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Biomedical subjects

I Komiya

Publications and source records attributed to I Komiya.

At least 19 recordsLinked to original sources
PubMed1992

[Forty-one cases of Cushing's syndrome: a comparison between Cushing's syndrome (adrenal adenoma) and Cushing's disease (adrenal hyperplasia)].

We experienced 41 cases of Cushing's syndrome (12 males and 29 females, 15 years old - 65 years old) during the last 20 years. These included 20 patients with unilateral adrenal adenoma (Cushing's syndrome), 19 patients with bilateral adrenal hyperplasia (Cushing's disease), one patient with adrenal carcinoma and one patient with primary adrenocortical nodular dysplasia (PAND). Moreover, these cases included some special ones, i.e. 5 cases with destructive thyroiditis after treatment, 2 cases with aggravation of arthritis after treatment, a case of Carney's complex with PAND, one case with paradoxical response to dexamethasone, and one case combined with empty sella syndrome. The most specific clinical signs were moon face (95% occurrence), hypertension (95%) and subcutaneous bruising (80%). Other significant signs were eye edema (66%), buffalo hump (68%), subcutaneous purpura (63%) and osteoporosis (49%). Skin striae was not a common sign in our cases (41%). Renal stone was observed in only 20% of our patients but was a significant sign in this syndrome. There was no difference in the occurrence of each clinical sign between Cushing's syndrome and Cushing's disease. The elevation of white blood cell count (WBC) and serum sodium, a decrease of serum potassium, and a decrease of reabsorption of phosphate (%TRP) were observed. Thyroid-stimulating hormone (TSH) and human growth hormone (HGH) were suppressed in patients with Cushing's syndrome and patients with Cushing's disease. These results were consistent with those of previous reports. However, luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin (PRL) were high in those patients with Cushing's syndrome and those with Cushing's disease. Oral glucose tolerance test was carried out in 34 patients before and after treatment. Thirty-one percent of those had diabetes mellitus and 26% had impaired glucose tolerance (IGT). The response of IRI in this test was high in patients with Cushing's syndrome and patients with Cushing's disease, and decreased 4 weeks after treatment in those with Cushing's syndrome but remained high in those with Cushing's disease. Plasma ACTH level and urinary 17-OHCS excretion were significantly higher in Cushing's disease than in Cushing's syndrome. During an 8mg-high-dose dexamethasone suppression test, urinary 17-OHCS excretion in 13 of 14 patients with Cushing's disease (93%) was suppressed by more than 50% of baseline on the second day of testing. However, all of 18 patients with Cushing's syndrome, who had an 8mg-dexamethasone suppression test, failed to suppress urinary 17-OHCS by 50% of baseline.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenoma↗
PubMed1992

Disappearance of thyrotropin-blocking antibodies and spontaneous recovery from hypothyroidism in autoimmune thyroiditis.

BACKGROUND: Hypothyroidism may result from the production of antibodies that block the actions of thyrotropin. How often these thyrotropin-blocking antibodies are a cause of hypothyroidism and whether their production may cease, causing hypothyroidism to disappear, have not been extensively studied. METHODS: We determined the frequency with which thyrotropin-blocking antibodies were present in 172 hypothyroid patients with goitrous autoimmune thyroiditis (Hashimoto's disease) and 64 hypothyroid patients with atrophic autoimmune thyroiditis (idiopathic primary hypothyroidism). For 6 to 11 years we then followed 21 of these patients who were found to have thyrotropin-blocking antibodies. They received levothyroxine therapy for 3.5 to 8 years, after which it was discontinued. At frequent intervals during this time we measured the patients' serum concentrations of thyroxine, triiodothyronine, thyrotropin, and thyrotropin-blocking antibodies (measured as immunoglobulins that inhibit thyrotropin binding and immunoglobulins that inhibit thyrotropin bioactivity). RESULTS: Thyrotropin-blocking antibodies were detected in 9 percent of the patients with goitrous autoimmune thyroiditis and in 25 percent of those with atrophic autoimmune thyroiditis. Among the 21 patients studied serially while receiving levothyroxine, thyrotropin-blocking antibodies disappeared in 15 (group 1), 7 of whom had goiter initially, and persisted in 6 (group 2), none of whom had goiter initially. Levothyroxine therapy was subsequently discontinued in these 21 patients. Six of those in group 1 (four with goiter) remained euthyroid (mean follow-up after discontinuation of therapy, 2.1 years), and nine became hypothyroid again within 3 months. All six patients in group 2 remained hypothyroid. CONCLUSIONS: Hypothyroidism in some patients with autoimmune thyroiditis may be due to thyrotropin-blocking antibodies. The production of thyrotropin-blocking antibodies may subside, producing remissions of hypothyroidism. Chronic autoimmune thyroiditis may therefore cause transient as well as permanent hypothyroidism.

Adult↗
PubMed1992

Studies on the association of NIDDM in Japanese patients with hyperthyroid Graves' disease.

We attempted to analyze the association of hyperthyroid Graves' disease with non-insulin-dependent diabetes mellitus (NIDDM). Forty-nine patients (23 males and 26 females; 7.6%) of a total of 647 patients with hyperthyroid Graves' disease had NIDDM, several years before or after Graves' disease was diagnosed. Only 1 patient had insulin-dependent diabetes mellitus. Compared with the general Japanese population (n = 9,133), the incidence of NIDDM (n = 348; 3.9%) in patients with Graves' disease was higher in all age groups. Only 4 patients (8.2%) of the 49 hyperthyroid patients with NIDDM had a history of being overweight (body mass index > 25). In contrast, 276 (79.9%) of the 348 diabetic patients were currently or previously overweight. Moreover, the incidence of a family history of diabetes (13 of the 49 hyperthyroid Graves' patients with NIDDM; 26.5%) was also lower in the patients with NIDDM in the general Japanese population (50% incidence). The male:female ration in patients with Graves' disease and NIDDM was 1:1.1; much different from that in the total Graves' disease population (1:4.1). Analysis of the HLA loci A, B, C, DR and DQ (35 determinations) in 35 hyperthyroid patients with NIDDM and in 386 subjects from the general population revealed a highly significant difference between them in the incidence of HLA-Cw4, -DR2, -DQw1, -DQw3 and -DQw4. This study suggests that there was an association of Graves' disease with NIDDM. A significant association of HLA-DR and -DQ loci was observed in hyperthyroid Graves' patients with NIDDM.

Adolescent↗
PubMed1992

Requirements of follicle structure for thyroid hormone synthesis; cytoskeletons and iodine metabolism in polarized monolayer cells on collagen gel and in double layered, follicle-forming cells.

Thyroid cells take up iodine and synthesize thyroid hormones. Thyroid cell polarity plays an important role in the uptake of iodine. However, we do not know whether polarity itself is enough for thyroid hormone synthesis or whether follicle structure is required for it. Using polarized monolayer porcine thyroid cells, cultured on collagen-coated filters, and double layered, follicle-forming cells, we analyzed the relationships of iodine metabolism and cell polarity (and follicle formation). We demonstrated that follicle structure was required for thyroid hormone synthesis. A quick-freezing and deep-etching method revealed the three-dimensional ultrastructures of cytoskeletons in the thyroid cells. On the collagen gel, the thyroid cells are reorganized into polarized monolayer cells; the basal cell membranes are in contact with the collagen gel and the apical ones face the culture medium. Actin microfilaments predominate under the apical cell membranes and intermediate filaments in the basal cytoplasm. The arrangement of these cytoskeletons determines the polarity of the cells. When the cells are cultured as double layers, follicle structures are reconstructed between the two monolayers. When apical cell membranes are in contact with other apical ones or when the cells are cultured as double layers, the cells are reorganized into follicles; the basal cell membranes are in contact with the collagen gel, and the apical ones face the follicle cavities. Actin microfilaments predominate at the apical cell membranes and intermediate filaments in the basal cytoplasm. Polarized thyroid cells transport iodine from the basal compartments to the apical ones, but cannot organify iodine into thyroid hormones. However, follicle-forming cells, cultured as double layers, take up iodine and organify it into thyroid hormones. Polarity is important for iodine uptake, and follicle structure is required for thyroid hormone synthesis.

Animals↗
PubMed1992

Ten-year follow-up of Japanese overweight subjects with impaired glucose tolerance: identification of a diabetes-prone subpopulation.

Ninety-four overweight subjects with normal glucose tolerance (NGT) or impaired glucose tolerance (IGT) were followed for 10 years. No one from the NGT group developed diabetes, however 32% of the IGT subjects did develop diabetes. Initial data of the IGT subjects who developed diabetes were significantly different from those who did not develop diabetes. Fasting, peak and/or sigma plasma glucose (PG), IRI and CPR at 180 minutes and CPR/IRI at 0 and 180 minutes were increased, and the peak time of PG was delayed; also the prevalence of a positive family history was higher, and the body weight heavier. Seventy-nine percent of IGT subjects with the initial sigma PG of greater than or equal to 40 mM or a positive family history developed diabetes whereas only 3% of those with sigma PG of less than 40 mM and a negative family history developed diabetes. Therefore, it might be considered that among the overweight adults with IGT, those with sigma PG of greater than or equal to 40 mM or a positive family history are diabetes prone and those with sigma PG of less than 40 mM and a negative family history are diabetes resistant.

Adult↗
PubMed1992

In vitro and in vivo effects of MDP-Lys(L18) on mouse megakaryocyte progenitor cells (CFU-Meg).

We investigated the in vitro and in vivo effects of MDP-Lys(L18), a derivative of muramyl dipeptide (MDP), on megakaryocyte progenitor cells (megakaryocyte colony-forming units, CFU-Meg) in the mouse bone marrow and spleen. When CFU-Meg culture was performed with a suboptimum concentration (2%) of pokeweed mitogen-stimulated mouse spleen-conditioned medium (PWM-SCM), addition of 0.1-20 micrograms/ml of MDP-Lys(L18) increased the number of megakaryocyte colonies. The size of the megakaryocyte colonies (the number of megakaryocytes per colony) was also significantly increased by the addition of MDP-Lys(L18) under the same culture conditions in comparison with cultures without MDP-Lys(L18). MDP-Lys(L18) itself did not stimulate megakaryocyte colony formation without PWM-SCM, and it failed to enhance megakaryocyte colony formation in cultures with an optimum PWM-SCM concentration (10%). Furthermore, no effect of MDP-Lys(L18) was observed in cultures of phagocytic cell-depleted bone marrow cells. However, MDP-Lys(L18) enhanced megakaryocyte colony formation in cultures of T-lymphocyte-depleted bone marrow cells. The culture supernatant from a macrophage cell line, J774.1, plus MDP-Lys(L18) enhanced in vitro megakaryocyte colony formation in cultures with a suboptimum PWM-SCM concentration. Although interleukin 1 (IL-1)beta in the culture supernatant of J774.1 plus MDP-Lys(L18) was increased in a dose-dependent manner in response to MDP-Lys(L18), the effect of the culture supernatant was not blocked by an anti-IL-1 antibody, and IL-1 beta failed to enhance megakaryocyte colony formation in the presence of suboptimum PWM-SCM levels. The enhancement of megakaryocyte colony formation by MDP-Lys(L18) could be neutralized, however, by an anti-interleukin 6 (IL-6) antibody. Intraperitoneal administration of MDP-Lys(L18) (100 micrograms daily for 3 days) significantly increased the number of bone marrow and spleen megakaryocyte colonies at 24 to 72 h after the final injection. These in vitro and in vivo observations strongly suggest that MDP-Lys(L18) indirectly enhances the proliferation and differentiation of mouse CFU-Meg via colony-stimulating factor(s) other than IL-1, probably as a result of the stimulation of macrophages to produce IL-6.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1991

Retroperitoneal neurilemoma presenting with humoral hypercalcemia associated with markedly elevated plasma prostaglandin levels.

A 72-year-old woman complaining of somnolence and thirst was diagnosed to have a hypercalcemic crisis (corrected serum calcium level, 17.4 mg/dl) associated with encephalopathy and nephropathy. Imaging diagnostic techniques demonstrated a retroperitoneal tumor at the median site of right renal pelvis. Hormonal studies revealed that plasma levels of thromboxane B2, prostaglandin (PG) E2, 6-keto prostaglandin F1 alpha (PGF1 alpha) and prostaglandin F2 alpha (PGF2 alpha) were markedly elevated. The tumor was successfully removed by operation; her serum calcium level and PG levels normalized without any treatment indicating that this case belongs to the category of humoral hypercalcemia of malignancy (HHM). Pathologically, this tumor was diagnosed to be a benign neurilemoma. Parathyroid hormone-related protein (PTHrP) radioimmunoassay and Northern blot hybridization for PTHrP mRNA were negative. The current case demonstrates that hypercalcemic crisis could be induced by a curable benign neurilemoma, and suggests that this HHM-like morbidity was associated with markedly elevated plasma PG levels.

Aged↗
PubMed1991

Interrelationship between insulin-like growth factor I-induced activation of the Na+/H(+)-antiporter and intracellular Ca(2+)-mobilization in thyroid cells.

Insulin-like growth factor I (IGF-I) increased cytoplamic pH (pHi) and cytoplasmic Ca2+ [( Ca2+]i) in cultured porcine thyroid cells. Inhibition of the Na+/H(+)-antiporter by dimethylamiloride or a reduction of external Na(+)-concentrations attenuates the increases in pHi and [Ca2+]i. The [Ca2+]i response to IGF-I is a pHi-dependent process. IGF-I activates Na+/H(+)-antiporter and alkalinizes thyroid cells. The resulting increase in pHi facilitates the [Ca2+]i response by adjusting the pHi closer to the pHi-optimum of the intracellular Ca(2+)-mobilizing system. One of the biological functions of IGF-I-induced activation of the Na+/H(+)-antiporter is to shift the pHi to an optimal value for the [Ca2+]i response.

Amiloride↗
PubMed1991

Superoxide anion hyperproduction by neutrophils in a case of myelodysplastic syndrome. Association with Sweet's syndrome and interstitial pneumonia.

The complication of Sweet's syndrome and interstitial pneumonia occurred in a patient with myelodysplastic syndrome. Superoxide anion production by the patient's neutrophils was considerably higher than that by neutrophils obtained from normal controls after stimulation with opsonized zymosan, phorbol myristate acetate, or myristic acid. Prednisone, which a potent inhibitor of superoxide anion production by neutrophils, dramatically improved the skin and pulmonary lesions, suggesting that they were parts of the same clinical spectrum associated with the superoxide anion hyperproduction.

Dermatitis↗
PubMed1991

Alloxan-induced DNA strand breaks in pancreatic islets. Evidence for H2O2 as an intermediate.

Alloxan exhibits the most potent diabetogenicity and has been used for induction of experimental diabetes mellitus. Understanding the mechanisms of action of the typical diabetogenic agent is important for elucidating the causes of diabetes. Okamoto (Okamoto, H. (1985) BioEssays 2, 15-21) proposed a model in which DNA fragmentation plays an important role for the development of diabetes. This DNA fragmentation is supposed to result from the accumulation of superoxide or hydroxyl radicals. However, direct evidence for this accumulation is lacking. Using rat pancreatic islets, we demonstrated that alloxan stimulated H2O2 generation, which induced DNA strand breaks. These findings support Okamoto's proposal that alloxan induces diabetes through the following biochemical events: alloxan----H2O2 generation----DNA strand breaks----diabetes mellitus. Perhaps this report constitutes the first demonstration of alloxan-stimulated H2O2 generation which could conceivably act as an intermediate for alloxan-induced DNA strand breaks.

Alloxan↗
PubMed1991

Gradual delay in glucose-induced first phase insulin secretion by the pancreatic islets of 7 week-, 6 month-, and 1 year-old rats.

The temporal profiles of insulin secretion by isolated pancreatic islets of male Wistar rats with various ages up to 1-year-old were studied using high glucose, potassium (K+) depolarization, and arginine as secretagogues. In the islets of 6-month-old rats, the onset and peak of glucose-induced first phase of insulin release were delayed for 1 min compared to those of 7--week-old rats. The onset and peak were further delayed for 1 min in the islets of 1-year-old rats. The onset of glucose-induced second phase of insulin secretion, and the onset and peak of K+ depolarization- and arginine-induced insulin release were not delayed in the islets of 6-month and 1-year-old rats. Glucose-stimulated increase in cytosolic free calcium ([Ca2+]i) seemed not delayed in the islets of 1-year-old rats. We conclude that the first phase of glucose-induced insulin release by the islets is selectively delayed as rat ages. It was suggested that the defect lies distal to the elevation of [Ca2+]i.

Aging↗
PubMed1991

Streptozocin- and alloxan-induced H2O2 generation and DNA fragmentation in pancreatic islets. H2O2 as mediator for DNA fragmentation.

Streptozocin (STZ) and alloxan (ALX) exhibit the most potent diabetogenicity and are used for induction of experimental diabetes mellitus. An understanding of the mechanisms of action of the typical diabetogenic agents is important for elucidating the causes of diabetes. Okamoto proposed a model in which DNA fragmentation plays an important role in the development of diabetes. DNA fragmentation supposedly results from the accumulation of superoxide or hydroxyl radicals. However, direct evidence for this accumulation is lacking. With isolated rat pancreatic islets in vitro, we demonstrated that STZ and ALX stimulated H2O2 generation and caused DNA fragmentation. Addition of STZ or ALX resulted in an increase in H2O2 generation. On DNA analysis, when incubated without STZ or ALX, DNA sedimented as a single peak; when incubated with STZ or ALX, DNA sedimented slower as a broad peak and was fragmented. Graded doses of STZ and ALX stimulated H2O2 generation and induced DNA fragmentation; their effects on H2O2 generation and DNA fragmentation were evident at a concentration of 0.1 mM and were maximal at 1 mM. Administration of STX or ALX to rats in vivo stimulated H2O2 generation and caused DNA fragmentation in pancreatic islets. H2O2 itself also induced DNA fragmentation. These findings may support Okamoto's proposal that STZ and ALX induce diabetes through the following biochemical events: STZ and ALX----H2O2 generation----DNA fragmentation----beta-cell destruction. This study may constitute the first demonstration of STZ- and ALX-stimulated H2O2 generation, which probably acts as a mediator of STZ- and ALX-induced DNA fragmentation.

Alloxan↗
PubMed1991

In vitro and in vivo antibacterial activities of ME1220 and ME1221, novel cephalosporins.

The antibacterial activities and serum pharmacokinetic properties of ME1220 and ME1221, new aminothiazolylalkoxyiminoacetylcephalosporins having an N-alkylpyridiniumthiomethyl side chain at C-3, were compared with those of cefpirome and ceftazidime. ME1220 and ME1221 exhibited broad antibacterial activity against Gram-positive and Gram-negative bacteria. The in vitro and in vivo activities of ME1220 were similar to cefpirome, while ME1221 was superior to ceftazidime against almost all test organisms except pseudomonas. On intravenous injection in rats, ME1220 and ME1221 were excreted mainly in the urine. ME1221 was excreted moderately in the bile and showed higher serum concentration and AUC than those of ME1220.

Animals↗
PubMed1990

Test for recovery from hypothyroidism during thyroxine therapy in Hashimoto's thyroiditis.

Hypothyroid patients with Hashimoto's thyroiditis usually receive lifelong thyroxine therapy. Some are known to recover thyroid function, but identification of these patients during continued thyroxine therapy has been impossible. 92 patients with hypothyroidism after Hashimoto's thyroiditis and 70 normal controls were studied. All controls but not patient before thyroxine was started had a normal thyroid response to thyroid stimulating hormone (TSH), circulating concentrations of which were increased by administration of 500 micrograms thyrotropin releasing hormone (TRH). During treatment with thyroxine, 22 patients recovered thyroid responsiveness to TSH, and when treatment was stopped these patients have remained euthyroid for 1-8 years, whereas all 70 who did not recover thyroid TSH responsiveness became hypothyroid within 3 months. Over 20% of patients with hypothyroidism after Hashimoto's thyroiditis may recover satisfactory thyroid function, and can be identified during thyroxine treatment by their thyroid response to TSH in a TRH test.

Adolescent↗
PubMed1990

Graves' disease following hypothyroidism due to Hashimoto's disease: studies of eight cases.

Hashimoto's and Graves' diseases represent the main two types of autoimmune thyroid disease. The combination of these two is well known. However, occurrence of Graves' disease after primary hypothyroidism is rare. We report seven patients with hypothyroidism due to Hashimoto's disease, who developed Graves' disease with hyperthyroidism. We also report one patient with hypothyroidism due to Hashimoto's disease, who continued to be hypothyroid even in the presence of TSAb (thyroid stimulating antibody). These patients were divided into three groups according to the changes in thyroid function and clinical course: (1) transient hyperthyroidism due to Graves' disease following hypothyroidism; (2) persistent hyperthyroidism due to Graves' disease following hypothyroidism; and (3) persistent hypothyroidism with positive TSAb. Such changes in thyroid function and clinical course seem to be decided by three factors: (1) TSAb and (2) TSBAb (thyroid stimulation blocking antibody) activities in the blood and (3) the responsiveness of the thyroid gland to TSAb. Seven patients had hyperthyroidism, when they had TSAb, which stimulated the thyroid gland; one of these seven patients had TSBAb during the hypothyroid state and TSAb during the hyperthyroid state, indicating that the alterations in the thyroid state related to the balance between the activities of TSAB and TSBAb. Another patient continued to be hypothyroid despite the presence of TSAb; his thyroid gland was not palpable and could not respond to TSAb.

Adult↗
PubMed1979

Re-evaluation of a possible high incidence of hypertension in hypothyroid patients.

In an attempt to re-evaluate a possible high incidence of hypertension in hypothyroid patients, blood pressure was measured in 38 slightly hypothyroid patients, in 17 moderate hypothyroid patients, and in 26 severe hypothyroid patients. The data were then compared with the findings in 73 known euthyroid subjects and in 1,601 possibly euthyroid subjects. Blood pressure and incidence of hypertension increased progressively with age in known euthyroid subjects and in possibly euthyroid subjects. Similarly, blood pressure increased progressively with age in slight and moderate hypothyroid patients, but the incidence of hypertension was high in the sixth decade in slightly hypothyroid patients for some unknown reason. In contrast, blood pressure and the incidence of hypertension were low in the fifth and sixth decades in severe hypothyroid patients. This low blood pressure was elevated slightly when Sv1 + Rv5 and C/T were shifted toward normal by T4 treatment for 3 to 4 months. It is suggested that the hypothyroid state does not accelerate the development of hypertension.

Adult↗