Chronic venous insufficiency is a complex disease that can result in severe sequelae including venous ulceration. Though the exact progression from chronic venous insufficiency to venous ulcer remains unclear, the high cost and burden of this disease on patients and society is quite clear. Sustained ambulatory venous pressures or venous hypertension plays an integral role in the development of venous ulceration and involves the failure of the calf muscle pump system. Standard of care involves compression therapy to assist the calf muscle pump. However, several cofactors may contribute to or exacerbate this disease and understanding their impact may provide insight into new treatment modalities. Nerve involvement, which may result in neuropathic pain and muscle dysfunction, alterations in mobility and a decrease in range of motion may lead to gait alterations all affecting calf muscle pump function. In this paper, we analyze these cofactors and discuss possible treatment options to target them. Physicians treating this disease should be aware of the numerous factors involved in its development. Exploring new treatment options may 1 day lessen the burden and suffering caused by venous insufficiency.
Systemic fungal infections pose a significant risk to patients following allogeneic hematopoietic cell transplantation (alloHCT). Voriconazole (Vfend®, Pfizer) is an oral second-generation triazole antifungal agent that offers broad spectrum of coverage against fungal species and is frequently utilized in the post-HCT setting. Herein, we describe five patients who were initially believed to be experiencing a flare of cutaneous chronic graft-versus-host disease (cGvHD), but who were actually exhibiting phototoxicity caused by voriconazole. A high index of suspicion for this adverse reaction in the post-alloHCT setting will prevent misdiagnosis and avoid inappropriate therapy for cGvHD.
Orofacial herpes is a widespread benign malady that is also commonly known as herpes labialis or cold sores. Herpes of this type is generally caused by herpes simplex virus type 1 (HSV-1) and, to a lesser degree, herpes simplex virus type 2 (HSV-2), both of which are DNA viruses. The clinical presentation of herpetic lesions is normally located on mucocutaneous areas of the face and may eventually erode and ulcerate, leaving wounds that are known to be difficult to successfully treat. Focus of treatment has been related to treatment of the viral infection, and limited attention has focused on the resultant wounds. Clinical observation and recent histologic evaluation has demonstrated these wounds to extend through a disrupted cutaneous basement membrane into the dermis, suggesting that HSV is capable of causing partial-thickness wounds. This observation suggests a role for occlusion in the treatment of herpetic-induced partial-thickness wounds because occlusion is well recognized as the treatment of choice for other types of partial-thickness wounds.
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