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Biomedical subjects

P Iglesias

Publications and source records attributed to P Iglesias.

At least 19 recordsLinked to original sources
PubMed2005

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↗
PubMed2005

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↗
PubMed2005

Comparison of two techniques of sputum induction in the diagnosis of pulmonary tuberculosis.

SETTING: Specialised tuberculosis out-patient clinic covering a population of 350 885. OBJECTIVES: To compare two techniques, ultrasonic nebuliser (UN) and Venturi-type face mask nebuliser (VFMN), for obtaining sputum in patients suspected of having active pulmonary tuberculosis (PTB) and who cannot expectorate, and to analyse the usefulness and cost of sputum induction with UN in a specialised medical practice. DESIGN: Prospective study from October 1997 until March 2000. RESULTS: Of 94 subjects who completed all tests, at least one sample of sputum was obtained from 89 (95.6%). UN provided adequate samples in 86 (93.4%) and VFMN in 66 (71%), a significant difference (P < 0.001). Among 43 patients diagnosed with active PTB, the diagnosis was confirmed in 39 with the samples obtained by sputum induction. Direct acid-fast bacilli smear was positive in 8 (19%). Direct costs were low and the technique can be performed on the day the patient attends the outpatient clinic. CONCLUSION: Sputum induction with an ultrasonic nebuliser was well-tolerated, of low cost, allows adequate samples to be obtained in the majority of patients who cannot produce sputum, and was more effective than the Venturi-type face mask.

Adolescent↗
PubMed2003

A novel mutation in the calcium-sensing receptor responsible for autosomal dominant hypocalcemia in a family with two uncommon parathyroid hormone polymorphisms.

A novel missense activating mutation in the extracellular calcium-sensing receptor (CaSR) is reported in this work. It was identified in three related subjects with the phenotypic features of autosomal dominant hypocalcemia (ADH). The proband, a 27-year-old woman, diagnosed as having hypoparathyroidism at 7 years of age and a history of seizures, showed the highest penetrance of the mutation. The remaining two affected members presented asymptomatic chronic hypocalcemia despite severe hypoparathyroidism associated with high levels of serum phosphate and calcium urinary excretion. The missense mutation (Glu(604)Lys) affected an amino acid residue in the C terminus of the cysteine-rich domain of the extracellular amino-terminal domain, which seems to be required for the coupling of ligand binding to the activation of intracellular signaling pathways. This genetic change cosegregated with hypocalcemia in all the individuals where the mutation was found. As parathyroid hormone (PTH) secretion is the regulatory target of the CaSR, polymorphism analysis of the PTH gene was carried out. PTH polymorphisms were analyzed in the kindred studied. Affected members for the Glu(604)Lys CaSR mutation which also carried the uncommon PTH alleles showed higher penetrance of the mutation, with more severe autosomal dominant hypocalcemia. These results suggested that the PTH gene could act as a modifier locus of ADH, affecting the penetrance of the activating CaSR mutation described.

Adolescent↗
PubMed2002

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↗
PubMed2001

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↗
PubMed2001

Serum insulin-like growth factor type 1, insulin-like growth factor-binding protein-1, and insulin-like growth factor-binding protein-3 concentrations in patients with thyroid dysfunction.

Thyroid hormones play a role in the regulation of insulin-like growth factor type 1 (IGF-1) and insulin-like growth factor-binding protein-3 (IGFBP-3) expression, and both IGF-1 and IGFBPs have been shown to be related to the function and growth of the thyroid. Our aim was to evaluate serum concentrations of IGF-1, IGFBP-1, and IGFBP-3 in patients with thyroid dysfunction before and after normalization of thyroid function. The study was performed in 86 patients with thyroid dysfunction (43 hyperthyroid and 43 hypothyroid patients) and 17 euthyroid subjects. Serum growth hormone (GH), insulin, IGF-1, IGFBP-1, and IGFBP-3 were measured in all patients before and after normalizing serum thyroid hormone concentrations. Hyperthyroid patients showed IGF-1 (198.8 +/- 17.0 microg/L) and IGFBP-3 levels (4.2 +/- 0.2 mg/L) similar to those found in the control group (217.9 +/- 20.3 microg/L and 4.2 +/- 0.3 mg/L, respectively). After therapy these levels significantly decreased to 156.6 + 11.1 microg/L (p < 0.01) and 3.3 +/- 0.1 mg/L (p < 0.001), respectively. IGFBP-1 concentrations were clearly higher than those found in controls (22.7+/- 2.6 vs. 5.7 +/- 1.5 microg/L, p < 0.001) and exhibited a significant reduction after therapy for thyroid hyperfunction (11.0 +/- 1.7 microg/L, p < 0.001). Patients with hypothyroidism showed serum concentrations of IGF-1 (161.5 +/- 13.1 microg/L, p < 0.05) and IGFBP-3 (3.2 +/- 0.3 microg/L, p < 0.05) significantly lower than those found in healthy volunteers. However, replacement therapy with levothyroxine did not induce any significant modification of these concentrations (152.6 +/- 10.6 microg/L and 3.2 +/- 0.2 mg/L, respectively). Similarly, patients with thyroid hypofunction exhibited raised levels of IGFBP-1 (15.5 +/- 0.9 microg/L, p < 0.05 vs. control group) that were significantly decreased after therapy (8.8 +/- 1.4 microg/L, p < 0.01). The results of the present study show that thyroid status affects GH/IGF axis. Hypothyroidism is associated with significant reductions of IGF-1 and IGFBP-3, and IGFBP-1 is elevated in both hypothyroidism and hyperthyroidism.

Adolescent↗
PubMed2000

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↗
PubMed2000

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↗
PubMed2000

Current management of acromegaly.

Acromegaly, a chronic disease of growth hormone (GH) hypersecretion, is most typically caused by a pituitary adenoma. Early diagnosis is critical for prompt intervention to prevent deleterious effects of prolonged exposure to elevated GH and insulin-like growth factor Type I (IGF-I) levels. Current therapy for acromegaly includes several options: surgery, radiotherapy and pharmacotherapy. Transsphenoidal adenomectomy remains a mainstay of therapy for acromegaly. Cure rates are high in microadenomas, but < 50% in macroadenomas. Conventional and stereotactic procedures for radiation therapy are also effective in decreasing GH levels in acromegalic patients, but they need years to normalise GH hypersecretion and carry with them the risk of hypopituitarism. The major classes of drugs currently used to treat acromegaly are dopamine agonists and analogues of somatostatin. Dopamine agonists bind to the D2 receptor and suppress GH hypersecretion in some patients with acromegaly. Their clinical effectiveness is modest, although promising results have been obtained with two novel compounds, quinagolide and cabergoline, that possess long duration of action. Somatostatin analogues have been shown to improve clinical symptoms of acromegaly, decrease hypersecretion of GH and IGF-I and reduce tumour volume in a clinically significant number of patients. Octreotide is administered by s.c. route several times a day, but the recently developed sustained release formulations (octreotide LAR and SR lanreotide) are administered only every 7-28 days by i.m. injections. The complications associated with somatostatin analogues are small, relative to the benefits. Lastly, compounds with a novel mechanism of action, the GH receptor antagonists, are presently under investigation.

Acromegaly↗
PubMed2000

Effects of acute infusion of erythropoietin on paradoxical responses of growth hormone to thyrotropin-releasing hormone in acromegalic patients.

OBJECTIVE: Our aim has been to evaluate the effects of i.v. infusion of recombinant human erythropoietin (rhEPO) on the responses of growth hormone (GH), prolactin (PRL) and thyrotropin (TSH) to thyrotropin-releasing hormone (TRH) stimulation in acromegalic patients. METHODS: We studied 16 patients (8 females, aged 29-68 years) with active acromegaly and 12 control subjects (7 females, 24-65 years). All participants were tested with TRH (400 microg i.v. as bolus) and with TRH plus rhEPO (40 U/kg at a constant infusion rate for 30 min, starting 15 min before TRH injection) on different days. Blood samples were obtained between -30 and 120 min for GH and PRL determinations, and between -30 and 90 min for TSH determinations. Hormone responses were studied by a time-averaged (area under the secretory curve (AUC)) and time-independent (peak values) analysis. RESULTS: Twelve patients exhibited a paradoxical GH reaction after TRH administration with great interindividual variability in GH levels. When patients were stimulated with rhEPO plus TRH there were no changes in the variability of GH responses or in the peak and AUC for GH secretion. Infusion with rhEPO did not induce any significant change in GH secretion in normal subjects. Baseline and TRH-stimulated PRL concentrations in patients did not differ from those values found in controls. When TRH was injected during the rhEPO infusion, a significant (P<0.05) increase in PRL concentrations at 15-120 min was found in acromegalic patients. Accordingly, the PRL peak and the AUC for PRL secretion were significantly increased in patients. Infusion with rhEPO had no effect on TRH-induced PRL release in control subjects. Baseline TSH concentrations, as well as the TSH peak and the AUC after TRH, were significantly lower in patients than in controls. Infusion with rhEPO modified neither the peak TSH reached nor the AUC for TSH secretion after TRH injection in acromegalic patients and in healthy volunteers. CONCLUSION: Results in patients with acromegaly suggest that (i) the paradoxical GH response to TRH is not modified by rhEPO infusion, (ii) rhEPO has no effect on TRH-induced TSH release, and (iii) acute rhEPO administration increases the TRH-induced PRL release in acromegalic patients.

Acromegaly↗