Prevalence and causes of functional disability in an elderly general population of Japanese: the Hisayama study

Background

There are limited data on the prevalence and causes of disability in the elderly general population in Japan.

Methods

In a population-based cross-sectional study of 1550 Japanese aged 65 years or older, we examined the prevalence of functional disability (defined as a Barthel Index score of ≤95) and its causes.

Results

A total of 311 of the participants had a disability (prevalence 20.1%). The prevalence of disability increased with age and doubled with every 5-year increment in age. Prevalence was higher in women than in men, especially among those aged 85 years or older. With respect to the cause of functional disability, dementia accounted for 23.5%, stroke for 24.7%, orthopedic disease for 12.9%, and other disease for 38.9% of cases in men; in women, the respective values were 35.8%, 9.3%, 31.0%, and 23.9%. Regarding age, dementia was the most frequent cause of disability in subjects aged 75 years or older, whereas stroke was most common in subjects aged 65 to 74 years. Approximately two-thirds of cases of total dependence were attributed to dementia in both sexes, whereas the main cause of slight or moderate/severe dependence was stroke in men and orthopedic disease in women. Among participants with total dependence, 94.8% resided in a hospital or health care facility.

Conclusions

Our findings indicate that functional disability is common among Japanese elderly adults and that its major cause is stroke in men and dementia in women.Key words: functional disability, dementia, stroke, prevalence, Japanese elderly     

Clinical role of serum programmed death ligand 1 in patients with hepatocellular carcinoma: Where does it come from?

Programmed death ligand 1 (PD-L1) is a key target for the treatment of several malignancies. The present study was conducted to clarify the role of serum PD-L1 in hepatocellular carcinoma (HCC). Serum PD-L1 (sPD-L1) was examined by an enzyme-linked immunosorbent assay in 153 patients with HCC who underwent curative hepatectomy at Kumamoto University in 2011–2016. The expression of PD-L1 in tissue (tPD-L1) was investigated by immunohistochemistry. The clinical roles of the PD-L1 expression in both serum and tissue were examined. The sPD-L1 was significantly elevated in HCC patients compared to patients without any malignant or inflammatory disease (234 vs. 93 pg/mL, p < 0.0001). The percentage of the tPD-L1-positive area (%tPD-L1) in the background liver was significantly higher than in the tumor (1.52% vs. 0.48%, p < 0.0001). The %tPD-L1 in the background liver but not in the tumor was significantly correlated with the sPD-L1 level (p = 0.0079). The sPD-L1, %tPD-L1 in the tumor, and %tPD-L1 in the background liver were not correlated with the overall survival after surgery. PD-L1-expressing cells in the background liver, but not in the tumor tissue, appeared to contribute to the sPD-L1 level. The sPD-L1 level may thus not indicate the tumor burden in patients with HCC.     

Association of serum cytokine concentrations with psychological symptoms in midlife women

OBJECTIVE: The purpose of the present study was to clarify the association of serum cytokine concentrations, determined using a multiplexed cytokine assay, with psychological symptoms in midlife women. METHODS: Fifty-three peri- and post-menopausal women with and without psychological symptoms in Greene's climacteric scale were enrolled in this study. Levels of 17 cytokines in serum samples were measured simultaneously using a multiplexed human cytokine assay. RESULTS: Serum interleukin (IL)-6 concentration in women with psychological symptoms (2.71+/-047 pg/ml) was significantly (p=0.009) higher than that in women without psychological symptoms (0.98+/-0.18 pg/ml). Serum IL-8 concentration in women with psychological symptoms (33.4+/-8.17 pg/ml) was also significantly (p=0.022) higher than that in women without psychological symptoms (7.87+/-1.64 pg/ml). In addition, serum IL-10 concentration in women with psychological symptoms (0.74+/-0.26 pg/ml) was significantly (p=0.048) higher than that in women without psychological symptoms (0.07+/-0.04 pg/ml). Tumor necrosis factor (TNF)-alpha in serum was detected only in women with psychological symptoms. Serum IL-2 concentration in women with psychological symptoms tended (p=0.066) to be higher than that in women without psychological symptoms. No significant differences were found between levels of other cytokines in women with and without psychological symptoms. CONCLUSION: Psychological stress manifested as climacteric symptoms in midlife women may be associated with increases in serum concentrations of IL-6, IL-8, IL-10, and TNF-alpha.     

Impact of parametric imaging on contrast-enhanced ultrasound of breast cancer

Purpose

To prospectively evaluate the usefulness of contrast-enhanced ultrasound (CEUS) using parametric imaging for breast cancer in a multicenter study.

Methods

A total of 65 patients with breast cancer were included in this study. CEUS was performed, and still images on peak time (S), accumulated images (A) and parametric images (P) were generated from the raw data. Four blind reviewers ranked the best visible images as first place, and determined second and third place consecutively. We compared the average ranking of each image. The maximal diameter of the tumor determined on ultrasonography and MRI was compared with the corresponding pathological maximal diameter for 48 of the 65 patients. The correlation between the diameter determined by two experts and two beginners was analyzed.

Results

The average rank of visibility was as follows: P, 1.44; A, 2.04; and S, 2.52. The correlation between each image and the pathology was as follows: P, r = 0.664; A, r = 0.630; S, r = 0.717; and MRI, r = 0.936. There were no significant differences among the correlation between the experts and beginners in each image.

Conclusions

The use of parametric imaging improves the visibility of CEUS. The maximal diameter of the tumor determined on CEUS correlates substantially with the pathology.

     

A patient of CD4-/CD8+ chronic T-cell leukemia associated with hypercalcemia.

A patient with chronic T-cell leukemia characterized by a suppressor phenotype is reported. A 71-year-old woman presented with symptoms and signs of hypercalcemia. Peripheral blood specimen showed abnormal lymphoid cells with an oval to cleaved nucleus, rather condensed chromatin, occasional prominent nucleolus, and basophilic cytoplasms with vacuoles which seems to be a T-cell counterpart of B-cell chronic lymphocytic leukemia with mixed cell types. The phenotype of these cells was CD4-, CD8+, CD5+, CD6+ with poor expression of CD3, CD7, and CD25. Southern blot analysis of T-cell receptor beta-chain gene revealed one allele rearranged band. The serum antibodies were positive against human T-cell leukemia virus, type I-associated antigens, but monoclonal integration of proviral DNA was not detected in the leukemic cells suggesting that she was just a carrier of this virus. Interestingly, serum PTH-related peptide (PRP) was elevated. The combination therapy with vincristine and prednisolone for leukemia decreased not only the number of leukemic cells but also the serum PRP levels. The clinical course was aggressive. She only responded transiently to treatments, and died of renal failure due to uncontrollable hypercalcemia six weeks after admission.     

Neurotoxic conversion of β-synuclein: a novel approach to generate a transgenic mouse model of synucleinopathies?

Many groups have generated α-synuclein (α-syn) transgenic (tg) mice as a rodent model for human synucleinopathies, including Parkinson’s disease and dementia with Lewy bodies (DLB). Indeed, some of the lines displayed limited evidence of neurodegeneration, such as α-syn deposits, compromised function of dopaminergic neurons, fibrillization of α-syn, and astrogliosis. However, none of them fully replicate the pathological features of synucleinopathies. To better understand the pathogenesis of the synucleinopathies and to develop new therapeutic strategies, improvement of the current version of α-syn tg mice may be required. We predict that β-synuclein (β-syn), the homologue of α-syn, might be a key molecule for this purpose. Although β-syn is a neuroprotective molecule counteracting the α-syn pathology in tg mice, it was previously shown that both β-syn and γ-synuclein were associated with axonal pathology in the hippocampus of sporadic cases of Parkinson’s disease and DLB. Furthermore, two missense mutations (P123H and V70M) of β-syn were recently identified in DLB. These mutants of β-syn were prone to aggregate in vitro and overexpression of these mutant β-syn proteins in neuroblastoma cells resulted in enhanced lysosomal pathology. Taken together, these results suggest that a toxic gain of function of β-syn might be involved in the pathogenesis of synucleinopathies. In this context, it is of considerable interest to determine if mutant β-syn-overexpressing tg mice could exhibit neuropathological features distinct from those in conventional α-syn tg mice. Furthermore, it is expected that a bigenic mouse model for mutant β-syn/α-syn might be characterized by a more accelerated phenotype of synucleinopathies.

     

Successful treatment with steroid and cyclosporine A in a patient with immunoglobulin A–proliferative glomerulonephritis with monoclonal immunoglobulin deposits

We report a case of glomerulonephritis with monoclonal immunoglobulin (Ig) A deposits as a form of monoclonal gammopathy of renal significance (MGRS) caused by monoclonal immunoglobulins without blood disorders in a 41‐year‐old woman. She developed lower leg oedema and was hospitalized because of nephrotic syndrome. Serum and urine were negative for M protein, and the free light chain κ/λ ratio was within the normal range. Renal histopathological findings included mesangial proliferation, endocapillary cell proliferation, and a double‐contour appearance of the capillary walls. Immunofluorescent staining indicated IgA and C3 deposits on the mesangium and capillary walls. Only λ chain and IgA1 deposits were noted. Fine granular sub‐endothelial deposits with no specific structure were observed under electron microscopy. The patient was diagnosed with IgA–proliferative glomerulonephritis with monoclonal immunoglobulin deposits (IgA‐PGNMID). The patient had decreased urine protein and sediment erythrocytes after she underwent two rounds of steroid pulse therapy and oral steroid therapy, but proteinuria and haematuria still remained. Four months later, the patient was administered 50 mg/day cyclosporine (CsA), and proteinuria and haematuria dramatically decreased. Only a few case reports have been published on IgA‐PGNMID. This case is rare in that the patient achieved successful treatment using a combination of steroids and CsA.     

Nursing Diagnoses and Interventions of Japanese Patients with End-Stage Breast Cancer Admitted for Different Care Purposes

PURPOSE: To clarify actual nursing diagnoses for and interventions given to patients with end-stage breast cancer admitted for different care purposes. METHODS: Nursing diagnoses, defining characteristics, related/risk factors, and nursing interventions were analyzed in a convenience sample of 150 patient records. FINDINGS: A total of 539 nursing diagnoses (96 labels) were documented. Frequently listed diagnoses were chronic pain, risk for infection, and activity intolerance. The most frequently used nursing diagnosis for the chemotherapy group was risk for infection. The nurses in this study rarely report any diagnoses related to death and dying. CONCLUSIONS: Nursing diagnoses and interventions differed depending on the purpose of admission. PRACTICE IMPLICATIONS: Oncology nurses need to consider the reasons for admission when making nursing diagnoses and interventions for patients with end-stage breast cancer.