.[234] However, in DI-SCLE, there are specific cutaneous lesions and systemic features are minimal or absent. Anti-histone antibodies are frequently present in DI-LE,[3] whereas anti Ro/SSA antibodies are more frequently positive in DI-SCLE.[2] It is also important to identify and differentiate this subset of patients from idiopathic SCLE (I-SCLE) as removal of the culprit drug is the mainstay of management in DI-SCLE. DI-SCLE usually has an older age of onset than I-SCLE.[34] Latent period between exposure to the drug and the onset of symptoms is 4 to 8 weeks.[2] The disease is more widespread, and involves areas that are usually spared by I-SCLE. Bullous, erythema multiforme–like lesions, purpura, necrotic-ulcerative lesions, malar rash, and the involvement of lower legs are more common in DI-SCLE.[34] Recently, one case of isoniazid-induced SCLE was described in a HIV-positive female.[5] In our patient, temporal correlation with the intake of drugs, widespread involvement including legs, erythema multiforme–like lesions, and eosinophilia suggested drug as a possible etiology. The patient did not meet the criteria for Rowell syndrome,[6] and SLE was ruled out because of lack of systemic involvement. The mainstay of treatment is the discontinuation of the culprit drug which leads to the resolution of lesions in a period of nearly 6 to 12 weeks.[4] Other treatment modalities are topical steroids, topical tacrolimus, hydroxychloroquine, and oral steroids.[2] Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

Are there distinct clinical and pathological features distinguishing idiopathic from drug-induced subacute cutaneous lupus erythematosus? A European retrospective multicenter study

Clinical and pathologic criteria to distinguish drug-induced subacute lupus erythematosus (DI-SCLE) from idiopathic (I-SCLE) are controversial. The aim of the survey was a retrospective analysis of a consistent number of iatrogenous and idiopathic SCLE cases, by means of clinical and histopathologic investigation. Eleven European university dermatology units collected all diagnosed cases from January 2000 to December 2016. Board-certified dermatopathologists reviewed the histopathologic specimens. Statistical analysis included Student t test, exact test of goodness-of-fit, Fisher's exact test, and the Cochran-Mantel-Haenszel test for repeated measures. Out of 232 patients, 67 (29%) belonged to the DI-SCLE group. Patients with DI-SCLE were significantly older and reported more systemic symptoms than those with I-SCLE. No statistical differences were found for presentation pattern or serology, while histopathology showed a significant association of mucin deposition (P=.000083), direct immunofluorescence positivity for granular immunoglobulin M, and C3 deposits on the basement membrane zone (P=.0041) for I-SCLE and of leukocytoclastic vasculitis (P=.0018) for DI-SCLE. This is a retrospective study. An integrated clinical and immunopathologic evaluation is useful to differentiate I-SCLE from DI-SCLE. Older age at onset and more frequent systemic symptoms characterize DI-SCLE. Mucin deposition and immunofluorescence findings are found in I-SCLE, and leukocytoclastic vasculitis is found in DI-SCLE.

Drug-induced subacute cutaneous lupus erythematosus secondary to intravenous immunoglobulin during the treatment of Castleman disease–associated paraneoplastic pemphigus

Drug-induced subacute cutaneous lupus erythematosus secondary to intravenous immunoglobulin during the treatment of Castleman disease–associated paraneoplastic pemphigus

462 Systemic fluorouracil causing subacute cutaneous lupus erythematosus

Case History: A 67-year-old woman with pancreatic adenocarcinoma presented with photosensitivity and pruritic photodistributed annular plaques over the bilateral extensor forearms and dorsal hands after her fourth cycle of FOLFIRINOX (folinic acid, fluorouracil, irinotecan, and oxaliplatin). Dermatopathology showed an interface dermatitis with a cuffed perivascular lymphocytic infiltrate and dermal mucin, suggestive of lupus erythematosus. Laboratory evaluation demonstrated an antinuclear antibody level of 8.0 U, anti-Ro IgG > 8.0 U, and anti-La IgG > 8.0 U. Systemic lupus was excluded given the lack of systemic symptoms, normal renal function, and normal urine studies. She was diagnosed with subacute cutaneous lupus erythematosus (SCLE) thought to be induced by systemic fluorouracil. Treatment and Follow-up: Photoprotection was advised, and she was treated with topical steroids while receiving three additional chemotherapy cycles. The eruption progressed to involve her back and chest and pruritus worsened, prompting cessation of fluorouracil from her treatment regimen. Five weeks after discontinuation of fluorouracil and while still receiving folinic acid, irinotecan, and oxaliplatin, the cutaneous eruption and associated pruritus resolved. Discussion: Drug-induced SCLE is most commonly associated with thiazides, terbinafine, calcium channel blockers, and angiotensin-converting enzyme inhibitors. Although several reports describe capecitabine, an oral fluorouracil prodrug, causing SCLE, only two descriptions of fluorouracil-induced SCLE exist in the literature. The pathophysiology underlying SCLE caused by fluorouracil is unclear although it has been postulated that fluorouracil preferentially targets epidermal basal cells leading to increased ultraviolet light-induced damage. The presence of anti-Ro antibody may also predispose individuals to fluorouracil-associated lupus erythematosus-like eruptions. Given the widespread use of fluorouracil and its prodrugs in oncologic management, both oncologists and dermatologists should be aware of the possibility of fluorouracil-induced SCLE.

Capecitabine-Induced Subacute Cutaneous Lupus Erythematosus in a Patient with Systemic Lupus Erythematosus

Capecitabine is a fluoropyrimidine chemotherapy prodrug of 5-fluorouracil (5-FU) used in the treatment of metastatic breast and colorectal cancers. Drug-induced subacute cutaneous lupus erythematosus (DI-SCLE) is a rare side effect of capecitabine therapy, with eight cases previously reported. We report a case of DI-SCLE in a patient with a documented history of systemic lupus erythematosus (SLE). This is the second documented case of DI-SCLE in a patient with a past medical history of SLE, and provides evidence that there may be an increased risk of DI-SCLE in these patients. Further research should examine whether patients with SLE are at greater risk for this adverse event.

Polekowy podostry skórny toczeń rumieniowaty indukowany amlodypiną

ENWEndNote BIBJabRef, Mendeley RISPapers, Reference Manager, RefWorks, Zotero AMA Kozłowska A, Woźniak Z, Maj J, Białynicki-Birula R. Drug-induced subacute cutaneous lupus erythematosus caused by amlodipine. Dermatology Review/Przegląd Dermatologiczny. 2018;105(2):298-306. doi:10.5114/dr.2018.75585. APA Kozłowska, A., Woźniak, Z., Maj, J., & Białynicki-Birula, R. (2018). Drug-induced subacute cutaneous lupus erythematosus caused by amlodipine. Dermatology Review/Przegląd Dermatologiczny, 105(2), 298-306. https://doi.org/10.5114/dr.2018.75585 Chicago Kozłowska, Agata, Zdzisław Woźniak, Joanna Maj, and Rafał Białynicki-Birula. 2018. "Drug-induced subacute cutaneous lupus erythematosus caused by amlodipine". Dermatology Review/Przegląd Dermatologiczny 105 (2): 298-306. doi:10.5114/dr.2018.75585. Harvard Kozłowska, A., Woźniak, Z., Maj, J., and Białynicki-Birula, R. (2018). Drug-induced subacute cutaneous lupus erythematosus caused by amlodipine. Dermatology Review/Przegląd Dermatologiczny, 105(2), pp.298-306. https://doi.org/10.5114/dr.2018.75585 MLA Kozłowska, Agata et al. "Drug-induced subacute cutaneous lupus erythematosus caused by amlodipine." Dermatology Review/Przegląd Dermatologiczny, vol. 105, no. 2, 2018, pp. 298-306. doi:10.5114/dr.2018.75585. Vancouver Kozłowska A, Woźniak Z, Maj J, Białynicki-Birula R. Drug-induced subacute cutaneous lupus erythematosus caused by amlodipine. Dermatology Review/Przegląd Dermatologiczny. 2018;105(2):298-306. doi:10.5114/dr.2018.75585.

Subacute Cutaneous Lupus Erythematosus: Clinical Characteristics, Disease Associations, Treatments, and Outcomes in a Series of 90 Patients at Mayo Clinic, 1996-2011

ObjectiveTo characterize the clinical presentation, laboratory studies, disease associations, and treatments of subacute cutaneous lupus erythematosus (SCLE). Patients and MethodsA retrospective review of 90 patients with SCLE at Mayo Clinic from January 1, 1996, through October 28, 2011, was performed. ResultsThe mean patient age at diagnosis was 61 years; 64 patients (71%) were women, and 11 cases (12%) were drug induced (1996-2000, no drug-induced cases; 2001-2005, 2 cases; 2006-2011, 9 cases). Seventeen of 59 patients (29%) with available data were smokers at the time of diagnosis. The SCLE lesions were photodistributed in 75 patients (83%), and 52 (58%) had papulosquamous morphologic findings. Anti-Ro/SS-A positivity was present in 84 of 85 patients tested (99%), whereas 32 of the 85 patients (38%) tested positive for anti-La/SS-B. Associated autoimmune connective tissue diseases included Sjögren syndrome (n=13, 14%) and systemic lupus erythematosus (SLE) (n=8, 9%). Eighteen patients (20%) had at least 4 American College of Rheumatology criteria for SLE; 1 had lupus nephritis, and none had neurologic or notable hematologic sequelae. The most common therapy was hydroxychloroquine, with a complete response noted in 34 of 46 patients (74%) with available follow-up data. ConclusionTwenty-eight percent of patients with SCLE (n=25) had an associated autoimmune connective tissue disease, although the severe sequelae of SLE, such as nephritis, were rare. The frequency of drug-induced SCLE increased during the study. Most patients responded to treatment with hydroxychloroquine.

Drug-induced cutaneous lupus erythematosus: 88 new cases.

An increasing number of drugs have been linked to drug-induced subacute cutaneous lupus erythematosus (DI-SCLE). The recognition and management of DI-SCLE can be challenging, as the condition may be triggered by different classes of drugs after variable lengths of time. To determine the proportion of patients with cutaneous lupus erythematosus (CLE) whose drugs are an inducing or aggravating factor. We conducted a retrospective chart review of patients diagnosed with CLE at a dermatological department over a 21-year period. We registered clinical, serological, and histological data with a focus on drug intake. Of 775 consecutive patients with a diagnosis of lupus erythematosus (LE) or suspected LE, a diagnosis of CLE could be confirmed in 448 patients. A total of 130 patients had a drug intake that could suggest DI-SCLE. In 88 cases, a drug was evaluated to be definitely, probably, or possibly triggering CLE using the Naranjo probability scale. The most common drugs involved were proton pump inhibitors (PPIs), thiazide diuretics, antifungals, chemotherapeutics, statins, and antiepileptics. The incubation period varied widely with a median of eight weeks. The characteristics of DI-SCLE patients were more widespread rash relative to the other patients, with inflamed skin lesions or atypical variants which could resemble erythema multiforme. We present 88 patients with DI-SCLE, which is the largest case series reported, to date. DI-SCLE represented 20% of patients with CLE seen at our department. We conclude that DI-SCLE should be considered in every case of SCLE.

An update in drug-induced subacute cutaneous lupus erythematosus

It has been over three decades sincethe first report of drug-induced subacute cutaneouslupus erythematosus (DI-SCLE) was described. Withan increasing variety of implicated drugs and thepotential for publication bias, we must consider: 1) hasthere been a change in drugs most often reported inDI-SCLE over time, and, 2) if so, of which drugs shouldclinicians be most suspicious in the setting of possibleDI-SCLE? To determine which drug(s) present thehighest risk for inducing DI-SCLE. The PubMed database was queried forreports of DI-SCLE from August, 2009 until May,2016. Cases reported in the English language wereorganized by drug class and compared with theresults of our previous review. From 55 selected publications, 95 qualifiedreports of DI-SCLE were identified. With theexception of a population-based study from Sweden,all other reports of DI-SCLE appeared as case reportsor small case series. Cases associated with protonpump inhibitors relative to all other medicationswere increased by 34.1%. Reports associated withantihypertensive and antifungal medicationsdecreased by 28.9% and 22.4%, respectively duringthis timeframe. The majority of new reports wereassociated with drugs not previously described.Greater than 70% of reports since August, 2009 werefrom European countries. The number of drugs associated withDI-SCLE is increasing. However, a form of publicationbias has likely contributed to this shift in reporting.There is a need for additional large, populationbasedstudies in this area.

Drug-Induced Subacute Cutaneous Lupus Erythematosus Associated with Proton Pump Inhibitors.

Subacute cutaneous lupus erythematosus (SCLE) is an autoimmune disease that may be induced by proton pump inhibitors (PPIs) in at-risk populations. The US FDA does not recognize SCLE as an adverse event associated with PPIs. We queried the FDA Adverse Event Reporting System database, which contains adverse event case reports submitted by the public as well as by industry, and analyzed the data to quantify passive pharmacovigilance signals for SCLE associated with PPIs. A disproportionality analysis of the signals yielded a significant association between SCLE and PPIs. Discontinuation of PPI resulted in remission, with PPI re-challenge causing SCLE to reoccur. A follow-up analysis also yielded a significant association between SCLE and H2 receptor antagonists. We conducted a brief literature survey of published case reports and studies to discern the validity of PPI-induced SCLE signals. Healthcare prescribers and patients should be made aware that SCLE can be induced by PPIs. In such cases, PPIs should be discontinued and alternative clinical treatment sought. Regulatory bodies such as the FDA should incorporate the adverse reaction in PPI prescription labels.

Immediate and Delayed Hypersensitivity Reactions to Proton Pump Inhibitors: Evaluation and Management.

PPIs are among the most commonly administered medications in the USA and are generally well tolerated. Immediate and delayed immune-mediated hypersensitivity reactions are rare but increasingly recognized adverse effects of proton pump inhibitors (PPIs). Immediate hypersensitivity reactions can occur due to IgE-mediated hypersensitivity to PPIs and can be evaluated by immediate hypersensitivity skin testing and oral provocation challenge testing. A desensitization protocol can be used when PPI use cannot be avoided in an allergic patient. Delayed hypersensitivity reactions to PPIs have also been reported. Occupational exposures causing cutaneous reactions to PPIs are the most commonly reported delayed hypersensitivity reaction, followed by drug-induced subacute cutaneous lupus erythematosus. This review presents a summary of the clinical presentation, diagnostic evaluation, and management of immune-mediated hypersensitivity reactions to PPIs.

Drug-Induced Lupus Erythematosus

Drug-induced lupus erythematosus is an autoimmune disorder, much like idiopathic systemic lupus erythematosus. As in idiopathic systemic lupus erythematosus, there is antibody generation and “accidental” attack on normal healthy tissues in drug-induced lupus erythematosus. Symptoms and signs often resolve upon discontinuation of the offending drug, making it an important diagnosis for healthcare providers to make. An increasingly large number of medications have been linked to drug-induced lupus erythematosus. Hydralazine, isoniazid, and procainamide are the most common medications known to cause drug-induced systemic lupus, whereas hydrochlorthiazide, diltiazem (and other calcium channel blockers), and terbinafine are the most common causative agents in drug-induced subacute cutaneous lupus erythematosus.

Subacute cutaneous lupus erythematosus induced by lansoprazole

A 48-year-old woman presented us with multiple annular erythematous-squamous plaques over trunk and limbs appeared 3 weeks before. There was no mucosal involvement. Her medical history included systemic lupus erythematosus (LES), diagnosed 3 years before and currently no longer treated, and gastroesophageal reflux for which she was in therapy with lansoprazole (30mg/daily) from 2months.Microscopy in 10 % potassium hydroxide and culture for mycoses was negative. Routine laboratory investigations were normal, antinuclear antibodies (ANA) negative, and anti-Ro/SSA antibodies positive (titer 1/80). Histology of an annular lesion showed atrophy of the epidermis, hydropic degeneration of the basal layer, edema in the upper dermis, and perivascular and periadnexial lymphohistiocytic infiltrate, consistent with subacute cutaneous lupus erythematosus (SCLE). A direct immunofluorescence test was negative. The patient received oral methylprednisolone (0.5 mg/kg/daily), topical steroids, and continued lansoprazolewith improvement but without complete resolution of the lesions. Therefore, lansoprazole was suspected to be responsible of the eruption and replaced by alginate and bicarbonate sodium with complete remission in a few days. Hence, diagnosis of drug-induced SCLE (DI-SCLE) was made. SCLE is a subtype of cutaneous lupus erythematosus that usually manifests as annular, psoriasiform lesions with limited systemic involvement and typically associated with positive ANA, anti-Ro/SSA, and anti-La/SSB antibodies. It may also be induced or exacerbated by drugs, including thiazide diuretics, calcium channel blockers, and also proton pump inhibitors (PPI) [1]. DI-SCLE does not differ clinically, histopathologically, or immunologically from idiopathic SCLE even though some authors have emphasized that DI-SCLE presented more disseminated cutaneous manifestations (as in our patient) and more frequent occurrence of malar rash and bullous, targetoid, and vasculitic lesions [1]. Patients with autoimmune diseases are more prone to druginduced or exacerbated SCLE [1], but the pathogenesis of DISCLE is not completely understood. However, it may be correlated to antimicrobial peptides (AMPs), small effector molecules of the innate immune system with well-known antimicrobial activity [2, 3]. In fact, several AMPs are increased in CLE at both gene and protein levels. In particular, AMPs were found to be significantly more highly induced in subacute CLE as compared with discoid LE and LE tumidus [2]. This might also explain the low prevalence of skin infections in CLE [2]. The selectivity of AMPs to bacterial cells relies on their cationic structures that are crucial for the interaction with negatively charged bacterial membranes [3]. Cathelicidins are a family of evolutionarily conserved AMPs, and hCAP-18 is the only cathelicidin in humans. Proteolytic cleavage of this preprotein releases a 37-residue known as LL-37 that is secreted by bone marrow cells, circulating leukocytes, and numerous types of epithelial tissues, such as skin. LL-37 could mediate innate immunity through regulating chemotaxis of leukocytes and production of cytokines at sites of infection/ inflammation as well as promoting re-epithelization during wound healing. LL-37 orients near the surface of phospholipid bilayers and forms oligomeric structures possessing the ability to disrupt cell membrane [3]. Depending on cellular context, autophagy may serve as a pro-death either pro-survival mechanism through p53 activation [3]. Human LL-37 and its derivatives may contribute to the control of immune-mediated inflammatory diseases through the regulation of proand antiinflammatory cytokines [4]. * Sanja Javor javor.med@gmail.com

Proton pump inhibitor‐induced subacute cutaneous lupus erythematosus

SummaryBackgroundDrug-induced subacute cutaneous lupus erythematosus (SCLE) has been known in the literature since 1985 and is increasingly recognized.ObjectivesTo identify and describe patients with proton pump inhibitor (PPI)-induced SCLE.MethodsA retrospective medical chart review of patients diagnosed with lupus erythematosus at the Department of Dermatology and Allergy Centre was carried out over a 19-year period. A causality assessment to PPI was performed using the Naranjo probability scale.ResultsTwenty-four patients with PPI-induced SCLE were identified (21 women and three men). Nineteen patients were newly identified cases, with a mean age of 61 years. These patients had 24 episodes of PPI-induced SCLE comprising lansoprazole (12), omeprazole (six), esomeprazole (four) and pantoprazole (two). Four patients had multiple episodes and three patients reacted to different PPIs. The incubation period was on average 8 months (range 1 week to 3·5 years) and the resolution period was on average 3 months (range 4 weeks to 8 months). Antinuclear antibodies were positive in 61% of tested patients, most frequently with a speckled pattern. Positive anti-Ro/SSA antibodies were found in 73%, anti-La/SSB antibodies in 33% and antihistone antibodies in 8% of tested patients at the time of the eruption. The skin rash was often widespread with a tendency to bullous lesions and focal skin necrosis.ConclusionsWe present the largest case series of PPI-induced SCLE reported to date, and our patient cohort reveals the lack of attention to this condition. The diagnosis may be suspected on the clinical picture, and most patients have anti-Ro/SSA antibodies, while antihistone antibodies have no value in the diagnostic process. Cross-reactivity can be seen between different PPIs.

Drug-Induced Subacute Cutaneous Lupus Erythematosus Associated with Nab-Paclitaxel Therapy

Drug-induced lupus erythematosus (dile) syndromes are documented complications of chemotherapeutic agents, including paclitaxel. Subacute cutaneous lupus erythematosus (scle) is a distinct dile syndrome presenting with characteristic annular or papulosquamous skin lesions in a photosensitive distribution with associated high anti-ssa titres. Previously, dile syndromes complicating paclitaxel therapy have been attributed to polyethoxylated castor oil (Kolliphor EL: BASF, Ludwigshafen, Germany), the biologic solvent included in the drug's original formulation (Taxol: Bristol-Myers Squibb, Montreal, QC), rather than the parent chemotherapy molecule. Here, we report a characteristic case of drug-induced scle complicating treatment with nanoparticle albumin bound (nab)-paclitaxel (Abraxane: Celgene, Summit, NJ, U.S.A.), a solvent-free taxane formulation. The pertinent English-language literature is also discussed. This case report is the first to link solvent-free paclitaxel with scle, and it suggests that the parent molecule is responsible for the reaction.

Subacute Cutaneous Lupus Erythematosus Induced by Chemotherapy

Several chemotherapeutic agents have been reported to induce subacute cutaneous lupus erythematosus (SCLE). To our knowledge, this is the first report to date of SCLE induced by monotherapeutic gemcitabine hydrochloride and includes a comprehensive review of all published cases of chemotherapeutic drug-induced SCLE. We describe a patient who developed a SCLE-like eruption after being administered gemcitabine and discuss 16 other published cases of chemotherapeutic drug-induced SCLE. This case and a review of the literature call attention to gemcitabine and other chemotherapeutic agents that have been reported to cause drug-induced SCLE. We also discuss the clinical features of the disease.

Drug-Induced Subacute Cutaneous Lupus Erythematosus—Filling the Gap in Knowledge

Drug-Induced Subacute Cutaneous Lupus Erythematosus—Filling the Gap in Knowledge