Patients with alcohol-related liver disease (ALD) might be at increased risk of acute pancreatitis (AP), but large-scale data are lacking.
Population-based cohort study using data from the Swedish National Patient Register on 37,062 patients with ALD from 1969 to 2020. Patients were matched to ≤10 general population comparators (n = 352,931). We used logistic regression to estimate the risk of acute or chronic pancreatitis prior to ALD diagnosis and Cox regression to estimate rates for hospitalization for AP after ALD diagnosis.
Median age at ALD diagnosis was 59 years; 72% were men, and 67% had cirrhosis at baseline. Overall, 7% had experienced pancreatitis before ALD diagnosis, resulting in 9-fold higher odds of pancreatitis compared to comparators. The 10-year cumulative incidence of hospitalization for AP was 2.7% (95%CI = 2.5–2.8) in ALD and 0.6% (95%CI = 0.58–0.63) in comparators, yielding an adjusted HR of 6.3 (95%CI = 5.8–6.9). Younger age, male sex, and diagnoses of alcohol use disorders and chronic obstructive pulmonary disease were independent risk factors for developing AP in ALD. Continued drinking after baseline was associated with a higher risk of AP (adjusted hazard ratio [aHR] 2.6, 95%CI = 2.29–2.85).
ALD is associated with 9-fold higher odds of prevalent pancreatitis compared to the general population. The hospitalization rate for AP following ALD diagnosis is 6-fold higher. About 10% of patients with ALD have or develop AP, suggesting that assessing history of pancreatitis and its sequelae might be relevant for patients with ALD.
A blood-based biomarker that accurately reflects neuronal injury in acute ischemic stroke could be an easily accessible and cost-effective complement to clinical and radiological evaluation. Here, we investigate whether plasma levels of the novel biomarker brain-derived tau (BD-tau) reflect cerebral infarct volumes and whether BD-tau can improve clinical outcome prediction.
The present study included 713 consecutive cases from two different hospital-based cohorts, the Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS) and SAHLSIS phase 2 (SAHLSIS2). Acute stroke severity was determined by the Scandinavian Stroke Scale converted to the National Institutes of Health stroke scale (NIHSS) in SAHLSIS and by the NIHSS in SAHLSIS2. All participants were assessed for functional outcome 3 months after stroke by the modified Rankin Scale, and 254 participants in SAHLSIS had quantitative neuroimaging available.
Plasma BD-tau concentrations and cerebral infarct volumes were highly correlated (ρ 0.72, p < 0.001). BD-tau improved the prognostic accuracy of suffering an unfavorable outcome over age and stroke severity in the whole cohort. However, the gain in predictive power was dependent on stroke severity and infarct location. The largest improvement was observed for mild ischemic strokes (NIHSS <5; area under the curve [AUC] = 0.73 for age + NIHSS versus AUC = 0.84 with addition of BD-tau; DeLong p 0.02), posterior circulation stroke (AUC = 0.75 vs. AUC = 0.84; DeLong p 0.06) and more specifically for infarcts in the brainstem/cerebellum (AUC = 0.74 vs. 0.87; DeLong p 0.009).
Plasma BD-tau can provide information on the extent of acute neuronal damage in ischemic stroke and adds prognostic value for outcome, especially for mild and posterior circulation strokes.
After age 85, the U.S. non-Hispanic Black population mortality rate becomes less than that of the White population (called the Black–White mortality crossover). It is not known how this survival advantage compares to Asian and Hispanic groups, and whether differences persist to age 100+ years.
The U.S. period life table data were extracted to obtain life expectancy at birth and at ages 70, 85, and 100 years according to year, sex, and race and ethnicity. Age-specific death rates and adult modal age at death were calculated. We computed period probabilities of survival to age 100, from ages 70, 80, and 90. Pseudo-birth cohort calculations were undertaken to enable comparison with period-based results.
In 2019, the Black–White mortality crossover occurred at 86–88 years and persisted at ages 100 and 100+. Life expectancies at age 100 for non-Hispanic Black, Hispanic, and Asian populations were similar and were significantly greater than the non-Hispanic White population. From 2006 to 2019, the probability of survival from 70 and 80 years to age 100 was highest for the Hispanic population, followed by non-Hispanic Black and then non-Hispanic White populations. Probability of survival from age 90 to 100 years was similar for all but the non-Hispanic White population, which had a comparatively lower probability of survival. When Asian population data became available in 2019, this population had the highest probability of survival to age 100, starting from ages 70, 80, and 90 years. Pseudo-cohort results displayed patterns consistent with those observed over calendar years.
Race- and ethnicity-based variation in mortality between ages 85 and 100+ years suggests differences in environmental and possibly genetic influences upon risk for exceptional longevity.
The frequent association between transthyretin wild-type (TTRwt) cardiac amyloidosis (CA) and aortic stenosis (AS) suggests a bidirectional relationship: TTRwt-CA could induce AS and vice versa. Systemic manifestations may highlight this interaction: systemic amyloidogenesis would lead to systemic symptoms, CA, and AS, whereas the myocardial stresses induced by degenerative AS might promote local amyloidogenesis without systemic symptoms. Carpal tunnel syndrome (CTS) is the most frequently reported extracardiac symptom. Through a comparison of TTRwt-CA patients with and without CTS, we sought to determine whether CTS serves as a reliable indicator of systemic involvement and its impact on cardiac and valvular characteristics.
A total of 411 consecutive patients with TTRwt-CA were included. CTS, present in 70.3%, was associated with a younger age (80 vs. 84 years, p < 0.001), more extracardiac symptoms, and advanced CA, with greater cardiac remodeling and a higher heart-to-mediastinum ratio (1.63 vs. 1.54; p = 0.012) compared to patients without CTS. AS was present in 21% and 31% of patients with and without CTS, respectively (p = 0.024). Except for AS, these associations remained significant after adjusting for confounding factors. In severe AS, patients with CTS exclusively exhibited low-flow low-gradient (LFLG) AS and less severe class of aortic valvular calcium score (5.6% vs. 60%; p = 0.006) compared to those without CTS.
Our findings suggest that CTS may delineate two phenotypes in TTRwt-CA: a systemic phenotype associated with advanced CA and poorly calcified LFLG AS, and a cardiac phenotype characterized by less severe CA and a mixed pattern of highly calcified AS, suggesting disparate pathophysiologies.
Research on Mesoamerican Nephropathy, chronic kidney disease of unknown cause and chronic kidney disease of nontraditional cause has been going on for more than 20 years. Thousands of manual workers, especially in agriculture, are affected. The disease has been reported in different countries and regions, not only from heat-stressed sugarcane cutters in Central America but also from other occupational groups with strenuous work in hot environments. The cause of this disease is still debated. A multitude of causative factors have been suggested, including agrochemicals, water quality, infections, and heavy metals. The evidence that heat stress is the major cause of kidney disease is convincing, whereas the support for alternative causes is weak. Associations between exposure and kidney damage are strong, consistent, and specific, occur after acute and chronic exposure, display dose-effect and dose–response relationships, are plausible, and coherent. Improving working conditions by providing hydration, rest, and shade to heat-stress-exposed workers is beneficial. Continued global warming will increase the number of people at risk for dangerous heat exposure and kidney disease.
Longitudinal studies investigating hormone therapy in transgender individuals are rare and often limited to 1- to 2-year follow-up periods.
We examined changes in body composition, muscle volumes, and fat distribution as well as muscle strength, arterial stiffness, and cardiometabolic biomarkers in both transgender men (TM; n = 17, age 25 ± 5 years) and transgender women (TW; n = 16, age 28 ± 5 years) at baseline and after 1 and 5–6 years of hormone therapy in a longitudinal prospective cohort design. Whole-body and regional fat and muscle volumes were analyzed using magnetic resonance imaging, and blood samples were taken.
Skeletal muscle size increased in TM (21% after 6 years) and decreased in TW (7% after 5 years). Muscle strength increased 18% after 6 years in TM (p = 0.003) but was statistically unchanged in TW. Muscle fat infiltration changed (p < 0.05) almost completely toward the affirmed sex phenotype after 1 year of therapy in both TM and TW. The most notable changes in fat volume distribution were that TW increased total adiposity but decreased visceral fat volume, whereas TM showed increased visceral fat (70%) and liver fat but relatively stable total adipose tissue levels. Although arterial stiffness and blood pressure did not change, there was a significant increase in triglyceride and LDL cholesterol levels and a decrease in HDL levels in TM after 6 years.
These unique longitudinal data underscore the importance of continued clinical monitoring of the long-term health effects of gender-affirming hormone therapy in both TW and, perhaps especially, TM.
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