ABSTRACT
Objective: The use of Botulinum toxin type A (Botox) for cosmetic procedures has become so prevalent that many patients do not always consider it to be a past surgical procedure, and it goes excluded from the medical record. Without the knowledge of prior Botox use, interpretation of facial nerve train-of-four testing may be inaccurate. Methods: We describe a 61-year-old woman with a history of multiple cosmetic procedures whose postoperative course was complicated by multiorgan system failure, requiring neuromuscular blockade while on mechanical ventilatory support. Results: Gauged by facial nerve stimulation, adequate neuromuscular blockade was assumed. However, patient-ventilator dyssynchrony motivated the decision to move the peripheral nerve stimulator to the ulnar nerve, where muscle twitches were observed. This indicated inadequate paralysis. Conclusions: This case report highlights the importance of monitoring neuromuscular function with ulnar nerve testing in patients with a history of cosmetic Botox procedures.
ABSTRACT
The epidermis increases pigmentation and epidermal thickness in response to ultraviolet exposure to protect against UV-associated carcinogenesis; however, the contribution of epidermal thickness has been debated. In a humanized skin mouse model that maintains interfollicular epidermal melanocytes, we found that forskolin, a small molecule that directly activates adenylyl cyclase and promotes cAMP generation, up-regulated epidermal eumelanin accumulation in fair-skinned melanocortin-1-receptor (Mc1r)-defective animals. Forskolin-induced pigmentation was associated with a reproducible expansion of epidermal thickness irrespective of melanization or the presence of epidermal melanocytes. Rather, forskolin-enhanced epidermal thickening was mediated through increased keratinocyte proliferation, indirectly through secreted factor(s) from cutaneous fibroblasts. We identified keratinocyte growth factor (Kgf) as a forskolin-induced fibroblast-derived cytokine that promoted keratinocyte proliferation, as forskolin induced Kgf expression both in the skin and in primary fibroblasts. Lastly, we found that even in the absence of pigmentation, forskolin-induced epidermal thickening significantly diminished the amount of UV-A and UV-B that passed through whole skin and reduced the amount of UV-B-associated epidermal sunburn cells. These findings suggest the possibility of pharmacologic-induced epidermal thickening as a novel UV-protective therapeutic intervention, particularly for individuals with defects in pigmentation and adaptive melanization.
