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We report the case of a 72-year-old man with history of ankylosing spondylitis, who, during the treatment with infliximab, developed painful, erythematous-violaceous plaques with later development of ulcers on his feet associated with cold exposure. Concomitantly with the appearance of these lesions, he presented increased antinuclear antibodies (ANA) titers, positivity for anti-DNA and IgM anticardiolipin antibodies, low complement levels, polyclonal hypergammaglobulinemia, and lymphopenia. He was diagnosed of chilblain lupus induced by infliximab, this agent was withdrawn and initiated treatment for chilblains with improvement of lesions. On reviewing of the literature, we found seven reported cases of tumor necrosis factor α (TNF-α) antagonists-induced chilblain lupus, all in rheumatoid arthritis patients and four of them with clinical and immunological characteristics available are presented and compared with our case. Although it is infrequent, chilblain lupus forms part of the spectrum of TNF-α antagonists-induced lupus erythematosus; usually is limited to skin without progression to systemic lupus erythematosus; presents ANA, anti-DNA, and antinucleosome antibodies positivity as more frequent immunological alterations; and responds appropriately to the specific treatment, TNF-α antagonists withdrawal being not necessary in almost all cases.

The number of people dependent on crack-cocaine in the UK has increased substantially in recent years. Some crack-cocaine users develop coarsening changes in the appearance of their hands after prolonged use of the drug. These changes have most often been recognized in females and include: (i) Perniosis with cold, numb hands, sometimes with perniotic hyperkeratosis over the knuckles.(ii) Finger pulp atrophy of the distal part of the pulps of some digits, especially the thumbs and index fingers.(iii) Claw-like curvature of the nails. As the distal pulp is lost, it can no longer splint the nail straight and so the nail curves, claw-like, and reminiscent of a parrot's beak as it clings to the new contour. As the pulp atrophy progresses, the nail eventually also becomes smaller.This triad may be due to ischemia consequent upon peripheral vasoconstriction induced by crack-cocaine. Early changes may resolve with abstinence. In the patients described the syndrome does not appear to be to related to intravenous drug usage. It may occur without concomitant use of heroin, whether smoked or via the intravenous route. The syndrome does not occur in all crack-cocaine users. It is hypothesized that those with a vasoreactive circulation (i.e., those with vasomotor instability/perniosis) are more susceptible to this reaction pattern. The syndrome consisting of the triad of perniosis, pulp atrophy and parrot-beaked clawing of the nails should alert the clinician to the possibility of prolonged crack-cocaine misuse.