SURVEY OF DUCHENNE TYPE AND CONGENITAL TYPE OF MUSCULAR DYSTROPHY IN SHIMANE, JAPAN 1

Similar documents
Creatine phosphokinase levels in the newborn

SERUM CREATINE PHOSPHOKINASE IN THE

Inheritance and the muscular dystrophies

Learn the steps to identify pediatric muscle weakness and signs of neuromuscular disease.

1/28/2019. OSF HealthCare INI Care Center Team. Neuromuscular Disease: Muscular Dystrophy. OSF HealthCare INI Care Center Team: Who are we?

Single Gene (Monogenic) Disorders. Mendelian Inheritance: Definitions. Mendelian Inheritance: Definitions

Atlas of Genetics and Cytogenetics in Oncology and Haematology

14 2 Human Chromosomes

Lecture 17: Human Genetics. I. Types of Genetic Disorders. A. Single gene disorders

Genetic diagnosis of limb girdle muscular dystrophy type 2A, A Case Report

Estimation of proportion of new mutants

Human Genetic Diseases (non mutation)

Unifactorial or Single Gene Disorders. Hanan Hamamy Department of Genetic Medicine and Development Geneva University Hospital

Human Genetics Notes:

Lab Activity Report: Mendelian Genetics - Genetic Disorders

Central nervous system involvement in progressive

SEX-LINKED INHERITANCE. Dr Rasime Kalkan

Lesson Overview. Human Chromosomes. Lesson Overview. Human Chromosomes

Mendelian Inheritance. Jurg Ott Columbia and Rockefeller Universities New York

Genetics. by their offspring. The study of the inheritance of traits is called.

Neonatal Hypotonia. Encephalopathy acute No encephalopathy. Neurology Chapter of IAP

2. A normal human germ cell before meiosis has how many nuclear chromosomes?


Human Heredity: The genetic transmission of characteristics from parent to offspring.

INTELLECTUAL IMPAIRMENT IN MUSCULAR DYSTROPHY

Myotubular (centronuclear) myopathy

The Brain Pathology in Fukuyama Type Congenital Muscular Dystrophy -CT and Autopsy Findings-

14 1 Human Heredity. Week 8 vocab Chapter 14

Effects of Inbreeding on Raven Matrices

Evaluation of the Hypotonic Infant and Child

Genetics. the of an organism. The traits of that organism can then be passed on to, on

What favorite organism of geneticists is described in the right-hand column?

Spinal Muscular Atrophy: Case Study. Spinal muscular atrophy (SMA) is a fairly common genetic disorder, affecting

Chapter 4 PEDIGREE ANALYSIS IN HUMAN GENETICS

Prevalence and mode of inheritance of major genetic eye diseases in China

Nemaline (rod) myopathies

Spinal Muscular Atrophy Newborn Screening

Pedigree Construction Notes

Red flags for clinical practice - guidance on indicators that your patient may have a genetic condition

Cardiac Considerations and Care in Children with Neuromuscular Disorders

Classifications of genetic disorders disorders

SMA IS A SEVERE NEUROLOGICAL DISORDER [1]

The Floppy Baby. Clare Betteridge

Gene Expression and Mutation

Gaucher disease 3/22/2009. Mendelian pedigree patterns. Autosomal-dominant inheritance

Genetics in Primary Care Curriculum Statement 6. Dr Dave Harniess PCME Stockport

MULTIPLE CHOICE. Choose the one alternative that best completes the statement or answers the question.

Human inherited diseases

Muscular Dystrophies. Pinki Munot Consultant Paediatric Neurologist Great Ormond Street Hospital Practical Neurology Study days April 2018

p and q can be thought of as probabilities of selecting the given alleles by

Genetic Conditions and Services: An Introduction

Profile, types, duration and severity of muscular dystrophy: a clinical study at a tertiary care hospital

Chapter 1: What is PKU?

Below are photos from a 6 month old child with Werdnig-Hoffman s disease.

Hypotonia Care Pathway Update: Diagnosis Garey Noritz, MD...

Clinical features, particularly those of the central nervous system, of patients with Becker s muscular dystrophy, including autopsied cases

Genetic Disorders. and. blood vessels the and. How many genes are affected by this deletion? Turner s Syndrome- An incomplete or missing chromosome

X Linked Inheritance. Information for Patients and Families. Illustrations by Rebecca J Kent

Community Genetics. Hanan Hamamy Department of Genetic Medicine & Development Geneva University Hospital

RECORDS OF DEA1" MUTISM IN NORTHERN IRELAND

- Aya Alomoush. - Talal Al-Zabin. - Belal Azab. 1 P a g e

Neuromuscular in the Pediatric Clinic: Recognition and Referral

Spinal Muscular Atrophy as a Focus Indication for Biomarker Development. Meg Winberg, PhD Spinal Muscular Atrophy Foundation February 26, 2007

GENETICS NOTES. Chapters 12, 13, 14, 15 16

A Lawyer s Perspective on Genetic Screening Performed by Cryobanks

Neurology. Access Center 24/7 access for referring physicians (866) 353-KIDS (5437)

Figure 1: Transmission of Wing Shape & Body Color Alleles: F0 Mating. Figure 1.1: Transmission of Wing Shape & Body Color Alleles: Expected F1 Outcome

Congenital hypothyroidism and your child

boys who are not walking by the age of 18 months.9 This age was selected because 97% of normal boys are walking,17 whereas only 50% of boys with

Approach to the Child with Developmental Delay

thorough physical and laboratory investigations fail to define the etiology of hearing loss. (2000, p. 16). In a report produced for the Maternal and

Clinical Summaries. CLN1 Disease, infantile onset and others

Mendelian Genetics and Beyond Chapter 4 Study Prompts

Centres of reference for rare diseases expectations based on Polish experience. Małgorzata Krajewska-Walasek

Clinical aspects of pterin disorders

Chapter 15 Notes 15.1: Mendelian inheritance chromosome theory of inheritance wild type 15.2: Sex-linked genes

X-linked Genetic Disorders

Disorders of Muscle. Disorders of Muscle. Muscle Groups Involved in Myopathy. Needle Examination of EMG. History. Muscle Biopsy

Lab Activity 36. Principles of Heredity. Portland Community College BI 233

Pathophysiology. Tutorial 1 Genetic Diseases

Genetic Disorders. PART ONE: Detecting Genetic Disorders. Amniocentesis Chorionic villus sampling Karyotype Triple Screen Blood Test

Pediatric Aspects of EDX

Roadmap. Inbreeding How inbred is a population? What are the consequences of inbreeding?

Immunohistochemical Study of Dystrophin Associated Glycoproteins in Limb-girdle Muscular Dystrophies

Genetics Questions: There are 15 questions in total. The answers can be found on the accompanying document

Basic Definitions. Dr. Mohammed Hussein Assi MBChB MSc DCH (UK) MRCPCH

Sialic Acid Storage Diseases

Problem set questions from Final Exam Human Genetics, Nondisjunction, and Cancer

(b) What is the allele frequency of the b allele in the new merged population on the island?

A rare case of muscular dystrophy with POMT2 and FKRP gene mutation. Present by : Ghasem Khazaei Supervisor :Dr Mina Mohammadi Sarband

Congenital myasthenic syndromes (CMS)

What is myotonic dystrophy?

GENETICS - NOTES-

Diseases of Muscle and Neuromuscular Junction

Hths 2231 Laboratory 3 Genetics

DMD Genetics: complicated, complex and critical to understand

Evidence for early impairment of verbal intelligence

Human Molecular Genetics Prof. S. Ganesh Department of Biological Sciences and Bioengineering Indian Institute of Technology, Kanpur

Page 1 CLINICAL (MEDICAL) GENETICS. Medical Genetics (M1 - M4) Medical Genetics within Core 2

Human beings contain tens of thousands of genes, the basic material for cell

Transcription:

Jap. J. Human Genet. 22, 43--47, 1977 SURVEY OF DUCHENNE TYPE AND CONGENITAL TYPE OF MUSCULAR DYSTROPHY IN SHIMANE, JAPAN 1 Kenzo TAKESHITA,* Kunio YOSHINO,* Tadashi KITAHARA,* Toshio NAKASHIMA,** and Noriko KATO** *Division of Child Neurology, Brain Research lnstitutep Tottori University School of Medicine, Yonago, Japan **National Matsue Hospital, Matsue, Japan Summary Duchenne muscular dystrophy and congenital muscular dystrophy (Fukuyama type) were analyzed clinically, genetically and epidemiologically in Shimane Prefecture in the Western Honshu Island of Japan. Cases were collected from all available sources and the diagnosis was reexamined by our group, yielding a total of 83 patients with various myopathies. Thirty-two patients with Duchenne muscular dystrophy were found. Their clinical manifestations were not different from cases occurring elsewhere in Japan. The incidence rate of this type was 20.8 x 10-5. Parental consanguinity of the cases was noted in 18.5~, considerably higher than control families. As to the Fukuyama type of congenital muscular dystrophy, 11 patients were identified. The incidence rate was 5.60 x 10-5. There was no doubt that an autosomal recessive pattern of inheritance was involved in these patients. The gene frequency was estimated as 0.0075. INTRODUCTION Duchenne muscular dystrophy and congenital muscular dystrophy are the most common and clinically severe myopathies in childhood. According to Araki (1967), the prevalence rate of progressive muscular dystrophy pooling all types is 2.6-5.5 x 10-5 in Japan, of which 44.5~ is classified as Duchenne type. Although far less frequent than Duchenne type, a congenital type of muscular dystrophy first reported by Fukuyama et al. (1960) is widely known among Japanese pediatricians. This type is supposed to be recessively heritable, but there is no report about its frequencies in the population. The present report describes clinical, genetic and epidemiologic patterns of the stated two types of muscular dystrophy in Shimane Prefecture, located in Western Honshu Island of Japan. Received July 23, 1977 1 This paper was partially presented at the 18th Annual Meeting of the Japanese Society of Pediatric Neurology, June 16, 1976.

44 K. TAKESHITA et al. MATERIALS AND METHODS In order to find patients possibly suffering from myopathies, questionnaires were sent to all the nurse-teachers in 118 infant schools, 318 primary schools and 141 junior high schools in Shimane Prefecture, asking whether there were individuals who had motor troubles like myopathies. In addition, records in two public institutions for children, three hospitals for handicapped children and two protecture institutions in Shimane Prefecture were also surveyed for similar cases. The population survey was done from January, 1975 through June, 1975. The provisional cases with suspected myopathy were collected from people of all ages. All patients were examined neurologically and electromyographically and serum levels of creatine-phosphokinase (CPK) were determined. Muscle biopsies were made for definite diagnosis in some cases. The medical examination was finished in November, 1975. RESULTS The questionnaires were all returned and yielded 104 provisional cases, whereas 58 cases were found in the record surveys. Reevaluation of the diagnosis revealed that a total of 83 patients were suffering from various types of muscular dystrophy as seen in Table 1. The population in Shimane Prefecture was 768,876 in 1975. The prevalence rate of muscular dystrophy, all types pooled, was approximately 10.7 x 10-5 for November, 1975. Duchenne muscular dystrophy Thirty-two Duchenne patients were found. All cases were males, their age ranged mostly 5-19. Clinically, (1) the mean age of onset was 4.7_+ 1.37 years, (2) all patients except one manifested the disease with gait disturbances as initial symptoms, (3) 23 bedpatients became unable to walk between 9-15 years of age, (4) pseudohypertrophy was seen in all patients, (5) subnormal intelligence was noted in 21 patients. Table 1. Numbers of patients with muscular dystrophy by type and sex and numbers of families of patients exhaustively collected in Shimane Prefecture, November, 1975. Duchenne type Congenital type Limb- Faciogirdle scapulo- Fukuyama Others humeral type type type Myotonic Others dystrophy Total Male 32 5 4 10 1 1 2 54 Female 0 6 1 12 2 2 5 29 Total 32 11 5 22 3 3 7 83 No. of 27 7 5 15 3 3 3 63 families

SURVEY OF MUSCULAR DYSTROPHY 45 Table 2. Incidence of Duchenne muscular dystrophy among male live-births between 1956-1970. Year of birth No. of male live-births No. of patients Incidence rate (10-~) 1956-1960 26, 992 7 259 1961-1965 29, 593 4 135 1966-1970 34, 572 8 231 Total 91,157 19 208 Table 3. Consanguineous marriages among parents of Duchenne muscular dystrophy and Fukuyama type congenital muscular dystrophy. Duchenne type Congenital type Control in Shimane No. of families 27 7 480 First-cousins 3 1 12 (2.5~) Half-cousins 2 1. 15 (3.1~) Second-cousins 0 0 3 (0. 6Yo) Total 5 (18.5~) 2 (28. 6Yo) 30 (6. 2~) When plotted against a map of the prefecture, the addresses of the patients revealed no focus of high incidence. Incidence rate of this type among the 91,157 male aged between 5 and 19 (born in 1956-1970 inclusive) was 20.8 x 10 -~ or about 1 in 4,800 male youths (Table 2). The rates did not change by year periods of the birth. All the patients were comprised in 27 families. Consanguinity up to second cousin mating was observed in 5 pairs of the parents (Table 3). Consanguinity rate was 18.5~ and the coefficient of inbreeding was 0.0092. According to the family patterns of the patients, 4 mothers were definite carriers, whereas 3 were probable and the remaining 20 were possible carriers. Fukuyama-type congenital muscular dystrophy A total of 16 patients were classified as having congenital myopathies. Eleven of the 16 patients, 5 males and 6 females, belonged to the group of Fukuyama-type congenital muscular dystrophy. Clinically, (1) all the patients were unable to walk alone, (2) muscular weakness were severe and proximally dominant, (3) facial muscular involvement, joint contractures and severe mental retardation were noted in all the patients. The geographical distribution of 11 patients revealed no particular pattern. Ten of 11 patients were aged from 5 to 19. Incidence of this group among a total of 178,457 population aged between 5 and 19 (born in 1956-1970) was 5.60 10-5 or about 1 in 18,000 youths (Table 4). All the patients were comprised in 7 famiiies. Consanguinity up to second cousin mating or more was observed in 2 pairs of parents (Table 3). Consanguinity rate was 29.6~ obviously elevated than the proportion in control parents from the same

46 K. TAKESHITA et al. Table 4. Incidence of Fukuyama type congenital muscular dystrophy among live-births between 1956-1970. Year of birth No. of live-births No. of patients (male:female) Incidence rate (10-5) 1956-1960 52,296 5 (3:2) 956 1961-1965 58,285 4 (0 : 4) 686 1966-1970 67, 876 1 (1 : 0) 179 Total 178, 457 10 (4 : 6) 560 population. Of a total of 18 sibs in 7 families 11 were patients. Segregation ratio, which was calculated according to Weinberg's formula, was found to be 0.0364, although its validity was questionable due to a small sample size. DISCUSSION Patterns of Duchenne type as well as Fukuyama type of muscular dystrophy, particularly their frequencies, were evaluated in Shimane Prefecture in Japan. As to the frequency of Duchenne type diversified figures have been published. A low incidence, namely 1 in 100,000 live births i.e., 1 in 50,000 live-born male infants, Was mentioned by Pearson (1973). Morton and Chung (1959) estimated the incidence for Wisconsin to be 1 in 3,000 live births. A similar figure can be computed from the studies of Stephens and Tyler of Utah (1951). Zellweger and Antonik (1975) also found 1 case in 3,300 male live births. In Japan, Miyazaki (1963) estimated the prevalence rate for Fukuoka City to be 4 x 10-5, which was similar to those from the studies of WaRon (1955). From records in the many public hospitals, Araki (1967) estimated the prevalence rate of progressive muscular dystrophy in Japan to be 2.6-5.5 x 10-5, of which 44.5~ had Duchenne muscular dystrophy. According to our work in Shimane Prefecture, the incidence of Duchenne muscular dystrophy was 20.8 x 10-5 or about 1 in 4,800 male youths. Assuming that all patients under the age of 19 had survived the disease, the estimates might be similar to the incidence among male live births. Duchenne muscular dystrophy is generally considered to be inherited as an X- linked recessive trait. HoWever, there have been a few reports of cases purportedly transmitted by an autosomal recessive gene. Miyoshi et al. (1975) estimated from their pooled data that X-linked recessive, new mutation and autosomal recessive types occurred with the proportion roughly 68 : 25 : 14. The consanguinity rate of 18.5~ encountered in the parents of our Duchenne patients was remarkably higher than 6.3~ in the control families. This may probably indicate that simple recessive cases were included in our material which were indistinguishable from X-linked Duchenne patients. Congenital muscular dystrophy reported by Fukuyama et al. (1960) is the most common type of congenital dystrophies observed in Japan. This is characterised

SURVEY OF MUSCULAR DYSTROPHY 47 by (1) transmission by an autosomal recessive gene, (2) slow progression, (3) proximal muscular weakness with facial muscular involvement, (4) early onset of joint cotractures, and (5) frequent mental retardation. All the patients so diagnosed in Shimane Prefecture exhibited typical picture of this group. Its incidence rate was estimated as 5.60 x 10-5 or about 1 in 18,000 youths, but as some patients might posssibly died without surviving until the age of 5, this figure is considered to be low. No data pertaining to the frequency of this disease was reported thus far. The consanguinity rate of 28.6~ in Fukuyama type was remarkably higher. The both sexes were nearly equally affected, and although acceptable segregation ratio was not available, there was little doubt that an autosomal recessive pattern of inheritance was involved in these patients. Based on records in many public hospitals, Kondo et al. (1974) made a genetic analysis of the disease and accepted the stated pattern of inheritance. They estimated the gene frequency of this type to be 0.94-1.56~. REFERENCES Araki, S. 1967. Myopathy in Japan. Special Issue of the 17th Annual Meeting of Japanese Society of Medicine, Vol. 4, pp. 1014-1015 (in Japanese). Fukuyama, Y., Kawazura, M and Haruna, H. 1960. A peculiar form of congenital progressive muscular dystrophy. Paediatr. Univ. Tokyo 4: 5-8. Kondo, K., Segawa, M and Fukuyama, Y. 1974. Genetics of congenital muscular dystrophy (Fukuyama). The 16th Annual Meeting of the Japanese Society of Pediatric Neurology. Miyazaki, T. 1963. A epidemiological, genetic and clinical study on the progressive muscular dystrophies. Fukuoka Acta Medica 54: 1007-1038. Miyoshi, K., Tada, Y., Sasaki, N., Iwasa, M. and Kawai, H. 1975. Genetics of muscular dystrophy. Neurol. Med. 3:113-122 (in Japanese). Morton, N. E. and Chung, C. S. 1959. Formal genetics of muscular dystrophy. Am. J. Human Genet. 11: 360-366. Pearson, C. M. 1973. Childhood pseudohypertrophic muscular dystrophy. In Birth Defects, Atlas and Compendium (D. Bergsma, ed.), Williams & Wilkins Co., Baltimore, p. 257. Stephens, F. E. and Tyler, F. H. 1951. Studies in disorders of the muscle. Am. J. Human Genet. 3: 111-116. Walton, J. N. and Gardner-Medwin, D. 1969. Progressive muscular dystrophy and the myotonic disorders. In Disorders of Voluntary Muscle (J. N. Walton, ed.), 2nd. ed., Churchill, London, p. 455. Walton, J. N. 1955. On the inheritance of muscular dystrophy. Ann. Human. Genet. 20: 1-7. Zellweger, H. and Antonik, A. 1975. Newborn screening for Duchenne muscular dystrophy. Pediatrics 55: 30-34.