Drug-induced bullous lichenoid eruption: a side effect of nivolumab triggered by the TLR agonist imiquimod

2021 ◽  
Vol 31 (1) ◽  
pp. 91-92
Author(s):  
Ingrid Costedoat ◽  
R. Vergara ◽  
Lea Dousset ◽  
Emilie Gerard ◽  
Sorilla Prey ◽  
...  
2018 ◽  
Vol 8 (2) ◽  
pp. 172-176
Author(s):  
Wasim Md Mohosin Ul Haque ◽  
Tabassum Samad ◽  
Muhammad Abdur Rahim ◽  
Shudhanshu Kumar Saha ◽  
Sarwar Iqbal

Drug induced encephalopathy is an established side effect of many drugs when used in a higher dose. Though we do not encounter this side effect frequently in our day to day practice, yet with renal impairment this is not uncommon. Even with a reduced dose many of these can precipitate encephalopathy in this special group of patients. We are presenting here a series of seven such cases of drug induced encephalopathy in patients with renal impairment.Birdem Med J 2018; 8(2): 172-176


2021 ◽  
pp. 662-666
Author(s):  
Mitra Barahimi ◽  
Scott Lee ◽  
Kindra Clark-Snustad

We report the case of a 51-year-old male with Crohn’s disease (CD) who developed a reproducible pustular rash after ustekinumab (UST) administration. The patient first presented with a pustular rash on his hands, body, extremities, and scalp starting 5 weeks after his initial weight-based UST induction. The rash resolved spontaneously, then recurred 4 weeks after his first subcutaneous maintenance dose of UST 90 mg. Biopsy of the affected area demonstrated subcorneal pustular dermatosis (SPD). UST was discontinued and the rash resolved. Unfortunately, the patient experienced clinical recurrence of CD, and given prior failure of multiple CD medications, UST was restarted with premedication. Two weeks after UST re-induction, the rash recurred, though less severe. Given improvement in CD symptoms, UST was continued and the rash managed with topical corticosteroids. This is the first case of drug-induced SPD associated with UST. One case report has previously described de novo pustular psoriasis associated with UST in a patient with CD and enteropathic arthritis. Notably, SPD and pustular psoriasis can be histologically indistinguishable. The development of a paradoxical psoriasiform rash is thought to be one of the few dose and duration dependent side effects of TNF-antagonist therapy but has not previously been established as a side effect of UST. This case demonstrates a new potential side effect of UST.


Author(s):  
Masaki Maehara ◽  
Masayasu Sugiyama

Sexual dysfunction (SD) is a common side effect of antipsychotics. The community pharmacist assessed a patient with SD and suggested a change in prescription from risperidone and haloperidol to aripiprazole that improved SD. This is the first report on amelioration of antipsychotic-induced SD by early intervention by community pharmacists.


2017 ◽  
Vol 2017 ◽  
pp. 1-7
Author(s):  
Dong Li ◽  
Aixin Li ◽  
Hairui Zhou ◽  
Xi Wang ◽  
Peng Li ◽  
...  

Drug-induced myopathy (DIM) is a rare side effect; however, the consequence could be fatal. There are few reports to systematically assess the underlying mechanism of DIM. In this study, we curated the comprehensive DIM drug list based on structured labeling products (SPLs) and carried out the analysis based on chemical structure space, drug protein interaction, side effect space, and transcriptomic profiling space. Some key features are enriched from each of analysis. Specifically, the similarity of DIM drugs is more significant than random chance, which shows that the chemical structure could distinguish the DIM-positive drugs from negatives. The cytochrome P450 (CYP) was identified to be shared by DIM drugs, which indicated the important role of metabolism in DIM. Three pathways including pathways in cancer, MAPK signaling pathway, and GnRH signaling pathway enriched based on transcriptomic analysis may explain the underlying mechanism of DIM. Although the DIM is the current focus of the study, the proposed approaches could be applied to other toxicity assessments and facilitate the safety evaluation.


2021 ◽  
Vol 16 ◽  
Author(s):  
Suryanarayana Challa Reddy ◽  
Naresh Midha ◽  
Vivek Chhabra ◽  
Deepak Kumar ◽  
Gopal Krishna Bohra

Background: DIGO or drug-induced gingival overgrowth occurs as a side effect of certain drugs. Until now, the etiology of drug-induced gingival overgrowth is not clearly understood. Among the calcium channel blockers, nifedipine has been shown to be most frequently associated with drug-induced gingival hyperplasia. Amlodipine is a comparatively newer calcium channel blocker that witha longer duration of action and lesser side effects as compared to nifedipine. There are only certain case reports of amlodipine-induced gum hyperplasia. Case presentation: We report a case of amlodipine-induced gum hyperplasia in a 66-year-old hypertensive patient taking amlodipine at a dose of 5 mg once a day. There was significant regression of gum hypertrophy after substitution of amlodipine by Losartan. Conclusion: Amlodipine is one of the commonly prescribed antihypertensive drugs, and gingival hyperplasia is one overlooked side effect in patients taking amlodipine. Awareness of this potential side effect of amlodipine may be helpful to reduce the anxiety of patients and the cost of diagnostic procedures.


2020 ◽  
Vol 13 (8) ◽  
pp. e235528 ◽  
Author(s):  
Layan El-khatib ◽  
Hussayn Alrayes ◽  
Omar Sallam ◽  
Ahmed Elbanna

Quinidine is one of the oldest antiarrhythmics known. Over the years, its use has decreased along with its side effects. Our case describes a 69-year-old woman with recurrent resistant ventricular tachycardia on Quinidine and Amiodarone who presented with acute liver toxicity. Drug-induced liver toxicity was at the top of our differential diagnosis list. Taking multiple factors into consideration, a decision was made to discontinue Quinidine, the patient’s symptoms and lab abnormalities resolved within 1 week, yielding the diagnosis of Quinidine hypersensitivity.


Author(s):  
Péter Farkas ◽  
Dávid Szatmári ◽  
Franciska Könczöl ◽  
Dénes Lőrinczy

AbstractSeveral kind of drugs—used in cancer treatments—such as cyclophosphamide (CP) can also trigger a disease classified as toxic polyneuropathy. Polyneuropathy is a simultaneous malfunction of several peripheral nerves, typical side effect of a cancer therapy. In our previous study, we used CP treated in vitro animal model (Guinea pig) with a comparable dosage and time handling of human protocol to show evidences of this drug-induced effects. We could show a dose-dependent difference between in Tm and ΔHcal of untreated and treated samples assigned to their intact muscle and nerve, blood plasma and red blood cells. In our current study we analyze this side effect on skeletal muscle actin (prepared from m. psoas of rabbit) by DSC (differential scanning calorimetry), to follow the possible consequence of drug treatment on the “activator” of muscle contraction. We have demonstrated that run of DSC curves, Tms together with the ΔHcal exhibit clear CP effect. In case of Ca2+ G actin it is manifested in a well separated second high denaturing temperature as a consequence of CP binding into the cleft. This way the nucleotide binding cleft with subdomains 1 and 3 becomes less flexible, indicating clear sensitivity to CP treatment. In F-actin samples, the main peak represents the thermal denaturation of subdomains 1 and 3, and the increased calorimetric enthalpy administrating Ca2+ as well as CP refers to a more rigid structure. These alterations can be the molecular background in the malfunction of muscle in case of polyneuropathy after CP treatment.


2009 ◽  
Vol 11 (1) ◽  
pp. 7-16 ◽  
Author(s):  
Susan G. Dorsey ◽  
Carmen C. Leitch ◽  
Cynthia L. Renn ◽  
Sherrie Lessans ◽  
Barbara A. Smith ◽  
...  

Painful peripheral neuropathy is a debilitating complication of the treatment of HIV with nucleoside reverse transcriptase inhibitors (NRTIs). Patients are living longer with these drugs; however many develop excruciating, unremitting, and often treatment-limiting neuropathy that is resistant to conventional pain management therapies. Improving patient comfort and quality of life is paramount and depends on a clearer understanding of this devastating side effect. The mechanisms underlying the development of NRTI-induced neuropathy, however, remain unclear. Using a mouse model of NRTI-induced neuropathy, the authors conducted an unbiased whole-genome microarray screen to identify molecular targets in the spinal dorsal horn, which is the location where integration of ascending sensory transmission and descending modulatory effects occur. Analysis of the microarray data identified a change in the gene giant axonal neuropathy 1 (Gan1). Mutation of this gene has been linked to the development of giant axonal neuropathy (GAN), a rare autosomal recessive condition characterized by a progressive sensorimotor neuropathy. Gan1 has not been previously linked to nerve pathologies in other populations. In this study, downregulation of the Gan1 gene and the gene protein product, gigaxonin, was validated via quantitative polymerase chain reaction ([qPCR] gene expression) and Western blot analyses (protein level). Our report is the first to suggest that Gan1 might be a novel molecular target in the development of NRTI-induced peripheral neuropathy with implications for new therapeutic approaches to preventing or reducing a significant side effect of HIV treatment.


2016 ◽  
Vol 7 (5) ◽  
pp. 135-137
Author(s):  
Robin George Manappallil ◽  
Vinod Krishnan

Etoricoxib  is  a  selective  cyclo-oxygenase  2  inhibitor,  commonly  used  in  treatment  of  rheumatoid  arthritis,  gout  and  back  pain.  Pretibial  edema  and  erythema,  gastric  irritation  and  risks  of  cardiovascular  and  cerebrovascular  thrombotic  events  are  some  of  the  reported  adverse  effects  due  to  etoricoxib.  This  case  report  is  regarding  a  patient  who  presented  with  wet  purpura  following  etoricoxib  intake.  Drug  induced  thrombocytopenia  is  an  unreported  side  effect  of  etoricoxib.Asian Journal of Medical Sciences Vol.7(5) 2016 135-137


1993 ◽  
Vol 60 (4) ◽  
pp. 354-356
Author(s):  
Y. Talmon ◽  
M. Guy ◽  
S. Eisenkraft ◽  
N. Guy

Three chronic paranoid schizophrenic patients were treated with clozapine, a new anti-psychotic agent. Retrograde ejaculation developed as a side-effect. Stopping the drug therapy or reducing the dosage caused the side-effect to disappear. Re-challenge caused the return of the side-effect. We discuss this rare side-effect to clozapine, and the pathophysiological mechanisms of ejaculation disturbances, with emphasis on those that are drug-induced.


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