No abstract

Male patients with AD, in contrast with female patients, fail to maintain a normal energy homeostasis even in the early stages of the disease, as shown by the decreased lean mass content in males AD compared to controls. Disruption of the normal compensatory modulation of ghrelin secretion might contribute to the metabolic changes observed in male patients with AD.

We investigated endothelial and in vivo platelet activation in a cohort of 52 patients with essential thrombocythemia (ET) and polycythemia vera (PV) before and after cytoreductive treatment, 22 healthy controls, and 17 patients with acute cerebrovascular ischemia (ACVI) and normal platelet counts. We measured platelet expression of CD62P and CD63 antigens and levels of soluble vascular cell adhesion molecule 1 (sVCAM-1). We found increased in vivo platelet activation in all patients with ET and PV, both before and after cytoreductive treatment, compared with controls. In patients with arterial thrombosis, platelet expression of CD62P, and in patients with erythromelalgia, expression of both markers was higher compared with expression in patients without thrombotic complications. In patients with ET and PV before and after treatment, sVCAM-1 expression was increased compared with expression in controls but also compared with expression in patients with ACVI and normal platelet counts. In patients with arterial thrombosis and erythromelalgia, in vivo platelet activation correlated with the level of sVCAM-1. Our findings indicated that in vivo platelet activation reflects intrinsic platelet defects in patients with ET and PV, persists after cytoreductive treatment, and results in endothelial damage, probably through release of angiogenic factors and/or activation of white blood cells.

Different attempts were made to identify the variables that may be involved in the clinical course of cerebrovascular ischemia. In the case of stroke with mild severity (SMS), the clinical significance of neuroendocrine changes as well as of post-stroke depression (PSD) remains unknown. We therefore evaluated the presence of neuroendocrine changes in the acute and post-acute phase of SMS, and their potential role during convalescence. Serum cortisol, T4, T3, FT4, FT3, TSH and PRL levels were measured in 17 euthyroid patients with stroke on admission (day 1), following morning (day 2), 7 days and 3 months later. TSH and PRL secretion after TRH test were measured. Stroke severity on admission was determined by Scandinavian Stroke Scale (SSS). Montgomery-Asberg Depression Rating Scale (Madrs) was used for assessment of post-stroke depression. On admission, TSH and T3, were within normal limits and were greater compared to values on day 2. Lower basal TSH and decreased TSH response to TRH on day 2, were associated with stroke of greater severity. Delta-PRL after TRH on day 2 was higher in patients who develop PSD. Changes in serum thyroid hormones in SMS, reflects those of non-thyroidal illness. A mild stimulation of hypothalamic-pituitary-adrenal axis was detected. We provide evidence that PRL response to TRH, in the acute phase of stroke may be used as an index for early detection of PSD.

Hyperthyroidism is characterized by hyperphagia and increased basal metabolic rate. Ghrelin peptide is implicated in food intake through activation of the orexigenic neuropeptide Y/agouti related protein in the arcuate nucleus of hypothalamus. Also different studies suggested that ghrelin might play a role in states of energy insufficiency, controlling body weight. We therefore evaluate ghrelin levels in severe hyperthyroidism before and after medical treatment when euthyroidism was achieved, in order to evaluate its possible role in the increase of appetite and in the metabolic changes observed in hyperthyroidism. Serum ghrelin and insulin levels were measured after an oral glucose tolerance test (OGTT), in 7 severe hyperthyroid female patients, before and after medical treatment when euthyroidism was achieved. Body mass index (BMI), percentage of body fat and lean mass was also estimated in hyperthyroidism as well as in euthyroidism. Basal insulin levels were statistically higher in hyperthyroid patients with respect to euthyroid state after treatment (p=0.02, t=3.379), while homeostasis model assessment (HOMA) index for insulin sensitivity was statistically higher in hyperthyroidism (group 1) compared to euthyroidism (group 2) (1.64+/-0.69 vs 0.78+/-0.44, p=0.019, t=3.389). Fasting ghrelin concentrations were significantly reduced in group 1 compared to group 2 (938+/-578 pg/ml vs 1402+/-566 pg/ml, p<0.05, t=-2.489). Oral glucose loading induced suppression of ghrelin level in both groups, but the area under the curve for ghrelin during the OGTT in euthyroidism was greater compared to hyperthyroidism (p=0.05, t=-2.485). After medical treatment, a statistically significant increase in BMI (23.1+/-4.3 vs 25.9+/-5.1) (p=0.007, t=-4.399) was also observed. In hyperthyroidism, basal ghrelin levels showed a negative correlation with BMI (p=0.042, r=-0.829), insulin (p<0.001, r=-1.000), and HOMA index (p=0.019, r=-0.886). No correlation was found between ghrelin levels and thyroid hormone values. Ghrelin levels are decreased in hyperthyroidism and increase when euthyroidism is achieved. BMI and insulin are the main factors that influence ghrelin concentration in hyperthyroidism. T3 and T4 levels do not influence ghrelin levels. There is no evidence that ghrelin is responsible for the increase appetite seen in hyperthyroidism.