Faculty Bibliography

Anetoderma is an uncommon dermatosis that manifests as discrete foci of well-circumscribed, atrophic skin. The condition can be idiopathic or can be secondary to a number of associated cutaneous diseases. Whereas the pathophysiologic mechanisms remain unknown, anetoderma results from diminished elastic fibers in the dermis. We present an unusual case of localized, lenticular anetoderma in a man with HIV, a history of syphilis, and lichen planus. Both of these infections have been associated with anetoderma. Although his lesions are vaguely reminiscent of a variant of syphilitic anetoderma described in the 1930s, they are confined to a smaller anatomic distribution, differ in size, and have a papular appearance. As anetoderma can develop in the context of infectious disease, a diagnosis of anetoderma should trigger a thorough examination and evaluation for treatable concomitant illnesses.

A 36-year-old African man from Guinea with a history of albinism presented with a many-year history of scaling and erythema of the face, neck, and arms. The patient had light eyes, hair, and skin. Physical examination showed extensive photodamage. A skin biopsy specimen from the posterior aspect of the lower leg showed a squamous-cell carcinoma in situ. The most common types of oculocutaneous albinism (OCA), OCA 1 and OCA 2, are autosomal recessive disorders of pigmentation that commonly affect the skin, hair, eyes, and ears. Photodamage and skin cancers plague patients with albinism. In Africa, where albinism is prevalent, albinos face a myriad of social and medical issues. Skin cancer surveillance is an important consideration for albinos, and sun protection is paramount.

Gorlin syndrome is an autosomal dominantly inherited disorder that results in numerous basal cell carcinomas as well as a number of other facial and skeletal findings. We present a patient with many classic features and review some of the treatment options available for these patients.

We present a 31-year-old woman with a ten-year history of a progressive macular eruption; one of her macules demonstrated a wheal when rubbed. A biopsy was consistent with telangiectasia macularis eruptiva perstans. There were no signs and symptoms of systemic involvement despite the large body surface area of involvement.

OBJECTIVE: The aim was to assess the level of systemic involvement and character of renal disease in patients with chronic cutaneous lupus erythematosus of the discoid lupus variety (hereafter referred to as 'discoid lupus') and features of systemic lupus erythematosus (SLE). Clinical confusion with other types of cutaneous lupus erythematosus complicates interpretation of some previously reported studies. METHODS: Over three years, sixteen patients met the diagnostic criteria of discoid lupus, positive anti-nuclear-antibody, and at least one extracutaneous manifestation. RESULTS: Most patients (14/16) were female, between 26 to 66 years old. Arthritis was the most common extracutaneous manifestation followed by Raynaud's phenomenon. The anti-nuclear-antibody was speckled in ten patients with titers ranging from 1:40 to 1:1280 IU/mL. Elevated levels of double-stranded-DNA in low titers were found in four patients, anti-Smith-antibody in four; anti-Sjogren-syndrome-A-antibody in seven, and anti-ribonucleoprotein-antibody in seven. Renal function markers were transiently high in some patients but normalized over time. Hematuria and/or proteinuria were present at some time in seven patients. The highest BUN and creatinine levels were 42 mg/dL and 1.5 mg/dL, respectively. One patient had membranous glomerulonephropathy class 5; however, discoid lupus developed well after the onset of renal disease during a time when renal function had returned to normal. CONCLUSION: Our observational data supports previous reports suggesting that patients with active discoid lupus rarely have progressive renal insufficiency. The mechanism for the development of discoid lupus may involve an immunologic mechanism that differs from that which produces severe organ involvement, especially advanced immune-complex-mediated renal disease. Patients with discoid lupus rarely have sustained high levels of antibodies to double-stranded-DNA. Discoid lupus appears to be a marker for a more benign lupus course. This clinical observation lays the groundwork for a larger prospective, longitudinal cohort study for further validation.

A 49-year-old man with advanced HIV/AIDS on anti-retroviral therapy (HAART) and trimethoprim-sulfamethoxazole (TMP-SMX) presented with a several-month history of pruritic, erythematous, lichenified papules that coalesced into hyperkeratotic plaques on the trunk and extremities in a sun-exposed distribution. He shortly thereafter developed a progressive depigmentation over more than 80 percent of his body surface area. A biopsy specimen of an erythematous plaque on the trunk showed a superficial and mid-dermal infiltrate of lymphocytes with eosinophils, most consistent with either chronic lichenoid drug eruption or atypical lymphoproliferative disorder (ACLD) of HIV. The patient's lichenoid skin disease has persisted despite discontinuation of TMP-SMX, although it has improved partially with administration of topical glucocorticoids and acitretin. His depigmentation has continued to progress. We discuss the overlapping diagnostic entities which may be comprised by this patient's clinical disease, and highlight a unique presentation of the complex interaction between HIV infection and the skin.

We report the case of a 63-year-old obese man with a rapid-onset of widespread acanthosis nigricans (AN) in the setting of having recently initiated treatment with niacin for dyslipidemia. Although obesity and insulin-resistance are risk factors for AN, AN associated with endocrine dysfunction tends to have a more gradual onset and limited involvement. Owing to our patient's age, the rapid onset, and extensive distribution of his eruption, we initially were concerned about paraneoplastic AN. However, an evaluation for a malignant condition was negative. The timing of the onset of our patient's eruption within several months of starting niacin therapy is consistent with niacin-induced AN. Niacin is known to cause rapidly progressive, widespread AN that is reversible upon discontinuation of the medication. We discuss the pathogenesis of AN, which is thought to be the final common manifestation of stimulation of different subtypes of tyrosine kinase receptors by various epidermal growth factors.

Lupus erythematosus tumidus (LET) is an uncommon variant of cutaneous lupus erythematosus. Lupus erythematodes tumidus is characterized by smooth, erythematous plaques on sun-exposed areas without surface changes, such as follicular plugs, atrophy, or scale. Histopathologic features include a lymphocytic, perivascular and periadnexal infiltrate with abundant interstitial, superficial, and deep dermal mucin without appreciable epidermal and vacuolar changes. Typically, LET is responsive to treatment with systemic antimalarials. We present a unique case of alopecia associated with LET, which was partially responsive to hydroxychloroquine. We also note that the plaque of LET is adjacent to the plaque of discoid lupus erythematosus.

Figure skaters, ice-hockey players and speed skaters experience a range of dermatologic conditions and tissue-related injuries on account of mechanical trauma, infectious pathogens, inflammatory processes and environmental factors related to these competitive pursuits. Sports medicine practitioners, family physicians, dermatologists and coaches should be familiar with these skin conditions to ensure timely and accurate diagnosis and management of affected athletes. This review is Part I of a subsequent companion review and provides a comprehensive review of mechanical dermatoses experienced by ice-skating athletes, including skater's nodules and its variants, pump bumps, piezogenic pedal papules, talon noir, skate/lace bite, friction bullae, corns and calluses, onychocryptosis, skater's toe and skate blade-induced lacerations. These injuries result from friction, shear forces, chronic pressure and collisions with surfaces that occur when athletes endure repetitive jump landings, accelerated starts and stops and other manoeuvres during rigorous training and competition. Ill-fitting skates, improper lacing techniques and insufficient lubrication or protective padding of the foot and ankle often contribute to the development of skin conditions that result from these physical and mechanical stresses. As we will explain, simple measures can frequently prevent the development of these conditions. The treatment of skater's nodules involves reduction in chronic stimulation of the malleoli, and the use of keratolytics and intralesional steroid injections; if malleolar bursitis develops, bursa aspirations may be required. Pump bumps, which result from repetitive friction posteriorly, can be prevented by wearing skates that fit correctly at the heel. Piezogenic pedal papules may be treated conservatively by using heel cups, compressive stockings and by reducing prolonged standing. Talon noir usually resolves without intervention within several weeks. The treatment of skate bite is centred on reducing compression by the skate tongue of the extensor tendons of the anterior ankle, which can be accomplished by use of proper lacing techniques, increasing pliability of the skate tongue and using protective padding, such as Bunga Pads. Anti-inflammatory medications and cold compresses can also help reduce inflammation. Friction bullae are best managed by careful lancing of painful blisters and application of petrolatum or protective dressings to accelerate healing; preventative measures include the use of well fitting skates, proper lacing techniques and moisture-wicking socks. Corns and calluses are similarly best prevented by the use of well fitted skates and orthotic devices. Symptomatic, debridement reduces the irritant effect of the thick epidermis, and can be accomplished by soaking the area in warm water followed by paring. Application of creams with high concentrations of urea or salicylic acid can also soften callosities. Cases of onychocryptosis benefit from warm soaks, antibiotic ointments and topical steroids to reduce inflammation, but sometimes chemical or surgical matricectomies are required. Preventative measures of both onychocryptosis and skater's toe include cutting toenails straight across to allow for a more equal distribution of forces within the toe box. Finally, the prevention and treatment of lacerations, which constitute a potentially fatal type of mechanical injury, require special protective gear and acute surgical intervention with appropriate suturing. The subsequent companion review of skin conditions in ice skaters will discuss infectious, inflammatory and cold-induced dermatoses, with continued emphasis on clinical presentation, diagnosis, treatment and prevention.