Patient navigation across the cancer care continuum: An overview of systematic reviews and emerging literature

Patient navigation is a strategy for overcoming barriers to reduce disparities and to improve access and outcomes. The aim of this umbrella review was to identify, critically appraise, synthesize, and present the best available evidence to inform policy and planning regarding patient navigation across the cancer continuum. Systematic reviews examining navigation in cancer care were identified in the Cochrane Central Register of Controlled Trials (CENTRAL), PubMed, Embase, Cumulative Index of Nursing and Allied Health (CINAHL), Epistemonikos, and Prospective Register of Systematic Reviews (PROSPERO) databases and in the gray literature from January 1, 2012, to April 19, 2022. Data were screened, extracted, and appraised independently by two authors. The JBI Critical Appraisal Checklist for Systematic Review and Research Syntheses was used for quality appraisal. Emerging literature up to May 25, 2022, was also explored to capture primary research published beyond the coverage of included systematic reviews. Of the 2062 unique records identified, 61 systematic reviews were included. Fifty-four reviews were quantitative or mixed-methods reviews, reporting on the effectiveness of cancer patient navigation, including 12 reviews reporting costs or cost-effectiveness outcomes. Seven qualitative reviews explored navigation needs, barriers, and experiences. In addition, 53 primary studies published since 2021 were included. Patient navigation is effective in improving participation in cancer screening and reducing the time from screening to diagnosis and from diagnosis to treatment initiation. Emerging evidence suggests that patient navigation improves quality of life and patient satisfaction with care in the survivorship phase and reduces hospital readmission in the active treatment and survivorship care phases. Palliative care data were extremely limited. Economic evaluations from the United States suggest the potential cost-effectiveness of navigation in screening programs.     

Neonatal Hemochromatosis, Renal Tubular Dysgenesis, and Hypocalvaria in a Neonate

We report a neonate with neonatal hemochromatosis (NH), renal tubular dysgenesis (RTD), and hypocalvaria. NH is a fatal condition of the newborn, characterized by severe idiopathic liver failure of intrauterine onset and siderosis, intra- and extrahepatic, with sparing of the reticuloendothelial system. RTD is characterized by short, abnormally developed cortical tubules that lack proximal tubule differentiation. Although both NH and RTD have been reported as entities with a genetic component, similar findings can be secondary to in utero insults. Hypocalvaria has been reported in association with fetal hypoxia including that secondary to angiotensin converting enzyme inhibitors. This 38-week-old infant died at 8.5 h. The small nodular liver weighed 44 g. Grossly, the kidneys were normal. Hypocalvaria was present. Microscopically, the hepatic parenchyma was distorted by fibrous tracts, proliferation of bile ducts, and abundant iron deposition in hepatocytes. Extrahepatic siderosis in the pancreas, myocardium, and other organs was consistent with NH. Proximal convoluted tubules were not seen on routine stains and markers for proximal tubules were negative. Previous reports have linked NH with RTD and RTD with hypocalvaria. This infant had all three of these rare conditions, which have been hypothesized or shown to be due to genetic factors, hypoxia, or drugs. The etiology in this case is unknown. Received May 20, 1997; accepted August 15, 1997.     

Organ donor screening using parallel nucleic acid testing allows assessment of transmission risk and assay results in real time

Expansion of the donor pool may lead to utilization of donors with risk factors for viral infections. Donor laboratory screening relies on serological and nucleic acid testing (NAT). The increased sensitivity of NAT in low prevalence populations may result in false‐positive results (FPR) and may cause unnecessary discard of organs.We developed a screening algorithm to deal, in real time, with potential FPR. Three NAT assays: COBAS AmpliScreen assay (CAS), AmpliPrep Total Nucleic Acid Isolation/CAS, and AmpliPrep/TaqMan assays, were validated and used in parallel for prospective screening of increased‐risk donors (IRD), and the probability of FPR was calculated. The lower limit of detection of this algorithm was 9.79, 21.02, and 4.31 IU/mL for human immunodeficiency virus‐1, hepatitis C virus, and hepatitis B virus, respectively, with an average turn‐around‐time of 7.67 h from sample receipt to result reporting. The probability that a donor is potentially infectious with two NAT concordant results was >90%. NAT screening of 35 IRD within 18 months resulted in transplantation of 102 additional organs that without screening would either not be used or used with restrictions in Australia. Using a parallel testing algorithm, real‐time confirmation of seropositive donors allows use of organs from IRD and safer expansion of the donor pool.     

Acute effect of smoking on the functional activity of alpha1-protease inhibitor in bronchoalveolar lavage fluid

To assess the acute effect of smoking on the functional activity of alpha1-protease inhibitor (alpha-Pl) in bronchoalveolar lavage (BAL), we studied 38 smokers (mean age 25 +/- 6.5 yr), who had 2 fiberoptic bronchoscopic lavages in sequence, the first after 8 h of abstinence from smoking, and the second at varying time intervals after smoking. Twenty-two smokers were tested before, and 10 min to 3 h after, smoking 2 medium-tar filter cigarettes; 16 smokers were were tested before, and 2 min to 60 min after, smoking 4 cigarettes. Eight nonsmoking volunteers had 2 BAL performed in sequence as control subjects. Initial BAL from control subjects and from smokers after 8 h of abstinence had similar alpha-Pl activity (mean 0.495 +/- SD 0.017 micrograms of pancreatic elastase/micrograms alpha-Pl, about 90% of the activity of purified alpha-Pl). After smoking, we did not find significant inactivation of alpha-Pl except in the 6 smokers lavaged 1 h after smoking 2 cigarettes, whose alpha-Pl activity decreased slightly to 90.0 +/- SD 10.6% of their initial activity (p less than 0.05). We also obtained BAL from 7 smokers only after smoking, and did not find inactivation of alpha-Pl. We conclude that in young healthy smokers: (1) alpha-Pl in BAL after 8 h of abstinence from smoking is active similar to nonsmoking control subjects, and (2) after smoking 2 to 4 cigarettes, there is no, or very limited, inactivation of alpha-Pl.