Search results for "Anhidrosis"

showing 6 items of 6 documents

Botulinum toxin A (Botox) and sweating-dose efficacy and comparison to other BoNT preparations.

2004

Abstract Background Botulinum toxin type A (BoNT/A) is 20–50 times more effective than Botulinum toxin type B (BoNT/B) concerning the treatment of muscular hypercontractions [Sloop, R.R., Cole, B.A., Escutin, R.O., 1997. Human response to botulinum toxin injection: type B compared with type A. Neurology 49, 189–194]. Botulinum toxins block motor nerves as well as autonomic fibres [Rand, M.J., Whaler, B.C., 1965. Impairment of sympathetic transmission by botulinum toxin. Nature 206, 588–591]. Objective Purpose of this study was to analyse the dose dependent reduction of sweating using the BoNT/A preparation Botox® and to compare the results with our earlier results analysing Dysport® [Braune…

AdultMalemedicine.medical_specialtyBotulinum ToxinsTime FactorsInjections SubcutaneousSweatingBotulinum toxin aCellular and Molecular NeuroscienceMedicineHumansBotulinum toxin type BAnhidrosisBotulinum Toxins Type AHypohidrosisDose-Response Relationship DrugEndocrine and Autonomic Systemsbusiness.industryStarchBotulinum toxinSurgerySudomotorDose–response relationshipThreshold doseNeuromuscular AgentsAnesthesiaFemaleNeurology (clinical)medicine.symptombusinessBotulinum toxin typemedicine.drugFollow-Up StudiesAutonomic neuroscience : basicclinical
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Heterotopic ossifications and Charcot joints: Congenital insensitivity to pain with anhidrosis (CIPA) and a novel NTRK1 gene mutation

2018

Abstract Congenital insensitivity to pain with anhidrosis (CIPA), also known as hereditary sensory and autonomic neuropathy type IV (HSAN-IV), is a rare and severe autosomal recessive disorder. We report on an adult female patient whose clinical findings during childhood were not recognized as CIPA. There was neither complete anhidrosis nor a recognizable sensitivity to heat. Tumorlike swellings of many joints and skeletal signs of Charcot neuropathy developed in adolescence which, together with a history of self-mutilation, led to a clinical suspicion of CIPA confirmed by identification of a novel homozygous variant c.1795G > T in the NTRK1 gene in blood lymphocytes. Both parents were hete…

AdultPremature Stop Codonmedicine.medical_specialtyPainmedicine.disease_causeYoung AdultCongenital insensitivity to pain with anhidrosisHereditary sensory and autonomic neuropathyGeneticsmedicineHumansGenetic Predisposition to DiseaseReceptor trkAAnhidrosisGenetics (clinical)HypohidrosisMutationAdult femalebusiness.industryOssification HeterotopicGeneral MedicineEuropean populationNTRK1 Genemedicine.diseaseDermatologyFemaleArthropathy Neurogenicmedicine.symptombusinessEuropean Journal of Medical Genetics
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Cutaneous complications of Anderson-Fabry disease.

2013

Anderson-Fabry disease is an X-linked lysosomal storage disorder caused by a defect in the -galactosidase A gene, which leads to the deficiency of the hydrolytic enzyme -galactosidase A. The consequent inability to catabolize glycosphingolipids causes progressive accumulation of globotriaosylceramide in the vascular endothelium throughout the body. Fatalities in the classical phenotype may usually occur as a consequence of cerebral, cardiac or renal disease. Dermatological manifestations are a relevant feature of Fabry disease and include angiokeratomas, telangiectasiae, lymphedema, anhidrosis or hypohidrosis and pseudo-acromegalic facial appearance. The actual causal treatment for Fabry …

MalePathologymedicine.medical_specialtySkin NeoplasmsGlobotriaosylceramideDiseaseDiagnosis Differentialchemistry.chemical_compoundDrug DiscoverymedicineHumansAge FactorEnzyme Replacement TherapySkin NeoplasmAnhidrosisSkinPharmacologySex CharacteristicsVascular diseasebusiness.industryAge FactorsEnzyme replacement therapySex Characteristicmedicine.diseaseFabry diseaseAngiokeratomaLymphedemachemistryalpha-GalactosidaseFabry DiseaseFemalemedicine.symptombusinessHumanAngiokeratomaCurrent pharmaceutical design
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Botulinum Toxin Type B Blocks Sudomotor Function Effectively: A 6 Month Follow Up

2003

This study analyzes the suppression of sweat gland activity by botulinum toxin type B. We injected botulinum toxin type B (between 2 and 1000 mouse units subcutaneously) in the lateral side of both lower legs in 15 healthy volunteers. Sweat tests were carried out before botulinum toxin type B injections, and at 3 wk, 3 mo, and 6 mo. We studied focal anhidrosis by iodine–starch staining and by capacitance hygrometry after carbachol iontophoresis, according to the quantitative sudomotor axon reflex test (QSART). Iodine starch staining indicated that a threshold dose of 8 mouse units botulinum toxin type B leads to anhidrotic skin spots (>4 cm2) after 3 wk. Duration of anhidrosis was prolonged…

Malemedicine.medical_specialtyCarbacholBotulinum ToxinsSweatingDermatologyBiochemistrySWEATSweat glandInternal medicinemedicineHumansHyperhidrosisAnhidrosisBotulinum Toxins Type AMolecular BiologyHypohidrosisLegIontophoresisStaining and Labelingbusiness.industryHyperhidrosisautonomic nervous systemStarchCell BiologySweat GlandsSudomotorEndocrinologymedicine.anatomical_structureAxon reflexFemalemedicine.symptombusinessiodine starch stainingbotulinum toxin Bmedicine.drugFollow-Up StudiesIodineJournal of Investigative Dermatology
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Mecanismo de activación del receptor de neurotrofinas TrkA

2022

234 págs, figuras y tablas

UNESCO::CIENCIAS DE LA VIDA::Biología moleculartropomyosin receptor kinase (TrkA):CIENCIAS DE LA VIDA::Neurociencias [UNESCO]UNESCO::CIENCIAS DE LA VIDA::Biología celularCongenital insensitivity to pain with anhidrosis (CIPA):CIENCIAS DE LA VIDA::Biología molecular [UNESCO]nerve growth factor (NGF)Neurotrofinasneurotrofinas:CIENCIAS DE LA VIDA::Biología celular [UNESCO]Nerve growth factor (NGF)UNESCO::CIENCIAS DE LA VIDA::NeurocienciasTropomyosin receptor kinase (TrkA)p75 neurotrophin receptor
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Psychiatrische und neuropsychologische Auffälligkeiten bei Patienten mit Morbus Fabry: Literaturübersicht

2005

Fabry Disease (FD) is an X-linked lysosomal storage disorder (prevalence about 1 : 100 000) caused by a genetic defect associated with a lack of alpha-galactosidase A (alpha-GAL) enzyme activity. As a consequence, neutral glycosphingolipides can not be cleaved and metabolized, and accumulate in lysosomes of several tissues, particularly in vascular endothelium and smooth muscle cells. The most prominent symptoms comprise pain attacks and acroparesthesia, angiokeratoma, corneal opacity, renal and cardiac dysfunction, hypo- and anhidrosis, gastrointestinal symptoms, and cerebrovascular dysfunction with vertigo, headache, and cerebral ischemia. Characteristic symptoms of FD can occur in male a…

medicine.medical_specialtyPathologybiologyEndotheliumbusiness.industryIschemiabiology.organism_classificationmedicine.diseaseFabry diseasePathophysiologyAngiokeratomaPsychiatry and Mental healthmedicine.anatomical_structureNeurologyVertigoInternal medicinemedicineCardiologyNeurology (clinical)Differential diagnosisAnhidrosismedicine.symptombusinessFortschritte der Neurologie · Psychiatrie
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