Sarcoidosis, Malignancy and Immune Checkpoint Blockade

Neurosarcoidosis following Immune Checkpoint Inhibition

“…Additionally, there are also a handful of reports describing patients with known sarcoidosis who later received ICPIs. Gaughan [13] summarized 2 series that included 5 patients with preexisting sarcoidosis treated with ICPIs and of which 2 patients experienced sarcoidosis exacerbations that were treated with corticosteroids.…”

Adalimumab as a successful alternative for the treatment of infliximab‐induced sarcoidosis

“…3 Anti-TNF drugs can spread the infection of P. acnes to other cells or organs 2 and increase the ratio of T-helpher (Th)1 to Th2 cells as well as the levels of IFN-c, which further contribute to granuloma formation. 1,4 Taken together, P. acnes infection and cytokine imbalance induced by IFX might have promoted the pathogenesis of sarcoidosis in our case. IFX is a chimeric monoclonal immunoglobulin (Ig)G1 antibody composed of human constant and murine variable regions, while ADA is a recombinant human IgG1 antibody.…”

“…As previous reports suggested, probucol is more useful for the treatment of xanthelasma palpebrarum than pravastatin. 4 Because the precise mechanisms of probucol are still unknown, several hypotheses have been suggested. 4 Among them, Fujita et al 4 suggested that probucol inhibits the uptake of degenerated low-density lipoprotein into macrophages, leading to a reduction of the xanthelasma.…”

“…4 Because the precise mechanisms of probucol are still unknown, several hypotheses have been suggested. 4 Among them, Fujita et al 4 suggested that probucol inhibits the uptake of degenerated low-density lipoprotein into macrophages, leading to a reduction of the xanthelasma. Indeed, several reports suggested the therapeutic effects of probucol for the treatment of xanthelasma.…”

“…In sarcoidosis, T-helper 1 cells generally produce IFN-c and IL-2, inducing macrophage activation and local inflammation. 4 Meanwhile, melanogenesis-related peptide-specific CD8 + T cells are involved in the pathogenesis of vitiligo. 5 Our case indicates that effector T cells may differ depending on the irAE type, CD4 + T cells in sarcoidosis and CD8 + T cells in vitiligo.…”