Biosecurity and the ornamental fish trade: A stakeholder perspective in England

The freshwater and marine ornamental fish industry is a primary route of hazard introduction and emergence, including aquatic animal diseases and non-native species. Prevention measures are key to reducing the risk of hazard incursion and establishment, but there is currently little understanding of the biosecurity practices and hazard responses implemented at post-border stages of the ornamental fish supply chain. This study addresses this knowledge gap, using questionnaires to collate information on actual biosecurity behaviours and hazard responses practised by ornamental fish retailers and hobbyist communities in England. Actual behaviours varied considerably within retailers and hobbyists, suggesting that reliance on preventative practices by individuals in the post-border stages of the ornamental fish supply chain is likely to be ineffective in minimizing the risk of hazard incursion and establishment. Resources should be allocated towards improving and enforcing robust pre- and at-border control measures, such as risk-based surveillance of ornamental fish imports at border controls. In addition, these findings should be used to implement targeted awareness-raising campaigns and help create directed training on biosecurity practices for individuals involved in the post-border stages of the ornamental supply chain

Monitoring quality of care in hepatocellular carcinoma: A modified delphi consensus

Although there are several established international guidelines on the management of hepatocellular carcinoma (HCC), there is limited information detailing specific indicators of good quality care. The aim of this study was to develop a core set of quality indicators (QIs) to underpin the management of HCC. We undertook a modified, two-round, Delphi consensus study comprising a working group and experts involved in the management of HCC as well as consumer representatives. QIs were derived from an extensive review of the literature. The role of the participants was to identify the most important and measurable QIs for inclusion in an HCC clinical quality registry. From an initial 94 QIs, 40 were proposed to the participants. Of these, 23 QIs ultimately met the inclusion criteria and were included in the final set. This included (a) nine related to the initial diagnosis and staging, including timing to diagnosis, required baseline clinical and laboratory assessments, prior surveillance for HCC, diagnostic imaging and pathology, tumor staging, and multidisciplinary care; (b) thirteen related to treatment and management, including role of antiviral therapy, timing to treatment, localized ablation and locoregional therapy, surgery, transplantation, systemic therapy, method of response assessment, and supportive care; and (c) one outcome assessment related to surgical mortality. Conclusion: We identified a core set of nationally agreed measurable QIs for the diagnosis, staging, and management of HCC. The adherence to these best practice QIs may lead to system-level improvement in quality of care and, ultimately, improvement in patient outcomes, including survival

Diabetes and hemochromatosis

Hereditary hemochromatosis is due, in most cases, to a common genetic mutation in the HFE gene which leads to the C282Y substitution, which in turn can result in end organ damage from iron overload. The major manifestations in advanced disease are skin pigmentation, diabetes ('bronzed diabetes') and cirrhosis of the liver. When present, these features are associated with a reduced life expectancy and the possibility of hepatocellular carcinoma. It may be considered as an endocrine disorder where, instead of insulin, the peptide hepcidin is deficient, leading to an unregulated increase in iron absorption from the intestine. When present, diabetes is due to a defect in beta cell function resulting from iron deposition in these cells. Increased insulin resistance may also be present in cases of advanced liver disease. Fortunately, patients are now more frequently being diagnosed at an earlier stage and have a good prognosis when appropriate treatment for the iron loading is instituted. In this situation, diabetes is less frequently seen. This review summarizes current knowledge about the pathogenesis of hereditary hemochromatosis, its association with diabetes mellitus and the management of these conditions

Allergy controls the population density of Necator americanus in the small intestine

Background & Aims: Nearly 700 million people remain infected with hookworms. Although allergy is intuitively linked to immunity against helminths, few positive examples have been characterized. Larval migration through the lungs has been considered the likely interface at which hookworm attrition occurs. As part of a study evaluating a potential role for hookworms in the modulation of human autoimmunity, we examined parasite migration and intestinal colonization. Methods: Capsule and conventional endoscopies supplemented the evaluation of healthy volunteers and Crohn’s disease patients recently inoculated with larvae of the human hookworm Necator americanus. Two healthy volunteers with a previously established and stable hookworm infection were inoculated with 50 larvae and had serial capsule endoscopies performed. Results: Eosinophilic enteritis developed in all subjects after the initial inoculation. Newly inoculated larvae in the 2 subjects with an established infection reliably reached the intestine within 4 weeks. Thereafter, the colony diminished to the host’s constitutive status quo because mostly immature worms failed to attach. The intensity of the eosinophilic response correlated negatively with the time available for hookworms to feed and positively with hookworm attrition. Conclusions: Necator larval migration to the intestine is uncontested. We propose that allergic inflammation purposefully degrades the hookworm’s bite, causing premature detachment, restricted feeding, and expulsion. This novel biological dynamic suggests a new paradigm of hookworm resistance

Transforming growth factor-β and toll-like receptor-4 polymorphisms are not associated with fibrosis in haemochromatosis

AIM: To investigate the role of genetic polymorphisms in the progression of hepatic fibrosis in hereditary haemochromatosis

Serum ferritin concentration predicts hepatic fibrosis better than hepatic iron concentration in human HFE-Haemochromatosis

Background & AimsFerritin is purported to have proinflammatory and profibrogenic effects on hepatic stellate cells. Thus, rather than acting as a passive indicator of hepatic iron concentration (HIC) in haemochromatosis, ferritin may directly influence fibrosis. This study evaluated whether serum ferritin is a better predictor of hepatic fibrosis compared to variables previously associated with increased fibrosis risk in haemochromatosis

Restrictive or Liberal Transfusion Strategy in Myocardial Infarction and Anemia

BACKGROUND: A strategy of administering a transfusion only when the hemoglobin level falls below 7 or 8 g per deciliter has been widely adopted. However, patients with acute myocardial infarction may benefit from a higher hemoglobin level. METHODS: In this phase 3, interventional trial, we randomly assigned patients with myocardial infarction and a hemoglobin level of less than 10 g per deciliter to a restrictive transfusion strategy (hemoglobin cutoff for transfusion, 7 or 8 g per deciliter) or a liberal transfusion strategy (hemoglobin cutoff, <10 g per deciliter). The primary outcome was a composite of myocardial infarction or death at 30 days. RESULTS: A total of 3504 patients were included in the primary analysis. The mean (±SD) number of red-cell units that were transfused was 0.7±1.6 in the restrictive-strategy group and 2.5±2.3 in the liberal-strategy group. The mean hemoglobin level was 1.3 to 1.6 g per deciliter lower in the restrictive-strategy group than in the liberal-strategy group on days 1 to 3 after randomization. A primary-outcome event occurred in 295 of 1749 patients (16.9%) in the restrictive-strategy group and in 255 of 1755 patients (14.5%) in the liberal-strategy group (risk ratio modeled with multiple imputation for incomplete follow-up, 1.15; 95% confidence interval [CI], 0.99 to 1.34; P = 0.07). Death occurred in 9.9% of the patients with the restrictive strategy and in 8.3% of the patients with the liberal strategy (risk ratio, 1.19; 95% CI, 0.96 to 1.47); myocardial infarction occurred in 8.5% and 7.2% of the patients, respectively (risk ratio, 1.19; 95% CI, 0.94 to 1.49). CONCLUSIONS: In patients with acute myocardial infarction and anemia, a liberal transfusion strategy did not significantly reduce the risk of recurrent myocardial infarction or death at 30 days. However, potential harms of a restrictive transfusion strategy cannot be excluded. (Funded by the National Heart, Lung, and Blood Institute and others; MINT ClinicalTrials.gov number, NCT02981407.)

Environmental and genetic modifiers of the progression to fibrosis and cirrhosis in hemochromatosis

Hereditary hemochromatosis is a genetic disorder of iron metabolism leading to inappropriate iron absorption and iron loading in various organs especially the liver. Despite the genetic mutation being relatively common in those of Anglo Celtic descent, cirrhosis of the liver occurs in only a small proportion of affected individuals. The risk of hepatic fibrosis and cirrhosis relates to the degree of iron loading with threshold hepatic iron concentrations being identified from population studies. However, other environmental and possibly genetic factors appear to modify this risk. Excess alcohol consumption appears to be one of the most important cofactors with steatosis and coexistent viral infection also implicated. Genetic polymorphisms in genes associated with fibrogenesis, antioxidant activity, and inflammation have been investigated in several different forms of chronic liver disease. The variability in the expression of these genes that predispose patients with hemochromatosis to increased risk of severe liver disease is the subject of ongoing investigations. Clearly the progression of iron loading to cirrhosis marks a crucial stage in the natural history of a patient's disease and therefore therapy and prognosis. This review explores recent developments in knowledge of environmental and genetic modifiers of this process