Many emerging studies have implicated the Janus kinase/signal transducer and activator of transcription (JAK-STAT) cytokine signalling mechanism in disease pathogenesis. This signalling pathway is involved in haematopoiesis and immune development. Mutations in genes regulating JAK-STAT signalling can cause common inflammatory disorders and myeloproliferative disorders. JAK and STAT inhibitors are new management tools for disorders such as myelofibrosis and rheumatoid arthritis. Evidence suggests that the cytokine components of the JAK-STAT pathways play a crucial role in common skin disorders, including psoriasis and atopic dermatitis. We present an overview for the clinical dermatologist of the significance of these signalling pathways in various skin disorders, and introduce the potential application of JAK and STAT inhibition as a new therapeutic tool in dermatology.

Pyoderma gangrenosum (PG) commonly occurs in association with various haematological and inflammatory disorders. We report a new association, a Janus kinase (JAK)2 mutation, in a 63-year-old patient with PG. We hypothesise that PG occurs by direct activation of JAK along with signal transducers and activators of transcription (STAT), a common mechanism involved in the pathogenesis of inflammatory and haematological diseases.

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A 65-year-old man presented with a 6-year history of a lesion on his left shin, which had rapidly doubled in size over a period of 6 months.On physical examination, a large, pigmented nodule, 10 · 14 mm in size, was seen on the patient's shin (Fig. 1a). It was not tender, and was doughy in consistency. Using dermatoscopy, an asymmetrical bluish-grey pigmented area was seen in the centre, while white to whitish-grey pigmented streaks were seen on the periphery of the lesion (Fig 1b). Laterally, there were few faint dotted blood vessels.The lesion was excised under local anaesthesia.