scholarly journals The Serotonin Syndrome: From Molecular Mechanisms to Clinical Practice

2019 ◽  
Vol 20 (9) ◽  
pp. 2288 ◽  
Author(s):  
James Francescangeli ◽  
Kunal Karamchandani ◽  
Meghan Powell ◽  
Anthony Bonavia
Keyword(s):  
Serotonin Syndrome ◽  
Molecular Mechanisms ◽  
Fatal Outcome ◽  
Major Depressive ◽  
Number Of Patients ◽  
Molecular Context ◽  
Life Threatening ◽  
Clinical Conditions ◽  
Pharmacologic Agents ◽  
Stimulation Of

The serotonin syndrome is a medication-induced condition resulting from serotonergic hyperactivity, usually involving antidepressant medications. As the number of patients experiencing medically-treated major depressive disorder increases, so does the population at risk for experiencing serotonin syndrome. Excessive synaptic stimulation of 5-HT2A receptors results in autonomic and neuromuscular aberrations with potentially life-threatening consequences. In this review, we will outline the molecular basis of the disease and describe how pharmacologic agents that are in common clinical use can interfere with normal serotonergic pathways to result in a potentially fatal outcome. Given that serotonin syndrome can imitate other clinical conditions, an understanding of the molecular context of this condition is essential for its detection and in order to prevent rapid clinical deterioration.

scholarly journals Experimental Serotonin Syndrome: Effects of GABA-ergic Medications and 5-HT2-Antagonists

2021 ◽  
Author(s):  
Rumen Nikolov ◽  
Kalina Koleva
Keyword(s):  
Animal Models ◽  
Mental Status ◽  
Autonomic Dysfunction ◽  
Serotonin Receptors ◽  
Serotonin Syndrome ◽  
Drug Effect ◽  
Adverse Drug Effect ◽  
Combined Administration ◽  
Life Threatening ◽  
Stimulation Of

Serotonin syndrome (SS) is a potentially life-threatening adverse drug effect that occurs after an overdose or combined administration of two or more drugs that increase the serotonin levels. In humans, SS is represented by a triad of symptoms including mental status changes, neuromuscular hyperactivity and autonomic dysfunction. The manifestations of the syndrome observed in rodents resemble the symptoms of SS in humans. Theoretically, SS can occur as a result of stimulation of any of the seven families of the serotonin receptors. However, most data support the involvement of 5-HT1A and 5-HT2A receptors. A number of studies indicate the effectiveness of 5-HT2 antagonists and GABA-ergic agents in the treatment of the hyperthermia and other symptoms of SS in rats. Therefore, animal models of SS may help to further elucidate the mechanism of its development and the possibilities for its treatment.

scholarly journals Transient Serotonin Syndrome by Concurrent Use of Electroconvulsive Therapy and Selective Serotonin Reuptake Inhibitor: A Case Report and Review of the Literature

2012 ◽  
Vol 2012 ◽  
pp. 1-3 ◽  
Author(s):  
Nagahisa Okamoto ◽  
Kota Sakamoto ◽  
Maki Yamada
Keyword(s):  
Electroconvulsive Therapy ◽  
Serotonin Syndrome ◽  
Neurological Symptoms ◽  
Major Depressive ◽  
Autonomic Nervous ◽  
Concurrent Use ◽  
Initial Session ◽  
Rare Side Effect ◽  
The Central Nervous System ◽  
Stimulation Of

The serotonin syndrome, which is characterized by psychiatric, autonomic nervous and neurological symptoms, is considered to be caused by excessive stimulation of the 5-HT1A and 5-HT2 receptors in the gray matter and spinal cord of the central nervous system, after the start of dosing or increase of the dose of a serotoninergic drug. There have been hardly any reports of induction of serotonin syndrome by electroconvulsive therapy (ECT) in combination with antidepressant. We present the case of a female patient with major depressive disorder (MDD) who developed transient serotonin syndrome soon after the first session of ECT in combination with paroxetine. Paroxetine was discontinued, and her psychiatric, autonomic nervous and neurological symptoms were gradually relieved and disappeared within 2 days. We performed the second ECT session 5 days after the initial session and performed 12 sessions of ECT without any changes in the procedure of ECT and anesthesia, but no symptoms of SS were observed. Finally, her MDD remitted. ECT might cause transiently increased blood-brain barrier (BBB) permeability and enhance the transmissivity of the antidepressant in BBB. Therefore, it is necessary to pay attention to rare side effect of serotonin syndrome by ECT in combination with antidepressant.

scholarly journals Clinical Relevance of Pharmacogenetics in Serotonin Syndrome

2020 ◽  
Vol 2020 ◽  
pp. 1-7 ◽  
Author(s):  
Dehuti Pandya ◽  
My Tran ◽  
Monica Verduzco-Gutierrez
Keyword(s):  
Serotonin Syndrome ◽  
Low Dose ◽  
Genetic Profile ◽  
Threatening Condition ◽  
Life Threatening ◽  
Additive Risk ◽  
Serotonergic Drugs ◽  
Higher Doses ◽  
Dose Change ◽  
Stimulation Of

Serotonin syndrome is a predictable life-threatening condition that is caused by serotonergic stimulation of the central and peripheral nervous systems. A patient’s genetic profile can amplify exposure risk as many serotonergic drugs are metabolized by CYP450 enzymes, and these enzymes may be altered in functionality. We report a case of an elderly man who presented with serotonin syndrome after a dose change in valproic acid 5 weeks prior. His medication list consisted of low-dose serotonergic agents, which is unusual as most cases of serotonin syndrome involve higher doses. A review of his pharmacogenetic profile is presented to retrospectively evaluate the additive risk for serotonin syndrome and implications on resuming serotonergic agents.

Clinical Significance of Lung Uptake in Liver Scanning

1986 ◽  
Vol 25 (01) ◽  
pp. 15-18 ◽  
Author(s):  
M. Luostarinen ◽  
M Vorne ◽  
T. Lantto
Keyword(s):  
Clinical Significance ◽  
Final Diagnosis ◽  
Reticuloendothelial System ◽  
Liver Imaging ◽  
Lung Uptake ◽  
Benign Diseases ◽  
Number Of Patients ◽  
Liver Image ◽  
Liver Scanning ◽  
Stimulation Of

Summary 99mTc tin colloid accumulated in the lungs in 102 patients during liver imaging both in malignant and benign diseases. The percentage of neoplastic diseases increased when the lung uptake became greater and only patients with malignant final diagnosis had marked lung uptake. Abnormal liver image was seen only in 23%, which disagrees highly with some earlier findings on a rather small number of patients. The cause of increased lung uptake was suggested to be the activation of the reticuloendothelial system (RES) by disease. The activation of the RES was stronger in malignant than in benign diseases. Some type of regional stimulation of the RES was suggested as being due to the location of the disease and both malignant and benign diseases of the chest region stimulated the pulmonary part of the RES more than other parts of the RES.

Ion Channel Remodelling in Atrial Fibrillation

2011 ◽  
Vol 7 (2) ◽  
pp. 97 ◽  
Author(s):  
Niels Voigt ◽  
Dobromir Dobrev ◽  
◽  
Keyword(s):  
Atrial Fibrillation ◽  
Ion Channel ◽  
Antiarrhythmic Drugs ◽  
Current Knowledge ◽  
Bleeding Complications ◽  
Large Size ◽  
Cardiovascular Morbidity And Mortality ◽  
Number Of Patients ◽  
Life Threatening ◽  
Underlying Mechanisms

Atrial fibrillation (AF) is the most common arrhythmia and is associated with substantial cardiovascular morbidity and mortality, with stroke being the most critical complication. Present drugs used for the therapy of AF (antiarrhythmics and anticoagulants) have major limitations, including incomplete efficacy, risks of life-threatening proarrhythmic events and bleeding complications. Non-pharmacological ablation procedures are efficient and apparently safe, but the very large size of the patient population allows ablation treatment of only a small number of patients. These limitations largely result from limited knowledge about the underlying mechanisms of AF and there is a hope that a better understanding of the molecular basis of AF may lead to the discovery of safer and more effective therapeutic targets. This article reviews the current knowledge about AF-related ion-channel remodelling and discusses how these alterations might affect the efficacy of antiarrhythmic drugs.

Periodontal Pathogens and Neuropsychiatric Health

2020 ◽  
Vol 20 (15) ◽  
pp. 1353-1397 ◽  
Author(s):  
Abhishek Wadhawan ◽  
Mark A. Reynolds ◽  
Hina Makkar ◽  
Alison J. Scott ◽  
Eileen Potocki ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Metabolic Diseases ◽  
Low Grade ◽  
Periodontal Pathogens ◽  
Synergistic Interactions ◽  
Brain Vasculature ◽  
Micro Rnas ◽  
Clinical Conditions ◽  
Low Grade Inflammation ◽  
Neuropsychiatric Illness

Increasing evidence incriminates low-grade inflammation in cardiovascular, metabolic diseases, and neuropsychiatric clinical conditions, all important causes of morbidity and mortality. One of the upstream and modifiable precipitants and perpetrators of inflammation is chronic periodontitis, a polymicrobial infection with Porphyromonas gingivalis (P. gingivalis) playing a central role in the disease pathogenesis. We review the association between P. gingivalis and cardiovascular, metabolic, and neuropsychiatric illness, and the molecular mechanisms potentially implicated in immune upregulation as well as downregulation induced by the pathogen. In addition to inflammation, translocation of the pathogens to the coronary and peripheral arteries, including brain vasculature, and gut and liver vasculature has important pathophysiological consequences. Distant effects via translocation rely on virulence factors of P. gingivalis such as gingipains, on its synergistic interactions with other pathogens, and on its capability to manipulate the immune system via several mechanisms, including its capacity to induce production of immune-downregulating micro-RNAs. Possible targets for intervention and drug development to manage distal consequences of infection with P. gingivalis are also reviewed.

Haemophagocytic Lymphohistiocytosis (HLH) in a case of Enteric Fever

2016 ◽  
Vol 5 (03) ◽  
pp. 4882
Author(s):  
Vineeta Pande ◽  
Agarkhedkar S. R. ◽  
Ayank Tandon* ◽  
Aditya Agarwal
Keyword(s):  
Inflammatory Reaction ◽  
Enteric Fever ◽  
Infectious Agent ◽  
Clinical Syndrome ◽  
Haemophagocytic Lymphohistiocytosis ◽  
Life Threatening ◽  
Stimulation Of

HLH is an uncommon, life threatening clinical syndrome cause by a severe hyper inflammatory reaction triggered by an infectious agent. The characteristic symptoms of HLH are due to the persistent stimulation of lymphocytes and histiocytes, leading to hyper-cytokinemia. We report a case of HLH in enteric fever in a13 year old female presenting with fever, lymphadenopathy and pancytopenia due an infection caused by Salmonella.

scholarly journals Impairing flow-mediated endothelial remodeling reduces extravasation of tumor cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Gautier Follain ◽  
Naël Osmani ◽  
Valentin Gensbittel ◽  
Nandini Asokan ◽  
Annabel Larnicol ◽  
...  
Keyword(s):  
Blood Flow ◽  
Tumor Cells ◽  
Molecular Mechanisms ◽  
Metastatic Progression ◽  
Metastatic Dissemination ◽  
Secondary Tumors ◽  
Flow Profiles ◽  
Endothelial Response ◽  
Life Threatening

AbstractTumor progression and metastatic dissemination are driven by cell-intrinsic and biomechanical cues that favor the growth of life-threatening secondary tumors. We recently identified pro-metastatic vascular regions with blood flow profiles that are permissive for the arrest of circulating tumor cells. We have further established that such flow profiles also control endothelial remodeling, which favors extravasation of arrested CTCs. Yet, how shear forces control endothelial remodeling is unknown. In the present work, we aimed at dissecting the cellular and molecular mechanisms driving blood flow-dependent endothelial remodeling. Transcriptomic analysis of endothelial cells revealed that blood flow enhanced VEGFR signaling, among others. Using a combination of in vitro microfluidics and intravital imaging in zebrafish embryos, we now demonstrate that the early flow-driven endothelial response can be prevented upon specific inhibition of VEGFR tyrosine kinase and subsequent signaling. Inhibitory targeting of VEGFRs reduced endothelial remodeling and subsequent metastatic extravasation. These results confirm the importance of VEGFR-dependent endothelial remodeling as a driving force of CTC extravasation and metastatic dissemination. Furthermore, the present work suggests that therapies targeting endothelial remodeling might be a relevant clinical strategy in order to impede metastatic progression.

scholarly journals Pathophysiology of Atherosclerotic Plaque Development-Contemporary Experience and New Directions in Research

2021 ◽  
Vol 22 (7) ◽  
pp. 3513
Author(s):  
Michal Kowara ◽  
Agnieszka Cudnoch-Jedrzejewska
Keyword(s):  
Atherosclerotic Plaque ◽  
Molecular Mechanisms ◽  
Cellular Heterogeneity ◽  
Ldl Oxidation ◽  
Plaque Development ◽  
New Directions ◽  
Life Threatening ◽  
Non Coding Rnas ◽  
Cellular Pathways ◽  
Key Aspects

Atherosclerotic plaque is the pathophysiological basis of important and life-threatening diseases such as myocardial infarction. Although key aspects of the process of atherosclerotic plaque development and progression such as local inflammation, LDL oxidation, macrophage activation, and necrotic core formation have already been discovered, many molecular mechanisms affecting this process are still to be revealed. This minireview aims to describe the current directions in research on atherogenesis and to summarize selected studies published in recent years—in particular, studies on novel cellular pathways, epigenetic regulations, the influence of hemodynamic parameters, as well as tissue and microorganism (microbiome) influence on atherosclerotic plaque development. Finally, some new and interesting ideas are proposed (immune cellular heterogeneity, non-coding RNAs, and immunometabolism) which will hopefully bring new discoveries in this area of investigation.

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