Search results for "Consanguinity"

showing 7 items of 37 documents

Autosomal recessive polycystic kidney disease: case report of a newborn with rare PKHD1 mutation, rapid renal enlargement and early fatal outcome

2020

Abstract Introduction Autosomal recessive polycystic kidney disease (ARPKD; MIM#263200) is one of the most frequent pediatric renal cystic diseases, with an incidence of 1:20,000. It is caused by mutations of the PKHD1 gene, on chromosome 6p12. The clinical spectrum is highly variable, ranging from late-onset milder forms to severe perinatal manifestations. The management of newborns with severe pulmonary insufficiency is challenging, and causes of early death are sepsis or respiratory failure. In cases of massive renal enlargement, early bilateral nephrectomy and peritoneal dialysis may reduce infant mortality. However, there is no conclusive data on the role of surgery, and decision-makin…

Pediatricsmedicine.medical_specialtyGenotype-phenotype correlationGenotypemedicine.medical_treatmentARPKDPulmonary insufficiencyReceptors Cell SurfaceCase ReportPeritoneal dialysisSepsis03 medical and health sciencesLiver diseaseConsanguinity0302 clinical medicineFatal OutcomeNext generation sequencingmedicineHumansGenetic Predisposition to DiseaseEthicPotter sequencePolycystic Kidney Autosomal RecessiveEthicsbusiness.industrylcsh:RJ1-570Infant Newbornlcsh:Pediatricsmedicine.diseaseAutosomal Recessive Polycystic Kidney DiseaseRespiratory failure030220 oncology & carcinogenesisMutationFemalebusiness030217 neurology & neurosurgeryInfant PrematureBilateral NephrectomyPotter sequence
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Lecithin-cholesterol-acyltransferase deficiency: autosomal recessive transmission in a large kindred.

2008

Thirty-four members of a single Sardinian kindred with lecithin-cholesterol-acyltransferase deficiency have been studied. The kindred spans four generations and the parents of the two affected siblings are blood relatives. Segregation of the acyltransferase deficiency gene in the family clearly demonstrated an autosomal recessive mode of inheritance. Thirteen family members, including all obligate heterozygotes, had roughly half-normal acyltransferase activities (mean +/- S.D. = 0.39 +/- 0.06 mU/ml) when compared to 17 intrafamilial controls and spouses (mean +/- S.D. = 0.72 +/- 0.09 mU/ml) and 40 blood donors from Marburg/Lahn (mean +/- S.D. =0.76 +/- 0.1 mU/ml). Characterization of the he…

Plasma lipoproteinMaleHeterozygoteThalassemiaLipoproteinsGenes RecessiveConsanguinityConsanguinityLecithin Cholesterol Acyltransferase DeficiencyGeneticsmedicineHumansGenetics (clinical)GeneticsLecithin cholesterol acyltransferase deficiencybiologyHeterozygote advantagemedicine.diseaseHypolipoproteinemiasPedigreeAcyltransferaseLecithin—cholesterol acyltransferasebiology.proteinThalassemiaFemaleHypolipoproteinemiaClinical genetics
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A homozygous mutation in the TUB gene associated with retinal dystrophy and obesity.

2013

Inherited retinal dystrophies are a major cause of childhood blindness. Here, we describe the identification of a homozygous frameshift mutation (c.1194_1195delAG, p.Arg398Serfs*9) in TUB in a child from a consanguineous UK Caucasian family investigated using autozygosity mapping and whole-exome sequencing. The proband presented with obesity, night blindness, decreased visual acuity, and electrophysiological features of a rod cone dystrophy. The mutation was also found in two of the proband's siblings with retinal dystrophy and resulted in mislocalization of the truncated protein. In contrast to known forms of retinal dystrophy, including those caused by mutations in the tubby-like protein …

ProbandMaleobesity030209 endocrinology & metabolismGenes RecessiveConsanguinityBiologymedicine.disease_causeWhite PeopleFrameshift mutation03 medical and health sciencesConsanguinity0302 clinical medicineRetinitis pigmentosaGeneticsRod-cone dystrophymedicineHomeostasisHumansretinal dystrophyTUBChildEye ProteinsFrameshift MutationGenetics (clinical)030304 developmental biologyAdaptor Proteins Signal TransducingGenetics0303 health sciencesMutationHomozygoteChildhood blindnessciliatubbyChromosome MappingProteinsmedicine.diseaseUnited Kingdom3. Good healthPedigreeBrief ReportsFemaleRetinal DystrophiesRetinitis Pigmentosa
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Autosomal recessive severe dwarfism in a Sicilian girl: a new form of osteodysplastic primordial dwarfism?

1996

A new type of osteodysplastic primordial dwarfism is delineated in a 5- year-old female child with severe growth retardation of prenatal onset, gross skeletal changes, a non-Seckel facial phenotype, and presumed autosomal recessive inheritance.

media_common.quotation_subjectgrowth retardationDwarfismDwarfismGenes RecessiveOsteodysplastic primordial dwarfismBiologyBone and BonesCraniofacial AbnormalitiesConsanguinitymedicineHumansAbnormalities MultipleGirlGenetics (clinical)media_commonGeneticsAutosomal recessive inheritanceGrowth retardationautosomal recessive inheritancemedicine.diseasePrenatal onsetOsteochondrodysplasiaRadiographyChild Preschoolosteodysplastic primordial dwarfismFemalesense organsAmerican journal of medical genetics
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Congenital secondary hypothyroidism caused by exon skipping due to a homozygous donor splice site mutation in the TSHbeta-subunit gene.

2002

Isolated TSH deficiency as a cause for congenital hypothyroidism is relatively uncommon. Even more rare is the identification of mutations in the TSHβ gene, only four of which have been identified. We here report a 4-month-old girl with isolated TSH deficiency born to consanguineous parents. Sequencing of the TSHβ-subunit gene revealed a homozygous G to A transition at position +5 of the donor splice site of intron 2. TSHβ gene transcript could not be obtained from fibroblasts or white blood cells by illegitimate amplification. Thus, to investigate further the mechanism leading to TSH deficiency in this patient, we used an in vitro exon-trapping system. The mutation at position +5 of the do…

medicine.medical_specialtyEndocrinology Diabetes and MetabolismClinical BiochemistryThyrotropinBiologymedicine.disease_causeBiochemistryExonConsanguinityEndocrinologyInternal medicinemedicineCongenital HypothyroidismMissense mutationHumansspliceRNA MessengerGeneGeneticsMutationSplice site mutationBiochemistry (medical)IntronInfantExonsExon skippingEndocrinologyMutationFemaleRNA Splice SitesThe Journal of clinical endocrinology and metabolism
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Newborn hearing-screening project using transient evoked otoacoustic emissions: western sicily experience

2006

Summary Objective To study the incidence of congenital sensorineural hearing loss in all newborns introducing a screen test with a protocol no expensive, with a good “screen sensitivity” that could let an earlier identification of hearing impairment beginning early intervention by 2 months of age and increasing the probability of having language development within the normal range of development. Methods The study was conducted in Sciacca hospital from the beginning of 2003 to our days and was carried out with transient evoked otoacoustic emission using the criteria for PASS or RETEST and considering eventual prenatal and perinatal risk factors. All the newborns were divided into four group…

medicine.medical_specialtymedicine.medical_treatmentHearing Loss SensorineuralOtoacoustic Emissions SpontaneousOtoacoustic emissionNewborn Hearing screeningAudiologyScreen testHearing screeningConsanguinityNeonatal Screeningotorhinolaryngologic diseasesmedicineHumansNormal rangeRehabilitationbusiness.industryIncidence (epidemiology)Hearing TestsIncidenceInfant NewbornGeneral Medicinemedicine.diseaseSettore MED/32 - AudiologiaSettore MED/31 - OtorinolaringoiatriaOtorhinolaryngologySpeech developmentItalyPediatrics Perinatology and Child HealthSensorineural hearing lossbusiness
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Does δ-sarcoglycan-associated autosomal-dominant cardiomyopathy exist?

2009

In this study we clinically and genetically characterize a consanguineous family with a homozygous novel missense mutation in the delta-sarcoglycan gene and a second delta-sarcoglycan mutation that has previously been reported to cause severe autosomal-dominant dilated cardiomyopathy. We identified a novel missense mutation in exon 6 (p.A131P) of the delta-sarcoglycan gene, which in a homozygous state leads to the clinical picture of a limb girdle muscular dystrophy. In four heterozygous carriers for the mutation, aged 3-64 years, a second sequence variant in exon 6 (p.S151A) of the delta-sarcoglycan gene was detected on the other allele. This second missense change had previously been repo…

musculoskeletal diseasesAdultCardiomyopathy DilatedMalemedicine.medical_specialtyAdolescentBiopsyDNA Mutational AnalysisCardiomyopathyMutation MissenseCompound heterozygosityArticleExonConsanguinityElectrocardiographyYoung AdultInternal medicineSarcoglycansGeneticsMedicineMissense mutationHumansMuscular dystrophyChildGenetics (clinical)Genes DominantGeneticsFamily Healthbusiness.industryMusclesMyocardiumDilated cardiomyopathyMiddle Agedmedicine.diseasePedigreeEndocrinologyEchocardiographyChild PreschoolMutation (genetic algorithm)FemalebusinessLimb-girdle muscular dystrophy
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