Cutaneous Sarcoidosis in a Patient with Severe Asthma treated with Omalizumab

Abstract

Omalizumab, a monoclonal anti-immunoglobulin E antibody, has been used as an effective treatment for severe asthma associated with atopy over the past decade. Sarcoidosis is an idiopathic granulomatous disorder in which first-line treatment is usually glucocorticoids. To the authors' knowledge, the present report describes the first case of an association between omalizumab therapy and revelation of cutaneous sarcoidosis with the withdrawal of systemic glucocorticoids. A 56-year-old woman with severe allergic asthma dependent on oral prednisone initiated omalizumab treatment. As her symptoms of asthma improved over the course of a year, her prednisone was gradually tapered. After being off glucocorticoids, she developed skin nodules that had biopsy characteristics of sarcoidosis. The present case illustrates the need to monitor closely for potential unmasking of glucocorticoid-responsive conditions when transitioning from systemic glucocorticoids to omalizumab therapy.

Drug‐induced sarcoidosis: an overview of the WHO pharmacovigilance database

“…Most of the drugs identified in this study have been associated with sarcoidosis in the literature and were represented by TNF‐alpha antagonists, interferons and immune checkpoint inhibitors . However, some drugs have rarely been reported as sarcoidosis inducers until now such as rituximab , omalizumab or ustekinumab . Other drugs have never been reported as being associated with sarcoidosis adverse events such as secukinumab or treprostinil.…”

Drug-induced sarcoidosis in a patient treated with an interleukin-1 receptor antagonist for hidradenitis suppurativa

“…Immune checkpoint inhibitors can induce sarcoidosis by modifying cytotoxic, Th1/17 and regulatory T-cell ratios 10, 21Table IDrugs that induce cutaneous sarcoidosis and proposed biologic mechanisms of inductionDrugBiologic mechanismIL-1Ra: anakinra 1 Unopposed type I IFN productionFailure of immune regulatory mechanismsImmunosuppression favoring infection with bacterium implicated in sarcoidosisInterferon-α 3 Induction of Th1 cytokinesanti-TNF agents4, 5: entanercept, 6 infliximab, 7 adalimumab 8 Unopposed type I IFN productionMove toward a Th1/Th17 profileDecreased TNF-mediated suppression of Treg expansion/activityAlteration in ratio of membrane bound to soluble TNFR2Process of anti-IFX antibody productionPredisposition secondary to genetic variation of TNF-α genePD-1 inhibitors: pembrolizumab, 9 nivolumab 10 Increased T-cell proliferative capacityNote: PD-1 up-regulation has also been associated with sarcoidosis with a proposed mechanism of decreased T-cell proliferative capacity leading to immunologic derangements conducive to sarcoidosis BRAF inhibitor: vemurafenib 11 Increased TNF-α and IFN-γ levelsNote: Study suggests patients who have sarcoidosis with vemurafenib therapy carry a better prognosisanti-CTLA4 mAb: ipilimumab 12 Enhanced T-cell responsesanti-IgE mAb: omalizumab 13 Decreased expression of dendritic cell IgE high affinity receptor/Th2 cytokine production with subsequent shift from Th2 to Th1 cytokine profileUnmasking of sarcoidosis with prednisone taper accompanying omalizumab treatment initiationFillers for aesthetic procedures: hyaluronic acid 14 Tissue injury and foreign body reaction to fillerInsulin15, 16Traumatic induction (Koebnerization) and foreign body reaction to materials introduced with insulin injectionInflammatory response to zinc component of insulin formulationBotulinum neurotoxin A 17 Foreign body reaction after deposition of crystalline preparation of botulinum neurotoxin A in the skinForeign body reactio...…”