Drug-induced parkinsonism

2021 ◽  
Vol 13 (6) ◽  
pp. 91-97
Author(s):  
T. M. Ostroumova ◽  
O. D. Ostroumova ◽  
A. S. Soloveva
Keyword(s):  
Adverse Reaction ◽  
Movement Disorder ◽  
Antipsychotic Drugs ◽  
Channel Blockers ◽  
Drug Induced ◽  
Anticholinergic Activity ◽  
Common Drug ◽  
Naranjo Algorithm ◽  
Treatment Onset ◽  
Monoamine Reuptake Inhibitors

Drug-induced parkinsonism (DIP) is the most common drug-induced movement disorder and is most commonly associated with antipsychotic drugs, monoamine reuptake inhibitors, and calcium channel blockers. DIP manifests as a typical movement disorder, which makes it practically indistinguishable from idiopathic Parkinson's disease (PD) and requires differential diagnosis. DIP symptoms develop fairly quickly (hours to weeks) after the antipsychotic is started or after the dose is increased. Therefore, DIP is predominantly a clinical diagnosis that must be kept in mind when a patient develops typical symptoms during treatment onset or increasing the dose of drugs that most often lead to such an adverse reaction (ADR). DIP evaluation includes using the Naranjo algorithm, which helps assess a causal relationship between drug intake and the development of parkinsonism symptoms. The primary DIP treatment is the reduction of the dose of the inducer drug, or its cancellation, or replacement with another drug. In patients with schizophrenia and antipsychotic-induced DIP, dose reduction, replacement with another medication, or prescription of a drug with anticholinergic activity may be possible. The awareness of the doctor and the patient about the possibility of developing this ADR is crucial in the prevention of DIP. Therefore, choosing a drug with the lowest risk of developing DIP is necessary for pharmacotherapy.

Heparin-induced Thrombocytopenia: Towards Consensus

1998 ◽  
Vol 79 (01) ◽  
pp. 1-7 ◽  
Author(s):  
Theodore Warkentin ◽  
Beng Chong ◽  
Andreas Greinacher
Keyword(s):  
Adverse Reaction ◽  
Treatment Approach ◽  
Diagnostic Testing ◽  
Optimal Treatment ◽  
Drug Induced ◽  
Danaparoid Sodium ◽  
Heparin Induced Thrombocytopenia ◽  
Thrombin Inhibition ◽  
Common Drug ◽  
Thrombotic Complications

SummaryHeparin-induced thrombocytopenia (HIT) is a drug-induced, immunoglobulin-mediated thrombocytopenic disorder that is important for at least three reasons. First, it is a relatively common drug-induced immunohematologic adverse reaction. Second, it is frequently complicated by life- and limb-threatening thrombotic complications. And third, there remains uncertainty about the optimal treatment approach for these patients. Recently, there has emerged increasing consensus on such important issues as the frequency, pathogenesis, and diagnostic testing, which we will summarize here. Further, a greater appreciation of the activation of the coagulation pathways in this syndrome indicate a rationale to treatment approaches that emphasize thrombin inhibition (eg. danaparoid sodium; hirudin and its analogues).

Delayed and Often Persistent

2016 ◽  
Author(s):  
Susan H. Fox
Keyword(s):  
Side Effects ◽  
Tardive Dyskinesia ◽  
Movement Disorder ◽  
Movement Disorders ◽  
Antipsychotic Drugs ◽  
Dopamine D2 Receptor ◽  
Treatment Options ◽  
D2 Receptor ◽  
Drug Induced ◽  
Tardive Dystonia

Tardive syndromes are drug-induced hyperkinetic movement disorders that occur as a consequence of dopamine D2 receptor antagonism/blockade. There are several types, including classical tardive dyskinesia, tardive dystonia, tardive tics, tardive myoclonus, and tardive tremor, and it is important to the management of these disorders that the type of movement disorder induced is identified. Tardive syndromes can occur with all antipsychotic drugs, including so-called atypical drugs. Patients taking these drugs should be evaluated frequently for side effects. Evaluating the nature of the movement (i.e., chorea or dystonia) is important because treatment options can differ according to the type of dyskinesia present.

Dyskinesias Associated with Tricyclic Antidepressants

1976 ◽  
Vol 128 (5) ◽  
pp. 490-493 ◽  
Author(s):  
William E. Fann ◽  
John L. Sullivan ◽  
Bruce W. Richman
Keyword(s):  
Side Effects ◽  
Tardive Dyskinesia ◽  
Movement Disorders ◽  
Antipsychotic Drugs ◽  
Tricyclic Antidepressants ◽  
Striatal Dopamine ◽  
Drug Induced ◽  
Anticholinergic Activity ◽  
Extrapyramidal Disorders

SummaryHyperkinetic movement disorders may occur as side effects of antipsychotic drugs; and a hyperdopaminergic state induced by the neuroleptic compounds is thought to be a cause of extrapyramidal disorders such as tardive dyskinesia. We have observed two cases of the dyskinetic syndrome in patients receiving tricyclic antidepressants (TCA). Because the TCA are known to have little effect on striatal dopamine but do share with the neuroleptics potent anticholinergic activity, these cases appear to support the hypothesis that the drug-induced hyperkinetic disorders are related to a diminution of CNS acetylcholine activity as well as to an increase in dopamine activity.

scholarly journals Antipsychotic Drug-Induced Movement Disorders

2003 ◽  
Vol 30 (S1) ◽  
pp. S101-S107 ◽  
Author(s):  
Pierre J. Blanchet
Keyword(s):  
Movement Disorders ◽  
Antipsychotic Drugs ◽  
Involuntary Movement ◽  
Short Review ◽  
Central Place ◽  
Channel Blockers ◽  
Motor Complications ◽  
Drug Induced ◽  
Receptor Blocking ◽  
High Index Of Suspicion

Very early in the process of diagnosing abnormal involuntary movement (AIM) disorders, one can be rewarded by keeping a high index of suspicion for possible drug-induced causes, not only through a complete list of current medications, but also identification of the drugs the patient used to take and other possible offending medications that might be available from family members and other sources. Among drug-induced movement disorders, antipsychotic drugs and other dopamine receptor blocking agents occupy a central place. Their various acute and tardive motor complications provide the template of this short review. Movement disorders caused by antidepressants, lithium, antiemetics, antiparkinsonian agents, anticonvulsants, calcium channel blockers, sympathomimetics and others are only briefly covered in table form.

scholarly journals Drugs associated with DIP

2021 ◽  
pp. 109-118
Author(s):  
T. M. Ostroumova ◽  
O. D. Ostroumova ◽  
A. S. Soloveva
Keyword(s):  
Relative Risk ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Antipsychotic Drugs ◽  
Lewy Bodies ◽  
Lithium Carbonate ◽  
Channel Blockers ◽  
Minimal Risk ◽  
Drug Induced ◽  
Extrapyramidal Disorders ◽  
Increased Risk

Drug-induced parkinsonism (DIP) is one of the most frequent extrapyramidal disorders that develops against the background of prescribing a large number of medications. Initially, DIP was described as an adverse drug reactions (ADRs) against the background of the use of antipsychotic drugs, but later recognized as ADRs of a number of other drugs, including prokinetics, antidepressants, calcium channel blockers and antiepileptic drugs. The relative risk of developing LIP on the background of taking typical antipsychotics increased by 2.92 times compared to patients who do not take these drugs. The risk of developing DIP in patients receiving flunarizine is increased by 2.75-4.07 times. The risk of DIP with the use of antidepressants is increased by 2.14 times, among the drugs of this group with an increased risk of DIP, the use of selective serotonin reuptake inhibitors is most often associated with DIP (relative risk 1.24). Among other antidepressants, there is evidence of the development of DIP against the background of the use of duloxetine, mirtazapine, amitriptyll clomipramine, venlafaxine, trazodone. Among anticonvulsants, DIP can rarely develop against the background of the appointment of valproic acid, gabapentin, pregabalin, carbamazepine, oxcarbazepine. The risk of DIP in patients receiving metoclopramide is extremely low (0.06%), but it is 2.16 times higher compared to people who do not take this drug. Among drugs from other groups, DIP can occur against the background of the use of lithium carbonate, tacrolimus, cyclosporine, amiodarone, captopril, amphotericin B. If DIP develops, it is necessary, if possible, to reduce the dose or cancel the inducer drug, or replace it with another drug with minimal risk of DIP. Symptoms of DIP most often regress within a few weeks or months after dose reduction or withdrawal of the drug inducer. If the symptoms persist longer, it is necessary to exclude the presence of Parkinson’s disease or dementia with with Lewy bodies.

Treatment Methods Conditioned by the Gravity of Drug-Induced Gingival Hyperplasias

2017 ◽  
Vol 68 (11) ◽  
pp. 2618-2622
Author(s):  
Alina Mihaela Calin ◽  
Mihaela Debita ◽  
Raluca Dragomir ◽  
Ovidiu Mihail Stefanescu ◽  
Cristian Budacu ◽  
...  
Keyword(s):  
Dental Treatment ◽  
Histopathological Examination ◽  
Transplant Rejection ◽  
Surgical Excision ◽  
Channel Blockers ◽  
Gingival Hyperplasia ◽  
Drug Induced ◽  
Treatment Methods ◽  
Systemic Medication ◽  
Bacterial Plaque

The first drug discovered to be involved in the development of gingival hyperplasia is phenytoin, which is indicated in the treatment of epileptic patients. The other drugs are calcium channel blockers with vasodilating effect. The most important one is Nifedipine, while Ciclosporin A, which is used as an immunosuppressant in the prevention of transplant rejection, causes gingival hyperplasia as a secondary effect. Gingival hyperplasia can reach an impressive volume, completely covering the dental crown and affecting the masticatory and physiognomic functions. The elucidation of the mechanism, by which drug-induced gingival hyperplasia occurs, favoring factors and the choice of conservative or surgical treatment methods, emphasizing the prophylactic treatment. The study batch was subject to intraoral and extraoral clinical examinations and the data were included in the dental treatment sheet of each patient, 11 patients aged over 60 years, who came to the Clinic ... in the period 2014-2016. The diagnosis was based on the anamnesis, the clinical aspect of the lesions and the histopathological examination. After the surgical excision of the hyperplasia affected area, recurrence was prevented by dispensarizing the patients and controlling the bacterial plaque through rigorous oral hygiene. Treatment depends on the severity of the lesions, as well as on the physionomic and masticatory functions. Conservative etiological therapy is attempted, by removing the bacterial plaque and local irritant factors, by reducing the dose of drugs, or by changing the systemic medication.

Non-chemotherapy drug-induced agranulocytosis in a tertiary hospital

2015 ◽  
Vol 35 (3) ◽  
pp. 244-250 ◽  
Author(s):  
R Navarro-Martínez ◽  
E Chover-Sierra ◽  
O Cauli
Keyword(s):  
Adverse Drug Reaction ◽  
Drug Reaction ◽  
Tertiary Hospital ◽  
Negative Association ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Drug Induced ◽  
Common Drug ◽  
Low Incidence ◽  
Stimulating Factor

Drug-induced agranulocytosis is a rare haematological disorder considered as severe adverse drug reaction. Due to its low incidence, the number of studies are low and the variability of clinical features and presentation in hospitalized patients is rarely described. Awe performed an observational, transversal and retrospective study in the haematology and toxicology unit in a tertiary hospital located in Spain (Valencia) (1996–2010) in order to assess its incidence, the drugs involved, the management and outcomes of drug-induced agranulocytosis. Twenty-one cases of agranulocytosis were retrieved. All of them presented severe and symptomatic agranulocytosis (fever and infection). The most common drug associated with drug-induced agranulocytosis was metamizole administration but other drugs belonging to different pharmacological classes as well (carbimazol, sulfasalazine, bisoprolol, itraconazole, amitryptiline, ketorolac and claritomicine+cefuroxime). No differences between sex and age were found in relationship with the manifestations or course of agranulocytosis. In contrast, a significantly negative association was found between age of patients and the percentage of increase in neutrophil count. Administration of human granulocyte colony-stimulating factor did not significantly enhance the recovery of the process or the restoration of leucocytes count, suggesting a limited utility in this type of agranulocytosis.

scholarly journals Drug-Induced Heart Failure (Part 2: Mechanisms of Development, Clinical Signs, Differential Diagnosis, Risk Factors, Treatment and Prevention)

2020 ◽  
Vol 8 (2) ◽  
pp. 57-65
Author(s):  
O. D. Ostroumova ◽  
I. V. Goloborodova
Keyword(s):  
Heart Failure ◽  
Beta Blockers ◽  
Clinical Signs ◽  
Clinical Manifestations ◽  
Left Ventricular ◽  
Clinical Syndrome ◽  
Channel Blockers ◽  
Drug Induced ◽  
Treatment And Prevention ◽  
Developing Heart

Heart failure is a complex clinical syndrome caused by an impaired pumping function of the heart muscle, etiologically associated with cardiovascular disease and, in the vast majority of cases, requiring complex therapeutic regimens and simultaneous prescription of several drugs. To date, we know several classes of drugs (including those used for heart failure) which can induce development/progression of heart failure in both patients with left ventricular dysfunction, and in patients who do not have cardiovascular diseases. The aim of the study was to analyse and systematize data on development mechanisms, as well as methods of prevention and treatment of drug-induced heart failure when using diff erent groups of drugs. It has been established that drug-induced heart failure is most often associated with the use of calcium channel blockers (verapamil, diltiazem, nifedipine), beta-blockers, antiarrhythmic drugs (disopyramide, fl ecainide, propafenone, amiodarone, ibutilide, dofetilide, dronedarone), anthracyclines (doxorubicin) and other antitumor drugs (trastuzumab, bevacizumab, infl iximab), hypoglycemic drugs (thiazolidinediones, saxagliptin, alogliptin), and nonsteroidal anti-infl ammatory drugs, including selective cyclooxygenase-2 inhibitors. The study revealed various mechanisms of heart failure development following drug treatment. In some patients, heart failure development is associated with the cardiotoxic eff ect of a particular drug, in others with adverse eff ects on hemodynamics. Much depends on risks of developing heart failure, including specifi c risks attributable to groups of drugs and individual drugs. The identifi cation of drugs that can contribute to the development/ progression of heart failure, and possible clinical manifestations of drug-induced heart failure, as well as provision of timely information to physicians, and engagement of clinical pharmacologists with the aim of optimizing treatment of patients can facilitate timely diagnosis, treatment and prevention of drug-induced heart failure. 

scholarly journals Drug-Induced Gingival Overgrowth in an 8-Year-Old Girl: A Case Report

2021 ◽  
Vol 13 (3) ◽  
pp. 109-112
Author(s):  
Parviz Torkzaban ◽  
Amir Talaie
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Case Report ◽  
Autoimmune Disease ◽  
Lupus Erythematosus ◽  
Immunological Tolerance ◽  
Systemic Autoimmune Disease ◽  
Channel Blockers ◽  
Systemic Lupus ◽  
Drug Induced ◽  
Gingival Overgrowth

Systemic lupus erythematosus is a systemic autoimmune disease that involves multi organs. Genetic, endocrine, immunological, and environmental factors influence the loss of immunological tolerance against self-antigens leading to the formation of pathogenic autoantibodies that cause tissue damage through multiple mechanisms. The gingival overgrowth can be caused by three factors: noninflammatory, hyperplastic reaction to the medication; chronic inflammatory hyperplasia; or a combined enlargement due to chronic inflammation and drug-induced hyperplasia. Drug-Induced Gingival Overgrowth is associated with the use of three major classes of drugs, namely anticonvulsants, calcium channel blockers, and immunosuppressants. Due to recent indications for these drugs, their use continues to grow.

scholarly journals A review on drug induced skin disorders: pathophysiology and therapeutics

2020 ◽  
Vol 6 (5) ◽  
pp. 715
Author(s):  
Priyanka N. ◽  
R. Srinivasan
Keyword(s):  
Adverse Drug Events ◽  
Treatment Approach ◽  
Current Evidence ◽  
Fixed Dose ◽  
Positive Outcomes ◽  
Skin Disorders ◽  
Drug Induced ◽  
Common Drug ◽  
Online Library ◽  
Risk And Benefit

<p class="abstract"><span lang="EN-US">Drugs are the central part of treatment of various disorders. The consequence of drug use may be either positive outcomes (clinical effect of the drug) or negative outcomes (adverse drug events). That is, it contains both risk and benefit. In recent years multiple disorders treated with many drugs by monotherapy or by fixed-dose therapy existing in the market which leads to increased drug-related problems one among that is drug-induced disorders. Morbidity and mortality have increased due to drug-induced disorders. This study was aimed to describe the various drugs induces skin disorders, its pathophysiology, diagnosis and treatment approach. We completed a review of the current evidence for various drug-induced skin disorders its causative drugs and therapeutic intervention of drug-induced skin disorders. A review through Medline, Embase, Pubmed, Wiley online library and selected studies related to drug-induced skin disorders. This is the comprehensive review of drug- induced skin disorders, designed to address prospectively its etiopathogenesis and clinical management. Penicillin, sulfa, phenyl-butazone, Tetracycline are the most common drug induces various skin disorders. There is not much significant differences in the clinical, histopathological or immuno-pathological features between various skin disorders and drug induced skin disorders. Hence knowing the etiopathology, and differential diagnosis is important to a proper treatment approach.</span></p>

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