Pathologic Upstaging of Cutaneous Melanoma After Mohs Micrographic Surgery.

BACKGROUND: Mohs micrographic surgery (MMS) is used for melanoma in situ (MIS) and thin invasive melanomas, particularly on the head and neck, during which a debulk section is typically prepared. Tumor upstaging occurs if the debulking specimen meets criteria for an increased tumor (T) stage per the American Joint Committee on Cancer 8th edition compared with the initial biopsy. Upstaging can alter survival and recurrence outcomes, resulting in increased patient morbidity and mortality. OBJECTIVE: To determine the rate of cutaneous melanoma upstaging during MMS. MATERIALS AND METHODS: A multicenter study was performed. Information from electronic medical records from 3 dermatologic surgeons performing MMS for cutaneous melanoma were logged from January 1, 2017 to December 31, 2021. Deidentified information regarding patient demographics and tumor characteristics was recorded. RESULTS: Three-hundred and ten cases of cutaneous melanoma treated with MMS were identified. 2.3% of cases were upstaged, ranging from T1a to T3a. No significant risk factors for upstaging were identified. CONCLUSION: Our data demonstrate a lower rate of cutaneous melanoma upstaging during MMS than the current literature. Differences may be accounted for because of differing patient populations, cutaneous melanoma detection at an earlier clinical stage, and evolving melanoma histologic criteria.

Earlobe Rejuvenation: A Review of Current Treatment Modalities.

BACKGROUND: As one of the defining features of the face, the ear influences perceptions of beauty. Despite its significance, comparatively little is known about rejuvenation options for the ear. OBJECTIVE: To provide a comprehensive review of minimally invasive options for earlobe rejuvenation. METHODS: & Materials: Cochrane, Embase, and PubMed were used to identify articles exploring minimally invasive treatments for ear rejuvenation. RESULTS: Topical medications, peels, fillers, lasers, photodynamic therapy, and dermabrasion are safe and efficacious for managing a variety of concerns related to earlobe aesthetics. CONCLUSION: Numerous minimally invasive treatment modalities are available for earlobe rejuvenation; further investigation is needed to design a grading system and treatment algorithm.

Empowering Residents to Address Socioeconomic Disparities in Dermatology.

Vulnerable communities are in tremendous need of specialized dermatologic care. Through exposure to unique patient populations during medical school curricula and residency training, creation of partnerships with existing advocacy networks, and technological innovation, dermatology residents can harness their skill set to aid marginalized communities.

Navigating the Evolving Landscape of the Dermatologic Workforce.

As dermatologists endeavor to meet growing patient demand, novel care models are transforming how the field is practiced. Physician extenders-which include physicians not board certified in dermatology, physician assistants, and nurse practitioners-can play a pivotal role in bridging health care disparities and reducing health care expenditures. Nevertheless, while the dermatologic workforce is adapting to evolving public needs, patient safety must remain the key priority when negotiating changes in scope of practice. Given that the current literature highlights concerning differences in diagnostic accuracy and procedural safety between different providers, further evidence is needed to help guide health care policies and care models.

Prognostic implications of normal or minimal urinary findings on long-term renal impairment in adults with Henoch-Schönlein purpura.

BACKGROUND: Renal involvement in adult Henoch-Schönlein purpura is a major cause of morbidity and can lead to significant long-term renal impairment. The prognostic significance of normal or minimal urinary abnormalities at diagnosis is unknown. OBJECTIVE: To assess the risk of long-term renal impairment in patients with Henoch-Schönlein purpura who present with normal or minimal urinary abnormalities. METHODS: Retrospective cohort study of adult Henoch-Schönlein purpura patients presenting with normal urinalysis results, microscopic hematuria, or low-grade proteinuria. Patients were followed for development of long-term renal impairment, with adjusting for comorbidities. RESULTS: Forty-seven patients were included, with median follow-up 73.9 months (interquartile range 35 to 98 months). Thirty-nine patients (83.0%) had abnormal urinalysis results, of whom 15 (38.5%) progressed to long-term renal impairment. In contrast, 8 patients (17%) had normal urinalysis results, of whom only 1 (12.5%) developed long-term renal impairment (adjusted hazard ratio 10.58; 95% confidence interval 1.18-94.73). Renal events occurred at a median 36.1 months (interquartile range 17.1 to 61 months) from diagnosis, earlier in patients with comorbidities compared with those with none, and in a constant event rate over time. LIMITATIONS: Small sample size. CONCLUSIONS: Microscopic hematuria and low-grade proteinuria at Henoch-Schönlein purpura diagnosis is a poor prognostic sign for the development of long-term renal impairment. This population should be targeted for prolonged surveillance.

Immune Privilege Collapse and Alopecia Development: Is Stress a Factor.

Hair is a defining mammalian feature that serves as a hallmark of human communication. Given the critical significance of hair in social, religious, and political contexts, it is important to understand factors that play a role in hair loss disorders. The hair follicle is an immune privileged site, and mounting evidence suggests that the collapse of immune privilege contributes to the pathogenesis of autoimmune hair loss disorders, including alopecia areata and lichen planopilaris. This review comprehensively appraises the current literature to shed light on mechanisms for immune privilege collapse, and examines the role of neurogenic stress in triggering this process.

New onset erythematous nodules in an elderly woman.

An 86-year- old woman with a history of recurrent bronchitis and giant cell arteritis presented for new onset, cyclic and migratory erythematous nodules associated with fatigue and weight loss. Although a systemic vasculitis was initially suspected, elevated inflammatory markers and symptoms persisted despite aggressive corticosteroid therapy. Excisional biopsy of one nodule showed dense suppurative and granulomatous inflammation that was rife with acid-fast bacilli. The patient was urgently admitted for empiric treatment of disseminated mycobacterial infection. Although T-SPOT Tuberculosis testing and direct mycobacterial PCR were negative, mass spectrometry demonstrated Mycobacterium chelonae. The patient was treated with a macrolide and quinolone combination regimen and then discharged to a rehabilitation facility.

Smear Campaign: Misattribution of Pancytopenia to a Tick-Borne Illness.

We report the case of a 51-year-old woman presenting with a targetoid rash and pancytopenia after a tick bite. Initial evaluation was notable for severe neutropenia on the complete blood cell count differential, a positive Lyme IgM antibody, and a peripheral blood smear demonstrating atypical lymphocytes. While her pancytopenia was initially attributed to tick-borne illness, peripheral flow cytometry showed 7% myeloblasts, and a bone marrow biopsy confirmed 60% blasts. The patient was ultimately diagnosed with acute myelogenous leukemia, in addition to early, localized Lyme disease. This case highlights the differential diagnosis for pancytopenia, cytopenia patterns for different tick-borne illnesses, the risk of premature closure in internal medicine, and management of Lyme disease in hosts with altered immunity.

Mutation of neuron-specific chromatin remodeling subunit BAF53b: rescue of plasticity and memory by manipulating actin remodeling.

Recent human exome-sequencing studies have implicated polymorphic Brg1-associated factor (BAF) complexes (mammalian SWI/SNF chromatin remodeling complexes) in several intellectual disabilities and cognitive disorders, including autism. However, it remains unclear how mutations in BAF complexes result in impaired cognitive function. Post-mitotic neurons express a neuron-specific assembly, nBAF, characterized by the neuron-specific subunit BAF53b. Subdomain 2 of BAF53b is essential for the differentiation of neuronal precursor cells into neurons. We generated transgenic mice lacking subdomain 2 of Baf53b (BAF53bΔSB2). Long-term synaptic potentiation (LTP) and long-term memory, both of which are associated with phosphorylation of the actin severing protein cofilin, were assessed in these animals. A phosphorylation mimic of cofilin was stereotaxically delivered into the hippocampus of BAF53bΔSB2 mice in an effort to rescue LTP and memory. BAF53bΔSB2 mutant mice show impairments in phosphorylation of synaptic cofilin, LTP, and memory. Both the synaptic plasticity and memory deficits are rescued by overexpression of a phosphorylation mimetic of cofilin. Baseline physiology and behavior were not affected by the mutation or the experimental treatment. This study suggests a potential link between nBAF function, actin cytoskeletal remodeling at the dendritic spine, and memory formation. This work shows that a targeted manipulation of synaptic function can rescue adult plasticity and memory deficits caused by manipulations of nBAF, and thereby provides potential novel avenues for therapeutic development for multiple intellectual disability disorders.

The neuron-specific chromatin regulatory subunit BAF53b is necessary for synaptic plasticity and memory.

Recent exome sequencing studies have implicated polymorphic Brg1-associated factor (BAF) complexes (mammalian SWI/SNF chromatin remodeling complexes) in several human intellectual disabilities and cognitive disorders. However, it is currently unknown how mutations in BAF complexes result in impaired cognitive function. Postmitotic neurons express a neuron-specific assembly, nBAF, characterized by the neuron-specific subunit BAF53b. Mice harboring selective genetic manipulations of BAF53b have severe defects in long-term memory and long-lasting forms of hippocampal synaptic plasticity. We rescued memory impairments in BAF53b mutant mice by reintroducing BAF53b in the adult hippocampus, which suggests a role for BAF53b beyond neuronal development. The defects in BAF53b mutant mice appeared to derive from alterations in gene expression that produce abnormal postsynaptic components, such as spine structure and function, and ultimately lead to deficits in synaptic plasticity. Our results provide new insight into the role of dominant mutations in subunits of BAF complexes in human intellectual and cognitive disorders.