Search

Taxanes are commonly used anticancer agents with a potential of producing an allergic or hypersensitivity reaction (HSR). We performed a randomized study to evaluate the value of a test dose given prior to the full dose of either paclitaxel or docetaxel.Patients were randomly assigned to either the administration of the full dose or to the prior administration of a 1 mg intravenous test dose of either paclitaxel or docetaxel. The primary endpoints were severity of the HSR and the cost of drug wastage due to a HSR.Two hundred and eighteen patients were randomized from three different treatment sites. The overall incidence of HSR was 6.5% and there was no significant difference in the incidence of HSR in either group. The mean HSR severity grade was 2.8 for patients without a test dose and 2.3 for those receiving a test dose. There was, however, a reduction in the wastage of taxane in the test dose arm. Wastage avoided in the test dose arm was $1573 per patient who had a HSR and $104 per patient treated with a taxane.Although a test dose may not reduce the severity of a HSR with the administration of a taxane, it does reduce the cost associated with drug wastage.

Ozone is a ubiquitous pollutant that can cause acute pulmonary inflammation, cellular injury and may contribute to the development or exacerbation of chronic lung diseases. Despite much research, the effects of ozone on humans and potential cellular mechanisms of injury are still uncertain. However, ozone has been reported to increase the formation of aldehydes that could react with cellular proteins. Therefore, the purpose of these studies was to determine whether 4-hydroxynonenal (HNE), a previously unidentified aldehyde product of ozone exposure, is formed in human subjects exposed to ozone, and whether the response of human alveolar macrophages (AM) following a 1-h exposure to 0.25 ppm ozone with moderate exercise could be mimicked by in vitro incubation of AM with HNE. Western analysis demonstrated increased HNE protein adducts in airway fluid and alveolar macrophages after ozone exposure. AM were examined for endotoxin (lipopolysaccharide [LPS])-stimulated interleukin-1 beta (IL-1 beta) release and expression of heat shock protein 72 (HSP72). Immediately after ozone exposure there was no change in HSP72, but a 5-fold increase occurred 4 h after exposure. By 18 h after exposure, HSP72 levels decreased to below comparable air-exposed levels. Immediately after ozone exposure there was no effect on IL-1 beta release stimulated by LPS. However, IL-1 beta release stimulated by LPS was significantly inhibited 4 h after ozone exposure. By 18 h after ozone exposure, IL-1 beta release stimulated by LPS returned to normal. Incubation of human AM in vitro with HNE induced HSP72 and blocked LPS-stimulated IL-1 beta release possibly by inhibiting interleukin converting enzyme. Consequently, the in vitro results and demonstration of HNE protein adducts following ozone exposure are consistent with HNE being involved in this process in vivo and suggest that the cellular toxic effects of ozone could be a result of thiol reactive aldehydes produced by ozone.

A case of complete urethral duplication in a child is presented. The malformation consisted of a normal urethra and another epispadial dorsal urethra ending at the dome of the bladder. This is a rare variant of this type of malformation. Incontinence was the surgical indication. The classification, embryology, diagnosis, indications for surgery and treatment of this anomaly are presented.