Use of granulocyte and monocyte adsorption apheresis in dermatology (Review)
Exp Ther Med 2022 Jun 24;24(2):536. doi: 10.3892/etm.2022.11463. eCollection 2022 Aug. DOI: 10.3892/etm.2022.11463
Adsorptive granulocyte and monocyte apheresis (GMA) is an extracorporeal treatment that selectively removes activated myeloid lineage leukocytes from peripheral blood. This technique consists of a column with cellulose acetate beads as absorptive leukocytapheresis carriers, and was initially used to treat ulcerative colitis. A literature search was conducted to extract recently published studies about the clinical efficacy of GMA in patients with different skin disorders, reporting information on demographics, clinical symptoms, treatment and clinical course. Dermatological diseases, in which GMA has been performed, include generalized pustular psoriasis, pyoderma gangrenosum, palmoplantar pustular psoriasis, Behcet’s disease, Sweet’s syndrome, adult-onset Still’s disease, impetigo herpetiformis, reactive arthritis, acne and hidradenitis suppurativa syndrome, cutaneous allergic vasculitis and systemic lupus erythematosus. In most patients, GMA was started after the failure of conventional therapeutic options and it was helpful in the majority of cases. Based on the information summarized, GMA could be considered a valid non-pharmacological treatment option for patients with several dermatological conditions, which are difficult to treat with other pharmacological preparations.
PASH syndrome; cutaneous allergic vasculitis; granulocyte and monocyte apheresis; neutrophilic dermatoses; reactive arthritis; systemic lupus erythematosus.
Leukocytapheresis for rheumatoid arthritis cases that are super-resistant to any class of biological drugs and tofacitinib
Many biological disease-modifying antirheumatic drugs (bDMARDs) and targeted synthetic DMARDs (tsDMARDs) are currently available as treatment options for rheumatoid arthritis (RA), but a subset of RA patients shows inadequate responses to any of these DMARDs. This phenomenon, which we call super-resistance, is becoming a serious concern. In this study, I present two cases of super-resistant RA in which patients failed to respond to treatment with bDMARDs of any class as well as to tsDMARD therapy with tofacitinib. In these cases, leukocytapheresis (LCAP), a treatment that removes overabundant leukocytes from the body, rapidly induced low disease activity and made patients subsequently responsive to previously ineffective DMARDs. My experience with the present cases suggests that LCAP is worth considering as an alternative therapeutic option for the management of RA patients with super-resistance to DMARD therapies.
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