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Biomedical subjects

Masaaki Inaba

Publications and source records attributed to Masaaki Inaba.

At least 19 recordsLinked to original sources
PubMed2007

Annual change in bone mineral density in predialysis patients with chronic renal failure: significance of a decrease in serum 1,25-dihydroxy-vitamin D.

Bone disease occurs in the predialysis phase of chronic renal failure (CRF). The aim of this study was to examine how a decrease in renal function affects annual bone mineral density (BMD) changes in predialysis CRF patients and to examine the factors that affect BMD. The BMD of the distal radius in 53 predialysis CRF patients (age, 61.3 +/- 10.8 years; serum creatinine 2.7 +/- 1.2 mg/dl) was measured by peripheral quantitative computed tomography (pQCT) twice with a 1-year interval. The total BMD of the radius significantly decreased over a year (P < 0.001), and both trabecular and cortical BMD showed a significant decrease. Significant positive correlations with BMD changes were found for estimated creatinine clearance (r = 0.375, P < 0.01) and baseline serum 1,25(OH)(2)D (r = 0.434, P < 0.005), indicating that BMD decreased to a greater extent with larger reductions in creatinine clearance and serum 1,25(OH)(2)D. Of several bone metabolic markers examined, baseline serum osteocalcin was significantly positively correlated with annual BMD changes (r = -0.276, P < 0.05). Multiple regression analysis showed that baseline serum 1,25(OH)(2)D (beta = 0.434) was a significant predictor of decreases in total and trabecular BMD (R (2) = 0.188, P < 0.01; and R (2) = 0.207, P < 0.01), independent of other confounding factors. These results indicate that BMD decreases as renal function deteriorates in predialysis CRF patients, and that osteocalcin is a clinically useful marker associated with the decrease in BMD. The serum 1,25(OH)(2)D level is the principal factor affecting BMD of the radius, suggesting that supplementation with an active form of vitamin D is of importance for predialysis CRF patients.

Aged↗
PubMed2007

Association of serum fetuin-A with carotid arterial stiffness.

OBJECTIVE: Fetuin-A is a circulating glycoprotein which is well characterized as an inhibitor of ectopic calcification. Vascular calcification commonly found in chronic kidney disease (CKD) patients is a predictor of cardiovascular death. Recently, several groups have demonstrated that low fetuin-A levels are associated with mortality in uraemic patients, possibly through regulation of vascular calcification. However, the physiological significance of fetuin-A in atherosclerosis remains unknown, except in specific conditions, such as vascular calcification in CKD patients. The objective of this study was to investigate the association between serum fetuin-A levels and arterial stiffness, a functional property of atherosclerosis, in healthy subjects. PATIENTS AND MEASUREMENTS: The study subjects comprised 141 healthy subjects. We measured serum fetuin-A levels and stiffness parameter beta for the common carotid artery, which was assessed by ultrasound using a phase-locked echo-tracking system. RESULTS: Simple regression analyses indicated that serum fetuin-A levels were significantly correlated with stiffness parameter beta (r = 0.200, P = 0.018). Multiple regression analyses showed that, besides age, fetuin-A (beta = 0.166, P = 0.033) independently contribute to the stiffness parameter beta (R(2) = 0.310, P < 0.0001). CONCLUSIONS: Serum fetuin-A level is associated with carotid arterial stiffness, independent of known atherogenic factors in healthy subjects.

Age Factors↗
PubMed2007

Central pulse wave velocity is responsible for increased brachial-ankle pulse wave velocity in subclinical hypothyroidism.

OBJECTIVE: Subclinical hypothyroidism affects 5-15% of the general population, and is associated with increased morbidity from cardiovascular disease. We recently reported a significant increase in brachial-ankle pulse wave velocity (baPWV), a parameter of arterial stiffening and an independent predictor for the presence of cardiovascular disease, in subclinical hypothyroidism. The current study was performed to assess which arterial segment is responsible for enhanced baPWV in subclinical hypothyroidism. PATIENTS AND METHODS: Central PWV (PWV in heart-femoral segments), peripheral PWV (PWV in femoral-ankle segments), and baPWV were measured in subclinical hypothyroid patients and normal subjects. RESULTS: Central PWV, baPWV, and peripheral PWV were significantly higher in subclinical hypothyroid patients than in normal subjects. BaPWV was significantly and positively correlated with central and peripheral PWV in both groups. However, a significant and positive correlation between central and peripheral PWV in normal subjects was not found in subclinical hypothyroid patients. Moreover, stepwise regression analysis showed that the association of central PWV with baPWV was stronger than that of peripheral PWV, whereas in normal subjects central PWV was not associated with baPWV. CONCLUSIONS: Our results demonstrate that central and peripheral PWV are significantly higher in subclinical hypothyroid patients, and that the increase in baPWV depends more strongly on central PWV than on peripheral PWV in these patients. This suggests that increased elastic arterial stiffening of the aorta, rather than of peripheral muscular arteries, might be more responsible for increased general arterial stiffening in subclinical hypothyroid patients.

Ankle↗
PubMed2006

Neutrophil-activating activity and platelet-activating factor synthesis in cytokine-stimulated endothelial cells: reduced activity in growth-arrested cells.

The reactivity of endothelial cells (ECs) to proinflammatory cytokines is critically important for the pathogenesis of vascular diseases. Here, we studied functional alterations of human ECs during culture under a confluent condition; i.e., the alterations of neutrophil-activating activity, platelet-activating factor (PAF) synthesis, and granulocyte-macrophage colony-stimulating factor (GM-CSF) production in cytokine-stimulated ECs. Human umbilical vein-derived ECs exhibited the increased activity in neutrophil activation, PAF synthesis, and GM-CSF production when stimulated by proinflammatory cytokines such as interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha). The activity of cytokine-stimulated ECs to stimulate superoxide release in human neutrophils and to produce PAF declined markedly in parallel as ECs became growth-arrested during culture under a confluent condition. By contrast, GM-CSF production induced by cytokine stimulation was modestly increased, and up-regulation of intercellular adhesion molecule-1 (ICAM-1) and activation of mitogen-activated protein kinases were not altered. The neutrophil-activating activity of cytokine-stimulated ECs was dependent on PAF synthesis and GM-CSF production from ECs. These findings indicate that the reduced neutrophil-activating activity in growth-arrested ECs may be, at least in part, ascribed to down-regulation of PAF synthesis.

Antibodies↗
PubMed2006

Laparoscopic adrenalectomy on a patient with primary aldosteronism during pregnancy.

A pregnant 26-year-old woman was referred for evaluation and management of progressive hypertension and hypokalemia at 14 weeks of gestation. Her plasma aldosterone level was markedly elevated and magnetic resonance imaging showed a right adrenal tumor. Primary aldosteronism due to an aldosterone producing-adenoma was diagnosed. Because of progressive severe hypertension, a laparoscopic adrenalectomy was performed at 17 weeks of gestation. The procedure was completed without complication, and plasma aldosterone and potassium levels rapidly improved post-operatively. However, her hypertension persisted and the growth retardation of the fetus was found. Regrettably, intrauterine fetal death was confirmed at 26 weeks of gestation. Histological examination of the placenta revealed that the placental artery had very thick walls which had apparently caused a critical failure in fetal blood flow. The optimal timing of laparoscopic surgery during pregnancy and perioperative management were subsequently discussed.

Adenoma↗
PubMed2006

Annual fat mass change is a significant predictor of mortality in female hemodialysis patients.

BACKGROUND: Although obesity confers an increased risk of mortality in the general population, it has been reported to be associated with improved survival in dialysis patients. However, the influence of fat mass change over time on mortality in dialysis patients has not been determined. METHODS: This relationship was examined in 190 female maintenance hemodialysis patients. Fat mass was measured twice with a 12-month interval, using dual energy X-ray absorptiometry (DEXA). The patients were followed up for 5 years, and predictors for all-cause death were examined using Kaplan-Meier analysis and Cox proportional hazards analyses. RESULTS: During the 5-year follow-up period, 65 patients died. Annual fat mass changes in the expired group tended to be greater than in the surviving group (-1.0 +/- 2.5 vs. -0.3 +/- 2.6 kg; P = 0.0776), although initial body fat mass was not significantly different. Kaplan-Meier analysis revealed that patients with decreased fat mass (N = 110) had a significantly lower survival rate, compared with those with increased fat mass (N = 80; P = 0.021). Multivariate Cox proportional hazards analyses demonstrated that annual fat mass change was a significant predictor of all-cause mortality after adjustments for confounding factors, such as age, serum albumin, serum creatinine, and the presence of diabetes. An increase in annual fat mass of 1 kg reduced mortality by 14.5%. CONCLUSIONS: These results demonstrate that the decrease in annual fat mass is a significant predictor for mortality in female hemodialysis patients. Fat mass change is also a useful parameter for measurement of nutritional status in hemodialysis patients.

Absorptiometry, Photon↗
PubMed2006

Simultaneous bilateral laparoscopic adrenalectomy for adrenocorticotropic hormone-independent macronodular adrenal hyerplasia: report of a case.

Cushing's syndrome caused by adrenocorticotropic hormone (ACTH)-independent macronodular adrenal hyperplasia (AIMAH) is an extremely rare disease, which shows bilateral macronodular adrenal hypertrophy and autonomous cortisol production. We herein report a case of AIMAH treated successfully by minimally invasive simultaneous bilateral laparoscopic adrenalectomy. A 73-year-old woman with hypertension, diabetes mellitus, and osteoporosis was referred to our hospital because of an incidentally found huge bilateral adrenal mass. An abdominal computed tomography scan showed large bilateral adrenal glands with multiple nodules. A diagnosis of AIMAH was made and a simultaneous bilateral laparoscopic adrenalectomy was thus performed. The total operation time was 310 min and blood loss was 70 g. Both glands were hypertrophic (right 5 x 3 cm, 48.5 g and left 4 x 2 cm, 39.2 g) and consisted of multiple golden yellow macronodules. The postoperative course was uneventful. A simultaneous bilateral adrenalectomy for AIMAH performed by an experienced surgical team is therefore considered to be a safe and minimally invasive procedure.

Adrenal Glands↗
PubMed2006

Direct in vitro evidence of the suppressive effect of cinacalcet HCl on parathyroid hormone secretion in human parathyroid cells with pathologically reduced calcium-sensing receptor levels.

Clinical studies have been performed to determine the effect of cinacalcet HCl (cinacalcet), an allosteric modulator of the calcium-sensing receptor (CaR), on primary hyperparathyroidism (PHPT) and secondary hyperparathyroidism of uremia (SHPT). However, no in vitro studies on human parathyroid cells have been reported to date. In this study, the inhibitory effect of cinacalcet on PTH secretion was analyzed in primary cultured parathyroid cells obtained from patients. The investigation involved three PHPT and three SHPT patients subjected to therapeutic parathyroidectomy. Notably, all SHPT patients were resistant to intravenous vitamin D analogue therapy. Removed parathyroid tumors were used for immunohistochemistry and parathyroid cell primary culture. Immunohistochemical analyses revealed diminished expression of CaR and vitamin D receptor (VDR) in all parathyroid tumors. PTH secretion from cultured parathyroid cells of PHPT and SHPT patients was suppressed by extracellular Ca2+ and cinacalcet in a dose-dependent manner. Rates of suppression of PTH secretion in PHPT and SHPT by cinacalcet (1000 nmol/l) were 61% +/- 21% and 61% +/- 19%, respectively. Cinacalcet demonstrates significant potency in the suppression of PTH secretion in primary cultured human parathyroid cells in vitro, despite reduced levels of the target protein, CaR. Data from this in vitro analysis support the clinical application of cinacalcet in PHPT and SHPT therapy.

Cinacalcet↗
PubMed2006

The association of plasma adiponectin level with carotid arterial stiffness.

Adiponectin plays important roles in protecting against both insulin resistance and the development of atherosclerosis. The aim of the present study was to investigate the clinical impact of plasma adiponectin on arterial stiffness, a functional property of atherosclerosis, in type 2 diabetic and nondiabetic subjects. We evaluated plasma adiponectin levels and stiffness index beta for the common carotid artery assessed by ultrasound using a phase-locked echo-tracking system for 98 type 2 diabetic subjects and 116 nondiabetic subjects as controls. Plasma adiponectin levels were significantly lower in the diabetic than in the nondiabetic group. The stiffness index beta was significantly higher in the diabetic than in the nondiabetic group. Plasma adiponectin level was significantly correlated with stiffness index beta in the group of all subjects (r=-0.189, P=.006) and the nondiabetic group (r=-0.187, P=.045), but not in the diabetic group (r=0.045, P=.665). On multiple regression analysis, plasma adiponectin level was found to be a significant independent contributor to stiffness index beta in the group of all subjects (beta=-0.232, P=.020) and the nondiabetic group (beta=-0.337, P=.016), but not in the diabetic group. In conclusion, adiponectin is significantly but weakly associated with carotid arterial stiffness independently of known atherogenic factors in the nondiabetic group and that of all subjects, although no significant association between these variables was found in the group of diabetic subjects.

Adiponectin↗
PubMed2006

Effect of adiponectin on carotid arterial stiffness in type 2 diabetic patients treated with pioglitazone and metformin.

Adiponectin, an adipocyte-specific plasma protein, has been reported to exhibit protective effects against atherosclerosis as well as an insulin-sensitizing effect. This study was designed to investigate the effect of adiponectin on carotid arterial stiffness in type 2 diabetic patients treated with pioglitazone and metformin. Twenty type 2 diabetic patients were enrolled and divided into 2 groups, a pioglitazone-treated group (n = 10) and a metformin-treated group (n = 10). Before and after intervention, plasma adiponectin levels were measured by enzyme-linked immunosorbent assay and carotid arterial stiffness was evaluated by the stiffness parameter beta, measured by ultrasound equipped with a phase-locked echo-tracking system. In the pioglitazone group, plasma adiponectin level significantly increased and stiffness parameter beta significantly decreased, whereas in the metformin group neither of these parameters changed significantly. The changes in stiffness parameter beta were significantly and inversely correlated with change in plasma adiponectin level after treatment with pioglitazone or metformin in the group of all subjects (r = -0.472, P = .036). In conclusion, the present study is the first to demonstrate that increase in adiponectin level after treatment with the insulin sensitizers pioglitazone and metformin may improve arterial stiffness in patients with type 2 diabetes mellitus.

Adiponectin↗
PubMed2006

Regulation of plasma fibroblast growth factor 23 by calcium in primary hyperparathyroidism.

OBJECTIVE: While the importance of fibroblast growth factor (FGF)-23 is established in phosphate-wasting disorders, little is known about the mechanisms regulating its circulating level. To investigate the role of parathyroid hormone (PTH) and calcium in FGF-23 metabolism, we examined plasma FGF-23 levels in patients with primary hyperparathyroidism (PHPT). PATIENTS AND METHODS: Fifty patients with PHPT and 52 controls were employed in this study. Plasma was obtained from 18 PHPT patients who underwent parathyroidectomy (PTX) on the first postoperative morning without vitamin D administration. Time-course samples were also obtained from 5 of 18 PTX patients without vitamin D analogs or calcium administration. The expression of Fgf23 on resected parathyroid glands was analyzed by reverse transcription (RT)-PCR and immunohistochemistry. RESULTS: FGF-23 was significantly elevated in PHPT patients compared with controls. FGF-23 levels were significantly correlated positively with serum corrected calcium and intact PTH levels, and negatively with creatinine clearance and inorganic phosphate, among which creatinine clearance and corrected calcium were independently associated factors. In 18 PTX patients, postoperative FGF-23 levels were significantly decreased compared with preoperative levels. Corrected-calcium levels were significantly decreased 1 h after PTX, and this was followed by a reduction in plasma FGF-23 levels in time-course study. In addition, postoperative FGF-23 levels in 18 PTX patients were significantly correlated with corrected calcium, consistent with a role of serum calcium as one of the major regulators of FGF-23. The absence of Fgf23 expression in parathyroid glands indicated that the parathyroid glands were not major sources of circulating FGF-23. CONCLUSIONS: Serum calcium may regulate circulating FGF-23 levels in PHPT.

Calcium↗
PubMed2006

[Bone metabolic marker; recent progress].

Measurement of bone markers has been established to supplement measurement of bone mineral density (BMD) in the diagnosis and treatment of osteoporosis. Bone marker provide a clinical useful mean to predict BMD reduction in near future, to assess fracture risk independent of BMD, to select therapeutic regimens for osteoporosis, to assess the effectiveness of drugs much earlier than BMD measurement. On the basis of the findings that a selective estrogen receptor modulator, raloxifene, showed a protective effect of bone fracture far more potent than its BMD-increasing effect, the hypothesis that bone marker indicates fracture risk independent of BMD has been raised and established.

Biomarkers↗
PubMed2006

Paraarticular trabecular bone loss at the ultradistal radius and increased arterial stiffening in postmenopausal patients with rheumatoid arthritis.

OBJECTIVE: We recently reported enhanced arterial thickening in patients with rheumatoid arthritis (RA) and the importance of increased bone resorption in this process. Our aim was to examine whether arterial stiffening, another aspect of atherosclerosis, is also increased in patients with RA, and to determine if it is an important risk factor. METHODS: The subjects were 47 patients with RA and 49 healthy controls, all postmenopausal women. Subjects having risk factors for atherosclerosis were excluded. Femoral-ankle (fa) pulse wave velocity (PWV) and brachial-ankle (ba) PWV were measured in all patients using a waveform analyzer. Bone mineral density (BMD) at the ultradistal radius was assessed by peripheral quantitative computed tomography. Inflammation markers (C-reactive protein, erythrocyte sedimentation rate, rheumatoid factor, platelet count) and bone resorption markers (urinary excretion of deoxypyridinoline and N-terminal telopeptide) were also measured. RESULTS: The median values of faPWV and baPWV in RA patients were 1124 cm/s [interquartile range (IQR) 1040-1175] and 1539 cm/s (IQR 1297-1738), respectively, which were significantly greater than the respective values of 982 cm/s (IQR 819-1054; p < 0.001) and 1322 cm/s (IQR 1112-1398; p = 0.004) in controls. In multiple regression analysis, the presence of RA emerged as an independent factor associated with the greater faPWV and baPWV when adjusted for age, blood pressure, and smoking. In RA patients alone, BMD in the trabecular bone component, but not for the total bone (cortical plus trabecular), at the ultradistal radius correlated significantly with both faPWV and baPWV. Multiple regression analysis showed that trabecular BMD at the distal radius was a significant factor independently associated with greater faPWV and baPWV when adjusted for age, blood pressure, and smoking. None of the measured inflammation markers or bone resorption markers correlated with either faPWV or baPWV in patients with RA. CONCLUSION: Patients with RA show increased arterial stiffening, in addition to the arterial thickening we have previously reported, supporting the notion of enhanced atherosclerosis in RA patients. Paraarticular bone loss in the trabecular bone component at the ultradistal radius is a factor significantly associated with increased arterial stiffening in RA patients.

Amino Acids↗
PubMed2006

[Bone abnormalities in diabetic hemodialysis patients].

In patients with end stage renal disease, metabolic bone abnormalities are frequently seen. Diabetes may affect bone metabolism through various mechanisms, including hyperglycemia, insulin deficiency, and accumulation of advanced glycation end-products. Bone disease in hemodialysis patients with diabetes mellitus is characterized by low bone turnover, resulting from either impaired secretion of parathyroid hormone or osteoblast dysfunction. The prevalence rate of vertebral fractures in diabetic hemodialysis patients was 32%, which was greater than that of non-diabetic hemodialysis patients (13%). In non-diabetic hemodialysis patients, those with vertebral fracture showed significantly lower bone mineral density in either lumbar spine or distal one third of radius than the respective value in those without fracture. However, in diabetic hemodialysis patients, neither bone mineral density in lumbar spine nor distal one third of radius was significantly lower in those with vertebral fracture than in those without.

Aged↗
PubMed2006

[Effect of aldose reductase on the abnormality of calcium metabolism in diabetic patients].

Bone disease in patients with type 2 diabetes mellitus (DM) is characterized by low bone turnover, resulting from either impaired secretion of parathyroid hormone or osteoblasts dysfunction. We have reported that intracellular sorbitol accumulation via. sorbitol pathway might be involved in the development of osteoblast dysfunction and osteoclast formation, as evidenced by either in vitro or in vivo study. The importance of metabolic pathway is further supported by the protective effect of aldose reductase inhibitor against the development of galactose-induced bone diseases in vivo and of functional impairments of human osteoblasts-like MG-63 cells. In conclusion, sorbotol pathway might be important in the development of low bone turnover disease in DM patients, and thus aldose reductase inhibitor might be clinically useful in the protection against the development of bone diseases in DM patients.

Aldehyde Reductase↗