Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of altered thyroid function on serum fructosamine concentrations was investigated in 31 untreated hyperthyroid patients, 18 short-term hypothyroid patients (i.e., 20 days after withdrawal of thyroid hormone suppressive therapy for thyroid cancer), 7 untreated long-term hypothyroid patients, and 25 age-matched normal controls. No differences in serum fructosamine concentrations were observed between hyperthyroid patients and normal controls; conversely, serum fructosamine concentrations were significantly higher both in short-term and in long-term hypothyroid patients than those found in normal controls. Furthermore, long-term hypothyroid patients showed significantly higher serum fructosamine concentrations than short-term hypothyroid patients. L-Thyroxine (L-T4), replacement therapy in two hypothyroid patients, resulted in a marked decrease in serum fructosamine concentrations. In seven hyperthyroid patients, the restoration of euthyroidism with antithyroid drug therapy was associated with no significant changes in serum fructosamine concentrations. The results of the present study indicate that hypothyroidism is associated with a marked increase in serum fructosamine concentrations. This alteration does not appear to be the consequence of gross abnormalities in plasma protein or glucose metabolism. The duration of hypothyroidism seems to be an important factor, even though the mechanism underlying this alteration remains at present unexplained. These results also suggest that caution must be used in the interpretation of elevated serum fructosamine concentrations as an index of the metabolic control of diabetes mellitus in the presence of hypothyroidism.
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PMID:The effect of altered thyroid function on serum fructosamine concentrations. 245 10

Since the approval of lithium use in treatment of acute mania, there have been numerous clinical trials of lithium in medical and psychiatric disorders. This paper gives a brief review of the literature on lithium trials in approximately fourteen medical conditions. These are: hyperthyroidism, metabolizing thyroid cancer, syndrome of inappropriate secretion of antidiuretic hormone, premenstrual tension syndrome, anorexia nervosa, Felty's syndrome, chemotherapy-induced neutropenia, aplastic anemia, seborrheic dermatitis, eczematoid dermatitis, cyclic vomiting, diabetes mellitus and asthma. Most of the case reports cited showed the efficacy of the side effects from lithium salt in the management of the symptoms and signs of these disorders, however, well-designed and controlled studies give negative results. The positive results are reported in the group of disorders having an underlying subdromal affective syndrome such as premenstrual tension syndrome and anorexia nervosa. Other encouraging reports include the effect of lithium to induce leucocytosis in Felty's syndrome and chemotherapy-induced neutropenia.
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PMID:A review of clinical trials of lithium in medicine. 639 35

Patients with diffusely increased uptake in both kidneys (often referred to as "host kidneys") on Tc-99m-MDP bone imaging were evaluated. Among 2056 patients reviewed, this finding was seen in 13 patients (0.63%): four with liver cirrhosis, two with lung cancer, one each with primary hepatoma, Hodgkin's disease, malignant lymphoma, thyroid cancer, leukemia, sideroblastic anemia and diabetes mellitus. Renal vascular disease and iron overload are considered to be the major causes of this finding.
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PMID:Diffusely increased Tc-99m-MDP uptake in both kidneys. 645 33

Thyroid cancer patients are treated with up to 9.9 GBq of 131I to ablate remnant thyroid tissue and/or any functioning metastases that may be present. Radioiodine therapy is repeated as often as required. However, only a small fraction of the 131I is taken up by remnant thyroid and metastases, the remainder being eliminated by the kidneys, which are therefore subject to irradiation. External radiation therapy to the kidneys is known to lead to nephritis and albuminuria. The study included 113 patients treated with one to four doses of 131I (1.1-9.9 GBq each dose) and followed up 1 month to more than 8 years later. Spot samples of urine were collected and microalbuminuria measured by in-house radioimmunoassay. Twelve patients had elevated levels (normal range up to 34 micrograms ml-1), but their clinical history revealed such predisposing factors as diabetes and/or hypertension and proteinuria before therapy commenced. The remaining patients had normoalbuminuria. Grouping the patients based on the total dose of 131I administered resulted in a median microalbuminuria of 2.4-12.9 micrograms ml-1. Hence, this study showed that the dose of 131I normally used in treating thyroid cancer does not increase microalbuminuria to any significant extent.
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PMID:Screening for microalbuminuria by RIA in 131I-treated thyroid cancer patients. 882 54

Retinoic acids (RAs), well characterized regulators of proliferation and differentiation, partly re-differentiate follicular thyroid carcinoma cell lines (FTC-133, FTC-238, and HTC-TSHr) as well as SV40-transfected immortalized thyroid cell lines (ori3 and 7751). This is indicated by the stimulation of type I 5'-deiodinase and other differentiation markers. As demonstrated by RT-PCR, electrophoretic mobility shift, and [3H]-retinoic acid binding assays, thyroid carcinoma cell lines express RA receptor mRNAs and functional ligand- and DNA-binding receptor proteins able to mediate RA-dependent signal transduction. Together, these properties make these thyroid-derived cell lines useful in vitro models for studying the effects of an RA re-differentiation therapy of thyroid cancer.
Exp Clin Endocrinol Diabetes 1996
PMID:Effects of retinoids and role of retinoic acid receptors in human thyroid carcinomas and cell lines derived therefrom. 898 Sep 93

Invasion and metastasis are the primary cause of death in patients with follicular thyroid cancer (FTC). The thyroid is a micro-economic system in which proliferation and differentiation was supposed to be under the major control of only a single hormone (thyroid stimulating hormone-TSH). It has shown, however, that a complex network of various growth factors regulates growth and invasion of thyroid cancer cells. A growing literature has established the close association between malignant tumor progression and growth regulatory aberrations in cancer cells. Most of these studies have focused on the phenomenon, that advanced and more aggressive tumors or metastases lost the sensitivity to growth inhibitors, such as transforming growth factor beta. These findings highlight two aberrations of growth regulation which may favour progression of malignant disease and acquisition of metastatic competence: (1) Resistance to growth factor inhibitors and (2) growth autonomy of metastatic follicular thyroid cancer cells.
Exp Clin Endocrinol Diabetes 1996
PMID:The regulation of proliferation and invasion in differentiated thyroid cancer by growth factors. 898 Sep 96

Oncogene amplification is frequent in many epithelial tumors and often associated with advanced tumor progression. In different epithelial neoplasias it helps to provide prognostic information on individual patients. The present study was performed to evaluate the hitherto unknown prevalence of INT-2 gene amplification and its potential usefulness as prognostic marker in patients with human thyroid cancer. We used differential quantitative polymerase chain reaction and fluorescent DNA technique as a reliable method to detect low copy-number amplification of oncogenes from archival carcinoma specimens. Sequences from the int-2 gene and the single copy gamma-interferon gene were amplified simultaneously by PCR and quantified on a fluorescence activated sequencer. Native tumor tissue from 63 patients with differentiated thyroid cancer (43 papillary, 3 oncocytary, and 17 follicular) and from 12 goiters was analyzed by differential quantitative polymerase chain reaction. The study group contained many far advanced tumors. 40% of tumors were recurrent, 35% were staged T4 tumors and 70% presented with lymph node metastases. The prevalence of INT-2 amplification was 12% for follicular and 7% for papillary carcinomas. In goiter tissue no amplification was found. Amplification was only 2-4fold in positive cases. Low grade amplification is of no apparent importance in differentiated thyroid cancer.
Exp Clin Endocrinol Diabetes 1996
PMID:INT-2 gene amplification in differentiated human thyroid cancer. 898 Oct 13

Thyroid cancer is a rare disease in childhood and adolescence. However, it represents the most frequent cancer type in this age group. Thyroid cancer amounts about 0.5%-1.5% of all malignancies in children and adolescents. In Germany 10-30 cases could be expected in a year. The most common histologic type for this age group is the differentiated thyroid cancer (DTC), i.e. the papillary and follicular subtypes (90%). In 10% of patients medullary thyroid cancer (MTC) will be diagnosed. DTC occur more often in girls than in boys (female/male-ratio 2:1), with a median age of about 12-13 years (yrs). An important aetiological factor of DTC is a former exposition to different kinds of radiation. In childhood and adolescence MTC mostly appears in patients suffering from the syndrome MEN-2, whereas the sporadic form is rare. As in DTC, more girls than boys can be diagnosed for MTC (female/male-ratio 2-3:1), with a median age about 10 yrs. The anaplastic/undifferentiated subtype occurs extremely rare. For all types of thyroid cancer the most important therapeutic approach is the surgical intervention. In most cases of DTC an optimal disease control could be achieved by radioiodine therapy. Prognosis of DTC in children and adolescents is favourable. However, therapeutic strategies and modalities reported in the literature are very different. In contrast, prognosis of MTC is rather poor, that of the anaplastic type is infaust. No other effective therapy option than surgery is available. To evaluate the therapeutic efficacy of a combined modality therapy by both radiotherapy and cytostatic drugs in children and adolescents with poor prognosis types of thyroid cancer, an interdisciplinary multicenter therapy study will now be started in Germany.
Exp Clin Endocrinol Diabetes 1997
PMID:Epidemiology and therapy of thyroid cancer in childhood and adolescence. 943 21

The recently cloned sodium-iodide symporter (NIS) represents a key molecule for thyroid function by efficiently accumulating iodide from the circulation into the thyrocyte against an electrochemical gradient. This uptake requires energy, is coupled to the action of Na+/K+-ATPase, and stimulated by TSH, the main hormone regulating thyroid-specific functions. NIS mutations are found in congenital hypothyroidism, and potential defects in the NIS gene, its expression, or function of the NIS protein are currently under investigation in various thyroid diseases. Increased NIS expression has been found in autonomous adenoma and Graves' disease, decreased levels of NIS protein and/or mRNA were observed in Hashimoto's disease, cold nodules, most thyroid cancers and cell lines derived therefrom. Autoantibodies directed against NIS have been identified in autoimmune thyroid disease and blocking antibodies isolated from sera of patients with Hashimoto's disease inhibit NIS function in NIS-transfected CHO cells. NIS mRNA expression can be up-regulated by retinoic acid in human thyroid carcinoma cell lines whereas retinoic acid treatment decreases NIS expression and function in differentiated rat thyroid FRTL-5 cells. Apart from thyrocytes, NIS is also expressed in other tissues known to transiently accumulate radioiodide, albeit at much lower levels, requiring RT-PCR for detection of the transcript. Diagnostic and therapeutic implications of the recent cloning of the human NIS gene such as development of NIS-directed drugs, ligands, antibodies, vaccines, gene therapeutic approaches combining NIS targeting and expression together with the long-established, efficient and safe method of radioiodide therapy are discussed both for application to thyroid related diseases and carcinoma, and non-thyroid benign and malignant diseases. Apart from these therapeutic and diagnostic perspectives the availability of the NIS gene will also open new opportunities to develop sensitive and homologous diagnostic test systems to identify factors involved in autoimmune thyroid disease, evolution of goitre, adenoma and thyroid cancer as well as NIS-directed new drugs. Advanced and sophisticated molecular diagnostic approaches (RT-PCR from fine needle aspirations, screening for mutations, analysis of gene defects) are already developed for NIS and will complement or overcome some established procedures in thyroid diagnostics.
Exp Clin Endocrinol Diabetes 1998
PMID:Implications of the molecular characterization of the sodium-iodide symporter (NIS). 986 44

The role of enhanced thyroid-stimulating hormone (TSH) secretion, in the aetiology of thyroid cancer is not totally consistent. Circumstances and conditions which cause (e.g., iodine deficiency, through suboptimal intake in water and food) or indicate (e.g., goitre) increased TSH secretion have been associated to increased risk of thyroid cancer, most notably follicular and anaplastic carcinomas. Elevated incidence and mortality rates of thyroid cancer, however, are also found in areas were iodine intake is high (Hawaii, Iceland). At least in some countries (Switzerland), a favourable impact of the introduction of iodized salt on mortality from thyroid cancer has been reported. Elsewhere, the correction of iodine deficiency has coincided with elevations of diagnostic standards (e.g., spread of thyroid scintigraphy, ultrasound, and fine-needle biopsy) and corresponding increases in incidence of papillary carcinomas, often clinically silent, thus hampering a distinction of the two phenomena. Upward trends of papillary carcinoma incidence have, however, been seen in most affluent countries, irrespective of the iodine status of the population.
Exp Clin Endocrinol Diabetes 1998
PMID:Iodine intake and thyroid carcinoma--a potential risk factor. 986 53


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