The Enlargement of Abdominal Lymph Nodes Is a Characteristic of Autoimmune Liver Disease

Background. The enlargement of lymph nodes is a common clinical sign in connective tissue disease (CTD) and viral hepatitis. In this research, we evaluated the incidence of enlarged lymph nodes in autoimmune liver diseases (AILD). Moreover, we identified the clinical significance of abdominal lymph node enlargement in AILD. Methods. The characteristics of abdominal lymph nodes, including their morphology and distribution, were assessed by ultrasonography and computed tomography in 125 patients with AILD, 54 with viral hepatitis, 135 with CTD, and 80 healthy controls. The pathological and laboratory results of 106 AILD patients were collected to analyze the association between lymphadenectasis and disease activity. Results. Enlargement of abdominal lymph nodes was found in 69.6% of patients with AILD, 63% of patients with viral hepatitis, 29.6% of patients with CTD, and 2% of healthy controls. Alkaline phosphatase (ALP), glutamate transpeptidase (GGT), and immunoglobulin M (IgM) levels were significantly increased in AILD patients with lymphadenectasis (LA) in contrast to patients without lymphadenectasis (NLA) (P<0.05). The pathological characteristics of inflammation, cholestasis, and focal necrosis were more common in the LA group than in the NLA group (P<0.05). As shown by multivariate logistic regression analysis, interface hepatitis (OR=3.651, P<0.05), cholestasis (OR=8.137, P<0.05), and focal necrosis (OR=5.212, P<0.05) were related to LA. Conclusions. The percentage of abdominal lymph node enlargement in AILD subjects was significantly higher than that in CTD subjects. Therefore, the enlargement of lymph nodes can represent a noninvasive indicator of histological and biochemical inflammation activity in AILD

Nitric Oxide Mediates Inflammation in Type II Diabetes Mellitus through the PPARγ/eNOS Signaling Pathway

Inflammation accounts for the process of type II diabetes mellitus (T2DM), the specific mechanism of which is still to be elucidated yet. Nitric oxide (NO), a critical inflammation regulator, the role of which is the inflammation of T2DM, is rarely reported. Therefore, our study is aimed at exploring the effect of NO on the inflammation in T2DM and the corresponding mechanism. We analyzed the NO levels in plasma samples from T2DM patients and paired healthy adults by Nitric Oxide Analyzer then measured the expression of inflammatory cytokines (C-reactive protein, heptoglobin, IL-1β, TNF-α, IL-6) in insulin-induced HepG2 cells treated with NO donor or NO scavenger, and the PPARγ, eNOS, C-reactive protein, heptoglobin, IL-1β, TNF-α, and IL-6 levels were detected by RT-PCR and western blot in insulin-induced HepG2 cells transfected with si-PPARγ. The results showed that excess NO increased the inflammation marker levels in T2DM, which is activated by the PPARγ/eNOS pathway. These findings will strengthen the understanding of NO in T2DM and provide a new target for the treatment of T2DM