Systemic Lupus erythematosus Exacerbated by Piroxicam

Roura, Margarida; López-Gil, Francisco; Umbert, Pablo

doi:10.1159/000247739

Cited by 28 publications

(6 citation statements)

References 9 publications

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“…SCLE skin lesions can occur in other clinical settings in which Ro ⁄SS-A autoantibody is seen, such as Sjögren syndrome and rheumatoid arthritis. 23 Our review revealed four patients with Sjögren syndrome who later developed DI-SCLE, [24][25][26] lending further support to the importance of the 8.1 ancestral haplotype immunogenetic background and Ro ⁄SS-A autoantibody production they both share. 27 The reverse is true as well.…”

Section: Are Histone Autoantibodies Significantly Associated With Drumentioning

confidence: 59%

“…The median incubation time was 6 weeks. The mean and median overall time 30 3 cases Nitrendipine 31 1 case Diuretics Hydrochorothiazide 3,10,22 10 cases Hydrochlorothiazide + triamterene 6 3 cases Chlorthiazide 5 2 cases Beta blockers Oxprenolol 32 4 cases Acebutolol 33 1 case Angiotensin-converting enzyme inhibitors Enalapril 10 2 cases Lisnopril 10 1 case Captopril 34 1 case Cilazapril 34 1 case Antifungals 30 of 117 reported cases: 25AE6% Terbinafine 12,14-16, [35][36][37] 29 cases Griseofulvin 13 1 case Chemotherapeutics 10 of 117 reported cases: 8AE5% Docetaxel 38 3 cases Paclitaxel 24, 38 3 cases Tamoxifen 39 2 cases Capecitabine 40, 41 2 cases Antihistamines 9 of 117 reported cases: 7AE7% Ranitidine 42 7 cases Brompheniramine 42 1 case Cinnarizine + thiethylperazine 43 1 case Immunomodulators 8 of 117 reported cases: 6AE8% Leflunomide 9,17,25, 44 5 cases Interferon a and b 10, 45 3 cases Antiepileptics 3 of 117 reported cases: 2AE6% Carbamazepine 46, 47 2 cases Phenytoin 48 1 case Statins 3 of 117 reported cases: 2AE6% Simvastatin 10, 49 2 cases Pravastatin 10 1 case Biologics 2 of 117 reported cases: 1AE7% Etanercept 50 1 case Efalizumab 51 1 case Proton pump inhibitors 2 of 117 reported cases: 1AE7% Lansoprazole 52 2 cases Nonsteroidal anti-inflammatory drugs 2 of 117 reported cases: 1AE7% Naproxen 53 1 case Piroxicam 26 1 case Hormone-altering drugs 2 of 117 reported cases: 1AE7% Leuprorelin 19 1 case Anastrozole 18 1 case Ultraviolet therapy 2 of 117 reported cases: 1AE7% PUVA 54 1 case PUVA and UVB 20 1 case Others 4 of 117 reported cases: 3AE4% Bupropion…”

Section: Resultsmentioning

confidence: 99%

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A systematic review of drug-induced subacute cutaneous lupus erythematosus

Rh³

et al. 2011

British Journal of Dermatology

140

266

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The initial appearance of subacute cutaneous lupus erythematosus (SCLE) skin lesions in conjunction with Ro/SS-A autoantibodies occurring as an adverse reaction to hydrochlorothiazide [i.e. drug-induced SCLE (DI-SCLE)] was first reported in 1985. Over the past decade an increasing number of drugs in different classes has been implicated as triggers for DI-SCLE. The management of DI-SCLE can be especially challenging in patients taking multiple medications capable of triggering DI-SCLE. Our objectives were to review the published English language literature on DI-SCLE and use the resulting summary data pool to address questions surrounding drug-induced SCLE and to develop guidelines that might be of value to clinicians in the diagnosis and management of DI-SCLE. A systematic review of the Medline/PubMed-cited literature on DI-SCLE up to August 2009 was performed. Our data collection and analysis strategies were prospectively designed to answer a series of questions related to the clinical, prognostic and pathogenetic significance of DI-SCLE. One hundred and seventeen cases of DI-SCLE were identified and reviewed. White women made up the large majority of cases, and the mean overall age was 58·0 years. Triggering drugs fell into a number of different classes, highlighted by antihypertensives and antifungals. Time intervals ('incubation period') between drug exposure and appearance of DI-SCLE varied greatly and were drug class dependent. Most cases of DI-SCLE spontaneously resolved within weeks of drug withdrawal. Ro/SS-A autoantibodies were present in 80% of the cases in which such data were reported and most remained positive after resolution of SCLE skin disease activity. No significant differences in the clinical, histopathological or immunopathological features between DI-SCLE and idiopathic SCLE were detected. There is now adequate published experience to suggest that DI-SCLE does not differ clinically, histopathologically or immunologically from idiopathic SCLE. It should be recognized as a distinct clinical constellation differing clinically and immunologically from the classical form of drug-induced systemic lupus erythematosus.

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Section: Are Histone Autoantibodies Significantly Associated With Drumentioning

confidence: 59%

Section: Resultsmentioning

confidence: 99%

A systematic review of drug-induced subacute cutaneous lupus erythematosus

Rh³

et al. 2011

British Journal of Dermatology

140

266

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“…These modulators may include immunosuppressive cytokines, such as IL-10 or VIP (25,26), but also lipid mediators of the PG family, such as PGE 2 , as demonstrated in the current study. Although PG were so far thought to mediate mainly proinflammatory effects, their involvement in IFN-a regulation may explain not only occasional reports about the induction of SLE-like symptoms by cyclooxygenase inhibitors (38), but also improvement of such symptoms by treatment with PGE 1 (39) and PGI analogs (40). Such beneficial effects have been mainly attributed to vasodilation and inhibition of thrombosis, whereas the effect of PG analogs on PDC-dependent IFN-a secretion and the costimulatory phenotype of PDC has so far not been considered.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin E2 Inhibits IFN-α Secretion and Th1 Costimulation by Human Plasmacytoid Dendritic Cells via E-Prostanoid 2 and E-Prostanoid 4 Receptor Engagement

Fabricius

Neubauer

Mandel

et al. 2009

The Journal of Immunology

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Plasmacytoid dendritic cell (PDC)-derived IFN-α plays a central role in antiviral defense and in Th1-driven autoimmune diseases, such as systemic lupus erythematosus (SLE). In the current study, we explored how PGE2 effects the phenotype of PDCs from healthy and SLE subjects. Although PGE2 is considered to mediate mainly proinflammatory effects, we show that PGE2 and PG analogs potently inhibit secretion of IFN-α by TLR-activated PDCs. This effect is mainly mediated by PG receptors E-prostanoid 2 and E-prostanoid 4 and involves inhibition of IFN regulatory factor 7 expression. Of note, profound IFN-α inhibition by PGE2 is also seen in PDCs from SLE subjects, independent of age, disease activity, and therapy. We show that TLR9-activated PDCs treated with PGE2 exhibit DC2-like characteristics with enhanced expression of CD86 and CD62L, and decreased expression of CD80 and MHC class I. Consequently, PGE2-treated PDCs suppress secretion of Th1 cytokines by T cells while increasing the secretion of Th2 cytokines. Prevention of CpG-induced CD62L downregulation by PGE2 suggests that it may induce the retreat of PDCs from inflamed tissues. Our data on the effects of PGE2 on PDCs may explain occasional reports about the induction of SLE-like symptoms by cyclooxygenase inhibitors as well as improvement of such symptoms by treatment with PG analogs. In conclusion, our data suggest that PGE2 and certain PG analogs, some of which are already in clinical use, should be evaluated as a novel and inexpensive treatment approach for patients with SLE and other IFN-α–dependent, Th1-driven autoimmune diseases.

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“…1 Although all nonsteroidals have been associated with photosensitive rashes, only piroxicam has been reported to be associated with phototoxicity with resulting lupus ares. 18 Even though the overwhelming majority of SLE patients taking ibuprofen have no adverse reactions, case reports of aplastic anaemia, 19 ulcerative proctitis 20 and aseptic meningitis have appeared. [21][22][23][24] The latter represents one manifestation of a distinct hypersensitivity reaction characterized by hypotension, fever, rigors, conjunctivitis, nausea, arthralgias, elevated liver function tests and aseptic meningitis.…”

Section: Toxicity Of Nsaids In Slementioning

confidence: 99%

Celecoxib for systemic lupus erythematosus: case series and literature review of the use of NSAIDs in SLE

Lander

Wallace

Weisman

2002

Lupus

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The primary objectives of this study were to evaluate the safety and efficacy of the cyclooxygenase-2 inhibitor celecoxib in systemic lupus erythematosus (SLE) patients both with and without a self-reported sulfa drug allergy and to review the literature on the use of nonsteroidal agents in SLE subjects. A retrospective review of medical records was performed for 50 SLE patients seen by a community-based rheumatologist and treated with open label celecoxib in doses of 200-400 mg/day for a period of 1-9 months. A MEDLINE search of all articles pertaining to the use of NSAIDs in patients with SLE since 1966 was undertaken. We noted that, in this cohort of celecoxib-treated SLE patients from an office rheumatology practice, the majority demonstrated some improvement, and little toxicity was observed. SLE patients with self-reported sulfa allergies were not more likely to have adverse reactions to celecoxib than non-sulfa allergic patients. The literature review performed herein reveals that, although NSAID toxicity should be a continuing concern in an SLE population, structural dissimilarities between celecoxib and the sulfonamide antimicrobials may make true cross-allergenicity less likely to be a clinical problem. These results suggest that patients with SLE can be safely and effectively treated with celecoxib; however, further studies are needed to assess the effectiveness and safety of all NSAIDs in SLE.

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Systemic Lupus erythematosus Exacerbated by Piroxicam

Cited by 28 publications

References 9 publications

A systematic review of drug-induced subacute cutaneous lupus erythematosus

A systematic review of drug-induced subacute cutaneous lupus erythematosus

Prostaglandin E2 Inhibits IFN-α Secretion and Th1 Costimulation by Human Plasmacytoid Dendritic Cells via E-Prostanoid 2 and E-Prostanoid 4 Receptor Engagement

Celecoxib for systemic lupus erythematosus: case series and literature review of the use of NSAIDs in SLE

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