tofacitinib has been researched along with Dermatitis* in 3 studies
3 other study(ies) available for tofacitinib and Dermatitis
| Article | Year |
|---|---|
Topical Janus kinase-signal transducers and activators of transcription inhibitor tofacitinib is effective in reducing nonatopic dermatitis chronic itch: A case series.
Topics: Dermatitis; Humans; Janus Kinases; Piperidines; Pruritus; Pyrimidines; Pyrroles | 2022 |
[Granulomatous rosacea-like dermatitis under therapy with tofacitinib].
The case of a 32-year-old female with ulcerative colitis who developed severe papulopustular dermatitis while undergoing treatment with the Janus kinase (JAK) inhibitor tofacitinib. Despite intensive topical therapy, treatment with oral corticosteroids and oral doxycycline was unable to achieve sufficient improvement. Hence, tofacitinib treatment needed to be discontinued. It is well known that the class of JAK inhibitors can cause infectious and allergic cutaneous side effects. However, sterile papulopustular dermatitis as a side-effect has rarely been reported to date.. Wir berichten von einer 32-jährigen Patientin mit Colitis ulcerosa, die unter Therapie mit dem JAK(Januskinase)-Inhibitor Tofacitinib eine massive papulopustulöse Dermatitis entwickelt hat. Trotz intensiver lokaltherapeutischer Maßnahmen und der Einnahme von Kortikosteroiden und Doxycyclin trat keine ausreichende Besserung ein, sodass die Tofacitinib-Behandlung beendet werden musste. Bekanntermaßen kann die Klasse der JAK-Inhibitoren zu infektiösen und allergischen Hautnebenwirkungen führen. Fälle von steriler papulopustulöse Dermatitis unter Therapie mit JAK-Inhibitoren sind allerdings bislang kaum berichtet worden. Topics: Adult; Dermatitis; Female; Humans; Piperidines; Pyrimidines; Pyrroles; Rosacea | 2021 |
Reversal of CD8 T-cell-mediated mucocutaneous graft-versus-host-like disease by the JAK inhibitor tofacitinib.
The utility of allogeneic hematopoietic stem cell transplantation is limited by graft-versus-host disease (GVHD), a significant cause of morbidity and mortality. Patients with GVHD exhibit cutaneous manifestations with histological features of interface dermatitis followed by scleroderma-like changes. JAK inhibitors represent a class of immunomodulatory drugs that inhibit signaling by multiple cytokines. Herein we report the effects of tofacitinib in a murine model of GVHD. Oral administration of tofacitinib prevented GVHD-like disease manifested by weight loss and mucocutaneous lesions. More importantly, tofacitinib was also effective in reversing established disease. Tofacitinib diminished the expansion and activation of murine CD8 T cells in this model, and had similar effects on IL-2-stimulated human CD8 T cells. Tofacitinib also inhibited the expression of IFN-γ-inducible chemoattractants by keratinocytes, and IFN-γ-inducible cell death of keratinocytes. Tofacitinib may be an effective drug for treatment against CD8 T-cell-mediated mucocutaneous diseases in patients with GVHD. Topics: Administration, Oral; Animals; Bone Marrow; CD4-Positive T-Lymphocytes; CD8-Positive T-Lymphocytes; Cell Line, Tumor; Cell Proliferation; Chemokines; Cytokines; Dermatitis; Gene Expression Regulation; Graft vs Host Disease; Hematopoietic Stem Cell Transplantation; Humans; Interleukin-2; Keratinocytes; Mice; Mice, Inbred C57BL; Piperidines; Protein Kinase Inhibitors; Pyrimidines; Pyrroles | 2014 |