scholarly journals Drug-Induced Cutaneous Toxicity

10.5772/64473 ◽  
2016 ◽  
Author(s):  
Katsuhiko Yoshizawa ◽  
Michiko Yuki ◽  
Airo Tsubura
Keyword(s):  
Drug Induced ◽  
Cutaneous Toxicity

scholarly journals Vemurafenib-Induced Toxic Epidermal Necrolysis: An Emerging Adverse Event

2018 ◽  
Vol 76 (3) ◽  
pp. 329-332
Author(s):  
Ana Filipe Monteiro ◽  
Margarida Rato ◽  
César Martins
Keyword(s):  
Toxic Epidermal Necrolysis ◽  
Metastatic Melanoma ◽  
Stage Iv ◽  
Maculopapular Rash ◽  
European Medicines Agency ◽  
Drug Induced ◽  
Cutaneous Toxicity ◽  
Life Threatening ◽  
Cutaneous Adverse Reactions ◽  
Continue Therapy

Vemurafenib, a selective inhibitor of the BRAF V600 mutation, is Food and Drug Administration and European Medicines Agency approved for the treatment of stage IV metastatic melanoma alone or in combination. Among the adverse effects, cutaneous toxicity is the most common. Most of these reactions such as maculopapular rash, photosensitivity and hyperkeratotic lesions are manageable, and the majority of patients are able to continue therapy. However, a few cases of life-threatening severe cutaneous adverse reactions have been reported and drug withdrawal is mandatory in these cases. Herein, we report a case of vemurafenib- -induced toxic epidermal necrolysis in a patient receiving therapy for metastatic melanoma. After several hospital complications, our patient survived to the drug-induced reaction and he is in remission for 2 years.

scholarly journals Drug-induced cutaneous toxicity

2008 ◽  
Vol 131 (4) ◽  
pp. 285-290 ◽  
Author(s):  
Katsuhiko Yoshizawa
Keyword(s):  
Drug Induced ◽  
Cutaneous Toxicity

Clinical Management of Cutaneous Toxicity of Anti-EGFR Agents

2007 ◽  
Vol 22 (1_suppl4) ◽  
pp. 53-61 ◽  
Author(s):  
M. Monti ◽  
S. Motta
Keyword(s):  
Adverse Reactions ◽  
Growth Factor Receptor ◽  
Signs And Symptoms ◽  
Skin Toxicity ◽  
Keratinocyte Differentiation ◽  
Clinical Approach ◽  
Drug Induced ◽  
Skin Reactions ◽  
Cutaneous Toxicity ◽  
Epidermal Growth

Cutaneous toxicity is the most evident adverse effect of epidermal growth factor receptor (EGFR) inhibitors because of the specific role played by EGFR in skin biophysiology. Dermatological adverse reactions, mainly folliculocentric, have been widely reported in the literature. However, the mechanism of these reactions is not well defined and their management is still a matter of debate. In this paper keratinocyte differentiation, activation and pathways regulating gene expression are reviewed in order to improve the understanding of adverse skin reactions and obtain success in their management. The authors had the opportunity to treat skin reactions induced by cetuximab in a cohort of patients affected by metastatic colorectal carcinoma. The aims of this clinical approach were to control the signs and symptoms of skin toxicity in order to avoid delay in cancer therapy and to use nondrug agents for the treatment of drug-induced skin reactions.

Early Development of Drug-Induced Hepatic Necrosis

1971 ◽  
Vol 29 ◽  
pp. 576-577
Author(s):  
F. G. Zaki ◽  
E. Detzi ◽  
C. H. Keysser
Keyword(s):  
Early Development ◽  
Hepatic Necrosis ◽  
Screening Tests ◽  
Dense Matrix ◽  
Sprague Dawley ◽  
Electron Microscopic ◽  
Drug Induced ◽  
Hepatocellular Damage ◽  
Sprague Dawley Rats ◽  
Microscopic Studies

This study represents the first in a series of investigations carried out to elucidate the mechanism(s) of early hepatocellular damage induced by drugs and other related compounds. During screening tests of CNS-active compounds in rats, it has been found that daily oral administration of one of these compounds at a dose level of 40 mg. per kg. of body weight induced diffuse massive hepatic necrosis within 7 weeks in Charles River Sprague Dawley rats of both sexes. Partial hepatectomy enhanced the development of this peculiar type of necrosis (3 weeks instead of 7) while treatment with phenobarbital prior to the administration of the drug delayed the appearance of necrosis but did not reduce its severity.Electron microscopic studies revealed that early development of this liver injury (2 days after the administration of the drug) appeared in the form of small dark osmiophilic vesicles located around the bile canaliculi of all hepatocytes (Fig. 1). These structures differed from the regular microbodies or the pericanalicular multivesicular bodies. They first appeared regularly rounded with electron dense matrix bound with a single membrane. After one week on the drug, these vesicles appeared vacuolated and resembled autophagosomes which soon developed whorls of concentric lamellae or cisterns characteristic of lysosomes (Fig. 2). These lysosomes were found, later on, scattered all over the hepatocytes.

Effect of piperacillin on morphology and viability of gram-negative bacteria

1984 ◽  
Vol 42 ◽  
pp. 218-219
Author(s):  
R. H. Liss
Keyword(s):  
Inhibitory Concentration ◽  
Cytoplasmic Membrane ◽  
Drug Binding ◽  
Gram Negative Bacteria ◽  
Bacterial Cells ◽  
Drug Induced ◽  
Penicillin Binding Proteins ◽  
Lactam Antibiotic ◽  
Drug Free ◽  
Tube Dilution

Piperacillip (PIP) is b-[D(-)-α-(4-ethy1-2,3-dioxo-l-piperzinylcar-bonylamino)-α-phenylacetamido]-penicillanate. The broad spectrum semisynthetic β-lactam antibiotic is believed to effect bactericidal activity through its affinity for penicillin-binding proteins (PBPs), enzymes on the bacterial cytoplasmic membrane that control elongation and septation during cell growth and division. The purpose of this study was to correlate penetration and binding of 14C-PIP in bacterial cells with drug-induced lethal changes assessed by microscopic, microbiologic and biochemical methods.The bacteria used were clinical isolates of Escherichia coli and Pseudomonas aeruginosa (Figure 1). Sensitivity to the drug was determined by serial tube dilution in Trypticase Soy Broth (BBL) at an inoculum of 104 organisms/ml; the minimum inhibitory concentration of piperacillin for both bacteria was 1 μg/ml. To assess drug binding to PBPs, the bacteria were incubated with 14C-PIP (5 μg/0.09 μCi/ml); controls, in drug-free medium.

Drug Induced Changes in Cell Organelles

1968 ◽  
Vol 26 ◽  
pp. 110-111
Author(s):  
Sarah A. Luse
Keyword(s):  
Clinical Medicine ◽  
Cell Organelles ◽  
Riboflavin Deficiency ◽  
Drug Induced ◽  
New Era ◽  
Health And Disease ◽  
In The Beginning ◽  
Cellular Pathology ◽  
Induced Changes ◽  
The Impact

In the mid-nineteenth century Virchow revolutionized pathology by introduction of the concept of “cellular pathology”. Today, a century later, this term has increasing significance in health and disease. We now are in the beginning of a new era in pathology, one which might well be termed “organelle pathology” or “subcellular pathology”. The impact of lysosomal diseases on clinical medicine exemplifies this role of pathology of organelles in elucidation of disease today.Another aspect of cell organelles of prime importance is their pathologic alteration by drugs, toxins, hormones and malnutrition. The sensitivity of cell organelles to minute alterations in their environment offers an accurate evaluation of the site of action of drugs in the study of both function and toxicity. Examples of mitochondrial lesions include the effect of DDD on the adrenal cortex, riboflavin deficiency on liver cells, elevated blood ammonia on the neuron and some 8-aminoquinolines on myocardium.

Acetaminophen: Macula densa hypersecretory activity by induced hepatotoxicity

1987 ◽  
Vol 45 ◽  
pp. 934-935
Author(s):  
S.S. Poolsawat ◽  
C.A. Huerta ◽  
S.TY. Lae ◽  
G.A. Miranda
Keyword(s):  
Cell Proliferation ◽  
Liver Function ◽  
Chronic Inflammation ◽  
Foam Cell ◽  
Term Effect ◽  
Short Term ◽  
Drug Induced ◽  
Experimental Induction ◽  
Tissue Alterations ◽  
Toxic Responses

Introduction. Experimental induction of altered histology by chemical toxins is of particular importance if its outcome resembles histopathological phenomena. Hepatotoxic drugs and chemicals are agents that can be converted by the liver into various metabolites which consequently evoke toxic responses. Very often, these drugs are intentionally administered to resolve an illness unrelated to liver function. Because of hepatic detoxification, the resulting metabolites are suggested to be integrated into the macromolecular processes of liver function and cause an array of cellular and tissue alterations, such as increased cytoplasmic lysis, centrilobular and localized necroses, chronic inflammation and “foam cell” proliferation of the hepatic sinusoids (1-4).Most experimentally drug-induced toxicity studies have concentrated primarily on the hepatic response, frequently overlooking other physiological phenomena which are directly related to liver function. Categorically, many studies have been short-term effect investigations which seldom have followed up the complications to other tissues and organs when the liver has failed to function normally.

Drug-Induced Movement Disorders

2015 ◽  
Vol 25 (2) ◽  
pp. 70-77
Author(s):  
Amy Lustig ◽  
Cesar Ruiz
Keyword(s):  
Movement Disorders ◽  
Medical Management ◽  
Disease Process ◽  
Underlying Disease ◽  
Extrapyramidal Symptoms ◽  
Drug Induced ◽  
General Overview ◽  
Management Approaches ◽  
Broad Understanding ◽  
Underlying Disease Process

The purpose of this article is to present a general overview of the features of drug-induced movement disorders (DIMDs) comprised by Parkinsonism and extrapyramidal symptoms. Speech-language pathologists (SLPs) who work with patients presenting with these issues must have a broad understanding of the underlying disease process. This article will provide a brief introduction to the neuropathophysiology of DIMDs, a discussion of the associated symptomatology, the pharmacology implicated in causing DIMDs, and the medical management approaches currently in use.

Drug-induced pemphigus foliaceus with features of pemphigus vulgaris

2001 ◽  
Vol 144 (2) ◽  
pp. 421-422 ◽  
Author(s):  
K. Ogata ◽  
H. Nakajima ◽  
M. Ikeda ◽  
Y. Yamamoto ◽  
M. Amagai ◽  
...  
Keyword(s):  
Pemphigus Vulgaris ◽  
Pemphigus Foliaceus ◽  
Drug Induced
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