2017
DOI: 10.1016/j.jdcr.2017.02.015
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Nivolumab-related cutaneous sarcoidosis in a patient with lung adenocarcinoma

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Cited by 70 publications
(51 citation statements)
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“…With systemic ICI therapies including ipilimumab (anti‐CTLA4), nivolumab, and pembrolizumab (anti‐PD1), a rare sarcoidosis‐like presentation has been described, characterized by noninfectious noncaseating granulomatous lymphadenopathy in a bilateral hilar and mediastinal distribution . A subset of cases manifests with a concomitant dermal sarcoid‐like granulomatous process . Even more relevant to the current report are three cases of subcutaneous panniculitis with a granulomatous component in patients treated with ICIs .…”
Section: Discussionmentioning
confidence: 77%
“…With systemic ICI therapies including ipilimumab (anti‐CTLA4), nivolumab, and pembrolizumab (anti‐PD1), a rare sarcoidosis‐like presentation has been described, characterized by noninfectious noncaseating granulomatous lymphadenopathy in a bilateral hilar and mediastinal distribution . A subset of cases manifests with a concomitant dermal sarcoid‐like granulomatous process . Even more relevant to the current report are three cases of subcutaneous panniculitis with a granulomatous component in patients treated with ICIs .…”
Section: Discussionmentioning
confidence: 77%
“…This reaction has been well documented in melanoma [3][4][5][6][7][8] but on rare occasion also in lung carcinoma. Concerning the few cases of lung cancer, none of them showed clear lymph node progression with sarcoid-like reaction, but rather a cutaneous form or unclear diagnosis [15,16]. In this case, the differential diagnosis is more challenging and has a greater impact on treatment strategy.…”
Section: Discussionmentioning
confidence: 89%
“…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...…”
Section: Discussionmentioning
confidence: 99%