Background Drug reaction with eosinophilia and systemic symptoms syndrome (DRESS) is a delayed infrequent potentially lifethreatening idiosyncratic drug reaction. Aromatic anticonvulsants and allopurinol are the most frequent causative agents. However, various reports of antibiotic-induced DRESS are available. In this review, we try to summarize reports of antibacterial antibiotic-induced DRESS focusing on characteristics of DRESS induced by each antibiotic group. Methods The data were collected by searching PubMed/MEDLINE and ScienceDirect. The keywords used as search terms were "DRESS syndrome," "drug-induced hypersensitivity syndrome (DIHS)," "antibiotics," "antimicrobial," and names of various antimicrobial groups. Finally, 254 relevant cases with a definite or probable diagnosis of DRESS based on RegiSCAR criteria were found until 30 May 2020 and reviewed. Results and conclusion Totally, 254 cases of antibacterial antibiotic-induced DRESS are reported. Most of them are related to antituberculosis drugs, vancomycin, and sulfonamides, respectively. Rash and fever were most frequent clinical findings. Eosinophilia and liver injury were the most reported hematologic and visceral organ involvement, respectively. Most of the patients are managed with systemic corticosteroids. The death occurred in 16 patients which most of them experienced liver or lung involvement. The reactivation of various viruses especially HHV-6 is reported in 33 cases. The mean latency period was 29 days. It is necessary to perform thorough epidemiological, genetic, and immunological studies, also systematic case review and causality assessment, as well as well-designed clinical trials for better management of antibiotic-induced DRESS.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) is the reason for this ongoing pandemic infection diseases termed coronavirus disease 2019 (COVID-19) that has emerged since early December 2019 in Wuhan City, Hubei Province, China. In this century, it is the worst threat to international health and the economy. After 4 months of COVID-19 outbreak, there is no certain and approved medicine against it. In this public health emergency, it makes sense to investigate the possible effects of old drugs and find drug repositioning that is efficient, economical, and riskless process. Old drugs that may be effective are from different pharmacological categories, antimalarials, anthelmintics, anti-protozoal, anti-HIVs, anti-influenza, antihepacivirus, antineoplastics, neutralizing antibodies, immunoglobulins, and interferons. In vitro, in vivo, or preliminary trials of these drugs in the treatment of COVID-19 have been encouraging, leading to new research projects and trials to find the best drug/s. In this review, we discuss the possible mechanisms of these drugs against COVID-19. Also, it should be mentioned that in this manuscript, we discuss preliminary rationales; however, clinical trial evidence is needed to prove them. COVID-19 therapy must be based on expert clinical experience and published literature and guidelines from major health organizations. Moreover, herein, we describe current evidence that may be changed in the future.

Acute severe carbon monoxide (CO) poisoning induces hypoxia that leads to cardiovascular and nervous systems disturbances. Different complex mechanisms lead to CO neurotoxicity including lipid peroxidation, inflammatory and immune-mediated reactions, myelin degeneration and finally neuronal apoptosis and necrosis. Granulocyte colony-stimulating factor (G-CSF) is considered to be a novel neuroprotective agent. In this study, we evaluated the efficacy of G-CSF therapy on CO neurotoxicity in rats with acute CO poisoning. Rats were exposed to 3000 ppm CO in air (0.3%) for 1 h, and then different doses (50,100, and 150 µg/kg) of G-CSF or normal saline were administrated intraperitoneally. Water content of brain as an indicator for total edema and blood brain barrier integrity (Evans blue extravasation) were evaluated. Malondialydehyde was determined in order to evaluate the effect of G-CSF on CO-induced lipid peroxidation in brain tissues. Also, the effect of G-CSF on myeloperoxidase activity in the brain tissue was evaluated. The effect of G-CSF administration on induced apoptosis in the brain was measured using TUNEL method. To evaluate the level of MBP, STAT3 and pSTAT3 and HO-1 proteins and the effect of G-CSF on these proteins Western blotting was carried out. G-CSF reduced water content of the edematous poisoned brains (100 µg/kg) and BBB permeability (100 and 150 µg/kg) (P < 0.05). G-CSF (150 µg/kg) reduced the MDA level in the brain tissues (P < 0.05 as compared to CO poisoned animals). G-CSF did not decrease the MPO activity after CO poisoning in any doses. G-CSF significantly reduced the number of apoptotic neurons and Caspase 3 protein levels in the brain. Western blotting results showed that G-CSF treatment enhanced expression of HO-1 and MBP, STAT3 and pSTAT3 proteins in the brain tissues. Based on our results, a single dose of G-CSF immediately after CO poisoning significantly attenuates CO neurotoxicity via different mechanisms. © 2015 Wiley Periodicals, Inc. Environ Toxicol 32: 37-47, 2017.

Obesity is an important feature of the metabolic syndrome and is associated with an increased risk of type 2 diabetes mellitus, cardiovascular disease, and some cancers. The aim of this study was to determine the relationship between body fat percentage and an imbalance of the prooxidant/antioxidant balance (PAB), serum superoxide dismutase (SOD1) and inflammation (serum hs‐CRP) and increase risk of metabolic syndrome and diabetes mellitus. In this study, 9154 individuals were recruited as part of the Mashhad Stroke and Heart Association Disorder (MASHAD) study. Subjects were categorized into two groups according to body fat percentage as defined >25% in male and > 30% in female, according to gender. Biochemical factors, including serum PAB, SOD1, and hs‐CRP were measured in all subjects. SPSS version 18 was used for statistical analyses for all. GraphPad Prism 6 for figures was used. Of total number of subjects (9154), 6748 (73.7%) were found to have a high body fat (BF) percentage. Serum hs‐CRP and PAB were significantly higher in individuals with a high BF percentage (P < 0.05) but SOD1 was not significantly different between the two groups (P > 0.05). BF percentage, serum PAB and serum hs‐CRP were significantly higher in individuals with metabolic syndrome and diabetes versus those without metabolic syndrome and diabetes mellitus (P < 0.05), however serum SOD1 was significantly lower in individuals with metabolic syndrome (P < 0.005). Oxidative stress and inflammation are two factors that may link the presence of high BF percentage with the development of metabolic syndrome, diabetes, and cardiovascular disease. © 2018 BioFactors, 45(1):35–42, 2019

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High‐density lipoprotein (HDL) function rather than level may better predict cardiovascular disease (CVD). However, the contribution of the impaired antioxidant function of HDL that is associated with increased HDL lipid peroxidation (HDLox) to the development of clinical CVD remains unclear. We have investigated the association between serum HDLox with incident CVD outcomes in Mashhad cohort. Three‐hundred and thirty individuals who had a median follow‐up period of 7 years were recruited as part of the cohort. The primary end point was cardiovascular event, including myocardial infarction, stable angina, unstable angina, or coronary revascularization. In both univariate/multivariate analyses adjusted for traditional CVD risk factors, HDLox was an independent risk factor for CVD (odds ratio, 1.62; 95% confidence interval, 1.41–1.86; p < 0.001). For every increase in HDLox by 0.1 unit, there was an increase in CVD risk by 1.62‐fold. In an adjusted analysis, there was a >2.5‐fold increase in cardiovascular risk in individuals with HDLox higher than cutoff point of 1.06 compared to those with lower scores, suggesting HDLox > 1.06 is related to the impaired HDL oxidant function and in turn exposed to elevated risk of CVD outcomes (hazard ratio, 2.72; 95% CI, 1.88–3.94). Higher HDLox is a surrogate measure of reduced HDL antioxidant function that positively associated with cardiovascular events in a population‐based cohort.

This study, to the best of our knowledge, showed for the first time that intraperitoneal administration of carbamazepine at clinically comparable doses during organogenesis can induce several eye malformations in mice. The implication of these results needs to be considered when carbamazepine is administered during human pregnancy.

IntroductionCopper (Cu) and zinc (Zn) are important trace elements that are also structural ions of superoxide dismutase (SOD), which reduce oxidative stress. Zinc deficiency and excess copper have been reported to be associated with inflammation. The human T-lymphotropic virus type 1 (HTLV-1) is a retrovirus, which is believed to cause systemic inflammation. The aim of this study is to measure levels of Zn, Cu, SOD, and prooxidant–antioxidant balance (PAB) in HTLV-1-positive patients and investigate the association between serum Zn and Cu concentrations and levels of oxidative stress in them.MethodsThe serum samples of 1,116 subjects who had participated in the “Mashhad Stroke and Heart Atherosclerotic Disorder” study, including 279 HTLV-1-positive and 837 HTLV-1-negative patients, were used. Levels of Zn, Cu, SOD, and PAB were measured.ResultsZinc and SOD levels were lower in the HTLV-1-positive group; however, the difference was statistically significant only for the level of SOD (P=0.003). On the other hand, levels of copper and PAB were significantly higher in HTLV-1 positive subjects; P=0.004 and P=0.002, respectively.ConclusionIn HTLV-infected patients, serum Zn concentration is lower and Cu concentration is higher than healthy controls. This altered situation might be either primary or secondary to HTLV-1 infection, which should be investigated in larger studies. We showed that SOD is significantly lower in HTLV-1-infected subjects. As in some other viruses that evolve different mechanisms to potentiate virus replication by changing the physiologic condition of host cells, HTLV-1 too probably decreases the activity of copper–zinc SOD1 by suppressing its gene.