[Analysis of clinical characteristics and risk factors for nosocomial mortality in patients with liver cirrhosis combined with atrial arrhythmia].

Objective: To analyze and explore the clinical characteristics and risk factors related to nosocomial mortality in patients with liver cirrhosis combined with atrial arrhythmia. Methods: 252 hospitalized patients with liver cirrhosis combined with atrial arrhythmia from January 2014 to December 2021 were enrolled, and their clinical characteristics were analyzed. The above-mentioned patients were divided into groups according to their nosocomial mortality rate. Among them, 45 nosocomial mortality cases were classified as the mortality group, and 207 survival cases were classified as the survival group. The differences in clinical data and laboratory data between the two groups were compared. The risk factors for nosocomial mortality in patients with liver cirrhosis combined with atrial arrhythmia were analyzed. The t-test, or rank-sum test, was used to compare measurement data. The chi-square test, or Fisher's exact probability method, was used to compare enumeration data. Multivariate analysis was performed by the logistic regression method. Results: Among the 252 cases, the male-to-female ratio was the same (male/female ratio: 126/126). The age range was 26 to 89 (66.77±10.46) years. Han ethnicity accounted for 79.5%. The main type of atrial arrhythmia was atrial fibrillation (P < 0.001). The main cause of liver cirrhosis was post-hepatitis B cirrhosis (56.3%). There were 57/72/123 cases of CTP grade A/B/C. The CTP and Model for End-Stage Liver Disease (MELD) scores were 10.30±1.77 and 18.0(11.0, 29.0), respectively. The nosocomial mortality rate was 17.9% (45/252). The overall incidence rate of complications in all patients was 89.28%, with complications occurring in the following order: 71.4% ascites, 71.0% hypersplenism, 64.7% spontaneous peritonitis, 64.3% esophageal gastric varices, 32.5% hepatorenal syndrome, 32.1% hepatic encephalopathy, and 26.2% esophageal gastric variceal bleeding. The incidence rate of new-onset atrial fibrillation in the nosocomial mortality group was 73.3%, which was much higher than the 44.0% rate in the survival group (P < 0.05). Multivariate logistic regression analysis showed that new-onset atrial fibrillation (OR=2.707, 95%CI 1.119 ~ 6.549), esophageal-gastric varices (OR=3.287, 95%CI 1.189 ~ 9.085), serum potassium (OR=3.820, 95%CI 1.532 ~ 9.526), and MELD score (OR=1.108, 95%CI 1.061~1.157) were independent risk factors for nosocomial mortality in patients with liver cirrhosis combined with atrial arrhythmia. Conclusion: Patients with cirrhosis combined with atrial arrhythmias have more severe liver function damage and are more likely to develop complications such as ascites, hypersplenism, and hepatorenal syndrome. New-onset atrial fibrillation, esophageal-gastric varices, hyperkalemia, and a high MELD score are risk factors for nosocomial mortality in patients with liver cirrhosis combined with atrial arrhythmia, so more attention should be paid to corresponding patients for timely symptomatic treatment.

[Advances in anticoagulant therapy for cirrhosis combined with atrial fibrillation].

Relevant research in recent years has demonstrated that the atrial fibrillation occurrence rate is significantly higher in patients with cirrhosis. The most common indication for long-term anticoagulant therapy is chronic atrial fibrillation. The use of anticoagulant therapy greatly reduces the incidence rate of ischemic stroke. Patients with cirrhosis combined with atrial fibrillation have an elevated risk of bleeding and embolism during anticoagulant therapy due to cirrhotic coagulopathy. At the same time, the liver of such patients will go through varying levels of metabolism and elimination while consuming currently approved anticoagulant drugs, thereby increasing the complexity of anticoagulant therapy. This article summarizes the clinical studies on the risks and benefits of anticoagulant therapy in order to provide a reference for patients with cirrhosis combined with atrial fibrillation.

Quality of vision and vision-related quality of life after Descemet membrane endothelial keratoplasty: a randomized clinical trial.

PURPOSE: To compare quality of vision and vision-related quality of life (QOL) in patients undergoing Descemet membrane endothelial keratoplasty (DMEK) or ultrathin Descemet stripping automated endothelial keratoplasty (DSAEK). METHODS: Fifty-four eyes of 54 patients with Fuchs' dystrophy from six corneal clinics in the Netherlands were randomized to DMEK or ultrathin DSAEK and examined preoperatively, and 3, 6 and 12 months postoperatively. Main outcome measures were corneal higher-order aberrations (HOAs), contrast sensitivity, straylight and vision-related QOL. RESULTS: Posterior corneal HOAs decreased after DMEK and increased after ultrathin DSAEK (p ≤ 0.001) 3 months after surgery and correlated positively with best spectacle-corrected visual acuity (12 months: r = 0.29, p = 0.04). Anterior and total corneal HOAs did not differ significantly between both techniques at any time point. Contrast sensitivity was better (p = 0.01), and straylight was lower (p = 0.01) 3 months after DMEK compared with ultrathin DSAEK; 95% confidence interval [CI] of log(cs) 1.10-1.35 versus 95% CI: 0.84 to 1.12, and 95% CI: log(s) 1.18 to 1.43 versus 95% CI: 1.41 to 1.66, respectively. Both were comparable at later time points. Vision-related QOL (scale 0-100) did not differ significantly between both groups at any time point and improved significantly at 3 months (ß = 12 [95% CI: 7 to 16]; p < 0.001), and subsequently between 3 and 12 months (ß = 5 [95% CI: 0 to 9]; p = 0.06). CONCLUSIONS: Descemet membrane endothelial keratoplasty (DMEK) results in lower posterior corneal HOAs compared with ultrathin DSAEK. Contrast sensitivity and straylight recover faster after DMEK but reach similar levels with both techniques at 1 year. Vision-related QOL improved significantly after surgery, but did not differ between both techniques.

Reflex lacrimation in patients with glaucoma and healthy control subjects by fluorophotometry.

PURPOSE: Steady state tear turnover (TTO), defined as TTO under normal physiological conditions, is significantly lower in patients with untreated glaucoma than in healthy control subjects. To obtain more information on the effect of glaucoma on lacrimation, a method for quantification of reflex lacrimation was developed and applied to patients with glaucoma or ocular hypertension and healthy control subjects. METHODS: After instillation of 2 microl of fluorescein (2%), the decay of fluorescein concentration in tears was measured by fluorophotometry over 10 minutes to determine steady state TTO. Then, reflex lacrimation was induced by stimulating the trigeminal nerve with ethanol vapor via the nostrils. Thereafter, the decay of fluorescein and corresponding steady state TTO were determined again. An index of reflex lacrimation, defined as the percentage decrease in fluorescein concentration as a result of stimulation, was calculated by forward and backward extrapolation of the steady state decay of the fluorescein concentration in tears, relative to the time of stimulation. RESULTS: The index of reflex lacrimation was determined in 16 patients with newly discovered but not yet treated glaucoma, 16 patients with untreated ocular hypertension, and 16 healthy control subjects. The values did not differ between groups (mean +/- SD, 67.0%+/-17.7%, 63.5%+/-21.3%, and 70.4%+/-19.6%, respectively; ANOVA, P>0.25). Surprisingly, the steady state TTO after stimulation was lower than that before stimulation in each group (ratio, 0.62+/-0.46; paired t-test, P<0.04). CONCLUSIONS: The method developed is appropriate for the quantification of reflex lacrimation. Reflex lacrimation is not influenced significantly by glaucoma or ocular hypertension. The decreased steady state TTO after reflex stimulation may be caused by exhaustion of the lacrimal glands after excessive reflex lacrimation, indicating that normal lacrimation probably also contains reflex tears.

HNK-1 antigens on uveal and cutaneous melanoma cell lines.

The HNK-1 epitope has been associated with the metastatic behaviour of uveal melanomas. We characterized HNK-1 antigens on four human uveal (primary and metastatic) and two primary cutaneous melanoma cell lines by immunocytochemistry and Western blot analysis. We also determined the involvement of the HNK-1 epitope in cell-cell interactions on a matrigel layer. Three uveal melanoma cell lines (one primary and two metastatic) and one cutaneous melanoma cell line showed HNK-1 expression by immunocytochemistry. On matrigel, only the HNK-1-positive cutaneous melanoma cell line Bowes grew in a honeycomb-like structure which disappeared after adding HNK-1 antibodies to the culture medium. Immunoblot analysis of the primary uveal melanoma cell line EOM-3 revealed five HNK-1-positive protein bands with apparent molecular weights of 200, 160, 115, 95 and 75 kDa. The cutaneous melanoma cell line Bowes showed three HNK-1-positive protein bands with apparent molecular weights of 150, 135 and 90 kDa. This study shows that two uveal (primary and metastatic) and one primary cutaneous melanoma cell lines express HNK-1 antigens on immunoblot. Only in the HNK-1-positive cutaneous melanoma cell line Bowes did the HNK-1 epitope have a function in intercellular adhesion. Although the primary uveal melanoma cell line EOM-3 showed a similar HNK-1 immunoreactivity, we could not demonstrate HNK-1-mediated cell adhesion. On immunoblot, the two cell lines displayed different HNK-1 antigens, which may explain the difference in cell adhesion.