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Aim: As the population ages, the proportion aged ≥75 years is expected to increase. Many studies on peroral endoscopic myotomy (POEM) as treatment for esophageal achalasia have already been reported; however, few studies have been designed on patients aged ≥75 years. The purpose of this study is to describe the characteristics of esophageal achalasia in patients >75 years and to evaluate the outcomes of POEM. Methods: This study included 121 patients who underwent POEM for esophageal achalasia, which was divided into the geriatric (n = 18) group aged ≥75 and the young (n = 103) group ≤74 years. The characteristics of esophageal achalasia and the short‐term outcomes after POEM in the geriatric group compared with the young group were retrospectively investigated. Results: The median age of the geriatric group was 78 years, and two patients were initially diagnosed with refractory pneumonia, and esophageal achalasia was initially overlooked. The preoperative Eckardt score of the geriatric group was significantly lower than that of the young group (4 vs. 6, P = 0.007), particularly in the regurgitation score. The Eckardt score and integrated relaxation pressure of both groups were significantly improved after POEM (P < 0.001). There were no cases of perioperative complications in the geriatric group. Conclusions: POEM for esophageal achalasia is a safe and effective treatment even in geriatric patients >75 years of age. In geriatric patients with recurrent or intractable pneumonia, it is important to rule out esophageal achalasia. Geriatr Gerontol Int 2021; 21: 788–793. [ABSTRACT FROM AUTHOR]

Background: The effectiveness of treatments for recurrent esophageal squamous cell carcinoma (ESCC), particularly chemotherapy and chemoradiotherapy (CRT), remains unclear in patients who have previously been administered the same drugs during neoadjuvant chemotherapy. Methods: In this retrospective study, 117 patients with recurrent thoracic ESCCs who had undergone curative resection were included. Patients were divided into two groups based on presurgical treatment: no presurgical treatment (n = 74), and neoadjuvant chemotherapy (n = 43). Prognosis after recurrence was analyzed differently in the group of patients who received CRT and chemotherapy for a recurrent site because of differences in recurrence patterns. Results: There were no differences in patterns and times to recurrence between the patients who underwent each presurgical treatment. For treatment of recurrence, CRT was administered to 66 patients, chemotherapy to 32, surgical resection to 5, and best supportive care to 14. In patients who underwent CRT for local recurrence, the survival rates of those administered neoadjuvant chemotherapy were similar to those who did not receive any presurgical treatment (P = 0.706). In patients who underwent chemotherapy for distant metastasis, the survival rates of those administered neoadjuvant chemotherapy were worse than in those who did not receive any presurgical treatment (P = 0.028). Conclusions: The effects of CRT for recurrent cancers are not influenced by neoadjuvant chemotherapy, even when using the same anticancer agent. Chemotherapy is an acceptable treatment for patients who do not receive presurgical treatment. [ABSTRACT FROM AUTHOR]

Objective: To investigate the point prevalence of major depressive disorder (MDD) as diagnosed by the Mini-International Neuropsychiatric Interview (M.I.N.I) in patients with rheumatoid arthritis (RA) and to determine whether MDD is related to features of RA disease, such as disease activity or physical dysfunction. Methods: Of the patients with RA who participated in the IORRA survey conducted in October 2005, 162 were evaluated using the M.I.N.I., the Center for Epidemiologic Studies-Depression (CES-D) scale, and the two-question depression screen for MDD. RA clinical features were obtained from the concomitant IORRA cohort database. Relationships between MDD and RA disease features were analyzed by the Wilcoxon rank sum test and Pearson's chi-square test. Results: The point prevalence of MDD as diagnosed by the M.I.N.I. was 6.8 % in our Japanese patients with RA. The percentage of depressive patients was determined to be 23.5, 17.3, or 7.4 % according to the CES-D scale with cut-off points of 16, 19, or 27, respectively, and 14.2 % according to the two-question depression screen. The best cut-off point for CES-D for risk of MDD diagnosed by M.I.N.I. in this study was determined to be 23, with 11.7 % depressive patients having the highest sum of sensitivity and specificity. No relationship between MDD and RA disease activity was detected. Conclusion: By using the well-established structural interview instrument M.I.N.I., we determined the point prevalence of MDD in the RA patients enrolled in this study to be 6.8 %, leading to the conclusion that concomitant MDD does not seem to influence disease activity in RA patients. [ABSTRACT FROM AUTHOR]

Biochemical factors play an important role in osteoarthritis (OA) pathogenesis. The purpose of this study is to clarify whether the dermatan sulfate (DS) levels in the synovial fluid of patients with knee OA are related to residual cartilage. Synovial fluid was obtained from 51 OA patients. Knee radiographs were evaluated with the Kellgren–Lawrence (K/L) grading scale. The levels of the following disaccharides were measured by high-performance liquid chromatography (HPLC): DS (DSΔDi4S), chondroitin 6-sulfate (CSΔDi6S), and chondroitin 4-sulfate (CSΔDi4S). The concentration of cartilage oligomeric matrix protein (COMP) was measured by a sandwich ELISA. The levels of DSΔDi4S in Grades 0 and I OA were significantly higher than levels in Grade II ( P = 0.0458), Grade III ( P < 0.0001) and Grade IV ( P < 0.0001), and we found strong relationships between the levels of DSΔDi4S and those of CSΔDi6S ( P < 0.0001, r = 0.705), CSΔDi4S ( P < 0.0001, r = 0.750), and COMP ( P < 0.0001, r = 0.699). We conclude that the presence of DSΔDi4S reflects proteoglycan metabolism in the residual articular cartilage of OA patients. This suggests that metabolism of the small leucine-rich repeat proteoglycans decorin and biglycan, which contain chains of DSΔDi4S, is similar to that of aggrecan. [ABSTRACT FROM AUTHOR]

We present two rheumatoid arthritis (RA) patients suffering from disturbances of the symphysis pubis. Radiography revealed one with pelvic ring disruption with symphysis pubis diastasis, and the other with osteolysis at both pubic rami and disruption of the superior aspect of the symphysis pubis. Both cases had received long-term corticosteroid therapy, including pulse therapy. We recommend reducing the corticosteroid dose to prevent disturbances of the symphysis pubis especially in RA patients on long-term steroid therapy. [ABSTRACT FROM AUTHOR]

Studies effects of benidipine hydrochloride on autonomic nervous activity in hypertensive patients with high and low-salt diets. Study methods and patients; Low and high frequency power spectrum of heart rate; Absence of difference in the antihypertensive effect of benidipine; Influence of benidipine on blood pressure and autonomic nervous activity.

Abstract: Background: The difference of arterial healing response following everolimus-eluting stent (EES) or sirolimus-eluting stent (SES) implantation in patients with ST-segment elevated myocardial infarction (STEMI) has not been compared in detail. Methods: Thirty-five patients with STEMI were randomly implanted with an EES or SES (23 EES, 12 SES). At seven months, neointimal thickness (NIT) and strut malapposition were evaluated by optical coherence tomography (OCT) and the grade and heterogeneity of neointimal coverage (NIC) and development of intra-stent thrombi were evaluated by angioscopy. Results: No significant differences were noted in clinical events experienced by the two groups, although one patient with an EES died following a papillary muscle rupture and one patient with a SES experienced sub-acute stent thrombosis. On OCT, although the EES implants showed a greater NIT than the SES implants (94.8±88.8μm vs 65.6±63.3μm, P<0.0001), both the EES and SES showed an excellent suppression of neointimal proliferation in the culprit lesion of STEMI. The frequency of uncovered and malapposed struts of EES was significantly lower than that of SES (2.7% vs. 15.7%, P<0.0001, 0.7% vs. 2.3%, P<0.0001, respectively). The ratio of stents fully covered with neointima of EES group was significantly higher than that of SES group (P=0.04). Angioscopic analysis also showed greater dominant NIC grade with homogenous NIC in EES than in SES (P=0.03, P=0.0002, respectively). The incidence of massive intra-stent thrombus of EES was lower than that of SES (P=0.05). Conclusion: For patients with STEMI, EES may promote better arterial healing response than SES. [Copyright &y& Elsevier]

Objectives: The purpose of this study was to explore a novel disease gene for hypertrophic cardiomyopathy (HCM) and to evaluate functional alterations caused by mutations. Background: Mutations in genes encoding myofilaments or Z-disc proteins of the cardiac sarcomere cause HCM, but the disease-causing mutations can be found in one-half of the patients, indicating that novel HCM-susceptibility genes await discovery. We studied a candidate gene, ankyrin repeat domain 1 (ANKRD1), encoding for the cardiac ankyrin repeat protein (CARP) that is a Z-disc component interacting with N2A domain of titin/connectin and N-terminal domain of myopalladin. Methods: We analyzed 384 HCM patients for mutations in ANKRD1 and in the N2A domain of titin/connectin gene (TTN). Interaction of CARP with titin/connectin or myopalladin was investigated using coimmunoprecipitation assay to demonstrate the functional alteration caused by ANKRD1 or TTN mutations. Functional abnormalities caused by the ANKRD1 mutations were also examined at the cellular level in neonatal rat cardiomyocytes. Results: Three ANKRD1 missense mutations, Pro52Ala, Thr123Met, and Ile280Val, were found in 3 patients. All mutations increased binding of CARP to both titin/connectin and myopalladin. In addition, TTN mutations, Arg8500His, and Arg8604Gln in the N2A domain were found in 2 patients, and these mutations increased binding of titin/connectin to CARP. Myc-tagged CARP showed that the mutations resulted in abnormal localization of CARP in cardiomyocytes. Conclusions: CARP abnormalities may be involved in the pathogenesis of HCM. [Copyright &y& Elsevier]