Increased Incidence of Giant Cell Arteritis After Introduction of a Live Varicella Zoster Virus Vaccine.

BACKGROUND: Varicella zoster virus (VZV) has been associated with giant cell arteritis (GCA). The introduction of a live attenuated vaccine against this virus (ZVL) might have changed the incidence of GCA. METHODS: The incidence of GCA was retrospectively measured using 2 matched cohorts seen in a regional health system located in the Midwestern United States: ZVL recipients from the years 2007 through 2015 following the introduction of the vaccine and nonrecipients from the years 2000 through 2015. RESULTS: In the ZVL cohort, a significant increase of GCA was associated with clinical criteria alone for the diagnosis of GCA (hazard ratio [HR], 2.70; 95% CI, 1.48-4.45; P = .004). In addition, using only pathologically confirmed GCA, the same matched cohort comparison analysis also found that ZVL recipients were at significantly higher risk than those who did not receive ZVL (HR, 2.70; 95% CI, 1.48-4.95; P = .001). CONCLUSION: Using a matched cohort, retrospective comparison, ZVL was associated with an increased incidence of GCA.

Sequential treatment failures in response to BRAF/MEK and immune checkpoint inhibitors mediated by MAP2K2 and B2M mutations in melanoma.

Although the treatment of metastatic melanoma has been significantly improved by both anti-BRAF/MEK and checkpoint immunotherapies, resistance to these treatment modalities remains a substantial clinical problem. Multiple clinical studies are addressing the optimal sequencing of these agents in larger patient cohorts, but successful long-term individualized treatment will likely require the elucidation of resistance mechanisms from post-progression samples. Here, we describe a patient with BRAF-V600E-positive metastatic melanoma who was sequentially treated with BRAF/MEK inhibitors (dabrafenib/trametinib) and checkpoint inhibitor immunotherapy (nivolumab, followed by pembrolizumab). After the emergence of resistance, whole exome sequencing was performed, implicating MAP2K2 and B2M mutations in loss of response to anti-BRAF/MEK and anti-PD1 therapies, respectively.

Recurrent strokes, central nervous system vasculitis, and acquired protein S deficiency secondary to varicella zoster in a child with AIDS.

A child with vertical transmission of human immunodeficiency virus refractory to therapy developed zoster-induced protein S deficiency and recurrent strokes. Extensive carotid arteritis was found postmortem. The carotid tissue was positive for herpes varicella zoster by polymerase chain reaction, as were immunofixation stains of the arterial wall.