Searches / Genetic Counseling (Geneva, Switzerland)[JOURNAL]

Genetic Counseling (Geneva, Switzerland)[JOURNAL]

Sun 200 papers
RSS

UHL'S ANOMALY AS A PART OF VACTERL ASSOCIATION.

Ertugrul I, Dogan V, Beken S … +4 more , Ozgur S, Okumuş N, Orün UA, Karademir S

Genet Couns · 2015 · PMID 26349203

Abstract loading — click title to view on PubMed.

PRENATAL DIAGNOSIS OF ISOLATED SCOLIOSIS WITH DOWN SYNDROME.

Arisoy R, Demirci O, Erdogdu E … +3 more , Pekin O, Kumru P, Aydin H

Genet Couns · 2015 · PMID 26349202

Abstract loading — click title to view on PubMed.

TURNER SYNDROME WITH 45,X/46,X,I(Xq)/47,X,I(Xq),I(Xq) KARYOTYPE.

Gorukmez O, Sag SO, Gulten T … +3 more , Gorukmez, Ture M, Yakut T

Genet Couns · 2015 · PMID 26349201

Abstract loading — click title to view on PubMed.

A TRISOMY 13 CASE PRESENTING WITH CONGENITAL DIAPHRAGMATIC HERNIA AND MICROPHTHALMIA.

Sahin S, Kutman KH, Bozkurt O … +6 more , Canpolat FE, Uras N, Oguz SS, Topcu V, Ozdemir O, Dilmen U

Genet Couns · 2015 · PMID 26349200

Abstract loading — click title to view on PubMed.

NOVEL MUTATION OF THE ELECTRON TRANSFERRING FLAVOPROTEIN DEHYDROGENASE (ETFDH) GENE IN THE ISOLATED MYOPATHIC FORM OF COENZYME q10 DEFICIENCY.

Gorukmez O, Gorukmez O, Sag SO … +3 more , Erdol S, Saglam H, Yakut T

Genet Couns · 2015 · PMID 26349199

Abstract loading — click title to view on PubMed.

CO-OCCURRENCE OF NEURAL TUBE DEFECT, THORACAL DEFECT AND OMPHALOCELE: A RARE CASE AND REVIEW OF THE LITERATURE.

Aydin BH, Arisoy R, Simsek H … +4 more , Erdogdu E, Geckinli B, Karaman A, Demirci O

Genet Couns · 2015 · PMID 26349198

Abstract loading — click title to view on PubMed.

THE SPECTRUM OF CLINICAL FEATURES ASSOCIATED WITH KLIPPEL-TRENAUNAY-WEBER SYNDROME.

Sahin ON, Atik T, Coğulu O … +1 more , Ozkinay F

Genet Couns · 2015 · PMID 26349197

Abstract loading — click title to view on PubMed.

PRENATAL DIAGNOSIS OF DE NOVO PERICENTRIC INVERSION INV(2)(p11.2z13).

Yakut S, Cetin Z, Sanhal C … +3 more , Karaman B, Mendilcioglu I, Karauzum SB

Genet Couns · 2015 · PMID 26349196

We here report a prenatal case with de novo pericentric inversion inv(2)(p11.2q13). A 20-years-old G1PO woman was referred for amniocentesis at 17 weeks of gestation, because of a positive second trimester screening test... We here report a prenatal case with de novo pericentric inversion inv(2)(p11.2q13). A 20-years-old G1PO woman was referred for amniocentesis at 17 weeks of gestation, because of a positive second trimester screening test for aneuploidy. A de novo pericentric inversion inv(2)(p11.2q13) was detected during conventional cytogenetic analysis. Array-CGH analysis of the fetus showed no subtle chromosomal imbalances at the breakpoints. Genetic counseling was given to the family and the family decided to continue the pregnancy. To our knowledge, our case is the third prenatally detected de novo case with inv(2)(p11.2q13), and also the first case in which molecular karyotyping analysis were also applied.

A VARIANT CASE OF 6p24 DELETION SYNDROME (OMIM #612582).

Ergin RN, Cigerciogullari E, Alanay Y … +1 more , Yayla M

Genet Couns · 2015 · PMID 26349195

The 6p24 deletion syndrome, a contiguous gene deletion syndrome is characterized by a wide spectrum of clinical presentations. In this case report we present an antenatal case of 6p 24 deletion syndrome variant involving... The 6p24 deletion syndrome, a contiguous gene deletion syndrome is characterized by a wide spectrum of clinical presentations. In this case report we present an antenatal case of 6p 24 deletion syndrome variant involving FOXC1 gene. First trimester fetal screening of a 34 year old pregnant female revealed ultrasonographic anomalies and chorionic villus sampling was performed to rule out any chromosomal anomaly. Cytogenetic examination resulted in normal 46,XY karyotype. In the following weeks further anomalies like cleft palate/lip, thick nuchal fold, ventral septal defect and low set ear were detected with ultrasonography. At 20 weeks of gestation, amniocentesis and whole genome array-CGH analysis revealed a 9.6 Mb interstitial deletion in the 6p25.2p24.1 region which has many genes including an important gene, FOXC1 and 119 Kb interstitial deletion at 9q22.31. The pregnancy was terminated. Postmortem morphological examination revealed turricephaly, hypertelorism, depressed nasal bridge, broad nasal tip, left sided cleft lip, low-set small ears, micrognathia, short neck, increased nuchal fold, short broad distal phalanges, broad thumbs, broad halluces and broad toes.

MEGALENCEPHALIC LEUKOENCEPHALOPATHY WITH SUBCORTICAL CYSTS WITH HOMOZYGOUS MUTATION (C.448DELC, P.LEU150 SER FSX11) ON EXON 6 OF MLC1 GENE.

Soysal Z, Okur M, Eroz R … +3 more , Gun E, Kocabay K, Besir FH

Genet Couns · 2015 · PMID 26349194

MLC or Van der Knaap disease is a rare entity, a rare and genetically heterogeneous cerebral white matter disease. It is characterized by the presence of macrocephaly, epilepsy and a slowly progressive spastic cerebellar... MLC or Van der Knaap disease is a rare entity, a rare and genetically heterogeneous cerebral white matter disease. It is characterized by the presence of macrocephaly, epilepsy and a slowly progressive spastic cerebellar syndrome. It is an autosomal recessive disease caused from mutations of MLC1 gene. In the current case report, a case with MLC who had a homozygous mutation (c.448delC, p.Leul50 ser fsX11) on exon 6 of MLC1 gene is presented.

RECURRENCE OF POMPE DISEASE IN FIRST COUSINS.

Lacombe D, Thambo JB, Fayon M … +2 more , Goizet C, Guffon N

Genet Couns · 2015 · PMID 26349193

We report on the cases of two first-degree non-consanguineous cousins with infantile-onset Pompe disease, a rare autosomal recessive disease. The first patient developed cardiorespiratory failure at age 1 year. When she... We report on the cases of two first-degree non-consanguineous cousins with infantile-onset Pompe disease, a rare autosomal recessive disease. The first patient developed cardiorespiratory failure at age 1 year. When she was 4 her male cousin developed hypotonia during his first month of life. Both infants had cardiac hypertrophy at diagnosis and shared the c.1927G>A missense mutation. Since a first degree cousin of an affected patient has 50 times the risk of developing the disease compared with unrelated infants and since cardiac hypertrophy is constant in affected infants, the combination of cardiac symptoms with a history of Pompe disease in a first degree cousin leads to a very high probability of having the condition. Clinically oriented screening based on simple diagnostic procedures such as echocardiogram and anamnesis could accelerate the initiation of enzyme replacement therapy of the deficient acid α-glucosidase which is critical to restoring cardiac function in affected infants.

A NOVEL MUTATION IN NPR2 GENE IN A PATIENT WITH ACROMESOMELIC DYSPLASIA, MAROTEAUX TYPE.

Sag SO, Gorukmez O, Topak A … +5 more , Gorukmez O, Ture M, Sahinturk S, Gulten T, Yakut T

Genet Couns · 2015 · PMID 26349192

Acromesomelic dysplasia, Maroteaux type (AMDM) is a rare autosomal recessive disease characterized by disproportionate shortening of skeletal elements, predominantly affecting the middle segments (forearms and forelegs)... Acromesomelic dysplasia, Maroteaux type (AMDM) is a rare autosomal recessive disease characterized by disproportionate shortening of skeletal elements, predominantly affecting the middle segments (forearms and forelegs) and distal segments (hands and feet) of appendicular skeleton. Furthermore it is related to axial skeleton and leads to wedging of vertebral bodies, with shorter dorsal margins than the ventral margins. Bartels et al. defined mutations in NPR2 gene, encoding natriuretic peptide receptor B (NPR-B), underlying Acromesomelic dysplasia, type Maroteaux. We present here molecular and clinical findings of a case with AMDM. In a patient, a novel homozygous mutation c.1435C>T p.R479X in exon 7 of NPR2 gene was found. Further testing confirmed the heterozygous carrier status of the parents. Our findings expand the spectrum of causative mutations in AMDM.

A NEW OBSERVATION OF 13q DELETION SYNDROME: SEVERE UNDESCRIBED FEATURES.

Garcia-Rodriguez E, Garcia-Garcia E, Perez-Sanchez A … +1 more , Pavon-Delgado A

Genet Couns · 2015 · PMID 26349191

A new observation of 13q deletion syndrome: severe undescribed features: 13q deletion syndrome is characterized by a wide phenotypic spectrum resulting from a partial deletion-of the long arm of chromosome 13. It consist... A new observation of 13q deletion syndrome: severe undescribed features: 13q deletion syndrome is characterized by a wide phenotypic spectrum resulting from a partial deletion-of the long arm of chromosome 13. It consists predominantly of mental and motor retardation, craniofacial dysmorphia, growth retardation, and several congenital malformations. We present a new case with 13q deletion syndrome phenotypically characterized by severe major malformations, some of them still undescribed, consisting of left diaphragmatic hernia, right pulmonary sequestration, hypoplastic left heart syndrome, pancreatic agenesis, polysplenia, and catastrophic central nervous system malformations: semilobar holoprosencephaly, occipital myelomeningocele, partial agenesis of the corpus callosum and agenesis of olfactory bulbs. Fluorescence in situ hybridization technique using the probe LSI D13S319 (13q1l4) SO/ LSI 13q34 SG determined partial monosomy of chromosome 13 in 39/100 cells (mosaicism).

INFLAMMATORY BOWEL DISEASE-LIKE PHENOTYPE IN A YOUNG GIRL WITH PROLIDASE DEFICIENCY: A NEW SPECTRUM OF CLINICAL MANIFESTATION.

Kuloglu Z, Kansu A, Serwas N … +4 more , Demir A, Yaman A, Ensari A, Boztug K

Genet Couns · 2015 · PMID 26349190

Prolidase deficiency (PD) is an inherited disorder associated with cutaneous ulcers, intellectual disability, unusual facial appearance, skeletal deformities, hematological anomalies, splenomegaly, and chronic infections... Prolidase deficiency (PD) is an inherited disorder associated with cutaneous ulcers, intellectual disability, unusual facial appearance, skeletal deformities, hematological anomalies, splenomegaly, and chronic infections. We report a girl with PD who presented with early inflammatory bowel disease (IBD). A 2-month-old girl with a dysmorphic face presented with recurrent respiratory tract infections, vomiting, diarrhea and hepatosplenomegaly. She had steatorrhea, abnormal liver enzymes, hypergammaglobulinemia, autoantibody positivity and steatohepatitis in liver biopsy. On follow-up, skin lesions, pruritus and developmental delay were added. At the age of 21 months, IBD was diagnosed with persistent diarrhea, fever, hypoalbuminemia, elevated inflammatory markers, fecal leukocytes and aphthous ulcers in colon. Remission was achieved with prednisone and continued with mesalasine. Thrombocytopenia developed after 3 years. Her findings prompted us to further investigations. PD as the underlying molecular cause of the disease was detected by exome sequencing. In conclusion, PD should be considered in the differential diagnosis of some IBD patients.

DETECTING PORCN MICRODELETIONS IN A LARGE FAMILY WITH FOCAL DERMAL HYPOPLASIA.

Seven M, Güven A, Bozoğlu TM … +1 more , Tolun A

Genet Couns · 2015 · PMID 26349189

Focal dermal hypoplasia (FDH), an X-linked dominant disease with a highly variable phenotype, presents mainly with congenital linear pigmentation of the skin, herniation of fat through the dermal defects and multiple pap... Focal dermal hypoplasia (FDH), an X-linked dominant disease with a highly variable phenotype, presents mainly with congenital linear pigmentation of the skin, herniation of fat through the dermal defects and multiple papillomas. PORCNmicrodeletions are identified in a total of 12 FDH patients to date. Routine molecular methods for detecting microdeletions have proven not to be effective, as patients also carry a normal allele. Additionally, methods using copy number estimations are labor-intensive, time-consuming and require expensive equipment. With respect to the molecular diagnosis of FDH, we aimed to investigate the inheritance of maternal disease allele in a three-generation FDH pedigree with seven affected members by using a simple yet efficient method. The strategy used in this study appeared to have the benefit of detecting all PORCN micro-deletions identified for FDH so far. The family with the largest number of related patients reported to date presented an opportunity to evaluate clinical variability, which was high, with the least affected and the most severely affected patients being half-sisters. The extensive intra-familial phenotypic variability observed in this FDH family suggests that genetic counselling should be part of management of this syndrome even in a family with a very mild case. The unique finding of IgA deficiency in the most severe case indicated that the feature could be a new characteristic of FDH.

CLINICAL VARIABILITY IN TWO SISTERS WITH KEUTEL SYNDROME DUE TO A HOMOZYGOUS MUTATION IN MGP GENE.

Tüysüz B, Cinar B, Laçiner S … +2 more , Onay H, Mittaz-Crettol L

Genet Couns · 2015 · PMID 26349188

Keutel syndrome (KS) is an autosomal recessive disease characterised by abnormal cartilage calcification, brachytelephalangism, peripheral pulmonary artery stenosis, hearing loss and midface retrusion. KS is caused by ho... Keutel syndrome (KS) is an autosomal recessive disease characterised by abnormal cartilage calcification, brachytelephalangism, peripheral pulmonary artery stenosis, hearing loss and midface retrusion. KS is caused by homozygous mutations in MGP, a gene encoding Matrix Gla protein which acts as a calcification inhibitor in extracellular matrix. We present two Turkish sisters (22 and 13 years old) who had abnormal cartilage calcification, brachytelephalangism, congenital heart defect and chronic asthmatic bronchitis. The patients were homozygous for c.62-2A>G (IVS1-2 A>G) mutation in MGP gene. Abnormal cartilage calcification, brachytelephalangism and midfacial retrusion are the hallmarks of KS. It was observed that the younger sister had striking cartilaginous calcifications, midfacial retrusion and severe brachytelephalangism while her older sister had mild costal cartilaginous calcifications and brachytelephalangism without any midfacial retrusion. Intrafamiliar clinical variability for KS has not been described previously.

MICROARRAY DELINEATION OF DE NOVO DUPLICATION 1q32q42 IN A CHILD SHOWING MULTIPLE ANOMALIES AND DYSMORPHISM.

Gorukmez O, Aydin H, Gorukmez O … +3 more , Sag SO, Kucukcongar A, Celayir FM

Genet Couns · 2015 · PMID 26349187

We present a 9 month-old baby girl with de novo pure interstitial duplication 1q. The girl has dysmorphic craniofacial features as well as neuromotor retardation, multiple subcutaneous solid tissue lesions, urogenital an... We present a 9 month-old baby girl with de novo pure interstitial duplication 1q. The girl has dysmorphic craniofacial features as well as neuromotor retardation, multiple subcutaneous solid tissue lesions, urogenital anomalies, cardiac defect, liver parenchyma heterogeneity and intracranial anomaly. The case of de novo duplication of 1q32q42 defined by G-banding and Microarray Comparative Genomic Hybridization (Microarray CGH) was presented with its clinical findings.

MOLAR TOOTH SIGN AND ACROCALLOSAL SYNDROME--A REPORT ON A POLISH FAMILY AND REVIEW OF KIF7 SYNDROMOLOGY.

Krajewska-Walasek M, Kugaudo M, Jędrzejowska M … +4 more , Cieślikowska A, Ichkou A, Attié-Bitach T, Jezela-Stanek A

Genet Couns · 2015 · PMID 26349186

Acrocallosal syndrome is a multiple congenital anomaly disorder characterized by postaxial and/or preaxial polydactyly, cutaneous syndactyly, macrocephaly, widely spaced eyes, absence or hypoplasia of the corpus callosum... Acrocallosal syndrome is a multiple congenital anomaly disorder characterized by postaxial and/or preaxial polydactyly, cutaneous syndactyly, macrocephaly, widely spaced eyes, absence or hypoplasia of the corpus callosum, and intellectual disability. It was first described by Albert Schinzel as early as in 1979, but the diagnosis of this syndrome still remains challenging. Here we report a family with 2 sibs with acrocallosal syndrome caused by novel mutations in KIF7. They present with features like molar tooth sign and hyperventilation that are not very typical in ACLS, but do occur in other ciliopathies, hence we also discuss the clinical heterogeneity of KIF7-associated disorders.

MULTIPLE CONGENITAL ANOMALIES IN A CHILD WITH 47,XY,+der(8;9)(p10;p10): A CASE REPORT.

Gorukmez O, Gorukmez O, Sag OS … +2 more , Yakut T, Gulten T

Genet Couns · 2015 · PMID 26349185

Complex small supernumerary marker chromosomes (sSMC) constitute one of the smallest subgroups of sSMC in general. Complex sSMC consist of chromosomal material derived from more than one chromosome. We report a complex s... Complex small supernumerary marker chromosomes (sSMC) constitute one of the smallest subgroups of sSMC in general. Complex sSMC consist of chromosomal material derived from more than one chromosome. We report a complex sSMC derived from chromosomes 9 and 8, characterized as der(8;9)(p10;p10) resulting from unbalanced transition of maternal balanced translocation. Besides dysmorphic face and mental-motor retardation, the patient had Dandy-Walker malformation (DWM) in cranial MR also. As far as we are concerned, this is the first complex sSMC case comprising short arms of 8th and 9th chromosomes.

A FEMALE PATIENT WITH DUPLICATION OF 7p13-pter ASSOCIATED WITH DEL 20p13pter RESULTING FROM MALSEGREGATED PATERNAL 7;20 BALANCED TRANSLOCATION.

Eid MO, Eid MM, Kamel AK … +2 more , El-Ruby M, Abdel-Salam GM

Genet Couns · 2015 · PMID 26349184

Duplication of the short arm of chromosome 7 is a genomic disorder presenting with distinctive facies including hypertelorism, large anterior fontanel, and intellectual disability. A 2½-year-old Egyptian girl was referre... Duplication of the short arm of chromosome 7 is a genomic disorder presenting with distinctive facies including hypertelorism, large anterior fontanel, and intellectual disability. A 2½-year-old Egyptian girl was referred because of cleft palate and dysmorphic features. She showed clinical manifestations of duplication of 7p, along with atypical features of corpus callosum hypogenesis and skeletal anomalies. Chromosome analyses revealed unbalanced translocations involving the short arms of chromosomes 7 and 20 due to malsegregation of a paternal balanced translocation 7;20. Fluorescence in situ hybridization analysis (FISH) of the female patient showed partial trisomy 7p and a subtelomeric monosomy 20p. Thus, the karyotype of our patient is 46,XX,der(20) (7pter --> 7p13::20p13 --> 20qter). In this report, we present the clinical phenotype of this patient with duplication of 7p and review the literature.
← Prev Page 6 of 10 Next →

About

Frequency
Sun
Papers found
200
RSS feed
Subscribe