• Title/Summary/Keyword: drug induced

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Drug-Induced Dyskinesia Treated with Korean Medicine: A Case Report

  • Soo Min Ryu;Jung Won Byun;You Jin Heo;Eun Yong Lee;Cham Kyul Lee;Na Young Jo;Jeong-Du Roh
    • Journal of Acupuncture Research
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    • v.40 no.2
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    • pp.150-155
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    • 2023
  • Drug-induced dyskinesia is an involuntary muscle movement caused by various dopamine receptor-blocking drug exposure, such as antipsychotics, antidepressants, and antiemetics. Causative drug removal is the main treatment for drug-induced dyskinesia whenever possible because its pathophysiology lacks a universally accepted mechanism; however, the symptoms can persist for years or decades in many patients even after causative drug removal. Herein, we present a case of drug-induced dyskinesia in a 61-year-old female patient who consumed medication for approximately 10 years for her depression, anxiety, and insomnia. Cervical and facial dyskinesia was suggested to be related to perphenazine and levosulpiride administration. The patient received acupuncture, pharmacopuncture, herbal medicine, and chuna treatment for 81 days during hospitalization. The symptoms were evaluated using the Abnormal Involuntary Movement Scale, Toronto Western Spasmodic Torticollis Rating Scale, Tsui's score, and Numeric Rating Scale, which revealed remarkable improvement, suggesting the effectiveness of combined Korean medicine for drug-induced dyskinesia.

Drug-Induced Dyskinesia Outpatient Suspected to be Induced by Risperidone Management with Yigan-san with Citri Pericarpium and Pinelliae Rhizoma (modified Yigan-san, Yokukan-san Kachimpihang), Electro-Acupuncture at GB34 (陽陵泉), and Stopping Suspected Medication: A Case Report (Risperidone으로 유발된 것으로 의심된 약물유발성 이상운동증에 대한 의심약물 중단 및 억간산가진피반하와 GB34(陽陵泉) 전침치료를 통한 외래기반 관리 : 증례보고)

  • Roh, Min-yeong;Jang, Seung-won;Kim, Hyun-ho;Han, Yang-hee;Leem, Jungtae
    • The Journal of Internal Korean Medicine
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    • v.40 no.6
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    • pp.1303-1310
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    • 2019
  • Objectives: Drug-induced Parkinsonism has similar symptoms to Parkinson's disease, but each has different causes. Drug-induced Parkinsonism accounts for the largest proportion of secondary Parkinsonism We report a outpatient case of drug-induced Parkinsonism after taking Risperidone, an atypical antipsychotic. Method: With discontinuing of antipsychotic drug, modified Yigan-san extract was administered for 12 weeks, and acupuncture and electroacupuncture procedures were performed 20 times. Results: Abnormal Involuntary Movement Scale (AIMS) score decreased from 23 to 3 during 59 days of treatment period without adverse events and worsening of depression. The Patient was highly satisfied. Conclusion: Modified Yigan-san and electroacupuncture (GB34) can be used as an treatment option in patients with drug-induced Parkinsonism.

A Case Report of Drug-Induced Parkinsonism Treated with Jodeung-san and Electro-acupuncture at GB34 (조등산(Diaoteng-san, Choto-san, 釣藤散)과 GB34(陽陵泉) 전침치료를 활용한 약인성파킨슨증후군 환자의 증례 1례)

  • Kim, Eun-ji;Song, Ho-joon;Kim, Hyun-ho;Han, Yang-hee;Leem, Jung-tae
    • The Journal of Internal Korean Medicine
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    • v.38 no.5
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    • pp.600-609
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    • 2017
  • Drug-induced Parkinsonism is the most frequently observed type among the cases of secondary Parkinsonism. Besides typical parkinsonian symptoms, such as tremor, rigidity and bradykinesia, drug-induced Parkinsonism manifests with additional simultaneous symptoms like orobuccolingual dyskinesia, mixed type of tremor (resting, action), and symmetry of expressions. We present a case of drug-induced Parkinsonism, affected by taking the antiulcer drug cimetidine. Jodeung-san extract (Choto-san, Tsumura Co. 10) was administered for 7 days and acupuncture (electronic, auricular, pharmacopuncture) was conducted 3 times. The clinical outcomes were then evaluated through the patient's global impression of change, visual analogue scale, and Hoehn and Yahr stage. After the treatment, the clinical features, such as tremor and orobuccolingual dyskinesia, disappeared. The combination of Jodeung-san and electro-acupuncture at GB34 could therefore be a remedy for the patients with drug-induced Parkinsonism.

Drug induced Pulmonary Edema (약물 유발성폐부종)

  • Sung, Si-Han;Jang, Hye-Young;Lim, Hoon
    • Journal of The Korean Society of Clinical Toxicology
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    • v.8 no.2
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    • pp.113-121
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    • 2010
  • Purpose: Drug-induced non-cardiogenic pulmonary edema has been reported on in a drug case series. For most of the agents that cause pulmonary edema, the pathogenic mechanisms that are responsible for the pulmonary edema remain unknown. We report here on the cases of suspected drug-induced pulmonary edema and we analyze the clinical characteristics. Methods: We reviewed the medical records of 1,345 patients who had drug adverse effects and drug poisoning from January 2005 to July 2010, and 480 of these patients were admitted to the EM Department. Among them, 17 patients developed abnormal chest radiological findings and they were analyzed for any clinical characteristics, the initial symptoms, securing the airway and the clinical results. Results: Seventeen patients out of 480 (3.54%) developed drug-induced abnormal chest radiographic pulmonary edema; they displayed initial symptoms that included mental change (41.2%), dyspnea (17.6%), vomiting (11.8%), etc, and some displayed no symptoms at all (11.8%). Only 3 patients out of the 11 who died or had severe pulmonary edema were able to obtain an advanced airway prior to their arrival to the EM Department. Clinical recovery was generally rapid and this was mostly completed within 6 hours. The mortality rate was 11.8% (2 of 17 patients), and the causative drugs were found to be propofol (35.3%, 6 of 17 patients), multiple drugs (41.2% or 7 out of 17) and one patient each with ephedrine, ethylene glycol, doxylamine and an unknown drug, respectively. Conclusion: Drug-induced pulmonary edema and deaths are not uncommon, and recovery is typically rapid with few long-term sequelae when drug administration is discontinued. Oxygen therapy and securing the airway must be performed during transportation for patients with pulmonary edema.

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Minocycline-Induced Autoimmune Hepatitis: A Rare But Important Cause of Drug-Induced Autoimmune Hepatitis

  • Harmon, Elizabeth G.;McConnie, Randolph;Kesavan, Anil
    • Pediatric Gastroenterology, Hepatology & Nutrition
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    • v.21 no.4
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    • pp.347-350
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    • 2018
  • Drug-induced autoimmune hepatitis (DIAIH) is an increasingly recognized form of drug-induced liver injury that leads to a condition similar to idiopathic autoimmune hepatitis. A number of drugs have been associated with DIAIH, minocycline is one of the most well characterized. Minocycline is a semisynthetic tetracycline antibiotic used in the treatment of acne vulgaris. Minocycline-induced autoimmune hepatitis presents with serologic and histologic features similar to idiopathic autoimmune hepatitis. However, the natural history and outcomes of these two conditions differ significantly. The majority of patients with minocycline-induced autoimmune hepatitis experience complete resolution of symptoms after withdrawal of the medication. Some patients may require a short course of steroids and rarely use of an immunomodulator to achieve resolution of disease. Recurrence of symptoms is rare and typically only occurs with reintroduction of minocycline. It is important for primary care providers to consider minocycline-induced autoimmune hepatitis when liver injury develops during minocycline therapy.

Review for Herbal Drug and Drug-Induced Liver Injury

  • Park, Bong-Ky;Son, Chang-Gue
    • The Journal of Korean Medicine
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    • v.31 no.3
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    • pp.128-132
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    • 2010
  • Objectives: This study aimed to review the general features of drug induced liver injury (DILI) and the important factors in consideration of herbal drugs and DILI. Methods: We reviewed general aspects of DILI such as classification, inducible factors, diagnosis methods, prevention, and the status of herbal drug-associated DILI via literature. Results: Besides the drug itself, genetic and environmental factors affect hepatic toxicity. There is a lack of definitive diagnoses of DILI by drugs, including herbal remedies. The possibility of herbal drug-associated DILI is exaggerated, and majority of herbal drug-derived hepatic injury could be easily prevented if Oriental doctors pay attention to this issue. Conclusion: This study can provide Oriental doctors an overview and be helpful in minimizing the episodes of hepatotoxicity in use of herbal drugs.

Ginsenoside Rb1 attenuates methamphetamine (METH)-induced neurotoxicity through the NR2B/ERK/CREB/BDNF signalings in vitro and in vivo models

  • Yang, Genmeng;Li, Juan;Peng, Yanxia;Shen, Baoyu;Li, Yuanyuan;Liu, Liu;Wang, Chan;Xu, Yue;Lin, Shucheng;Zhang, Shuwei;Tan, Yi;Zhang, Huijie;Zeng, Xiaofeng;Li, Qi;Lu, Gang
    • Journal of Ginseng Research
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    • v.46 no.3
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    • pp.426-434
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    • 2022
  • Aim: This study investigates the effects of ginsenoside Rb1 (GsRb1) on methamphetamine (METH)-induced toxicity in SH-SY5Y neuroblastoma cells and METH-induced conditioned place preference (CPP) in adult Sprague-Dawley rats. It also examines whether GsRb1 can regulate these effects through the NR2B/ERK/CREB/BDNF signaling pathways. Methods: SH-SY5Y cells were pretreated with GsRb1 (20 mM and 40 mM) for 1 h, followed by METH treatment (2 mM) for 24 h. Rats were treated with METH (2 mg/kg) or saline on alternating days for 10 days to allow CPP to be examined. GsRb1 (5, 10, and 20 mg/kg) was injected intraperitoneally 1 h before METH or saline. Western blot was used to examine the protein expression of NR2B, ERK, P-ERK, CREB, P-CREB, and BDNF in the SH-SY5Y cells and the rats' hippocampus, nucleus accumbens (NAc), and prefrontal cortex (PFC). Results: METH dose-dependently reduced the viability of SH-SY5Y cells. Pretreatment of cells with 40 µM of GsRb1 increased cell viability and reduced the expression of METH-induced NR2B, p-ERK, p-CREB and BDNF. GsRb1 also attenuated the expression of METH CPP in a dose-dependent manner in rats. Further, GsRb1 dose-dependently reduced the expression of METH-induced NR2B, p-ERK, p-CREB, and BDNF in the PFC, hippocampus, and NAc of rats. Conclusion: GsRb1 regulated METH-induced neurotoxicity in vitro and METH-induced CPP through the NR2B/ERK/CREB/BDNF regulatory pathway. GsRb1 could be a therapeutic target for treating METH-induced neurotoxicity or METH addiction.

Gene Expression Analysis for Statin-induced Cytotoxicity from Rat Primary Hepatocytes

  • Ko, Moon-Jeong;Ahn, Joon-Ik;Shin, Hee-Jung;Kim, Hye-Soo;Chung, Hye-Joo;Jeong, Ho-Sang
    • Genomics & Informatics
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    • v.8 no.1
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    • pp.41-49
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    • 2010
  • Statins are competitive inhibitors of hydroxy-3-methyl glutaryl coenzyme A (HMG-CoA) reductase and used most frequently to reduce plasma cholesterol levels and to decrease cardiovascular events. However, statins also have been reported to have undesirable side effects such as myotoxicity and hepatotoxicity associated with their intrinsic efficacy mechanisms. Clinical studies recurrently reported that statin therapy elevated the level of liver enzymes such as ALT and AST in patients suggesting possible liver toxicity due to statins. This observation has been drawn great attention since statins are the most prescribed drugs and statin-therapy was extended to a larger number of high-risk patients. Here we employed rat primary hepatocytes and microarray technique to understand underlying mechanism responsible for statin-induced liver toxicity on cell level. We isolated genes whose expressions were commonly modulated by statin treatments and examined their biological functions. It is of interest that those genes have function related to response to stress in particular immunity and defense in cells. Our study provided the basic information on cellular mechanism of statin-induced cytotoxicity and may serve for finding indicator genes of statin -induced toxicity in rat primary hepatocytes.

A Review on Chemical-Induced Inflammatory Bowel Disease Models in Rodents

  • Randhawa, Puneet Kaur;Singh, Kavinder;Singh, Nirmal;Jaggi, Amteshwar Singh
    • The Korean Journal of Physiology and Pharmacology
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    • v.18 no.4
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    • pp.279-288
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    • 2014
  • Ulcerative colitis and Crohn's disease are a set of chronic, idiopathic, immunological and relapsing inflammatory disorders of the gastrointestinal tract referred to as inflammatory bowel disorder (IBD). Although the etiological factors involved in the perpetuation of IBD remain uncertain, development of various animal models provides new insights to unveil the onset and the progression of IBD. Various chemical-induced colitis models are widely used on laboratory scale. Furthermore, these models closely mimic morphological, histopathological and symptomatical features of human IBD. Among the chemical-induced colitis models, trinitrobenzene sulfonic acid (TNBS)-induced colitis, oxazolone induced-colitis and dextran sulphate sodium (DSS)-induced colitis models are most widely used. TNBS elicits Th-1 driven immune response, whereas oxazolone predominantly exhibits immune response of Th-2 phenotype. DSS-induced colitis model also induces changes in Th-1/Th-2 cytokine profile. The present review discusses the methodology and rationale of using various chemical-induced colitis models for evaluating the pathogenesis of IBD.