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Biomedical subjects

J J Díez

Publications and source records attributed to J J Díez.

At least 19 recordsLinked to original sources

Acute and persistent iatrogenic Cushing's syndrome after a single dose of triamcinolone acetonide.

Iatrogenic Cushing's syndrome is a well-known adverse effect of glucocorticoids. It usually develops after prolonged exposure to excessive amounts of synthetic glucocorticolds. The development of iatrogenic Cushing's syndrome (ICS) after a single and low dose of synthetic glucocorticoid is an exceptional event. Up to now, only a few number of cases have been associated with triamcinolone acetonide and they have always been related to local administration. We report, for the first time, a patient who developed ICS after a single low dose of parenterally (im) administered triamcinolone acetonide. She was a 45-yr-old woman who referred to us because of cushingoid appearance, whose hormonal determinations were suggestive of secondary adrenal insufficiency. Clinical features were developed one month after the administration of a 40 mg single-dose of im triamcinolone acetonide because of acute laryngitis. Endocrinological evaluation confirmed the hypothalamic-pituitary-adrenal (HPA) axis suppression. Eight months later, cushingoid phenotype had completely disappeared and HPA function had spontaneously recovered. We review clinical features and comment on the possible pathogenic mechanisms of this particular and new form of ICS.

Cushing Syndrome↗

Ambulatory blood pressure monitoring in patients with hyperthyroidism before and after control of thyroid function.

BACKGROUND AND OBJECTIVE: Thyroid hormones have pronounced effects on the cardiovascular system. Thyrotoxicosis affects blood pressure (BP), modifying both diastolic (DBP) and systolic (SBP) pressures. There are no studies examining BP with ambulatory blood pressure monitoring (ABPM) in hyperthyroidism before and after control of thyroid function. Our aims were (1) to analyse ABPM in a group of normotensive hyperthyroid patients before and after normalizing circulating thyroid hormones and (2) to compare these results with those obtained in a group of euthyroid subjects. PATIENTS AND MEASUREMENTS: We studied 20 normotensive hyperthyroid subjects [18 women; age (mean +/- SEM) 49.0 +/- 3.0 years] and 15 healthy subjects. Patients were evaluated by ABPM over 24 h, at diagnosis and after therapy (n = 18). RESULTS: The average 24-h, daytime and night-time SBP was significantly greater in hyperthyroid patients than in controls with no significant differences in DBP. Circadian BP rhythm, estimated by the difference between mean values of SBP, DBP and mean BP during daytime and night-time, was unchanged. The average 24-h and daytime SBP significantly decreased after normalizing thyroid function in the 18 hyperthyroid evaluated patients. Daytime SBP and DBP were higher than night-time values both before and after control of thyroid function. However, no differences in circadian BP rhythm were observed. CONCLUSIONS: Normotensive hyperthyroid patients exhibit higher ambulatory SBP throughout 24 h than normotensive euthyroid subjects. Control of hyperthyroidism decreases ambulatory SBP values. Mean nocturnal fall in BP is comparable in normotensive hyperthyroid patients and control subjects.

Antithyroid Agents↗

Prevalence of thyroid dysfunction in adults over age 60 years from an urban community.

Thyroid dysfunction affects a considerable portion of the elder population. The aim of the present study has been to assess the prevalence of thyroid dysfunction in adult healthy subjects over age 60 years from our population. We performed a descriptive, cross-sectional study in the setting of a sanitary area in an urban community in Madrid (Spain). Serum concentrations of thyrotropin (TSH) and free thyroxine (FT4) were determined by an electrochemiluminescency assay in all participants after antecubital venous sampling. A second examination, including the measurement of triiodothyronine and thyroid autoantibodies, was performed in subjects with abnormal results. A total of 127 women and 167 men, aged 60 to 84 years, were studied. We identified 6 subjects (all women) with hypothyroidism (2.04 %) and 19 (6 women, 13 men) with hyperthyroidism (6.46 %, 95 %CI 3.65 - 9.27 %). There were 3 cases (1.02 %) of subclinical and 3 cases (1.02 %) of overt hypothyroidism. In the hyperthyroid group only one patient (0.34 %) showed overt hyperthyroidism. TSH test did not detect erroneously any case of hypothyroidism or hyperthyroidism, although one patient with hyperthyroidism was not diagnosed by this test. FT4 test detected erroneously two cases of hypothyroidism; however, it was the only way to detect the patient with overt hyperthyroidism. In conclusion, in our population over age 60 years the prevalence of hypothyroidism was 2.04 % and that of hyperthyroidism 6.46 % (95 %CI 3.65 - 9.27 %). The total prevalence of thyroid dysfunction was, therefore, 8.50 % (95 %CI 5.31 - 11.69). Our data suggest that TSH test is probably enough to screen for thyroid dysfunction in adults over age 60 years.

Aged↗

Somatostatin analogs in the treatment of medullary thyroid carcinoma.

The medical therapy for advanced or metastatic medullary thyroid carcinoma has not been fully established. Somatostatin analogs have been used with variable success in the therapy of a few patients with medullary thyroid carcinoma. In the present study, we evaluated the effects of somatostatin analog therapy on calcitonin (ct) and carcinoembryonic antigen in patients with advanced medullary thyroid carcinoma. Five patients (2 men and 3 women, aged 35-57 yr) with post-operative recurrent medullary thyroid carcinoma received somatostatin analog therapy for 12 weeks. All had been previously treated with total thyroidectomy and lymphadenectomy. Four of them showed positive uptake in (111)In-pentetreotide scanning. One patient was treated with sc octreotide (100 microg/8 h), 3 patients received im slow release lanreotide (30 mg/14 days), and a further one received im octreotide LAR (30 mg/28 days). Serum samples for ct and carcinoembryonic antigen were obtained at 0, 1, 2, 4, 8 and 12 weeks of therapy. Therapy was well-tolerated in general, with minimal side-effects. One patient died after the first month of therapy because of advanced disease. Another patient showed normalization of his ct and carcinoembryonic antigen concentrations at the second week of therapy, maintaining elevated values thereafter. No clinically relevant changes in serum concentrations of ct and carcinoembryonic antigen were observed in the rest of the patients. One patient with positive (111)In-pentetreotide scan, showed no uptake after somatostatin analog therapy. No significant decrease in the size of metastases was evident in the remaining patients. In conclusion, therapy with different formulations of octreotide and lanreotide does not seem to modify serum concentrations of ct and carcinoembryonic antigen in patients with recurrent medullary thyroid carcinoma.

Adult↗

Reduction of lung distensibility in acromegaly after suppression of growth hormone hypersecretion.

Whether the growth of the lungs in acromegaly is due to alveolar hypertrophy or alveolar hyperplasia is a subject of debate. To discriminate these hypotheses, we compared pulmonary distensibility and diffusing capacity among 11 patients with active acromegaly and 11 matched control subjects, evaluating the response of pulmonary distensibility and diffusing capacity to suppression of growth hormone (GH) hypersecretion. We performed lineal and exponential analyses of quasistatic pressure-volume curves. Patients with active acromegaly had a greater TLC, lung compliance, and shape constant, K, than did normal subjects. We found no significant differences between the study groups in carbon monoxide diffusing capacity or diffusing capacity per unit of alveolar volume. After treatment, patients with inactive acromegaly showed a reduced TLC (6.95 +/- 1.40 [mean +/- SD] L versus 6.35 +/- 1.23 L), reduced lung compliance (3.61 +/- 0.90 L/kPa versus 2.36 +/- 0.79 L/ kPa), reduced K coefficient (2.62 +/- 0.65 kPa(-)(1) versus 1.35 +/- 0.40 kPa(-)(1)), and increased maximal recoil pressure (1.74 +/- 0.38 kPa versus 2.28 +/- 0.25 kPa). We conclude that the increased lung distensibility with normal diffusion capacity demonstrated in patients with active acromegaly, which was partly reversible after suppression of GH hypersecretion, suggests that lung growth in acromegaly may result from an increase in alveolar size.

Acromegaly↗

Growth hormone responses to oral glucose and intravenous thyrotropin-releasing hormone in acromegalic patients treated by slow-release lanreotide.

The aim of this study was to assess GH response to oral glucose tolerance test (OGTT) and TRH stimulation test in a group of 10 patients with active post-operative acromegaly before and after long-term slow-release (SR) lanreotide therapy (30 mg im every 10-14 days). Seven patients (2 males, 5 females, 29-71 yr), who during therapy maintained plasma GH and IGF-I concentrations under 5 microg/l and 450 microg/l, respectively, were considered as responders and studied for 24 (1 patient) to 36 months (6 patients). Three patients (1 male, 2 females, 46-61 yr) with levels of GH and IGF-I above those values were studied for 12 months. The OGTT (75 g po) and TRH test (400 microg iv) were repeated before and after 6, 12, 24 and 36 months. The GH response to OGTT was abnormal (nadir: >2 microg/l) at 6 and 12 months in poorly responsive patients. This response was normalized in all responsive patients. Nonetheless, 2 responsive patients showed abnormal GH values after OGTT once each throughout the 36-month study period. The GH response to TRH was characterized by great variability and exhibited unpredictable behavior throughout the study period both in responsive and in poorly responsive patients. Only 2 patients in the responsive group showed persistent normal GH levels (peak: < or =5 microg/l) after TRH for 3 yr. In conclusion, SR lanreotide treatment gave rise to a correct control of GH hypersecretion and to a normalization of GH response to oral glucose in 7 out of 10 patients, although it did not abolish the paradoxical reaction of GH to TRH in all responders. The effect of SR lanreotide on GH response to glucose tolerance test was not paralleled by GH response to TRH.

Acromegaly↗

Cholinergic modulation of growth hormone responses to growth hormone-releasing hormone in uraemic patients on peritoneal dialysis.

BACKGROUND: Hypothalamic cholinergic neurotransmission plays a major role in the regulation of GH secretion. Pyridostigmine, a cholinesterase inhibitor, is able to decrease hypothalamic somatostatinergic tone and release GH in normal subjects. Blockade of muscarinic receptor with pirenzepine blunts the GH release in several clinical situations. However, little information is available on the role played by central cholinergic pathways in GH regulation in uraemic patients. OBJECTIVE: We aimed to assess GH responses to GHRH after pretreatment with pyridostigmine and pirenzepine in a group of uraemic patients undergoing peritoneal dialysis (PD). GH responses of the patients treated with recombinant human erythropeitin (rhEPO) were compared to patients without treatment. DESIGN: We studied 14 male patients on PD and nine control subjects. All subjects underwent three endocrine test in random order after an overnight fast. Each subject received GHRH (100 microg, i.v. in bolus at 0 minutes). Sixty minutes before the injection of GHRH subjects were given oral placebo, pyridostigmine (120 mg), or pirenzepine (100 mg). MEASUREMENTS: Blood samples for GH were collected at -60, 0, 15, 30, 45, 60 and 90 minutes The hormonal secretory responses were studied by a time-averaged (area under the curves, AUC) and time-independent (peak values) analysis. RESULTS: Baseline GH concentrations were similar in patients and controls. GH responses to placebo plus GHRH were also comparable in patients and controls (peak 26.6 +/- 3.8 vs. 33.2 +/- 4.4 mU/l, AUC 28.2 +/- 3.4 vs. 27.8 +/- 4.6 mU/h/l). Pyridostigmine administration induced a significant potentiation of GH responses to GHRH both in patients (peak 43.2 +/- 5.2 mU/l, AUC 47.6 +/- 6.0 mU/h/l; P < 0.01) and in control subjects (peak 79.2 +/- 8.6 mU/l, AUC 78.0 +/- 9.4 mU/h/l; P < 0.01). However, the increment in GH peak and AUC was significantly (P < 0.05) greater in controls in relation to values found in patients. Pirenzepine administration induced an abolishment of GH release after GHRH stimulation both in PD patients (peak 5.4 +/- 2.6 mU/l, AUC 6.0 +/- 2.4 mU/h/l; P < 0.01) and in healthy controls (peak 3.8 +/- 0.6 mU/l, AUC 4.0 +/- 0.4 mU/h/l; P < 0.05). Responses to pyridostigmine plus GHRH and pirenzepine plus GHRH were similar in patients on chronic therapy with recombinant human erythropeitin and in patients without rhEPO therapy. CONCLUSION: These results suggest that the cholinergic regulation of GH release is preserved in uraemic patients on peritoneal dialysis. The significantly lower increase in GH response to GHRH induced by pyridostigmine suggests that cholinergic stimulatory tone is attenuated in patients in relation to control subjects. Long-term therapy with rhEPO seems not to affect GH responses to cholinergic stimulation or blockade.

Adult↗

Short-term recombinant human growth hormone therapy does not modify growth hormone, thyrotropin and prolactin responses to thyrotropin-releasing hormone in adult dialysis patients.

BACKGROUND: We recently have reported the first randomized, controlled study on the effects of short-term recombinant human growth hormone (rhGH|| therapy on the nutritional status of a group of malnourished adult dialysis patients. In order to evaluate whether rhGH administration exerts any influence on GH, thyrotropin (TSH|| and prolactin (PRL|| responses to TSH-releasing hormone (TRH||, we assessed these responses before and after rhGH therapy. METHODS: GH, PRL and TSH responses to TRH before and 1 month after rhGH therapy in a group of adult dialysis patients were evaluated. Seventeen dialysis patients (11 on continuous ambulatory peritoneal dialysis/six on haemodialysis|| were studied (rhGH group, n=8; control group, n=9||. In the rhGH group, 0.2 IU/kg/day rhGH was administered subcutaneously. Each patient was tested with TRH (400 microg bolus i.v.|| on two separate occasions, just before and immediately after the treatment period. RESULTS: rhGH treatment did not modify baseline serum GH concentrations (6.6+/-2.7 vs 4.1+/-1.1 microg/l||, paradoxical GH responses to TRH (six out of eight patients||, GH peak (11.9+/-4.6 vs 11.2+/-5.3 microg/l, NS|| or area under the secretory curve of GH (GH AUC; 19.1+/-4.5 vs 12.1+/-3.1 microg/h/l||. Both basal PRL (35.5+/-7.1 vs 36.7+/-8.6 microg/l|| and TSH (2.3+/-1.1 vs 2.8+/-1.7 mU/l|| concentrations, as well as their responses to TRH stimulation (PRL peak, 59.9+/-16.6 vs 59. 5+/-11.8 microg/l; TSH peak, 6.2+/-2.6 vs 7.1+/-3.9 mU/l||, were also unaffected by rhGH therapy. CONCLUSION: These results suggest that short-term rhGH therapy does not significantly influence the magnitude of the somatotropic, lactotropic or thyrotropic response to TRH in adult dialysis patients. However, this finding has to be interpreted with caution due to the two different patient groups included in this study.

Adult↗