Faculty Bibliography

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.

We describe a 73-year-old woman with a long-standing history of annular, hyperkeratotic papules that began on the palms and soles and gradually spread to her trunk, extremities, and face. The clinical presentation and biopsy findings were consistent with PPPD, which is a rare subtype of porokeratosis that begins on the palms and soles and gradually spreads to the trunk and extremities. Owing to the risk of malignant degeneration in porokeratosis, patients should be closely monitored with total body skin examinations. There is no definitive treatment for PPPD. Oral retinoids are sometimes helpful although relapses are common after discontinuation of therapy

A 61-year-old woman with systemic lupus erythematosus and Sjogren syndrome presented with a two-month history of symptomatic nodules on the buttocks and thighs that progressed to involve the dorsal aspects of the hands. On examination, infiltrative papules, nodules, and plaques were present in these regions. Biopsy specimens demonstrated granulomatous inflammation and acid-fast bacilli with the use of a Fite stain, although a culture and polymerase chain reaction analysis were negative. The patient continues to improve on long-term clarithromycin therapy. Atypical mycobacterial infections are becoming more common, especially in immunocompromised patients. Antimicrobial therapy, either with a single agent or multiple agents, often is prolonged. A high index of suspicion is warranted in immunocompromised patients, which includes those with connective-tissue diseases that are active or that require immunosuppression. In these patients, the differential diagnosis includes infectious as well as inflammatory, reactive, or neoplastic processes

Laugier Hunziker syndrome is a rare disorder that is characterized by adult-onset hyperpigmented macules of the lips, oral cavity, and fingertips. Longitudinal melanonychia is present in the majority of cases. We present a 45-year-old woman with adult-onset hyperpigmented macules of the oral cavity as well as linear melanonychia that involved multiple fingernails. The history, clinical examination, and paucity of laboratory abnormalities or systemic findings support a diagnosis of Laugier Hunziker syndrome

Thalidomide and analogues are a class of immunomodulatory drugs or IMiDS. Thalidomide was initially approved by the U.S. Food and Drug Administation for treatment of erythema nodosum in leprosy and is now approved for multiple myeloma as well. A second generation IMiD, lenalidomide, is also approved for multiple myeloma and refractory myelodysplastic syndrome. Discovery of this class of drugs has been serendipitous and empirical, as the drug targets have been unknown. In this review, the authors integrate recent identification of drug targets of IMiDS, which include the inducible form of nitric oxide synthase (iNOS), Rho GTPase and caspase-1, with the developments in the understanding of the molecular biology of human inflammatory, infectious and neoplastic skin disorders. Because thalidomide reemerged through leprosy, the original disease classified by the T cell, the authors have also emphasized advances in the understanding of T-cell subsets in human skin disorders.

Sarcoidosis is a noncaseating granulomatous disease, likely of autoimmune etiology, that causes inflammation and tissue damage in multiple organs, most commonly the lung, but also skin, and lymph nodes. Reduced dendritic cell (DC) function in sarcoidosis peripheral blood compared with peripheral blood from control subjects suggests that blunted end organ cellular immunity may contribute to sarcoidosis pathogenesis. Successful treatment of sarcoidosis with tumor necrosis factor (TNF) inhibitors, which modulate DC maturation and migration, has also been reported. Together, these observations suggest that DCs may be important mediators of sarcoidosis immunology. This review focuses on the phenotype and function of DCs in the lung, skin, blood, and lymph node of patients with sarcoidosis. We conclude that DCs in end organs are phenotypically and functionally immature (anergic), while DCs in the lymph node are mature and polarize pathogenic Th1 T cells. The success of TNF inhibitors is thus likely secondary to inhibition of DC-mediated Th1 polarization in the lymph node

BACKGROUND: Sarcoidosis affects the central nervous system more frequently than previously appreciated. The diagnosis of neurosarcoidosis is often delayed, potentially leading to serious complications. Symptoms, when present, are not specific, may be subtle and resemble those of other neurologic diseases. REVIEW SUMMARY: During the past decade, significant progress has been made in understanding the epidemiology and pathophysiology of neurosarcoidosis, as well as the ability to diagnose and treat this disease. Studies have shown that the optimal diagnostic imaging modality for neurosarcoidosis is magnetic resonance imaging with gadolinium as it enhances visualization of granulomatous infiltration in neural tissue. Subclinical neurosarcoidosis may not be uncommon in patients with sarcoidosis. It is now evident that neurosarcoidosis does not invariably present as a catastrophic event. Adverse effects associated with high-dose systemic corticosteroids, the standard therapy, have discouraged practitioners from initiating treatment in the absence of significant symptomatic neurologic disease. However, other immunosuppressive agents as well newer biologic agents have emerged as an effective, well-tolerated therapeutic alternative to corticosteroids, which are often effective in corticosteroid-recalcitrant cases. CONCLUSION: Neurologists should be aware of the varying presentations of neurosarcoidosis since early recognition of neurologic involvement in patients with undiagnosed or proven sarcoidosis is currently possible and critical to the prevention of disabling complications