The Identification and Validation of Neural Tube Defects in the General Practice Research Database

Total Page:16

File Type:pdf, Size:1020Kb

The Identification and Validation of Neural Tube Defects in the General Practice Research Database THE IDENTIFICATION AND VALIDATION OF NEURAL TUBE DEFECTS IN THE GENERAL PRACTICE RESEARCH DATABASE Scott T. Devine A dissertation submitted to the faculty of the University of North Carolina at Chapel Hill in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the School of Public Health (Epidemiology). Chapel Hill 2007 Approved by Advisor: Suzanne West Reader: Elizabeth Andrews Reader: Patricia Tennis Reader: John Thorp Reader: Andrew Olshan © 2007 Scott T Devine ALL RIGHTS RESERVED - ii- ABSTRACT Scott T. Devine The Identification And Validation Of Neural Tube Defects In The General Practice Research Database (Under the direction of Dr. Suzanne West) Background: Our objectives were to develop an algorithm for the identification of pregnancies in the General Practice Research Database (GPRD) that could be used to study birth outcomes and pregnancy and to determine if the GPRD could be used to identify cases of neural tube defects (NTDs). Methods: We constructed a pregnancy identification algorithm to identify pregnancies in 15 to 45 year old women between January 1, 1987 and September 14, 2004. The algorithm was evaluated for accuracy through a series of alternate analyses and reviews of electronic records. We then created electronic case definitions of anencephaly, encephalocele, meningocele and spina bifida and used them to identify potential NTD cases. We validated cases by querying general practitioners (GPs) via questionnaire. Results: We analyzed 98,922,326 records from 980,474 individuals and identified 255,400 women who had a total of 374,878 pregnancies. There were 271,613 full-term live births, 2,106 pre- or post-term births, 1,191 multi-fetus deliveries, 55,614 spontaneous abortions or miscarriages, 43,264 elective terminations, 7 stillbirths in combination with a live birth, and 1,083 stillbirths or fetal deaths. A marker of pregnancy care was identifiable for 330,153 pregnancies, eighty-four percent of which had data available at least 180 days prior to the first marker of pregnancy care. From the same population of 980,474 individuals, 217 NTD cases were identified. We attempted to validate all 217 NTD cases and 165 GP - iii- questionnaires were returned. We validated a NTD diagnosis for 117 cases, giving our electronic case definitions a positive predictive value of 0.71. The positive predictive value varied by NTD type: 0.81 for anencephaly, 0.83 for cephalocele, 0.64 for meningocele, and 0.47 for spina bifida. Conclusions: We were successful in identifying a large number of pregnancies in the GPRD. Our use of a hierarchical approach to identify pregnancy outcomes builds upon the methods suggested in previous work, while implementing additional steps to minimize potential misclassification of pregnancy outcomes. Our NTD identification algorithm was useful in identifying three of the four types of NTDs studied. Additional information is necessary to accurately identify cases of spina bifida. - iv- DEDICATION To my wife Julie and my son Adam. I could not have done this without their love and support. - v- ACKNOWLEDGEMENTS Thank you to Dr. Suzanne West for her leadership throughout this process. I would like to thank the Center for Education and Research of Therapeutics for their financial support of this project. Thank you to all the members of my dissertation committee for their time and effort for the past four years. Thank you to Susan Eaton from the General Practice Research Database for her guidance through the learning of the nuances of the database. I would also like to thank Dr. Newell McElwee for his support and mentorship throughout my dissertation journey. Finally, I would like to thank Dr. Harry Guess who supported this project from the beginning. - vi- TABLE OF CONTENTS ABSTRACT.................................................................................................................................................iii DEDICATION..............................................................................................................................................v ACKNOWLEDGEMENTS........................................................................................................................vi TABLE OF CONTENTS...........................................................................................................................vii LIST OF TABLES......................................................................................................................................xii LIST OF FIGURES...................................................................................................................................xiv LIST OF ABBREVIATIONS..................................................................................................................xvii Chapter Page I. INTRODUCTION.................................................................................................................................1 II. REVIEW OF THE LITERATURE.....................................................................................................2 A. Neural Tube Defects........................................................................................................................2 1. Biology............................................................................................................................................2 2. The Role Of Folic Acid .................................................................................................................3 3. Genetic Risk Factors ......................................................................................................................7 4. Maternal Factors.............................................................................................................................9 5. Medications ..................................................................................................................................11 6. Other Risk Factors........................................................................................................................13 B. Clinical Definitions........................................................................................................................13 1. Anencephaly .................................................................................................................................14 2. Encephalocele...............................................................................................................................15 3. Spina Bifida And Meningocele ...................................................................................................16 - vii- C. Prenatal Diagnostic And/Or Screening Tests: .............................................................................18 1. Alpha-fetoprotein .........................................................................................................................18 2. Amniocentesis ..............................................................................................................................19 3. Ultrasonography ...........................................................................................................................21 4. Current UK Guidelines For NTD Screening..............................................................................22 D. NTD Monitoring In The UK.........................................................................................................23 1. The National Congenital Anomaly System................................................................................24 2. The European Concerted Action On Congenital Anomalies And Twins.................................25 3. Differences Between NCAS And EUROCAT Systems............................................................26 E. The GPRD ......................................................................................................................................28 1. Introduction ..................................................................................................................................28 2. The Mother-Baby Linkage ..........................................................................................................30 3. Previous Birth Defect Research In The GPRD ..........................................................................32 4. Previous Pregnancy Research Using The GPRD.......................................................................35 III. STATEMENT OF SPECIFIC AIMS ..............................................................................................37 A. Hypotheses .....................................................................................................................................37 B. Rationale.........................................................................................................................................37 C. Research Questions And Specific Aims.......................................................................................41 IV. METHODS .......................................................................................................................................43 A. Overview Of Methods Used..........................................................................................................43 B. Data Used .......................................................................................................................................44 C. Procedure For Pregnancy Identification.......................................................................................47
Recommended publications
  • In This Issue
    THE JOURNAL OF THE AAPA VOLUME 8 ISSUE 4 2018 IN THIS ISSUE Peer-Reviewed 1 CE Quiz & Peer-Reviewed Manuscript: New Malignant Transformation of Childhood Malignant Transformation of Burn Wound with Metastasis: A Case CE Article Report Childhood Burn Wound with 3 Letter from the Editor Metastasis: A Case Report N. Dominic Alessio, PA(ASCP)CM 6 CE Quiz & Peer-Reviewed Manuscript: Breast Cancer Metastasis to the Colon Detroit Medical Center, Detroit, MI Presenting After Fifteen Years Fellow members were given the opportunity to apply for a travel grant to attend an upcoming Fall Conference or Spring Meeting of 8 Peer-Reviewed Manuscript: their choice. Fellows were required to write a manuscript, and the Aurora Diagnostics Pathologists’ Assistant four winning entries received a grant valued at up to $1800 (full week Breast Specimen Handling Best Practice Guideline registration + $1000 to help cover travel expenses). Congratulations, Dominic, on your winning submission! 11 44th Annual Continuing Education Conference Recap Abstract 12 44th Annual Continuing Education Marjolin’s ulcer is a rare and aggressive form of cutaneous squamous cell carcinoma Conference Photos (SCC) which forms through malignant transformation of chronically irritated previous injury, such as incompletely healed burns, ulcers, and other wounds. Although similar in 17 8th Annual Spring Meeting microscopic morphology, Marjolin’s ulcer is unique from other cutaneous SCCs in many other significant characteristics. The carcinoma often appears decades after the initial 18 Board of Trustees Chair’s Report trauma, but once present it follows a rapid course of growth and metastasis. In the current case study, a male in his mid-30s with history of extensive burns as a child presented 21 Gross Photo Unknown to the Emergency Department complaining of a large, open wound on his lower back.
    [Show full text]
  • Description Treatment
    Description Megalencephaly, also called macrencephaly, is a condition in which an infant or child has an abnormally large, heavy, and usually malfunctioning brain. By definition, the brain weight is greater than average for the age and gender of the child. Head enlargement may be evident at birth or the head may become abnormally large in the early years of life. Megalencephaly is thought to be related to a disturbance in the regulation of cell production in the brain. In normal development, neuron proliferation - the process in which nerve cells divide to form new generations of cells - is regulated so that the correct number of cells is produced in the proper place at the appropriate time. In a megalencephalic brain, too many cells are produced either during development or progressively as part of another disorder, such as one of the neurofibromatoses or leukodystrophies. Symptoms of megalencephaly include delayed development, seizures, and corticospinal (brain cortex and spinal cord) dysfunction. Megalencephaly affects males more often than females. Unilateral megalencephaly or hemimegalencephaly is a rare condition that is characterized by the enlargement of one side of the brain. Children with this disorder may have a large, asymmetrical head accompanied by seizures, partial paralysis, and impaired cognitive development. Megalencephaly is different from macrocephaly (also called megacephaly or megalocephaly), which describes a big head, and which doesn’t necessarily indicate abnormality. Large head size is passed down through the generations in some families. Treatment There is no standard treatment for megalencephaly. Treatment will depend upon the disorder with which the megalencephaly is associated and will address individual symptoms and disabilities.
    [Show full text]
  • Hamilton Radiologu Nuchal Translucencey
    PATIENT INFORMATION Advice regarding your 12 week scan Nuchal Translucency HAMILTON RADIOLOGY MEDICAL IMAGING SPECIALISTS YOU’RE IN SAFE HANDS A Few Facts . • The vast majority of babies are born normal. • All women, whatever their age, have a small risk of delivering a baby with physical and/or intellectual impairment. • In some cases the impairment is due to a chromosome abnormality such as Downs Syndrome (Trisomy 21). • The programme will only accept foetuses with a crown rump length between 4.5 and 8.3cm ie within the 11+2 days – 13 weeks 6 days period. Optimal time for this scan is 12–13 weeks. • The scan gives an estimate of the risk for Downs Syndrome. To know for sure whether or not the foetus has a chromosomal abnormality, an invasive test is needed (chorionic villus sampling or amniocentesis). • However, invasive tests carry a small risk of causing miscarriage (1%). • The early scan allows detection of some, but not all, physical defects. A further scan at 19–20 weeks is recommended. Risk for Downs Syndrome The table to the right shows how the chance of having a baby with Downs Syndrome increases with age. The First Trimester Scan At the 12 week scan we confi rm that the foetus is alive and we assess the gestational age by measuring the crown-rump length. We can look for major physical defects, measure nuchal translucency thickness and calculate your baby’s chance of Downs Syndrome based on the scan fi ndings and your age. Occasionally the foetus is not well seen on the abdominal scan and it may be necessary to perform a transvaginal scan.
    [Show full text]
  • Monoamniotic Twins: What Should Be the Optimal Antenatal Management?
    Monoamniotic Twins: What Should Be the Optimal Antenatal Management? Ashis K. Sau1, Kate Langford1, Catherine Elliott1, Lin L. Su2, and Darryl J. Maxwell1 1Fetal Medicine Unit, St.Thomas’ Hospital, London, UK 2National University Hospital, Singapore onoamniotic twinning is a rare event with an incidence of London with a high proportion of socially deprived and M1% of all monozygotic twins and associated with a high black, Asian or mixed race peoples. Management protocols fetal morbidity and mortality. Confident early diagnosis is possi- ble, but optimal management is not yet established. This article employed were those of early detection of chorionicity and presents the experience of a single centre in managing all amnionicity, 2-weekly serial ultrasound surveillance and monoamniotic twins diagnosed during 1994–2000. Seven pairs early delivery by elective cesarean section at around 32 of monoamniotic twins were identified for analysis. All were weeks gestation. From 1997, a formal twin ultrasound sur- managed in accord with a unit protocol that involved early diag- veillance clinic was established and first trimester nuchal nosis, serial ultrasound examination and elective early delivery. In four cases, the detection of monoamnionicity was made translucency screening was performed. The same fetal med- during a first trimester nuchal scan. Discordance for structural icine consultant had clinical input into the management of abnormality was found in three cases where the co-twin was all cases. A summary of the cases can be seen in Table 1. normal. Cord entanglement was detected antenatally in four cases. Two pairs of twins died before 20 weeks. One of these Case 1 had early onset twin–twin transfusion syndrome.
    [Show full text]
  • Megalencephaly and Macrocephaly
    277 Megalencephaly and Macrocephaly KellenD.Winden,MD,PhD1 Christopher J. Yuskaitis, MD, PhD1 Annapurna Poduri, MD, MPH2 1 Department of Neurology, Boston Children’s Hospital, Boston, Address for correspondence Annapurna Poduri, Epilepsy Genetics Massachusetts Program, Division of Epilepsy and Clinical Electrophysiology, 2 Epilepsy Genetics Program, Division of Epilepsy and Clinical Department of Neurology, Fegan 9, Boston Children’s Hospital, 300 Electrophysiology, Department of Neurology, Boston Children’s Longwood Avenue, Boston, MA 02115 Hospital, Boston, Massachusetts (e-mail: [email protected]). Semin Neurol 2015;35:277–287. Abstract Megalencephaly is a developmental disorder characterized by brain overgrowth secondary to increased size and/or numbers of neurons and glia. These disorders can be divided into metabolic and developmental categories based on their molecular etiologies. Metabolic megalencephalies are mostly caused by genetic defects in cellular metabolism, whereas developmental megalencephalies have recently been shown to be caused by alterations in signaling pathways that regulate neuronal replication, growth, and migration. These disorders often lead to epilepsy, developmental disabilities, and Keywords behavioral problems; specific disorders have associations with overgrowth or abnor- ► megalencephaly malities in other tissues. The molecular underpinnings of many of these disorders are ► hemimegalencephaly now understood, providing insight into how dysregulation of critical pathways leads to ►
    [Show full text]
  • Low-Lying Placenta
    LOW- LYING PLACENTA LOW-LYING PLACENTA WHAT IS PLACENTA PRAEVIA? The placenta develops along with the baby in the uterus (womb) during pregnancy. It connects the baby with the mother’s blood system and provides the baby with its source of oxygen and nourishment. The placenta is delivered after the baby and is also called the afterbirth. In some women the placenta attaches low in the uterus and may be near, or cover a part, or lie over the cervix (entrance to the womb). If it is shown in early ultrasound scans, it is called a low-lying placenta. In most cases, the placenta moves upwards as the uterus enlarges. For some women the placenta continues to lie in the lower part of the uterus in the last months of pregnancy. This condition is known as placenta praevia. If the placenta covers the cervix, this is known as major placenta praevia. Normal Placenta Placenta Praevia Major Placenta Praevia WHAT ARE THE RISKS TO MY BABY AND ME? When the placenta is in the lower part of the womb, there is a risk that you may bleed in the second half of pregnancy. Bleeding from placenta praevia can be heavy, and so put the life of the mother and baby at risk. However, deaths from placenta praevia are rare. You are more likely to need a caesarean section because the placenta is in the way of your baby being born. HOW IS PLACENTA PRAEVIA DIAGNOSED? A low-lying placenta may be suspected during the routine 20-week ultrasound scan. Most women who have a low-lying placenta at the routine 20-week scan will not go on to have a low-lying placenta later in the pregnancy – only 1 in 10 go on to have a placenta praevia.
    [Show full text]
  • Polymicrogyria (PMG) ‘Many–Small–Folds’
    Polymicrogyria Dr Andrew Fry Clinical Senior Lecturer in Medical Genetics Institute of Medical Genetics, Cardiff [email protected] Polymicrogyria (PMG) ‘Many–small–folds’ • PMG is heterogeneous – in aetiology and phenotype • A disorder of post-migrational cortical organisation. PMG often appears thick on MRI with blurring of the grey-white matter boundary Normal PMG On MRI PMG looks thick but the cortex is actually thin – with folded, fused gyri Courtesy of Dr Jeff Golden, Pen State Unv, Philadelphia PMG is often confused with pachygyria (lissencephaly) Thick cortex (10 – 20mm) Axial MRI 4 cortical layers Lissencephaly Polymicrogyria Cerebrum Classical lissencephaly is due Many small gyri – often to under-migration. fused together. Axial MRI image at 7T showing morphological aspects of PMG. Guerrini & Dobyns Malformations of cortical development: clinical features and genetic causes. Lancet Neurol. 2014 Jul; 13(7): 710–726. PMG - aetiology Pregnancy history • Intrauterine hypoxic/ischemic brain injury (e.g. death of twin) • Intrauterine infection (e.g. CMV, Zika virus) TORCH, CMV PCR, [+deafness & cerebral calcification] CT scan • Metabolic (e.g. Zellweger syndrome, glycine encephalopathy) VLCFA, metabolic Ix • Genetic: Family history Familial recurrence (XL, AD, AR) Chromosomal abnormalities (e.g. 1p36 del, 22q11.2 del) Syndromic (e.g. Aicardi syndrome, Kabuki syndrome) Examin - Monogenic (e.g. TUBB2B, TUBA1A, GPR56) Array ation CGH Gene test/Panel/WES/WGS A cohort of 121 PMG patients Aim: To explore the natural history of PMG and identify new genes. Recruited: • 99 unrelated patients • 22 patients from 10 families 87% White British, 53% male ~92% sporadic cases (NB. ascertainment bias) Sporadic PMG • Array CGH, single gene and gene panel testing - then a subset (n=57) had trio-WES.
    [Show full text]
  • Screening for Trisomy 21 in Denmark; Evaluation of the Current and Possible Future Strategies
    Faculty of Health Sciences University of Copenhagen Screening for trisomy 21 in Denmark; Evaluation of the current and possible future strategies PhD thesis Charlotte Kvist Ekelund Academic supervisors Ann Tabor, professor, DMSc, Department of Fetal Medicine, Rigshospitalet, University of Copenhagen Olav Bjørn Petersen, PhD, consultant, Department of Obstetrics, Aarhus University Hospital Ida Vogel, DMSc, Head of Department of Clinical Genetics, Aarhus University Hospital Evaluation committee Katja Bilardo, Professor, Head Fetal Medicine Unit, Department of Obstetrics & Gynaecology, University Medical Center Groningen, The Netherlands Michael Christiansen, Head of Molecular Diagnostics, Statens Serum Institute, Copenhagen Lone Krebs, DMSc, Associate professor, consultant, Department of Gynecology and Obstetrics, Holbæk Sygehus, University of Copenhagen The PhD defence will take place Friday the 13th of April 2012, Auditorium B, Teilum, Rigshospitalet, Copenhagen. Acknowledgement This thesis was made possible by help from a number of fantastic supervisors and colleagues. First and foremost, I owe my deepest thanks to Professor Ann Tabor. Thank you for sharing your interest and knowledge in first trimester screening with me, for your professional and personal guidance, for always having time and for showing your confidence in me from the very beginning of the project. Your constructive and focused attitude is admirable and to me you have been an extremely inspiring mentor within all aspects of life. I am greatly indebted to Olav Bjørn Petersen, MD, PhD, one of the most enthusiastic and optimistic persons I know. Your positive attitude, support and encouragement have really helped me through the challenging phases of the project. And my sincere thanks to Ida Vogel, MD, DMSc for taking part in the project, for everything you taught me many years ago and for still being there.
    [Show full text]
  • Guide to Learning in Maternal-Fetal Medicine
    GUIDE TO LEARNING IN MATERNAL-FETAL MEDICINE First in Women’s Health The Division of Maternal-Fetal Medicine of The American Board of Obstetrics and Gynecology, Inc. 2915 Vine Street Dallas, TX 75204 Direct questions to: ABOG Fellowship Department 214.871.1619 (Main Line) 214.721.7526 (Fellowship Line) 214.871.1943 (Fax) [email protected] www.abog.org Revised 4/2018 1 TABLE OF CONTENTS I. INTRODUCTION ........................................................................................................................ 3 II. DEFINITION OF A MATERNAL-FETAL MEDICINE SUBSPECIALIST .................................... 3 III. OBJECTIVES ............................................................................................................................ 3 IV. GENERAL CONSIDERATIONS ................................................................................................ 3 V. ENDOCRINOLOGY OF PREGNANCY ..................................................................................... 4 VI. PHYSIOLOGY ........................................................................................................................... 6 VII. BIOCHEMISTRY ........................................................................................................................ 9 VIII. PHARMACOLOGY .................................................................................................................... 9 IX. PATHOLOGY .........................................................................................................................
    [Show full text]
  • Gtg-No-20B-Breech-Presentation.Pdf
    Guideline No. 20b December 2006 THE MANAGEMENT OF BREECH PRESENTATION This is the third edition of the guideline originally published in 1999 and revised in 2001 under the same title. 1. Purpose and scope The aim of this guideline is to provide up-to-date information on methods of delivery for women with breech presentation. The scope is confined to decision making regarding the route of delivery and choice of various techniques used during delivery. It does not include antenatal or postnatal care. External cephalic version is the topic of a separate RCOG Green-top Guideline No. 20a: ECV and Reducing the Incidence of Breech Presentation. 2. Background The incidence of breech presentation decreases from about 20% at 28 weeks of gestation to 3–4% at term, as most babies turn spontaneously to the cephalic presentation. This appears to be an active process whereby a normally formed and active baby adopts the position of ‘best fit’ in a normal intrauterine space. Persistent breech presentation may be associated with abnormalities of the baby, the amniotic fluid volume, the placental localisation or the uterus. It may be due to an otherwise insignificant factor such as cornual placental position or it may apparently be due to chance. There is higher perinatal mortality and morbidity with breech than cephalic presentation, due principally to prematurity, congenital malformations and birth asphyxia or trauma.1,2 Caesarean section for breech presentation has been suggested as a way of reducing the associated perinatal problems2,3 and in many countries in Northern Europe and North America caesarean section has become the normal mode of breech delivery.
    [Show full text]
  • Efficacy of Genetic Testing in Cases of Ambiguous Genitalia
    EFFICACY OF GENETIC TESTING IN CASES OF AMBIGUOUS GENITALIA DETECTED ON PRENATAL! ULTRASOUND ! ! ! by! EVELYN ROSE! CRAWFORD ! ! Submitted in partial fulfillment of !the requirements for the degree of Master of! Science ! ! ! Thesis Advisor: Larisa! Baumanis, MS ! ! Genetic Counseling! Department !of Genetics CASE WESTERN RESERVE! UNIVERSITY ! ! ! ! ! ! ! August, 2014 ! ! CASE WESTERN RESERVE! UNIVERSITY SCHOOL OF GRADUATE! STUDIES We hereby approve! the thesis of: Evelyn Rose! Crawford candidate for the degree of !Master of Science degree.* ! ! Larisa Baumanis, MS (Committee Chair) ! Anne Matthews, RN, PhD ! Noam Lazebnik, MD ! Aditi Parikh, MD ! Sara Debanne, PhD ! ! ! ! Date of Defense June 20, 2014 ! ! ! ! ! *We also certify that written approval has been obtained for any proprietary material contained therein !2 ! ! ! TABLE OF CONTENTS List of Tables 4 List of Figures 5 Acknowledgements 6 Abstract 7 Introduction 8 Purpose of Study & Specific Aims 10 Background 11 Detection of Ambiguous Genitalia on Prenatal Ultrasound 11 Current use of Genetic testing in determining a specific diagnosis 13 The Importance of Prenatal Diagnosis in Cases of Ambiguous Genitalia 18 Significance for genetic counselors 19 Conclusions 20 Methodology 22 Systematic Review of the Literature 22 Chart Review 27 Algorithm & Analysis 29 Results 31 Analysis 52 Discussion 55 Appendix I: First Review Matrix Organization and summary of literature review articles 62 Appendix II: Second Review Matrix Organization and summary of case studies from the literature review 78 Appendix III: Third Review Matrix Organization and summary of chart review cases 94 References 102 !3 LIST OF TABLES ! !Table 1: Keyword Combinations for Literature Search 22 !Table 2: Example First Review Matrix 25 !Table 3: Example Second Review Matrix 25 !Table 4: Protocol Key 26 !Table 5: Example Third Review Matrix 29 Table 6: Imaging characteristics to differentiate cloacal exstrophy, bladder !exstrophy and cloacal malformation (Calvo-Garcia et al.
    [Show full text]
  • Prioritization of Health Services
    PRIORITIZATION OF HEALTH SERVICES A Report to the Governor and the 74th Oregon Legislative Assembly Oregon Health Services Commission Office for Oregon Health Policy and Research Department of Administrative Services 2007 TABLE OF CONTENTS List of Figures . iii Health Services Commission and Staff . .v Acknowledgments . .vii Executive Summary . ix CHAPTER ONE: A HISTORY OF HEALTH SERVICES PRIORITIZATION UNDER THE OREGON HEALTH PLAN Enabling Legislatiion . 3 Early Prioritization Efforts . 3 Gaining Waiver Approval . 5 Impact . 6 CHAPTER TWO: PRIORITIZATION OF HEALTH SERVICES FOR 2008-09 Charge to the Health Services Commission . .. 25 Biennial Review of the Prioritized List . 26 A New Prioritization Methodology . 26 Public Input . 36 Next Steps . 36 Interim Modifications to the Prioritized List . 37 Technical Changes . 38 Advancements in Medical Technology . .42 CHAPTER THREE: CLARIFICATIONS TO THE PRIORITIZED LIST OF HEALTH SERVICES Practice Guidelines . 47 Age-Related Macular Degeneration (AMD) . 47 Chronic Anal Fissure . 48 Comfort Care . 48 Complicated Hernias . 49 Diagnostic Services Not Appearing on the Prioritized List . 49 Non-Prenatal Genetic Testing . 49 Tuberculosis Blood Test . 51 Early Childhood Mental Health . 52 Adjustment Reactions In Early Childhood . 52 Attention Deficit and Hyperactivity Disorders in Early Childhood . 53 Disruptive Behavior Disorders In Early Childhood . 54 Mental Health Problems In Early Childhood Related To Neglect Or Abuse . 54 Mood Disorders in Early Childhood . 55 Erythropoietin . 55 Mastocytosis . 56 Obesity . 56 Bariatric Surgery . 56 Non-Surgical Management of Obesity . 58 PET Scans . 58 Prenatal Screening for Down Syndrome . 59 Prophylactic Breast Removal . 59 Psoriasis . 59 Reabilitative Therapies . 60 i TABLE OF CONTENTS (Cont’d) CHAPTER THREE: CLARIFICATIONS TO THE PRIORITIZED LIST OF HEALTH SERVICES (CONT’D) Practice Guidelines (Cont’d) Sinus Surgery .
    [Show full text]