A Retrospective Study Analyzing the Appropriateness of Initial Treatment of Clostridium difficile in Patients with Active Malignancy.

BACKGROUND: Clostridium difficile infection (CDI) is the leading cause of hospital-associated gastrointestinal illness. Previous studies reported that patients with active malignancy are at high risk for CDIs, and yet they are still classified as nonsevere CDI and initially treated with metronidazole. Our aim is to investigate the need for the escalation of antibiotic therapy in patients with CDI and active cancer treated with oral metronidazole versus oral vancomycin. METHODS: This is a retrospective study of adult patients admitted with CDI and any underlying active malignancy at Beaumont Hospital, Royal Oak, Michigan, from January 2008 to December 2014. Inclusion criteria included age > 18 years old, polymerase chain reaction- (PCR-) proven CDI, and active malignancy. RESULTS: 197 patients were included in the final analysis. 44.8% of the metronidazole group required escalation of therapy compared to 15.2% in the vancomycin group (p value = 0.001). 29.8% of the combination group (metronidazole and vancomycin) underwent deescalation of antibiotics, which was significantly higher compared to 2.2% of patients in the vancomycin group (p value < 0.001). DISCUSSION: Our results support the initial use of vancomycin or a combination (metronidazole and vancomycin) versus metronidazole in patients with CDI and active malignancy.

Drug-induced pulmonary arterial hypertension: a review.

Pulmonary arterial hypertension (PAH) is a subgroup of PH patients characterized hemodynamically by the presence of pre-capillary PH, defined by a pulmonary artery wedge pressure (PAWP) ≤15 mmHg and a PVR >3 Wood units (WU) in the absence of other causes of pre-capillary PH. According to the current classification, PAH can be associated with exposure to certain drugs or toxins such as anorectic agents, amphetamines, or selective serotonin reuptake inhibitors. With the improvement in awareness and recognition of the drug-induced PAH, it allowed the identification of additional drugs associated with an increased risk for the development of PAH. The supposed mechanism is an increase in the serotonin levels or activation of serotonin receptors that has been demonstrated to act as a growth factor for the pulmonary artery smooth muscle cells and cause progressive obliteration of the pulmonary vasculature. PAH remains a rare complication of several drugs, suggesting possible individual susceptibility, and further studies are needed to identify patients at risk of drug-induced PAH.