Cabergoline Withdrawal Before and After Menopause : Outcomes in Microprolactinomas

Natural course of prolactinomas after menopause is not fully elucidated. The aim of this study was to compare recurrence rate after cabergoline withdrawal in premenopausal vs. postmenopausal women with microprolactinoma. Sixty-two women with microprolactinoma treated with cabergoline for at least 1 year and followed for 2 years after drug withdrawal were retrospectively selected. Patients were divided into two groups: 48 patients stopped cabergoline before menopause ("PRE" group), while 14 after menopause ("POST" group). Recurrence was defined by prolactin levels above normal, confirmed on two occasions. Overall, 39/62 women relapsed. Patients who relapsed apparently had higher prolactin before withdrawal (median 216.2, range 21.2-464.3 mIU/L) compared with those in long-term remission (94.3, 29.7-402.8 mIU/L; p < 0.05), and the risk of recurrence seemed lower in POST women (4/14, 29%) than in PRE ones (35/48, 73%, p < 0.005, OR 0.149, 95% CI 0.040-0.558). However, none of the factors (prolactin before withdrawal, menopausal status, treatment duration, complete adenoma regression) showed a correlation with recurrence risk in multivariate analysis. The best strategy able to optimize CBG treatment and withdrawal's outcomes is still to be defined in microprolactinomas. Postmenopausal status cannot reliably predict long-term remission, and follow-up is needed also in women of this age

Evaluation of pituitary function after infectious meningitis in childhood

Background: A number of studies of adults have shown that pituitary deficiencies can develop in a considerable proportion of subjects during the acute phase of meningitis or years after the infection has disappeared. The results of the very few studies of the impact of pediatric meningitis on hypothalamic-pituitary function are conflicting.Methods: In order to determine the incidence of pituitary dysfunction in children with central nervous system infection, we evaluated pituitary function and anthropometric parameters in 19 children with meningitis of different etiologies (15 males; mean age \ub1 standard deviation [SD] at pituitary evaluation, 5.9 \ub1 4.0\ua0years; mean time from the acute event \ub1 SD, 18 \ub1 10\ua0months).Results: All of the subjects had a normal stature and growth velocity for their age and gender, and none of them was obese. On the basis of Tanner's reference charts, 17 subjects (13 boys and all four girls) were pre-pubertal; two boys were in Tanner stage 2. None of the subjects had central hypothyroidism. All of the patients had normal serum of insulin growth factor (IGF)-I and prolactin. Their sex steroid and gonadotropin levels were concordant with their age and pubertal status. Early morning urine osmolality and serum electrolyte levels showed no signs of diabetes insipidus. All of the patients had normal plasma adrenocorticotropic hormone (ACTH) levels. Peak cortisol responses to the standard dose Synacthen test (SDST) were normal in all cases.Conclusions: The results showed that hypopituitarism following infectious meningitis appears to be infrequent in childhood and children's pituitary glands seem to be less vulnerable to damage than those of adults

Efficacy and safety of growth hormone treatment in children with short stature: the Italian cohort of the GeNeSIS clinical study

Purpose: We examined auxological changes in growth hormone (GH)-treated children in Italy using data from the Italian cohort of the multinational observational Genetics and Neuroendocrinology of Short Stature International Study (GeNeSIS) of pediatric patients requiring GH treatment. Methods: We studied 711 children (median baseline age 9.6 years). Diagnosis associated with short stature was as determined by the investigator. Height standard deviation score (SDS) was evaluated yearly until final or near-final height (n = 78). Adverse events were assessed in all GH-treated patients. Results: The diagnosis resulting in GH treatment was GH deficiency (GHD) in 85.5 % of patients, followed by Turner syndrome (TS 6.6 %). Median starting GH dose was higher in patients with TS (0.30 mg/kg/week) than patients with GHD (0.23 mg/kg/week). Median (interquartile range) GH treatment duration was 2.6 (0.6\u20133.7) years. Mean (95 % confidence interval) final height SDS gain was 2.00 (1.27\u20132.73) for patients with organic GHD (n = 18) and 1.19 (0.97\u20131.40) for patients with idiopathic GHD (n = 41), but lower for patients with TS, 0.37 ( 120.03 to 0.77, n = 13). Final height SDS was > 122 for 94 % of organic GHD, 88 % of idiopathic GHD and 62 % of TS patients. Mean age at GH start was lower for organic GHD patients, and treatment duration was longer than for other groups, resulting in greater mean final height gain. GH-related adverse events occurred mainly in patients diagnosed with idiopathic GHD. Conclusions: Data from the Italian cohort of GeNeSIS showed auxological changes and safety of GH therapy consistent with results from international surveillance databases

Craniofaringioma ed altri tumori parasellari

La ghiandola ipofisaria pu\uf2 essere sede di processi espansivi di natura diversa dagli adenomi che originano dalle cellule endocrine e comprendono processi patologici sia neoplastici che non neoplastici. Tra i primi il pi\uf9 importante per incidenza e rilevanza \ue8 sicuramente il craniofaringioma, tumore dal comportamento aggressivo che origina da residui della tasca di Rathke. Il capitolo ne tratta l'epidemiologia, l'anatomia patologica, la presentazione clinica, la diagnosi, la terapia ed il follow-up

A 2019 update on TSH-secreting pituitary adenomas

Thyrotropin-secreting pituitary adenomas (TSH-omas) present with signs and symptoms of hyperthyroidism and they are characterized by elevated serum levels of free thyroid hormones with measurable TSH levels. TSH-omas are very infrequent, accounting for less than 1% of all pituitary adenomas, thus representing a very rare cause of hyperthyroidism. For this reason, data collected on these rare disorders are relatively few, but some new researches shed new light on the etiopathogenesis, the diagnosis and the treatment of such a remarkable disease. Since the same biochemical picture is present in the syndromes of thyroid hormone resistance (RTH), in particular in the form of pituitary RTH, failure in distinguishing these clinical entities may lead to improper patient management. Conversely, early diagnosis and correct treatment of TSH-omas may prevent the occurrence of neurological and endocrinological complications, thus leading to a better rate of cure. In the present short review article, the most relevant recent advances in the pathophysiology of TSH-omas are described

Obesity : impact of infections and response to vaccines

Obesity is a common condition that has rapidly increased in both the industrialised and developing world in recent decades. Obese individuals show increased risk factors for severe infections and significant immune system dysregulation that may impair the immune response to vaccines. The main aim of this paper was to review the current knowledge regarding the association between obesity and the risk and outcome of infections as well as immune response to vaccines. The results showed that obesity is a highly complex clinical condition in which the functions of several organ and body systems, including the immune system, are modified. However, only a small minority of the biological mechanisms that lead to reduced host defences have been elucidated. Relevant efforts for future research should focus on obese children, as the available data on this population are scarce compared with the adult population. Even if most vaccines are given in the first months of life when obesity is rare, some vaccines require booster doses at preschool age, and other vaccines, such as the influenza vaccine, are recommended yearly in the obese population, but it is not known whether response to vaccines of obese patients is impaired. The reduced immune response of obese patients to vaccination can be deleterious not only for the patient but also for the community

Ipotiroidismo centrale: diagnosi, patogenesi e terapia sostitutiva

L\u2019ipotiroidismo centrale (IC) \ue8 un raro difetto di produzione degli ormoni tiroidei dovuto ad un\u2019insufficiente stimolazione da parte della tireotropina (TSH) di una ghiandola tiroidea normale. La sua diagnosi pu\uf2 essere molto semplice in pazienti con evidenti manifestazioni di malattie ipotalamo-ipofisarie, ma pu\uf2 essere difficile nei casi in cui queste manifestazioni sono assenti o modeste. Tale difficolt\ue0 deriva soprattutto dalla perdita dell\u2019elevato potere diagnostico che la misurazione del TSH ha nei casi di malattie che colpiscono primariamente la ghiandola tiroidea. Infatti, i centri coinvolti nel meccanismo di feedback sono lesi nei pazienti con IC e i livelli circolanti di TSH possono essere bassi, normali o modestamente elevati. L\u2019origine del difetto pu\uf2 coinvolgere in maniera variabile sia l\u2019ipofisi che l\u2019ipotalamo ed essere di tipo genetico, con insorgenza dell\u2019IC in et\ue0 neonatale o infantile, o secondaria alla presenza di alterazioni acquisite della regione ipotalamo-ipofisaria, con insorgenza pi\uf9 frequente in et\ue0 adulta. La terapia dell\u2019IC si basa sull\u2019utilizzo della l-tiroxina a dosi sostitutive. I fattori che possono interferire nell\u2019assorbimento, nel metabolismo della l-tiroxina sono particolarmente numerosi nei pazienti con IC e il raggiungimento del dosaggio ottimale pu\uf2 essere difficoltoso nella maggioranza dei pazienti a causa della impossibilit\ue0 di utilizzare il TSH come parametro utile per il monitoraggio. Tutti questi argomenti sono affrontati in questo articolo con lo scopo di indicare i metodi pi\uf9 idonei per la diagnosi e il monitoraggio dei pazienti con IC