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

The aim of the study was to answer the questions: 1) does the prolactin secretion in the TRH test (0.4 mg i.v.) differ in haemodialyzed patients with diabetes nephropathy in the end stage renal failure in comparison to haemodialyzed chronic renal failure patients with non-diabetic nephropathy and healthy subjects; 2) does the opiate receptors blockade with naloxone (2 mg i.v.) modify the prolactin secretion during the TRH test in those patients. 39 subjects were studied. The patients were divided into three groups: group I: 12 haemodialyzed patients with IDDM and diabetic nephropathy in the end stage renal failure, group II: 15 haemodialyzed chronic renal patients with non-diabetic nephropathy and the control group: 12 healthy persons. The basic prolactin secretion and area over basic value (AOBV) of the prolactin were estimated. Prolactin concentration was measured by LIA. 1) The basic prolactin secretion was significantly higher in the patients with chronic renal failure. 2) The basic prolactin secretion in IDDM patients with diabetic nephropathy in the end stage renal failure treated with haemodialysis was significantly lower than in haemodialyzed patients with chronic renal failure of non-diabetic etiology. 3) TRH and TRH with naloxone caused significant increase of prolactin secretion in all investigated groups, but the increase is significantly lower in chronic renal failure patients than in healthy subjects. 4) Naloxone decreases significantly the prolactin secretion during TRH test only in haemodialyzed patients with chronic renal failure of non-diabetic etiology.
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PMID:[Effects of opiate receptor blockade with naloxone on prolactin (PRL) secretion in patients with diabetes type I (IDDM) with chronic renal failure treated with hemodialysis (HD)]. 912 1

We investigated the effects of diabetes mellitus on the hypothalamo-hypophysial-thyroid axis in male (R x U) F1 and R-Amsterdam rats, which were found to respond to streptozotocin (STZ)-induced diabetes mellitus with no or marked increases, respectively, in plasma corticosterone. Males received STZ (65 mg/kg i.v.) or vehicle, and were killed 1, 2 or 3 weeks later. At all times studied, STZ-induced diabetes mellitus resulted in reduced plasma TSH, thyroxine (T4) and 3,5,3'-tri-iodothyronine (T3). Since the dialyzable T4 fraction increased after STZ, probably as a result of decreased T4-binding prealbumin, plasma free T4 was not altered during diabetes. In contrast, both free T3 and its dialyzable fraction decreased during diabetes, which was associated with an increase in T4-binding globulin. Hepatic activity of type I deiodinase decreased and T4 UDP-glucuronyltransferase increased after STZ treatment. Thus, the lowered plasma T3 during diabetes may be due to decreased hepatic T4 to T3 conversion. Median eminence content of TRH increased after STZ, suggesting that hypothalamic TRH release is reduced during diabetes and that this is not caused by impaired synthesis or axonal transport of TRH to the median eminence. Hypothalamic proTRH mRNA did not change in diabetic (R x U) F1 rats during the period of observation, but was lower in R-Amsterdam rats 3 weeks after STZ. Similarly, pituitary TSH and TSH beta mRNA had decreased in R-Amsterdam rats by 1 week after STZ treatment, but did not change in (R x U) F1 rats. The difference between the responses in diabetic R-Amsterdam and (R x U) F1 rats may be explained on the basis of plasma corticosterone levels which increased in R-Amsterdam rats only. Hypothalamic TRH content was not affected by diabetes mellitus, but the hypothalami of diabetic rats released less TRH in vitro than those of control rats. Moreover, insulin had a positive effect on TRH release in vitro. In conclusion, the reduced hypothalamic TRH release during diabetes is probably not caused by decreases in TRH synthesis or transport to the median eminence, but seems to be due to impaired TRH release from the median eminence which may be related to the lack of insulin. Inhibition of proTRH and TSH beta gene expression in diabetic R-Amsterdam rats is not a primary event but appears to be secondary to enhanced adrenal activity in these animals during diabetes.
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PMID:Possible role of corticosterone in the down-regulation of the hypothalamo-hypophysial-thyroid axis in streptozotocin-induced diabetes mellitus in rats. 916 15

The case history of a 54-year-old male suffering from pituitary macroadenoma with suprasellar extension is reported. A TRH-test with 200 micrograms i.v. was followed by severe headache and vomiting after 60', and by development of ophthalmoplegia on the following day. Hyperdens patches on the CT scan showed haemorrhage into the tumor. A chromophobic adenoma with macroscopic and histological signs of haemorrhage was removed via the transsphenoidal route. In the postoperative period the ophthalmoplegia gradually disappeared but central hypoadrenia and hypothyroidism occurred. This is the second case in the literature showing that TRH alone and in a low dose may cause pituitary tumor apoplexy. It is concluded that TRH-testing is a risk for the patient with pituitary apoplexy. If, due to the size of the tumor the patients have to be operated on in any case, and the test is not of essential diagnostic value, the TRH-test should be done only in selected cases. Its use in the postoperative evaluation however is without risk for the patients.
Exp Clin Endocrinol Diabetes 1997
PMID:Apoplexy of a pituitary macroadenoma as a severe complication of preoperative thyrotropin-releasing hormone (TRH) testing. 928 12

We report a rare case of Cushing's syndrome due to bilateral adrenocortical adenomas in a 45-year-old female. She suffered from diabetes mellitus and hypertension for a decade, but her appearance was not Cushingoid. The plasma cortisol level in the morning was at the upper limit of the normal range, but did not show a diurnal rhythm or was suppressed by 1 mg of dexamethasone. The plasma level of ACTH was undetectable, and it failed to respond to human CRH (hCRH). Plasma cortisol responded well to synthetic ACTH. The urinary 17-OHCS level was high, and was not suppressed by 4 mg of dexamethasone. While these findings were consistent with a diagnosis of adrenocortical adenoma, computed tomography showed several nodules in both adrenal glands that suggested the presence of huge nodular adrenocortical hyperplasia or bilateral adrenocortical adenomas. Bilateral adrenalectomy demonstrated the presence of three adenomas, two in the right and one in the left adrenal. Analysis of the extract from each adenoma revealed that two of the three produced an excess amount of cortisol. Magnetic resonance imaging (MRI) of the brain suggested the presence of pituitary adenoma. Prior to adrenalectomy, TSH, GH or LH showed a low response to TRH, GHRH or LHRH, respectively. Since normal responses were restored after bilateral adrenalectomy, these abnormalities were attributed to hypercortisolemia.
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PMID:A rare case of Cushing's syndrome due to bilateral adrenocortical adenomas. 944 86

About 90% of all functional thyroid autonomies (FTA) are euthyroid for a prolonged period of time. It is estimated that more than 10% of goiter patients in iodine deficient regions and less than 10% in iodine rich areas have evidence of FTA. After the age of 40, the risk of hyperthyroidism decompensation gradually increases. This risk rises with increasing thyroid volume, nodularity and patient age. In the elderly, hyperthyroidism also occurs in the absence of goiter. After decades of iodine deficiency, especially the intake of unphysiologically high iodine concentrations may result in increased frequencies of hyperthyroidism. In iodine deficient regions, almost half of all cases of hyperthyroidism are FTA related. Following elimination of iodine deficiency, the rate of hyperthyroidism may be reduced below 10%. This will not affect the prevalence of immunogenic hyperthyroidism. The most reliable evidence of FTA is produced using the TcTU supp. test. The highly sensitive TSH0 and the TRH test are 2.5 times less sensitive. Thus, they may still indicate euthyroidism in scintigraphically compensated or decompensated FTA. The TSH0 screening is only recommended with a view to an improved cost/benefit ratio in the elderly, females above the age of 40, and ill persons. Acutely ill and psychiatric patients should be excluded. Already 1 year after the introduction of iodine into the medical treatment of thyroid disorders, Coindet reported in 1821 his epidemiologically relevant clinical observation of an increase in hyperthyroidism, predominantly of the functional autonomy type. In the meantime, detailed and universally accepted knowledge has become available on the pathogenesis and pathophysiology of functional thyroid autonomy (Gerber et al., 1985). Data on the epidemiology of functional autonomy continue to apply only to the regional population they are based on. They allow to draw conclusions on the prevalence and natural course of functional thyroid autonomy (FTA). The different forms and prevalence rates of hyperthyroidism reflect the severity and duration of the nutritional iodine deficiency on one hand and the quality of iodine prophylaxis on the other.
Exp Clin Endocrinol Diabetes 1998
PMID:Epidemiology of functional autonomy. 986 90

Determination of thyrotropin (TSH) by sensitive immunometric assays is currently judged as the most sensitive and also most cost-effective first-line approach to thyroid function testing. Further improvement of assay sensitivity has led to the description of third generation TSH assays with a functional sensitivity in the range of 0.01 to 0.02 mU/l. In the present study, we analyzed interassay precision profiles of a commercially available third generation assay (ACS:180 TSH-3) and documented the critical role of the time span used for the assessment of a method's functional sensitivity. By using a standardized approach with five serum pools measured in 30 different runs across a 6-week period, functional sensitivity was calculated as 0.015 mU/l. The TSH concentrations measured by two different third generation assays (ACS: 180 TSH-3 and Elecsys TSH) in samples from healthy blood donors were highly correlated (r = 0.76, n = 252). In some samples, however, discordant results were obtained. Euthyroid reference intervals were determined as 0.30-3.68 mU/l for the ACS:180 TSH-3 assay and as 0.36-3.64 mU/l for the Elecsys TSH assay. Reevaluation of reference intervals including only TPOAb or TgAb negative samples resulted in almost the same reference ranges. Measuring TSH concentrations in various patient populations, third generation assay turned out to be advantageous in the following clinical situations. (a) In patients with mildly suppressed but well detectable TSH concentrations due to functional thyroid autonomy (0.03-0.3 mU/l), overt hyperthyroidism can be excluded by third generation TSH measurement alone without the need of additional thyroid hormone measurements; (b) in patients receiving long term suppressive T4 treatment after thyroidectomy for differentiated thyroid cancer, measurement of basal TSH by third generation assays allow accurate monitoring of hormone therapy without the need for TRH testing; (c) in most patients with severe nonthyroidal illnesses and decreased TSH levels, TSH concentrations measured by third generation assays are only moderately suppressed and can be clearly discriminated from undetectable levels in overt hyperthyroidism. In conclusion, the use of third generation TSH assays is recommended in specialized clinical laboratories frequently analyzing samples taken in one of those clinical situations.
Exp Clin Endocrinol Diabetes 1998
PMID:Utility of third generation thyrotropin assays in thyroid function testing. 986 93

The thyrotropin-releasing hormone stimulation test (TRH test) is commonly used as part of the endocrine evaluation after pituitary surgery. However, some patients with a normal thyrotropin (TSH) response to TRH after pituitary surgery develop central hypothyroidism during follow-up. On the other hand, hypothyroidism does not necessarily ensue in patients with a blunted TSH response. As TSH is secreted in a pulsatile fashion with maximum secretion in the early morning, we investigated whether measurement of the nocturnal TSH surge is useful for predicting development of thyrotropic function after pituitary surgery. Serum TSH concentrations were measured at hourly intervals from 16.00 h to 06.00 h in 13 healthy volunteers and in 10 patients within 2 weeks after pituitary surgery. A standard TRH test using i.v. injection of 200 microg synthetic TRH was performed the next morning. Three and six months later thyroid function was reassessed in all patients by measuring thyroid hormones and TSH. Healthy volunteers showed a clear nocturnal TSH surge from a nadir of 0.55 +/- 0.27 microIU/ml at 18.00 h to a peak concentration of 1.82 +/- 0.97 microU/ml at 06.00 h (p = 0.0015). DeltaTSH during TRH test was 6.31 +/- 2.27 microIU/ml. In contrast, following pituitary surgery, patients invariably showed a blunted nocturnal increase in TSH concentration, which was 0.27 +/- 0.20 microIU/ml at 18.00 h and 0.33 +/- 0.26 microIU/ml at 06.00 h (p = 0.044). DeltaTSH during TRH test was 1.99 +/- 2.51 microIU/ml and was subnormal in 8 out of 10 patients. Levothyroxine supplementation was initiated in two of these patients, because free T4 levels were also subnormal and clinical hypothyroidism was present. In the remaining patients with subnormal TRH response, no case of central hypothyroidism was identified at the follow-up visits after 3 and 6 months. We conclude from these data that both nocturnal TSH surge and TRH test are subnormal after pituitary surgery and do not indicate that central hypothyroidism will develop.
Exp Clin Endocrinol Diabetes 1999
PMID:Blunted nocturnal TSH surge does not indicate central hypothyroidism in patients after pituitary surgery. 1007 63

A pituitary tumor with suprasellar extension was found by magnetic resonance imaging (MRI) in a male with diabetes mellitus. Endocrine examination revealed high plasma follicle-stimulating hormone (FSH) and alpha-subunit levels, which increased with administration of thyrotropin (TSH)-releasing hormone (TRH). Plasma luteinizing hormone (LH) and testosterone levels were low. Pituitary gonadotropin producing tumor was diagnosed. Because the patient refused surgery, bromocriptine was administered and plasma FSH and alpha-subunit rapidly decreased; on MRI the tumor size was gradually reduced. When pituitary operation is not feasible, bromocriptine is one choice of treatment.
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PMID:Reduction of plasma gonadotropin levels and pituitary tumor size by treatment with bromocriptine in a patient with gonadotropinoma. 1033 39

Thyrotropin releasing hormone (TRH) is therapeutically effective in experimental and clinical spinal injury. The effects of TRH on diabetic neuropathy are not known. The aim of the present study was to investigate the electrophysiological effects of TRH in the streptozotocin diabetic rats. Three groups of rats were studied, non-diabetic control (n = 10), diabetic controls (n = 8), and TRH treated diabetic rats (n = 9). Administration of TRH or saline and electrophysiological measurements were performed 4 weeks after induction of diabetes. TRH was given intraperitoneally in a dose of 600 microg (3 ml). Nerve conduction velocity (NCV), measured in caudal nerve, and N1 latency of somatosensory evoked potentials (SEP) were measured 75 min after injection of TRH or serum saline. SEP latencies were 28.1 +/- 0.6, 29.4 +/- 0.8, 27.8 +/- 1.1 ms, in normal, diabetic and diabetic TRH-treated groups, and NCV values were 28.1 +/- 0.8, 23.8 +/- 0.4, and 27.9 +/- 0.7 m/s respectively. NCV was significantly reduced in the diabetic group compared to normals (P < 0.05). but then improved by TRH treatment (P < 0.05). Our findings suggest that TRH has an acute effect on peripheral neuropathy in experimental streptozotocin diabetes in the rat.
Diabetes Res Clin Pract 1999 May
PMID:Beneficial effect of thyrotropin-releasing hormone on neuropathy in diabetic rats. 1041 27

Previous data have indicated that organ-specific and non-organ-specific autoimmune diseases may occur in the same patient. We report here our study on the type and prevalence of endocrine autoimmune diseases in undifferentiated connective tissue disease (UCTD). A retrospective analysis revealed five out of 75 UCTD cases (6.6%) with cytology-verified autoimmune thyroiditis (associated with insulin-dependent diabetes mellitus in one case). Other UCTD patients had Graves' disease (one case), non-toxic multinodular goitre (two cases) and central hypothyroidism (one case). In a prospective study, thyroid function was evaluated in 15 consecutive UCTD patients with neither clinical nor laboratory signs of thyroid involvement. Basal and post-TRH stimulation TSH levels were significantly higher in UCTD patients than in healthy subjects.
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PMID:Autoimmune thyroid diseases in patients with undifferentiated connective tissue disease. 1075 98


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