ABSTRACT
Rebound pain (RP) remains a challenge in ambulatory surgery, characterized by severe pain upon resolution of a peripheral nerve block (PNB). Intravenous (IV) administration of Dexamethasone (DEXA) potentiates PNB analgesic effect and reduces RP incidence although preventive effective dose remains undetermined. This retrospective analysis evaluates the preventive effect of IV DEXA on RP in outpatients undergoing upper limb surgery under axillary block. DEXA was divided into high (HD > 0.1 mg/kg) or low (LD < 0.1 mg/kg) doses. RP was defined as severe pain (NRS ≥ 7/10) within 24 h of PNB resolution. DEXA HD and LD patients were matched with control patients without DEXA (n = 55) from a previous randomized controlled study. Records of 118 DEXA patients were analyzed (DEXA dose ranged from 0.05 to 0.12 mg/kg). Intraoperative IV DEXA was associated with a significant reduction of the pain felt when PNB wore off as well as to a significant reduction of RP incidence (n = 27/118, 23% vs. 47% in controls, p = 0.002) with no effect related to the dose administered (p = 0.053). Our results support the administration of intraoperative DEXA as a preventive measure to reduce the occurrence of RP.
ABSTRACT
BACKGROUND: Kisspeptin (encoded by the KISS1 gene in humans) is an excitatory neuromodulatory peptide implicated in multiple homeostatic systems, including anti-oxidation, glucose homeostasis, nutrition, locomotion, etc. Therefore, in the current obesity epidemic, kisspeptin is gaining increasing interest as a research objective. AIM: To construct an updated interactome of genetic obesity, including the kisspeptin signal transduction pathway. METHODS: Kisspeptin and obesity-related genes or gene products were extracted from the biomedical literature, and a network of functional associations was created. RESULTS: The generated network contains 101 nodes corresponding to gene/gene products with known and/or predicted interactions. In this interactome, KISS1 and KISS1R are connected directly to the luteinizing hormone receptor (LHCGR), gonadotropin-releasing hormone receptor (GNRH1), and indirectly, through the latter, to proopiomelanocortin (POMC), glucagon, leptin (LEP), and/or pro-protein convertase subtilisin/kexin-type 1 (PCSK1), all of which are critically implicated in obesity disorders. CONCLUSIONS: Our updated obesidome includes kisspeptin and its connections to the genetic obesity signalosome with 12 major hubs: glucagon (GCG), insulin (INS), arginine vasopressin (AVP), G protein subunit beta 1 (GNB1) and proopiomelanocortin (POMC), melanocortin 4 receptor (MC4R), leptin (LEP), gonadotropin-releasing hormone 1 (GNRH1), adrenoceptor beta 2 and 3 (ADRB2-3), glucagon-like peptide 1 receptor (GLP1R), and melanocortin 3 receptor (MC3R) genes were identified as major "hubs" for genetic obesity, providing novel insight into the body's energy homeostasis.
