Choroidal Changes in Patients with Diabetic Retinopathy: A Retrospective Study.

This study aimed to investigate the characteristic choroidal changes in patients with diabetic retinopathy and identify factors affecting choroidal thickness (CTh), choroidal vascular index (CVI), and choriocapillaris flow. We retrospectively analyzed 79 eyes of 48 patients with diabetes between August 2021 and February 2022. We collected laboratory data, including HbA1c, serum creatinine, blood urea nitrogen, triglyceride, total cholesterol, high-density lipoprotein, and low-density lipoprotein (LDL) levels. Optical coherence tomography images of the foveal avascular zone, retinal vascular density, choroidal flow, retinal thickness, CTh, and CVI were analyzed. Possible determining factors affecting CTh, CVI, and choriocapillaris flow were analyzed using nonparametric multivariate analysis. LDL (p < 0.001) positively correlated with CTh, whereas CVI (p = 0.007) was negatively correlated with CTh in diabetic patients with diabetes. We also identified a negative correlation between choriocapillaris flow and deep parafoveal retinal vessel density in patients with low-grade diabetic retinopathy (DR), which diminished in those with more advanced DR. Our study provides further information on the changes in choroidal structure and blood flow in patients with diabetes.

Measuring serum total and free indoxyl sulfate and p-cresyl sulfate in chronic kidney disease using UPLC-MS/MS.

Chronic kidney disease (CKD) is a complex disorder that affects multiple organs and increases the risk of cardiovascular complications. CKD affects approximately 12% of the population in Taiwan. Loss of kidney function leads to accumulation of potentially toxic compounds such as indoxyl sulfate (IS) and p-cresyl sulfate (pCS), two protein-bound uremic solutes that can stimulate the progression of CKD. The aim of this study was to assess whether IS and pCS levels were correlated with CKD stage. We developed and validated a method for quantitating total and free IS and pCS in serum by ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). Serum samples were pretreated using protein precipitation with acetonitrile containing stable isotope-labeled IS and pCS as internal standards. After centrifugation, the supernatant was diluted and injected into a UPLC-MS/MS system. Analyte concentrations were calculated from the calibration curve and ion ratios between the analyte and the internal standard. The calibration curves were linear with a correlation coefficient of >0.999; the analytical measurement range was 0.05-5 mg/L. The limit of quantitation of this assay was 0.05 mg/L for both analytes. The reference interval was ≤0.05-1.15 mg/L for total-form IS, ≤0.05-5.33 mg/L for total-form pCS, ≤0.05 mg/L for free-form IS, and ≤0.12 mg/L for free-form pCS. A positive correlation was observed between analyte concentration and CKD stage. Our sensitive UPLC-MS/MS method for quantifying total and free-form IS and pCS in serum can be used to monitor the progression of CKD in clinical settings, identify patients at risk, and facilitate development of further therapies for this devastating disease.

Reduction in Hospital-Wide Clinical Laboratory Specimen Identification Errors following Process Interventions: A 10-Year Retrospective Observational Study.

BACKGROUND: Accurate patient identification and specimen labeling at the time of collection are crucial steps in the prevention of medical errors, thereby improving patient safety. METHODS: All patient specimen identification errors that occurred in the outpatient department (OPD), emergency department (ED), and inpatient department (IPD) of a 3,800-bed academic medical center in Taiwan were documented and analyzed retrospectively from 2005 to 2014. To reduce such errors, the following series of strategies were implemented: a restrictive specimen acceptance policy for the ED and IPD in 2006; a computer-assisted barcode positive patient identification system for the ED and IPD in 2007 and 2010, and automated sample labeling combined with electronic identification systems introduced to the OPD in 2009. RESULTS: Of the 2000345 specimens collected in 2005, 1023 (0.0511%) were identified as having patient identification errors, compared with 58 errors (0.0015%) among 3761238 specimens collected in 2014, after serial interventions; this represents a 97% relative reduction. The total number (rate) of institutional identification errors contributed from the ED, IPD, and OPD over a 10-year period were 423 (0.1058%), 556 (0.0587%), and 44 (0.0067%) errors before the interventions, and 3 (0.0007%), 52 (0.0045%) and 3 (0.0001%) after interventions, representing relative 99%, 92% and 98% reductions, respectively. CONCLUSIONS: Accurate patient identification is a challenge of patient safety in different health settings. The data collected in our study indicate that a restrictive specimen acceptance policy, computer-generated positive identification systems, and interdisciplinary cooperation can significantly reduce patient identification errors.

[Significance of the mitochondrial D-loop alterations in hyperplastic pancreatic ductal cells in the vicinity of pancreatic cancer coexisting with chronic pancreatitis].

OBJECTIVE: To explore the significance of mitochondrial D-loop alterations in hyperplastic pancreatic ductal cells in vicinity of pancreatic cancer coexisting with chronic pancreatitis. METHODS: Malignant lesions and foci of pancreatic ductal intraepithelial neoplasia of the pancreas and paired normal gastric mucosal epithelial cells from the same patients, respectively, were assessed by polymerase chain reaction. Somatic point mutations and sequence variants of D-loop were searched by direct sequencing of the mitochondrial genome. D-loops were sequenced by BLAST to identify their mutations. RESULTS: Eleven of 12 pancreatic cancers displayed at least one D-loop variants and one tumor presented heteroplasmy. There was an apparent increase in incidence of D-loop mutational rate from PanIN1 (33.3%) to PanIN3 (75%, P < 0.01). CONCLUSION: Mitochondrial D-loop alterations in the pancreas occur in the earliest premalignant lesions and exhibite an increasing occurence that parallels histological severity. These alterations may serve as a valuable marker to follow the histopathological progression of the lesions. Large number of further studies are required to clarify clinical implications of the mitochondrial DNA alterations.