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.

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.

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.

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 OLANZAPINE INDUCED BRUXISM

2021 ◽  
Vol 10 (5) ◽  
pp. 3597-3600
Author(s):  
Tathagata Roy
Keyword(s):  
Selective Serotonin Reuptake Inhibitors ◽  
Antipsychotic Drugs ◽  
Healthcare Professionals ◽  
Causality Assessment ◽  
Drug Induced ◽  
Clinical Complications ◽  
Hematological Tests ◽  
Probable Relation

Iatrogenic or drug induced disease is of great clinical significance in therapeutics. Treatment with antidepressants like selective serotonin reuptake inhibitors (SSRIs) and antipsychotics reveal Bruxism (excessive grinding and clenching of the teeth) as such type of iatrogenic disease, however it is rarely found with atypical antipsychotic drugs like Olanzapine. A 50-year male patient, suffering from schizophrenia was under regular antipsychotic medication receiving Tab. Olanzapine 5 mg O.D., Tab. Clonazepam 0.5 mg O.D. regularly for past 25 years. Recently he gradually developed excessive grinding and clenching of teeth despite of any dental and ENT clinical complications. Biochemical and hematological tests also showed normal result. On admission with the complication of bruxism, tab. Olanzapine dose was reduced to 2.5 mg OD, however even after dose reduction there was not much improvement in bruxism. On the 4th day of the admission tab. Olanzapine has been substituted with tab. Clozapine 50 mg TDS. After 1 week of withdrawal of Olanzapine there was no complain of bruxism and he was discharged. On follow up after 1month the complication was occasional. Causality assessment revealed a probable relation between Olanzapine and Bruxism. Though among the atypical neuroleptics, extrapyramidal side effects are thought to be less common with olanzapine, but it may cause fatal consequences. Therefore, this case study and proper investigation may be helpful in designing the treatment strategy in more effective way and also aware all the healthcare professionals to monitor the patients on neuroleptics.

scholarly journals Understanding the Effects of Antipsychotics on Appetite Control

2022 ◽  
Vol 8 ◽  
Author(s):  
Sayani Mukherjee ◽  
Silje Skrede ◽  
Edward Milbank ◽  
Ramaroson Andriantsitohaina ◽  
Miguel López ◽  
...  
Keyword(s):  
Side Effects ◽  
Receptor Binding ◽  
First Generation ◽  
Antipsychotic Drugs ◽  
Molecular Mechanisms ◽  
Extrapyramidal Side Effects ◽  
Appetite Control ◽  
Drug Induced ◽  
Increased Risk

Antipsychotic drugs (APDs) represent a cornerstone in the treatment of schizophrenia and other psychoses. The effectiveness of the first generation (typical) APDs are hampered by so-called extrapyramidal side effects, and they have gradually been replaced by second (atypical) and third-generation APDs, with less extrapyramidal side effects and, in some cases, improved efficacy. However, the use of many of the current APDs has been limited due to their propensity to stimulate appetite, weight gain, and increased risk for developing type 2 diabetes and cardiovascular disease in this patient group. The mechanisms behind the appetite-stimulating effects of the various APDs are not fully elucidated, partly because their diverse receptor binding profiles may affect different downstream pathways. It is critical to identify the molecular mechanisms underlying drug-induced hyperphagia, both because this may lead to the development of new APDs, with lower appetite-stimulating effects but also because such insight may provide new knowledge about appetite regulation in general. Hence, in this review, we discuss the receptor binding profile of various APDs in relation to the potential mechanisms by which they affect appetite.

scholarly journals Gingival Enlargement in Antihypertensive Medication

2009 ◽  
Vol 48 (174) ◽  
pp. 149-52 ◽  
Author(s):  
Shaili Pradhan ◽  
P Mishra
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blockers ◽  
Antihypertensive Medication ◽  
Channel Blocker ◽  
Antihypertensive Agents ◽  
Channel Blockers ◽  
Drug Induced ◽  
Probing Depth ◽  
Increased Risk ◽  
Gingival Enlargement

Introduction: Drug-induced gingival enlargement is a well documented side effect with the use of phenytoin, cyclosporine and calcium channel blockers. The prevalence of gingival enlargement induced by calcium channel blockers is uncertain. Several studies show confl icting results ranging from 20% to 83%. This study was conducted to determine the prevalence of gingival enlargement in patients taking antihypertensive medication. Methods: All consecutive patients on antihypertensive agents attending the Dental OPD were studied. The prevalence of drug induced gingival enlargement was determined. The periodontal condition of all subjects were assessed including plaque index and probing depth. Results: Total 81.2% of subjects taking antihypertensive were seen to have signifi cant enlargement. Among them 71.1% were taking calcium channel blocker, 21.5% were taking ACE Inhibitors, and 7.4% were taking β- blockers. Conclusions:Patients taking antihypertensive agents are at increased risk for gingival enlargement and infl ammation is an important cofactor for the expression of this effect.Key Words: anti-hypertensive drugs, gingival enlargement

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.

scholarly journals The Catecholaldehyde Hypothesis for the Pathogenesis of Catecholaminergic Neurodegeneration: What We Know and What We Do Not Know

2021 ◽  
Vol 22 (11) ◽  
pp. 5999
Author(s):  
David S. Goldstein
Keyword(s):  
Lewy Bodies ◽  
Alpha Synuclein ◽  
Future Research ◽  
Catecholamine Metabolism ◽  
Secondary Effects ◽  
Drug Induced ◽  
Neuronal Homeostasis ◽  
Mitochondrial Functions ◽  
Environmental Agents ◽  
Spontaneous Oxidation

3,4-Dihydroxyphenylacetaldehyde (DOPAL) is the focus of the catecholaldehyde hypothesis for the pathogenesis of Parkinson’s disease and other Lewy body diseases. The catecholaldehyde is produced via oxidative deamination catalyzed by monoamine oxidase (MAO) acting on cytoplasmic dopamine. DOPAL is autotoxic, in that it can harm the same cells in which it is produced. Normally, DOPAL is detoxified by aldehyde dehydrogenase (ALDH)-mediated conversion to 3,4-dihydroxyphenylacetic acid (DOPAC), which rapidly exits the neurons. Genetic, environmental, or drug-induced manipulations of ALDH that build up DOPAL promote catecholaminergic neurodegeneration. A concept derived from the catecholaldehyde hypothesis imputes deleterious interactions between DOPAL and the protein alpha-synuclein (αS), a major component of Lewy bodies. DOPAL potently oligomerizes αS, and αS oligomers impede vesicular and mitochondrial functions, shifting the fate of cytoplasmic dopamine toward the MAO-catalyzed formation of DOPAL—destabilizing vicious cycles. Direct and indirect effects of DOPAL and of DOPAL-induced misfolded proteins could “freeze” intraneuronal reactions, plasticity of which is required for neuronal homeostasis. The extent to which DOPAL toxicity is mediated by interactions with αS, and vice versa, is poorly understood. Because of numerous secondary effects such as augmented spontaneous oxidation of dopamine by MAO inhibition, there has been insufficient testing of the catecholaldehyde hypothesis in animal models. The clinical pathophysiological significance of genetics, emotional stress, environmental agents, and interactions with numerous proteins relevant to the catecholaldehyde hypothesis are matters for future research. The imposing complexity of intraneuronal catecholamine metabolism seems to require a computational modeling approach to elucidate clinical pathogenetic mechanisms and devise pathophysiology-based, individualized treatments.

scholarly journals Hemoglobin A1c and preoperative glycemia as a decision tool to help minimise sternal wound complications: a retrospective study in OPCAB patients

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Jef Van den Eynde ◽  
Abel Van Vlasselaer ◽  
Annoushka Laenen ◽  
Delphine Szecel ◽  
Bart Meuris ◽  
...  
Keyword(s):  
Retrospective Study ◽  
Hemoglobin A1c ◽  
Clinical Decision Making ◽  
Artery Bypass ◽  
Clinical Decision ◽  
Wound Complications ◽  
Minimal Risk ◽  
Off Pump ◽  
Increased Risk ◽  
Diabetes Patients

Abstract Background Poor glycemic control has been associated with an increased risk of wound complications after various types of operations. However, it remains unclear how hemoglobin A1c (HbA1c) and preoperative glycemia can be used in clinical decision-making to prevent sternal wound complications (SWC) following off-pump coronary artery bypass grafting (OPCAB). Methods We conducted a retrospective study of 1774 consecutive patients who underwent OPCAB surgery between January 2010 and November 2016. A new four-grade classification for SWC was used. The associations of HbA1c and preoperative glycemia with incidence and grade of SWC were analysed using logistic regression analysis and proportional odds models, respectively. Results During a median follow-up of 326 days (interquartile range (IQR) 21–1261 days), SWC occurred in 133/1316 (10%) of non-diabetes and 82/458 (18%) of diabetes patients (p < 0.001). Higher HbA1c was significantly associated with a higher incidence of SWC (odds ratio, OR 1.24 per 1% increase, 95% confidence interval, CI 1.04;1.48, p = 0.016) as well as a higher grade of SWC (OR 1.25, 95% CI 1.06;1.48, p = 0.010). There was no association between glycemia and incidence (p = 0.539) nor grade (p = 0.607) of SWC. Significant modifiers of these effects were found: HbA1c was associated with SWC in diabetes patients younger than 70 years (OR 1.41, 95% CI 1.17;1.71, p < 0.001), whereas it was not in those older than 70 years. Glycemia was associated with SWC in patients who underwent non-urgent surgery (OR 2.48, 95% CI 1.26;4.88, p = 0.009), in diabetes patients who received skeletonised grafts (OR 4.83, 95% CI 1.28;18.17, p = 0.020), and in diabetes patients with a BMI < 30 (OR 2.19, 95% CI 1.01;4.76, p = 0.047), whereas it was not in the counterparts of these groups. Conclusions Under certain conditions, HbA1c and glycemia are associated SWC following OPCAB. These findings are helpful in planning the procedure with minimal risk of SWC.

scholarly journals Bittersweet: infective complications of drug-induced glycosuria in patients with diabetes mellitus on SGLT2-inhibitors: two case reports

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Caroline Bartolo ◽  
Victoria Hall ◽  
N. Deborah Friedman ◽  
Chloe Lanyon ◽  
Andrew Fuller ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Fungal Infections ◽  
Case Reports ◽  
Sglt2 Inhibitor ◽  
Sglt2 Inhibitors ◽  
Urogenital Tract ◽  
Hypoglycemic Agents ◽  
Drug Induced ◽  
First Case ◽  
Increased Risk

Abstract Background Sodium-glucose co-transporter 2 (SGLT2) inhibitors are novel hypoglycemic agents which reduce reabsorption of glucose at the renal proximal tubule, resulting in significant glycosuria and increased risk of genital mycotic infections (GMI). These infections are typically not severe as reported in large systematic reviews and meta-analyses of the medications. These reviews have also demonstrated significant cardiovascular benefits through other mechanisms of action, making them attractive options for the management of Type 2 diabetes mellitus (T2DM). We present two cases with underlying abnormalities of the urogenital tract in which the GMI were complicated and necessitated cessation of the SGLT2 inhibitor. Case presentations Both cases are patients with T2DM on empagliflozin, an SGLT2 inhibitor. The first case is a 64 year old man with Candida albicans balanitis and candidemia who was found to have an obstructing renal calculus and prostatic abscess requiring operative management. The second case describes a 72 year old man with Candida glabrata candidemia who was found to have prostatomegaly, balanitis xerotica obliterans with significant urethral stricture and bladder diverticulae. His treatment was more complex due to fluconazole resistance and concerns about urinary tract penetration of other antifungals. Both patients recovered following prolonged courses of antifungal therapy and in both cases the SGLT2 inhibitor was ceased. Conclusions Despite their cardiovascular benefits, SGLT2 inhibitors can be associated with complicated fungal infections including candidemia and patients with anatomical abnormalities of the urogenital tract may be more susceptible to these infections as demonstrated in these cases. Clinicians should be aware of their mechanism of action and associated risk of infection and prior to prescription, assessment of urogenital anatomical abnormalities should be performed to identify patients who may be at risk of complicated infection.

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