RESUMO
Lipedematous scalp (LS) and lipedematous alopecia (LA) are uncommon dermatological conditions characterized by lipid accumulation within scalp tissue, leading to a thickened and boggy scalp. While the exact cause remains elusive, these conditions are believed to be on a spectrum of the same underlying disease process. LS/LA patients can experience dysesthesia of the scalp, but LA is associated with additional hair growth abnormalities. The pathogenesis remains poorly understood, with some cases suggesting a link to hormone leptin dysregulation and/or hyperlipidemia. We present a 73-year-old African American female with a medical history of hypertension, hyperlipidemia, and partial thyroidectomy who presented to the clinic with a two-week history of an itchy, burning 'rash' on the scalp. Physical examination showed normal hair density, but palpation revealed scalp edema and diffuse bogginess. While blood tests were mostly normal, she had an elevated antinuclear antibodies (ANA) titer (1:160). A punch biopsy revealed lichenification, but subsequent non-contrast magnetic resonance angiography (MRA) showed increased scalp fat tissue measuring up to 11 mm, confirming the diagnosis of LS. The patient was reassured that this finding was benign; however, she continued to experience dysesthesia. Our patient experienced minimal relief with topical steroids, leading to the consideration of intralesional steroid injections. The case highlights the importance of recognizing and managing LS as a distinct dermatological entity that requires further research to elucidate underlying mechanisms and establish standardized treatment protocols for this condition.
RESUMO
Dynamin-1 (DNM1) consolidates memory through synaptic transmission and modulation and has been explored as a therapeutic target in Alzheimer's disease. Through a two-prong approach, this study examined its role in cancer-related cognitive impairment (CRCI) pathogenesis using human and animal models. The human study recruited newly diagnosed, chemotherapy-naïve adolescent and young adult cancer and non-cancer controls to complete a cognitive instrument (FACT-Cog) and blood draws for up to three time points. Concurrently, a syngeneic young-adult WT (C57BL/6 female) mouse model of breast cancer was developed to study DNM1 expression in the brain. Samples from eighty-six participants with 30 adolescent and young adult (AYA) cancer and 56 non-cancer participants were analyzed. DNM1 levels were significantly lower among cancer participants compared to non-cancer prior to treatment. While receiving cancer treatment, cognitively impaired patients were found with a significant downregulation of DNM1, but not among those without impairment. In murine breast cancer-bearing mice receiving chemotherapy, we consistently found a significant decline in DNM1 immunoreactivity in the hippocampal CA1 and CA3 subregions. Observed in both human and animal studies, the downregulation of DNM1 is linked with the onset of CRCI. Future research should explore the potential of DNM1 in CRCI pathogenesis and therapeutics development.