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Biomedical subjects

D Inoue

Publications and source records attributed to D Inoue.

At least 37 records · Page 2Linked to original sources
PubMed1998

Potent inhibitory effect of troglitazone on carotid arterial wall thickness in type 2 diabetes.

There is increasing evidence that insulin resistance may be causally related to atherosclerosis. The measurement of common carotid arterial intimal and medial complex thickness (IMT) by B-mode ultrasound technique has been recognized as a powerful and non-invasive method to evaluate early atherosclerotic lesions. We investigated the effect of treatment with troglitazone, an insulin sensitizer, on IMT in a total of 135 Japanese subjects with type 2 diabetes. Troglitazone (400 mg daily) was administered for 6 months in 57 patients. Compared to control group (n = 78), the group given troglitazone showed a significant decrease in IMT as early as 3 months after the administration (IMT change: -0.080[SE 0.016] mm vs. control 0.027[SE 0.007] mm, P < 0.001). The decrease in IMT was also found after 6 months, although further decrease was not observed. Both HbA1c and postprandial serum triglycerides were decreased after troglitazone, but there was no statistically significant relation between a decrease in IMT and those in HbA1c or postprandial triglycerides. These findings indicate that troglitazone has a potent inhibitory effect on progression of early atherosclerotic lesions probably through the decreased insulin resistance in type 2 diabetes.

Carotid Arteries↗
PubMed1998

Improved cardiac function after catheter ablation in a patient with type B Wolff-Parkinson-White syndrome with an old myocardial infarction.

A 67-year-old man was admitted to hospital for the treatment of exertional dyspnea. He suffered from congestive heart failure due to an old inferior myocardial infarction with type B Wolff-Parkinson-White syndrome. Asynchronous wall motion caused by pre-excitation through a right-side bypass tract caused his cardiac function to deteriorate. Catheter ablation of the bypass tract increased the ejection fraction, and improved his symptoms, prior to surgical revascularization.

Aged↗
PubMed1998

Low bone mineral density in a case of mosaicism Klinefelter syndrome: rapid response to testosterone therapy.

Male hypogonadism has been recognized as one of the major causes of secondary osteoporosis, but most cases seem to be left undiagnosed. We report a 54-year-old case of mosaicism Klinefelter syndrome lacking typical clinical features such as tall stature or low intelligence, who was found to have marked decrease in lumbar bone mineral density (BMD: 0.686 g/cm2) during treatment of diabetes mellitus. In investigation for etiologies of secondary osteoporosis, he was diagnosed as having mosaicism Klinefelter syndrome (XXY/XY/XX). Although he was infertile, he lacked typical clinical features of Klinefelter syndrome. Testosterone replacement was started, which resulted in an increase in BMD up to 0.712 g/cm2 two months after the initiation of therapy. The fact that BMD increased shortly after the initiation of testosterone replacement therapy in the present case supported a beneficial effect of testosterone on BMD, as recently suggested in idiopathic hypogonadotropic hypogonadism. Although the present case was diagnosed as having mosaicism Klinefelter syndrome by investigating etiologies for osteoporosis, it may be stressed that male hypogonadism, in general, should be adequately suspected in the presence of infertility and from the findings of physical examination.

Bone Density↗
PubMed1998

A case of aldosterone-producing adenoma with severe postoperative hyperkalemia.

It is known that some patients with primary aldosteronism show postoperative hyperkalemia, which is due to inability of the adrenal gland to secrete sufficient amounts of aldosterone. However, hyperkalemia is generally neither severe nor prolonged, in which replacement therapy with mineralocorticoid is seldom necessary. We report a case of a 46-year-old woman with an aldosterone-producing adenoma associated with severe postoperative hyperkalemia. After unilateral adrenalectomy, the patient showed episodes of severe hyperkalemia for four months, which required not only cation-exchange resin, but also mineralocorticoid replacement. Plasma aldosterone concentration (PAC) was low, although PAC was increased after rapid ACTH test. Histological examination indicated the presence of adrenocortical tumor and paradoxical hyperplasia of zona glomerulosa in the adjacent adrenal. Immunohistochemistry demonstrated that the enzymes involved in aldosterone synthesis, such as cholesterol side chain cleavage (P-450scc), 3beta-hydroxysteroid dehydrogenase (3beta-HSD), and 21-hydroxylase (P-450c21), or the enzyme involved in glucocorticoid synthesis, 11beta-hydroxylase (P-450c11beta), were expressed in the tumor, but they were completely absent in zona glomerulosa of the adjacent adrenal. These findings were consistent with the patterns of primary aldosteronism. Serum potassium level was gradually decreased with concomitant increase in PAC. These results suggest that severe postoperative hyperkalemia of the present case was attributable to severe suppression of aldosterone synthesis in the adjacent and contralateral adrenal, which resulted in slow recovery of aldosterone secretion. It is plausible that aldosterone synthesis of adjacent and contralateral adrenal glands is severely impaired in some cases with primary aldosteronism, as glucocorticoid synthesis in Cushing syndrome.

Adenoma↗
PubMed1998

[Recent advances in biology of bone resorption].

Bone resorption is a unique process which requires function of highly specialized cells, i.e., osteoclasts, Osteoclasts are terminally differentiated multinuclear cells that originate from multipotent hematopoietic stem cells and are closely related to the monocyte/macrophage lineage. Recent advances in molecular biological techniques and development of useful experimental systems both in vitro and in vivo have made it possible to identify several factors essential to osteoclast differentiation or function under physiological and/or pathological conditions. Such factors include transcription factors such as c-Fos and PU.1, cytokines such as IL-6 and TNF-alpha, and other various molecules such as tyrosine kinases and adhesion molecules. This review will focus on recent progress in our understanding of osteoclast biology.

Animals↗
PubMed1997

Identification of an osteoclast transcription factor that binds to the human T cell leukemia virus type I-long terminal repeat enhancer element.

Transgenic mice expressing human T cell leukemia virus type I (HTLV-I)-tax under the control of HTLV-I-long terminal repeat (LTR) promoter develop skeletal abnormalities with high bone turnover and myelofibrosis. In these animals, Tax is highly expressed in bone with a pattern of expression restricted to osteoclasts and spindle-shaped cells within the endosteal myelofibrosis. To test the hypothesis that lineage-specific transcription factors promote transgene expression from the HTLV-I-LTR in osteoclasts, we first examined tax expression in transgenic bone marrow cultures. Expression was dependent on 1alpha,25-dihydroxycholecalciferol and coincided with tartrate-resistant acid phosphatase (TRAP) expression, a marker of osteoclast differentiation. Furthermore, Tax was expressed in vitronectin receptor-positive mononuclear precursors as well as in mature osteoclast-like cells (OCLs). Consistent with our hypothesis, electrophoretic mobility shift assays revealed the presence of an OCL nuclear factor (NFOC-1) that binds to the LTR 21-base pair direct repeat, a region critical for the promoter activity. This binding is further enhanced by Tax. Since NFOC-1 is absent in macrophages and conserved in osteoclasts among species including human, such a factor may play a role in lineage determination and/or in expression of the differentiated osteoclast phenotype.

Acid Phosphatase↗
PubMed1997

Bcl-2 lies downstream of parathyroid hormone-related peptide in a signaling pathway that regulates chondrocyte maturation during skeletal development.

Parathyroid hormone-related peptide (PTHrP) appears to play a major role in skeletal development. Targeted disruption of the PTHrP gene in mice causes skeletal dysplasia with accelerated chondrocyte maturation (Amizuka, N., H. Warshawsky, J.E. Henderson, D. Goltzman, and A.C. Karaplis. 1994. J. Cell Biol. 126:1611-1623; Karaplis, A.C., A. Luz, J. Glowacki, R.T. Bronson, V.L.J. Tybulewicz, H.M. Kronenberg, and R.C. Mulligan. 1994. Genes Dev. 8: 277-289). A constitutively active mutant PTH/PTHrP receptor has been found in Jansen-type human metaphyseal chondrodysplasia, a disease characterized by delayed skeletal maturation (Schipani, E., K. Kruse, and H. Jüppner. 1995. Science (Wash. DC). 268:98-100). The molecular mechanisms by which PTHrP affects this developmental program remain, however, poorly understood. We report here that PTHrP increases the expression of Bcl-2, a protein that controls programmed cell death in several cell types, in growth plate chondrocytes both in vitro and in vivo, leading to delays in their maturation towards hypertrophy and apoptotic cell death. Consequently, overexpression of PTHrP under the control of the collagen II promoter in transgenic mice resulted in marked delays in skeletal development. As anticipated from these results, deletion of the gene encoding Bcl-2 leads to accelerated maturation of chondrocytes and shortening of long bones. Thus, Bcl-2 lies downstream of PTHrP in a pathway that controls chondrocyte maturation and skeletal development.

Animals↗
PubMed1997

Comparative analysis of clonality and pathology in primary and secondary hyperparathyroidism.

Parathyroid adenoma and hyperplasia are the most common causes for hyperparathyroidism, and distinction between them is controversial based on the current criteria for pathological diagnosis. We studied the clonality of hyperparathyroidism and its correlation with the pathological features, analysing 39 female patients with hyperparathyroidism. Clonality was successfully detected in 12 heterozygous cases by PCR amplification of PGK-1 gene. The 12 cases yielded 14 hypercellular glands, 8 affected by primary and 6 by secondary hyperparathyroidism. The results revealed that 7 of the 8 glands with primary hyperparathyroidism showed monoclonal proliferation. Only 1 gland pathologically diagnosed as adenoma showed a polyclonal pattern. In the 4 cases with secondary hyperparathyroidism, at least one monoclonal tumour was detected in each case. Our data indicate that monoclonal tumours are more common than expected in both primary and secondary hyperparathyroidism. Monoclonal tumours and polyclonal hyperplasia can co-exist in the same patient. Comparative study of the clonality and the pathological features showed that the clonality was consistent with the diagnosis of parathyroid adenoma, whereas it was in conflict with the diagnosis of hyperplasia with multigland involvement. One of the reasons for this is that we are ignorant of the true natures of hyperparathyroidism with multigland involvement.

Cell Line↗
PubMed1997

A case of sarcoid reaction associated with papillary thyroid carcinoma.

Sarcoid reaction, a granulomatous lesion similar to those seen in sarcoidosis, has been reported to be associated with various disorders. Here we describe a 54-year-old woman, who was diagnosed with sarcoid reaction associated with papillary carcinoma of the thyroid. Her history included total thyroidectomy with radical neck dissection for a papillary carcinoma of the thyroid. She was found to have a right subclavian mass. Dissection of the mass was performed for the diagnosis of metastatic papillary carcinoma to the lymph node, but the pathological examination showed granuloma without caseation as well as metastasis to the lymph node. Polymerase chain reaction (PCR) of the specimen excluded a possibility of Mycobacterium infection. There was no supporting evidence for systemic sarcoidosis in this patient; the patient showed no skin, eye, or lung lesions, or bilateral hilar lymphadenopathy, and she did not show increase in serum gamma-globulin or in plasma angiotensin-converting enzyme (ACE) levels, or increased CD4/CD8 ratio of lymphocytes obtained from bronchoalveolar lavage. These findings suggest that the present case had sarcoid reaction associated with papillary carcinoma. Although sarcoid reaction has been reported to be associated with various malignancies, only five cases, to our knowledge, are reported in the literature, which were associated with papillary carcinoma.

Carcinoma, Papillary↗
PubMed1997

A case of nonfunctioning pituitary adenoma resembling so-called silent corticotroph adenoma.

It has been indicated that some subsets of clinically nonfunctioning pituitary adenoma exhibit immunohistochemical and ultrastructural features of somatotroph or corticotroph cells, which are described as silent somatotroph and corticotroph adenomas, respectively. We here describe a 70-year-old woman with nonfunctioning pituitary adenoma presenting with visual disturbance. None of the pituitary hormones show abnormal finding. Magnetic resonance imaging study revealed a pituitary tumor which developed inferiorly into the sphenoidal sinus. Tumor resection was performed by a transsphenoidal approach, and resulted in a partial resection of the tumor. The specimen indicated chromophobic adenoma. Immunohistochemical examination revealed a characteristic distribution pattern of cytokeratin staining for ACTH cell adenoma, although immunostaining for ACTH was only weakly positive. After the operation, only ACTH secretion was impaired, requiring replacement therapy with glucocorticoid. Bromocriptine was administered in order to prevent the recurrence of the tumor. It remains to be elucidated whether the present case could be classified as silent corticotroph adenoma, which was originally indicated to have aggressive characteristics, i.e., progressive visual defect, high incidence of infarction and frequent recurrence.

Adenoma, Chromophobe↗
PubMed1997

Effectiveness of a short-term steroid treatment on the reduction in goiter size in antithyroid drug-treated patients with Graves' disease.

Reduction of goiter size is one of the criteria necessary to determine clinical remission in antithyroid drug (ATD)-treated Graves' patients. To facilitate goiter reduction or to achieve quick remission, a short-term steroid treatment was administered to 5 Graves' patients. These patients had been treated with ATD for a considerable period of time, had maintained euthyroidism with negative or weak thyrotropin-binding inhibitor immunoglobulin (TBII), but still had an enlarged goiter and remained T3 unsuppressive. Betamethazone was initially given 1.5 mg daily and then gradually tapered to 0 mg for 3 months. Compared to the 6-month observation period or the pre-medication period, goiter reduction exceeding 0.7 cm was achieved in all 5 patients during the steroid treatment. These reductions partly reversed to an extent smaller than pre-treatment levels in 2 patients, but continuous goiter reductions were observed for at least 3 months after steroid cessation in 3 patients. In 2 of these reduced goiter patients, T3 suppressibility was confirmed, and they were diagnosed in remission. During steroid administration, serum T3 and TSH concentrations were lowered but reversed shortly, serum fT4 concentrations did not change, and TBII levels became negative in all patients including the 2 with weak positive values before the treatment. In conclusion, a short-term steroid treatment for goitrous ATD-treated Graves' patients appears promising in achieving goiter reduction or remission.

Adult↗