Frequency of OBI among patients with autoimmune hepatitis

Autoimmune hepatitis (AIH) is recognized as a serious disease in which the body's immune system attacks liver cells so untreated patients may consequently suffer from liver cirrhosis, hepatocellular carcinoma (HCC) and liver failure. The role of viral infection may be involved in AIH. Presence of anti-HBc alone is a predictive signal of potential OBI. Thus, this study was conducted to evaluate the rate OBI among the patients with AIH. Methods: The sera of 20 consecutive patients with AIH were collected and tested for LFT (ALT, AST, ALP elevation), Immunoglobulin (IgG) level, bilirubin, anti-LKM-1, ASMA, ANA in titer, HBsAg, HBcIgG. The patients' sera were also tested for HBV DNA by nested PCR and Real-time PCR. Results: Out of 20 patients, 10 (50) were males and 10 (50) females. The patients' ages ranged from 25 to 71 years with the mean age of 44.5±13.4. All patients' had elevated abnormal ALT and AST but their level of alkaline phosphatase was normal among the patients. All patients had IgG level>1.5 times upper than the normal limit. The patients' sera were negative for HBsAg and HBV DNA (by nested PCR and real-time PCR). Only 2 (10) females with AHI type 1 (positive ANA, ASMA in titers >1:100 were positive for HBcIgG while no OBI detection was found among the males (p=0.005). All diagnosis of the AHI was confirmed by pathologist. The level of ALT, AST among the cases with positive and negative OBI were (p=0.000) and (p=0.003), respectively. Conclusion: In the present study, two OBI female patients with type 1 AIH were positive for anti-HBc but negative for HBsAg and HBV DNA. With regard to the consequences of OBI, prior to prophylactic treatment, it is recommended to screen HBV markers including anti-HBc in all diagnosed patients with AIH. © 2020 Asian Pacific Organization for Cancer Prevention

Effects of long-term low-dose oxygen supplementation on the epithelial function, collagen metabolism and interstitial fibrogenesis in the guinea pig lung

<p>Abstract</p> <p>Background</p> <p>The patient population receiving long-term oxygen therapy has increased with the rising morbidity of COPD. Although high-dose oxygen induces pulmonary edema and interstitial fibrosis, potential lung injury caused by long-term exposure to low-dose oxygen has not been fully analyzed. This study was designed to clarify the effects of long-term low-dose oxygen inhalation on pulmonary epithelial function, edema formation, collagen metabolism, and alveolar fibrosis.</p> <p>Methods</p> <p>Guinea pigs (n = 159) were exposed to either 21% or 40% oxygen for a maximum of 16 weeks, and to 90% oxygen for a maximum of 120 hours. Clearance of inhaled technetium-labeled diethylene triamine pentaacetate (Tc-DTPA) and bronchoalveolar lavage fluid-to-serum ratio (BAL/Serum) of albumin (ALB) were used as markers of epithelial permeability. Lung wet-to-dry weight ratio (W/D) was measured to evaluate pulmonary edema, and types I and III collagenolytic activities and hydroxyproline content in the lung were analyzed as indices of collagen metabolism. Pulmonary fibrotic state was evaluated by histological quantification of fibrous tissue area stained with aniline blue.</p> <p>Results</p> <p>The clearance of Tc-DTPA was higher with 2 week exposure to 40% oxygen, while BAL/Serum Alb and W/D did not differ between the 40% and 21% groups. In the 40% oxygen group, type I collagenolytic activities at 2 and 4 weeks and type III collagenolytic activity at 2 weeks were increased. Hydroxyproline and fibrous tissue area were also increased at 2 weeks. No discernible injury was histologically observed in the 40% group, while progressive alveolar damage was observed in the 90% group.</p> <p>Conclusion</p> <p>These results indicate that epithelial function is damaged, collagen metabolism is affected, and both breakdown of collagen fibrils and fibrogenesis are transiently induced even with low-dose 40% oxygen exposure. However, these changes are successfully compensated even with continuous exposure to low-dose oxygen. We conclude that long-term low-dose oxygen exposure does not significantly induce permanent lung injury in guinea pigs.</p

Estimation of the acoustic impedance of lung versus level of inflation for different species and ages of animals

In a previous study, it was hypothesized that ultrasound-induced lung damage was related to the transfer of ultrasonic energy into the lungs (W. D. O’Brien et al. 2002, “Ultrasound-induced lung hemorrhage: Role of acoustic boundary conditions at the pleural surface,” J. Acoust. Soc. Am. 111, 1102–1109). From this study a technique was developed to: 1) estimate the impedance (Mrayl) of fresh, excised, ex vivo rat lung versus its level of inflation (cm H2O) and 2) predict the fraction of ultrasonic energy transmitted into the lung (M. Oelze et al. 2003, “Impedance measurements of ex vivo rat lung at different volumes of inflation.” J. Acoust. Soc. Am. 114, 3384–3393). In the current study, the same technique was used to estimate the frequency-dependent impedance of lungs from rats, rabbits, and pigs of various ages. Impedance values were estimated from lungs under deflation (atmospheric pressure, 0 cm H2O) and three volumes of inflation pressure [7 cm H2O (5 cm H2O for pigs), 10 cm H2O, and 15 cm H2O]. Lungs were scanned in a tank of degassed 37 °C water. The frequency-dependent acoustic pressure reflection coefficient was determined over a frequency range of 3.5–10 MHz. From the reflection coefficient, the frequency-dependent lung impedance was calculated with values ranging from an average of 1.4 Mrayl in deflated lungs (atmospheric pressure) to 0.1 Mrayl for fully inflated lungs (15 cm H2O). Across all species, deflated lung (i.e., approximately 7% of the total lung capacity) had impedance values closer to tissue values, suggesting that more acoustic energy was transmitted into the lung under deflated conditions. Finally, the impedance values of deflated lungs from different species at different ages were compared with the thresholds for ultrasound-induced lung damage. The comparison revealed that increases in ultrasonic energy transmission corresponded to lower injury threshold values