Egy hazai matematikai felmérés eredményei nemzetközi összehasonlításban

<p><b>Comparisons of the effect of different dipeptidyl peptidase-4 inhibitor treatment for 1 year on adjusted mean changes in fasting plasma glucose (FPG) (A) and glycated hemoglobin (HbA</b>_<b>1</b><b>c) (B) in the patients with a low and high hemoglobin glycation index (HGI).</b> Factors included in the analysis of variance statistical model were baseline oral anti-diabetes drugs, age, sex and renal function. VI = vildagliptin (n = 24 in the low HGI and n = 36 in the high HGI groups), LI = linagliptin (n = 33 in the low HGI and n = 31 in the high HGI groups), SA = saxagliptin (n = 45 in low HGI and n = 64 in the high HGI groups), SI = sitagliptin (n = 97 in the low HGI and n = 138 in the high HGI group). Error bars represent 95% confidence interval (CI). p-value for between-group difference. (To convert glucose to millimoles per liter, multiply by 0.0555)</p

Serum Uric Acid and Progression of Kidney Disease: A Longitudinal Analysis and Mini-Review

<div><p>Background</p><p>Increasing evidence supports the association between hyperuricemia and incident chronic kidney disease (CKD); however, there are conflicting data regarding the role of hyperuricemia in the progression of CKD. This study retrospectively assessed the longitudinal association between uric acid (UA) level and CKD progression in a Chinese population lived in Taiwan.</p><p>Methods</p><p>Patients with physician diagnosis of hyperuricemia or receiving urate-lowering therapy between 2003 and 2005 were identified in the electronic medical records (EMR) of a tertiary medical center and were followed up until December 31, 2011. Patients were divided into four UA categories at the cut-off 6, 8, and 10 mg/dL. CKD progression was estimated by the change of estimated glomerular filtration rate (eGFR) in the linear mixed models. Kidney failure was defined as an eGFR less than 15 mL/min/1.73 m² or requiring renal replacement therapy.</p><p>Results</p><p>A total of 739 patients were analyzed. In the full-adjusted model, patients with a baseline UA level ≥6 mg/dL had greater decline in eGFR ((<i>β</i> = -9.6, 95% CI -16.1, -3.1), comparing to those with a UA level less than 6 mg/dL. When stratifying patients into four UA categories, all three hyperuricemia categories (UA6-8, 8–10, ≥10 mg/dL) associated with a greater decline in eGFR over the follow-up period with an increasing dose-response, comparing to the lowest UA category. The risk of progression to renal failure increased 7% (hazard ratio 1.07, 95% CI 1.00, 1.14) for each 1mg/dL increase in baseline UA level. The influences of hyperuricemia on eGFR decline and the risk of kidney failure were more prominent in patients without proteinuria than those with proteinuria.</p><p>Conclusion</p><p>Our study showed a higher uric acid level is associated with a significant rapid decline in eGFR and a higher risk of kidney failure, particularly in patients without proteinuria. Our findings suggest hyperuricemia is a potential modifiable factor of CKD progression.</p></div

Characteristics of hyperuricemic patients stratified by baseline serum uric acid categories^*.

<p>Characteristics of hyperuricemic patients stratified by baseline serum uric acid categories^{<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0170393#t001fn001" target="_blank">*</a>}.</p

The distribution of the proportion of baseline hyperuricemic status (by cut-off values of 6, 8, and 10mg/dL) across CKD stages.

<p>The distribution of the proportion of baseline hyperuricemic status (by cut-off values of 6, 8, and 10mg/dL) across CKD stages.</p

Violin plot of the distribution of baseline serum uric acid levels by CKD stages.

<p>The violin is a mirrored density plot with a boxplot of the baseline uric acid concentrations inside. Black dots represented the group mean and outliers in each CKD category.</p

Studies of serum uric acid level in the progression of kidney function and the development of kidney failure.

<p>Studies of serum uric acid level in the progression of kidney function and the development of kidney failure.</p

The risk of CKD progression to kidney failure (eGFR <15 ml/min) for each 1 mg/dL increase in uric acid level.

<p>The risk of CKD progression to kidney failure (eGFR <15 ml/min) for each 1 mg/dL increase in uric acid level.</p

Effect of acute pancreatitis on the risk of developing osteoporosis: A nationwide cohort study

<div><p>Purpose</p><p>Chronic exocrine pancreatic insufficiency can lead to osteoporosis. However, the incidence and risk of osteoporosis after acute inflammation of pancreas remained known. Thus, we conducted a population-based cohort study to clarify the association between acute pancreatitis (AP) and osteoporosis.</p><p>Methods</p><p>Patients newly diagnosed with AP with index date between 2000 and 2011 were identified from the National Health Insurance Research Database. Osteoporosis were defined according to the International Classification of Diseases, Ninth Revision, Clinical Modification codes. We applied age-, sex-, and comorbidities-adjusted variable Cox proportional hazard models for assessing the association between AP and osteoporosis. Moreover, these models were used to adjust for the influences of patient characteristics and comorbidities.</p><p>Results</p><p>In this study, 4,016 patients were included in the AP cohort (males, 67.9%; mean age, 51.8 years) and 4,016 matched controls in the non-AP cohort. After a mean follow-up period of 4.97 and 5.21 years in the AP and non-AP cohorts, respectively, the incidence of osteoporosis was 8.22 per 1000 person-years in the AP cohort. The AP cohort had a higher risk [adjusted hazard ratio (aHR) = 1.27, 95% confidence interval (CI) = 1.02–1.58] of osteoporosis than did the non-AP cohort. The risk of osteoporosis was highest in the female patients of the AP cohort (aHR = 2.26, 95% CI = 1.85–2.76) and patients aged 50–64 years (aHR = 4.14, 95% CI = 3.13–5.47).</p><p>Conclusion</p><p>AP patients are at a risk of osteoporosis, especially female gender and age 50–64 years. Those with > 3 episodes of AP had highest significant risk of developing osteoporosis.</p></div

Characteristics between subjects with and without acute pancreatitis.

<p>Characteristics between subjects with and without acute pancreatitis.</p

Table_1_The Impact of Alcohol Consumption on Cognitive Impairment in Patients With Diabetes, Hypertension, or Chronic Kidney Disease.DOCX

To investigate the impact of alcohol use on the risk of cognitive impairment in older adults with chronic illness, we used the Digit Symbol Substitution Test (DSST) to evaluate cognitive function in older adults (≥ 60 years) in the National Health and Nutrition Examination Survey. Participants were categorized as light drinkers, moderate and heavy drinkers. Logistic regression analyses were used to explore associations between cognitive impairment and alcohol drinking in patients with or without diabetes, hypertension, and chronic kidney disease (CKD). Multivariate analysis showed that alcohol heavy drinkers was significantly associated with a higher risk of cognitive impairment in patients with hypertension (aOR 6.089, 95% CI 1.318–28.13) and CKD (aOR 6.324, 95% CI 1.158–34.52) compared with light drinkers. The dose-response analyses revealed that moderate to heavy alcohol use was associated with a higher risk of cognitive decline in patients with diabetes and CKD, heavy drinking increased the risk of cognitive impairment in patients with hypertension. The impacts of alcohol drinking on cognitive impairment are significantly different in patients with different comorbidities.</p