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H Koshiyama

Publications and source records attributed to H Koshiyama.

At least 19 recordsLinked to original sources
PubMed2006

Drugs share antidiabetic and antiatherosclerotic actions through "the common soil".

There have been increasing evidences that atherosclerosis is not the result of diabetes mellitus, but that both type 2 diabetes mellitus and atherosclerosis may share common pathogenesis, as Stern proposed as 'common soil' hypothesis in 1995. There are several candidates for 'common soil', such as insulin resistance, vascular inflammation and endothelial dysfunction. Recently many of clinical studies have indicated that some drugs can prevent or delay the development of cardiovascular diseases (CVD). Furthermore, many studies have suggested that some classes of drugs may prevent the development of type 2 diabetes. It is to be noted that most of the drugs may have both actions, i.e., to prevent development of new diabetes and to prevent CVD. Furthermore, they are reported to inhibit inflammation or endothelial dysfunction. Taken together, it is hypothesized that the drug which may have antiatherogenetic action may also have antidiabetic action, and vice versa. This hypothesis may provide the new insights into perspectives of drug development both to prevent type 2 diabetes and to prevent CVD.

Atherosclerosis↗
PubMed2001

Positional dissociation between the genetic mutation responsible for pseudohypoparathyroidism type Ib and the associated methylation defect at exon A/B: evidence for a long-range regulatory element within the imprinted GNAS1 locus.

Pseudohypoparathyroidism type Ib (PHP-Ib) is a paternally imprinted disorder which maps to a region on chromosome 20q13.3 that comprises GNAS1 at its telomeric boundary. Exon A/B of this gene was recently shown to display a loss of methylation in several PHP-Ib patients. In nine unrelated PHP-Ib kindreds, in whom haplotype analysis and mode of inheritance provided no evidence against linkage to this chromosomal region, we confirmed lack of exon A/B methylation for affected individuals, while unaffected carriers showed no epigenetic abnormality at this locus. However, affected individuals in one kindred (Y2) displayed additional methylation defects involving exons NESP55, AS and XL, and unaffected carriers in this family showed an abnormal methylation at exon NESP55, but not at other exons. Taken together, current evidence thus suggests that distinct mutations within or close to GNAS1 can lead to PHP-Ib and the associated epigenetic changes. To further delineate the telomeric boundary of the PHP-Ib locus, the previously reported kindred F, in which patient F-V/51 is recombinant within GNAS1, was investigated with several new markers and direct nucleotide sequence analysis. These studies revealed that F-V/51 remains recombinant at a single nucleotide polymorphism (SNP) located 1.2 kb upstream of XL. No heterozygous mutation was identified between exon XL and an SNP approximately 8 kb upstream of NESP55, where this affected individual becomes linked, suggesting that the genetic defect responsible for parathyroid hormone resistance in kindred F, and probably other PHP-Ib patients, is located >or=56 kb centromeric of the abnormally methylated exon A/B. A region upstream of the known coding exons of GNAS1 is therefore predicted to exert, presumably through imprinting of exon A/B, long-range effects on G(s)alpha expression.

Chromosome Mapping↗
PubMed2001

Lymphocytic hypophysitis: its expanding features.

Lymphocytic hypophysitis is classically defined as an inflammatory disorder confined to adenohypophysis. However, it has recently been indicated that infundibuloneurohypophysitis underlies some subsets of central diabetes insipidus (DI). Therefore, lymphocytic hypophysitis can be considered a syndrome including disorders of both the anterior pituitary (lymphocytic adenohypophysitis) and the posterior pituitary (lymphocytic infundibuloneurohypophysitis). We describe a 77-yr-old woman with lymphocytic hypophysitis presenting with headache, diplopia, general malaise and appetite loss. Head magnetic resonance imaging (MRI) demonstrated pituitary swelling and dura mater thickening on the dorsum sella. Endocrinological investigations revealed both anterior and posterior pituitary dysfunction associated with primary hypothyroidism due to Hashimoto's thyroiditis. Headache and diplopia spontaneously disappeared, and anterior pituitary dysfunction, general malaise and appetite loss improved after taking 10 mg hydrocortisone daily, although ACTH hyposecretion persisted. Pituitary swelling was thereafter reduced but the dura mater thickening persisted. We suggest that this case may represent a variant of lymphocytic hypophysitis in which chronic inflammatory process involves both the anterior and the posterior pituitary gland, infundibulum, dura mater on the dorsum sella and cavernous sinus. Regarding expanding features of lymphocytic hypophysitis, it may be considered a syndrome including heterogeneous disorders, of which the pathogenesis remains to be elucidated.

Aged↗
PubMed2001

Rapid progress of acute suppurative cholangitis to secondary sclerosing cholangitis sequentially followed-up by endoscopic retrograde cholangiography.

A 66-year-old man was admitted to our hospital because of right hypochondralgia and fever after colonic polypectomy. Endoscopic examination revealed purulent bile excretion from the duodenal papilla orifice; based on this finding, acute suppurative cholangitis was diagnosed. An endoscopic retrograde cholangiography revealed no abnormality in the biliary tree. However, chronic cholestasis persisted, and endoscopic cholangiography performed 4 months later disclosed a beaded appearance of the intrahepatic bile ducts; this sign is a characteristic finding of sclerosing cholangitis. This is the first report of rapid progression of acute suppurative cholangitis to secondary sclerosing cholangitis sequentially followed-up by endoscopic retrograde cholangiography.

Acute Disease↗
PubMed2001

Rapid communication: inhibitory effect of pioglitazone on carotid arterial wall thickness in type 2 diabetes.

There have been increasing evidences that thiazolidinediones, peroxisome proliferator-activated receptor gamma (PPARgamma) agonists, may have some antiatherogenic actions. We have previously reported that troglitazone has a potent inhibitory effect on common carotid arterial intima-media thickness (IMT) in subjects with type 2 diabetes. However, some studies suggested a possibility that PPARgamma activators may have protoatherogenic actions, raising concern about their detrimental effects in diabetic subjects. In the present study, we investigated the effect of treatment with pioglitazone, another PPARgamma agonist, on IMT in a total of 106 Japanese subjects with type 2 diabetes. Pioglitazone (30 mg daily) was administered for 6 months in 53 patients. Compared to control group (n = 53), the group given pioglitazone showed a significant decrease in IMT as early as 3 months after the administration. The decrease in IMT was also found after 6 months (IMT change: -0.084[SE 0.023] mm vs. control 0.022[SE 0.006] mm, P < 0.001), although the difference between those after 3 and 6 months did not reach any statistical significance. These findings indicate that thiazolidinediones cause an inhibition of early atherosclerotic process PPARgamma activation.

Arteriosclerosis↗
PubMed2001

Case of adrenocorticotropic hormone-independent macronodular adrenal hyperplasia with possible adrenal hypersensitivity to angiotensin II.

With increasing case reports, it has been indicated that some cases with adrenocorticotropic hormone (ACTH)-independent macronodular adrenal hyperplasia (AIMAH) show abnormal responses in cortisol to various stimulation tests. Here we report a case of AIMAH that showed an aberrant response to angiotensin II via AT1 receptor in cortisol hypersecretion. A 53-yr-old man was admitted to our division seeking further examinations for the possible diagnosis of Cushing's syndrome. He had hypertension, diabetes mellitus, and physical stigmata, such as moon face and central obesity. His plasma ACTH level was undetectable, and plasma cortisol level was high. Plasma cortisol showed no normal diurnal rhythm and was not suppressed after the administration of 8 mg of dexamethasone. Abdominal computed tomography demonstrated nodular enlargement of bilateral adrenal glands. He was diagnosed with Cushing's syndrome owing to AIMAH. An injection of arginine vasopressin (AVP) increased plasma cortisol and aldosterone levels, whereas ACTH remained undetectable. After 4 h in an upright position, plasma cortisol and aldosterone levels were increased. Pretreatment with candesartan, angiotensin II receptor AT1 antagonist, blocked the increase in plasma cortisol level. These results suggested a possibility of adrenal hypersensitivity to angiotensin II and AVP in cortisol secretion. Bilateral laparoscopic adrenalectomy was performed. The histological findings of the specimen were compatible with AIMAH. In summary, we have made the first report on a case of AIMAH with possible hypersensitivity to angiotensin II.

Adrenal Glands↗
PubMed2000

Thyrotropin regulation of cyclic adenosine monophosphate production in human coronary artery smooth muscle cells.

Thyroid disease has been associated with the occurrence of pathophysiologic changes in the vasculature that may result in part from altered serum thyroid hormone and serum lipid levels. Thyrotropin (TSH) levels are also altered in thyroid disease, but a direct effect of TSH on vascular smooth muscle has not previously been considered. In the present study, human coronary artery smooth muscle cells (CASMC) were induced into two morphologically distinct forms by culturing in either (1) growth factor supplemented, 0.5% serum medium (SmGM-3) or (2) basal medium (SmBM) plus 10% fetal bovine serum (FBS). Intracellular cyclic adenosine monophosphate (cAMP) accumulation was determined by radioimmunoassay after exposure to increasing doses of bovine TSH. Cells grown in SmBM/10% FBS for 3 days exhibited a dose-dependent increase in intracellular cAMP that reached a level 10 times higher than baseline at the highest dose examined (100 mIU/mL). In contrast, cells grown in SmGM-3 medium exhibited no change in intracellular cAMP on exposure to increasing TSII. Low serum (0.5% FBS) reduced the ability of TSH to stimulate cAMP above the control value in CASMC. Pretreatment of CASMC with either transforming growth factor-beta1 (TGF-beta1) or tumor necrosis factor-alpha (TNF-alpha) lowered basal levels of cAMP production, but did not inhibit the ability of TSH to stimulate cAMP production. Human, but not rat aortic smooth muscle cells in culture also responded to TSH with a significant increase in cAMP. The results of this study suggest that TSH may exert direct effects on vascular smooth muscle mediated by adenylate cyclase activation that could conceivably affect the progression of vascular disease associated with thyroid dysfunction.

Actins↗
PubMed2000

Decrease in carotid intima-media thickness after 1-year therapy with etidronate for osteopenia associated with type 2 diabetes.

It has been suggested that bisphosphonates may have some antiatherogenic actions in experimental animals or in vitro, but their effects on the atherogenic process in humans has not been reported. In the present study the effect of etidronate treatment on carotid arterial intima-media thickness was prospectively examined in 57 subjects with type 2 diabetes associated with osteopenia. After 1 yr of therapy with cyclical etidronate (200 mg/day for 2 weeks every 3 months), intima-media thickness showed a decrease (mean +/- SE, 0.038 +/- 0.011 mm), which was significantly different from a change in 57 control subjects (0.023 +/- 0.015 mm; P < 0.005). Cardiovascular parameters were not changed after etidronate treatment. These findings suggest that etidronate in clinical dosage may have an antiatherogenic action, at least in type 2 diabetes, although its mechanisms remain to be elucidated.

Bone Diseases, Metabolic↗
PubMed1999

Lymphocytic hypophysitis presenting with diabetes insipidus: MR findings.

It has been thought that neurohypophysial involvement manifesting as central diabetes insipidus in lymphocytic hypophysitis is rare. The radiological and clinicopathological features of two cases represent a variant of lymphocytic adenohypophysitis and/or lymphocytic infundibulo-neurohypophysitis are discussed.

Diabetes Insipidus↗
PubMed1999

Medial plantar nerve conduction velocities among patients with vibration syndrome due to chain-saw work.

OBJECTIVE: The present study examined the effect of the vibration syndrome (VS) on the peripheral nervous system in the lower extremities. METHODS: Thirty-eight patients with VS due to previous exposure to vibration from chain-saw work and 55 age-matched controls were examined for sensory nerve conduction velocities in the medial plantar nerve (SCV-P). The patient group was divided into two subgroups, one with (n=19) and the other without vibration-induced white finger (VWF; n=19). RESULTS: Analysis of variance of SCV-P for the three groups showed significant difference (F(2,89)=10.65, P < 0.0001). A significant difference was found between the controls and the VWF(+) group (P < 0.0001) but not between the controls and the VWF(-) group (P=0.0508) by multiple comparison using Scheffe's method. CONCLUSION: These findings suggest that VS affects the peripheral nervous system function in the lower extremities via mediation of circulatory disturbance manifested as VWF.

Action Potentials↗
PubMed1999

Effect of calcium channel blocker amlodipine on the intimal-medial thickness of carotid arterial wall in type 2 diabetes.

Although several reports have suggested that calcium channel blockers may inhibit progression of atherosclerosis in animals, it is still controversial whether they have any clinically significant antiatherogenic action in humans. The measurement of intimal-medial thickness (IMT) of the common carotid artery by B-mode ultrasound technique has been recognized as a powerful and noninvasive method to evaluate early atherosclerotic lesions. We investigated the effect of treatment with amlodipine, a powerful calcium channel blocker, on IMT. Twenty-two hypertensive patients with type 2 diabetes were enrolled in a prospective open study. An amlodipine group (amlodipine, 5 mg; n = 11) and a control group receiving angiotensin-converting enzyme inhibitors (n = 11) were studied before and 6 months after treatment. Amlodipine treatment caused a significant decrease in IMT compared with control (-0.052 +/- 0.017 vs. 0.011 +/- 0.021 mm; p < 0.05). Although the exact mechanisms remain to be elucidated, our preliminary result suggests that amlodipine has an antiatherogenic action in type 2 diabetes.

Aged↗