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Prevention, Identification and Management of Postoperative Hypoparathyroidism
Salvatore Lazzara,Alberto Barbera,Guido Nicola Zanghì,Francesco Freni,Grazia Pagano,Andrea Cogliandolo,Ozer Makay,Gianlorenzo Dionigi 대한갑상선-내분비외과학회 2018 The Koreran journal of Endocrine Surgery Vol.18 No.2
The objective of this article is to detail and present our experience on the incidence and management of parathyroid dysfunction after thyroid surgery. Selective evaluation of original articles and reviews that were retrieved by a PubMed search over the years 1990 to 2018, as well as of the recommendations of medical societies including the American, European and Asian Thyroid/Endocrine Associations. The literature presents several contributions, with controversial results. The recommended management for the diagnosis and treatment of parathyroid dysfunction after bilateral thyroid surgery or recurrent surgery consists of an intact parathyroid hormone (iPTH) determination 12–24 hours after surgery and calcium substitution in iPTH <15 pg/mL, no substitution with iPTH ≥15 pg/mL. This procedure is safe for the patient and is accepted by patients and social insurances (for short hospital stay).
Treatment Decision Making in Papillary Thyroid Microcarcinoma
Giuseppe Navarra,Guido Nicola Zanghì,Francesco Freni,Bruno Galletti,Francesco Galletti,Grazia Pagano,Andrea Cogliandolo,Alberto Barbera,Salvatore Lazzara,Gianlorenzo Dionigi 대한갑상선-내분비외과학회 2018 The Koreran journal of Endocrine Surgery Vol.18 No.2
The objective of this article is to detail the treatment for papillary thyroid microcarcinoma (PTMC). The literature presents only few contributions, with controversial results, about comparison between ‘active surveillance’ and surgery. Hemithyroidectomy is the treatment of choice for PTMC. Thyroidectomy is indicated in cases of multifocality, extrathyroid tumor growth, and familial PTMCs. Active surveillance can only be done under well-defined and controlled conditions. Collected findings and agreements with the patient must be precisely documented, also for medico-legal reasons. An observation of PTMC seems most appropriate for patients >60 years of age. In the case of observation of a PTMC, a lifelong examination of the tumor disease must be carried out, since tumor growth or metastases can still occur after 10–15 years. The follow-up periods for the ‘active surveillance’ proposed from the literature review are too short to conclude this as a real alternative.
Fogelgren, Ben,Zuo, Xiaofeng,Buonato, Janine M.,Vasilyev, Aleksandr,Baek, Jeong-In,Choi, Soo Young,Chacon-Heszele, Maria F.,Palmyre, Auré,lien,Polgar, Noemi,Drummond, Iain,Park, Kwon Moo,Lazzara American Physiological Society 2014 American Journal of Physiology Vol.307 No.12
<P>Acute kidney injury is common and has a high mortality rate, and no effective treatment exists other than supportive care. Using cell culture models, we previously demonstrated that exocyst Sec10 overexpression reduced damage to renal tubule cells and speeded recovery and that the protective effect was mediated by higher basal levels of mitogen-activated protein kinase (MAPK) signaling. The exocyst, a highly-conserved eight-protein complex, is known for regulating protein trafficking. Here we show that the exocyst biochemically interacts with the epidermal growth factor receptor (EGFR), which is upstream of MAPK, and Sec10-overexpressing cells express greater levels of phosphorylated (active) ERK, the final step in the MAPK pathway, in response to EGF stimulation. EGFR endocytosis, which has been linked to activation of the MAPK pathway, increases in Sec10-overexpressing cells, and gefitinib, a specific EGFR inhibitor, and Dynasore, a dynamin inhibitor, both reduce EGFR endocytosis. In turn, inhibition of the MAPK pathway reduces ligand-mediated EGFR endocytosis, suggesting a potential feedback of elevated ERK activity on EGFR endocytosis. Gefitinib also decreases MAPK signaling in Sec10-overexpressing cells to levels seen in control cells and, demonstrating a causal role for EGFR, reverses the protective effect of Sec10 overexpression following cell injury in vitro. Finally, using an in vivo zebrafish model of acute kidney injury, morpholino-induced knockdown of <I>sec10</I> increases renal tubule cell susceptibility to injury. Taken together, these results suggest that the exocyst, acting through EGFR, endocytosis, and the MAPK pathway is a candidate therapeutic target for acute kidney injury.</P>