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Biomedical subjects

F Otsuka

Publications and source records attributed to F Otsuka.

At least 91 records · Page 5Linked to original sources
PubMed1998

Reversible hypothyroidism in empty sella syndrome: a case report.

A 33 year-old Japanese woman complained of generalized fatigue, recurrent infections and gradual weight loss 1 year after her first delivery. During delivery, no excessive bleeding or change in blood pressure was noted. On endocrinologic examination 2 years after delivery, she was found to have severe adrenal insufficiency and hypothyroidism. Pituitary function tests revealed impaired responses of ACTH, PRL and gonadotropins, and normal response of GH. TSH response to TRH was delayed but not exaggerated. Cranial magnetic resonance imaging showed an empty sella. The adrenal glands were responsive to extrinsic ACTH, and adequately accumulated 123I-aldosterol. Antipituitary and antithyroid autoantibodies were detected in her serum. She was diagnosed with partial hypopituitarism associated with empty sella syndrome. Approximately 2 months after administration of cortisone acetate 25 mg/ day her general condition was noticeably improved, with normalization of thyroid function and improvement of gonadotropin responses to GnRH. This case suggests that a physiologic dose of glucocorticoid is necessary to maintain not only thyroid function but also some of the remaining pituitary functions in patients with empty sella syndrome manifesting hypopituitarism.

Adult↗
PubMed1998

Pituitary apoplexy induced by a combined anterior pituitary test: case report and literature review.

We report the case of a 31-year-old woman with a pituitary adenoma who suffered symptomatic pituitary apoplexy. The patient developed a severe headache 2 min after undergoing a combined anterior pituitary function (CAP) test. Emergent computed tomography revealed a hemorrhagic pituitary tumor with evidence of a small subarachnoid hemorrhage. The headache improved spontaneously within half a day. Transsphenoidal surgery was performed 4 days later. Histologic examination demonstrated that the tumor was an eosinophilic adenoma with areas of diffuse hemorrhage. Although pituitary apoplexy caused by endocrinological testing has been reported in only 28 patients, apoplexy caused by a CAP test has been reported in only 1 patient. All of the previous cases had pituitary macroadenomas, 69% of which were involved in suprasellar extension. Non-functioning adenomas (24%) and prolactinomas (24%) were the most often affected by endocrine stimulation tests. With respect to the stimulants of pituitary adenomas, gonadotropin-releasing hormone (76%), TSH-releasing hormone (69%), and insulin (34%) were primarily responsible for the apoplexy. This case report with the literature review suggests that routine testing on pituitary function should be ordered cautiously given the risk of possible apoplexy.

Adult↗
PubMed1998

Sheehan's syndrome of more than 30 years' duration: an endocrine and MRI study of 6 cases.

The endocrine function and pituitary imaging in Sheehan's syndrome more than 30 years after causative events were evaluated. Magnetic resonance imaging (MRI), a combined anterior pituitary test, plasma vasopressin-to-osmolality adaptation study, and antithyroid and antipituitary cell antibody measurement were performed in 6 women with Sheehan's syndrome. The interval from delivery to the onset of symptoms of hormonal deficiency ranged from 3 to 32 years. Since clinical onset, all had received glucocorticoid and thyroid replacement therapy. Cranial MRI examination showed an "empty sella" in 5 cases. Among these, 2 of 5 (40%) demonstrated panhypopituitarism and the other 3 (60%) maintained gonadotropin response. The pituitary gland was normally discernible but with a low-intensity lesion on T1-weighted images in a patient who maintained PRL and gonadotropin responses. Posterior pituitary function was abnormal in 3 of 6 (50%) despite the absence of polyuria. No antipituitary antibodies were detected in any of the cases. Thyroid peroxidase antibody was negative in all cases, but antithyroglobulin antibody was detected in 2 of 6 (33%). Thyroid-stimulating antibody was not detected, but one case had an anti-TSH antibody. Thirty years after the initial events, most patients with Sheehan's syndrome showed signs of an empty sella on MRI, all having noticeable suppression of anterior and/or posterior pituitary hormones with no related autoimmunity.

Aged↗
PubMed1998

Hypocalcemia due to spontaneous infarction of parathyroid adenoma and osteomalacia in a patient with primary hyperparathyroidism.

A 49 year-old Japanese woman had subjected enlargement of a cervical tumor, and also suffered two bone fractures in 2 years. The cervical tumor had enlarged further in the month prior to admission, becoming warm and tender. Endocrinological examination revealed that the serum intact PTH concentration was remarkably high at 400 pg/mL despite the low serum calcium concentration, and that the serum vitamin Ds concentration was decreased. Bone roentgenograms revealed severe osteolytic changes compatible with osteitis fibrosa cystica and a pathologic fracture of the humerus. Under a diagnosis of primary hyperparathyroidism, parathyroidectomy was performed, followed by fixation surgery for the pathologic fracture. Histologically, the cervical tumor was a parathyroid chief-cell adenoma with massive necrosis, and the bone pathology by iliac bone biopsy revealed the existence of osteomalacia. She was treated with calcium, vitamins D and K2 and calcitonin after the surgery. This case is a rare condition manifesting hypocalcemia with catastrophic osteoporosis under the coexistence of spontaneous infarction of parathyroid adenoma with osteomalacia, suggesting that the clinical features of hyperparathyroidism are modified by both the autoparathyroidiectomy and the existence of osteomalacia due to vitamin D deficiency.

Adenoma↗
PubMed1998

Cushing's syndrome due to unilateral adrenocortical hyperplasia.

A 49-year-old woman with Cushing's syndrome due to unilateral adrenal hyperplasia is presented. She had developed obesity and menopause for 2 years, but no hypertension or hypertrichosis was observed. Although plasma adrenocorticotropin and serum cortisol levels were within normal ranges, the circadian rhythm has completely disappeared. Free thyroxine and triiodothyronine levels were decreased. Adrenocorticotropin did not respond to corticotropin-releasing hormone, and urinary excretion of 17-hydroxycorticosteroids was not suppressed by dexamethasone. Abdominal computed tomography and 131I-Adosterol scintigraphy demonstrated a unilateral functioning mass in the left adrenal gland. The resected left adrenal mass was pathologically diagnosed as the rare condition of adrenocortical nodular hyperplasia.

17-Hydroxycorticosteroids↗
PubMed1998

Renal AT1 receptor: autoradiographic localization and quantification in rat.

To elucidate the precise localization of angiotensin II (Ang II) type 1 (AT1) receptors in the kidney, we utilized in vitro macro- and micro-autoradiography (ARG) of [3H]-Ang II bindings to the Wistar rat kidney in the presence of L-158,809, a specific non-peptide AT1 receptor antagonist. Besides, we estimated the density of renal AT1 receptors using the quantification of macro-ARG. The density of [3H]-Ang II binding to renal tissue was concentration-dependent in both renal cortex and medulla. Although the addition with 500 nM arginine vasopressin and 500 nM atrial natriuretic peptide had no effect on [3H]-Ang II, the total binding of [3H] Ang II completely displaced by the addition with 500 nM unlabeled Ang II or L-158,809. Macro-ARG revealed that the amount of both Ang II and AT1 receptors in the renal medulla greatly exceeded those in the renal cortex. In the medulla, the density of these receptors was not localized on the outer medulla but was confirmed mainly to the inner medulla, especially to the inner zone and longitudinal bands. Since the density and localization of AT1 receptors was consistent with that of total Ang II receptors, it appears that AT1 receptors comprise most of the Ang II receptors in the kidney. Micro-ARG revealed that Ang II receptors were mainly located in the glomerulus and proximal tubules of the renal cortex, as well as on the circumferences of vessels and the vasa recta of the renal medulla. The present study established a method for ARG of AT1 receptors in the kidney as well as a method for quantifying the macro-ARG.

Angiotensin I↗
PubMed1998

Renal AT1 receptor: computerized quantification in spontaneously hypertensive rats and DOCA-salt rats.

To assess the involvement of angiotensin II (Ang II) in the regulation of blood pressure, we investigated the alterations of renal Ang II type 1 (AT1) receptors in two different models of hypertension; i.e., in spontaneously hypertensive rats (SHR) and deoxycorticosterone acetate (DOCA)-salt hypertensive rats by using the method for quantification of in vitro macro-autoradiography (ARG). In the SHR model, although the number of cortical AT1 receptors equaled that of Wistar Kyoto (WKY) rats at 4 and 12 weeks of age, the number of medullary AT1 receptors in the 4-week-old SHR animals was significantly lower than that in age-matched WKY rats, and increased by 12 weeks of age. The renal AT1 receptor number in DOCA-salt hypertensive rats was significantly higher than that in control rats. The amount of these receptors also increased with age in both DOCA-salt hypertensive rats and control rats. These findings indicate that the development of medullary AT1 receptors in early stages of hypertension in the SHR model differs from that in WKY rats or DOCA-salt hypertensive rats. This suggests that renal AT1 receptors may contribute to the hypertension seen in the SHR group. The renal AT1 receptors appear to be up-regulated in early stages of DOCA-salt-induced hypertension as well.

Age Factors↗
PubMed1997

Effects of OPC-21268, a vasopressin V1-receptor antagonist, on expression of growth factors from glomeruli in spontaneously hypertensive rats.

To assess the chronic in vivo effects of OPC-21268, a vasopressin-V1 receptor antagonist, on renal injury, we investigated the mRNA expressions of platelet-derived growth factor (PDGF) B-chain, transforming growth factor (TGF)-beta1 and proliferating cell nuclear antigen (PCNA) in the glomeruli of spontaneously hypertensive rats (SHR) treated with OPC-21268 for 3 weeks. SHR aged 10 weeks were given 2% NaCl in drinking water for 3 weeks. The OPC group was fed a 0.5% OPC-21268-containing diet for 3 weeks and the control group was given a normal diet. There were no significant changes in the time course of systolic blood pressure, heart rate, urine volume, or urinary sodium, protein and N-acetyl-beta-glucosaminidase (NAG) excretion between the two groups. Serum electrolytes, protein and creatinine levels also did not differ between the groups. The mRNA expressions of PDGF B-chain, TGF-beta1 and PCNA in the glomerulus were examined using reverse transcriptase-polymerase chain reaction (RT-PCR) methods. The mRNA expressions of PDGF B-chain and PCNA among these were significantly suppressed in the OPC group. No significant differences in renal histology including the organ weights were found between the two groups; however, the glomerular size tended to be enlarged in the OPC group. These findings suggest that chronic V1-receptor blockade directly inhibits the glomerular proliferative injury of salt-loaded SHR at the established hypertension stage.

Acetylglucosaminidase↗
PubMed1997

Effect of regional myocardial perfusion abnormalities on regional myocardial early diastolic function in patients with hypertrophic cardiomyopathy.

Nonuniform hypertrophy of the left ventricle is an important factor in regional diastolic dysfunction in patients with hypertrophic cardiomyopathy (HCM). However, the effect of myocardial perfusion abnormalities on regional diastolic dysfunction has not been established in patients with HCM. We investigated the relationship between regional myocardial perfusion abnormalities and regional early diastolic function in 31 patients with HCM and 8 control patients. Short-axis images of the left ventricle recorded by cine magnetic resonance imaging were divided into ten blocks. The time-to-peak-wall-thickness-thinning rate (TPWR) and the wall thickness were measured in each block. Of the 310 blocks from the patients with HCM, 242 (78%) showed normal thallium-201 uptake (group 1), 40 (13%) showed slightly decreased uptake (group 2), and 28 (9%) showed markedly decreased uptake (group 3). There was no difference in the regional wall thickness among the three groups. The TPWR was longer in patients with HCM than in control patients. It was significantly longer in group 3 (190+/-45ms) than in group 1 (167+/-36 ms) and group 2 (160+/-31 ms). (P < 0.01). The linear regression slope of the relationship between the TPWR and the regional wall thickness was significantly steeper in group 3 than in groups 1 and 2 (P < 0.05). In conclusion, abnormalities in regional myocardial perfusion, in addition to regional hypertrophy, contributed to the regional early diastolic dysfunction in patients with HCM.

Adult↗
PubMed1997

Interleukin-1 and lipopolysaccharide enhance intercellular adhesion molecule-1 expression in cell lines of human squamous cell carcinoma.

We show that in two cell lines of human squamous cell carcinoma (SCC) which slightly express intercellular adhesion molecule-1 (ICAM-1), the expression is enhanced not only by interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) but also by interleukin-1 (IL-1) and lipopolysaccharide (LPS). This expression is totally dependent on the increase of ICAM-1 mRNA. This evidence contrasts with previously reported findings indicating that, in human cultured keratinocytes, ICAM-1 expression is induced by IFN-gamma and TNF-alpha, and not by either IL-1 or LPS. This result suggests that various cytokines or agents easily enhance ICAM-1 expression in SCC cell lines, and may explain the clinical finding that ICAM-1 expression increases according to the progression of malignant tumors.

Actins↗
PubMed1997

Peripheral blood neutrophil rheology measured by micropore filtration reflects Behçet's disease activity well.

Activated neutrophils take a long time to pass through a narrow lumen like a micropore, and are supposed to play a deteriorating effect on microcirculation. Although the activation of neutrophils has been demonstrated in Behçet's disease, nobody analyzes the clinical activity of the disease by means of the rheological measure of neutrophils activity. Using a micropore (pore diameter 5 microns) filtration technique, we measured the filtration time of peripheral blood neutrophils, as a rheological measure of their activity, in order to determine the clinical activity of Behçet's disease. Twenty-one patients with Behçet's disease and 14 healthy control individuals were enrolled in the study. Symptoms and signs exhibited in the patients led us to distinguish the Behçet's disease into inactive and active cases. The latter were further differentiated into cases with absent symptoms and with present symptoms. Neutrophil filtration times were 11.5 +/- 4.8 s in the active cases with present symptoms, which were significantly (P < 0.05) larger than those (7.4 +/- 1.9 s) in the active cases with absent symptoms. The latter filtration times were further significantly (P < 0.001) larger than values (3.7 +/- 1.3 s) in the inactive cases and also those (4.8 +/- 1.2 s) in control subjects. Furthermore, increases in the filtration time obtained immediately after the exposure of cells to the chemotactic peptide formyl-methionyl-leucyl-phenylalanine (FMLP: 10 nM) were significantly (P < 0.01) larger in the active cases with present symptoms than those in the active cases with absent symptoms. The latter were also larger, but not significantly, than those in the inactive cases, and were significantly (P < 0.01) larger than those in control subjects. The present results demonstrate that the micropore filtration method reflects well the rheological activity of neutrophils as well as the clinical status of Behçet's disease. This method is much better than the measurement of O2 production to differentiate between active cases with absent symptoms and inactive patients or even control individuals. Furthermore, it is more sensitive and useful than laboratory data like the CRP value or the number of peripheral blood neutrophils.

Adolescent↗
PubMed1997

Eosinophil-colony stimulating activity in blister fluid of bullous pemphigoid.

We examined eosinophil-colony stimulating activity in blister fluid or serum obtained from patients with bullous pemphigoid using the methylcellulose semi-solid hematopoietic stem cell culture system, and demonstrated that the blister fluid of patients with bullous pemphigoid generated strong eosinophil-colony stimulating activity. This evidence suggests that eosinophil-colony stimulating activity in blister fluid probably influences the induction of eosinophilia in bullous pemphigoid.

Aged↗
PubMed1997

Leiomyoblastoma and leiomyomatosis of the small intestine in a case of von Recklinghausen's disease.

A 70-year-old patient with von Recklinghausen's neurofibromatosis 1 (NF1) developed a stomach ulcer and underwent a total gasterectomy. During the laparotomy, a leiomyoblastoma and multiple leiomyomas, which were histologically diagnosed as such later, were found in the small intestine and resected. It is quite possible that the association of gastrointestinal leiomyomas and NF1 is more than coincidental. It is thus important to take this complication into account in clinical treatment of patients with NF1.

Aged↗
PubMed1997

A case of recessive X-linked ichthyosis: scale-specific abnormalities of lipid composition may explain the pathogenesis of the skin manifestation.

We analyzed the lipid content of the scales, red blood cells, and plasma from a recessive X-linked icthyosis patient. The patient's scales accumulated cholesterol sulfate, had decreased levels of free sterols, sterol esters and sphingolipids, and lacked phospholipids. Although the accumulation of cholesterol sulfate was found in the patient's red blood cells and plasma as well as in the scales, other lipid composition abnormalities were specific for scales. Such scale-specific abnormal lipid composition may explain the pathogenesis of generalized hyperkeratosis and abnormal scaling of the disease.

Adult↗