Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Mais filtros








Base de dados
Intervalo de ano de publicação
1.
Biochim Biophys Acta Mol Basis Dis ; 1870(6): 167275, 2024 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-38844112

RESUMO

Albumin infusions improve circulatory and renal function in patients with decompensated cirrhosis. However, there is no convincing evidence that hypoalbuminemia contributes to ascites formation in liver cirrhosis. The aim of our study is to determine the exact role of hypoalbuminemia in the formation of ascites caused by liver cirrhosis and its underlying mechanism. Clinical profiles of patients with liver cirrhosis retrospectively analyzed. The details of albumin involved in ascites formation were investigated in rat model and murine model. Statistical analysis demonstrated hypoalbuminemia was an independent risk factor for ascites formation in patients with liver cirrhosis (OR = 0.722, P < 0.001). In carbon tetrachloride (CCl4)-induced rat model of liver cirrhosis, a significant reduction in serum albumin was observed in rats with ascites (13.37 g/L) compared with rats without ascites (21.43 g/L, P < 0.001). In thioacetamide (TAA)-treated mice, ascites amount of heterozygous albumin (Alb+/-) mice (112.0 mg) was larger than that of wild-type (Alb+/+) mice (58.46 mg, P < 0.001). In CCl4-induced chronic liver injury, ascites amounts of Alb+/- or Alb+/+ mice were 80.00 mg or 48.46 mg (P = 0.001). Further study demonstrated 24-h urinary sodium excretion in Alb+/- mice was lower than that of Alb+/+ mice in TAA/CCl4-induce murine models of liver cirrhosis. Additionally, serum sodium concentration of Alb+/- mice was lower than that of Alb+/+ mice. In cirrhotic mice, higher level of antidiuretic hormone was observed in Alb+/- mice compared with the control; and renal aquaporin (AQP2) expression in Alb+/- mice was significantly higher than that of WT mice. These revealed hypoalbuminemia contributed to the occurrence of ascites in liver cirrhosis through sodium and water retention.


Assuntos
Ascite , Hipoalbuminemia , Cirrose Hepática , Sódio , Animais , Hipoalbuminemia/metabolismo , Hipoalbuminemia/patologia , Ascite/metabolismo , Ascite/patologia , Sódio/metabolismo , Sódio/urina , Camundongos , Masculino , Humanos , Cirrose Hepática/metabolismo , Cirrose Hepática/patologia , Cirrose Hepática/complicações , Cirrose Hepática/genética , Feminino , Ratos , Tetracloreto de Carbono/toxicidade , Tetracloreto de Carbono/efeitos adversos , Pessoa de Meia-Idade , Aquaporina 2/metabolismo , Aquaporina 2/genética , Modelos Animais de Doenças , Estudos Retrospectivos , Albumina Sérica/metabolismo , Tioacetamida , Água/metabolismo , Idoso
2.
BMC Pediatr ; 24(1): 203, 2024 Mar 22.
Artigo em Inglês | MEDLINE | ID: mdl-38519924

RESUMO

Langerhans cell histiocytosis (LCH) involving the gastrointestinal tract is a rare condition for which clinical experience is limited. We describe the cases of two patients who initially presented with chronic diarrhoea, hypoproteinaemia, and intermittent fever. These findings suggest that in cases of refractory diarrhoea accompanied by recurrent hypoalbuminaemia, especially with abdominal rash, LCH should be considered. Gastrointestinal endoscopy, biopsy, and imaging studies are essential for obtaining a definitive diagnosis. This approach might be helpful for the early recognition of gastrointestinal tract involvement in LCH.


Assuntos
Histiocitose de Células de Langerhans , Hipoalbuminemia , Criança , Humanos , Hipoalbuminemia/complicações , Hipoalbuminemia/patologia , Histiocitose de Células de Langerhans/complicações , Histiocitose de Células de Langerhans/diagnóstico , Histiocitose de Células de Langerhans/patologia , Trato Gastrointestinal/patologia , Biópsia , Diarreia/complicações
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA