Search results for "Hereditary"

showing 10 items of 650 documents

Aplasia of the retinal vessels combined with optic nerve hypoplasia, neonatal epileptic seizures, and lactic acidosis due to mitochondrial complex I …

1992

A newborn male with mitochondrial complex I deficiency suffered from neonatal epileptic seizures, which later developed into infantile spasms. The infant was blind due to aplasia of the retinal vessels and hypoplasia of the optic nerve. There was congenital lactic acidosis, which persisted in later life. The boy was microcephalic and retarded. Muscular hypotonia later shifted to spasticity. Succinic acid was increased in urine. We assume that the aplasia of the retinal vessels is due to damage of the retinal ganglion cells caused by the mitochondrial disease in the first 3 to 4 months of pregnancy.

Malecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyCongenital lactic acidosisRetinal ganglionInternal medicineMedicineHumansNADH NADPH OxidoreductasesOptic nerve hypoplasiaRetinaElectron Transport Complex IEpilepsybusiness.industryInfant NewbornBrainRetinal VesselsOptic NerveAplasiamedicine.diseaseHypoplasiaMitochondriabody regionsEndocrinologymedicine.anatomical_structureLactic acidosisPediatrics Perinatology and Child HealthOptic nerveAcidosis LacticbusinessTomography X-Ray ComputedEuropean journal of pediatrics
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Patient-reported impact of Charcot-Marie-Tooth disease: protocol for a real-world digital lifestyle study

2021

Abstract Background Charcot-Marie-Tooth disease (CMT) is a rare, chronic, progressive motor and sensory neuropathy that affects the peripheral nervous system, leading to progressive, predominantly distal muscle weakness, atrophy, sensory loss and progressive limb dysfunction. As with many rare diseases, there is a lack of patient-reported data with which to understand and address patient needs. This study aims to explore the real-world impact of CMT from the patient perspective. Methods This is a prospective, digital lifestyle study of at least 2,000 people with CMT, >18 years, resident in the following countries: France, Germany, Italy, Spain, the UK and the USA. Participants will be re…

Malecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyDemographicsDiseaseUnmet needs03 medical and health sciencesTooth disease0302 clinical medicinePhysical medicine and rehabilitationCharcot-Marie-Tooth DiseaseMedicineHumans030212 general & internal medicineobservationalPatient Reported Outcome MeasuresProspective StudiesLife StyleSelection (genetic algorithm)Protocol (science)business.industryIdentifierpatient-reported outcomesinternationalburden of illnessObservational studyFemaleNeurology (clinical)business030217 neurology & neurosurgery
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ABO Blood Group and Inhibitor Risk in Severe Hemophilia A Patients: A Study from the Italian Association of Hemophilia Centers

2021

AbstractConsidering the profound influence exerted by the ABO blood group system on hemostasis, mainly through the von Willebrand factor and factor VIII (FVIII) complex, we have conducted a study evaluating the possible role of blood type on the risk of inhibitor development in hemophilia A. A total of 287 consecutive Caucasian patients with severe hemophilia A (202 without FVIII inhibitors and 85 with FVIII inhibitors) followed at seven Italian Hemophilia Treatment Centers belonging to the Italian Association of Hemophilia Centers (AICE) were included in the study. A higher prevalence of O blood group was detected in patients without inhibitors as compared in inhibitor patients (55 vs. 30.…

Malecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyHemophilia ASevere hemophilia AABO Blood-Group SystemVon Willebrand factorhemic and lymphatic diseasesInternal medicineABO blood group systemABO blood group; hemophilia; inhibitors; risk factorshemophiliainhibitorsHumansMedicinerisk factorsIn patientBlood typebiologybusiness.industryABO blood groupHematologyinhibitorItalyHemostasisbiology.proteinFemaleCardiology and Cardiovascular Medicinebusiness
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The risk of recurrent cardiovascular events in patients with increased plasma homocysteine levels is reduced by short but not long-term therapy with …

2006

Hyperhomocysteinemia is considered an independent risk factor for atherosclerosis, atherothrombosis and Venous ThromboEmbolism (VTE) [1], [2] and [3]. Normal total plasma homocysteine concentrations range from 5 to 15 μmol/L in the fasting state. Hyperhomocysteinemia is classified as moderate (homocysteine concentration, 15 to 30 μmol/L), intermediate (> 30 to 100 μmol/L), and severe (> 100 μmol/L) on the basis of concentrations measured during fasting. Although severe hyperhomocysteinemia is rare, mild hyperhomocysteinemia occurs in approximately 5% to 7% of the general population. In this case, patients are typically asymptomatic until the third or fourth decade of life when premature Cor…

Malecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyHyperhomocysteinemiaTime FactorsHomocysteinePopulationHyperhomocysteinemiaGastroenterologyAsymptomaticchemistry.chemical_compoundFolic AcidRecurrenceRisk FactorsInternal medicineMedicineHumansIn patientRisk factoreducationHomocysteineAgededucation.field_of_studybusiness.industrynutritional and metabolic diseasesHematologyMiddle Agedmedicine.diseaseB vitaminsEndocrinologyTreatment OutcomechemistryCardiovascular DiseasesVitamin B ComplexPlasma homocysteineFemalemedicine.symptombusinessThrombosis research
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Missense mutations in the coagulation factor XII (Hageman factor) gene in hereditary angioedema with normal C1 inhibitor.

2006

Hereditary angioedema is characterized by recurrent skin swelling, abdominal pain attacks, and potentially life-threatening upper airway obstruction. The two classic types are both caused by mutations within the complement C1 inhibitor gene. A recently described new type does not show a deficiency of C1 inhibitor and affects almost exclusively women. We screened twenty unrelated index patients with this new type of hereditary angioedema for mutations in the coagulation factor XII gene. Two different missense mutations were identified in exactly the same position within exon 9 of the F12 gene. 'Mutation 1' (1032C-->A), encountered in five patients, predicts a threonine-to-lysine substitution…

Malemedicine.medical_specialtyGenetic LinkageBiophysicsMutation MissenseCoagulation Factor XIImedicine.disease_causeBiochemistryC1-inhibitorInternal medicinemedicineMissense mutationHumansHereditary Angioedema Type IIIAngioedemaMolecular BiologyMutationFactor XIIAngioedemabiologyChemistryCell Biologymedicine.diseasePedigreeEndocrinologyHereditary angioedemaImmunologyFactor XIIbiology.proteinFemalemedicine.symptomComplement C1 Inhibitor ProteinBiochemical and biophysical research communications
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A new heterozygous mutation (L338N) in the human Gsalpha (GNAS1) gene as a cause for congenital hypothyroidism in Albright's hereditary osteodystroph…

2003

OBJECTIVE: To identify the molecular defect by which psychomotor retardation is caused in two brothers with congenital hypothyroidism who received adequate treatment with l-thyroxine. CASE REPORT: A six-year-old boy presented with psychomotor retardation and congenital primary hypothyroidism (CH). The patient had a normal blood thyrotrophin (TSH) level on neonatal screening, but low total serum thyroxine and triiodothyronine concentrations prompting thyroid hormone substitution shortly after birth. Nevertheless, psychomotor development was retarded and the patient underwent further investigation. Typical features of Albright's hereditary osteodystrophy (AHO) such as round face, obesity, and…

Malemedicine.medical_specialtyHeterozygoteGenotypeEndocrinology Diabetes and MetabolismThyrotropinFibrous Dysplasia PolyostoticEndocrinologyHypothyroidismInternal medicinemedicineGTP-Binding Protein alpha Subunits GsHumansOsteodystrophyChildAlbright's hereditary osteodystrophyPseudohypoparathyroidismPsychomotor retardationbusiness.industryThyroidErythrocyte MembranePrimary hypothyroidismGeneral MedicineSequence Analysis DNAmedicine.diseaseCongenital hypothyroidismPedigreeThyroxineEndocrinologymedicine.anatomical_structureMutationTriiodothyroninePseudopseudohypoparathyroidismCalciummedicine.symptomMetacarpusPsychomotor DisordersbusinessEuropean journal of endocrinology
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Hereditary Angioedema with Normal C1 Inhibitor

2013

Until recently it was assumed that hereditary angioedema was a disease that results exclusively from a genetic deficiency of the C1 inhibitor. In 2000, families with hereditary angioedema, normal C1 inhibitor activity, and protein in plasma were described. Since then, numerous patients and families with that condition have been reported. Most of the patients were women. In many of the affected women, oral contraceptives, hormone replacement therapy containing estrogens, and pregnancies triggered the clinical symptoms. In some families mutations in the coagulation factor XII (Hageman factor) gene were detected.

Malemedicine.medical_specialtyImmunologyCoagulation Factor XIIC1-inhibitorDiagnosis DifferentialPregnancyRisk FactorsInternal medicinemedicineHumansImmunology and AllergyHereditary Angioedema Type IIIAngioedemaFactor XIIbiologyAngioedemabusiness.industryAngioedemas Hereditarymedicine.diseaseEndocrinologyTransgender hormone therapyFactor XIIMutationHereditary angioedemabiology.proteinFemaleDifferential diagnosismedicine.symptombusinessComplement C1 Inhibitor ProteinImmunology and Allergy Clinics of North America
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Corneo-scleral contact lenses in an uncommon case of keratoconus with high hyperopia and astigmatism

2017

Purpose: To analyse the visual quality achieved by fitting corneo-scleral contact lenses (CScL) in an uncommon case of bilateral keratoconus, high hyperopia and astigmatism. Methods: A 45-year-old man presented for eye examination due to the unsatisfactory quality of his vision wearing soft toric contact lenses. He presented high hyperopia and astigmatism with bilateral keratoconus. He was fitted with CScL to correct his irregular astigmatism and ocular aberrations. A diagnostic trial set was used in the fitting process and he was assessed according to standardised fitting methodology. Visual acuity, corneal topography, biometry and ocular aberrations were evaluated. The follow-up period wa…

Malemedicine.medical_specialtyKeratoconusCorneal Wavefront AberrationVisual acuityCorneal ectasiagenetic structuresContact LensesVisual AcuityAstigmatismKeratoconusCornea03 medical and health sciences0302 clinical medicineProsthesis FittingOphthalmologyCorneamedicineHumansHigh orderIrregular astigmatismmedicine.diagnostic_testbusiness.industryAstigmatismCorneal TopographyEye Diseases HereditaryCorneoscleral contact lensGeneral MedicineMiddle Agedmedicine.diseaseCorneal topographyeye diseasesOphthalmologyHyperopiamedicine.anatomical_structureEye examination030221 ophthalmology & optometrysense organsmedicine.symptombusinessSclera030217 neurology & neurosurgeryOptometry
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Prognostic Role of Late Gadolinium Enhancement in Patients With Hypertrophic Cardiomyopathy and Low-to-Intermediate Sudden Cardiac Death Risk Score

2019

Sudden cardiac death (SCD) is the most life-threating complication of hypertrophic cardiomyopathy. Guidelines of the European Society of Cardiology (ESC) suggest the implantation of an implantable cardioverter defibrillator in primary prevention according to a 5-year risk SCD score >= 6%. The aim of the study is to evaluate the prognostic role of late gadolinium enhancement (LGE) in patients with a 5-year risk SCD score <6%. In this multicenter study, we performed cardiac magnetic resonance in 354 consecutive hypertrophic cardiomy-opathy patients (257 males, range of age 54 +/- 17) with a risk SCD score <6% (302 with <4% and 52 with >= 4 and <6% risk). Hard cardiac events,…

Malemedicine.medical_treatmentLeftCardiomyopathyContrast MediaGadolinium030204 cardiovascular system & hematologyVentricular Function Left030218 nuclear medicine & medical imagingSudden cardiac death0302 clinical medicineRisk Factorshemic and lymphatic diseasesVentricular FunctionFramingham Risk Scoremedicine.diagnostic_testIncidenceHypertrophic cardiomyopathyMiddle AgedImplantable cardioverter-defibrillatorPrognosisMagnetic Resonance ImagingHypertrophic Cardiomyopathy Sudden Cardiac Death.DeathSurvival RateItalyCineCardiologyFemaleCardiology and Cardiovascular MedicineCardiaccongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyCardiomyopathyHeart VentriclesMagnetic Resonance Imaging CineRisk Assessment03 medical and health sciencesInternal medicinemedicineHumanscardiovascular diseasesRetrospective Studiesbusiness.industryMyocardiumMagnetic resonance imagingRetrospective cohort studyCardiomyopathy HypertrophicCardiomyopathy Hypertrophic; Contrast Media; Death Sudden Cardiac; Female; Follow-Up Studies; Gadolinium; Heart Ventricles; Humans; Incidence; Italy; Magnetic Resonance Imaging Cine; Male; Middle Aged; Myocardium; Prognosis; ROC Curve; Retrospective Studies; Risk Assessment; Risk Factors; Survival Rate; Ventricular Function Leftmedicine.diseaseSuddenSudden cardiac deathDeath Sudden CardiacROC CurveHypertrophicComplicationbusinessFollow-Up Studies
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Overlapping phenotypes between SHORT and Noonan syndromes in patients with PTPN11 pathogenic variants

2020

Overlapping syndromes such as Noonan, Cardio-Facio-Cutaneous, Noonan syndrome (NS) with multiple lentigines and Costello syndromes are genetically heterogeneous conditions sharing a dysregulation of the RAS/mitogen-activated protein kinase (MAPK) pathway and are known collectively as the RASopathies. PTPN11 was the first disease-causing gene identified in NS and remains the more prevalent. We report seven patients from three families presenting heterozygous missense variants in PTPN11 probably responsible for a disease phenotype distinct from the classical Noonan syndrome. The clinical presentation and common features of these seven cases overlap with the SHORT syndrome. The latter is the c…

Malemusculoskeletal diseases0301 basic medicineMAPK/ERK pathwaycongenital hereditary and neonatal diseases and abnormalitiesMAP Kinase Signaling SystemProtein Tyrosine Phosphatase Non-Receptor Type 11030105 genetics & heredityBiologyGene productPhosphatidylinositol 3-Kinases03 medical and health sciencesMetabolic DiseasesGeneticsmedicineHumansMissense mutationskin and connective tissue diseasesProtein kinase BGrowth DisordersGenetics (clinical)GeneticsGenetic heterogeneityNoonan SyndromeGenetic Variationmedicine.diseasePTPN11NephrocalcinosisPhenotype030104 developmental biologySHORT syndromeHypercalcemiaNoonan syndromeFemaleMitogen-Activated Protein KinasesSignal TransductionClinical Genetics
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