2nd Annual San Diego Dermatology Symposium®
A Live Virtual Experience
June 11-13, 2021
A Live Virtual Experience
June 11-13, 2021
Natasha Mesinkovska, M.D.
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Dr. Mesinkovska began her lecture on scarring alopecia with a review of central centrifugal cicatricial alopecia (CCCA), which affects up to 15% of black women. CCCA is characterized by persistent hair loss that begins in the central crown of the scalp and widens over time. Complaints of burning and itching of the scalp may be early clues to the diagnosis, but Dr. Mesinkovska points out that CCCA is often initially mistaken for androgenetic alopecia due to subtle presentation in the early stages. CCCA is a fibroproliferative disorder characterized by aberrant scarring, which may relate to its association with uterine fibroids. A recently described gene variant, PADI3, is present in 25% of patients. The mainstays of treatment are topical and intralesional steroids; other proposed therapeutics include topical metformin 10% and platelet-rich plasma (PRP).
Dr. Mesinkovska then discussed frontal fibrosing alopecia (FFA). In addition to band-like scarring alopecia along the anterior hairline, patients with FFA may have loss of eyebrows (80%) or eyelashes (14%), as well as characteristic facial papules. Other associations include thyroid disease and possibly low levels of DHEAS and androstenedione. There is ongoing debate regarding the association of FFA with certain topicals including sunscreens (both chemical sunscreens and titanium dioxide), and further studies are needed. Treatment of FFA involves topical and intralesional steroids; oral therapeutics include hydroxychloroquine, pioglitazone, finasteride, and low-dose isotretinoin (particularly in patients with facial papules). Dr. Mesinkovska shared her philosophy for the use of PRP in scarring alopecia, stating that she considers PRP for early, active scarring hair loss, but does not use PRP for burnt-out disease. |
Sergei Grando, MD, PhD, DSc
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Dr. Grando began with a review of the clinical presentation and diagnosis of these entities. Pemphigus vulgaris (PV), characterized by autoantibodies against desmogleins 1 and 3, presents with irregularly shaped, fragile bullae leading to shallow erosions that do not heal (in contrast to aphthous ulcers and oral HSV, which do heal). Pemphigus foliaceous (PF), characterized by autoantibodies against desmoglein 1, typically does not have a mucosal component and presents on the skin with superficial, wet erosions. Dr. Grando briefly discussed his work demonstrating potential pathogenicity of certain non-desmoglein antibodies to explain the clinical presentation of patients in whom anti-desmoglein antibodies are negative. He then reviewed bullous pemphigoid (BP), which presents with tense bullae and is caused by auto-antibodies against basement membrane zone proteins BP180 and BP230.
Finally, Dr. Grando gave a review of his multidrug treatment protocol. The tenets of the protocol are 1) increasing resistance of keratinocytes to autoantibodies, 2) eliminating autoantibodies, and 3) preventing autoantibody production. He described a protocol involving concurrent use of prednisone, doxycycline + nicotinamide, IVIG, and rituximab, with tapering of prednisone over the first 6 months and continuation of the other for 2 years. He reports a relapse rate of 12% after 5 years with this regimen, compared with a 32% relapse rate in patients treated with the prednisone + rituximab regimen recently approved by the FDA. Dr. Grando maintained that maintenance therapy with IVIG + rituximab should be continued for at least 2 years to prevent relapse, arguing that relapses during this period may aggravate autoimmunity and induce new autoantibody formation, thereby resetting the clock for a possible cure. |
Sheila Fallon-Friedlander, M.D.
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This lecture on infantile hemangiomas (IH) highlighted important points for management of “little ones with big bumps.” Risk factors for IH include prematurity, female gender, and low birthweight, among others. While the majority of IHs follow a benign course, it is important for dermatologists to identify lesions at higher risk for complications and those that merit further workup. Dr. Friedlander noted that the diagnosis of IH is not always immediately obvious, and the differential diagnosis may include vascular malformations (venous, lymphatic, or mixed), vascular tumors (such as tufted angioma and kaposiform hemangioendothelioma), dysraphism (encephalocele, meningocele), and malignancy (rhabdomyosarcoma, myofibroma). If the diagnosis is in question, she recommends having the patient return in 3-4 weeks to see how the lesion evolves. Complications of IH can include compression of vital structures, bleeding, necrosis, scarring, and disfigurement. Lesions at risk for such complications should be treated. Dr. Friedlander also reviewed PHACE and LUMBAR syndromes, which should be suspected for large and/or segmental IHs located on the face and lumbosacral regions, respectively. Suspicion for any of these entities merits further workup. She also touched on diffuse neonatal hemangiomatosis, which should be suspected for babies with > 5 cutaneous hemangiomas.
Dr. Friedlander reviewed the treatment options and emphasized that one size does not fit all when managing IHs. She recommended reviewing the recent clinical practice guidelines for the management of IH and discussed the utility of the Infantile Hemangioma Referral Score (IHReS), a highly sensitive tool for practitioners deciding when an infant should be referred for management of their IH. |
Jashin Wu, M.D.
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Dr. Wu reviewed that for patients already on systemic immunosuppressive agents but have not tested positive or exhibited signs/symptoms of COVID-19, there is insufficient evidence to stop systemic immunosuppressive agents. If the patient is positive for COVID-19 or exhibits signs/symptoms, one should discontinue or postpone the systemic immunosuppressive agents until the patient recovers from COVID-19. He said one may can re-initiate the systemic immunosuppressive therapy after the patient has completely recovered from COVID-19.
For patients not on systemic immunosuppressive agents but are at high-risk for catching COVID-19, he recommended to consider deferring initiation of immunosuppressive agents. Two recent studies from Canada and Italy do not indicate that systemic therapy for psoriasis increases risk of COVID-19 infection. |