Ruth F Walters

Elastic fiber pattern in scleroderma/morphea

Background: Scleroderma/morphea is characterized by expansion of the dermis with thickened collagen bundles and loss of CD34+ dermal dendrocytes. Variable elastic fiber changes have been described, but to our knowledge, no systematic study of the elastic fiber pattern correlated with CD34 expression has been reported.

Acquired perforating calcific collagenosis after topical calcium chloride exposure.

A 24‐year‐old healthy man presented with a 6‐week history of numerous umbilicated coalescing erythematous papules with some scale and crust on his anterior medial thighs. The eruption began 1 to 2 weeks after he spilled calcium chloride rock salts on his pants while salting the sidewalk during a snow storm. The salts dissolved and remained in contact with his skin for at least 4 hours until he was able to change clothes. A skin biopsy shows thick and thin collagen fibers with partial calcification in the papillary and upper reticular dermis associated with a sparse infiltrate of neutrophils, lymphocytes and mononuclear histiocytes. There are foci of transepidermal elimination of calcified fibers with adjacent epidermal hyperplasia and ortho‐ and parakeratosis. Von Kossa stain highlights calcification of the fibers, and trichrome stain confirms the fibers are collagen. A Verhoeff‐van Gieson stain shows no abnormality of elastic fibers. The patient was treated with topical betametasone diproprionate cream twice daily for 3 weeks, as well as a short course of oral levofloxacin and topical gentamicin cream. The lesions resolved over 3 weeks with residual scarring. We report a unique case of acquired perforating calcific collagenosis secondary to topical calcium chloride exposure.

Topical drug-induced subacute cutaneous lupus erythematosus isolated to the hands

Subacute cutaneous lupus erythematosus (SCLE) is a well-defined subtype of lupus erythematosus, characterised by photosensitivity, annular and/or psoriasiform lesions, variable systemic involvement and presence of circulating SSA/anti-Ro antibodies. SCLE may be idiopathic or drug-induced. Both the idiopathic and drug-induced forms of SCLE are analogous in their clinical, serological and histological features. Drug-induced SCLE has been reported with various oral agents, but to our knowledge this is the first reported case due to a topical medication. A 34-year-old female foot masseuse presented with a 2-month history of scaly, erythematous lesions isolated to the dorsal hands and interdigital spaces. She had used topical terbinafine, a topical antifungal cream, to her clients’ feet for a number of years. ANA and anti-SSA/Ro antibodies were positive. Physical examination, serology and histopathology were consistent with SCLE. We propose that our patients unique presentation of SCLE may be explained by a prolonged occupational exposure to topical terbinafine as a foot masseuse. While oral terbinafine is a drug known to cause drug-induced SCLE, to our knowledge, this is the first topically induced form of the disease.