Tramadol and the occurrence of seizures: a systematic review and meta-analysis

Abstract

Introduction: Tramadol is a synthetic opioid which is commonly used around the world to relieve moderate to severe pain. One of the serious possible complications of its use is seizures. The present study aims to investigate and summarize the studies related to tramadol and occurrences of seizures after tramadol use and factors influencing these seizures.

Methodology: Our systematic review is compliant with PRISMA guidelines. Two researchers systematically searched PubMed/Medline, Web of Sciences, and Scopus. Cohort, case-control, cross-sectional studies, and clinical trials. The risk of bias was assessed using the Newcastle–Ottawa Scale After article quality assessment, a fixed or random model, as appropriate, was used to pool the results in a meta-analysis. Heterogeneity between the studies was assessed with using I-square and Q-test. Forest plots demonstrating the point and pooled estimates were drawn.

Results: A total of 51 articles with total sample size of 101 770 patients were included. The results showed that seizure event rate in the subgroups of tramadol poisoning, therapeutic dosage of tramadol, and tramadol abusers was 38% (95% CI: 27–49%), 3% (95% CI: 2–3%), 37% (95% CI: 12–62%), respectively. Tramadol dose was significantly higher in the patients with seizures than those without (mean differences: 0.82, CI 95%: 0.17–1.46). The odds for occurrence of seizures were significantly associated with male gender (pooled OR: 2.24, CI 95%: 1.80–2.77). Naloxone administration was not associated to the occurrence of seizures (pooled OR: 0.47, 95% CI: 0.15–1.49).

Conclusions: Our results demonstrate that the occurrence of seizures in patients exposed to tramadol are dose-dependent and related to male gender, but not related to naloxone administration. Given that, most of the evidence derives from studies utilizing a cross-sectional design, the association of tramadol with seizures should not be considered to be definitively established     

Prenatal exposure to misoprostol and congenital anomalies: systematic review and meta-analysis

The present systematic review was proposed with the objective of estimating the risk of congenital anomalies and other adverse events in children exposed to misoprostol during fetal life. The data source consisted of case–control studies that analyzed the effect of prenatal exposure to misoprostol on the pregnancy outcome, which were located in electronic databases and published up to June 2005. The outcomes of interest included congenital anomalies, fetal death, low birth weight and prematurity. The odds ratios (OR) for the individual studies were pooled by meta-analysis. Sensitivity tests and heterogeneity analysis were performed. Four studies involving 4899 cases of congenital anomalies and 5742 controls were included in accordance with the selection criteria. None of the studies analyzed other adverse effects from misoprostol on the outcome from gestation. Increased risks of congenital anomalies related to misoprostol use were found for any congenital defect (OR = 3.56; 95% CI: 0.98–12.98), Möbius sequence (OR = 25.31; 95% CI: 11.11–57.66) and terminal transverse limb defects (OR = 11.86; 95% CI: 4.86–28.90). In conclusion, prenatal exposure to misoprostol is associated with an increased risk of Möbius sequence and terminal transverse limb defects.     

Measles immunity in children: the 1985 national immunisation survey

In April 1985 a national immunisation survey was conducted, in the course of which blood samples were collected from approximately 3000 randomly selected children throughout the country. The study sample comprised approximately 1000 new school entrants, 1000 standard three pupils, and 1000 form four students. The sera were tested for morbilli antibody using an ELISA technique. Twenty-one percent of the five year olds lacked antibody, suggesting that an overall immunisation rate of about 80% is being achieved. Fourteen percent of the 15 year olds lacked antibody, suggesting that this rate of immunisation is partially interfering with the circulation of the wild virus. We conclude that a sizeable pool of susceptible adolescents is accumulating at a time when some wild virus activity still persists, and anticipate a shift in the peak age of measles infection from the 5-9 to the 10-15 age group. This unfortunate side effect of the national immunisation programme could be minimised by improving immunisation uptake in young childhood. Suggestions are made as to how this could be achieved.     

Hepatitis B in New Zealand children: the 1985 national immunisation survey

In April 1985 a national immunisation survey was conducted, in the course of which blood samples were collected from 3000 randomly selected children throughout the country. There were 1000 new school entrants (mean age 5 years), 1000 standard 3 pupils (mean age 10 years), and 1000 form 4 students (mean age 15 years). The sera were tested for hepatitis B surface antigen, antibody to hepatitis B surface antigen, and antibody to hepatitis B core antigen, by ELISA. The prevalence of infection rose with age until by 15 years of age 13.1% of the study population (8.2% of the European and 42.0% of the Maori children) were marker positive. At all ages, Maori children were five times more likely to be positive for any marker, and approximately thirteen times more likely to be positive for antigen (actively infected), than the European children. Even when the data had been standardised for age and race, children resident in the eastern North Island were still almost three times more at risk than children in the South Island. Children in the remaining areas of the North Island were at approximately equal degrees of risk, intermediate between the high and low endemic areas mentioned. We conclude that universal childhood immunisation is necessary to control horizontal transmission of heptatis B virus in New Zealand.     

Encephalopathy after high-dose Ifosfamide: a retrospective cohort study and review of the literature

BACKGROUND: Encephalopathy occurs in 10-40% of patients treated with high-dose ifosfamide. Proposed risk factors for encephalopathy include hepatic or renal dysfunction, brain metastases, electrolyte imbalances and drug-drug interactions. OBJECTIVE: The purpose of this retrospective cohort study and literature review was to estimate the prevalence of encephalopathy, identify characteristics associated with encephalopathy and evaluate the effectiveness of methylthioninium chloride (methylene blue) in its prevention. STUDY DESIGN AND METHODS: A total of 19 patients received high-dose ifosfamide for soft tissue sarcoma during a 4-year period at our medical centre. Eight patients developed encephalopathy based on adverse drug event (ADE) reports submitted by a clinical pharmacist. These reports incorporate the Naranjo probability scale, which is used to assess the likelihood that a change in clinical status is the result of an ADE rather than the result of other factors, such as progression of disease. The demographics, concurrent medication therapy, co-existing illnesses and laboratory parameters were documented from the medical records. We also conducted a review of the literature by searching MEDLINE (1996-October 2007). MAIN OUTCOME AND RESULTS: A total of 19 patients received high-dose ifosfamide; eight patients experienced encephalopathy (group I, 42%) and 11 patients did not experience encephalopathy (group II, 58%). More women than men developed encephalopathy (group I, 87.5% vs group II, 27.3%). Serum albumin (group I, 3.1 +/- 0.3 vs group II, 3.6 +/- 0.3 g/dL), haemoglobin (10.5 +/- 1.5 vs 12.4 +/- 1.7 g/dL) and total bilirubin (0.5 +/- 0.2 vs 0.8 +/- 0.3 mg/dL) levels were substantially lower in patients with encephalopathy, whereas the ratio of actual bodyweight to the ideal bodyweight (1.4 +/- 0.3 vs 1.1 +/- 0.2) was substantially higher in these patients. Five (62.5%) patients received a subsequent cycle of high-dose ifosfamide; all of these patients received methylthioninium chloride to minimize the risk of encephalopathy. All of these patients developed encephalopathy. Other reports have found that hypoalbuminaemia is associated with encephalopathy and that methylthioninium chloride does not prevent ifosfamide-induced encephalopathy. CONCLUSIONS: In summary, female sex, low total bilirubin, albumin and haemoglobin levels, and obesity appear to be associated with ifosfamide-induced encephalopathy. Methylthioninium chloride did not appear to prevent encephalopathy with subsequent doses of high-dose ifosfamide.     

Publication misconduct and plagiarism retractions: a systematic,retrospective study

Abstract

Objectives:

To investigate whether plagiarism is more prevalent in publications retracted from the medical literature when first authors are affiliated with lower-income countries versus higher-income countries. Secondary objectives included investigating other factors associated with plagiarism (e.g., national language of the first author’s country affiliation, publication type, journal ranking).     

Reporting quality in systematic reviews of in vitro studies: a systematic review

Background: Systematic reviews (SRs) and/or meta-analyses of in vitro research have an important role in establishing the foundation for clinical studies. In this study, we aimed to evaluate the reporting quality of SRs of in vitro studies using the PRISMA checklist.

Method: Four databases were searched including PubMed, Virtual Health Library (VHL), Web of Science (ISI) and Scopus. The search was limited from 2006 to 2016 to include all SRs and/or meta-analyses (MAs) of pure in vitro studies. The evaluation of reporting quality was done using the PRISMA checklist.

Results: Out of 7702 search results, 65 SRs were included and evaluated with the PRISMA checklist. Overall, the mean overall quality score of reported items of the PRISMA checklist was 68%. We have noticed an increasing pattern in the numbers of published SRs of in vitro studies over the last 10 years. In contrast, the reporting quality was not significantly improved over the same period (p?=?.363). There was a positive but not significant correlation between the overall quality score and the journal impact factor of the included studies.

Conclusions: The adherence of SRs of in vitro studies to the PRISMA guidelines was poor. Therefore, we believe that using reporting guidelines and journals paying attention to this fact will improve the quality of SRs of in vitro studies.     

Training in motivational interviewing: a systematic review

Motivational interviewing (MI), an evidence-based counseling approach, has received much recognition from a wide variety of health care professionals. Because of the rising interest in MI, there is increasing demand for training in this counseling approach. The MI training community has answered this call and as a result placed much emphasis on studying the MI training process. The purpose of this article is to provide a systematic review of the published research on MI training. Our goal is to provide a consolidated account of MI trainings outlining the populations receiving training, methods used, and training outcomes. We also identify which aspects of the (W. R. Miller & T. B. Moyers, 2006) eight stages of learning MI each study addressed. Recommendations for advancing the MI training research are highlighted.     

Pharmacogenetics in colorectal cancer: a systematic review

Pharmacological treatment of colorectal cancer has improved survival rates in recent years. Individual genetic variation in genes associated with metabolism and targets of commonly used drugs can be responsible for variability in treatment outcome and toxicity. Diverse study designs have been used and heterogeneous end points evaluated by studies assessing the association of genetic markers with treatment outcome. We conducted this systematic review, including 51 studies, to present a comprehensive overview and draw further conclusions. To facilitate comparison of reported study results, risk estimates for observed genetic variants in 33 key genes are presented using defined reference categories and recalculated risk estimates based on data provided in original publications, where necessary. Overall, evidence indicates associations of the UGT1A1(*) 28 variant genotype with toxicity after irinotecan treatment, mutations in GSTP1-105 with improved treatment outcome and the XPD-751 variant genotype with poor treatment outcome after oxaliplatin treatment, and amplification of the EGFR gene with improved treatment outcome after therapy with monoclonal antibodies. Adequately powered prospective investigations designed specifically for pharmacogenetics are needed.     

Dopamine in anorexia nervosa: a systematic review

Anorexia nervosa (AN) is a chronic relapsing psychiatric disorder with a largely unknown pathophysiology. Dopamine has been implicated in the pathophysiology of the disorder by preclinical and clinical evidence. Preclinical studies have examined two main characteristics of AN: reduction in food intake (diet restriction) and hyperactivity. Diet restriction has been associated with reduced dopamine levels in the hypothalamus, hippocampus, and the dorsal striatum. Animal hyperactivity following diet restriction has been linked to increased dopamine in the hypothalamus. Increased dopamine in the nucleus accumbens was associated with food administration, but not food expectation. Tyrosine and dopaminergic antagonists normalized anorexia-like behaviors in animal models of AN, but did not restore body weight. Clinical studies on the etiology of AN have produced contradictory findings. Cerebrospinal fluid concentrations of dopamine and its metabolites have been reported to be decreased or normal under conditions of low weight, whereas they tended to normalize when the weight was restored. Plasma and urinary levels of dopamine and its metabolites have been found to be normal, increased, and decreased. Neuroendocrine studies suggest that dopaminergic neurotransmission is increased in AN. However, recent neuroimaging studies lend support to the increase in binding of dopaminergic receptors in the striatum, which favors the opposite theory that intrasynaptic dopamine is indeed decreased. Genetic studies implicate dopamine D2 receptors, the dopamine transporter, and the enzyme COMT. There are promising results with respect to the use of atypical antipsychotics against symptoms of AN beyond weight gain, but further trials are required.     

Nano-hydroxyapatite use in dentistry: a systematic review

Abstract

Nano-hydroxyapatite (nano-HA) is a material with multiple uses due to its biocompatibility and its resemblance to the nonorganic bone structure. It is used in various dental domains such as implantology, surgery, periodontology, esthetics and prevention. The aim of this study is to provide a wide understanding of nano-HA and to promote treatments based on nanomaterials in dentistry. A search in two data bases, Scopus, and PubMED, was conducted over a 5?years period. We chose a 5?years period because this revealed the most recent published studies with the key words ‘nano-HA’ and ‘dentistry’. A number of 32 studies were included in this systematic review. In implantology the main use of nano-HA was as a coating material for titanium implants and its effect was assessed in the matter of osteointegration and inflammatory response as well as antibacterial activity. In tissue engineering the use of nano-HA was directed to surgery and periodontology and this material was assessed mainly as a grafting material. In esthetics and prevention its use was mainly focused on dentinal hypersensitivity treatment, remineralizing potential and as bleaching co-agent. Nano-HA is a relatively novel material with outstanding physical, chemical, mechanical and biological properties that makes it suitable for multiple interventions. It outperformed most of the classic materials used in implantology and surgery but it should be further investigated for bone engineering and caries prevention therapy.     

Serotonergic genes and suicide: A systematic review

Suicide is one of the leading causes of death in the world. Its aetiology is complex and diverse, however, epidemiological studies show that suicidal behavior is partly heritable. Neurobiological evidence implicates serotonergic dysfunction in suicidality, stimulating genetic research to focus on genes related to the serotonergic system. In this paper, we review evidence from studies examining the association between various serotonergic genes (Tryptophan Hydroxylase genes: TPH1; TPH2, Serotonin Transporter gene: 5-HTTLPR in SLC6A4, Serotonin Receptor genes: HTR1A, HTR2A, HTR1B, HTR2C and Monoamine Oxidase A gene: MAOA) and suicidal behavior. The data show associations between variation on the TPH1 gene and 5-HTTLPR gene and violent suicidal behavior in Caucasian populations, with the least inconsistencies. Results are mixed for the TPH2 gene and serotonin receptor genes, but for some genes, studies that include haplotypic analyses or that examine a larger coding region of the genes tend to provide more reliable results. Findings on endophenotypes of suicidality, such as aggression and impulsivity traits, show positive associations for the TPH1, HTR2A, and MAOA genes, but need further replication, since negative associations are also occasionally reported. Since genes can only partially explain suicidal risk, several studies during the past decade have tried to incorporate environmental factors in the susceptibility model. Studies to date show that variation on the 5-HTTLPR, MAOA and HTR2A gene can interact with stressful life events to increase risk for suicidal behavior. Limitations of case-control studies are discussed and future considerations are put forward with regard to endophenotypic measurements and gene–environment interactions.