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Journal of the American Veterinary... Nov 2016
Topics: Anaphylaxis; Animals; Arrhythmias, Cardiac; Bees; Diphenhydramine; Dog Diseases; Dogs; Electrocardiography; Heart Rate; Histamine Antagonists; Insect Bites and Stings; Male
PubMed: 27823376
DOI: 10.2460/javma.249.10.1138 -
Blood Transfusion = Trasfusione Del... Jul 2014
Review
Topics: Administration, Intravenous; Anaphylaxis; Anti-Allergic Agents; Diphenhydramine; Drug Hypersensitivity; Humans; Iron
PubMed: 25074787
DOI: 10.2450/2014.0094-14 -
Drug Discoveries & Therapeutics Nov 2022Cetirizine, a second-generation antihistamine, and diphenhydramine, a first-generation antihistamine, are among the most widely used anti-allergic drugs. In addition to...
Cetirizine, a second-generation antihistamine, and diphenhydramine, a first-generation antihistamine, are among the most widely used anti-allergic drugs. In addition to longer duration of action and less incidence of sedative side effects, recent clinical studies also indicate a higher potency of cetirizine than diphenhydramine in the treatment or prevention of allergic disorders. In the present study, using the differential-interference contrast (DIC) microscopy, we examined the effects of cetirizine and diphenhydramine (1 μM to 1 mM) on the degranulation from rat peritoneal mast cells. Using fluorescence imaging of a water-soluble dye, lucifer yellow, we also examined their effects on the deformation of the plasma membrane. At relatively higher concentrations (100 μM, 1 mM), both cetirizine and diphenhydramine significantly reduced the numbers of degranulating mast cells. Of note, at 1 mM, cetirizine more markedly reduced the number than diphenhydramine, almost entirely suppressing the degranulation of mast cells. Additionally, 1 mM cetirizine and levocetirizine, another second-generation antihistamine, almost totally inhibited the process of exocytosis in mast cells and washed out the trapping of the lucifer yellow on the cell surface, while diphenhydramine and chlorpheniramine, another first-generation antihistamine, did not. This study provided in vitro evidence for the first time that cetirizine more potently inhibited the process of exocytosis in mast cells than diphenhydramine, indicating its higher potency as a mast cell-stabilizer. Such mast cell-stabilizing property of cetirizine could be ascribed to its counteracting effect on the plasma membrane deformation in degranulating mast cells.
Topics: Rats; Animals; Cetirizine; Diphenhydramine; Mast Cells; Histamine H1 Antagonists; Anti-Allergic Agents
PubMed: 36261390
DOI: 10.5582/ddt.2022.01067 -
BMJ Case Reports Sep 2020SARS-CoV-2, the virus responsible for COVID-19, binds to the ACE2 receptors. ACE2 is thought to counterbalance ACE in the renin-angiotensin system. While presently it is...
SARS-CoV-2, the virus responsible for COVID-19, binds to the ACE2 receptors. ACE2 is thought to counterbalance ACE in the renin-angiotensin system. While presently it is advised that patients should continue to use ACE inhibitors or angiotensin receptor blockers, questions still remain as to whether adverse effects are potentiated by the virus. Here, we report a case of a 57-year-old man, unknowingly with COVID-19, who presented to the emergency department with tongue swelling, shortness of breath and difficulty in speaking following 4 months taking benazepril, an ACE inhibitor. Finally, we also describe possible pathways that exist for SARS-CoV-2 to interact with the mechanism behind angioedema.
Topics: Angioedema; Angiotensin-Converting Enzyme Inhibitors; Anti-Allergic Agents; Benzazepines; Betacoronavirus; COVID-19; Coronavirus Infections; Diagnosis, Differential; Diphenhydramine; Famotidine; Histamine H2 Antagonists; Humans; Male; Middle Aged; Pandemics; Pneumonia, Viral; SARS-CoV-2; Tranexamic Acid
PubMed: 32912894
DOI: 10.1136/bcr-2020-237888 -
Japanese Journal of Pharmacology Jun 1972
The influence of monoamine oxidase inhibitors and some other antidepressants on the anti-parkinsonian activity of sub-effective doses of diphenylhydramine in rats and mice.
Topics: Animals; Antidepressive Agents; Catatonia; Diphenhydramine; Humans; Mice; Monoamine Oxidase Inhibitors; Nortriptyline; Parasympatholytics; Parkinson Disease; Parkinson Disease, Secondary; Perphenazine; Phenelzine; Rats; Tremorine
PubMed: 4539394
DOI: 10.1254/jjp.22.301 -
The Journal of Investigative... Nov 2001Histamine-1 (H1) antihistamines are the first-line drug for the treatment of urticaria. Major progress has been achieved in recent years both in the understanding of... (Review)
Review
Histamine-1 (H1) antihistamines are the first-line drug for the treatment of urticaria. Major progress has been achieved in recent years both in the understanding of their ligands, the H1-histamine receptors, and therefore in the mechanisms of their pharmacologic effects, as well as in the development of safer antihistamines with low or no sedating effects and no interactions on the level of potassium channels leading to QT-prolongations and interactions on the level of cytochrome P450 isoenzymes. This development has brought antihistamines very close to the ideal antihistamines that are desired by clinicians to treat most types of urticaria in patients who have to take these drugs for a long time.
Topics: Cyclizine; Cytochrome P-450 Enzyme System; Diphenhydramine; Electrocardiography; Histamine H1 Antagonists; Humans; Promethazine; Pyrilamine; Urticaria
PubMed: 11764306
DOI: 10.1046/j.0022-202x.2001.00032.x -
The Journal of Neuroscience : the... Aug 2016T-helper 17 (Th17) cells play an important role in the pathogenesis of multiple sclerosis (MS), an autoimmune demyelinating disease that affects the CNS. In the present...
UNLABELLED
T-helper 17 (Th17) cells play an important role in the pathogenesis of multiple sclerosis (MS), an autoimmune demyelinating disease that affects the CNS. In the present study, MicroRNA sequencing (miRNA-seq) was performed in mouse Th0 and Th17 cells to determine the critical miRNAs that are related to Th17 differentiation. We found that miR-30a was significantly downregulated during mouse Th17 differentiation. In addition, the level of miR-30a in CD4(+) T cells from peripheral blood of MS patients and experimental autoimmune encephalomyelitis (EAE) animal models was also decreased and inversely correlated with the expression of interleukin 17a, the canonical cytokine of Th17 cells. Moreover, overexpression of miR-30a inhibited Th17 differentiation and prevented the full development of EAE, whereas interference of miR-30a promoted Th17 differentiation. Mechanism studies showed that miR-30a reduced IRF4 expression by specifically binding with the 3'-untranslated region. Through screening of 640 different Food and Drug Administration (FDA)-approved drugs, we found that disulfiram and diphenhydramine hydrochloride were effective candidates for inhibiting Th17 differentiation and ameliorating EAE development through upregulating miR-30a. To our knowledge, the present work is not only the first miRNA-seq study focusing on Th17 differentiation, but also the first chemical screening for FDA-approved drugs that inhibit Th17 differentiation through regulating miRNA expression.
SIGNIFICANCE STATEMENT
The present work is the first miRNA sequencing (miRNA-seq) study focusing on T-helper 17 (Th17) differentiation. By miRNA deep sequencing, we found that miR-30a was downregulated during Th17 differentiation. miR-30a was also decreased in CD4(+) T cells from multiple sclerosis patients and experimental autoimmune encephalomyelitis (EAE) mice. miR-30a reduced IRF4 expression by specific binding with the 3'-untranslated region and thus suppressed Th17 differentiation and prevented the full development of EAE. Interestingly, by performing a chemical screen with Food and Drug Administration-approved small-molecule drugs, we found that disulfiram and diphenhydramine upregulated miR-30a and suppressed Th17-associated autoimmune demyelination.
Topics: Animals; Case-Control Studies; Cell Differentiation; Cells, Cultured; Diphenhydramine; Disease Models, Animal; Disulfiram; Encephalomyelitis, Autoimmune, Experimental; Female; HEK293 Cells; Humans; Interferon Regulatory Factors; Interleukin-17; Male; Mice; Mice, Inbred C57BL; MicroRNAs; Myelin Proteolipid Protein; Myelin-Oligodendrocyte Glycoprotein; Peptide Fragments; Statistics, Nonparametric; Transfection; Up-Regulation
PubMed: 27581464
DOI: 10.1523/JNEUROSCI.4587-15.2016 -
The Pan African Medical Journal 2022Acute dystonia has notably been a challenge in the emergency unit. Drug-induced dystonia is reported in a limited number of cases in the literature. Rarely,...
Acute dystonia has notably been a challenge in the emergency unit. Drug-induced dystonia is reported in a limited number of cases in the literature. Rarely, diphenhydramine was found to be the culprit. We report the case of a 25-year-old female patient who developed an acute dystonic reaction following the administration of 25 mg of intravenous diphenhydramine as a treatment for an allergic reaction. The patient was given 5 mg diazepam, admitted for monitoring, and discharged home. Diphenhydramine-induced acute dystonia is a user drug-induced threatening reaction that warrants further investigation on the metabolism of these drugs and the contributing phenotypes to this adverse reaction.
Topics: Female; Humans; Dystonia; Diphenhydramine; Hypersensitivity
PubMed: 36405657
DOI: 10.11604/pamj.2022.42.289.35167 -
Annals of Oncology : Official Journal... Sep 2009
Topics: Adult; Anti-Allergic Agents; Anti-Inflammatory Agents; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Agents; Carcinoma, Squamous Cell; Cetuximab; Dexamethasone; Diphenhydramine; Humans; Laryngeal Neoplasms; Male; Meningitis, Aseptic; Middle Aged; Premedication; Tonsillar Neoplasms
PubMed: 19643807
DOI: 10.1093/annonc/mdp382 -
Revista Brasileira de Anestesiologia 2010Since atracurium can cause hypotension in humans, the hemodynamic effects of atracurium and cisatracurium as well as the hemodynamic protection of diphenhydramine and... (Comparative Study)
Comparative Study
BACKGROUND AND OBJECTIVES
Since atracurium can cause hypotension in humans, the hemodynamic effects of atracurium and cisatracurium as well as the hemodynamic protection of diphenhydramine and cimetidine were investigated in rats.
METHODS
1) Wistar rats were anesthetized with sodium pentobarbital and prepared according to Brown et al. to evaluate different doses of atracurium and cisatracurium in the reduction of T4/T1 equal or greater than 95%. 2) Assessment of the hemodynamic changes caused by the intravenous administration of atracurium and cisatracurium by monitoring the blood pressure in the carotid artery and the electrocardiogram of rats. 3) Observation of the hemodynamic protection of prior treatment with the intravenous administration of diphenhydramine (2 mg.kg(-1)) and/or cimetidine (4 mg.kg(-1)).
STATISTICAL ANALYSIS
Student t test and ANOVA.
RESULTS
Doses of 1 mg.kg(-1) and 0.25 mg.kg(-1) of atracurium and cisatracurium respectively did not change the mean arterial pressure (MAP). Doses of 4 mg.kg(-1) of atracurium and cisatracurium decreased MAP to 62.8 +/- 4.5% and 82.5 +/- 2.3% respectively when compared to control levels. When the rats were pre-treated with diphenhydramine and cimetidine, diastolic pressure was reduced to 95.4% +/- 2.5%. With cimetidine, diastolic pressure was reduced to 82.7 +/- 8.4% when compared to the control group. The effects on systolic and diastolic blood pressure were reflected in the levels of MAP.
CONCLUSIONS
The isolated administration of diphenhydramine and cimetidine did not prevent the reduction in mean arterial pressure induced by atracurium. However, the association of both drugs was able to prevent the hemodynamic effects of atracurium. The doses of cisatracurium used in this study did not cause a reduction in blood pressure significant enough to justify the use of the preventive measures used in the atracurium groups.
Topics: Animals; Atracurium; Cimetidine; Diphenhydramine; Female; Hemodynamics; Histamine H1 Antagonists; Histamine H2 Antagonists; Male; Neuromuscular Blocking Agents; Neuromuscular Nondepolarizing Agents; Rats; Rats, Wistar
PubMed: 20169263
DOI: 10.1016/s0034-7094(10)70006-4