Hyperprolactinemia in acromegalic patients may result either from cosecretion of growth hormone and prolactin by the tumour or from pituitary stalk compression. The occurrence of both conditions is possible. This study was designed aiming 1) to estimate the prevalence of each cause of hyperprolactinemia and its respective clinical course; 2) to compare the outcomes of patients with tumours staining only for growth hormone against tumours staining for both growth hormone and prolactin. 75 acromegalic patients submitted to transsphenoidal surgery between 1989 and 2018 were included. Patients were divided based on preoperative prolactin levels and immunostaining pattern. Statistical analysis was performed with SPSS version 23. Hyperprolactinemia was documented in 22 out of 36 patients (61%). Stalk compression was the only underlying cause of hyperprolactinemia in 45% of cases. The levels of prolactin were not associated with the immunostaining pattern for prolactin. Clinical differences were not observed between hyperprolactinemic and normoprolactinemic patients, except for a higher frequency of cavernous sinus invasion (64% vs 29%, p=0,064), that reached the level of significance for the subgroup with macroadenomas staining exclusively for growth hormone (p=0,031). In the present series, no clinical differences were noticed between patients with tumours staining only for growth hormone or staining for both growth hormone and prolactin. Hyperprolactinemia resulting from stalk compression is likely to anticipate a less favourable course of disease, since it is associated with larger tumours and a higher frequency of cavernous sinus invasion. On the contrary, positive immunostaining for prolactin was not a marker of worse prognosis.
Background: The role played by Helicobacter pylori in the sinuses, and its association with the same organism's gastric infection, are still unclear. Methods: In order to compare H.pylori colonization patterns in the nose and stomach we conducted a cohort analysis of 14 patients, eligible for sinus surgery due to chronic medically refractory rhinosinusitis, who were tested for simultaneous presence of H. pylori, by histology, culture and polymerase chain reaction, in pathologic sinus tissue collected during surgery and in gastric mucosa obtained through gastroduodenal endoscopy. Results: H. pylori DNA was found in the sinus mucosa of 15.4% of patients with chronic rhinosinusitis, and all of them showed concurrent H. pylori stomach infection. Sinus colonization was not found without simultaneous gastric colonization, although most patients with gastric infection did not have the bacterial DNA in their sinuses. H. pylori's presence in the nose was not associated with local inflammatory status, and no cultures could be obtained from any of the sinus tissue samples, including those positive for H. pylori DNA. Conclusions: Only H. pylori DNA, and not the culturable active form of the microorganism, could be found in the sinus mucosa of some patients with H. pylori gastric infection. We could not find evidence, however, that the bacterium's presence in the nose contributes to local mucosal inflammation.
Skin aging is a continuous process that affects skin appearance and function manifesting by several outcomes such as wrinkling and sagging. Researchers have identified impacting environmental factors (sun exposure, smoking, etc.) and several molecular mechanisms leading to skin aging. Recently, genome wide association studies (GWAS) have led to new insights into the molecular mechanisms of skin aging. Since individual SNP associations in GWAS explain only a small fraction of the genetic impact in complex polygenic phenotypes, we applied the Gene Set Enrichment Analysis on the genotype data obtained from 502 verywell characterized women to identify biological pathways associated with four major outcomes of skin aging, namely photoaging, solar lentigines, wrinkling, and sagging. This analysis revealed new relevant pathways and genes, some likely specific of skin aging such as the WNT7B and PRKCA genes in the "melanogenesis" pathway, some likely involved in global aging such as the DDB1 gene in the "nucleotide excision repair" pathway, not picked up in the previously published GWAS. Overall, our results suggest that photoaging, solar lentigines, wrinkling, and sagging involve specific molecular mechanisms such as "proteasome" and "mTOR signaling pathway" but also shared molecular mechanisms such as "nucleotide excision repair".
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