Objective
To investigate the relationship of serum high-sensitivity cardiac troponin I (hs-cTnI) with left ventricular structure and function in elderly hemodialysis patients.
Methods
92 elderly patients undergoing maintenance hemodialysis at our hemodialysis center were selected between January, 2015 and June, 2018. Their clinical data were collected. Their cardiac structure and function were measured by echocardiography.
Results
The serum hs-cTnI increased in 32 patients, and was normal in 60 patients. The proportions of the patients with III- IV grade cardiac function and left ventricular hypertrophy (LVH) were significantly higher in the elevated hs-cTnI group than in the normal hs-cTnI group (78.12% vs. 21.67% and 87.50% vs. 63.33%, both P<0.05). There were statistical differences in hemoglobin, serum albumin, brain natriuretic peptide (BNP) , and high sensitivity C reactive protein (hsCRP) between the two groups. Compared to the normal hs-cTnI group, the elevated hs-cTnI group had significantly larger left ventricular diameter (LVD) , left ventricular mass index (LVMI) and the ratio of mitral early diastolic peak flow and mitral annular early diastolic velocity (E/E’) (all P<0.05). The fractional shortening (FS) and left ventricular ejection fraction (EF) in the elevated hs-cTnI group were significantly lower than those in the normal hs-cTnI group (P<0.05). Hs-cTnI positively correlated with hsCRP, BNP, LVD, LVMI, and E/E', and negatively with serum albumin, EF, and FS. Age, hemoglobin, LVMI, and E/E' were significant indicators of high hs-cTnI level in the multivariate logistic regression. The areas under the ROC curve for the diagnosis of LVH, left ventricular systolic insufficiency, and left ventricular diastolic dysfunction by hs-cTn I were 0.697, 0.884, and 0.917, respectively.
Conclusions
The serum hs-cTnI level of elderly patients undergoing hemodialysis relates to their left ventricular structure and function. Measurement of serum hs-cTnI is helpful to evaluate LVH and left ventricular systolic and diastolic function in elderly patients undergoing hemodialysis.
Key words:
High-sensitivity cardiac troponin I; Left ventricle; Hemodialysis; Heart failure
This study is aimed at evaluating the relationship between leukocyte telomere length (LTL) and mitochondrial DNA copy number (mtDNAcn) in a noninterventional rural community of China with different glucose tolerance statuses. In addition, we investigate whether the indicators of oxidative stress and inflammation were involved and identify mediators among them. A total of 450 subjects in rural China were included and divided into two groups according to a 75 g oral glucose tolerance test (OGTT): the abnormal glucose metabolism (AGM, n=257, 57.1%) group and the normal glucose tolerance (NGT, n=193, 42.9%) group. Indicators of oxidative stress (superoxide dismutase (SOD) and glutathione reductase (GR)) and inflammatory indices (tumor necrosis factor α (TNF α ) and interleukin-6 (IL-6)) were all determined by ELISA. LTL and mtDNAcn were measured using a real-time PCR assay. Linear regressions were used to adjust for covariates that might affect the relationship between LTL and mtDNAcn. Mediation analyses were utilized to evaluate the mediators. In the AGM, LTL was correlated with mtDNAcn (r=0.214, p=0.001), but no correlation was found in the NGT. The association between LTL and mtDNAcn was weakened after adjusting for inflammatory factors in the AGM (p=0.087). LTL and mtDNAcn were both inversely related to HbA1c, IL-6, TNF α , and SOD activity. Mediation analysis demonstrated that TNF α was a significant mediator in the telomere-mitochondrial interactome in the AGM. This result suggests that inflammation and oxidative stress may play a vital role in telomere shortening as well as mitochondrial dysfunction. In the subjects with hyperglycemia, a significant positive correlation is observed between LTL and mtDNAcn, which is probably mediated by TNF α . TNF α may be considered a potential therapeutic target against aging-related disease in hyperglycemia.
Abstract Objective To investigate the clinical characteristics of patients with multiple endocrine neoplasia type 1 (MEN1)-related insulinoma and their relationship with specific biochemical changes and to summarize the features of treatment options for the Chinese population with this disease and the impact on long-term prognosis. Methods “MEN1” and “insulinoma” were used when searching the Peking Union Medical College Hospital (PUMCH) medical record retrieval system to obtain clinical information about patients. We identified patients diagnosed with MEN1-associated insulinoma based on endocrinological, radiological, and pathological examinations, and subsequently analyzed their clinical data. Results A total of 55 patients with MEN1-associated insulinoma were included, including 29 (52.7%) men and 26 (47.3%) women. The parathyroid gland was the most commonly affected (78.2%), followed by the pituitary gland (69.1%) and adrenal gland (16.4%). Insulinoma was the first manifestation of MEN1 in at least 23.6% (13/55) of patients. Nineteen (34.5%) patients presented with initial symptoms of hypoglycemia before the age of 22 years. Among the 24 Patients with high serum calcium (Ca) had significantly lower serum insulin levels than those with normal serum Ca levels ( p < 0.001) during hypoglycemic episodes. However, serum C-peptide level at 0.5 h and serum insulin level at 1 h was higher in patients with hypercalcemia than in patients with normal serum Ca levels in the oral glucose tolerance test (OGTT), although the differences were not statistically significant. Multifocal pancreatic neuroendocrine tumors (pNETs) were present in 38 (69.1%) patients; most of them (55.6%, 20/36) underwent multiple enucleations, and 45% (9/20) had a postoperative recurrence. Five patients (10%) who underwent distal pancreatectomy developed pancreatic insufficiency after an average of seven years. patients who underwent genetic testing, 23 (95.8%) were positive for MEN1 mutation, with mutations most commonly found in exons 2 (21.7%) and 3 (13%). Conclusions In our study, the rates of postoperative recurrence and long-term complications in patients with MEN1 with multifocal pNETs were significantly different from those in other international centers and might be related to the choice of surgical method. In addition, elevated serum Ca levels in patients with primary hyperparathyroidism may affect insulin secretion.
Objectives: Cardiomyopathies are diseases of heart muscle caused by mutations in cytoskeletal genes. Disease severity and penetrance vary greatly among patients carrying the same mutation(s) and single-gene variants often do not reliably predict cardiomyopathy phenotypes.
Background: The chromosome 10q21-q23 locus was previously associated to familial dilated cardiomyopathy (DCM), arrhythmias, heart failure, Wolff-Parkinson-White (WPW) syndrome, mitral valve prolapse (MVP) and/or mitral regurgitation (MR). However, the exact variants responsible for heterogeneous DCM and arrhythmia phenotypes remained unknown.
Methods: A large family of 62 members was re-studied using whole exome and direct sequencing. Phenotypegenotype correlation and systems genetics analysis were performed.
Results: We identified missense KCNMA1-M744T, ANXA11-I457V, and DYDC2-P123R variants at 10q21-q23. The proband and ten family members carried ANXA11-I457V and DYDC2-P123R identified in cis (digenicheterozygosity). Seven digenic carriers were affected including DCM (n=3), heart failure (n=1), left ventricular dysfunction (n=3), arrhythmia (n=2), MVP (n=2) and MR (n=3). A single KCNMA1-M744T variant was identified in 11 individuals, including 4 affected with MVP or MR (n=4), ventricular arrhythmia (n=2), and WPW (n=1). All three variants were identified in three family members and all were affected. Rare variants in cardiomyopathy-related genes such as CORIN-I52V, TTN-S21630P, TRPM7-Y537H, OTX1-H301del and FLNC-N47Swere identified in affected individuals.
Conclusion: This study facilitated the family-based predictive and personalized approach in identifying disease causative basis in patients with familial DCM and their relatives “at risk”. Different variant combinations of transKCNMA1-M744T, cis-ANXA11-I457V and DYDC2-P123R identified at 10q21-q23 underlie the clinical heterogeneity of familial DCM. Rare variants identified beyond the 10q21-q23 were predicted to modify the function of KCNMA1, ANXA11, andDYDC2 that may serve as the genetic modifiers in intra- and inter-familial phenotypic variability
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