Clinical presentation of verruca vulgaris in HIV.

BACKGROUND: Immunocompromised patients, including those with human immunodeficiency virus (HIV), have been observed to have verrucae that are more extensive and treatment-resistant compared to those in immunocompetent patients. However, there is a critical lack of data in the current literature on the characteristics of verruca vulgaris in individuals with HIV. METHODS: This retrospective chart review included a cohort of HIV-positive individuals and a control group of immunocompetent individuals presenting to an outpatient, county hospital-based dermatology clinic for evaluation of verruca vulgaris between the years of 2016 and 2018. Clinical characteristics, including gender, age, last CD4 count, viral load, antiretroviral therapy adherence, and total number and location of lesions were recorded. RESULTS: A total of 66 patients (33 HIV-positive, 33 immunocompetent) were included in the study. HIV-positive status was significantly associated with a higher total number of lesions (42% of immunocompromised patients versus 21% of immunocompetent patients presented with four or more lesions, P=0.04) as well as location of lesions on the face, scalp, and neck (51.5% versus 9.1%, P<0.001). CONCLUSIONS: HIV-positive status may be associated not only with a higher burden of verruca vulgaris lesions but also a higher number of lesions in locations at or above the neck.

Ischemic but not pharmacological preconditioning requires protein synthesis.

BACKGROUND: Ischemic preconditioning (IPC) and pharmacological preconditioning (PPC) have both been shown to confer cardioprotective effects. However, the role of protein synthesis in preconditioning is unclear. METHODS AND RESULTS: Isolated rabbit hearts were treated with cycloheximide (CHx, 10 micromol/L), a protein synthesis inhibitor at the translational level, before 2 cycles of IPC (5 minutes of global ischemia/5 minutes of reperfusion, n=6) or PPC by pinacidil (PIN, 10 micromol/L; n=6), an ATP-sensitive potassium channel opener. Six rabbit hearts received actinomycin D (Act D, 20 micromol/L; n=6), a protein synthesis inhibitor at the transcriptional level, before IPC. The left anterior descending coronary artery was then occluded for 60 minutes and reperfused for 120 minutes. Control hearts received no treatment before prolonged ischemia (n=6). Left ventricular pressure, action potential duration, and coronary flow were measured. Infarct size is expressed as a percentage of the area at risk. IPC (n=6) and PIN (n=8) hearts experienced reduced infarct size compared with control hearts (22+/-3% and 27+/-2% versus 46+/-3%, IPC and PIN versus control; P:<0.01). Translational blockade (CHx) reversed the IPC infarct size reduction effect (22+/-3% versus 48+/-4%, IPC versus CHx+IPC; P:<0.01) but not the effects of pinacidil (27+/-2% versus 29+/-3%, PIN versus CHx+PIN; P:=NS). Transcriptional blockade (Act D) did not abolish the IPC effect (23+/-5% versus 22+/-3%, Act D+IPC versus IPC; P:=NS). There were no significant differences in electromechanical function consequent to CHx and Act D treatment. CONCLUSIONS: These findings suggest an important role for protein synthesis in the mechanism for IPC-mediated protection at the translational level, which may be different from PPC.