RESUMO
Liver sinusoidal endothelial cells (LSECs) are crucial to the maintenance of hepatic homeostasis under physiologic conditions, while under the conditions of pathological liver damage, LSEC can respond to the damage by changing their structure through the process called capillarization, thereby aggravating liver damage. In addition, the interaction between LSEC and other cells in the liver plays a certain role in the development and progression of liver fibrosis, especially the interaction between LSEC and hepatic stellate cells, which are the primary effector cells of liver fibrosis. This article mainly elaborates on the role of LSEC in the development and progression of liver fibrosis during chronic liver injury.
RESUMO
Objective To explore the risk of pituitary dysfunction for spontaneous subarachnoid hemor -rhage( s-SAH) patients and to evaluate its correlation with clinical data .Methods 63 cases of patients with s-SAH were selected.Indicators(serum adrenocorti cotrophic hormone (ACTH), growth hormone(GH), insulin-like growth factor-1(IGF-1), thyroid stimulating hormone(TSH), thyroxine(T4), triiodothyronine(T3), folli-cle-stimulating hormone(FSH), luteinizing hormone(LH), total testosterone(in males), estradiol(in females) and prolactin)dynamic observation were tested 7 days, 1 year, 2 years, 3 years after the onset.Results Thirty patients( 47.6%) had some type of pituitary dysfunction .ACTH deficiency was the most frequent disorder (14.3%), followed by GH deficiency(12.7%), hypogonadatrophic(6.3%), hypothyroidism(3.2%)and high prolactin(1.6%).six patients(9.5%)showed deficiencies in more than one axis .Hormone deficiency was relat-ed to vasospasm, Fisher grade 4(P<0.05)and recovery time.Conclusions A greater incidence of hormone de-ficiency after s-SAH was related with vasospasm , Fisher grade and recovery time .Follow-up time should be ex-tended.