Search

BACKGROUND: Venous thromboembolism (VTE) is the second leading cause of death in patients with cancer. Patient characteristics, cancer type, treatments, and biomarkers can help to predict those at high risk for VTE. Several oncology guidelines recommend against routine thromboprophylaxis in ambulatory patients with cancer but recommend its consideration in those at high risk. Newer data suggest that direct oral anticoagulants (DOACs) may be safe and effective options to reduce the incidence of VTE in patients with cancer. OBJECTIVE: To review the management of VTE in patients with cancer, including prophylaxis and treatment, based on recently published randomized clinical trials, with a focus on DOACs. DISCUSSION: The PROTECHT and SAVE-ONCO clinical trials demonstrated statistically significant reductions in the incidence of VTE with low-molecular-weight heparin (LMWH) as primary prevention in ambulatory patients with cancer; however, the magnitude of VTE reduction did not prompt a change in clinical practice guidelines. The AVERT and CASSINI clinical trials enrolled patients with a Khorana risk score =2 and demonstrated that DOACs are safe and effective options to reduce VTE risk. The SELECT-D, Hokusai VTE Cancer, and ADAM VTE clinical trials compared the use of DOACs and LMWH in the prevention of VTE recurrence in patients with cancer. The results demonstrated that DOACs were more effective than LMWH but with an increased risk for bleeding in some patients. CONCLUSION: A concerted effort should be made by all healthcare professionals caring for ambulatory patients with cancer to screen patients for VTE risk factors and to consider interventions if clinically appropriate. [ABSTRACT FROM AUTHOR]

Several reviews are presented for national parks in the U.S. including the Devil's Den State Park, the Hot Springs National Park and the Crowley's Ridge State Park.

Sunset Crater volcano, located ~25 km northeast of downtown Flagstaff (Arizona, USA) in the San Francisco volcanic field, represents an interesting case of highly explosive monogenetic volcanism. Sunset Crater is a young (ca. 1085 CE) scoria cone, ~290 m high, that produced 0.52 km³ dense rock equivalent (DRE) of basaltic magma (0.16, 0.12, and 0.24 km³ DRE for the scoria cone, lava flows, and tephra deposit, respectively). The activity developed in three distinct phases: an initial fissure phase, followed by a highly explosive phase, and a final low-explosivity waning phase. The first phase was characterized by the opening of a 10-kmlong fissure, which produced the Gyp Crater spatter mounds and the Vent 512 lava flow ~10 km SE of the main scoria cone, followed by lava fountaining activity that produced the first tephra layer (unit 1, 0.01 km³ DRE). During the second highly explosive phase, the activity migrated to the northwest to evolve into a single-vent eruption, which formed the main scoria cone. The central vent activity was initially characterized by variable eruptive styles, which started the process of cone building, including deposition of a second tephra layer (unit 2, 0.01 km³ DRE), and the effusion of the two main lava flows (Bonito and Kana'a). Following the initiation of effusive activity, the eruption increased in explosivity to produce three subplinian tephra layers from the central vent (units 3, 4, and 5), which emitted more than 0.22 km³ DRE of basalt, with associated eruption columns >20 km high. By the end of this phase, the Kana'a lava flow was almost completely emplaced, but the Bonito flow continued to grow, forming a 3-km-diameter flow field. A final waning phase produced several tephra units, commonly discontinuous and reworked, with <0.01 km3 DRE cumulative volume. The comparatively large volume of tephra, the high eruptive columns, and high mass eruption rates make Sunset Crater the most explosive monogenetic eruption studied to date (volcano explosivity index [VEI] 3-4). Sunset Crater volcano represents an interesting case of monogenetic volcanism in that its activity was characterized by highly explosive eruptive phases up to subplinian in scale and intermittent episodes of lava effusion that heavily affected prehistoric communities in the area. Explosive basaltic volcanism should be considered when assessing volcanic hazards in continental settings, such as in the western United States. [ABSTRACT FROM AUTHOR]

Fluoropyrimidine chemotherapy is a primary component of many solid tumor treatment regimens, particularly those for gastrointestinal malignancies. Approximately one-third of patients receiving fluoropyrimidine-based chemotherapies experience serious adverse effects. This risk is substantially higher in patients carrying DPYD genetic variants, which cause reduced fluoropyrimidine metabolism and inactivation (ie, dihydropyridine dehydrogenase [DPD] deficiency). Despite the known relationship between DPD deficiency and severe toxicity risk, including drug-related fatalities, pretreatment DPYD testing is not standard of care in the United States. We developed an in-house DPYD genotyping test that detects 5 clinically actionable variants associated with DPD deficiency, and genotyped 827 patients receiving fluoropyrimidines, of which 49 (6%) were identified as heterozygous carriers. We highlight 3 unique cases: (1) a patient with a false-negative result from a commercial laboratory that only tested for the c.1905 + 1G>A (*2A) variant, (2) a White patient in whom the c.557A>G variant (typically observed in people of African ancestry) was detected, and (3) a patient with the rare c.1679T>G (*13) variant. Lastly, we evaluated which DPYD variants are detected by commercial laboratories offering DPYD genotyping in the United States and found 6 of 13 (46%) did not test for all 5 variants included on our panel. We estimated that 20.4% to 81.6% of DPYD heterozygous carriers identified on our panel would have had a false-negative result if tested by 1 of these 6 laboratories. The sensitivity and negative predictive value of the diagnostic tests from these laboratories ranged from 18.4% to 79.6% and 95.1% to 98.7%, respectively. These cases underscore the importance of comprehensive DPYD genotyping to accurately identify patients with DPD deficiency who may require lower fluoropyrimidine doses to mitigate severe toxicities and hospitalizations. Clinicians should be aware of test limitations and variability in variant detection by commercial laboratories, and seek assistance by pharmacogenetic experts or available resources for test selection and result interpretation.