Two episodes of life-threatening anaphylaxis in the same patient to a chlorhexidine–sulphadiazine-coated central venous catheter

Abstract

Chlorhexidine allergy has been described in the literature, mainly in Japanese individuals. Most reactions have been limited to the skin, mild in severity and a result of chlorhexidine containing solutions such as 'Savlon' (Novartis Consumer Health, Horesham, UK). We describe what we believe is the first reported case of anaphylaxis in a European patient to a chlorhexidine- sulphadiazine-coated central venous catheter.

Adenoid cystic carcinoma: A review of recent advances, molecular targets, and clinical trials

“…Another finding is that ACC tumors frequently produce high levels of the receptor tyrosine kinase c‐KIT (Figure 2) and variably overexpress other growth factor receptors, including fibroblast growth factor receptor 1 (FGFR1), epidermal growth factor receptor (EGFR), and/or human epidermal receptor‐2 (HER‐2) 2, 21, 22, 23. Although each of these receptors has the potential to generate oncogenic growth factor signals, mutational activation or overexpression because of gene amplification of the cognate genes is rare 24, 25. Thus, autocrine stimulation of these receptors is believed to lead to constitutive signaling.…”

“…ACC tumors exhibit nonrandom gains or losses of specific chromosome regions, including what may be an ACC‐specific deletion of chromosome 1p35–36. Other frequent deletions are located at 6q24, 12q, and 14q 23, 24, 25. However, the most intriguing alteration is a translocation between chromosomes 6q and 9p [(6;9)(q22–23;p23–24)].…”

“…Interestingly, tumor suppressor genes and oncogenes that are frequently mutated in other cancers were uncommon. For example, the p53 tumor suppressor gene was mutated in only 3 of the 84 tumors in the 2 studies, whereas RAS or phosphotidylinositol‐3‐kinase (PI3K) growth factor signaling proteins were mutated in only 7 24, 25. Although a number of mutations were unique or only in a small fraction of the tumors, the altered genes could be grouped together by their potential to disrupt specific cellular functions or biochemical pathways.…”

“…Although a number of mutations were unique or only in a small fraction of the tumors, the altered genes could be grouped together by their potential to disrupt specific cellular functions or biochemical pathways. This included those that interact with the MYB transcription network, but also genes that influence chromatin remodeling, DNA damage/checkpoint responses, signaling pathways regulated by fibroblast growth factor (FGF)‐insulin‐like growth factor‐PI3K, protein kinase A pathway, or Notch 24, 25, 35, 36. Understanding the specific contribution of each mutation to tumorigenesis might lead to novel pathways for targeted therapy.…”

“…These disappointing results suggest that the overexpressed c‐KIT receptors are not actively signaling in ACC cells or are not the major drivers of the malignant phenotype. Additionally, it is now clear from sequencing data that ACC tumors express wild‐type c‐KIT 24, 25, 66, 68, 69…”