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Relevant bibliographies by topics / Drug induced abnormalities

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Academic literature on the topic 'Drug induced abnormalities'

Author: Grafiati

Published: 4 June 2021

Last updated: 12 February 2022

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Journal articles on the topic "Drug induced abnormalities"

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Kozik, Teri M., Mary G. Carey, Salah S. Al-Zaiti, and Michele M. Pelter. "Drug Induced ECG Abnormalities." American Journal of Critical Care 24, no. 4 (2015): 365–66. http://dx.doi.org/10.4037/ajcc2015712.

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Piraccini, Bianca Maria, Matilde Iorizzo, and Antonella Tosti. "Drug-Induced Nail Abnormalities." American Journal of Clinical Dermatology 4, no. 1 (2003): 31–37. http://dx.doi.org/10.2165/00128071-200304010-00004.

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Piraccini, Bianca Maria, Matilde Iorizzo, Angela Antonucci, and Antonella Tosti. "Drug-induced nail abnormalities." Expert Opinion on Drug Safety 3, no. 1 (2004): 57–65. http://dx.doi.org/10.1517/14740338.3.1.57.

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Patton, W. Nigel, and Stephen B. Duffull. "Idiosyncratic Drug-Induced Haematological Abnormalities." Drug Safety 11, no. 6 (1994): 445–62. http://dx.doi.org/10.2165/00002018-199411060-00006.

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Gitlin, Norman. "DRUG-INDUCED HEPATIC VASCULAR ABNORMALITIES." Clinics in Liver Disease 2, no. 3 (1998): 591–606. http://dx.doi.org/10.1016/s1089-3261(05)70028-3.

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Mintzer, David M., Shira N. Billet, and Lauren Chmielewski. "Drug-Induced Hematologic Syndromes." Advances in Hematology 2009 (2009): 1–11. http://dx.doi.org/10.1155/2009/495863.

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Objective. Drugs can induce almost the entire spectrum of hematologic disorders, affecting white cells, red cells, platelets, and the coagulation system. This paper aims to emphasize the broad range of drug-induced hematological syndromes and to highlight some of the newer drugs and syndromes.Methods. Medline literature on drug-induced hematologic syndromes was reviewed. Most reports and reviews focus on individual drugs or cytopenias.Results. Drug-induced syndromes include hemolytic anemias, methemoglobinemia, red cell aplasia, sideroblastic anemia, megaloblastic anemia, polycythemia, aplasti

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Kokot, Franciszek, and Lidia Hyla‑Klekot. "Drug‑induced abnormalities of potassium metabolism." Polish Archives of Internal Medicine 118, no. 7-8 (2008): 431–34. http://dx.doi.org/10.20452/pamw.442.

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Frazier, Kendall S. "Drug-induced Physeal Abnormalities in Preclinical Toxicity Studies." Toxicologic Pathology 45, no. 7 (2017): 869–75. http://dx.doi.org/10.1177/0192623317713319.

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Most toxic physeal changes are characterized microscopically by altered chondrocyte development, proliferation, or maturation in the growth plate and eventually result in disordered appositional bone growth. Many therapeutic drugs directly or indirectly target proteins involved in chondrocytic differentiation and maturation pathways, so toxic physeal injury has become increasingly common in preclinical toxicologic pathology. While physeal dysplasia has been associated with several different drug classes including bisphosphonates, vascular endothelial growth factor receptor inhibitors, fibrobla

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Sidhu, Harbir S., Nanda Venkatanarasimha, Gauraang Bhatnagar, Varut Vardhanabhuti, Bruce M. Fox, and Sri Priya Suresh. "Imaging Features of Therapeutic Drug–induced Musculoskeletal Abnormalities." RadioGraphics 32, no. 1 (2012): 105–27. http://dx.doi.org/10.1148/rg.321115041.

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Vasic, Nada, Branislava Milenkovic, Dragica Pesut, Ruza Stevic, and Dragana Jovanovic. "Drug induced lung disease - amiodarone in focus." Medical review 67, no. 9-10 (2014): 334–37. http://dx.doi.org/10.2298/mpns1410334v.

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More than 380 medications are known to cause pulmonary toxicity. Selected drugs that are important causes of pulmonary toxicity fall into the following classes: cytotoxic, cardiovascular, anti-inflammatory, antimicrobial, illicit drugs, miscellaneous. The adverse reactions can involve the pulmonary parenchyma, pleura, the airways, pulmonary vascular system, and mediastinum. Drug-induced lung diseases have no pathognomonic clinical, laboratory, physical, radiographic or histological findings. A drug-induced lung disease is usually considered a diagnosis of exclusion of other diseases. The diagn

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Dissertations / Theses on the topic "Drug induced abnormalities"

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Wide, Katarina. "Children exposed to antiepileptic drugs in utero : clinical and epidemiological aspects on growth, development and occurrence of malformations /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4320-6/.

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Van, Gend Tania Anli. "Effect of a South African medicinal plant on antiretroviral drug induced abnormalities in rats." Thesis, Nelson Mandela Metropolitan University, 2008. http://hdl.handle.net/10948/1080.

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The worldwide AIDS epidemic is known to have had a profoundly negative social, economic and personal impact and has taken a heavy toll on existing health care systems, particularly in developing countries. South Africa is experiencing an HIV epidemic with enormous social and economic consequences. Lopinavir/ritonavir antiretroviral treatment has been accredited with having a significantly positive effect and is a key advance in controlling HIV morbidity and mortality. An indigenous South African medicinal plant, Sutherlandia frutescens, known for its anti-diabetic properties and immune-boostin

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Teär, Fahnehjelm Kristina. "Posterior ocular malformations in children : teratological aspects /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-470-4.

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Yan, Jin 1972. "The mechanisms of hydroxyurea induced developmental toxicity in the organogenesis stage mouse embryo /." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115897.

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Hydroxyurea was used as a model teratogen to investigate the role of oxidative stress and stress-response pathways in mediating developmental toxicity. When administered to pregnant mice during early organogenesis, hydroxyurea induced fetal death and growth retardation, as well as external and skeletal malformations. The malformed fetuses displayed hindlimb, vertebral column, and tail defects. Hydroxyurea treatment enhanced the production of 4-hydroxynonenal, a lipid peroxidation end product, in malformation sensitive regions of the embryo. Depletion of glutathione, a major cellular antioxidan

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Caumo, Débora Tomazi Moreira. "Limiares auditivos em altas frequências em pacientes com fibrose cística : revisão sistemática." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2016. http://hdl.handle.net/10183/148122.

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Introdução: A audiometria de altas frequências pode contribuir para a detecção precoce de alterações auditivas causadas por medicações ototóxicas. No tratamento dos pacientes com fibrose cística, existem muitos fármacos ototóxicos que são amplamente utilizados. A detecção precoce de alterações auditivas deve permitir que estas sejam identificadas antes que o dano atinja as frequências da fala. A lesão causada pela ototoxicidade é irreversível, trazendo importantes consequências sociais e psicológicas. Nas crianças, a perda auditiva, mesmo restrita às altas frequências, pode afetar o desenvolvi

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Larouche, Geneviève. "Understanding the role of superoxide in mediating the teratogenicity of hydroxyurea." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116029.

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Hydroxyurea is a teratogen; treatment of dams during organogenesis causes various malformations. Administration of a free radical scavenger ameliorates the embryotoxicity of hydroxyurea, suggesting that oxidative stress mediates this toxicity. The goal of this thesis was to test the hypothesis that superoxide, a reactive oxygen species, is involved. Superoxide dismutase 1 (SOD1) is an antioxidant enzyme that converts superoxide to hydrogen peroxide. To elucidate the role of superoxide in mediating hydroxyurea teratogenicity, dams that were wildtype or hemizygous for hSOD1 were treated on gesta

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Gnanabakthan, Naveen. "Understanding the basis of 5-Bromo-2'-deoxuridine teratogen specificity in organogenesis stage mouse embryos." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112624.

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5-Bromo-2'-deoxyuridine (BrdU), a thymidine analogue, is genotoxic and teratogenic. The exposure of mouse embryos to BrdU at doses that cause malformations induces oxidative stress and an embryonic stress response characterized by an increase in c-Fos dependent AP-1 DNA binding. The goal of this thesis was to test the hypothesis that development is disturbed at sites where BrdU is incorporated into DNA, triggering oxidative stress and c-Fos induction. Gestation day 9 CD-1 mice were treated with BrdU and embryos were obtained for immunolocalization of BrdU, 8-oxoguanine, a biomarker for oxidati

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Magnusson, Linda L. "Parental exposures and occurrence of adverse pregnancy outcomes and childhood atopic diseases /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-673-5/.

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Libório, Alexandre Braga. "Rosiglitazona, agonista do PPAR-y \"Peroxisome Proliferator-Activated Receptor-y\" reverte a nefrotoxicidade induzida pelo tenofovir-DF." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-12092008-130850/.

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Introdução: A nefrotoxicidade dos antiretrovirais constituem atualmente fator importante na morbidade e mortalidade de pacientes com HIV. O tenofovir DF (TDF) se enquadra em um dos antiretrovirais mais lesivos ao rim. Conhecer seu mecanismo de nefrotoxicidade e estudar medidas protetoras podem melhorar seu uso clínico. Material e Métodos: Ratos foram tratados durante 30 dias com uma de duas doses de TDF (50 ou 300mg/Kg de dieta), sendo que um grupo teve adicionado em sua dieta maleato de rosiglitazona (RSG) na dose de 92mg/Kg de dieta nos últimos 15 dias. Após esse período, os ratos foram colo

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"Effects of hyperglycemia and caffeine on early embryogenesis in whole rat embryo culture." 2001. http://library.cuhk.edu.hk/record=b5890919.

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by Chiu Pui Yu.<br>Thesis (M.Phil.)--Chinese University of Hong Kong, 2001.<br>Includes bibliographical references (leaves 86-118).<br>Abstracts in English and Chinese.<br>Title Page --- p.i<br>Abstract --- p.ii-iv<br>Acknowledgement --- p.v<br>Table of Contents --- p.vi-viii<br>List of Tables --- p.ix<br>List of Figures --- p.x-xii<br>List of Abbreviations --- p.xiii<br>Chapter Section I: --- Introduction<br>Chapter Chapter 1: --- Overview --- p.1-2<br>Chapter Chapter 2: --- Teratogenic Effects of Hyperglycemia<br>Chapter 2.1 --- What is Hyperglycemia --- p.3<br>Chapter 2.2 --- Tera

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Books on the topic "Drug induced abnormalities"

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Chemically induced birth defects. 3rd ed. Marcel Dekker, 2000.

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Chemically induced birth defects. 2nd ed. Dekker, 1993.

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Chemically induced birth defects. M. Dekker, 1985.

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Persaud, T. V. N. Environmental causes of human birth defects. C.C. Thomas, 1990.

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Catalog of teratogenic agents. 8th ed. Johns Hopkins University Press, 1995.

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Catalog of teratogenic agents. 5th ed. Johns Hopkins University Press, 1986.

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Catalog of teratogenic agents. 6th ed. Johns Hopkins University Press, 1989.

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Catalog of teratogenic agents. 7th ed. Johns Hopkins University Press, 1992.

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Shepard, Thomas H. Catalog of teratogenic agents. 9th ed. Johns Hopkins University Press, 1998.

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DES/diethylstilbestrol: New perspectives. MTP Press, 1986.

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Book chapters on the topic "Drug induced abnormalities"

1

Tosti, Antonella, Ralph Daniel, Bianca Maria Piraccini, and Matilde Iorizzo. "Drug-Induced Nail Abnormalities." In Color Atlas of Nails. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-79050-1_17.

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"Drug-induced hair abnormalities." In Diagnosis and Treatment of Hair Disorders. CRC Press, 2005. http://dx.doi.org/10.1201/b14444-11.

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Henry, Travis S., and Brent P. Little. "Drug-Induced Lung Disease." In Chest Imaging. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780199858064.003.0070.

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Almost any medication may result in a reaction within the lungs. These reactions are often variable and include diffuse alveolar damage, organizing pneumonia, eosinophilic pneumonia, hypersensitivity reaction, interstitial pneumonitis/fibrosis, alveolar hemorrhage, pulmonary vasculitis/pulmonary hypertension, bronchiolitis obliterans, or a sarcoid-like reaction. Because these reactions may mimic their idiopathic counterparts, yet may respond to drug cessation or alternative therapies, suspicion must be high in patients with pulmonary findings who are on certain medications. This chapter will focus on the spectrum of drug reactions with the lungs. Amiodarone-related pulmonary abnormalities will also be discussed.

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De Matteis, Francesco. "Drug-Induced Abnormalities of Liver Heme Biosynthesis." In Hepatotoxicology. CRC Press, 2020. http://dx.doi.org/10.1201/9780367812041-10.

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Abekawa, Tomohiro. "Methamphetamine-Induced Behavioral Abnormalities and Neuronal Apoptosis." In Neuropathology of Drug Addictions and Substance Misuse. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-800212-4.00013-3.

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Carter, Stuart, Lisa Dunkley, and Ade Adebajo. "Miscellaneous conditions presenting to the rheumatologist." In Oxford Textbook of Medicine, edited by Richard A. Watts. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0465.

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Musculoskeletal symptoms can occur in a variety of diseases, or as drug side effects. Presentations and conditions discussed in this section include: multisystem diseases (e.g. adult-onset Still’s disease, acute sarcoid arthritis, and amyloidosis); paraneoplastic syndromes (e.g. hypertrophic pulmonary osteoarthropathy, remitting seronegative symmetrical synovitis with pitting oedema, and tumour-induced osteomalacia); skin manifestations of rheumatic disease (e.g. panniculitis, neutrophilic dermatoses, and multicentric reticulohistiocytosis); primary joint pathology and synovial disorders (e.g. pigmented vilonodular synovitis, synovial osteochondromatosis, Charcot joint); rheumatic manifestations of haematological disease (e.g. haemophilia, sickle cell disease, leukaemia, lymphoma, and polyneuropathy, organomegaly, endocrinopathy, M-protein, and skin abnormalities); rheumatic manifestations of metabolic disease (e.g. hereditary haemochromatosis, Wilson’s disease); disorders of the spine and axial skeleton (e.g. Tietze’s syndrome, diffuse idiopathic skeletal hyperostosis, and alkaptonuria); drug-induced rheumatic syndromes (e.g. statin-induced myopathy, drug-induced tendinopathy, drug-induced lupus, and allopurinol hypersensitivity).

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Powers, Amy, and Leslie Silberstein. "Acquired haemolytic anaemia." In Oxford Textbook of Medicine, edited by Chris Hatton and Deborah Hay. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0542.

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Premature destruction of red cells occurs through two primary mechanisms: (1) decreased erythrocyte deformability that leads to red cell sequestration and extravascular haemolysis in the spleen and other components of the reticuloendothelial system—may be caused by membrane defects, metabolic abnormalities, exogenous oxidizing agents, or pathological antibodies; and (2) red cell membrane damage and intravascular haemolysis—may be caused by exposure to pathological antibodies, activated complement, mechanical forces, chemicals, and infectious agents. Congenital haemolytic anaemias—congenital disorders resulting in a haemolytic anaemia include (1) disorders of the red cell membrane such as hereditary spherocytosis and hereditary elliptocytosis; (2) disorders of red cell enzymes such as glucose-6-phosphate dehydrogenase deficiency and pyruvate kinase deficiency; and (3) disorders of globin structure. Acquired immune haemolytic anaemias—immune haemolysis may occur when IgG, IgM, or IgA antibodies and/or complement bind to the erythrocyte surface. Autoimmune haemolytic anaemias—these are best classified according to the temperature at which the antibody optimally binds to the erythrocyte: warm autoimmune haemolytic anaemia, cold agglutinin-mediated autoimmune haemolytic anaemia, paroxysmal cold haemoglobinuria, and mixed type autoimmune haemolytic anaemia. Drug-induced haemolytic anaemia—haemolysis can be caused by drugs that induce a positive DAT. Drug-induced antibodies may be drug dependent or drug independent depending on whether the presence of the drug is required for their detection. Alloimmune haemolytic anaemias—these include acute haemolytic transfusion reactions and other conditions such as delayed haemolytic transfusion reactions, passenger lymphocyte haemolysis, and haemolytic disease of the newborn. Acquired nonimmune haemolytic anaemias and microangiopathic haemolytic anaemia are also discussed in this chapter.

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Mitchell, David A., Laura Mitchell, and Lorna McCaul. "Oral medicine." In Oxford Handbook of Clinical Dentistry. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199679850.003.0010.

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Contents. Bacterial infections of the mouth. Viral infections of the mouth. Oral candidosis (candidiasis). Recurrent aphthous stomatitis (ulcers). Vesiculo-bullous lesions—intraepithelial. Vesiculo-bullous lesions—subepithelial. White patches. Pigmented lesions of the mouth. Premalignant lesions. Oral cancer. Abnormalities of the lips and tongue. Salivary gland disease—1. Salivary gland disease—2. Drug-induced lesions of the mouth. Facial pain. Oral manifestations of skin disease. Oral manifestations of gastrointestinal disease. Oral manifestations of haematological disease. Oral manifestations of endocrine disease. Oral manifestations of neurological disease. Oral manifestations of HIV infection and AIDS. Cervico-facial lymphadenopathy. An approach to oral ulcers. Temporomandibular pain—dysfunction/facial arthromyalgia.

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Sagata, Noriaki, Yasunari Sakai, and Takahiro A. Kato. "Clarifying the Pathophysiological Mechanisms of Neuronal Abnormalities of NF1 by Induced-Neuronal (iN) Cells from Human Fibroblasts." In Neurofibromatosis [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.98817.

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Direct conversion techniques, which generate induced-neuronal (iN) cells from human fibroblasts in less than two weeks, are expected to discover unknown neuronal phenotypes of neuropsychiatric disorders. Here, we present unique gene expression and cell morphology profiles in iN cells derived from neurofibromatosis type 1 (NF1) patients. NF1 is a single-gene multifaceted disorder with relatively high co-occurrence of autism spectrum disorder (ASD). Adenylyl cyclase (AC) dysfunction is one of the candidate pathways in abnormal neuronal development in the brains of NF1 patients. In our study, microarray-based transcriptomic analysis of iN cells from healthy controls (males) and NF1 patients (males) revealed significantly different gene expression of 149 (110 were upregulated and 39 were downregulated). In iN cells derived from NF1 patients (NF1-iN cells), there was a change in the expression level of 90 genes with the addition of forskolin, an AC activator. Furthermore, treatment with forskolin dramatically changed the cell morphology, especially that of NF1-iN cells, from flat-form to spherical-form. Current pilot data indicate the potential therapeutic effect of forskolin or AC activators on neuronal growth in NF1 patients. Further translational research is needed to validate the pilot findings for future drug development of ASD.

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Scott, Rebecca, T. M. Tan, and S. R. Bloom. "Hormones and the gastrointestinal tract." In Oxford Textbook of Medicine, edited by Jack Satsangi. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0296.

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The gastrointestinal tract is the largest endocrine organ in the body, with its component cells dispersed along its length rather than being clustered in glands. More than 20 gut peptides integrate gastrointestinal function by regulating the actions of the epithelium, muscles, and nerves; they also affect the growth and development of the gut and have a major role in appetite control. They mostly work in an autocrine or paracrine manner. Gastrointestinal hormones include the gastrin–cholecystokinin family, the secretin superfamily, preproglucagon derivatives, the motilin–ghrelin family, the pancreatic polypeptide-fold family, and various other gut peptides. Gastrointestinal and other diseases may cause abnormalities of these gut peptides, for example: (1) achlorhydria (from atrophic gastritis or drug-induced) causes elevation of circulating gastrin; (2) malabsorptive conditions are associated with a decrease in the amount of peptides produced in the affected region, and a compensatory elevation of other peptides; and (3) obesity is associated with orexigenic (appetite-stimulating) and less satiating hormonal changes, and the beneficial effects of bariatric surgery are partly explained through alterations in gut hormones.

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Conference papers on the topic "Drug induced abnormalities"

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Khodor, N., G. Carrault, P. L'hostis, H. Amoud, M. Khalil, and A. Hernandez. "New T-wave parameters describing repolarization abnormalities induced by drug." In 2014 Middle East Conference on Biomedical Engineering (MECBME). IEEE, 2014. http://dx.doi.org/10.1109/mecbme.2014.6783248.

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Nadine, Khodor, Carrault Guy, Amoud Hassan, Khalil Mohamad, L'hostis Philippe, and Hernandez Alfredo. "Evaluation of T-wave morphology parameters in drug-induced repolarization abnormalities." In 2013 2nd International Conference on Advances in Biomedical Engineering (ICABME). IEEE, 2013. http://dx.doi.org/10.1109/icabme.2013.6648883.

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Couderc, JP, M. Vaglio, X. Xia, S. McNitt, and O. Hyrien. "Electrocardiographic Method for Identifying Drug-induced Repolarization Abnormalities Associated with a Reduction of the Rapidly Activating Delayed Rectifier Potassium Current." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.260492.

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Couderc, JP, M. Vaglio, X. Xia, S. McNitt, and O. Hyrien. "Electrocardiographic Method for Identifying Drug-induced Repolarization Abnormalities Associated with a Reduction of the Rapidly Activating Delayed Rectifier Potassium Current." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.4398329.

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Maggi, A., M. Abbadini, R. Salemi, J. Pangrazzi, P. G. Pagella, and M. B. Donati. "DERMATAN SULPHATE PREVENTS VENOUS THROMBOSIS IN RATS WITHOUT INCREASING BLEEDING." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643245.

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Studies have suggested that endogenous proteoglycans, structurally similar to heparin, contribute to the “non-thrombogenicity” of the vascular wall. Our studies concentrated on Dermatan Sulphate (DS-MF 701) Heparin Sulphate (HS) and Standard Heparin (SH), all from Mediolanum Farmaceutici. The antithrombotic potential of these GAGs was evaluated in a well established model of venous thrombosis consisting in the ligature of the vena cava, 15 min after i.v. administration of the drug. A dose response-curve was obtained for DS (0.25-4 mg/kg), HS (1 -5 mg/kg) and SH (0.5-2 mg/kg).At the dose of 2 m

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Patel, R., and R. Bick. "PLATELET DYSFUNCTION INDUCED BY TETRAHYDROCANNABINOL." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644877.

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Many drugs and other agents have been reported to induce platelet dysfunction and clinical bleedability; however, tetrahydrocannabinol (marijuana) has thus far not been reported. The patient herein described is a 28-year-old Caucasian female who wasreferred for evaluation of easy and spontaneous bruising. On history, the patient related that for a three-month period she had been developing spontaneous ecchymoses of the extremities and torso. She denied any medication other than heavy marijuana use. Hemostasis evaluation revealed her to have a normal prothrombin time, partial thromboplastin tim

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