Journal of Investigative Medicine

Cirrhosis is diagnosed in patients of all ages and is the end result of many different diseases. The aim of this study was to characterize clinical and ethnic features of adult patients who were admitted to the hospital at different (young/old) ages and examine associations between age and ethnicity within these groups.

In this retrospective analysis of a diverse cohort of 2017 patients with a clinical diagnosis of cirrhosis between January 2001 and December 2011, we focused on age, ethnicity, and outcome of patients with cirrhosis.

We identified 219 patients younger than the age of 40 years, including 87 (11%) of 802 white, 31 (6%) of 550 African American, and 89 (16%) of 550 Hispanic patients (P < 0.001). Ethnicity and causes of cirrhosis were found to have a significant correlation with age. Overall, Hispanic and white patients together were more than twice as likely to be diagnosed with cirrhosis at an age younger than 40 years compared with African American patients (P < 0.001). Autoimmune hepatitis caused cirrhosis at a younger age regardless of ethnicity (P < 0.001), whereas cryptogenic/nonalcoholic fatty liver disease/nonalcoholic steatohepatitis was more likely identified at an older age (P = 0.008). African American patients with cirrhosis due to either alcohol or hepatitis C virus were older than Hispanic (P < 0.001 and P = 0.003, respectively) and white patients (P < 0.001 and P < 0.001, respectively) at presentation. Finally, younger patients admitted with cirrhosis had a higher in-hospital mortality rate (P < 0.001).

The data suggest an association between ethnicity and age of cirrhosis diagnosis, both overall and in patients with certain cirrhosis etiologies. This work raises the possibility of an ethnic and/or genetic basis for cirrhosis.

Accumulating evidence shows that gradual loss of white matter integrity plays an important role in the development of Alzheimer disease (AD).

The aim of this research was to study the microstructural integrity of white matter in AD in vivo.

Global fractional anisotropy, global axial diffusivity (AxD), and global radial diffusivity (RD) were analyzed in subjects with normal controls (NC), mild cognitive impairment (MCI), and AD using Alzheimer's Disease Neuroimaging Initiative data (total N = 210). We further compared specific white matter tracts among the 3 groups.

Compared with the NC group, the MCI group had significantly increased global AxD and global RD. Compared with the NC and MCI groups, the AD group had significantly decreased global fractional anisotropy, increased global AxD, and increased global RD. With regard to specific white matter tracts, in the MCI group, we found increased AxD and increased RD in the external capsule, part of the lateral cholinergic pathway, in addition to the tracts connecting the limbic regions, predominantly in the left hemisphere. In the AD group, white matter abnormalities were widespread, including in the external capsule (cholinergic pathway) and limbic region tracts as well as tracts connecting anterior to posterior regions bilaterally.

The radiographic manifestation of damaged white matter microstructural integrity in the cholinergic pathway in MCI patients may provide a rational basis for the use of cholinesterase inhibitor drugs in the MCI stage of AD.

Recent studies suggest an important role for leptin in respiratory immune responses and pathogenesis of inflammatory respiratory diseases. There has been an interest to explore whether leptin plays any role in the pathogenesis of chronic obstructive pulmonary disease (COPD).

We conducted a population-based study to evaluate the relationship between serum leptin and COPD in the third US National Health and Nutrition Examination Survey participants.

Our study group was constituted by 6415 adults who had fasting serum leptin and underwent spirometry measurement.

Serum leptin levels were compared (1) between subjects with normal lung function and those with COPD and (2) among COPD subjects with different severities.

Among male participants, 2257 were controls, and 680 had COPD. Compared with controls, COPD subjects were older (62 vs 43 years) and had higher prevalence of smokers (78% vs 58%), lower body mass index (BMI) (26.3 vs 26.9), and higher serum leptin levels (6.6 vs 5.9). For female participants, 2918 were controls, and 560 had COPD. Those with COPD were older (60 vs 43 years) and had lower BMI (26.9 vs 27.7). No differences in serum leptin levels were observed. The independent predictors of COPD in both sexes were age, BMI, and smoking, but not serum leptin. There were no differences in serum leptin among COPD subjects with different severities.

We did not find any significant difference in the levels of serum leptin in subjects with COPD. Our data provide indirect evidence against a major role for serum leptin in the pathogenesis of COPD in humans.

Chronic obstructive pulmonary disease (COPD) results from an abnormal inflammatory response of the lungs to noxious particles or gases. Serum soluble urokinase-type plasminogen activator receptor (suPAR) is a glycoprotein secreted during infections and inflammation. The main goal of this study was to evaluate the serum suPAR level in stable COPD patients compared with a control group.

Forty-six stable COPD patients and 41 control subjects were included in the study. Blood samples were collected from 46 stable COPD patients (40 men, 6 women; mean [SD] age, 55.92 [7.91] years; the forced expiratory volume in 1 second, 45.32% [19.1%] of predicted). Forty-one healthy subjects were selected as control subjects and were matched to COPD patients with respect to age and body mass index. Serum suPAR and plasma fibrinogen levels were measured in stable COPD patients and control subjects.

Serum suPAR levels of the COPD patients were significantly higher than those of the control subjects (4.94 [2.79] and 2.40 [2.01] ng/mL, respectively; P < 0.001). Plasma fibrinogen levels of the COPD patients were significantly higher than those of the control subjects (406.77 [172.6] and 336.53 [96.1] g/L, respectively; P < 0.05).

Our study indicated that serum suPAR may play an important role in the inflammatory process of COPD, and this increase may be particularly large for patients in Global Initiative for Chronic Obstructive Lung Disease stages III and IV. Serum suPAR and plasma fibrinogen level measurements may be useful for the evaluation of stable COPD.