Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 5 de 5
Filtrar
Mais filtros

Base de dados
Tipo de documento
País de afiliação
Intervalo de ano de publicação
1.
Diabetes Metab Res Rev ; 33(8)2017 11.
Artigo em Inglês | MEDLINE | ID: mdl-28730683

RESUMO

Presence of fat in the pancreas increases the risk of metabolic co-morbidities. Detection and quantification of pancreatic fat is not a routine clinical practice, at least in part because of need to use expensive imaging techniques. We aimed to systematically review common markers of pancreatic fat in blood and to investigate differences in these markers associated with fatty pancreas. The search was conducted in 3 databases (EMBASE, Scopus, and MEDLINE). Studies in humans were eligible for inclusion if they reported on biological markers and percentage of pancreatic fat or fatty pancreas prevalence. Data were pooled for correlation and effect size meta-analysis. A total of 17 studies including 11 967 individuals were eligible for meta-analysis. Markers of lipid metabolism, including circulating triglycerides (r = 0.38 [95% confidence interval (CI) 0.31, 0.46]) and high-density lipoprotein cholesterol (r = -0.33 [95% CI -0.35, -0.31]), and markers of glucose metabolism, including glycated haemoglobin (r = 0.39 [95% CI 0.30, 0.48], insulin (r = 0.38 [95% CI 0.33, 0.43]), and homeostasis model assessment-insulin resistance (r = 0.37 [95% CI 0.30, 0.44], yielded the best correlations with percentage of pancreatic fat. Further, effect size analysis showed large and medium effects for the above markers of lipid and glucose metabolism. Circulating levels of triglycerides and glycated haemoglobin appear to be the best currently available markers of pancreatic fat. The approach of non-invasive and accurate detection of pancreatic fat by blood analysis should be further explored in the future, by investigating other potential biological markers of pancreatic fat.


Assuntos
Tecido Adiposo/metabolismo , Pâncreas/metabolismo , Biomarcadores/sangue , HDL-Colesterol/sangue , Humanos , Resistência à Insulina/fisiologia , Metabolismo dos Lipídeos/fisiologia , Lipídeos/sangue , Triglicerídeos/sangue
2.
Am J Physiol Gastrointest Liver Physiol ; 311(1): G50-8, 2016 07 01.
Artigo em Inglês | MEDLINE | ID: mdl-27173509

RESUMO

Abnormal glucose metabolism is present in almost 40% of patients after acute pancreatitis, but its pathophysiology has been poorly investigated. Pancreatic hormone derangements have been sparingly studied to date, and their relationship with abnormal glucose metabolism is largely unknown. The aim was to investigate the associations between pancreatic hormones and glucose metabolism after acute pancreatitis, including the effect of potential confounders. This was a cross-sectional study of 83 adult patients after acute pancreatitis. Fasting venous blood was collected from all patients and used for analysis of insulin, glucagon, pancreatic polypeptide, amylin, somatostatin, C-peptide, glucose, and hemoglobin A1c. Statistical analyses were conducted using the modified Poisson regression, multivariable linear regression, and Spearman's correlation. Age, sex, body mass index, recurrence of acute pancreatitis, duration from first attack, severity, and etiology were adjusted for. Increased insulin was significantly associated with abnormal glucose metabolism after acute pancreatitis, in both unadjusted (P = 0.038) and adjusted (P = 0.001) analyses. Patients with abnormal glucose metabolism also had significantly decreased pancreatic polypeptide (P = 0.001) and increased amylin (P = 0.047) in adjusted analyses. Somatostatin, C-peptide, and glucagon were not changed significantly in both unadjusted and adjusted analyses. Increased insulin resistance and reduced insulin clearance may be important components of hyperinsulinemic compensation in patients after acute pancreatitis. Increased amylin and reduced pancreatic polypeptide fasting levels characterize impaired glucose homeostasis. Clinical studies investigating islet-cell hormonal responses to mixed-nutrient meal testing and euglycemic-hyperinsulinemic clamps are now warranted for further insights into the role of pancreatic hormones in glucose metabolism derangements secondary to pancreatic diseases.


Assuntos
Glicemia/metabolismo , Hormônios Pancreáticos/sangue , Pancreatite/sangue , Pancreatite/enzimologia , Doença Aguda , Adulto , Idoso , Biomarcadores/sangue , Distribuição de Qui-Quadrado , Estudos Transversais , Jejum/sangue , Feminino , Glucagon/sangue , Hemoglobinas Glicadas/metabolismo , Humanos , Hiperinsulinismo/sangue , Hiperinsulinismo/etiologia , Insulina/sangue , Resistência à Insulina , Polipeptídeo Amiloide das Ilhotas Pancreáticas/sangue , Modelos Lineares , Masculino , Pessoa de Meia-Idade , Análise Multivariada , Polipeptídeo Pancreático/sangue , Pancreatite/complicações , Pancreatite/diagnóstico , Somatostatina/sangue
3.
Expert Rev Gastroenterol Hepatol ; 12(8): 757-766, 2018 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-29972077

RESUMO

INTRODUCTION: The pancreas plays a central role in metabolism and is involved in the pathogenesis of several diseases. Pancreas volume is a holistic quantitative measure of pancreas size but the clinical relevance of pancreas volumetry is poorly understood. Areas covered: The aim was to systematically review studies in adults that used computed tomography or magnetic resonance imaging to measure pancreas volume in health and disease, to determine normal pancreas volume range, and to quantify changes in pancreas volume that are associated with disease. Expert commentary: The normal pancreas volume range in adults is 71-83 cm3, with no statistically significant difference between men and women. Type 2 diabetes and type 1 diabetes are associated with a progressively reduced pancreas volume. Overweight and obesity are associated with a progressively increased pancreas volume. There is a paucity of studies on pancreas volume in the setting of diseases of the exocrine pancreas, which should become a research priority in the future.


Assuntos
Pâncreas/anatomia & histologia , Pâncreas/patologia , Pancreatopatias/diagnóstico por imagem , Complicações do Diabetes/complicações , Voluntários Saudáveis , Humanos , Imageamento por Ressonância Magnética , Tamanho do Órgão , Sobrepeso/complicações , Pâncreas/diagnóstico por imagem , Pancreatopatias/etiologia , Pancreatopatias/patologia , Valores de Referência , Tomografia Computadorizada por Raios X
4.
Metabolism ; 69: 1-13, 2017 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-28285638

RESUMO

OBJECTIVE: Growing evidence suggests that individuals with excessive fat in the pancreas are at an increased risk of chronic metabolic disorders. The aim was to systematically review studies on non-alcoholic fatty pancreas disease (NAFPD) with a view to determine its prevalence, associations with metabolic co-morbidities, and to suggest normal pancreatic fat percentage threshold. METHODS: Three electronic databases (MEDLINE, Scopus, and Embase) were queried. Studies in humans were eligible for inclusion if they provided data on NAFPD and/or pancreatic fat percentage. Where possible, data were pooled using random-effects meta-analysis and the effect of covariates analysed using meta-regression. RESULTS: Pooling data on pancreatic fat percentage from nine studies (1209 healthy individuals who underwent magnetic resonance imaging), yielded the weighted mean and weighted standard deviation of 4.48% and 0.87%, respectively. Pooling data on NAFPD from eleven studies (12,675 individuals), yielded the pooled prevalence of 33% (95% confidence interval, 24% - 41%). Meta-regression analysis showed that the prevalence of NAFPD was independent of age and sex. The presence of NAFPD was associated with a significantly increased risk of arterial hypertension (risk ratio 1.67; 95% confidence interval, 1.32-2.10; p<0.0001), diabetes mellitus (risk ratio 2.08; 95% confidence interval, 1.44-3.00; p=0.0001), and metabolic syndrome (risk ratio 2.37; 95% confidence interval, 2.07-2.71; p<0.0001). CONCLUSION: The findings indicate that NAFPD is a frequent clinical entity, associated with significantly increased risk of metabolic syndrome and its components. The normal pancreatic fat cut-off point of 6.2% may be recommended for use in future prospective studies.


Assuntos
Gorduras/metabolismo , Metabolismo dos Lipídeos/genética , Pâncreas/metabolismo , Pancreatopatias/genética , Animais , Humanos , Doenças Metabólicas/complicações , Doenças Metabólicas/epidemiologia , Doenças Metabólicas/genética , Pâncreas/patologia , Pancreatopatias/epidemiologia , Pancreatopatias/patologia , Prevalência
5.
Medicine (Baltimore) ; 95(5): e2463, 2016 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-26844455

RESUMO

Gastrointestinal (GI) dysmotility is a common complication in acute, critically ill, postoperative, and chronic patients that may lead to impaired nutrient delivery, poor clinical, and patient-reported outcomes. Several pharmacological and nonpharmacological interventions to treat GI dysmotility were investigated in dozens of clinical studies. However, they often yielded conflicting results, at least in part, because various (nonstandardized) definitions of GI dysmotility were used and methodological quality of studies was poor. While a universally accepted definition of GI dysmotility is yet to be developed, a systematic analysis of data derived from double-blind placebo-controlled randomized trials may provide robust data on absolute and relative effectiveness of various interventions as the study outcome (GI motility) was assessed in the least biased manner.To systematically review data from double-blind placebo-controlled randomized trials to determine and compare the effectiveness of interventions that affect GI motility.Three electronic databases (MEDLINE, SCOPUS, and EMBASE) were searched. A random effects model was used for meta-analysis. The summary estimates were reported as mean difference (MD) with the corresponding 95% confidence interval (CI).A total of 38 double-blind placebo-controlled randomized trials involving 2371 patients were eligible for inclusion in the systematic review. These studies investigated a total of 20 different interventions, of which 6 interventions were meta-analyzed. Of them, the use of dopamine receptor antagonists (MD, -8.99; 95% CI, -17.72 to -0.27; P = 0.04) and macrolides (MD, -26.04; 95% CI, -51.25 to -0.82; P = 0.04) significantly improved GI motility compared with the placebo group. The use of botulism toxin significantly impaired GI motility compared with the placebo group (MD, 5.31; 95% CI, -0.04 to 10.67; P = 0.05). Other interventions (dietary factors, probiotics, hormones) did not affect GI motility.Based on the best available data and taking into account the safety profile of each class of intervention, dopamine receptor antagonists and macrolides significantly improve GI motility and are medications of choice in treating GI dysmotility.


Assuntos
Antagonistas dos Receptores de Dopamina D2/uso terapêutico , Gastroenteropatias/tratamento farmacológico , Motilidade Gastrointestinal/efeitos dos fármacos , Macrolídeos/uso terapêutico , Método Duplo-Cego , Humanos , Ensaios Clínicos Controlados Aleatórios como Assunto
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA