Bevacizumab, a humanized monoclonal antibody against vascular endothelial growth factor (VEGF), is an angiogenesis inhibitor used to treat a variety of cancers, including lung, colon, cervical, ovarian, and renal cancers as well as glioblastoma.  A significant adverse effect associated with its use is one of thromboembolic events. We report a case of a 74-year-old male with diagnosis of glioblastoma multiforme treated with partial resection, radiation, temozolomide, and bevacizumab. He presented to a plastic surgeon with a several week history of asymptomatic crusted hemorrhagic ulcers and purpuric patches on the lower legs shortly following the initiation of bevacizumab. A biopsy showed an occlusive pauci-inflammatory thrombogenic vasculopathy associated with ischemic epidermal and dermal changes and accompanied by extensive vascular C5b-9 (complement C5b-9 membrane attack complex) deposition. Bevacizumab has been associated with thrombotic complications including atypical hemolytic uremic syndrome and arterial and venous thrombosis. C5b-9 may be the factor most important in the mechanism of vascular thrombosis given the extent of deposition in our index case. Thrombotic events in the skin associated with bevacizumab therapy are without precedent and dermatologists should be aware of this potential complication.

• Epidermal nevi (EN) are benign congenital skin lesions derived from a postzygotic mutation in a subset of pluripotential embryonic cells (mosaicism).

• The lesions tend to arrange in a whirlwind pattern representing the migration of the pluripotent cells, known as lines of Blaschko.

• The distribution and extent of EN varies greatly ranging from a single linear lesion to systemic involvement.

• More extensive lesions are highly associated with musculoskeletal and nervous system abnormalities, making up what is known as Epidermal Nevus Syndrome.

• Not only do the extent of the lesions vary greatly, but so do the underlying genetic mutations demonstrating the difficulties in defining a clear phenotype-genotype model.

• These mutations include FGFR3, PIK3CA, and HRAS

Acquired zinc deficiency can develop as a consequence of poor nutritional intake or from dependence on total parenteral nutrition. Acquired zinc deficiency dermatitis classically manifests with erosions and scaly plaques in a periorificial and acral distribution. We present a case of a woman on parenteral nutrition who presented with bullous acrodermatitis mimicking pemphigus foliaceus histopathologically. This case highlights clinical and histopathologic variants of zinc deficiency that may lead to a delay in diagnosis.