Journal of clinical medicine research最新文献

Background: An individual's simple subjective feeling of having poor sleep quality usually occurs in combination with short sleep duration. Previous studies have mainly investigated the association between simple subjective sleep quality and blood pressure in a general population without considering the complicated issue regarding poor sleep quality and short sleep duration. The aim of this study was therefore to investigate whether poor sleep quality was associated with increased blood pressure in individuals with optimal sleep duration.

Methods: A cross-sectional study was conducted on 169 residents aged ≥ 18 years who lived in a remote island of Okinawa, Japan. The participants had a sleep duration of 6 - 7.9 h/day on weekdays and were not taking either sleep medication or antihypertensive medication. Analysis of covariance was used to compare systolic and diastolic blood pressures in the participants grouped according to simple subjective sleep quality.

Results: Of the 169 participants, 51 (30.2%) reported that their sleep quality was poor. After adjustment for age, sex, and other potential confounders including sleep duration within optimal levels, the participants aged ≤ 49 years had mean (95% confidence interval) systolic and diastolic blood pressures (mm Hg) of 121.0 (114.7 - 127.3) and 68.7 (63.8 - 73.6) in the good sleep quality group, and 127.8 (120.7 - 134.9) and 71.8 (66.2 - 77.3) in the poor sleep quality group (P = 0.01 and P = 0.14, respectively). However, in those aged ≥ 50 years, the corresponding means were 130.6 (121.3 - 139.8) and 79.1 (73.5 - 84.7) in the good-quality group and 126.9 (114.6 - 139.2) and 78.0 (70.5 - 85.4) in the poor-quality group (P = 0.43 and P = 0.68, respectively). There was a statistically significant interaction between simple subjective sleep quality and age for systolic blood pressure (P value for interaction = 0.04).

Conclusions: This study showed that an individual's simple subjective feeling of poor sleep quality was associated with increased systolic blood pressure in participants aged ≤ 49 years with optimal sleep duration. These findings highlight the importance of easily assessing simple subjective sleep quality in clinical settings even in individuals with optimal sleep duration, in order to prevent and manage hypertension.

Background: Our hospital is a designated emergency hospital and accepts many patients with out-of-hospital cardiac arrest (OHCA). Previously, after receiving a direct call from emergency services to request acceptance of an OHCA patient, the emergency room (ER) chief nurse notified medical staff. However, this method delayed ER preparations, so a Code Blue system (CB) was introduced in which the pending arrival of an OHCA patient was broadcast throughout the hospital.

Methods: In this study, we retrospectively analyzed the impact of introducing CB at our hospital on OHCA patient prognosis to examine whether the introduction of CB is clinically meaningful. We compared consecutive cases treated before introduction of the CB (March 3, 2022, to March 22, 2023) with those treated afterwards (March 23, 2023, to July 23, 2024).

Results: A total of 30 cases per group were included. The mean number of medical staff present at admissions increased significantly from 5.4 ± 0.6 to 15.0 ± 3.0 (P < 0.001). Although not statistically significant, the introduction of the CB increased the return of spontaneous circulation (ROSC) rate from 20% to 30%, survival to discharge rate from 3% to 10%, and social reintegration rate from 0% to 3%. ROSC occurred in 15 patients. Among OHCA patients with cardiac disease, the ROSC rate tended to increase from 0% to 43% (P = 0.055). In addition, in OHCA patients with cardiac disease whose electrocardiogram initially showed ventricular fibrillation or pulseless electrical activity, the ROSC rate increased from 0% to 100%. ROSC tended to be influenced by the total number of staff and physicians present and the number of staff such as medical clerks, clinical engineers, and radiology technicians (P = 0.095, 0.076, 0.088, respectively).

Conclusions: Introduction of a CB may increase the ROSC rate and the number of patients surviving to discharge. It also appears to improve the quality of medical care by quickly gathering all necessary medical staff so that they can perform their predefined roles.

Long-term survival has improved in kidney transplant recipients (KTRs) due to effective surgical techniques and anti-rejection therapies. Chronic immunosuppression associated with it has led to several types of skin cancers leading to substantial morbidity and mortality. Structured patient education including sun protective behaviors, regular dermatological surveillance, nicotinamide, long-chain omega-3 polyunsaturated fatty acids (PUFAs), early switch to mammalian target of rapamycin inhibitors (mTORis), combining them with low-dose calcineurin inhibitors (CNIs), can decrease the cancer risk. Checkpoint inhibitors (CPIs) are the major backbone of the treatment of advanced skin cancers. Unfortunately, these agents can increase the risk of graft rejection. Prospective studies done so far looking at combining steroids with CPI in treatment of skin cancer in KTRs have shown mixed results. Adoption of the weight-based approach of CPI has shown to decrease the amount of drug exposure with acceptable outcomes in the general population, which is something that can be studied in KTRs with skin cancer. Also, it is reasonable to consider surveillance allograft biopsies in KTRs receiving CPIs to detect early subclinical rejection. More studies are needed to develop guidelines to safely treat this population with minimal graft rejection. We conducted a comprehensive literature review from PubMed on skin cancer in kidney transplant patients, focusing on incidence, risk factors, protective behaviors, financial and treatment implications, especially with regards to CPIs therapy. We also discussed potential newer treatment options that will decrease skin cancer risk, as well as graft rejection.

Background: Abdominal aortic calcification (AAC) is a critical indicator of cardiovascular risk, particularly in patients with chronic kidney disease (CKD). Traditional classification systems may underestimate the risk in those with moderate CKD. This study aimed to evaluate the association between CKD risk categories - defined by both estimated glomerular filtration rate (eGFR) and albuminuria - and the prevalence of severe AAC.

Methods: This cross-sectional study analyzed data from the National Health and Nutrition Examination Survey (NHANES) 2013-2014. We included adults aged ≥ 40 years who underwent imaging for AAC assessment, excluding pregnant individuals and those without AAC scores. Survey-weighted and multivariate logistic regression was employed to assess the relationship between CKD risk categories and severe AAC, adjusting for age, hypertension, and smoking history. Subgroup analyses were conducted to explore variability across demographic and clinical subgroups.

Results: We analyzed data from 3,140 participants in the NHANES, 423 (13.4%) of whom had severe AAC. The cohort was categorized into CKD risk categories 1 through 4, with the majority (76%) in stage 1. Severe AAC was more prevalent among older individuals and those with traditional cardiovascular risk factors. Initial unadjusted analyses revealed that CKD category 2 was associated with a nearly fourfold increase in severe AAC (odds ratio (OR): 3.93), while categories 3 and 4 showed 3.75-fold and over 10-fold increases, respectively (all P < 0.01). However, after adjusting for confounders, categories 2 and 4 showed higher risks of severe AAC compared to category 1, but these associations did not reach statistical significance (OR: 1.72, 95% confidence interval (CI): 0.90 - 1.86, P = 0.06 and OR: 5.70, 95% CI: 0.85 - 38.00, P = 0.07, respectively).

Conclusion: Our study offers insights that may complement the current reliance on eGFR and albuminuria in risk stratification, highlighting that CKD category 2, defined by mildly reduced eGFR and albuminuria, may be a potential marker for severe AAC. Although statistical significance was narrowly missed after full adjustment, the clinical implications remain significant, advocating for more aggressive cardiovascular risk management in this population. This understanding may contribute to evolving approaches in CKD-related cardiovascular risk assessment and inform potential intervention strategies.

Background: Salivary α-amylase plays a crucial role in the glucose metabolism. However, postprandial salivary α-amylase activity (SAA) and its relationship with blood glucose (BG) are poorly understood. Therefore, we investigated SAA and BG after starch loading in healthy young women.

Methods: In 60 healthy non-obese young women, we investigated SAA, BG, and blood 3-hydroxybutyrate (3HB) after the consumption of 150 g rice (starch 48.8 g). Participants were classified into two groups based on the changes (Δ) in SAA from baseline at 60 min: small- and large-increase in ΔSAA groups (SI-ΔSAA and LI-ΔSAA).

Results: BG levels were significantly higher at 60, 90, and 120 min in participants with SI-ΔSAA (n = 31) than LI-ΔSAA (n = 29). Baseline 3HB concentration was also higher in participants with SI-ΔSAA. ΔSAA at 60 min was most closely and inversely correlated with BG and ΔBG at 90 min (r = -0.53 and -0.50, both P < 0.0001). Generalized linear model analysis also indicated that ΔSAA at 60 min was the most predictive of ΔBG at 90 min.

Conclusions: Higher levels of BG and ΔBG were observed after starch loading in healthy young women with smaller increase in salivary amylase, suggesting another crucial role of postprandial salivary amylase for the postprandial glucose metabolism.

Background: The aim of the present study was to conduct a prospective observational study to explore the effects of imeglimin on systemic energy metabolism/body composition and to identify potential mitochondria-related biomarkers of the efficacy of the drug in clinical settings.

Methods: In this prospective observational study, 16 participants with type 2 diabetes mellitus in the diabetes clinic of Kyoto University Hospital were enrolled. Individuals were started on imeglimin as monotherapy or add-on therapy.

Results: After 3 months under imeglimin treatment, there was no significant change in basal metabolism or body composition. However, serum levels of growth differentiation factor 15 (GDF15) were higher while those of serum fibroblast growth factor 21 and urine 8-hydroxy-2'-deoxyguanosine were not changed. Additional in vitro examination revealed that imeglimin induces GDF15 protein release from human hepatocytes.

Conclusions: Three-month imeglimin treatment increased serum GDF15 levels in clinical type 2 diabetes mellitus patients along with little change in basal metabolism or body composition, suggesting GDF15 as a potential marker for the efficacy of imeglimin.

Sodium-glucose cotransporter 2 (SGLT2) inhibitors, initially developed for type 2 diabetes, have emerged as a promising treatment for heart failure with reduced ejection fraction (HFrEF). They show significant cardiovascular benefits, including reduced cardiovascular mortality and heart failure hospitalizations. This review consolidates knowledge on the efficacy of SGLT2 inhibitors in HFrEF, focusing on their mechanisms of action, clinical benefits, and patient outcomes. To consolidate existing knowledge on the efficacy of SGLT2 inhibitors in reducing cardiovascular mortality in HFrEF, with an emphasis on pathophysiology, clinical benefits, and patient outcomes, major medical databases such as PubMed, Scopus, and Web of Science were reviewed, prioritizing research published from 2020 to 2024. Key studies and clinical trials, including DAPA-HF and EMPEROR-Reduced, were analyzed to understand the impacts of SGLT2 inhibitors on HFrEF management. The review highlights the multifaceted mechanisms by which SGLT2 inhibitors exert their cardiovascular benefits, including osmotic diuresis, natriuresis, improved myocardial energetics, and anti-inflammatory and antifibrotic effects. Clinical trials have consistently demonstrated significant reductions in cardiovascular mortality and hospitalizations among HFrEF patients treated with SGLT2 inhibitors. These benefits are observed across diverse demographic and clinical subgroups, indicating their broad applicability in clinical practice. SGLT2 inhibitors significantly advance HFrEF management, reducing cardiovascular mortality and hospitalizations. However, gaps remain in long-term outcomes, early diagnostic indicators, and mechanisms of action. Future research should address these gaps and explore personalized medicine to optimize treatment. Integrating SGLT2 inhibitors into standard HFrEF management guidelines, supported by updated policies and educational initiatives for healthcare providers, will be crucial to maximize their therapeutic potential and improve patient outcomes.

Background: Despite sharing common pathophysiological risk factors, the relationship between gallstones and depression requires further evidence for a clearer understanding. This study combines the National Health and Nutrition Examination Survey 2017 - 2020 observational data and Mendelian randomization (MR) analysis to shed light on the potential correlation between these conditions.

Methods: By analyzing the National Health and Nutrition Examination Survey 2017 - 2020 data through weighted multivariable-adjusted logistic regression, we examined the association between depression and gallstone risk. MR was subsequently applied, utilizing genetic instruments from a large genome-wide association study on depression (excluding 23andMe, 500,199 participants) and gallstone data (28,627 cases, 348,373 controls), employing the main inverse variance-weighted method alongside other MR methods to explore the causal relationship. Sensitivity analyses validated the study's conclusions.

Results: Among the 5,303 National Health and Nutrition Examination Survey participants, a significant association was found between depressive symptoms and increased gallstone risk (initial odds ratio (OR) = 2.001; 95% confidence interval (CI) = 1.523 - 2.598; P < 0.001), with the association persisting after comprehensive adjustments (final OR = 1.687; 95% CI = 1.261 - 2.234; P < 0.001). MR findings also indicated a causal link between genetically predicted depression and higher gallstone risk (OR = 1.164; 95% CI = 1.053 - 1.286; P = 0.003).

Conclusions: Depression is significantly associated with a higher risk of gallstones, supported by genetic evidence suggesting a causal link. These findings highlight the importance of considering depression in gallstone risk assessments and management strategies.

In the pharmacologic treatment of primary aldosteronism (PA), titration of mineralocorticoid receptor antagonist (MRA) dosing is necessary to reverse the renin suppression caused by high aldosterone levels. However, we often encounter cases in which the plasma renin activity (PRA) does not achieve the target level, even with the maximum dose of MRA. In this setting, sacubitril/valsartan, a combination of a neprilysin inhibitor and an angiotensin II type 1 receptor blocker that is approved for use as adjunctive therapy with an MRA, has been reported to inhibit aldosterone secretion both in vitro and in vivo. If sacubitril/valsartan proves to be effective in this context, it may offer a promising treatment for PA. However, there are few reports on the use of sacubitril/valsartan in this disease. We used add-on sacubitril/valsartan in three patients with PA, in whom blood pressure was insufficiently reduced and PRA remained suppressed despite administering the maximum dose of MRA. With the addition of sacubitril/valsartan, the decrease in plasma aldosterone concentration (PAC) was more marked than the increase in PRA. Because MRAs do not suppress aldosterone production but instead act by blocking mineralocorticoid receptors, use of these agents actually promotes the renin-angiotensin system and leads to increased PAC resulting from positive feedback. The pathological significance of the phenomenon whereby PAC increases with MRA administration but decreases with the addition of sacubitril/valsartan is unclear. In PA, more effective treatment may be possible by suppressing aldosterone with sacubitril/valsartan and blocking the action of aldosterone with MRAs.