Objective: Traumatic brain injury (TBI) is a devastating public health problem that may result in hypopituitarism. However, the mechanisms responsible for hypothalamic-pituitary dysfunction due to TBI are still unclear. Although the antibodies against neurons have been demonstrated in injured animal studies, investigations regarding the occurrence of antipituitary antibodies (APAs) in patients with TBI are lacking in the literature. In order to investigate whether autoimmune mechanisms could play a role in the pituitary dysfunction after TBI, we have planned this study aimed at investigating the presence of APA at the third year of TBI and association between the TBI-induced hypopituitarism and APA. Patients and design: Twenty-nine (25 males and 4 females; age 36.5G2.3 years) patients who had completed a 3-year follow-up after TBI were included in the present study. APA and pituitary function were evaluated in all the patients 3 years after TBI; moreover, APAs were tested also in sera of 60 age-/sexmatched normal controls. The APAs were investigated by an indirect immunofluorescence method. Results: APAs were detected in 13 out of the 29 TBI patients (44.8%), but in none of the normal controls. Pituitary dysfunction development ratio was significantly higher in APA-positive patients (46.2%) when compared with APA-negative ones (12.5%; PZ0.04). There was a significant association between APA positivity and hypopituitarism due to TBI (odds ratio: 2.25, 95% confidence intervals 1.1-4.6). Moreover, there was a significant positive correlation (rZ0.74, PZ0.004) between APA titer ratio and peak GH response to GHRHCGH related peptide (GHRP)-6 test, suggesting that high APA titers were associated with low GH response to GHRHCGHRP-6 test. Conclusions: This study shows for the first time the presence of the APA in TBI patients 3 years after head trauma. Moreover, present investigation indicates preliminary evidence that APA may be associated with the development of TBI-induced pituitary dysfunction, thus suggesting that autoimmunity may contribute in the development of TBI-induced hypopituitarism. The presence of the association between APA and TBIinduced hypopituitarism may provide a new point of view in this field and promote further clinical and experimental studies.European Journal of Endocrinology 159 7-13

BackgroundWestern dietary pattern is included among the environmental dietary factors involved in the pathogenesis of psoriasis. Nutritional data collection methods and gender differences might affect the association between diet and psoriasis. The 7-day food records is considered the “gold standard” of self-administered food frequency questionnaires. In this study, we evaluated the differences in the dietary intake, anthropometric measurements and cardio-metabolic risk profile in a group of psoriatic patients compared with an age and Body Mass Index (BMI)-matched control group. In addition, in the group of psoriatic patients we investigated the association between the dietary intake and clinical severity of psoriasis.MethodsCross-sectional case control observational study. A total of 82 adult males, 41 treatment-naïve patients with psoriasis and 41 healthy subjects matched for age and BMI were included in the study. The clinical severity of psoriasis was by assessed by Psoriasis Area and Severity Index (PASI) score. The dietary interview data were collected by a 7-day food records. Anthropometric measures, glucose and lipid profile, liver function tests and C-reactive protein levels were measured. Homeostasis Model Assessment of Insulin Resistance (HoMA-IR), Visceral Adiposity Index (VAI) and the Fatty Liver Index (FLI) were calculated.ResultsPsoriatic patients consumed a higher percentage of total and simple carbohydrates, total fat, polyunsaturated fatty acid (PUFA) and n-6/n-3 PUFAs ratio, and cholesterol, while the consumption of protein, complex carbohydrates, monounsaturated fatty acid (MUFA), n-3 PUFA and fiber was lower than in the control group. In addition, psoriatic patients presented altered anthropometric measurements, glucose and lipid profile, liver function tests, and elevated values of HoMA-IR, VAI and FLI. PASI score well correlated with anthropometric measures, glucose and lipid profile, liver function tests, cardio-metabolic indices, and the dietary components, except for protein and total carbohydrates. At logistic regression analysis between PASI score and MUFA, MetS presence was well predicted only by higher PASI score (OR = 1.794; p = 0.002; CI 1.242–2.591). At multiple regression analysis, MUFA was the best predictor of PASI score (r2 = 0.387, β = −0.635, t = −5.127, p < 0.001).ConclusionDifferences in dietary intake were observed in adult male psoriatic patients compared with the controls. These differences were associated to the severity of the psoriasis and cardio-metabolic risk. FLI represented an early indicator of the cardio-metabolic risk profile in psoriatic patients, and dietary MUFA were major predictor of the clinical severity of psoriasis, while the association between psoriasis and metabolic syndrome appeared to be independent of MUFA intake. The low MUFA consumption might act as a possible adjunctive mechanism in increasing the inflammation milieu of psoriatic patients.

APA measurement by immunofluorescence may help to predict the occurrence of hypopituitarism but only when considering the immunostaining pattern and their titers. Combined evaluation of these parameters allows identifying patients at higher risk for pituitary autoimmune dysfunction, thus requiring a strict pituitary surveillance to disclose a preclinical phase of hypopituitarism and possibly interrupt therapeutically the progression to clinically overt disease.

The findings in hyperthyroid patients with Graves' orbitopathy (GO) of antibodies against antigens shared between the thyroid and orbit, such as the TSH-receptor (TRAb) and a novel protein G2s (G2sAb), suggested a possible common therapeutic strategy. However, the gold therapeutic standard for hyperthyrodism in these patients remains still unsettled and is mainly based on personal experience. Studies on the effect of total thyroidectomy (TT) alone or followed by radioiodine ablation (RAI) of thyroid remnants showed often conflicting results. This longitudinal study was aimed at evaluating the influence of TT alone or followed by post-surgical RAI with respect to methimazole treatment on the activity and severity of GO in patients with hyperthyroidism and GO. Sixty consecutive patients with Graves' disease and mild/moderate GO were studied and grouped as follows: group 1, including 25 patients (16F, 9M) undergoing TT alone; group 2, including 10 patients (8F, 2M) undergoing TT followed by RAI for histological evidence of differentiated thyroid cancer; group 3, including 25 patients (18F, 7M) euthyroid under methimazole therapy, studied as controls. Clinical study of ophthalmopathy and measurements of TRAb and G2sAb were performed in all patients at start of the study (time of TT for group 1 and RAI after TT for group 2 and of the first finding of euthyroidism under methimazole treatment for group 3) and after 6, 12, 24 months. Patients of both groups 1 and 2 showed an early significant decrease and a further progressive reduction of the activity and severity of GO with a disappearance of TRAb and a decrease of G2sAb levels during the follow-up, without statistically significant differences between the two groups. Patients in group 3 showed a much later and less marked improvement of GO with persistence of TRAb and G2sAb positivity, even if with reduction of TRAb levels at 12 and 24 months. Our results suggest that in Graves' patients with large goiter or relapse of hyperthyroidism and mild/moderate GO, TT alone could be an advisable choice to treat hyperthyroidism also improving GO with reduction of cost/benefit ratio.

Our results suggest that in patients with selective idiopathic hypopituitarism, detection of APA or AHA could better characterize an autoimmune process involving the pituitary or hypothalamus, respectively. In particular, detection of antibodies targeting selectively ACTH-secreting or corticotrophin-releasing hormone-secreting cells may differentiate, respectively secondary from tertiary variants of autoimmune hypoadrenalism.

The occurrence of CDI in patients with lymphocytic hypophysitis seems due to an autoimmune hypothalamic involvement rather than an expansion of the pituitary inflammatory process. To search for AVP antibody in these patients may help to identify those of them prone to develop an autoimmune CDI. The detection of AHA targeting CRH-secreting cells in some patients with GH/ACTH deficiency but with APA targeting only GH-secreting cells indicates that an autoimmune aggression to hypothalamus is jointly responsible for their hypopituitarism.

LYH (lymphocytic hypophysitis) is an autoimmune disease of the pituitary gland which can present with varying degrees of pituitary hormonal impairment and/or with symptoms related to pituitary enlargement. In this review, we provide an overview of the epidemiology, diagnosis, pathogenesis, treatment, and the role of organ-specific and antipituitary antibodies as potential markers of LYH. In addition, although the mechanisms underlying LYH are not completely understood, the role of prolactin, which plays an important part in maintaining immune system homoeostasis and is increased in the disease, is considered.

A possible autoimmune aggression to pituitary somatotrophs has been suggested by the occurrence of antipituitary antibodies (APA) directed against GH-secreting cells in some cases of GH deficiency (GHD) both in adults and in children and in some patients with autoimmune poliendocrine syndrome. We also detected APA in some patients with idiopathic short stature (ISS) and suggested that the presence of these antibodies could identify those of them prone to develop GHD. In fact, patients with ISS, resulted positive for APA at the first observation, during a longitudinal follow-up showed an impaired GH response to the stimuli in subsequent years suggestive of acquired GHD. Also in such patients we demonstrated that the target of APA were the somatotrophs and that an autoimmune attack to these cells may be the underlying cause of hormonal impairment in several children with GHD positive for APA. In this connection we suggested that in these patients an early iso-hormonal therapy with recombinant GH may be useful to interrupt or delay the progression towards a clinical GHD.