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1.
Calcif Tissue Int ; 88(3): 231-7, 2011 Mar.
Article in English | MEDLINE | ID: mdl-21207016

ABSTRACT

Osteocalcin (OC) has been proposed as a regulator of insulin sensitivity in both humans and other animals. Primary hyperparathyroidism (PHPT) is characterized by high OC levels and insulin resistance. The aim of this study was to evaluate whether in PHPT the link between OC levels and blood markers of insulin resistance was maintained. In a consecutive series of 219 adult PHPT patients, serum OC as well as fasting insulin and glucose levels were measured. Insulin sensitivity was estimated by homeostatic model assessment (HOMA2-S%). The same parameters were evaluated in a subgroup of 45 patients after parathyroidectomy (PTX). PHPT patients were characterized by markedly high OC levels. After subdividing them according to glucose tolerance, it was found that OC was similar in subjects with normal glucose tolerance (NGT) and impaired glucose tolerance (IGT), while diabetic subjects had lower serum OC than those with NGT (P < 0.02) or IGT (P < 0.04). OC was negatively associated with fasting glucose and positively associated with HOMA2-S%. OC independently predicted HOMA2-S% in a multivariate analysis. In the subgroup of surgically cured PHPT patients, OC levels significantly decreased after PTX, while HOMA2-S% did not change. Our findings indicate that in PHPT there is a positive relationship between OC and glucose metabolism, OC being one of the predictors of insulin sensitivity. However, data in surgically cured patients, showing OC normalization in spite of unchanged HOMA2-S%, suggest that OC does not likely play a major role in affecting insulin sensitivity in PHPT.


Subject(s)
Hyperparathyroidism, Primary/blood , Hyperparathyroidism, Primary/metabolism , Insulin Resistance/physiology , Osteocalcin/blood , Adult , Aged , Body Mass Index , Case-Control Studies , Cross-Sectional Studies , Female , Glucose Intolerance/blood , Glucose Intolerance/complications , Glucose Intolerance/metabolism , Humans , Hyperparathyroidism, Primary/complications , Hyperparathyroidism, Primary/surgery , Male , Middle Aged , Parathyroidectomy , Retrospective Studies
2.
J Endocrinol Invest ; 30(4): RC9-RC12, 2007 Apr.
Article in English | MEDLINE | ID: mdl-17556860

ABSTRACT

Recent evidence suggests that patients with traumatic brain injury (TBI) are at substantial risk of hypopituitarism. The pathomechanisms, however, are not completely understood yet. Little is known about the association of morphological changes in the sella region with pituitary function in TBI. In this study, we assessed morphological abnormalities of the sella region in patients with TBI and their relation to endocrine function. We studied magnetic resonance (MR) or computed tomography (CT) scans of 22 patients with TBI [17 men, 5 women, age (mean+/-SD) 43.5+/-10.6 yr, time after trauma 17.4 +/-15.0 yr]. Of these, 15 patients had some degree of hypopituitarism. We found abnormalities of the sella region in 80% of the patients with hypopituitarism and 29% of those without hypopituitarism (Fisher's exact test, p=0.032). The most common abnormality was loss of volume or empty sella, followed by native signal inhomogeneities, perfusion deficit, and lack of neurohypophyseal signal. Our results indicate that pituitary imaging abnormalities are more common in TBI patients with hypopituitarism than those without. Both immediate trauma-induced pathology as necrosis and hemorrhage as well as multifactorial mid- to long-term changes may underlie these abnormalities.


Subject(s)
Brain Injuries/complications , Hypopituitarism/diagnosis , Hypopituitarism/etiology , Pituitary Diseases/diagnosis , Pituitary Diseases/etiology , Pituitary Gland/diagnostic imaging , Adult , Brain Injuries/diagnostic imaging , Female , Humans , Male , Middle Aged , Radiography , Retrospective Studies , Time Factors
3.
Eur J Endocrinol ; 155(4): 559-66, 2006 Oct.
Article in English | MEDLINE | ID: mdl-16990655

ABSTRACT

OBJECTIVE: Hypopituitarism frequently follows pituitary neurosurgery (NS) and/or irradiation. However, the frequency of hypothalamic-pituitary dysfunction after NS of non-pituitary intracranial tumors is unclear. The aim of this study was to assess the presence of endocrine alterations in patients operated on for intracranial tumors. DESIGN: This is a retrospective study. METHODS: We studied 68 consecutive adult patients (28 female, 40 male, age 45.0 +/- 1.8 years; body mass index (BMI): 26.5 +/- 0.6) with intracranial tumors who underwent NS only (n = 17) or in combination with radiotherapy (RT) and/or chemotherapy (CT) (n = 51). In all subjects, basal endocrine parameters and the GH response to GHRH + arginine test (using BMI-dependent cut offs) were evaluated. RESULTS: In 20.6% of the patients, peripheral endocrinopathy related to CT and/or RT was present. Hypopituitarism was found in 38.2% of the patients. Total pituitary hormone, multiple pituitary hormone, and isolated pituitary hormone deficits were present in 16.2, 5.8, and 16.2% respectively. The most common pituitary deficits were, in decreasing order: LH/FSH 29.4%, GH 27.9%, ACTH 19.1%, TSH 17.7%, and diabetes insipidus 4.4%. Hyperprolactinemia was present in 13.2%. The prevalence of hypopituitarism was higher in patients who underwent NS only and with tumors located closely to the sella turcica, but a substantial proportion of patients with tumors not directly neighboring the sella also showed hypopituitarism. CONCLUSIONS: Hypopituitarism frequently occurs after NS for intracranial tumors. Also, exposure of these patients to CT and/or RT is frequently associated with peripheral endocrinopathies. Thus, endocrine evaluation and follow-up of patients treated for intracranial tumors should be performed on a regular basis.


Subject(s)
Brain Neoplasms/complications , Brain Neoplasms/surgery , Endocrine System Diseases/etiology , Hypothalamo-Hypophyseal System/physiology , Adult , Aged , Brain Neoplasms/epidemiology , Endocrine System Diseases/epidemiology , Female , Humans , Hypopituitarism/epidemiology , Hypopituitarism/etiology , Male , Middle Aged , Pituitary Hormones/deficiency , Retrospective Studies
4.
J Endocrinol Invest ; 28(10 Suppl): 28-32, 2005.
Article in English | MEDLINE | ID: mdl-16550719

ABSTRACT

GH deficient (GHD) adult patients, either from child- or adulthood onset, have impaired health (impairment in body composition and structure functions as well as derangement in lipoprotein and in carbohydrate metabolism leading to increased cardiovascular morbidity), which improves with GH replacement. For patients with childhood-onset GHD, the so called "transition phase", defined as the period between reaching the final height and the completion of the development of such organs, can be considered as the most important phase of life for the development of important target organs: heart, bones and muscles. Particularly, children with GHD may not attain the peak bone mass (PBM) at the time of discontinuation of GH therapy, as the complete achievement of PBM is likely reached later on, during the transition phase to adulthood. In addition, patients with GHD generally have a delayed timing of PBM compared to normal individuals. GH treatment should be continued until the attainment of PBM, independently of the final height achieved. Individual titration of the recombinant human GH (rhGH) dose is recommended, and measurement of IGF-I levels is needed for monitoring the adequacy of replacement. The GH dose for replacement in the transition adolescent is still higher than in adulthood; after puberty, the rhGH dose should be progressively decreased in the following years (probably up to 25 yr of age) in order to obtain the achievement of optimal PBM.


Subject(s)
Aging , Bone Density/drug effects , Bone and Bones/drug effects , Dwarfism, Pituitary/drug therapy , Human Growth Hormone/therapeutic use , Adolescent , Adult , Body Height/drug effects , Bone Density/physiology , Bone Development/drug effects , Bone and Bones/metabolism , Bone and Bones/pathology , Bone and Bones/physiopathology , Child , Dose-Response Relationship, Drug , Dwarfism, Pituitary/pathology , Dwarfism, Pituitary/physiopathology , Female , Heart/drug effects , Heart/growth & development , Human Growth Hormone/pharmacology , Humans , Insulin-Like Growth Factor I/analysis , Male , Muscle Development/drug effects , Recombinant Proteins/pharmacology , Recombinant Proteins/therapeutic use
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