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Biomedical subjects

Masaaki Inaba

Publications and source records attributed to Masaaki Inaba.

At least 55 records · Page 3Linked to original sources
PubMed2005

The significance of thyroid blood flow at the inferior thyroid artery as a predictor for early Graves' disease relapse.

OBJECTIVE: We investigated the clinical usefulness of thyroid blood-flow measurement in predicting relapse of Graves' disease (GD) in comparison with known risk factors for GD relapse. MEASUREMENT: Thyroid blood flow was measured in pulsed Doppler mode at the inferior thyroid artery (ITA), and the peak systolic velocity (PSV) calculated. PATIENTS: ITA-PSV was measured in euthyroid GD patients (n = 79) immediately before withdrawal of anti-thyroid drug (ATD) and in healthy subjects (n = 17). RESULTS: In the 79 euthyroid GD patients, the values of free triiodothyronine (FT3), TSH receptor autoantibody (TRAb), ITA-PSV and thyroid volume were significantly higher in the relapse group (n = 40) than in the nonrelapse group (n = 39) and the Youden index of ITA-PSV was significantly higher than that of FT3, TSH, TRAb and vascular endothelial growth factor (VEGF). CONCLUSION: ITA-PSV may assist in the prediction of early GD relapse after ATD withdrawal.

Adolescent↗
PubMed2005

Introduction to sevelamer hydrochloride and its clinical effects.

Sevelamer hydrochloride (SH) is widely used for the treatment of hyperphosphatemia in patients with renal failure who are on maintenance hemodialysis. In this study, we investigated the clinical effects of SH, administered as either monotherapy or combined with a calcium carbonate formulation, on the metabolism of calcium (Ca) and phosphorus (P) in patients who had been taking a Ca-based binder. Patients were divided into three groups (i): switched completely from a Ca-based binder to SH (complete switch); (ii) dosage of the Ca-based binder was reduced, and SH introduced (partial switch); and (iii) dosage of the Ca-based binder was not reduced and SH introduced (combination therapy). We also examined the effects of the introduction of SH on the lipid profile and parathyroid hormone (PTH) concentration. Comparison between groups of the numbers of successfully treated cases (reaching target concentrations of serum P=5.5 mg/dL and Ca x P product=55 mg2/dL2 within 6 months of treatment) showed that the likelihood of reaching target levels was higher if Ca-based binder was maintained as much as possible (combination therapy>partial changeover>complete changeover). Furthermore, treatment with SH decreased total cholesterol and non-HDL cholesterol concentrations significantly, and also increased HDL cholesterol and PTH concentrations compared to pre-treatment. These results suggest that when a calcium carbonate formulation is already in use, as far as compliance allows, the dosage should not be reduced when SH is added. Despite its beneficial effects on the lipid and PTH concentrations, preventing an excessive increase in the PTH concentration is essential when using SH.

Adult↗
PubMed2005

Increased levels of serum osteoprotegerin in hypothyroid patients and its normalization with restoration of normal thyroid function.

Hypothyroidism is associated with increased morbidity from cardiovascular disease, and an increase in serum osteoprotegerin (OPG) has recently been reported to be associated with the severity of coronary heart disease and cardiovascular mortality. The present study was designed to examine whether hypothyroidism causes an increase in serum OPG, and to determine whether levothyroxine (L-T4) replacement therapy might suppress serum OPG levels in hypothyroid patients. Fifty-three hypothyroid patients with chronic thyroiditis and age- and sex-matched normal control subjects were examined for the levels of serum OPG and plasma von Willebrand factor (vWF), a vascular injury marker. Thirty-seven of the hypothyroid patients were further monitored for changes in these markers during 1 year in a euthyroid state induced by L-T4 replacement therapy. Baseline OPG was significantly higher in hypothyroid patients than in normal controls (4.51 +/- 0.50 vs 3.72 +/- 0.23 pmol/l (mean +/- S.E.); P = 0.0182). In multivariate analysis, baseline OPG was significantly associated with baseline levels of TSH (r = 0.280, P = 0.0162) and vWF (r = 0.626, P < 0.0001). During one year of L-T4 replacement therapy, hypothyroid patients showed a significant decrease in OPG levels from 4.35 +/- 0.51 to 3.48 +/- 0.26 pmol/l (P = 0.0166), a level comparable to normal controls. The change in serum OPG levels during L-T4 replacement therapy was significantly and independently associated in a negative fashion with baseline vWF (r = -0.503, P = 0.0014). This study suggested that the severity of hypothyroidism and vascular injury might have important independent roles in increasing the serum OPG level in hypothyroid patients. Furthermore, it was demonstrated that a sustained euthyroid state might have the potential to decrease the serum OPG level in hypothyroid patients and that the degree of vascular injury in the hypothyroid state is independently associated with a decrease in serum OPG during a 1-year normalization of thyroid function.

Female↗
PubMed2005

Relationship between parathyroid calcium-sensing receptor expression and potency of the calcimimetic, cinacalcet, in suppressing parathyroid hormone secretion in an in vivo murine model of primary hyperparathyroidism.

Cinacalcet HCl, an allosteric modulator of the calcium-sensing receptor (CaR), has recently been approved for the treatment of secondary hyperparathyroidism in patients with chronic kidney disease on dialysis, due to its suppressive effect on parathyroid hormone (PTH) secretion. Although cinacalcet's effects in patients with primary and secondary hyperparathyroidism have been reported, the crucial relationship between the effect of calcimimetics and CaR expression on the parathyroid glands requires better understanding. To investigate its suppressive effect on PTH secretion in primary hyperparathyroidism, in which hypercalcemia may already have stimulated considerable CaR activity, we investigated the effect of cinacalcet HCl on PTH-cyclin D1 transgenic mice (PC2 mice), a model of primary hyperparathyroidism with hypo-expression of CaR on their parathyroid glands. A single administration of 30 mg/kg body weight (BW) of cinacalcet HCl significantly suppressed serum calcium (Ca) levels 2 h after administration in 65- to 85-week-old PC2 mice with chronic biochemical hyperparathyroidism. The percentage reduction in serum PTH was significantly correlated with CaR hypo-expression in the parathyroid glands. In older PC2 mice (93-99 weeks old) with advanced hyperparathyroidism, serum Ca and PTH levels were not suppressed by 30 mg cinacalcet HCl/kg. However, serum Ca and PTH levels were significantly suppressed by 100 mg/kg of cinacalcet HCl, suggesting that higher doses of this compound could overcome severe hyperparathyroidism. To conclude, cinacalcet HCl demonstrated potency in a murine model of primary hyperparathyroidism in spite of any presumed endogenous CaR activation by hypercalcemia and hypo-expression of CaR in the parathyroid glands.

Aging↗
PubMed2005

Hypercalcemia in a patient with primary hyperparathyroidism and acromegaly: distinct roles of growth hormone and parathyroid hormone in the development of hypercalcemia.

We herein report a case of primary hyperparathyroidism associated with acromegaly. Although serum parathyroid hormone (PTH) levels increased after the resection of a pituitary adenoma, levels of serum 1a, 25-dihydroxyvitamin D [1, 25(OH)2D] decreased but remained above the normal upper limit. After resection of a parathyroid adenoma, serum PTH, 1, 25(OH)2D, calcium (Ca), and phosphate were all normalized. Since serum 1, 25(OH)2D levels decreased in spite of the increase in serum PTH levels after normalization of levels of growth hormone (GH), GH may have contributed to the elevation of serum 1, 25(OH)2D. It is therefore suggested that the mechanism by which elevation of serum 1, 25(OH)2D occurred in the present case may involve an increase in serum GH distinct from the PTH-mediated pathway.

Acromegaly↗
PubMed2005

Platelet-monocyte aggregates are independently associated with occurrence of carotid plaques in type 2 diabetic patients.

Recent evidence suggests important roles for platelet activation in the progression of atherosclerosis. We have recently shown that P-selectin expression or the presence of platelet-monocyte aggregates, a well-characterized marker of platelet activation, is associated with carotid atherosclerosis in the general population. It is not clear, however, whether platelet activation is also associated with carotid atherosclerosis in patients with type 2 diabetes. In the present study, we measured circulating levels of platelet-monocyte aggregates in 120 patients with type 2 diabetes and 120 age- and gender-matched non-diabetic subjects, and examined their association with carotid atherosclerosis determined by arterial ultrasound. The percentage of platelet-monocyte aggregates was analyzed by CD41-positivity determined by whole-blood flow cytometry. Diabetic subjects (7.73 +/- 4.04%, mean +/- SD) showed significantly higher percentages of platelet-monocyte aggregates than non-diabetic subjects (6.03 +/- 4.38%). The percentage of these aggregates was significantly and positively correlated with HbA(1c) in both diabetic and non-diabetic subjects, with the association independent of other clinical factors. Logistic multiple regression analyses revealed that platelet-monocyte aggregates were significantly associated with the presence of carotid plaques independent of the status of glycemic control in diabetic subjects. Thus, an increase in platelet-monocyte aggregation in type 2 diabetic patients appears to be involved in the pathophysiology of carotid atherosclerosis.

Aged↗
PubMed2005

[Ibandronate as a new therapeutic agent for osteoporosis].

Ibandronate, a second generation amino-bisphosphonate has a high potency as much as the third generation bisphosphonates. Therefore this compound can be characteristically administrated by means of bolus intravenous injection. Moreover it is the first bisphosphonate prospectively shown antifracture efficacy for the intermittent administration in a randomized, controlled clinical trial.

Administration, Oral↗
PubMed2005

[Metabolic syndrome and magnesium].

With westernization of lifestyle in Japanese people, dietary intake of Mg by grain, barley, seaweed, vegetable, and nuts has been remarkably diminished. Resultantly, Japanese people might develop hypomagnesemia easily. Likewise, upon drastic change of Japanese lifestyle, metabolic syndrome has been increasing a bigger problem of Japanese health in recent days, probably resulting from various causes, such as increasing intake of animal fat, exercise insufficiency, and accumulation of various stresses. People with metabolic syndrome are often complicated with obesity, hypertension, hyperglycemia, and hyperlipidemia, and thus be susceptible to cardiovascular events. Hypomagnesemia may cause an increase of vascular tonus by intracellular magnesium depletion, resulting in an increase of blood pressure. Furthermore, it might cause impaired insulin secretion, insulin resistance, and hyperlipidemia, and finally leading to the development of metabolic syndrome. Therefore, the importance of magnesium intake for the maintenance of health should be increasingly recognized.

Arteriosclerosis↗
PubMed2005

[Correlation of serum Bio-intact PTH (1-84) and parathyroid gland size in hemodialysed patients].

Bio-intact parathyroid hormone (Bio-PTH) assay, which measures exclusively intact PTH (1-84) molecule, provides a better assay for estimating parathyroid function in hemodialysis (HD) patients, whereas intact PTH (I-PTH) assay cross-react with PTH (7-84) as well as PTH (1-84). We have found that PTH (7-84) accumulated into serum of hemodialysis patients due probably to its impaired excretion into urine. We have reported that parathyroid gland size is one of major predictor for vitamin D responsiveness in secondary hyperparathyroidism. Therefore, we investigated whether serum Bio-PTH, in comparison with serum I-PTH, may provide a relevant assay to estimate parathyroid function as evidence by its correlation with parathyroid gland size on ultrasound examination.

Biomarkers↗
PubMed2005

[Effects of parathyroid hormone gene polymorphism on cardiovascular mortality].

It is well-known that secondary hyperparathyroidism of uremia influences not only bone and mineral metabolism but also cardiovascular complications. Here we reported the effects of the level of serum intact PTH and its gene polymorphism on cardiovascular and non-cardiovascular mortality in hemodialysis patients. We analyzed the association between clinico-molecular parameters and 3-year survival in 508 hemodialysis patients among whom 90 patients died. The multivariate Cox proportional hazards models showed that the presence of diabetes mellitus, levels of albumin and intact PTH, and BstB I genotype were indicated as independent predictors of cardiovascular mortality, whereas age and albumin level were indicated as those of non-cardiovascular mortality, suggesting that the level of intact PTH and its gene polymorphism effect cardiovascular mortality in hemodialysis patients.

Cardiovascular Diseases↗
PubMed2005

[Acute response of serum PTH and bone markers after injection of 1alpha,25 (OH)2D3 and 22-oxacalcitrol in hemodialysis patient].

Time-course changes of serum PTH and various bone markers were compared after injection of 1alpha,25 (OH)(2)D(3) with that of 22-oxacalcitriol (OCT) in hemodialysis patients. Five patients (M/F; 3/2, mean ages of 61.6 years) were enrolled into the present study. Oral administration of vitamin D(3) derivatives was stopped at least one week before initiation of vitamin injection. After 1 week of single intravenous injection of OCT (5 microg), 1alpha,25 (OH)(2)D(3) (0.5 microg) was followed. Serum levels of intact PTH, intact osteocalcin, bone alkaline phosphatase, cross-linked N-telopeptides of type I collagen, calcium, and phosphate were measured before, 24h, and 48 h after injections of vitamin D(3) derivatives. Significant difference did not exist in time-course changes of serum PTH, any of bone markers, calcium and phosphate between after OCT and 1alpha,25 (OH)(2)D(3) injection. In conclusion, the present study may not support the presence of significant direct effect of vitamin D(3) derivatives on bone metabolism in hemodialysis patients.

Aged↗
PubMed2005

[Clinical significance of PTH (1-84) and PTH (7-84) in patients with predialysis chronic renal failure in relation to bone metabolism markers].

Serum levels of parathyroid hormone (PTH) in predialysis patients with chronic renal failure (CRF) were measured using both the "intact PTH" and "bio PTH" assays, and serum levels of PTH (7-84) were assessed by subtracting bio PTH from intact PTH. The PTH values measured by the two assays were strongly correlated, and were also significantly positively correlated with both bone formation and resorption markers. PTH (7-84) was significantly positively correlated with both the intact PTH and bio PTH, and was also significantly positively correlated with the bone metabolism markers. There is no significant relationship between bio PTH/PTH (7-84) ratio and bone metabolism markers. In conclusion, bio PTH and intact PTH assays have similar clinical significance in predialysis CRF patients. The PTH (7-84) and even the ration of bio-PTH/PTH (7-84) have little specific clinical effect on bone metabolism.

Aged↗
PubMed2005

[Effect of calcium on N-terminal truncation of PTH in human parathyroid cells].

Serum PTH (7-84) is accumulated in patients with secondary hyperparathyroidism. It is also known that serum calcium (Ca) increases the generation of N-terminally truncated forms of parathyroid hormone (PTH). In this study, we examined whether accumulation of PTH (7-84) fraction is a parathyroid glandular origin or not by using primary cultured parathyroid cells from patients with primary and secondary hyperparathyroidism. The Bio-PTH/I-PTH ratio, indicating the ratio of PTH (1-84) to the sum of (1-84) PTH and N-terminally truncated fragment, was suppressed by increase in extracellular Ca2+ concentration for both cultured parathyroid cells prepared from parathyroid adenomas and uremia-associated secondary hyperparathyroidism. There is no difference between the ratios in primary and secondary hyperparathyroidism. These findings suggest that N-terminal truncation is regulated by extracellular Ca2+ concentration in parathyroid cells, but accumulation of PTH (7-84) fragments in patients with secondary hyperparathyroidism is mainly caused by uremia.

Calcium↗
PubMed2005

[Significance of serum PTH (7-84) as a reliable nutritional marker in hemodialysis patients].

To evaluate the significance of serum PTH (7-84) in hemodialysis patients, correlation of the serum PTH (7-84) level with various nutritional markers was investigated in HD patients. Serum PTH was determined in 170 male HD patients by either a Bio intact PTH assay or a second-generation intact PTH assay. The level of bone formation markers and bone resorption markers were also measured. Lean body mass in trunk region was measured by dual X-ray absorptiometry. The serum PTH (7-84) level was obtained for the difference between serum I-PTH and Bio-PTH. Serum PTH (1-84) was directly obtained from the serum Bio-PTH value. Serum PTH (7-84) correlated significantly with nutritional markers such as body weight, albumin, PCR, TAC BUN, BUN, phosphate and lean body mass in trunk, whereas PTH (1-84) only correlated with phosphate. The correlation of serum PTH (7-84) with bone metabolic markers was no less significant than that for PTH (1-84). The results suggest that serum level of PTH (7-84) may provide clinically useful information, not only of the bone metabolic state but also of the nutritional state in HD patients, in sharp contrast to the exclusive correlation of PTH (1-84) with bone metabolic state.

Biomarkers↗
PubMed2005

[Vascular calcification in advanced secondary hyperparathyroidism].

Cardiovascular disease is one of the largest cause of mortality in maintenance hemodialysis patients. Vascular calcifications frequently encountered in hemodialysis patients. In advanced uremic secondary hyperparathyroidism model mice, vascular calcifications were observed in their aorta, by Kossa staining. This mouse model may be a useful model to study vascular calcification in maintenance hemodialysis patients.

Animals↗