Economic progress as cancer risk factor. II: Why is overall cancer risk higher in more developed countries?

Analysis of data on cancer incidence rates in different countries at different time periods revealed positive association between overall cancer risk and economic progress. Typical explanations of this phenomenon involve improved cancer diagnostics and elevated exposure to carcinogens in industrial countries. Here we provide evidence from human and experimental animal studies suggesting that some other factors associated with high economic development and Western life style may primarily increase the proportion of susceptible to cancer individuals in a population and thus contribute to elevated cancer risks in industrial countries. These factors include (but not limited to): (i) better medical and living conditions that “relax” environmental selection and increase share of individuals prone to chronic inflammation; (ii) several medicines and foods that are not carcinogenic themselves but affect the metabolism of established carcinogens; (iii) nutrition enriched with growth factors; (iv) delayed childbirth. The latter two factors may favor an increase in both cancer incidence rate and longevity in a population. This implies the presence of a trade-off between cancer and aging: factors that postpone aging may simultaneously enhance organism’s susceptibility to several cancers. Key words: cancer risk, individual susceptibility, economic progress, aging

Serum N-Terminal Type III Procollagen Propeptide: An Indicator of Growth Hormone Excess and Response to Treatment in Feline Hypersomatotropism

BACKGROUND: N‐terminal type III procollagen propeptide (PIIINP) is a biomarker of soft tissue proliferation. Hypersomatotropism (HS) is associated with soft tissue proliferation. HYPOTHESIS: Serum PIIINP is increased in cats with HS and decreases with effective treatment, and may be an additional tool in the diagnosis and treatment of feline HS. ANIMALS: Cats with uncomplicated diabetes mellitus (DM; n = 30) and with HS‐induced DM (HSDM; n = 30). Pre‐ and posttreatment samples were available from 5 cats undergoing radiotherapy (RT) and 16 cats undergoing hypophysectomy (HPX). METHODS: Retrospective and prospective cross‐sectional study. Analytical performance of a serum PIIINP ELISA was assessed and validated for use in cats. PIIINP and insulin‐like growth factor 1 (IGF‐1) radioimmunoassays (RIA) were performed pre‐ and post‐treatment in cats with DM and HSDM. PIIINP and IGF‐1 were compared between cats treated by RT and HPX. RESULTS: Serum PIIINP concentrations were significantly higher (P < .001) in HSDM cats (median, 19.6 ng/mL; range, 1.7–27.9) compared to DM cats (median, 5.0 ng/mL; range, 2.1–10.4). A cut‐off of 10.5 ng/mL allowed differentiation between DM and HSDM cats with 87% sensitivity and 100% specificity (area under the curve [AUC], 0.91; 95% confidence interval [CI], 0.82‐1). After RT, PIIINP increased significantly (P = .043) with no significant change in IGF‐1 concentrations. After HPX, serum PIIINP (P = .034) and IGF‐1 concentrations (P < .001) decreased significantly. CONCLUSION AND CLINICAL IMPORTANCE: PIIINP concentrations are increased in cats with untreated HSDM compared to those with DM, demonstrating the effect of excess GH on soft tissue. PIIINP concentrations decreased after HPX in most HSDM cats

Economic evaluation of a clinical protocol for diagnosing emergency patients with suspected pulmonary embolism

BACKGROUND: The objective of this paper is to estimate the amount of cost-savings to the Australian health care system from implementing an evidence-based clinical protocol for diagnosing emergency patients with suspected pulmonary embolism (PE) at the Emergency department of a Victorian public hospital with 50,000 presentations in 2001–2002. METHODS: A cost-minimisation study used the data collected in a controlled clinical trial of a clinical protocol for diagnosing patients with suspected PE. Thenumber and type of diagnostic tests in a historic cohort of 185 randomly selected patients, who presented to the emergency department with suspectedPE during an eight month period prior to the clinical trial (January 2002 -August 2002) were compared with the number and type of diagnostic tests in745 patients, who presented to the emergency department with suspected PE from November 2002 to August 2003. Current Medicare fees per test were usedas unit costs to calculate the mean aggregated cost of diagnostic investigation per patient in both study groups. A t-test was used to estimate the statistical significance of the difference in the cost of resources used for diagnosing PE in the control and in the intervention group. RESULTS: The trial demonstrated that diagnosing PE using an evidence-based clinical protocol was as effective as the existing clinical practice. The clinical protocol offers the advantage of reducing the use of diagnostic imaging, resulting in an average cost savings of at least $59.30 per patient. CONCLUSION: Extrapolating the observed cost-savings of$59.30 per patient to the wholeof Australia could potentially result in annual savings between $3.1 million to$3.7 million

Management of hyperkalemia in the acutely ill patient.

PURPOSE:To review the mechanisms of action, expected efficacy and side effects of strategies to control hyperkalemia in acutely ill patients. METHODS:We searched MEDLINE and EMBASE for relevant papers published in English between Jan 1, 1938, and July 1, 2018, in accordance with the PRISMA Statement using the following terms: "hyperkalemia," "intensive care," "acute kidney injury," "acute kidney failure," "hyperkalemia treatment," "renal replacement therapy," "dialysis," "sodium bicarbonate," "emergency," "acute." Reports from within the past 10&nbsp;years were selected preferentially, together with highly relevant older publications. RESULTS:Hyperkalemia is a potentially life-threatening electrolyte abnormality and may cause cardiac electrophysiological disturbances in the acutely ill patient. Frequently used therapies for hyperkalemia may, however, also be associated with morbidity. Therapeutics may include the simultaneous administration of insulin and glucose (associated with frequent dysglycemic complications), β-2 agonists (associated with potential cardiac ischemia and arrhythmias), hypertonic sodium bicarbonate infusion in the acidotic patient (representing a large hypertonic sodium load) and renal replacement therapy (effective but invasive). Potassium-lowering drugs can cause rapid decrease in serum potassium level leading to cardiac hyperexcitability and rhythm disorders. CONCLUSIONS:Treatment of hyperkalemia should not only focus on the ability of specific therapies to lower serum potassium level but also on their potential side effects. Tailoring treatment to the patient condition and situation may limit the risks

Преклинический атеросклероз: эндотелиальная дисфункция, комплекс интима-медиа, сосудистая жесткость

Preclinical atherosclerosis is an acute problem of contemporary medicine with significant effects on cardiovascular morbidity and mortality. Targeting strategy to tackle atherosclerotic disease at incipient clinical stages is undertaken to achieve a significant reduction in major cardiovascular events and reliance on an early assessment of serum markers of endothelial dysfunction and other noninvasive indicators of asymptomatic atherosclerotic arterial disease, such as the intimae-media thickness and arterial stiffness.Преклинический атеросклероз является острой проблемой современной медицины и обладает значительным влиянием на сердечно- сосудистую заболеваемость и смертность. Ориентация стратегии борьбы с атеросклеротической болезнью на преклинических стадиях нацелена на достижение значительного снижения основных сердечно-сосудистых осложнений и основана на ранней оценке сывороточных маркеров эндотелиальной дисфункции и на других неинвазивных показателях бессимптомного атеросклеротического поражения артерий, таких как толщина комплекса интима-медиа и жесткость сосудистых стенок

Guidelines for the prevention and treatment of venous thromboembolism in non-surgically treated cancer patients

Guidelines for the prevention and treatment of venous thromboembolism (VTE) are aimed to improve patients’ safety and quality of life by appropriate prophylaxis and treatment of deep venous thrombosis (DVT) and pulmonary embolism (PE). These guidelines relate to adult cancer patients treated non-surgically. Recommendations included in those guidelines do not relate to paediatric patients. The guidelines presented here directed to physicians and other healthcare professionals taking care of mentioned patients: clinical oncologists, haematologists, radiotherapists, pulmonologists, oncological gynaecologists, internal medicine physicians, and GPs. Venous thromboembolism (VTE) comprises a serious problem in oncology because it is the most common complication as well as the second most common cause of cancer-related deaths. The term “venous thromboembolism” includes the cases of DVT and PE; however, the former is a primary event and the latter is a secondary result. Active malignant disease classifies patients to a group with at least moderate risk of VTE. D-dimer levels could be increased in cancer patients without concomitant VTE. D-dimer levels below cut-off value (negative D-dimer) do not exclude VTE in cancer patients. In patients with active malignant disease with clinical symptoms suggesting VTE ultrasound (US) examination of deep veins or computed tomography angiography (angio-CT) should be performed, depending on the symptoms. Low-molecular-weight heparins (LMWH) are the drugs of choice in prevention and treatment of VTE in cancer patients. Antithrombotic treatment in cancer patients with DVT does not differ from treatment of cancer patients with PE, except clear indications to thrombolytic therapy. Cancer patients with clinical symptoms suggesting PE (dyspnoea, chest pain or tachycardia) are per definition classified into the group of moderate or high clinical probability of PE. The majority of PE cases account for embolism, which do not warrant thrombolytic treatment and should be treated with LMWH, UFH, or fondaparinux; LMWHs are the treatment of choice in cancer patients with VTE. Cancer patients have increased risk of recurrence of VTE. Available evidence does not justify the use of antithrombotic drugs to prolong survival in cancer patients

Presumed Neuroglycopenia Caused by Severe Hypoglycemia in Horses.

BackgroundNeuroglycopenia refers to a shortage of glucose in the brain resulting in neuronal dysfunction and death if left untreated. Presumed neuroglycopenia has not been described in horses.ObjectiveTo report neurological signs in horses with presumed neuroglycopenia as the result of severe hypoglycemia.AnimalsNinety horses (hours to 28 years of age) diagnosed with hypoglycemia (blood glucose concentration &lt; 75 mg/dL [&lt; 4.2 mmol/L]).MethodsRetrospective study. Electronic medical records were searched. Signalment, history, complaint, clinical signs, laboratory findings including CSF analysis, electroencephalogram, clinical or definitive diagnosis, and outcome were recorded. Kruskal-Wallis analysis of variance and logistic regression were used to investigate association between blood glucose concentration and data extracted. Statistical significance was set at P &lt; 0.05.ResultsThirty-eight and 52 horses had mild (50-74 mg/dL [2.8-4.1 mmol/L]), and severe hypoglycemia (&lt; 50 mg/dL [&lt; 2.8 mmol/L]), respectively. Most common causes of hypoglycemia included liver and gastrointestinal (40%) disease, sepsis (33%), neoplasia (7%), and insulin-induced (4%). Most common neurologic deficits included obtundation (100%), seizures (42%), and disorientation (22%). CSF-glucose was severely low (mean 2.5 mg/dL [0.1 mmol/L], median 0 mg/dL). Paroxysmal discharges in support of seizures were identified in the occipital (visual) and parietal (closest to temporal-auditory) cortical regions upon EEG examination (8/8 horses).Conclusions and clinical importanceNeuroglycopenia is presumed to occur in horses as the result of severe hypoglycemia. Subclinical seizures, and intermittent blindness and deafness of cortical origin can occur. Severe altered state of consciousness and seizures can be observed at a blood glucose cut-off value of &lt; 42 mg/dL (&lt; 2.3 mmol/L)