Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypothyroidism in patients with diabetes mellitus is usually primary though rarely secondary hypothyroidism has occurred. An 11 6/12 year old white female developed diabetes mellitus at 8 6/12 years of age. She received treatment up to 40 units NPH daily with adequate control and normal growth. Hypothyroidism was diagnosed after a 3 month history of lethargy, constipation, dryness of skin and decreasing insulin requirement to 10 units NPH per day. Physical examination was entirely normal, except for dry skin. Serum levels of free thyroxine, thyroxine, T3 resin uptake, were low as was 131I uptake. Primary hypothyroidism was ruled out by the absence of goitre, absent antithyroid antibodies, low basal TSH levels and increased 131I uptake after TSH administration. Serum TSH levels rose 4-fold in respone to intravenous TRH administration. The patient was treated with 0.15 mg daily of L-thyroxine with very good response. This report describes a patient with juvenile diabetes mellitus and isolated TSH deficiency with hypothyroidism of probably hypothalamic origin, an association not previously described in children.
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PMID:Isolated thyrotrophin deficiency in diabetes mellitus. 57 89

We randomly administered thyrotropin-releasing hormone (200 micrograms, as an i.v. bolus) or control saline (in isovolumic amount) to 30 male diabetic subjects (23 IDDM, 7 NIDDM) in fair metabolic control (HbA1 9.7 +/- 0.3%, means +/- SEM) and to 12 healthy male controls on two different mornings. While GH in the basal state was similar in IDDM, NIDDM and normal subjects, TRH administration evoked a significant GH release only in a single IDDM individual. The only GH-responder to TRH was a newly-diagnosed (two weeks) IDDM patient, still with a high glycated hemoglobin level (HbA1 11.1%), despite normal plasma glucose levels. Saline infusion did not affect GH concentrations either in normals or in diabetics. Exaggerated GH responses to TRH are uncommon in diabetic patients in good metabolic conditions.
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PMID:Inappropriate growth-hormone (GH) response to thyrotropin-releasing hormone (TRH) occurs infrequently in well-regulated diabetes mellitus. 211 57

GH release is abnormally regulated in insulin-dependent diabetes (IDDM), and paradoxical stimulation of GH release after TRH has been reported. However, overnight GH pulsatility is increased in IDDM, and it may be difficult to distinguish TRH-stimulated release from spontaneous secretory episodes. To resolve this question, we carried out two overnight GH profiles followed by either TRH or saline control tests in six adolescents with IDDM; ages 11.4-14.7 years, duration IDDM 2.4-6.7 years. A rise in GH was seen in four of six following TRH, but with no consistent pattern. A rise was also seen in four of six following saline. Peak GH levels were similar after TRH and saline (19.3 +/- 4.4 vs 25.8 +/- 5.5 mU/l; mean +/- SEM). Mean blood glucose was no different during TRH and saline tests (9.5 +/- 1.6 vs 7.5 +/- 0.6 mmol/l). The two subjects who had an early GH peak after TRH were those in whom GH levels had already begun to rise, suggesting the coincident occurrence of a spontaneous GH pulse. The timing of the next GH pulse could be predicted equally well after TRH and saline from the overnight secretory profile using autocorrelation. Paradoxical GH stimulation after TRH is not seen in adolescents with IDDM, but apparent responses may be due to timing coincident with the increased spontaneous pulsatility.
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PMID:Spontaneous growth hormone (GH) pulsatility is the major determinant of GH release after thyrotrophin-releasing hormone in adolescent diabetics. 251 49

It is well known that muscarinic cholinergic blockade either reduces or abolishes stimulated GH release in normal subjects. In this study we have investigated whether cholinergic muscarinic blockade could reduce the GH responses to GRF 1-29 and TRH in acromegalic subjects. Eight acromegalic subjects underwent two GRF tests (GRF 1-29, 1 microgram/kg i.v.) with and without pirenzepine (0.6 mg/kg, i.v.). A further four of these patients received TRH (200 micrograms/kg, i.v.) on separate occasions with and without pirenzepine (0.6 mg/kg, i.v.). Cholinergic muscarinic blockade did not alter the GH responses to GRF and TRH in patients with acromegaly. These findings are in contrast with previous data reported on the effects of cholinergic blockade on stimulated GH levels in normal subjects and in patients with type I diabetes mellitus and are compatible with the view that somatotroph adenomas are functionally disconnected from hypothalamic control mechanisms.
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PMID:Lack of effect of muscarinic cholinergic blockade on the GH responses to GRF 1-29 and TRH in acromegalic subjects. 287 6

In 3737 subjects without clinically thyroid disorders we evaluated the incidence of thyroid microsomal and thyroglobulin antibodies. These autoantibodies were found in 7% of a normal population, in 9% of patients with various non-autoimmune diseases, and in 11-16% of groups who either had or were at risk for autoimmune diseases: patients with IDDM, vitiligo, alopecia areata, idiopathic hypoparathyroidism, Addison's disease, and first-degree relatives of IDDM patients. Functional thyroid evaluation with TRH test was performed in 197 seropositive subjects and 144 seronegative controls. One-quarter (26%) of the subjects with thyroid autoantibodies showed functional abnormalities on TRH testing, whereas only 2.8% of the 144 seronegative controls showed subclinical hypothyroidism. After an observation period of 12-44 months, 102 persistently seropositive subjects were reassessed and 31% of them showed an impairment in TRH test response.
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PMID:Thyroid autoantibodies: a good marker for the study of symptomless autoimmune thyroiditis. 356 35

The basal and TRH-induced prolactin (PRL) and TSH secretions were examined in 14 children aged 4 to 13 years with newly diagnosed insulin dependent diabetes (IDD) within three weeks after diagnosis. Basal PRL levels did not differ from the values of control. In response to TRH, 6 out of 14 patients showed an exaggerated PRL response and 8 a normal PRL response. The basal and TRH-induced TSH secretions were normal, while plasma triiodothyronine (T3) and thyroxine (T4) concentrations were significantly (p less than 0.001, p less than 0.02) lower in patients than in controls. These findings suggest that a significant proportion of children with newly diagnosed IDD has an exaggerated PRL response to TRH, and TSH secretion remains unchanged despite significant decreases of circulating thyroid hormone levels.
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PMID:Plasma prolactin response to thyrotropin releasing hormone in children with newly diagnosed insulin dependent diabetes. 640 63

Growth hormone (GH) response was studied in 8 insulin-dependent and 7 non-insulin-dependent diabetics after stimulation with L-Dopa (500 mg orally) and TRH (0.2 mg iv.). L-Dopa induced a clear GH response in insulin-dependent diabetes (IDDM) and in the control group while in non-insulin-dependent diabetes (NIDDM) peak GH levels were lower (P less than 0.05) and 4 of 7 subjects failed to respond to L-Dopa stimulation. TRH had no effect on GH levels in NIDDM and in the controls. Insulin-dependent diabetics responded to TRH stimulation and GH levels at 20 and 30 min were significantly higher as compared with NIDDM and the control group. The degree of hyperglycemia seemed not to influence GH response. The highest GH levels were noted in two patients with proliferative retinopathy. It is suggested that TRH-induced GH release may be a characteristic feature in some patients with IDDM.
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PMID:TRH-induced growth hormone release in insulin-dependent diabetes mellitus. 644 6

Significant high titres (1:400-1:25,600) of circulating thyroid microsomal antibodies (MCHA) were found in the sera of 5 out of 59 non-ketoacidotic, insulin-dependent diabetic (IDDM) patients (mean age 14.5 years). Among these five patients (four females, one male), all of whom were over 11 years, two also had thyroglobulin antibodies. Increased thyrotropin (TSH) response to TRH was found in 3/5 MCHA positive patients and in 3/54 without circulating MCHA. Serum thyroxine (T4) and free T4 (FT4) average values were significantly lower (P less than 0.01 and P less than 0.001) in diabetics (7.1 +/- 1.8 micrograms/dl and 10.2 +/- 3.1 pg/ml, means +/- SD) as compared to normal sex and age matched controls (8.9 +/- 1.9 micrograms/dl and 12.2 +/- 2.2 pg/ml, respectively). T4 and FT4 values were inversely related to the duration of the disease. Subnormal T4 values were found in six (five females and one male) patients, four of whom had subnormal FT4 values. No patient had low triiodothyronine (T3) and high reverse T3 (rT3) values, i.e. none displayed the biochemical pattern of the 'low T3 syndrome' described with ketoacidotic status. This indicates also a satisfactory compensation of IDDM in all the patients. At the time of study no patient (including also those with circulating MCHA and TGHA and with TSH hyper-response to TRH) showed either thyroid size enlargement or clinical features of thyroid dysfunction including impaired growth and bone age retardation.
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PMID:Circulating thyroid antibodies and thyroid function studies in children and adolescents with insulin-dependent diabetes mellitus. 648 76

Fifteen IDDM patients were evaluated for thyroid hormone abnormalities before and after control of diabetes mellitus/ketoacidosis. Blood sugar mean +/- SEM mg/dl on admission was 430 +/- 20.3 and after therapy fasting and post prandial blood sugar values were 120 +/- 14.5 and 150 +/- 20.2 respectively. GHb mean +/- SEM % on admission was 15.2 +/- 0.36. Serum T3 mean +/- SEM ng/dl of 0.36 +/- 0.04 was in hypothyroid range and rT3 mean +/- SEM ng/ml 0.40 +/- 0.6 was significantly raised (P < 0.001) before therapy. After metabolic control both T3 and rT3 became normal. T4 concentration mean +/- SEM meg/dl of 5.5 +/- 0.7 was well within normal range before therapy and rose to mean +/- SEM mcg/dl 8.8 +/- 0.5 after therapy (P < 0.01). TSH response to TRH was blunted in uncontrolled state. It is concluded that peripheral changes in T3, T4 and rT3 (low T3, high rT3 and low or normal T4) occurred in uncontrolled diabetic state during ketoacidosis. TSH response to TRH was blunted due to suppression of hypothalamic pituitary thyroid axis which takes more than a week for complete recovery.
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PMID:Thyroid hormones in diabetic ketoacidosis before and after therapy. 830 Apr 81

Disturbances of prolactin secretion occur both in the chronic renal failure and in diabetes mellitus. The study aimed to investigate if the diabetic nephropathy as a cause of chronic renal failure disturbs prolactin secretion. The study was conducted in 5 groups of patients: group I-12 patients with IDDM without diabetic nephropathy; group II-12 patients with IDDM with diabetic nephropathy treated conservatively; group III-16 patients with chronic renal failure of non-diabetic origin; group IV-12 patients with IDDM with end stage renal failure in the course of diabetic nephropathy treated with haemodialysis; group V-16 patients with end stage renal failure of non diabetic origin treated with haemodialysis. 12 healthy subjects served as the control group. In all investigated groups as well as in the control group the TRH test was performed. The mean serum prolactin concentration was estimated in the investigated groups just before the intravenous TRH injection and then after 15, 30, 45, 60 and 120 minutes. The mean area over the basic value (AOBV) of prolactin was also assessed. The patients with IDDM without diabetic nephropathy did not differ from healthy subjects both in the basic and TRH induced prolactin secretion. Basic and TRH induced prolactin secretion in patients with diabetic nephropathy both conservatively treated and treated with haemodialysis were lower than in patients with the same stage of chronic renal failure of non-diabetic origin.
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PMID:[Prolactin secretion in diabetic nephropathy of patients with diabetes mellitus type I (IDDM)]. 867 6


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