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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine variations of serum creatinine level immediately after percutaneous angioplasty for renal artery stenosis. After technical success of unilateral or bilateral percutaneous angioplasty for renal artery stenosis in 91 patients (mean age 62.7 years) in whom ioxaglate was always used (90 to 300 ml, mean 195), serum creatinine levels immediately before and 48 hours after dilatation were compared. In the whole population, no significant variation was observed in the overall population. No significant difference was observed between unilateral and bilateral renal angioplasty. The volume of contrast media did not influence creatinine level, nor did iodine injection performed during (n = 4) or more than 3 days before angioplasty. A significant difference was observed with or without diabetes mellitus (n = 15, p = 0.05). In patients without diabetes mellitus technically successful percutaneous angioplasty for renal artery stenosis when using ioxaglate do not significant alter serum creatinine level 48 hours later.
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PMID:[Evolution of serum creatinine level 48 hours after angioplasty for renal artery stenosis in 91 patients]. 876 47

We report here a rare case of 47 XXY/46 XY mosaic Klinefelter's syndrome associated with multiple endocrine disorders. A 35-year-old male admitted for the evaluation of renal dysfunction and recurrent bone fractures was diagnosed as having Klinefelter's syndrome by endocrinological examinations and sex chromosome analysis. He has suffered from diabetes mellitus for more than ten years. The serum FSH and LH levels were high together with low free testosterone and estradiol levels. There was a discrepancy between basal serum GH and somatomedin-C levels. On admission, thyroid function revealed thyrotoxicosis with low radioactive iodine uptake and negative thyroid autoantibodies. During hospitalization, serum FT3 and FT4 levels were gradually decreased and serum TSH levels became elevated, leading to the diagnosis of subacute thyroiditis. Serum ACTH levels showed high basal levels with delayed, exaggerated responses to insulin-induced hypoglycemia. Rapid ACTH test (1-24ACTH 0.25 mg) showed low cortisol responses and many of the adrenocortical steroids in plasma and urine were low or low normal. Furthermore, bone mineral density (BMD) by DEXA showed marked osteoporosis. Possible mechanisms underlying these varied endocrine disorders remain to be elucidated.
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PMID:47 XXY/46 XY mosaic Klinefelter's syndrome presenting with multiple endocrine abnormalities. 879 55

In 1992 we performed a prospective study with 300 patients after thyroid resection. Indication for the operation was a benign nodular goiter in 280 cases, Graves' disease in 11 cases and a differentiated thyroid carcinoma in 9 cases. 269 patients (89.6%) returned for a follow-up visit which contained an ultrasound of the thyroid region and a determination of the serum thyrotropin concentration. Patients with less than 10 ml had a thyroxine replacement of 100 yg daily for six months. This therapy was discontinued for the next three months and they received their follow-up nine months after the operation. All other patients with benign diseases had their follow-up without thyroxine replacement eight weeks after the operation. The mean remnant volume was 2.4 ml for selective resected lobes, 0.8 ml after near total resection and 0.2 ml after lobectomy. We found residual or recurrent nodular tissue in 7.2% of the partially resected lobes. Visualization of the recurrent nerve and ligation of the inferior thyroid artery reduced the risk of nodular tissue in the remnant thyroid tissue significantly. Only 153 patients (62%) were treated according to our postoperative treatment schedule. Thyroxine replacement therapy was given to 96 patients at the time of their follow-up. 34% of the patients without replacement therapy had signs of insufficient hormone production of the remnant thyroid tissue. However, 22% of the patients under thyroxine replacement therapy showed signs of iatrogenic subclinical hyperthyroidism. We found a significant correlation between the volume of the remnant tissue and the serum thyrotropin concentration in patients without continuous thyroxine replacement. The corresponding calculated volume for a functionally potent remnant thyroid volume was 7.3 ml. This value was significantly higher in patients with both inferior thyroid arteries ligated at 9.8 ml. An individual postoperative therapy with iodine and/or thyroxine, which results in neither a high rate of thyrotropin elevation nor an unnescessary and undesirable part of the patients with suppressed serum thyrotropin concentrations is an indispensable component of the surgical treatment of benign nodular thyroid disease in areas of endemic iodine deficiency. As a result of this study we changed our postoperative treatment schedule. Patients with less than 10 ml remnant thyroid volume will have a continuous replacement therapy with a reduced dose of 75 yg thyroxine daily.
Exp Clin Endocrinol Diabetes 1996
PMID:Thyroid morphology and function after surgical treatment of thyroid diseases. 881 46

Abnormalities in postthymic T cell development in the BB/W rat model of autoimmune insulin-dependent diabetes mellitus (IDDM) result in part from a lymphopenia (lyp) gene defect. To better characterize these abnormalities, the phenotypes of T cells from diabetes-prone (DP) and diabetes-resistant (DR) coisogenic rats were analyzed by multiparameter flow immunocytometry (FCM). Marked decreases in the numbers of Thy1- RT6+ T cells, most of which are CD8+, were documented in DP rats by live-gating. Conversely, an approximately 3-fold increase was observed in the percentage of Thy1+ RT6- T cells, which normally serve as the precursors of both Thy1- RT6+ and Thy1- RT6- T cell subsets in rats. These results suggested that, at a minimum, an arrest in maturation of the Thy1+ precursors of RT6+ T cells occurs postthymically in DP rats. To determine more precisely the stage(s) in T cell development at which lymphopenia occurs, the export and fate of recent thymic emigrants (RTE's) and their immediate descendants in DP rats was traced after intrathymic (i.t.) labelling with fluorescein isothiocyanate (FITC). The results showed that in DP, as compared with DR, rats: 1) 5-fold fewer RTE's are exported from the thymus per 24 hr; 2) more than 80% of the RTE's are CD4+; 3) most of the immediate descendants of RTE's disappear from the peripheral lymphoid tissues within one week after export from the thymus; and 4) few of the descendants of the RTE's that do survive differentiate into RT6+ T cells. Staining with propidium iodide revealed that a significantly higher proportion of Thy1+ T cells in DP than in DR rats are in cycle (S/G2/M), thereby accounting for their disproportionately high numbers relative to RTE's. These results indicate that, in addition to defective thymic export, most of the immediate descendants of RTE's in DP rats undergo non-productive proliferation and death at the time (3-7 days postthymic) at which their counterparts in DR rats differentiate into Thy1- RT6+ T cells. The resulting deficiency of immunoregulatory T cells, acting in concert with defective intrathymic selection of effector T cell precursors, appears to conspire to markedly enhance the predisposition of DP rats to autoimmunity.
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PMID:Abnormalities in the export and fate of recent thymic emigrants in diabetes-prone BB/W rats. 893 86

Excess iodine ingestion has been implicated in induction and exacerbation of autoimmune thyroiditis in human populations and animal models. We studied the time course and sex-related differences in iodine-induced autoimmune thyroiditis in NOD-H-2h4 mice. This strain, derived from a cross of NOD with B10.A(4R), spontaneously develops autoimmune thyroiditis but not diabetes. NOD-H-2h4 mice were given either plain water or water with 0.05% iodine for 8 weeks. Approximately 54% of female and 70% of male iodine-treated mice developed thyroid lesions, whereas only 1 of 20 control animals had thyroiditis at this time. Levels of serum thyroxin (T4) were similar in the treatment and control groups. Thyroglobulin-specific antibodies were present in the iodine-treated group after 8 weeks of treatment but antibodies to thyroid peroxidase were not apparent in the serum of any of the animals. Levels of thyroglobulin antibodies increased throughout the 8-week iodine ingestion period; however, no correlation was seen between the levels of total thyroglobulin antibodies and the degree of thyroid infiltration at the time of autopsy. The thyroglobulin antibodies consisted primarily of IgG2a, IgG2b, and IgM antibodies with no detectable IgA, IgG1, or IgG3 thyroglobulin-specific antibodies. The presence of IgG2b thyroglobulin-specific antibodies correlated well with the presence of thyroid lesions.
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PMID:Iodine-induced autoimmune thyroiditis in NOD-H-2h4 mice. 893 7

Interleukin-1 beta has been implicated as a pathogenic factor in the development of autoimmune thyroiditis. When given for 5 days to normal non-diabetes-prone Wistar Kyoto rats, it decreased plasma concentrations of total tri-iodothyronine and thyroxine and increased plasma TSH. These effects were not prevented by co-injection of nitroarginine methyl ester or aminoguanidine, inhibitors of NO synthases. Exposure to interleukin-1 beta dose-dependently reduced iodine uptake in FRTL-5 cells, but had no effect on thyroglobulin secretion. Nitrite was not detected in the FRTL-5 cell culture media after exposure to interleukin-1 beta. However, reverse transcription PCR analysis of mRNA isolated from interleukin-1 beta-exposed FRTL-5 cells revealed a transitory expression of the inducible NO synthase, which was markedly lower than inducible NO synthase induction in interleukin-1 beta-exposed isolated rat islets of Langerhans. Co-incubation with the NO synthase inhibitor NG-monomethylarginine did not ameliorate the effect of interleukin-1 beta on FRTL-5 cell iodine uptake. Furthermore, we demonstrate that daily injections of interleukin-1 beta for 13 weeks aggravated spontaneous thyroiditis and induced severe hypothyroidism in non-diabetic diabetes-prone BB rats. The data suggest that NO does not mediate interleukin-1 beta-induced inhibition of rat thyroid function in vivo or in vitro in FRTL-5 cells, and the induction of hypothyroidism by interleukin-1 beta in diabetes-prone BB rats is speculated to be due to exacerbation of recruitment and activation of intrathyroidal mononuclear cells.
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PMID:Interleukin-1 beta inhibits rat thyroid cell function in vivo and in vitro by an NO-independent mechanism and induces hypothyroidism and accelerated thyroiditis in diabetes-prone BB rats. 894 79

In order to investigate the effect of iodized oil administration on the thyroid status of male hypothyroid children and adolescents residing in an area of iodine deficiency, 32 apparently normal school boys with increased serum TSH, aged 7 to 15 years, were given a single intramuscular injection of 480 mg iodized oil. Four months after injection, serum T4 increased from 60 +/- 23 to 118 +/- 24 nmol/l and serum TSH decreased from 39 +/- 33 to 2.5 +/- 1.2 mU/l. Serum T4 remained unchanged while a further decline in TSH to 1.3 +/- 0.9 and 1.4 +/- 1.3 mU/l was observed 7 and 12 months after injection, respectively. There was a small but significant reduction in serum T3, FT3I as well as in the prevalence and severity of goiter 1 year following iodine treatment. Neither the age of the subject nor the severity of hypothyroidism affected the thyroid response to iodine treatment. It is concluded that iodized oil injection is an effective and convenient treatment for goitrous hypothyroid youngsters in iodine deficient areas.
Exp Clin Endocrinol Diabetes 1996
PMID:Treatment of goitrous hypothyroidism with iodized oil supplementation in an area of iodine deficiency. 895 74

Within the last decades multiple iodolipid-classes have been identified in thyroid tissue. For a long time they have been supposed to be involved in thyroid autoregulation, but for the time being no specific compounds could be isolated. A new approach was stimulated by the finding that thyroid cells were able to iodinate polyunsaturated fatty acids to form iodolactones and by the identification of alpha-iodohexadecanal (alpha-IHDA) as the major compound of an iodolipid fraction. alpha-IHDA exerts multiple inhibitory effects on adenylate cyclase, NADPH-oxidase and thyroid peroxidase. Therefore, it is speculated as a mediator of the Wolff-Chaikoff-effekt and to be involved in the autoregulation of specific thyroid functions mediated by the cyclic adenosine-3',5'-monophosphate (cAMP)-pathway. Meanwhile 6-iodo-5-hydroxy-8,11,14-eicosatrienoic acid delta-lactone (delta-iodolactone) has been identified in human thyroid tissue and it could be demonstrated that this iodoeicosanoid specifically inhibits signal transduction pathways induced by local growth factors such as epidermal growth factor (EGF) and basic fibroblast growth factor (bFGF). Therefore, delta-iodol-actones seem to act as mediators of iodine, especially in the autoregulation of cAMP-independent thyroid cell proliferation. We will summarize these important new findings and discuss the role of these iodolipids on thyroid cell growth regulation.
Exp Clin Endocrinol Diabetes 1996
PMID:Iodolactones and iodoaldehydes--mediators of iodine in thyroid autoregulation. 898 Oct

The present study was initiated to characterize thyrotropin receptor (TSH-R) expression in thyroids from patients with Graves' disease, as well as parameters that influence TSH-R expression either causally, such as interferon-gamma (IFN-gamma), the leading candidate among the cytokines thought to play a key role in the initiation of autoimmune thyroid disease, or therapeutically, such as iodide, which is used to prepare patients for surgery. Our data show that there is an average 4-fold increase of TSH-R mRNA levels in the thyroids of Graves' patients coming to surgery, which is paralleled by an increase in TSH-R protein levels and TSH binding capacity. The increase does not appear to be related to IFN-gamma since IFN-gamma transcripts are barely detectable in most Graves' patients. Iodide treatment causes a 2-fold decrease in TSH-R expression in association with significant decreases in major histocompatibility complex (MHC) class I and class II gene expression. These last data are compatible with a recently enunciated "transcription factor hypothesis" according to which abnormally high TSH-R and MHC class I and class II gene expression in Graves' thyroids are the result of a loss of the normal negative regulation of these genes necessary to allow the normal growth and function of the gland, yet preserve self-tolerance.
Exp Clin Endocrinol Diabetes 1996
PMID:Iodide, cytokines and TSH-receptor expression in Graves' disease. 898 Oct 6

While congenital hypothyroidism in 80-90% of the affected individuals is caused by thyroid dysgenesis (athyrosis, ectopy or hypoplasia), hypothyroidism in patients with a thyroid gland of normal position and size can be due to regulatory or enzymatic defects of thyroid hormone biosynthesis. Beside defects of thyroglobulinsynthesis, defects of the sodium-iodide-transporter or the TSH-receptor, a defect of the thyroidperoxidase, the key-enzyme of thyroid hormone biosynthesis, can cause a total iodide organification defect and thereby congenital hypothyroidism. We screened 14 of 103 patients (13.6%) with non familial congenital hypothyroidism and a normally developed thyroid gland detected by the newborn screening program with the PCR-SSCP (single-stranded-conformational-polymorphism) technique for mutations in the exons 2, 8, 9, 10 and 14 of the human thyroperoxidase gene, and in which mutations had been described previously in Dutch and Brazilian families with total organification defects. Most of the previously reported mutations were found in exons 8, 9 and 10 which code for the caralytic part of the enzyme. In two patients a GGCC-duplication in exon 8 was detected leading to a premature stop codon in exon 9. While one patient without neonatal goiter was homozygous for this mutation, the second patient was only heterozygous thus demanding another mutation on the second TPO-allel to explain the phenotype. Since the GGCC duplication is easily demonstrable by a NaeI digestion, because it creates a restriction site for this enzyme, screening for this mutation is indicated since it is easy to perform. In contrast to the perchlorate discharge test molecular genetic studies are less invasive, but as useful in making a definitive diagnosis in the individual patient. Furthermore it is the first feasible step to study the etiology and epidemiology of the so far only putative defects of thyroid hormone biosynthesis leading to congenital hypothyroidism.
Exp Clin Endocrinol Diabetes 1996
PMID:Screening for mutations of the human thyroid peroxidase gene in patients with congenital hypothyroidism. 898 Oct 18


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