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How advanced aging influences clinical laboratory results
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PATHOLOGY UPDATE 2009 ABSTRACT PUBLICATION
is reflected in the claims experience of the Avant Mutual Group Limited, in terms of high numbers and/or high costs of claims. In 2007 Avant undertook a detailed analysis of notified incidents pertaining to missed or delayed diagnosis of cutaneous melanoma.3 In this study 22% of cases involved pathologists, with nearly a third of the cases relating to a histological diagnostic error. A number of systems errors led to a failure of reports to reach the treating practitioners. Following this study, Avant has introduced a new approach to quality improvement in health care the Melanoma Clinical Risk Modification Program. In consultation with a range of Australian medical specialists, including pathologists, a framework of risk modification guidelines for recognising melanoma were developed. These guidelines were developed using an action research method which elicits feedback from current clinical practice. These guidelines are distinct from clinical practice guidelines and are intended to raise the practitioners’ awareness of their particular risk in managing patients with melanoma. They provide practical tools to assess the capacity to manage risks in daily practice. The pathology component of the risk modification guidelines, the associated practice audit and related resources will be showcased in the poster. Importantly, the use of active clinical review and the benefits of targeted and meaningful communication between pathologists, surgeons, skin clinics, dermatologists and general practitioners will be discussed. References: 1 AIHW and AACR. Cancer in Australia 2001. Canberra: AIHW and AACR, 2001. 2 AIHW and AACR. Cancer in Australia: An Overview 2006. Canberra: AIHW and AACR, 2007. 3 Williamson JB, Graham S, Clark RB. ‘‘Hot Issues’’ Study No. 2. Melanoma Medical Defence Outlook 2007; 14: 6-11.
SCREENING FOR ALZHEIMER’S PATHOLOGY THROUGH NANOBIOSENSORS Amir Nazem1, G. Ali Mansoori2 1 Mashhad University of Medical Sciences, Iran 2 Bio and Chemical Engineering, University of Illinois at Chicago, USA Introduction: The insidious and irreversible progression of Alzheimer’s disease (AD) leads to a diagnosis of AD, often so late that nothing more than a symptomatic treatment is available. There is a focus on inventing methods for very early detection of AD, in order to cease the neurodegeneration process very shortly after the culprit molecular processes have started. Aims: To evaluate the applications of nanotechnology in screening for Alzheimer’s disease. Methods: During this study, a thorough research was done on nanotechnology diagnostic methods. The results underwent several stages of evaluation and scrutiny by authors and their expert colleagues. Results: The main obstacles against designing a biochemical screening test for AD include the lack of one single biomarker for AD, very low concentrations of AD biomarkers and the lack of AD specific biomarker in plasma. Nanotechnology detection methodologies are capable of detecting ultra low concentrations of different biomarkers simultaneously. Bio-barcode assay and ‘localised surface plasmon resonance’ nanosensor, are the two suggested nanobiosensors for early diagnosis of AD. Conclusions: In this review, in addition to evaluating the mentioned nanotechnology tools, we have analysed the potentials of different nanobiosensors in screening for AD pathology. These nanobiosensors include cantilever arrays and nanoparticle technologies.
HOW ADVANCED AGING INFLUENCES CLINICAL LABORATORY RESULTS La´szlo´ R E Salgo´ University of Szeged, Hungary During normal aging, the biological structural changes merely narrow: the functional capacity, the residual homeostasis, is sufficient for a healthy lifestyle. Changes in elderly patients are generally poor symptoms, and clinical laboratory diagnoses are therefore of great importance. The aim of the author is to present age-dependent changes in some of the more important laboratory parameters. The levels of some compounds tend to rise, e.g., leptin, glucose, homocysteine, prostate-specific antigen, sex hormone bindingglobulin, atrial natriuretic peptide, etc. This may be explained not only by enhanced production, but also by enhanced breakdown and excretion; the levels of other compounds may remain relatively constant, e.g., IgA, IgG, prolactin, the blood pH, etc.; and the levels of yet others may by decreased, e.g., albumin, total body calcium, phosphorus, iron, potassium, creatinine in the urine, renal plasma flow and glomerular filtration rate, vitamin D, oestrogen, aldosterone, testosterone, dehydroepiandrosterone and sulfate, etc. There are also differences (can be marked) between men and women (sex-related), and genetic influences. The author considers that, instead of cross-sectional analyses, it would be more correct to carry out longitudinal analyses in investigations of state among the elderly.
RCPA Quality Assurance Programs Pty Ltd Congress Grant JUVENILE POLYMYOSITIS OR PAEDIATRIC MUSCULAR DYSTROPHY: A DETAILED REANALYSIS OF 13 CASES C E D’Arcy1,2, M M Ryan3, C A McLean1,2 1 Faculty of Medicine, Nursing and Health Sciences, Monash University, Melbourne; 2 Department of Anatomical Pathology, The Alfred Hospital, Melbourne; 3 Neurosciences Department, Royal Children’s Hospital, Melbourne, Victoria, Australia There has been much debate about the existence of juvenile polymyositis (JPM) as an entity distinct from muscular dystrophy (MD). Recent advances in techniques allow for more accurate identification of muscle disorders. Aim: To re-analyse the clinical features and muscle tissue of biopsy specimens from 13 children initially given a diagnosis of JPM, to determine whether an underlying dystrophy is present. Methods: Thirteen cases previously diagnosed with JPM were reanalysed using morphology, immunoperoxidase studies, Western blotting and molecular genetic analysis and compared with cases of adult polymyositis (n 8) and Duchenne muscular dystrophy (n 4). Results: All 13 cases had clinical outcomes consistent with a MD. Endomysial inflammatory infiltrates, predominantly CD68 macrophages, CD3 and CD4 T cells, were present in muscle
PATHOLOGY UPDATE 2009 ABSTRACT PUBLICATION
is reflected in the claims experience of the Avant Mutual Group Limited, in terms of high numbers and/or high costs of claims. In 2007 Avant undertook a detailed analysis of notified incidents pertaining to missed or delayed diagnosis of cutaneous melanoma.3 In this study 22% of cases involved pathologists, with nearly a third of the cases relating to a histological diagnostic error. A number of systems errors led to a failure of reports to reach the treating practitioners. Following this study, Avant has introduced a new approach to quality improvement in health care the Melanoma Clinical Risk Modification Program. In consultation with a range of Australian medical specialists, including pathologists, a framework of risk modification guidelines for recognising melanoma were developed. These guidelines were developed using an action research method which elicits feedback from current clinical practice. These guidelines are distinct from clinical practice guidelines and are intended to raise the practitioners’ awareness of their particular risk in managing patients with melanoma. They provide practical tools to assess the capacity to manage risks in daily practice. The pathology component of the risk modification guidelines, the associated practice audit and related resources will be showcased in the poster. Importantly, the use of active clinical review and the benefits of targeted and meaningful communication between pathologists, surgeons, skin clinics, dermatologists and general practitioners will be discussed. References: 1 AIHW and AACR. Cancer in Australia 2001. Canberra: AIHW and AACR, 2001. 2 AIHW and AACR. Cancer in Australia: An Overview 2006. Canberra: AIHW and AACR, 2007. 3 Williamson JB, Graham S, Clark RB. ‘‘Hot Issues’’ Study No. 2. Melanoma Medical Defence Outlook 2007; 14: 6-11.
SCREENING FOR ALZHEIMER’S PATHOLOGY THROUGH NANOBIOSENSORS Amir Nazem1, G. Ali Mansoori2 1 Mashhad University of Medical Sciences, Iran 2 Bio and Chemical Engineering, University of Illinois at Chicago, USA Introduction: The insidious and irreversible progression of Alzheimer’s disease (AD) leads to a diagnosis of AD, often so late that nothing more than a symptomatic treatment is available. There is a focus on inventing methods for very early detection of AD, in order to cease the neurodegeneration process very shortly after the culprit molecular processes have started. Aims: To evaluate the applications of nanotechnology in screening for Alzheimer’s disease. Methods: During this study, a thorough research was done on nanotechnology diagnostic methods. The results underwent several stages of evaluation and scrutiny by authors and their expert colleagues. Results: The main obstacles against designing a biochemical screening test for AD include the lack of one single biomarker for AD, very low concentrations of AD biomarkers and the lack of AD specific biomarker in plasma. Nanotechnology detection methodologies are capable of detecting ultra low concentrations of different biomarkers simultaneously. Bio-barcode assay and ‘localised surface plasmon resonance’ nanosensor, are the two suggested nanobiosensors for early diagnosis of AD. Conclusions: In this review, in addition to evaluating the mentioned nanotechnology tools, we have analysed the potentials of different nanobiosensors in screening for AD pathology. These nanobiosensors include cantilever arrays and nanoparticle technologies.
HOW ADVANCED AGING INFLUENCES CLINICAL LABORATORY RESULTS La´szlo´ R E Salgo´ University of Szeged, Hungary During normal aging, the biological structural changes merely narrow: the functional capacity, the residual homeostasis, is sufficient for a healthy lifestyle. Changes in elderly patients are generally poor symptoms, and clinical laboratory diagnoses are therefore of great importance. The aim of the author is to present age-dependent changes in some of the more important laboratory parameters. The levels of some compounds tend to rise, e.g., leptin, glucose, homocysteine, prostate-specific antigen, sex hormone bindingglobulin, atrial natriuretic peptide, etc. This may be explained not only by enhanced production, but also by enhanced breakdown and excretion; the levels of other compounds may remain relatively constant, e.g., IgA, IgG, prolactin, the blood pH, etc.; and the levels of yet others may by decreased, e.g., albumin, total body calcium, phosphorus, iron, potassium, creatinine in the urine, renal plasma flow and glomerular filtration rate, vitamin D, oestrogen, aldosterone, testosterone, dehydroepiandrosterone and sulfate, etc. There are also differences (can be marked) between men and women (sex-related), and genetic influences. The author considers that, instead of cross-sectional analyses, it would be more correct to carry out longitudinal analyses in investigations of state among the elderly.
RCPA Quality Assurance Programs Pty Ltd Congress Grant JUVENILE POLYMYOSITIS OR PAEDIATRIC MUSCULAR DYSTROPHY: A DETAILED REANALYSIS OF 13 CASES C E D’Arcy1,2, M M Ryan3, C A McLean1,2 1 Faculty of Medicine, Nursing and Health Sciences, Monash University, Melbourne; 2 Department of Anatomical Pathology, The Alfred Hospital, Melbourne; 3 Neurosciences Department, Royal Children’s Hospital, Melbourne, Victoria, Australia There has been much debate about the existence of juvenile polymyositis (JPM) as an entity distinct from muscular dystrophy (MD). Recent advances in techniques allow for more accurate identification of muscle disorders. Aim: To re-analyse the clinical features and muscle tissue of biopsy specimens from 13 children initially given a diagnosis of JPM, to determine whether an underlying dystrophy is present. Methods: Thirteen cases previously diagnosed with JPM were reanalysed using morphology, immunoperoxidase studies, Western blotting and molecular genetic analysis and compared with cases of adult polymyositis (n 8) and Duchenne muscular dystrophy (n 4). Results: All 13 cases had clinical outcomes consistent with a MD. Endomysial inflammatory infiltrates, predominantly CD68 macrophages, CD3 and CD4 T cells, were present in muscle