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[PMID]:27778639
[Au] Autor:Arnold AC; Garland EM; Celedonio JE; Raj SR; Abumrad NN; Biaggioni I; Robertson D; Luther JM; Shibao CA
[Ad] Endereço:Department of Neural and Behavioral Sciences, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033.
[Ti] Título:Hyperinsulinemia and Insulin Resistance in Dopamine ß-Hydroxylase Deficiency.
[So] Source:J Clin Endocrinol Metab;102(1):10-14, 2017 Jan 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Context: Dopamine ß-hydroxylase (DBH) deficiency is a rare genetic disorder characterized by failure to convert dopamine to norepinephrine. DBH-deficient patients lack sympathetic adrenergic function and are therefore predisposed to orthostatic hypotension. DBH-deficient mice exhibit hyperinsulinemia, lower plasma glucose levels, and insulin resistance due to loss of tonic sympathetic inhibition of insulin secretion. The impact of DBH deficiency on glucose homeostasis in humans is unknown. Case Description: We describe the metabolic profile of an adolescent female DBH-deficient patient. The patient underwent genetic testing, cardiovascular autonomic function testing, and evaluation of insulin secretion and sensitivity with hyperglycemic clamp under treatment-naive conditions. All procedures were repeated after 1 year of treatment with the norepinephrine prodrug droxidopa (300 mg, 3 times a day). Genetic testing showed a homozygous mutation in the DBH gene (rs74853476). Under treatment-naive conditions, she had undetectable plasma epinephrine and norepinephrine levels, resulting in sympathetic noradrenergic failure and orthostatic hypotension (-32 mm Hg supine to seated). She had high adiposity (41%) and fasting plasma insulin levels (25 µU/mL), with normal glucose (91 mg/dL). Hyperglycemic clamp revealed increased glucose-stimulated insulin secretion and insulin resistance. Droxidopa restored plasma norepinephrine and improved orthostatic tolerance, with modest effects on glucose homeostasis. Conclusions: We provide evidence for impairment in cardiovascular autonomic regulation, hyperinsulinemia, enhanced glucose-stimulated insulin secretion, and insulin resistance in a DBH-deficient patient. These metabolic derangements were not corrected by chronic droxidopa treatment. These findings provide insight into the pathophysiology and treatment of DBH deficiency and into the importance of catecholaminergic mechanisms to resting metabolism.
[Mh] Termos MeSH primário: Doenças do Sistema Nervoso Autônomo/complicações
Dopamina beta-Hidroxilase/deficiência
Hiperinsulinismo/etiologia
Resistência à Insulina
Norepinefrina/deficiência
[Mh] Termos MeSH secundário: Adolescente
Animais
Droxidopa/uso terapêutico
Feminino
Seres Humanos
Hiperinsulinismo/diagnóstico
Hiperinsulinismo/tratamento farmacológico
Insulina/metabolismo
Camundongos
Prognóstico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insulin); EC 1.14.17.1 (Dopamine beta-Hydroxylase); J7A92W69L7 (Droxidopa); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2016-3274


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[PMID]:28455315
[Au] Autor:Lundholm MD; Rooney M; Maas MB; Attarian H; Prabhakaran S
[Ad] Endereço:From the Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL.
[Ti] Título:Wake-Up Stroke Is Associated With Greater Nocturnal Mean Arterial Pressure Variability.
[So] Source:Stroke;48(6):1668-1670, 2017 06.
[Is] ISSN:1524-4628
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: Wake-up strokes (WUS) account for ≈20% to 30% of ischemic strokes. Studies have shown that increased autonomic instability as measured by blood pressure variability (BPV) is greater in stroke patients than nonstroke patients, but no studies have compared BPV in WUS versus non-WUS patients. METHODS: From a single-center prospective registry, we identified consecutive ischemic stroke patients. BPV was calculated as the coefficient of variation of the mean arterial pressure during the first 24 hours after hospitalization. We assessed 24-hour BPV as a continuous measure and in quartiles in WUS versus non-WUS patients using univariable and multivariable statistics. RESULTS: Among 369 patients (64.9±16.5 years; 50.1% male; 64.7% white), 78 were WUS (21.1%). Clinical characteristics and medical history were not different between WUS and non-WUS patients except WUS patients were older (69.0 versus 63.8 years; =0.015) and more frequently had previous ischemic stroke (29.5% versus 17.2%; =0.012). Initial 24-hour BPV (11.77 versus 10.76; =0.098) was similar between groups. However, WUS patients had greater nocturnal BPV (10.50 versus 8.95; =0.030), whereas daytime BPV was similar between groups (10.96 versus 10.47, =0.459). In multivariate analysis, the highest quartile (≥11.48 mm Hg) of nocturnal BPV was independently associated with WUS (adjusted odds ratio, 1.95; confidence interval, 1.13-3.39; =0.017). CONCLUSIONS: In this single-center study, we observed that greater nocturnal BPV during the first 24 hours after hospitalization occurred in WUS than non-WUS patients. Nocturnal autonomic instability warrants further study as a potential mechanism of WUS.
[Mh] Termos MeSH primário: Pressão Arterial/fisiologia
Doenças do Sistema Nervoso Autônomo/fisiopatologia
Isquemia Encefálica/fisiopatologia
Sono/fisiologia
Acidente Vascular Cerebral/fisiopatologia
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Doenças do Sistema Nervoso Autônomo/complicações
Isquemia Encefálica/etiologia
Feminino
Hospitalização
Seres Humanos
Masculino
Meia-Idade
Sistema de Registros
Acidente Vascular Cerebral/etiologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE
[do] DOI:10.1161/STROKEAHA.116.016202


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[PMID]:27779568
[Au] Autor:Santoro N; Allshouse A; Neal-Perry G; Pal L; Lobo RA; Naftolin F; Black DM; Brinton EA; Budoff MJ; Cedars MI; Dowling NM; Dunn M; Gleason CE; Hodis HN; Isaac B; Magnani M; Manson JE; Miller VM; Taylor HS; Wharton W; Wolff E; Zepeda V; Harman SM
[Ad] Endereço:1Department of Obstetrics & Gynecology 2Department of Biostatistics, University of Colorado School of Medicine, Aurora, CO 3Department of Obstetrics, Gynecology & Women's Health and Neurosciences, Albert Einstein College of Medicine, Bronx, NY 4Department of Obstetrics & Gynecology, Yale University School of Medicine, New Haven, CT 5Department of Obstetrics & Gynecology, Columbia University College of Physicians and Surgeons, New York, NY 6Department of Obstetrics & Gynecology, New York University School of Medicine, New York, NY 7Department of Epidemiology & Biostatistics, University of California at San Francisco, San Francisco, CA 8Utah Foundation for Biomedical Research, Salt Lake City, UT 9Department of Cardiology, Los Angeles Biomedical Research Institute at Harbor UCLA, Torrance, CA 10Department of Obstetrics & Gynecology, University of California at San Francisco, San Francisco, CA 11Departments of Biostatistics and Medical Informatics, University of Wisconsin, Madison, WI 12Kronos Longevity Research Institute, Phoenix, AZ 13Department of Medicine and Public Health, University of Wisconsin, Madison, WI 14Atherosclerosis Research Unit, University of Southern California, Los Angeles, CA 15Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 16Departments of Surgery and Physiology & Biomedical Engineering, Mayo Clinic, Rochester, MN 17Department of Neurology, Emory University, Atlanta, GA 18Department of Reproductive Biology and Medicine, National Institutes of Health, Bethesda, MD 19Department of Medicine, Endocrine Division, Phoenix VA Health Care System, Phoenix, AZ.
[Ti] Título:Longitudinal changes in menopausal symptoms comparing women randomized to low-dose oral conjugated estrogens or transdermal estradiol plus micronized progesterone versus placebo: the Kronos Early Estrogen Prevention Study.
[So] Source:Menopause;24(3):238-246, 2017 Mar.
[Is] ISSN:1530-0374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The objective of the present study was to compare the efficacy of two forms of menopausal hormone therapy in alleviating vasomotor symptoms, insomnia, and irritability in early postmenopausal women during 4 years. METHODS: A total of 727 women, aged 42 to 58, within 3 years of their final menstrual period, were randomized to receive oral conjugated estrogens (o-CEE) 0.45 mg (n = 230) or transdermal estradiol (t-E2) 50 µg (n = 225; both with micronized progesterone 200 mg for 12 d each mo), or placebos (PBOs; n = 275). Menopausal symptoms were recorded at screening and at 6, 12, 24, 36, and 48 months postrandomization. Differences in proportions of women with symptoms at baseline and at each follow-up time point were compared by treatment arm using exact χ tests in an intent-to-treat analysis. Differences in treatment effect by race/ethnicity and body mass index were tested using generalized linear mixed effects modeling. RESULTS: Moderate to severe hot flashes (from 44% at baseline to 28.3% for PBO, 7.4% for t-E2, and 4.2% for o-CEE) and night sweats (from 35% at baseline to 19% for PBO, 5.3% for t-E2, and 4.7% for o-CEE) were reduced significantly by 6 months in women randomized to either active hormone compared with PBO (P < 0.001 for both symptoms), with no significant differences between the active treatment arms. Insomnia and irritability decreased from baseline to 6 months postrandomization in all groups. There was an intermittent reduction in insomnia in both active treatment arms versus PBO, with o-CEE being more effective than PBO at 36 and 48 months (P = 0.002 and 0.05) and t-E2 being more effective than PBO at 48 months (P = 0.004). Neither hormone treatment significantly affected irritability compared with PBO. Symptom relief for active treatment versus PBO was not significantly modified by body mass index or race/ethnicity. CONCLUSIONS: Recently postmenopausal women had similar and substantial reductions in hot flashes and night sweats with lower-than-conventional doses of oral or transdermal estrogen. These reductions were sustained during 4 years. Insomnia was intermittently reduced compared with PBO for both hormone regimens.
[Mh] Termos MeSH primário: Estrogênios/administração & dosagem
Fogachos/tratamento farmacológico
Humor Irritável/efeitos dos fármacos
Progestinas/administração & dosagem
Distúrbios do Início e da Manutenção do Sono/tratamento farmacológico
[Mh] Termos MeSH secundário: Administração Cutânea
Administração Oral
Adulto
Doenças do Sistema Nervoso Autônomo/tratamento farmacológico
Doenças do Sistema Nervoso Autônomo/etiologia
Quimioterapia Combinada
Estradiol/administração & dosagem
Terapia de Reposição de Estrogênios/métodos
Estrogênios Conjugados (USP)/administração & dosagem
Feminino
Fogachos/etiologia
Seres Humanos
Estudos Longitudinais
Meia-Idade
Pós-Menopausa/efeitos dos fármacos
Progesterona/administração & dosagem
Distúrbios do Início e da Manutenção do Sono/etiologia
Resultado do Tratamento
Sistema Vasomotor/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Estrogens); 0 (Estrogens, Conjugated (USP)); 0 (Progestins); 4G7DS2Q64Y (Progesterone); 4TI98Z838E (Estradiol)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1097/GME.0000000000000756


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[PMID]:27770590
[Au] Autor:Cho YH; Craig ME; Januszewski AS; Benitez-Aguirre P; Hing S; Jenkins AJ; Donaghue KC
[Ad] Endereço:Institute of Endocrinology and Diabetes, Children's Hospital at Westmead, Westmead, Australia.
[Ti] Título:Higher skin autofluorescence in young people with Type 1 diabetes and microvascular complications.
[So] Source:Diabet Med;34(4):543-550, 2017 Apr.
[Is] ISSN:1464-5491
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIM: To test the hypothesis that non-invasive skin autofluorescence, a measure of advanced glycation end products, would provide a surrogate measure of long-term glycaemia and be associated with early markers of microvascular complications in adolescents with Type 1 diabetes. METHODS: Forearm skin autofluorescence (arbitrary units) was measured in a cross-sectional study of 135 adolescents with Type 1 diabetes [mean ± sd age 15.6 ± 2.1 years, diabetes duration 8.7 ± 3.5 years, HbA 72 ± 16 mmol/mol (8.7 ± 1.5%)]. Retinopathy, assessed using seven-field stereoscopic fundal photography, was defined as ≥1 microaneurysm or haemorrhage. Cardiac autonomic function was measured by standard deviation of consecutive RR intervals on a 10-min continuous electrocardiogram recording, as a measure of heart rate variability. RESULTS: Skin autofluorescence was significantly associated with age (R = 0.15; P < 0.001). Age- and gender-adjusted skin autofluorescence was associated with concurrent HbA (R = 0.32; P < 0.001) and HbA over the previous 2.5-10 years (R = 0.34-0.43; P < 0.002). Age- and gender-adjusted mean skin autofluorescence was higher in adolescents with retinopathy vs those without retinopathy [mean 1.38 (95% CI 1.29, 1.48) vs 1.22 (95% CI 1.17, 1.26) arbitrary units; P = 0.002]. In multivariable analysis, retinopathy was significantly associated with skin autofluorescence, adjusted for duration (R = 0.19; P = 0.03). Cardiac autonomic dysfunction was also independently associated with skin autofluorescence (R = 0.11; P = 0.006). CONCLUSIONS: Higher skin autofluorescence is associated with retinopathy and cardiac autonomic dysfunction in adolescents with Type 1 diabetes. The relationship between skin autofluorescence and previous glycaemia may provide insight into metabolic memory. Longitudinal studies will determine the utility of skin autofluorescence as a non-invasive screening tool to predict future microvascular complications.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 1/fisiopatologia
Angiopatias Diabéticas/diagnóstico por imagem
Retinopatia Diabética/diagnóstico por imagem
Microaneurisma/diagnóstico por imagem
Hemorragia Retiniana/diagnóstico por imagem
Pele/diagnóstico por imagem
[Mh] Termos MeSH secundário: Adolescente
Doenças do Sistema Nervoso Autônomo/etiologia
Doenças do Sistema Nervoso Autônomo/fisiopatologia
Diabetes Mellitus Tipo 1/complicações
Diabetes Mellitus Tipo 1/metabolismo
Angiopatias Diabéticas/etiologia
Angiopatias Diabéticas/fisiopatologia
Retinopatia Diabética/etiologia
Retinopatia Diabética/fisiopatologia
Eletrocardiografia
Feminino
Fundo de Olho
Hemoglobina A Glicada/metabolismo
Frequência Cardíaca
Seres Humanos
Masculino
Microaneurisma/etiologia
Microaneurisma/fisiopatologia
Análise Multivariada
Imagem Óptica
Hemorragia Retiniana/etiologia
Hemorragia Retiniana/fisiopatologia
Pele/irrigação sanguínea
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glycated Hemoglobin A); 0 (hemoglobin A1c protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE
[do] DOI:10.1111/dme.13280


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[PMID]:29187690
[Au] Autor:Yokoi K; Ando T; Ishikawa S
[Ad] Endereço:Department of Neurology, Anjo Kosei Hospital.
[Ti] Título:[Treatment for paroxysmal sympathetic hyperactivity in amyotrophic lateral sclerosis patient].
[So] Source:Rinsho Shinkeigaku;57(12):782-784, 2017 Dec 27.
[Is] ISSN:1882-0654
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:We report a case of an 80-year-old man who contracted amyotrophic lateral sclerosis (ALS) 15 years ago, was put on a ventilator 8 years ago, and became locked in 3 years ago. Two years ago, he began to suffer from sudden symptoms of paroxysmal sympathetic hyperactivity (PSH) attacks (hot flushes, abnormal sweating, tachycardia, and increased blood pressure). One day, he developed multiple-organ failure. This failure healed in a few days, but PSH attacks remained. His catecholamine levels were abnormal: adrenaline, 215 pg/ml; noradrenaline, 5,960 pg/ml; and dopamine, 606 pg/ml. Diazepam was administered, which decreased both the number of PSH attacks and the catecholamine levels. When the dose was increased to 3 mg, the attacks stopped, whereas when the dose was reduced to 2 mg, the attacks relapsed. When the dose of 3 mg was continued, there was no relapse of the attacks and no re-rise in the catecholamine levels. These results show that diazepam alone has an effect on PSH attacks in ALS.
[Mh] Termos MeSH primário: Esclerose Amiotrófica Lateral/complicações
Doenças do Sistema Nervoso Autônomo/tratamento farmacológico
Doenças do Sistema Nervoso Autônomo/etiologia
Diazepam/uso terapêutico
[Mh] Termos MeSH secundário: Idoso de 80 Anos ou mais
Doenças do Sistema Nervoso Autônomo/metabolismo
Catecolaminas/metabolismo
Seres Humanos
Masculino
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Catecholamines); Q3JTX2Q7TU (Diazepam)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.5692/clinicalneurol.cn-001093


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[PMID]:28911152
[Au] Autor:Seaquist ER; Moheet A; Kumar A; Deelchand DK; Terpstra M; Kubisiak K; Eberly LE; Henry PG; Joers JM; Öz G
[Ad] Endereço:Division of Diabetes, Endocrinology and Metabolism, Department of Medicine, University of Minnesota, Minneapolis, Minnesota 55455.
[Ti] Título:Hypothalamic Glucose Transport in Humans During Experimentally Induced Hypoglycemia-Associated Autonomic Failure.
[So] Source:J Clin Endocrinol Metab;102(9):3571-3580, 2017 Sep 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Context: Upregulated brain glucose transport in response to recurrent hypoglycemia may contribute to the development of hypoglycemia-associated autonomic failure (HAAF) and impaired awareness of hypoglycemia. Whether recurrent hypoglycemia alters glucose transport in the hypothalamus is unknown. Objective: To test the hypothesis that hypothalamic glucose transport will increase in healthy volunteers preconditioned with recurrent hypoglycemia to induce HAAF. Setting: University medical center. Design and Participants: Thirteen healthy subjects underwent paired euglycemic and hypoglycemic preconditioning studies separated by at least 1 month. Following preconditioning, hypothalamic glucose transport was measured by magnetic resonance spectroscopy (MRS) in the afternoon on day 2 of each preconditioning protocol. Outcome Measure: The ratio of maximal transport rate to cerebral metabolic rate of glucose (Tmax/CMRglc), obtained from MRS-measured glucose in the hypothalamus as a function of plasma glucose. Results: HAAF was successfully induced based on lower epinephrine, glucagon, and cortisol during the third vs first hypoglycemic preconditioning clamp (P ≤ 0.01). Hypothalamic glucose transport was not different following recurrent euglycemia vs hypoglycemia (Tmax/CMRglc 1.62 ± 0.09 after euglycemia preconditioning and 1.75 ± 0.14 after hypoglycemia preconditioning; P was not significant). Hypothalamic glucose concentrations measured by MRS were not different following the two preconditioning protocols. Conclusions: Glucose transport kinetics in the hypothalamus of healthy humans with experimentally induced HAAF were not different from those measured without HAAF. Future studies of patients with diabetes and impaired awareness of hypoglycemia will be necessary to determine if the existence of the diabetes state is required for this adaptation to hypoglycemia to occur.
[Mh] Termos MeSH primário: Doenças do Sistema Nervoso Autônomo/fisiopatologia
Glucose/metabolismo
Hipoglicemia/sangue
Hipotálamo/metabolismo
Insuficiência Autonômica Pura/sangue
[Mh] Termos MeSH secundário: Adulto
Doenças do Sistema Nervoso Autônomo/sangue
Feminino
Seres Humanos
Hipoglicemia/fisiopatologia
Infusões Intravenosas
Insulina/administração & dosagem
Masculino
Modelos Teóricos
Insuficiência Autonômica Pura/fisiopatologia
Valores de Referência
Amostragem
Análise Espectral
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insulin); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2017-00477


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[PMID]:28863200
[Au] Autor:Thornton K; Mitchell MO
[Ad] Endereço:Highland Hospital Family Medicine Residency, University of Rochester School of Medicine and Dentistry, NY, USA. Email: Kristen_Thornton@URMC.Rochester.edu.
[Ti] Título:Autonomic dysfunction: A guide for FPs.
[So] Source:J Fam Pract;66(9):539-543, 2017 Sep.
[Is] ISSN:1533-7294
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Impotence, bladder dysfunction, GI symptoms, and orthostatic hypotension can signal autonomic dysfunction. Here's what you'll see and how to respond.
[Mh] Termos MeSH primário: Doenças do Sistema Nervoso Autônomo/diagnóstico
Doenças do Sistema Nervoso Autônomo/terapia
Medicina de Família e Comunidade/normas
Guias de Prática Clínica como Assunto
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Feminino
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170902
[St] Status:MEDLINE


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[PMID]:28816118
[Au] Autor:Meyfroidt G; Baguley IJ; Menon DK
[Ad] Endereço:Department of Intensive Care Medicine, University Hospitals Leuven, Leuven, Belgium.
[Ti] Título:Paroxysmal sympathetic hyperactivity: the storm after acute brain injury.
[So] Source:Lancet Neurol;16(9):721-729, 2017 Sep.
[Is] ISSN:1474-4465
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A substantial minority of patients who survive an acquired brain injury develop a state of sympathetic hyperactivity that can persist for weeks or months, consisting of periodic episodes of increased heart rate and blood pressure, sweating, hyperthermia, and motor posturing, often in response to external stimuli. The unifying term for the syndrome-paroxysmal sympathetic hyperactivity (PSH)-and clear diagnostic criteria defined by expert consensus were only recently established. PSH has predominantly been described after traumatic brain injury (TBI), in which it is associated with worse outcomes. The pathophysiology of the condition is not completely understood, although most researchers consider it to be a disconnection syndrome with paroxysms driven by a loss of inhibitory control over excitatory autonomic centres. Although therapeutic strategies to alleviate sympathetic outbursts have been proposed, their effects on PSH are inconsistent between patients and their influence on outcome is unknown. Combinations of drugs are frequently used and are chosen on the basis of local custom, rather than on objective evidence. New rigorous tools for diagnosis could allow better characterisation of PSH to enable stratification of patients for future therapeutic trials.
[Mh] Termos MeSH primário: Doenças do Sistema Nervoso Autônomo/fisiopatologia
Lesões Encefálicas/fisiopatologia
Sistema Nervoso Simpático/fisiopatologia
[Mh] Termos MeSH secundário: Doenças do Sistema Nervoso Autônomo/diagnóstico
Doenças do Sistema Nervoso Autônomo/etiologia
Doenças do Sistema Nervoso Autônomo/terapia
Lesões Encefálicas/complicações
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170904
[Lr] Data última revisão:
170904
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170818
[St] Status:MEDLINE


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[PMID]:28732007
[Au] Autor:Anderson WD; DeCicco D; Schwaber JS; Vadigepalli R
[Ad] Endereço:Daniel Baugh Institute for Functional Genomics and Computational Biology, Department of Pathology, Anatomy, and Cell Biology, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA, USA.
[Ti] Título:A data-driven modeling approach to identify disease-specific multi-organ networks driving physiological dysregulation.
[So] Source:PLoS Comput Biol;13(7):e1005627, 2017 Jul.
[Is] ISSN:1553-7358
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Multiple physiological systems interact throughout the development of a complex disease. Knowledge of the dynamics and connectivity of interactions across physiological systems could facilitate the prevention or mitigation of organ damage underlying complex diseases, many of which are currently refractory to available therapeutics (e.g., hypertension). We studied the regulatory interactions operating within and across organs throughout disease development by integrating in vivo analysis of gene expression dynamics with a reverse engineering approach to infer data-driven dynamic network models of multi-organ gene regulatory influences. We obtained experimental data on the expression of 22 genes across five organs, over a time span that encompassed the development of autonomic nervous system dysfunction and hypertension. We pursued a unique approach for identification of continuous-time models that jointly described the dynamics and structure of multi-organ networks by estimating a sparse subset of ∼12,000 possible gene regulatory interactions. Our analyses revealed that an autonomic dysfunction-specific multi-organ sequence of gene expression activation patterns was associated with a distinct gene regulatory network. We analyzed the model structures for adaptation motifs, and identified disease-specific network motifs involving genes that exhibited aberrant temporal dynamics. Bioinformatic analyses identified disease-specific single nucleotide variants within or near transcription factor binding sites upstream of key genes implicated in maintaining physiological homeostasis. Our approach illustrates a novel framework for investigating the pathogenesis through model-based analysis of multi-organ system dynamics and network properties. Our results yielded novel candidate molecular targets driving the development of cardiovascular disease, metabolic syndrome, and immune dysfunction.
[Mh] Termos MeSH primário: Doenças do Sistema Nervoso Autônomo/fisiopatologia
Doenças Cardiovasculares/fisiopatologia
Biologia Computacional/métodos
Redes Reguladoras de Genes/fisiologia
Modelos Biológicos
[Mh] Termos MeSH secundário: Glândulas Suprarrenais/fisiopatologia
Animais
Tronco Encefálico/fisiopatologia
Perfilação da Expressão Gênica
Rim/fisiopatologia
Masculino
Modelos Estatísticos
Ratos
Ratos Endogâmicos SHR
Ratos Endogâmicos WKY
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170722
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pcbi.1005627


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[PMID]:28676377
[Au] Autor:Németh N; Putz Z; Istenes I; Körei AE; Vági OE; Kempler M; Gandhi R; Jermendy G; Tesfaye S; Tabák ÁG; Kempler P
[Ad] Endereço:1st Department of Internal Medicine, Semmelweis University, Budapest, Hungary. Electronic address: nora.nemeth@yahoo.com.
[Ti] Título:Is there a connection between postprandial hyperglycemia and IGT related sensory nerve dysfunction?
[So] Source:Nutr Metab Cardiovasc Dis;27(7):609-614, 2017 Jul.
[Is] ISSN:1590-3729
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND AIMS: To assess the risk factors for sensory nerve dysfunction in subjects with isolated impaired glucose tolerance (IGT). METHODS AND RESULTS: Seventy-two people with isolated IGT (WHO 1999 criteria) and 39 gender and age-matched healthy volunteers underwent detailed clinical and neurological assessment including quantitative sensory testing using the Neurometer device (current perception threshold measurement on four limbs at three different frequencies). Sensory nerve dysfunction was defined as at least two abnormalities on any frequencies on the upper or lower limbs. Sensory nerve dysfunction was more prevalent among subjects with IGT compared to controls (58.3 vs. 10.3%, OR: 11.23, 95%CI: 3.57-35.35). This association was not influenced by BMI, systolic and diastolic blood pressure, heart rate and autonomic neuropathy (multiple adjusted OR: 13.87, 95%CI: 3.18-60.58), but further adjustment for glycaemic measures abolished the association (OR: 1.58, 95%CI: 0.07-35.68). Assessing the components of glycaemic measures separately, the association between sensory nerve dysfunction and IGT was not affected by HbA1c (OR: 13.94, 95%CI: 1.84-105.5). It was, however, substantially attenuated by fasting plasma glucose (OR: 6.75, 95%CI: 1.33-34.27) while the significance was lost after adjustment for 120 min postload glucose level (OR: 3.76, 95%CI: 0.26-54.10). In the pooled population assessed, independent determinants of sensory nerve dysfunction were older age, 120 min glucose, higher height and cardiovascular autonomic neuropathy at near significance. CONCLUSIONS: Sensory nerve dysfunction amongst subjects with IGT was not explained by cardiovascular covariates, only by glycaemic measures. In addition to 120 min glucose, cardiovascular autonomic neuropathy at borderline significance, age, and height were the independent determinants of sensory nerve dysfunction.
[Mh] Termos MeSH primário: Doenças do Sistema Nervoso Autônomo/etiologia
Glicemia/metabolismo
Hiperglicemia/complicações
Extremidade Inferior/inervação
Doenças do Sistema Nervoso Periférico/etiologia
Período Pós-Prandial
Células Receptoras Sensoriais
Extremidade Superior/inervação
[Mh] Termos MeSH secundário: Adulto
Doenças do Sistema Nervoso Autônomo/diagnóstico
Doenças do Sistema Nervoso Autônomo/fisiopatologia
Biomarcadores
Estudos de Casos e Controles
Distribuição de Qui-Quadrado
Estudos Transversais
Estimulação Elétrica
Feminino
Teste de Tolerância a Glucose
Seres Humanos
Hiperglicemia/sangue
Hiperglicemia/diagnóstico
Modelos Logísticos
Masculino
Meia-Idade
Exame Neurológico/métodos
Razão de Chances
Doenças do Sistema Nervoso Periférico/diagnóstico
Doenças do Sistema Nervoso Periférico/fisiopatologia
Fatores de Risco
Limiar Sensorial
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Blood Glucose)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170706
[St] Status:MEDLINE



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