Hypoparathyroidism is a rare endocrine disorder characterized by low serum calcium and parathyroid hormone levels. The most common cause is parathyroid iatrogenic surgical removal. However, innumerous and rarer conditions can cause hypoparathyroidism. The authors describe a 27-year-old man that presented in emergency department with confusion, amnesia and decreased attention span. A cerebral computed tomography revealed bilateral extensive calcification in the basal ganglia. A complete work-up revealed low serum calcium, high serum phosphorus and low parathyroid hormone, leading to the diagnosis of idiopathic primary hypoparathyroidism. Initial intravenous therapy with calcium gluconate and calcitriol was administered, with clinical and analytical improvement. The authors describe a rare condition, with an exuberant cerebral presentation and extreme hypocalcemia, which did not directly correlate to the severity of symptoms. Not only this is a treatable disorder that may have catastrophic results if overlooked but also its symptoms may be completely reversed with prompt treatment.

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Here, we hypothesized that modulating the plasmatic levels of 5-HT through a tryptophan-rich diet we could inhibit prostatic growth.METHODS: C57BL6 adult male mice were divided in 2 groups, Group 1: fed with a normal diet and Group 2: fed with, for a 3-month period. After the sacrifice of the mice, the prostate was dissected and weighted. By ELISA, prostatic 5-HT concentration was determined and by Western Blot, AR expression was evaluated in both groups.RESULTS: We observed that mice fed with a tryptophan-rich diet for 3 months present a significant reduction in the prostatic weight comparatively to mice fed with normal diet (fig1). Intra-prostatic 5-HT concentration was significantly increased in mice fed with a tryptophanrich diet (fig2). Furthermore, we demonstrated that the expression of AR in prostatic tissue from mice who underwent tryptophan supplementation was inferior to the AR expression in the normal diet group (fig3).CONCLUSIONS: Modulating diet through tryptophan enrichment, with the consequent increase in prostatic serotonin, decreases prostate size and down-regulates AR. These results suggests that a tryptophan rich diet could be potential used to prevent or treat BPH.

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histology, immunohistochemistry, western blot analyses and quantitative PCR. In vitro effects of GHRH were tested on human prostate epithelial (BPH-1) and stromal (WPMY-1) cell lines.RESULTS: Carrageenan-induced prostatitis (CIP) produced a 73.2% increase in weights of the ventral prostate lobes which was reduced by 19.2% in rats treated with MIA-690. Vimentin staining showed thickening of the stromal compartment which effect was also suppressed by GHRH antagonists. Western blot analysis demonstrated an increase in GHRH, COX2 and TGF-b1 levels by inflammation and suppression by MIA-690. Prostatic IGF-1 levels measured by ELISA were increased by 65% in CIP and were suppressed to control level by GHRH antagonist. A qPCR array analysis of genes related to EMT revealed upregulation in several genes including collagens, matrix metalloproteinase 9, Snail1, TGF-b1 and vimentin by inflammation and downregulation by treatment with MIA-690. In vitro, GHRH stimulated the phosphorylation of EGF and IGF receptors and upregulated the level of TGF-b1 in BPH-1 cells but had no measurable effects on WPMY-1 stromal cells.CONCLUSIONS: Our current findings strongly indicate that GHRH is a key molecular player in inflammation-induced prostate enlargement via its direct action on epithelial cells. The effect of GHRH antagonists on stromal cells may be the consequence of their effect on epithelial growth factor production. Consequently, GHRH antagonists could be clinically useful to treat early and advanced stages of BPH due to their anti-proliferative and anti-inflammatory activities.

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