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[PMID]:29287886
[Au] Autor:Samdani S; Jain A; Meena V; Meena CB
[Ad] Endereço:Department of Otorhinolaryngology (ENT), Sawai Man Singh Medical College and Attached Group of Hospitals, Jaipur, Rajasthan, India.
[Ti] Título:Cardiac complications in diphtheria and predictors of outcomes.
[So] Source:Int J Pediatr Otorhinolaryngol;104:76-78, 2018 Jan.
[Is] ISSN:1872-8464
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To study the cardiac complications in diphtheria patients and to study the predictors of outcomes. STUDY DESIGN: Single centre prospective analysis of cardiac complications in diphtheria patients. RESULTS: In this study, there were 60 patients diagnosed with diphtheria with ECG changes. The ECG changes seen were sinus tachycardia (68.3%), T wave inversion (20%), ST segment depression (13.3%), right bundle branch block (5%), multiple atrial ectopics (3.3%). The case fatality rate in our study was 25% (15 patients). High CPK-MB, myoglobulin and cardiac troponin levels were associated with cardiac mortality. In our study, cardiac troponin T had the highest sensitivity (80%) and CK-MB had the highest specificity (95.56%). CONCLUSION: Cardiac involvement is a common complication of infection with C. diphtheria and is associated with high mortality. As diphtheria can be prevented by adequate vaccination, efforts should be maximized for high vaccine coverage with booster doses.
[Mh] Termos MeSH primário: Difteria/complicações
Cardiopatias/etiologia
[Mh] Termos MeSH secundário: Adolescente
Biomarcadores
Criança
Pré-Escolar
Creatina Quinase
Eletrocardiografia
Feminino
Cardiopatias/epidemiologia
Seres Humanos
Lactente
Masculino
Estudos Prospectivos
Sensibilidade e Especificidade
Troponina T
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Troponin T); EC 2.7.3.2 (Creatine Kinase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171231
[St] Status:MEDLINE


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[PMID]:29289268
[Au] Autor:Kamal F; Snook L; Saikumar JH
[Ad] Endereço:University of Tennessee Health Science Center (FK, JS), Memphis, Memphis, Tennessee. Electronic address: fkamal1@uthsc.edu.
[Ti] Título:Rhabdomyolysis-Associated Acute Kidney Injury With Normal Creatine Phosphokinase.
[So] Source:Am J Med Sci;355(1):84-87, 2018 Jan.
[Is] ISSN:1538-2990
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Rhabdomyolysis is a syndrome characterized by the breakdown of skeletal muscle and leakage of intracellular myocyte contents, such as creatine phosphokinase (CPK) and myoglobin, into the interstitial space and plasma resulting in acute kidney injury (AKI). Elevated CPK of at least 5 times the upper limit of normal is an important diagnostic marker of Rhabdomyolysis. We present a case of rhabdomyolysis with severe AKI with a normal CPK at presentation. A 32-year-old man presented with acute respiratory failure and AKI after an overdose of recreational drugs. Urinalysis at presentation showed trace amounts of blood, identified as rare red blood cells under microscopy. CPK was 156 U/L at presentation. Workup for glomerulonephritis and vasculitis was negative. He was initiated on renal replacement therapy, and a kidney biopsy showed severe acute tubular injury with positive myoglobin casts. Supportive management and renal replacement therapy was provided, and renal function spontaneously improved after a few weeks. This is an uncommon clinical presentation of severe rhabdomyolysis complicated by AKI. This suggests that CPK alone may not be a sensitive marker for rhabdomyolysis-induced AKI in some cases.
[Mh] Termos MeSH primário: Lesão Renal Aguda
Creatina Quinase/sangue
Overdose de Drogas
Terapia de Substituição Renal
Rabdomiólise
Drogas Ilícitas/efeitos adversos
[Mh] Termos MeSH secundário: Lesão Renal Aguda/sangue
Lesão Renal Aguda/induzido quimicamente
Lesão Renal Aguda/terapia
Adulto
Biomarcadores/sangue
Overdose de Drogas/sangue
Overdose de Drogas/complicações
Overdose de Drogas/terapia
Seres Humanos
Masculino
Rabdomiólise/sangue
Rabdomiólise/induzido quimicamente
Rabdomiólise/terapia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Street Drugs); EC 2.7.3.2 (Creatine Kinase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180101
[St] Status:MEDLINE


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[PMID]:28456776
[Au] Autor:Verbickas V; Baranauskiene N; Eimantas N; Kamandulis S; Rutkauskas S; Satkunskiene D; Sadauskas S; Brazaitis M; Skurvydas A
[Ad] Endereço:Institute of Sports Science and Innovation, Lithuanian Sports University, Kaunas, Lithuania. v.verbickas@gmail.com.
[Ti] Título:Effect of sprint cycling and stretch-shortening cycle exercises on the neuromuscular, immune and stress indicators in young men.
[So] Source:J Physiol Pharmacol;68(1):125-132, 2017 02.
[Is] ISSN:1899-1505
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Selection of optimal physical load is essential for desired adaptation including health benefits. We hypothesized that neuromuscular, immune and stress indicators will be higher after energy demanding sprint interval exercise (SIE) than to mechanically demanding stretch-shortening cycle exercise (SSE). The main aim of this study was to assess and compare the kinetics of blood brain-derived neurotrophic factor (BDNF), norepinephrine (NE) and cortisol (as stress indicators) and proinflammatory (IL-6) and anti-inflammatory (IL-10) cytokines within 24 hours after metabolically demanding SIE and after muscle damage inducing SSE. Twenty healthy physically active young men randomly assigned to two equal groups to complete 12 bouts of 5 s stationary cycling sprints every 3 min (SIE) or 200 drop-jumps with 30 s interval between each jump (SSE), respectively. Quadriceps muscle maximal voluntary contraction torque and voluntary activation and soreness were measured and blood samples collected before and 2 min, 1 hour, 12 hours and 24 hours after the SIE and SSE. The BDNF, cortisol, IL-6 and NE levels increased more at 2 min after SIE than SSE (P < 0.05); however, the IL-10 level did not differ between SIE and SSE. BDNF and cortisol levels were decreased at 24 h after both SIE and especially after SSE. The higher was the initial BDNF level, the greater was its decrease at 24 h after both type of exercise. Before exercise BDNF level correlated closely with the change in central fatigue (decrease in voluntary activation) after both SIE and SSE. We thus conclude that both metabolically demanding SIE and muscle damage inflicting SSE induced long-lasting decrease in circulating BDNF which may not promote brain health. The level of circulating BDNF, but not cortisol, IL-6, IL-10 or NE, was associated with changes in central motor fatigue.
[Mh] Termos MeSH primário: Ciclismo/fisiologia
Exercício/fisiologia
[Mh] Termos MeSH secundário: Adulto
Fator Neurotrófico Derivado do Encéfalo/sangue
Creatina Quinase/sangue
Seres Humanos
Hidrocortisona/sangue
Interleucina-10/sangue
Interleucina-6/sangue
Masculino
Contração Muscular
Fadiga Muscular/imunologia
Fadiga Muscular/fisiologia
Norepinefrina/sangue
Músculo Quadríceps/fisiologia
Adulto Jovem
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Brain-Derived Neurotrophic Factor); 0 (IL10 protein, human); 0 (IL6 protein, human); 0 (Interleukin-6); 0 (brain-derived neurotrophic factor, human); 130068-27-8 (Interleukin-10); EC 2.7.3.2 (Creatine Kinase); WI4X0X7BPJ (Hydrocortisone); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


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[PMID]:28143367
[Au] Autor:Neto GR; Novaes JS; Salerno VP; Gonçalves MM; Batista GR; Cirilo-Sousa MS
[Ad] Endereço:a Department of Physical Education , Associate Graduate Program in Physical Education UPE/UFPB , João Pessoa , Brazil.
[Ti] Título:Does a resistance exercise session with continuous or intermittent blood flow restriction promote muscle damage and increase oxidative stress?
[So] Source:J Sports Sci;36(1):104-110, 2018 Jan.
[Is] ISSN:1466-447X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to compare the effect of low-load resistance exercise (LLRE) with continuous and intermittent blood flow restriction (BFR) on the creatine kinase (CK), lactate dehydrogenase (LDH), protein carbonyl (PC), thiobarbituric acid-reactive substance (TBARS) and uric acid (UA) levels in military men. The study included 10 recreationally trained men aged 19 ± 0.82 years who underwent the following experimental protocols in random order on separate days (72-96 h): 4 LLRE sessions at a 20% 1RM (one-repetition maximum [1RM]) with continuous BFR (LLRE + CBFR); 4 LLRE sessions at 20% 1RM with intermittent BFR (LLRE + IBFR) and 4 high-intensity resistance exercise (HIRE) sessions at 80% 1RM. The CK and LDH (markers of muscle damage) levels were measured before exercise (BE), 24 h post-exercise and 48 h post-exercise, and the PC, TBARS and UA (markers of oxidative stress) levels were measured BE and immediately after each exercise session. There was a significant increase in CK in the HIRE 24 post-exercise samples compared with the LLRE + CBFR and LLRE + IBFR (P = 0.035, P = 0.036, respectively), as well as between HIRE 48 post-exercise and LLRE + CBFR (P = 0.049). Additionally, there was a significant increase in CK in the LLRE + CBFR samples BE and immediately after each exercise (Δ = 21.9%) and in the HIRE samples BE and immediately after each exercise, BE and 24 post-exercise, and BE and 48 post-exercise (Δ values of 35%, 177.6%, and 177.6%, respectively). However, there were no significant changes in LDH, PC, TBARS, and UA between the protocols (P > 0.05). Therefore, a physical exercise session with continuous or intermittent BFR did not promote muscle damage; moreover, neither protocol seemed to affect the oxidative stress markers.
[Mh] Termos MeSH primário: Músculo Esquelético/irrigação sanguínea
Músculo Esquelético/lesões
Estresse Oxidativo/fisiologia
Fluxo Sanguíneo Regional/fisiologia
Treinamento de Resistência/métodos
[Mh] Termos MeSH secundário: Biomarcadores/sangue
Creatina Quinase/sangue
Seres Humanos
L-Lactato Desidrogenase/sangue
Masculino
Militares
Força Muscular/fisiologia
Músculo Esquelético/fisiologia
Carbonilação Proteica
Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo
Ácido Úrico/sangue
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Thiobarbituric Acid Reactive Substances); 268B43MJ25 (Uric Acid); EC 1.1.1.27 (L-Lactate Dehydrogenase); EC 2.7.3.2 (Creatine Kinase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170202
[St] Status:MEDLINE
[do] DOI:10.1080/02640414.2017.1283430


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[PMID]:29304153
[Au] Autor:Barszcz M; Taciak M; Tusnio A; Skomial J
[Ad] Endereço:Department of Animal Nutrition, The Kielanowski Institute of Animal Physiology and Nutrition, Polish Academy of Sciences, Jablonna, Poland.
[Ti] Título:Effects of dietary level of tannic acid and protein on internal organ weights and biochemical blood parameters of rats.
[So] Source:PLoS One;13(1):e0190769, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tannic acid (TA) is a polyphenolic compound with a health-promoting potential for humans. It is hypothesised that TA effects on the relative weight of internal organs and biochemical blood indices are modified by dietary protein level in rats. The study involved 72 rats divided into 12 groups fed diets with 10 or 18% of crude protein (CP) and supplemented with 0, 0.25, 0.5, 1, 1.5 or 2% of TA. After 3 weeks of feeding, the relative weight of the caecum was greater in rats fed TA diets, while feeding diets with 10% of CP increased the relative weight of the stomach, small intestine and caecum, but decreased that of kidneys and spleen. Albumin concentration was higher in rats fed 0.25% and 0.5% TA diets than in rats given the 2% TA diets. The 2% TA diets reduced creatine kinase (CK) activity compared to non-supplemented diets and those with 0.5, 1 and 1.5% of TA. Rats fed the 10% CP diets had a higher activity of alkaline phosphatase, amylase, and γ-glutamyltransferase as well as the concentration of iron and cholesterol, but lower that of urea and uric acid. The interaction affected only cholinesterase activity. In conclusion, TA induced caecal hypertrophy and could act as a cardioprotective agent, as demonstrated by reduced CK activity, but these effects were not modified by dietary protein level.
[Mh] Termos MeSH primário: Dieta
Proteínas na Dieta
Taninos
[Mh] Termos MeSH secundário: Animais
Ceco/anatomia & histologia
Colesterol/sangue
Colinesterases/sangue
Creatina Quinase/sangue
Intestino Delgado/anatomia & histologia
Rim/anatomia & histologia
Masculino
Tamanho do Órgão
Ratos Endogâmicos WF
Albumina Sérica
Baço/anatomia & histologia
Estômago/anatomia & histologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Dietary Proteins); 0 (Serum Albumin); 0 (Tannins); 97C5T2UQ7J (Cholesterol); EC 2.7.3.2 (Creatine Kinase); EC 3.1.1.8 (Cholinesterases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180210
[Lr] Data última revisão:
180210
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190769


  6 / 23102 MEDLINE  
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[PMID]:29287112
[Au] Autor:Warren EB; Aicher AE; Fessel JP; Konradi C
[Ad] Endereço:Department of Pharmacology, Vanderbilt University, Nashville, Tennessee, United States of America.
[Ti] Título:Mitochondrial DNA depletion by ethidium bromide decreases neuronal mitochondrial creatine kinase: Implications for striatal energy metabolism.
[So] Source:PLoS One;12(12):e0190456, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mitochondrial DNA (mtDNA), the discrete genome which encodes subunits of the mitochondrial respiratory chain, is present at highly variable copy numbers across cell types. Though severe mtDNA depletion dramatically reduces mitochondrial function, the impact of tissue-specific mtDNA reduction remains debated. Previously, our lab identified reduced mtDNA quantity in the putamen of Parkinson's Disease (PD) patients who had developed L-DOPA Induced Dyskinesia (LID), compared to PD patients who had not developed LID and healthy subjects. Here, we present the consequences of mtDNA depletion by ethidium bromide (EtBr) treatment on the bioenergetic function of primary cultured neurons, astrocytes and neuron-enriched cocultures from rat striatum. We report that EtBr inhibition of mtDNA replication and transcription consistently reduces mitochondrial oxygen consumption, and that neurons are significantly more sensitive to EtBr than astrocytes. EtBr also increases glycolytic activity in astrocytes, whereas in neurons it reduces the expression of mitochondrial creatine kinase mRNA and levels of phosphocreatine. Further, we show that mitochondrial creatine kinase mRNA is similarly downregulated in dyskinetic PD patients, compared to both non-dyskinetic PD patients and healthy subjects. Our data support a hypothesis that reduced striatal mtDNA contributes to energetic dysregulation in the dyskinetic striatum by destabilizing the energy buffering system of the phosphocreatine/creatine shuttle.
[Mh] Termos MeSH primário: Corpo Estriado/metabolismo
Creatina Quinase/metabolismo
DNA Mitocondrial/metabolismo
Metabolismo Energético
Etídio/farmacologia
Mitocôndrias/enzimologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Glicólise
Seres Humanos
Consumo de Oxigênio
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (DNA, Mitochondrial); EC 2.7.3.2 (Creatine Kinase); EN464416SI (Ethidium)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171230
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190456


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[PMID]:29178655
[Au] Autor:Laughlin RS; Niu Z; Wieben E; Milone M
[Ad] Endereço:Department of Neurology, Mayo Clinic, Rochester, Minnesota.
[Ti] Título:RYR1 causing distal myopathy.
[So] Source:Mol Genet Genomic Med;5(6):800-804, 2017 11.
[Is] ISSN:2324-9269
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Congenital myopathies due to ryanodine receptor (RYR1) mutations are increasingly identified and correlate with a wide range of phenotypes, most commonly that of malignant hyperthermia susceptibility and central cores on muscle biopsy with rare reports of distal muscle weakness, but in the setting of early onset global weakness. METHODS: We report a case of a patient presenting with childhood onset hand stiffness and adult onset progressive hand weakness and jaw contractures discovered to have two variants in the RYR1 gene. RESULTS: The patient manifested with distal upper limb weakness which progressed to involve the distal lower limb, proximal upper limb, as well as the face in addition to limited jaw opening. Creatine kinase was mildly elevated with EMG findings supporting a myopathy. Muscle biopsy showed features consistent with centronuclear myopathy. Whole exome sequencing revealed a novel heterozygous pathogenic variant in RYR1 (c.12315_12328delAGAAATCCAGTTCC, p.Glu4106Alafs*8), and a heterozygous missense variant (c.10648C>T, p.Arg3550Trp) of unknown significance in compound heterozygous state. CONCLUSION: We expand the spectrum of RYR1-related myopathy with the description of a novel phenotype in an adult patient presenting with hand weakness and suggest considering RYR1 analysis in the diagnosis of distal myopathies.
[Mh] Termos MeSH primário: Miopatias Distais/genética
Canal de Liberação de Cálcio do Receptor de Rianodina/genética
[Mh] Termos MeSH secundário: Adulto
Creatina Quinase/metabolismo
Análise Mutacional de DNA
Miopatias Distais/diagnóstico
Eletromiografia
Heterozigoto
Seres Humanos
Anormalidades Maxilomandibulares/fisiopatologia
Masculino
Músculo Esquelético/patologia
Linhagem
Fenótipo
Polimorfismo de Nucleotídeo Único
Extremidade Superior/fisiopatologia
Sequenciamento Completo do Exoma
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ryanodine Receptor Calcium Release Channel); EC 2.7.3.2 (Creatine Kinase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1002/mgg3.338


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[PMID]:28747620
[Au] Autor:Finsterer J; Aliyev R
[Ad] Endereço:Department of Neurology, Krankenanstalt Rudolfstiftung, Vienna, Austria.
[Ti] Título:Chronic Inflammatory Demyelinating Polyneuropathy Variant with Creatine-Kinase Elevation and Vanishing Effect of Immunoglobulins.
[So] Source:Am J Case Rep;18:834-838, 2017 Jul 27.
[Is] ISSN:1941-5923
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND Whether creatine-kinase (CK) is elevated or not in chronic inflammatory demyelinating polyneuropathy (CIDP) and its variants is not comprehensively investigated. CASE REPORT We report the case of a 47-year-old male who developed weakness of the left lower leg and the right index finger at age 42 years. At age 44 years, paresthesias and dysesthesias of both lower legs and mild right lower leg weakness additionally developed. CK was recurrently elevated since age 42 years but paraprotein and anti-myelin-associated glycoprotein (MAG)-antibodies were negative. Nerve conduction studies at age 43 years showed an axonal and demyelinating lesion with conduction blocks. Cerebrospinal fluid (CSF) investigations revealed mild pleocytosis and elevated protein, which is why CIDP variant was diagnosed. Immunoglobulins were administered with success. Because of recurrent relapses, immunoglobulins were increased at age 45 years, resulting in stabilization. Currently, the patient is infusing immunoglobulins subcutaneously himself. CONCLUSIONS CIDP variants may go along with CK elevation, an axonal lesion, pleocytosis, and asymmetry of the lesion. A vanishing effect of immunoglobulins over time may be characteristic of CIDP variants.
[Mh] Termos MeSH primário: Creatina Quinase/sangue
Imunoglobulinas Intravenosas/uso terapêutico
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/tratamento farmacológico
[Mh] Termos MeSH secundário: Seres Humanos
Masculino
Meia-Idade
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/sangue
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/diagnóstico
Recidiva
Autoadministração
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunoglobulins, Intravenous); EC 2.7.3.2 (Creatine Kinase)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171201
[Lr] Data última revisão:
171201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE


  9 / 23102 MEDLINE  
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[PMID]:29095275
[Au] Autor:Hwang HE; Hsu TR; Lee YH; Wang HK; Chiou HJ; Niu DM
[Ad] Endereço:aDepartment of Radiology bDepartment of Pediatrics, Taipei Veterans General Hospital, Taipei, Taiwan.
[Ti] Título:Muscle ultrasound: A useful tool in newborn screening for infantile onset pompe disease.
[So] Source:Medicine (Baltimore);96(44):e8415, 2017 Nov.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Our study aimed to evaluate the utility of muscle ultrasound in newborn screening of infantile-onset Pompe disease (IOPD) and to establish a system of severity grading. We retrospectively selected 35 patients with initial low acid alpha-glucosidase (GAA) activity and collected data including muscle ultrasound features, GAA gene mutation, activity/performance, and pathological and laboratory findings. The echogenicity of 6 muscles (the bilateral vastus intermedius, rectus femoris, and sartorius muscles) was compared to that of epimysium on ultrasound and rated either 1 (normal), 2 (mildly increased), or 3 (obviously increased). These grades were used to divide patients into 3 groups. IOPD was present in none of the grade-1 patients, 5 of 9 grade-2 patients, and 5 of 5 grade-3 patients (P < .001). Comparing grade-2 plus grade-3 patients to grade-1 patients, muscle ultrasound detected IOPD with a sensitivity and specificity of 100.0% (95% confidence interval [CI]: 69.2%-100%) and 84.0% (95% CI: 63.9%-95.5%), respectively. The mean number of affected muscles was larger in grade-3 patients than in grade-2 patients (4.2 vs. 2.0, P = .005). Mean alanine transaminase (ALT), aspartate transaminase (AST), creatine kinase (CK), and lactate dehydrogenase (LDH) levels were differed significantly different between grade-3 and grade-1 patients (P < .001). Because it permits direct visualization of injured muscles, muscle ultrasound can be used to screen for IOPD. Our echogenicity grades of muscle injury also correlate well with serum levels of muscle-injury biochemical markers.
[Mh] Termos MeSH primário: Doença de Depósito de Glicogênio Tipo II/diagnóstico por imagem
Triagem Neonatal/métodos
Músculo Quadríceps/diagnóstico por imagem
Índice de Gravidade de Doença
Ultrassonografia/métodos
[Mh] Termos MeSH secundário: Alanina Transaminase/sangue
Aspartato Aminotransferases
Biomarcadores/sangue
Creatina Quinase/sangue
Feminino
Doença de Depósito de Glicogênio Tipo II/sangue
Seres Humanos
Recém-Nascido
L-Lactato Desidrogenase/sangue
Masculino
Estudos Retrospectivos
alfa-Glucosidases/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Biomarkers); EC 1.1.1.27 (L-Lactate Dehydrogenase); EC 2.6.1.1 (Aspartate Aminotransferases); EC 2.6.1.2 (Alanine Transaminase); EC 2.7.3.2 (Creatine Kinase); EC 3.2.1.20 (alpha-Glucosidases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171103
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008415


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[PMID]:28953679
[Au] Autor:Zhang F; Kanzali P; Rubin V; Paras C; Goldman J
[Ad] Endereço:aDepartment of Internal Medicine, Brookdale University Hospital and Medical Center, Brooklyn bRoss University School of Medicine, Portsmouth, Dominica cDivision of Endocrinology, Brookdale University Hospital and Medical Center, Brooklyn, New York.
[Ti] Título:Neuroleptic malignant syndrome with thyroid disorder: An unusual case report.
[So] Source:Medicine (Baltimore);96(39):e8191, 2017 Sep.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Neuroleptic malignant syndrome (NMS) is a life threatening neurologic emergency associated with neuroleptic or antipsychotic agent use. NMS is rarely related to thyroid disease. PATIENT CONCERNS: We report a case of NMS in a 66-year-old male with past medical history of paranoid schizophrenia on chlorpromazine, diabetes, hypertension and asthma, who presented with a humeral fracture after a fall. Patient developed hyperpyrexia, altered consciousness, autonomic instability, elevated serum creatine kinase (CK) without rigidity. DIAGNOSES: CT head and workup for infection were negative. Electroencephalogram (EEG) showed generalized slow wave activity. Ultrasound revealed a large goiter with nodules. INTERVENTIONS: Chlorpromazine was stopped due to concern of NMS. Patient was treated with cooling, fluid and electrolyte maintenance. OUTCOMES: Patient slowly improved and CK level normalized. Thyroid-stimulating hormone (TSH) level trended down from 10.2 mIU/L to 0.02 mIU/L. Patient was discharged with aripiprazole. LESSONS: Hypothyroidism predisposes patients to NMS by altering central dopaminergic systems. The typical symptoms may be masked by hypothyroidism. Thyroid dysfunction should be excluded in all patients with NMS. Discontinuing antipsychotic agents decreases TSH levels which maybe due to the negative feedback of dopaminergic activity. This is the first case report describing dramatic changes in TSH after discontinuing chlorpromazine in NMS.
[Mh] Termos MeSH primário: Aripiprazol
Clorpromazina
Hipotireoidismo
Síndrome Maligna Neuroléptica
Esquizofrenia Paranoide
Nódulo da Glândula Tireoide/diagnóstico por imagem
[Mh] Termos MeSH secundário: Idoso
Antipsicóticos/administração & dosagem
Antipsicóticos/efeitos adversos
Aripiprazol/administração & dosagem
Aripiprazol/efeitos adversos
Clorpromazina/administração & dosagem
Clorpromazina/efeitos adversos
Creatina Quinase/análise
Diagnóstico Diferencial
Substituição de Medicamentos/métodos
Hidratação/métodos
Seres Humanos
Hipotireoidismo/complicações
Hipotireoidismo/diagnóstico
Hipotireoidismo/terapia
Masculino
Síndrome Maligna Neuroléptica/diagnóstico
Síndrome Maligna Neuroléptica/etiologia
Síndrome Maligna Neuroléptica/fisiopatologia
Síndrome Maligna Neuroléptica/terapia
Esquizofrenia Paranoide/complicações
Esquizofrenia Paranoide/tratamento farmacológico
Tireotropina/análise
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antipsychotic Agents); 82VFR53I78 (Aripiprazole); 9002-71-5 (Thyrotropin); EC 2.7.3.2 (Creatine Kinase); U42B7VYA4P (Chlorpromazine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170928
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008191



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