Methaemoglobinaemia Associated With Mixed Cocaine and Amphetamine Overdose: A Case Report.

Methaemoglobinaemia is a rare disorder characterized by increased levels of methaemoglobin, a form of haemoglobin with oxidized iron that cannot efficiently bind oxygen. This leads to inadequate oxygen delivery to tissues with various clinical manifestations from asymptomatic to severe persistent hypoxia, CNS symptoms, and cardiovascular collapse. Acquired methaemoglobinaemia is typically a sudden condition, often resulting from poisoning by specific drugs and compounds, which can potentially have fatal consequences. We present a case of a patient who came with severe methaemoglobinaemia due to intoxication with cocaine and amphetamine.

Perioperative use of ketamine infusion versus dexmedetomidine infusion for analgesia in obese patients undergoing bariatric surgery: a double-blinded three-armed randomized controlled trial.

BACKGROUND: Bariatric surgery depends on the development of novel anesthetic techniques to reduce the incidence of complications and improve postoperative outcomes. Ketamine and dexmedetomidine have been used for perioperative analgesia and we hypothesized that they would decrease postoperative morphine requirements. The objective of this trial is to study whether choice of ketamine or dexmedetomidine infusion would affect postoperative total morphine consumption. METHODS: Ninety patients were equally randomized into three groups. The ketamine group received a bolus dose (0.3 mg/kg) of ketamine over 10 min, followed by an infusion of the same drug (0.3 mg/kg/h). The dexmedetomidine group received a bolus dose (0.5 mcg/kg) of dexmedetomidine over 10 min, followed by an infusion of this drug (0.5 mg/kg/h). The control group received a saline infusion. All infusions were given till 10 min before the end of surgeries. Intraoperative fentanyl was given when patient developed hypertension and tachycardia despite adequate anesthesia and muscle relaxation. Postoperative pain was managed by a rescue dose of 4 mg of IV morphine, with a minimum interval of 6 h between morphine doses if the numerical rating scale (NRS) score was ≥ 4. The primary outcome was the total morphine dose, and the secondary outcomes were intraoperative fentanyl requirement, time to extubation, postoperative nausea and vomiting (PONV), NRS scores, and modified observer's agitation/sedation scale (MOASS) scores. RESULTS: Compared with ketamine, dexmedetomidine decreased the need for fentanyl intraoperatively (160 ± 42 µg), shortened the time to extubation (3 ± 1 min), and improved MOASS and PONV scores. In turn, ketamine decreased postoperative NRS scores and the need for morphine (3 ± 3 mg). CONCLUSIONS: Dexmedetomidine treatment was associated with lower fentanyl doses, a shorter time to extubation, and better MOASS and PONV scores. Ketamine treatment was associated with significantly lower NRS scores and morphine doses. These results indicated that dexmedetomidine effectively decreased intraoperative fentanyl requirement and the time to extubation, while ketamine decreased the need for morphine. TRIAL REGISTRATION: This trail was registered on the clinicaltrials.gov registry (NCT04576975) on October 6, 2020.

The effects of adjunctive use of a desiccant agent in the treatment of stage III periodontitis (Randomized controlled clinical trial).

Introduction: Several bacterial species inhabiting the dental plaque biofilms are associated with periodontitis. Objective: The main objective of this study was to compare the efficacy of the desiccant agent HYBENX (HBX) as an adjunct to scaling and root planning (SRPX) versus scaling and root planning (SRP) alone in the treatment of periodontitis. Materials and Methods: The study sample comprised 25 patients with periodontitis stage Ш (grades A and B). Each maxillary quadrant was randomly allocated to two groups: SRPX group, including 25 quadrants treated with SRP plus HYBENX, and SRP group, including 25 quadrants treated with SRP alone. The following clinical periodontal parameters were recorded at baseline (immediately after treatment, T0), and 1 month (T1), 3 months (T3), and 6 months (T6) after treatment: probing pocket depth (PPD), relative attachment level (RAL), plaque index (PLI), gingival index (GI), gingival height (GH), and bleeding on probing index (BOP). Results: Comparisons within each study group showed that all clinical parameters significantly improved (P < 0.001) at all follow-up intervals. In contrast, a statistically significant difference (P < 0.001) was observed in RAL, PPD, BOP, and GI indices at all follow-up intervals between the SRPX and SRP groups. In contrast, no significant differences (P > 0.05) were found in GH and PLI between the study groups. Conclusion: Both treatment groups showed improved periodontal parameters. However, applying desiccant gel as an adjunct to SRP was significantly effective in the treatment of stage III periodontitis.

MicroRNA Expression Influences Methylmercury-Induced Lipid Accumulation and Mitochondrial Toxicity in Caenorhabditis elegans.

Metabolic effects of methylmercury (MeHg) are gaining wider attention. We have previously shown that MeHg causes lipid dysregulation in Caenorhabditis elegans (C. elegans), leading to altered gene expression, increased triglyceride levels and lipid storage, and altered feeding behaviors. Transcriptional regulators, such as transcription factors and microRNAs (miRNAs), have been shown to regulate lipid storage, serum triglycerides, and adipogenic gene expression in human and rodent models of metabolic diseases. As we recently investigated adipogenic transcription factors induced by MeHg, we were, therefore, interested in whether MeHg may also regulate miRNA sequences to cause metabolic dysfunction. Lipid dysregulation, as measured by triglyceride levels, lipid storage sites, and feeding behaviors, was assessed in wild-type (N2) worms and in transgenic worms that either were sensitive to miRNA expression or were unable to process miRNAs. Worms that were sensitive to the miRNA expression were protected from MeHg-induced lipid dysregulation. In contrast, the mutant worms that were unable to process miRNAs had exacerbated MeHg-induced lipid dysregulation. Concurrent with differential lipid homeostasis, miRNA-expression mutants had altered MeHg-induced mitochondrial toxicity as compared to N2, with the miRNA-sensitive mutants showing mitochondrial protection and the miRNA-processing mutants showing increased mitotoxicity. Taken together, our data demonstrate that the expression of miRNAs is an important determinant in MeHg toxicity and MeHg-induced metabolic dysfunction in C. elegans.

Methylmercury-Induced Metabolic Alterations in Caenorhabditis elegans Are Diet-Dependent.

Methylmercury (MeHg) is a well-known neurotoxicant; however, its role in metabolic diseases has been gaining wider attention. Chronic exposure to MeHg in human populations shows an association with diabetes mellitus and metabolic syndrome (MS). As the incidences of both obesity and MS are on the rise globally, it is important to understand the potential role of MeHg in the development of the disease. There is a dearth of information on dietary interactions between MeHg and lipids, which play an important role in developing MS. We have previously shown that MeHg increases food seeking behaviors, lipid levels, fat storage, and pro-adipogenic gene expression in C. elegans fed the standard OP50 Escherichia coli diet. However, we hypothesized that these metabolic changes could be prevented if the worms were fed a bacterial diet lower in lipid content. We tested whether C. elegans developed metabolic alterations in response to MeHg if they were fed two alternative E. coli strains (HT115 and HB101) that are known absorb significantly less lipids from their media. Additionally, to explore the effect of a high-lipid and high-cholesterol diet on MeHg-induced metabolic dysfunction, we supplemented the OP50 strain with twice the standard concentration of cholesterol in the nematode growth media. Wild-type worms fed either the HB101 or HT115 diet were more resistant to MeHg than the worms fed the OP50 diet, showing a significant right-hand shift in the dose-response survival curve. Worms fed the OP50 diet supplemented with cholesterol were more sensitive to MeHg, showing a significant left-hand shift in the dose-response survival curve. Changes in sensitivity to MeHg by differential diet were not due to altered MeHg intake in the worms as measured by inductively coupled mass spectrometry. Worms fed the low-fat diets showed protection from MeHg-induced metabolic changes, including decreased food consumption, lower triglyceride content, and lower fat storage than the worms fed either of the higher-fat diets. Oxidative stress is a common characteristic of both MeHg exposure and high-fat diets. Worms fed either OP50 or OP50 supplemented with cholesterol and treated with MeHg had significantly higher levels of reactive oxygen species, carbonylated proteins, and loss of glutathione than the worms fed the HT115 or HB101 low-lipid diets. Taken together, our data suggest a synergistic effect of MeHg and dietary lipid levels on MeHg toxicity and fat metabolism in C. elegans, which may affect the ability of MeHg to cause metabolic dysfunction.