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[PMID]:28674042
[Au] Autor:Bongers EMHF; Shelton LM; Milatz S; Verkaart S; Bech AP; Schoots J; Cornelissen EAM; Bleich M; Hoenderop JGJ; Wetzels JFM; Lugtenberg D; Nijenhuis T
[Ad] Endereço:Departments of Human Genetics.
[Ti] Título:A Novel Hypokalemic-Alkalotic Salt-Losing Tubulopathy in Patients with Mutations.
[So] Source:J Am Soc Nephrol;28(10):3118-3128, 2017 Oct.
[Is] ISSN:1533-3450
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mice lacking distal tubular expression of , the gene encoding the tight junction protein Claudin-10, show enhanced paracellular magnesium and calcium permeability and reduced sodium permeability in the thick ascending limb (TAL), leading to a urine concentrating defect. However, the function of renal Claudin-10 in humans remains undetermined. We identified and characterized mutations in two patients with a hypokalemic-alkalotic salt-losing nephropathy. The first patient was diagnosed with Bartter syndrome (BS) >30 years ago. At re-evaluation, we observed hypocalciuria and hypercalcemia, suggesting Gitelman syndrome (GS). However, serum magnesium was in the upper normal to hypermagnesemic range, thiazide responsiveness was not blunted, and genetic analyses did not show mutations in genes associated with GS or BS. Whole-exome sequencing revealed compound heterozygous sequence variants [c.446C>G (p.Pro149Arg) and c.465-1G>A (p.Glu157_Tyr192del)]. The patient had reduced urinary concentrating ability, with a preserved aquaporin-2 response to desmopressin and an intact response to furosemide. These findings were not in line with any other known salt-losing nephropathy. Subsequently, we identified a second unrelated patient showing a similar phenotype, in whom we detected compound heterozygous sequence variants [c.446C>G (p.(Pro149Arg) and c.217G>A (p.Asp73Asn)]. Cell surface biotinylation and immunofluorescence experiments in cells expressing the encoded mutants showed that only one mutation caused significant differences in Claudin-10 membrane localization and tight junction strand formation, indicating that these alterations do not fully explain the phenotype. These data suggest that pathogenic mutations affect TAL paracellular ion transport and cause a novel tight junction disease characterized by a non-BS, non-GS autosomal recessive hypokalemic-alkalotic salt-losing phenotype.
[Mh] Termos MeSH primário: Alcalose/genética
Claudinas/genética
Hipopotassemia/genética
Erros Inatos do Transporte Tubular Renal/genética
[Mh] Termos MeSH secundário: Adolescente
Feminino
Seres Humanos
Masculino
Adulto Jovem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Claudins); 0 (claudin 10)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170705
[St] Status:MEDLINE
[do] DOI:10.1681/ASN.2016080881


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[PMID]:28550912
[Au] Autor:Nissen M; Cernaianu G; Thränhardt R; Vahdad MR; Barenberg K; Tröbs RB
[Ad] Endereço:Department of Pediatric Surgery, St. Mary's Hospital, St. Elisabeth Group, Ruhr-University of Bochum, Herne, Germany. Electronic address: matthias.nissen@elisabethgruppe.de.
[Ti] Título:Does metabolic alkalosis influence cerebral oxygenation in infantile hypertrophic pyloric stenosis?
[So] Source:J Surg Res;212:229-237, 2017 May 15.
[Is] ISSN:1095-8673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: This pilot study focuses on regional tissue oxygenation (rSO ) in patients with infantile hypertrophic pyloric stenosis in a perioperative setting. To investigate the influence of enhanced metabolic alkalosis (MA) on cerebral (c-rSO ) and renal (r-rSO ) tissue oxygenation, two-site near-infrared spectroscopy (NIRS) technology was applied. MATERIALS AND METHODS: Perioperative c-rSO , r-rSO , capillary blood gases, and electrolytes from 12 infants were retrospectively compared before and after correction of MA at admission (T1), before surgery (T2), and after surgery (T3). RESULTS: Correction of MA was associated with an alteration of cerebral oxygenation without affecting renal oxygenation. When compared to T1, 5-min mean (± standard deviation) c-rSO increased after correction of MA at T2 (72.74 ± 4.60% versus 77.89 ± 5.84%; P = 0.058), reaching significance at T3 (80.79 ± 5.29%; P = 0.003). Furthermore, relative 30-min c-rSO values at first 3 h of metabolic compensation were significantly lowered compared with postsurgical states at 16 and 24 h. Cerebral oxygenation was positively correlated with levels of sodium (r = 0.37; P = 0.03) and inversely correlated with levels of bicarbonate (r = -0.34; P = 0.05) and base excess (r = -0.36; P = 0.04). Analysis of preoperative and postoperative cerebral and renal hypoxic burden yielded no differences. However, a negative correlation (r = -0.40; P = 0.03) regarding hematocrite and mean r-rSO , indirectly indicative of an increased renal blood flow under hemodilution, was obtained. CONCLUSIONS: NIRS seems suitable for the detection of a transiently impaired cerebral oxygenation under state of pronounced MA in infants with infantile hypertrophic pyloric stenosis. Correction of MA led to normalization of c-rSO . NIRS technology constitutes a promising tool for optimizing perioperative management, especially in the context of a possible diminished neurodevelopmental outcome after pyloromyotomy.
[Mh] Termos MeSH primário: Alcalose/metabolismo
Encéfalo/metabolismo
Rim/metabolismo
Oxigênio/metabolismo
Estenose Pilórica Hipertrófica/fisiopatologia
[Mh] Termos MeSH secundário: Alcalose/etiologia
Alcalose/terapia
Biomarcadores/metabolismo
Feminino
Seres Humanos
Lactente
Recém-Nascido
Masculino
Período Perioperatório
Projetos Piloto
Estenose Pilórica Hipertrófica/cirurgia
Estudos Retrospectivos
Espectroscopia de Luz Próxima ao Infravermelho
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Biomarkers); S88TT14065 (Oxygen)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170913
[Lr] Data última revisão:
170913
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170529
[St] Status:MEDLINE


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[PMID]:28501971
[Au] Autor:Jiménez JV; Carrillo-Pérez DL; Rosado-Canto R; García-Juárez I; Torre A; Kershenobich D; Carrillo-Maravilla E
[Ad] Endereço:Department of Internal Medicine, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Tlalpan, 14080, Mexico City, Mexico.
[Ti] Título:Electrolyte and Acid-Base Disturbances in End-Stage Liver Disease: A Physiopathological Approach.
[So] Source:Dig Dis Sci;62(8):1855-1871, 2017 Aug.
[Is] ISSN:1573-2568
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Electrolyte and acid-base disturbances are frequent in patients with end-stage liver disease; the underlying physiopathological mechanisms are often complex and represent a diagnostic and therapeutic challenge to the physician. Usually, these disorders do not develop in compensated cirrhotic patients, but with the onset of the classic complications of cirrhosis such as ascites, renal failure, spontaneous bacterial peritonitis and variceal bleeding, multiple electrolyte, and acid-base disturbances emerge. Hyponatremia parallels ascites formation and is a well-known trigger of hepatic encephalopathy; its management in this particular population poses a risky challenge due to the high susceptibility of cirrhotic patients to osmotic demyelination. Hypokalemia is common in the setting of cirrhosis: multiple potassium wasting mechanisms both inherent to the disease and resulting from its management make these patients particularly susceptible to potassium depletion even in the setting of normokalemia. Acid-base disturbances range from classical respiratory alkalosis to high anion gap metabolic acidosis, almost comprising the full acid-base spectrum. Because most electrolyte and acid-base disturbances are managed in terms of their underlying trigger factors, a systematic physiopathological approach to their diagnosis and treatment is required.
[Mh] Termos MeSH primário: Desequilíbrio Ácido-Base/fisiopatologia
Doença Hepática Terminal/fisiopatologia
Desequilíbrio Hidroeletrolítico/fisiopatologia
[Mh] Termos MeSH secundário: Desequilíbrio Ácido-Base/etiologia
Alcalose/etiologia
Alcalose/fisiopatologia
Progressão da Doença
Doença Hepática Terminal/complicações
Seres Humanos
Hipopotassemia/etiologia
Hipopotassemia/fisiopatologia
Hiponatremia/etiologia
Hiponatremia/fisiopatologia
Desequilíbrio Hidroeletrolítico/etiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170515
[St] Status:MEDLINE
[do] DOI:10.1007/s10620-017-4597-8


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[PMID]:28280973
[Au] Autor:Deb SK; Gough LA; Sparks SA; McNaughton LR
[Ad] Endereço:Department of Sport and Physical Activity, Edge Hill University, St Helen's Road, Ormskirk, L39 4QP, UK.
[Ti] Título:Determinants of curvature constant (W') of the power duration relationship under normoxia and hypoxia: the effect of pre-exercise alkalosis.
[So] Source:Eur J Appl Physiol;117(5):901-912, 2017 May.
[Is] ISSN:1439-6327
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: This study investigated the effect of induced alkalosis on the curvature constant (W') of the power-duration relationship under normoxic and hypoxic conditions. METHODS: Eleven trained cyclists (mean ± SD) Age: 32 ± 7.2 years; body mass (bm): 77.0 ± 9.2 kg; VO : 59.2 ± 6.8 ml·kg ·min completed seven laboratory visits which involved the determination of individual time to peak alkalosis following sodium bicarbonate (NaHCO ) ingestion, an environment specific ramp test (e.g. normoxia and hypoxia) and four x 3 min critical power (CP) tests under different experimental conditions. Participants completed four trials: alkalosis normoxia (ALN); placebo normoxia (PLN); alkalosis hypoxia (ALH); and placebo hypoxia (PLH). Pre-exercise administration of 0.3 g.kg BM of NaHCO was used to induce alkalosis. Environmental conditions were set at either normobaric hypoxia (FiO : 14.5%) or normoxia (FiO : 20.93%). RESULTS: An increase in W' was observed with pre-exercise alkalosis under both normoxic (PLN: 15.1 ± 6.2 kJ vs. ALN: 17.4 ± 5.1 kJ; P = 0.006) and hypoxic conditions (ALN: 15.2 ± 4.9 kJ vs. ALN: 17.9 ± 5.2 kJ; P < 0.001). Pre-exercise alkalosis resulted in a larger reduction in bicarbonate ion (HCO ) concentrations during exercise in both environmental conditions (p < 0.001) and a greater blood lactate accumulation under hypoxia (P = 0.012). CONCLUSION: Pre-exercise alkalosis substantially increased W' and, therefore, may determine tolerance to exercise above CP under normoxic and hypoxic conditions. This may be due to NaHCO increasing HCO buffering capacity to delay exercise-induced acidosis, which may, therefore, enhance anaerobic energy contribution.
[Mh] Termos MeSH primário: Alcalose/metabolismo
Tolerância ao Exercício
Exercício
Hipóxia/metabolismo
[Mh] Termos MeSH secundário: Adulto
Alcalose/etiologia
Alcalose/fisiopatologia
Limiar Anaeróbio
Seres Humanos
Hipóxia/fisiopatologia
Masculino
Consumo de Oxigênio
Bicarbonato de Sódio/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
8MDF5V39QO (Sodium Bicarbonate)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170311
[St] Status:MEDLINE
[do] DOI:10.1007/s00421-017-3574-4


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[PMID]:28045915
[Au] Autor:Kreü S; Jazrawi A; Miller J; Baigi A; Chew M
[Ad] Endereço:Institute for Clinical Sciences Malmö, Lund University, Lund, Sweden.
[Ti] Título:Alkalosis in Critically Ill Patients with Severe Sepsis and Septic Shock.
[So] Source:PLoS One;12(1):e0168563, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Although metabolic alkalosis is a common occurrence in intensive care units (ICUs), no study has evaluated its prevalence or outcomes in patients with severe sepsis or septic shock. METHODS: This is a retrospective cohort study of critically ill patients suffering from severe sepsis and septic shock admitted to the ICUs of Halmstad and Varberg County hospitals. From 910 patient records, 627 patients met the inclusion criteria. We investigated the relationship between metabolic alkalosis and mortality. Further, we studied the relationship between metabolic alkalosis and ICU length of stay (LOS). RESULTS: Metabolic alkalosis was associated with decreased 30-day and 12-month mortalities. This effect was however lost when a multivariate analysis was conducted, correcting for age, gender, pH on admission, base excess (BE) on admission, Simplified Acute Physiology Score III (SAPS III) and acute kidney injury (AKI). We then analyzed for any dose-response effect between the severity of metabolic alkalosis and mortality and found no relationship. Bivariate analysis showed that metabolic alkalosis had a significant effect on the length of ICU stay. When adjusting for age, sex, pH at admission, BE at admission, SAPS III and AKI in a multivariate analysis, metabolic alkalosis significantly contributed to prolonged ICU length of stay. In two separate sensitivity analyses pure metabolic alkalosis and late metabolic alkalosis (time of onset >48 hours) were the only significant predictor of increased ICU length of stay. CONCLUSION: Metabolic alkalosis did not have any effect on 30-day and 12-month mortalities after adjusting for age, sex, SAPS III-score, pH and BE on admission and AKI in a multivariate analysis. The presence of metabolic alkalosis was independently associated with an increased ICU length of stay.
[Mh] Termos MeSH primário: Alcalose/sangue
Estado Terminal/epidemiologia
Sepse/sangue
Choque Séptico/sangue
[Mh] Termos MeSH secundário: Lesão Renal Aguda/complicações
Idoso
Feminino
Mortalidade Hospitalar
Seres Humanos
Concentração de Íons de Hidrogênio
Unidades de Terapia Intensiva
Tempo de Internação
Masculino
Meia-Idade
Análise Multivariada
Prevalência
Estudos Retrospectivos
Índice de Gravidade de Doença
Resultado do Tratamento
[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:170104
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0168563


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[PMID]:27914757
[Au] Autor:Foy DS; de Morais HA
[Ad] Endereço:College of Veterinary Medicine, Midwestern University, 5715 West Utopia Road, Glendale, AZ 85308, USA. Electronic address: dfoy1@midwestern.edu.
[Ti] Título:A Quick Reference on Metabolic Alkalosis.
[So] Source:Vet Clin North Am Small Anim Pract;47(2):197-200, 2017 Mar.
[Is] ISSN:1878-1306
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Metabolic alkalemia is characterized by an increase in bicarbonate concentration and base excess, an increase in pH, and a compensatory increase in carbon dioxide pressure. This article outlines indications for analysis, reference ranges, causes, and clinical signs of metabolic alkalosis. Algorithms for evaluation of patients with acid-base disorders and metabolic alkalosis are included.
[Mh] Termos MeSH primário: Alcalose/veterinária
Doenças do Gato/etiologia
Doenças do Cão/etiologia
[Mh] Termos MeSH secundário: Desequilíbrio Ácido-Base
Alcalose/diagnóstico
Alcalose/etiologia
Animais
Bicarbonatos/metabolismo
Doenças do Gato/diagnóstico
Gatos
Doenças do Cão/diagnóstico
Cães
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Bicarbonates)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170721
[Lr] Data última revisão:
170721
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161205
[St] Status:MEDLINE


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[PMID]:27804847
[Au] Autor:Schwartz L; Supuran CT; Alfarouk KO
[Ad] Endereço:Assistance Publique des Hopitaux de Paris,France.
[Ti] Título:The Warburg Effect and the Hallmarks of Cancer.
[So] Source:Anticancer Agents Med Chem;17(2):164-170, 2017.
[Is] ISSN:1875-5992
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:It is a longstanding debate whether cancer is one disease or a set of very diverse diseases. The goal of this paper is to suggest strongly that most of (if not all) the hallmarks of cancer could be the consequence of the Warburg's effect. As a result of the metabolic impairment of the oxidative phosphorylation, there is a decrease in ATP concentration. To compensate the reduced energy yield, there is massive glucose uptake, anaerobic glycolysis, with an up-regulation of the Pentose Phosphate Pathway resulting in increased biosynthesis leading to increased cell division and local pressure. This increased pressure is responsible for the fractal shape of the tumor, the secretion of collagen by the fibroblasts and plays a critical role in metastatic spread. The massive extrusion of lactic acid contributes to the extracellular acidity and the activation of the immune system. The decreased oxidative phosphorylation leads to impairment in CO2 levels inside and outside the cell, with increased intracellular alkalosis and contribution of carbonic acid to extracellular acidosis-mediated by at least two cancer-associated carbonic anhydrase isoforms. The increased intracellular alkalosis is a strong mitogenic signal, which bypasses most inhibitory signals. Mitochondrial disappearance (such as seen in very aggressive tumors) is a consequence of mitochondrial swelling, itself a result of decreased ATP concentration. The transmembrane pumps, which extrude, from the mitochondria, ions, and water, are ATP-dependant. Therapy aiming at increasing both the number and the efficacy of mitochondria could be very useful.
[Mh] Termos MeSH primário: Trifosfato de Adenosina/metabolismo
Glucose/metabolismo
Neoplasias/metabolismo
Fosforilação Oxidativa
[Mh] Termos MeSH secundário: Acidose/metabolismo
Alcalose/metabolismo
Animais
Dióxido de Carbono/metabolismo
Proliferação Celular
Citratos/metabolismo
Glicólise
Seres Humanos
Mitocôndrias/metabolismo
Mitocôndrias/patologia
Neoplasias/patologia
Via de Pentose Fosfato
Ácido Tióctico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Citrates); 142M471B3J (Carbon Dioxide); 73Y7P0K73Y (Thioctic Acid); 8L70Q75FXE (Adenosine Triphosphate); 8W94T9026R (hydroxycitric acid); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170531
[Lr] Data última revisão:
170531
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161103
[St] Status:MEDLINE


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[PMID]:27752015
[Au] Autor:Gandhi K; Prasad D; Malhotra V; Agrawal D
[Ad] Endereço:Department of Nephrology, Sawai Man Singh Hospital, Jaipur, Rajasthan, India.
[Ti] Título:Gitelman's syndrome presenting with hypocalcemic tetany and hypokalemic periodic paralysis.
[So] Source:Saudi J Kidney Dis Transpl;27(5):1026-1028, 2016 Sep-Oct.
[Is] ISSN:1319-2442
[Cp] País de publicação:Saudi Arabia
[La] Idioma:eng
[Ab] Resumo:Gitelman's syndrome is an autosomal recessive renal tubular disorder characterized by hypomagnesemia, hypokalemia, hypocalciuria, and metabolic alkalosis. Hypocalcemic tetany as a presentation of Gitelman's syndrome has rarely been reported in literature. We report a rare case of Gitelman's syndrome presenting with hypocalcemic tetany along with hypokalemic periodic paralysis. A 17-year-old female was admitted to our hospital with a history of perioral numbness and carpal spasms of five days duration with progressive quadriparesis developing over a period of few hours. Past history was significant for three episodes of transient lower limb weakness. On examination, blood pressure was 110/70 mm Hg. Chvostek's sign and Trousseau's sign were positive. Neurologically, she was fully oriented. She had Grade 3 power in all the four limbs with intact sensation. Laboratory tests showed hypocalcemia (7.8 mg/dL), hypokalemia (2.2 mEq/L), hypomagnesemia (0.9 mEq/L), and hypocalciuria (104 mg/day). Arterial blood gas showed mild metabolic alkalosis with respiratory compensation. Thus, a clinical diagnosis of GS was made. The patient made a remarkable recovery after the correction of electrolyte imbalance. The aim of this case report is to re-emphasize the fact that hypocalcemia can rarely occur in Gitelman's syndrome.
[Mh] Termos MeSH primário: Síndrome de Gitelman
Paralisia Periódica Hipopotassêmica
Tetania
[Mh] Termos MeSH secundário: Adolescente
Alcalose
Síndrome de Bartter
Feminino
Seres Humanos
Hipopotassemia
[Pt] Tipo de publicação:CASE REPORTS
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170831
[Lr] Data última revisão:
170831
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161019
[St] Status:MEDLINE
[do] DOI:10.4103/1319-2442.190881


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[PMID]:27748700
[Au] Autor:López C; Alcaraz AJ; Toledo B; Cortejoso L; Gil-Ruiz MA
[Ad] Endereço:1Division of Neonatal Critical Care, Gregorio Marañón General University Hospital, Madrid, Spain.2Department of Pediatrics, Getafe University Hospital, Universidad Europea de Madrid, Research Network on Maternal and Child Health and Development, Getafe, Madrid, Spain.3Red SAMID, Spain.4Division of Pediatric Critical Care, Gregorio Marañon General University Hospital, Madrid, Spain.5Hospital Pharmacy Service, Gregorio Marañón General University Hospital, Madrid, Spain.
[Ti] Título:Acetazolamide Therapy for Metabolic Alkalosis in Pediatric Intensive Care Patients.
[So] Source:Pediatr Crit Care Med;17(12):e551-e558, 2016 Dec.
[Is] ISSN:1529-7535
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Patients in PICUs frequently present hypochloremic metabolic alkalosis secondary to loop diuretic treatment, especially those undergoing cardiac surgery. This study evaluates the effectiveness of acetazolamide therapy for metabolic alkalosis in PICU patients. DESIGN: Retrospective, observational study. SETTING: A tertiary care children's hospital PICU. PATIENTS: Children receiving at least a 2-day course of enteral acetazolamide. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Demographic variables, diuretic treatment and doses of acetazolamide, urine output, serum electrolytes, urea and creatinine, acid-base excess, pH, and use of mechanical ventilation during treatment were collected. Patients were studied according to their pathology (postoperative cardiac surgery, decompensated heart failure, or respiratory disease). A total of 78 episodes in 58 patients were identified: 48 were carried out in cardiac postoperative patients, 22 in decompensated heart failure, and eight in respiratory patients. All patients received loop diuretics. A decrease in pH and PCO2 in the first 72 hours, a decrease in serum HCO3 (mean, 4.65 ± 4.83; p < 0.001), and an increase in anion gap values were observed. Urine output increased in cardiac postoperative patients (4.5 ± 2.2 vs 5.1 ± 2.0; p = 0.020), whereas diuretic treatment was reduced in cardiac patients. There was no significant difference in serum electrolytes, blood urea, creatinine, nor chloride after the administration of acetazolamide from baseline. Acetazolamide treatment was well tolerated in all patients. CONCLUSIONS: Acetazolamide decreases serum HCO3 and PCO2 in PICU cardiac patients with metabolic alkalosis secondary to diuretic therapy. Cardiac postoperative patients present a significant increase in urine output after acetazolamide treatment.
[Mh] Termos MeSH primário: Acetazolamida/uso terapêutico
Alcalose/tratamento farmacológico
Inibidores da Anidrase Carbônica/uso terapêutico
Cuidados Críticos/métodos
[Mh] Termos MeSH secundário: Adolescente
Criança
Pré-Escolar
Esquema de Medicação
Feminino
Seres Humanos
Lactente
Recém-Nascido
Unidades de Terapia Intensiva Pediátrica
Modelos Lineares
Masculino
Estudos Retrospectivos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Carbonic Anhydrase Inhibitors); O3FX965V0I (Acetazolamide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161018
[St] Status:MEDLINE


  10 / 3333 MEDLINE  
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[PMID]:27697198
[Au] Autor:Koh C; Minns A; Rosen P
[Ad] Endereço:Division of Medical Toxicology, Department of Emergency Medicine, University of California, San Diego, San Diego, California.
[Ti] Título:A Practical Approach to the Ethanol-Intoxicated Patient in the Emergency Department.
[So] Source:J Emerg Med;51(4):463-464, 2016 Oct.
[Is] ISSN:0736-4679
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Intoxicação Alcoólica/complicações
Alcalose/complicações
[Mh] Termos MeSH secundário: Alcalose/diagnóstico
Alcalose/tratamento farmacológico
Deficiência de Vitaminas/complicações
Deficiência de Vitaminas/tratamento farmacológico
Desidratação/complicações
Desidratação/terapia
Serviço Hospitalar de Emergência
Hidratação
Seres Humanos
Hipoglicemia/complicações
Hipoglicemia/tratamento farmacológico
[Pt] Tipo de publicação:EDITORIAL
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171114
[Lr] Data última revisão:
171114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161005
[St] Status:MEDLINE



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