SIADH: A Serious Side Effect of Psychotropic Drugs

1987 ◽  
Vol 16 (4) ◽  
pp. 401-407 ◽  
Author(s):  
Jambur Ananth ◽  
Keh-Ming Lin
Keyword(s):  
Psychotropic Drugs ◽  
Side Effect ◽  
Neurological Symptoms ◽  
The Other ◽  
Drug Induced

In this communication two cases of possibly drug induced hyponatremia secondary to amitriptyline and thioridazine have been reported. What is particularly important is the fact that in one, irreversible neurological symptoms were left as sequelae and in the other, the patient was in a coma and thus suffered from a potentially lethal complication. The physicians should be aware of this disturbing side effect while treating their patients with antidepressant and neuroleptic medications.

Medications associated with development of drug-induced depression

2020 ◽  
Vol 1 (11) ◽  
pp. 36-45
Author(s):  
O. D. Ostroumova ◽  
C. V. Batyukina ◽  
E. Yu. Ebzeeva ◽  
N. A. Shatalova
Keyword(s):  
Psychotropic Drugs ◽  
Side Effect ◽  
Antineoplastic Agents ◽  
Controversial Issues ◽  
Drug Induced ◽  
Reactive Depression ◽  
External Influences ◽  
Depressive Syndromes ◽  
Hypolipidemic Drugs ◽  
Antiparkinsonian Drugs

More than 60 % of all depressive syndromes are reactive depression, which occurs in response to internal and external influences. One of the variants of reactive depression is drug-induced (drug-induced) or iatrogenic depression, which is a possible side effect of a number of medications. Depressogenic effect is described in both psychotropic and somatotropic drugs. Depressions that occur when using psychotropic drugs are most often associated with the duration of administration and large doses of the drug. Some antihypertensive, antiarrhythmic, hypolipidemic drugs, antibiotics, hormones, antiparkinsonian drugs and antineoplastic agents are most often mentioned in the series of somatotropic drugs that have a depressogenic effect. Drug-induced depression is one of the most controversial issues. this article presents a systematization of available literature data on depression associated with taking various drugs.

scholarly journals Drug Induced Encephalopathy in Patients with Chronic Kidney Disease: A Case Series

2018 ◽  
Vol 8 (2) ◽  
pp. 172-176
Author(s):  
Wasim Md Mohosin Ul Haque ◽  
Tabassum Samad ◽  
Muhammad Abdur Rahim ◽  
Shudhanshu Kumar Saha ◽  
Sarwar Iqbal
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renal Impairment ◽  
Side Effect ◽  
Case Series ◽  
Special Group ◽  
Drug Induced ◽  
Reduced Dose

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

scholarly journals Pustular Rash in Crohn’s Patient on Ustekinumab Raises Concern for Drug-Induced Paradoxical Psoriasis

2021 ◽  
pp. 662-666
Author(s):  
Mitra Barahimi ◽  
Scott Lee ◽  
Kindra Clark-Snustad
Keyword(s):  
Side Effect ◽  
De Novo ◽  
Pustular Psoriasis ◽  
Initial Weight ◽  
Drug Induced ◽  
Clinical Recurrence ◽  
Potential Side Effect ◽  
First Case ◽  
Tnf Antagonist ◽  
Subcorneal Pustular Dermatosis

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.

scholarly journals A community pharmacist's intervention in antipsychotic drug-induced sexual dysfunction in a patient with schizophrenia

2020 ◽  
Author(s):  
Masaki Maehara ◽  
Masayasu Sugiyama
Keyword(s):  
Early Intervention ◽  
Sexual Dysfunction ◽  
Antipsychotic Drug ◽  
Community Pharmacist ◽  
Side Effect ◽  
Community Pharmacists ◽  
Common Side Effect ◽  
Drug Induced ◽  
First Report

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.

scholarly journals Uncover the Underlying Mechanism of Drug-Induced Myopathy by Using Systems Biology Approaches

2017 ◽  
Vol 2017 ◽  
pp. 1-7
Author(s):  
Dong Li ◽  
Aixin Li ◽  
Hairui Zhou ◽  
Xi Wang ◽  
Peng Li ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Side Effect ◽  
Chemical Structure ◽  
Safety Evaluation ◽  
Underlying Mechanism ◽  
Mapk Signaling ◽  
Drug Induced ◽  
Drug List ◽  
Rare Side Effect

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.

Amlodipine Induced Gum Hypertrophy – A Rare Case Report

2021 ◽  
Vol 16 ◽  
Author(s):  
Suryanarayana Challa Reddy ◽  
Naresh Midha ◽  
Vivek Chhabra ◽  
Deepak Kumar ◽  
Gopal Krishna Bohra
Keyword(s):  
Calcium Channel ◽  
Side Effect ◽  
Antihypertensive Drugs ◽  
Case Reports ◽  
Diagnostic Procedures ◽  
Channel Blockers ◽  
Gingival Hyperplasia ◽  
Drug Induced ◽  
Duration Of Action ◽  
Gingival Overgrowth

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.

Direct metabolic effects of isoproterenol and propranolol in ischemic myocardium of the dog

1980 ◽  
Vol 239 (4) ◽  
pp. H469-H469
Author(s):  
Michael Goodlett ◽  
Kyran Dowling ◽  
Lynne J. Eddy ◽  
James M. Downey
Keyword(s):  
High Energy ◽  
Ischemic Myocardium ◽  
The Other ◽  
Energy Utilization ◽  
Metabolic Effects ◽  
Low Flow ◽  
High Energy Phosphate ◽  
Drug Induced ◽  
Flow Rates ◽  
Induced Changes

The effect of either isoproterenol or propranolol on the metabolism of ischemic myocardium was examined. To ensure that all changes were due to changes in metabolism and not drug-induced changes in residual flow to the ischemic regions, we devised a preparation in which two coronary branches on the same heart were simultaneously perfused at a low flow rate. Microsphere measurements verified that the two ischemic regions were receiving identical blood flow rates. One branch received an infusion of 0.9% NaCl and the other received the drug. After 1 h both regions were biopsied and the high-energy phosphate levels in each region were determined. ATP and phosphocreatine each fell to about 50% of their starting values in the 0.9% NaCl-treated regions, and isoproterenol did not further depress the high-energy phosphate concentrations. Propranolol, on the other hand, significantly preserved the high-energy phosphate concentrations. We conclude that although isoproterenol seemed incapable of accelerating energy utilization in ischemic myocardium, propranolol is apparently capable of reducing it.

scholarly journals Psychotropic drug-induced genetic-epigenetic modulation of CRTC1 gene is associated with early weight gain in a prospective study of psychiatric patients

2019 ◽  
Vol 11 (1) ◽  
Author(s):  
Aurélie Delacrétaz ◽  
Anaïs Glatard ◽  
Céline Dubath ◽  
Mehdi Gholam-Rezaee ◽  
Jose Vicente Sanchez-Mut ◽  
...  
Keyword(s):  
Weight Gain ◽  
Side Effects ◽  
Prospective Study ◽  
Psychotropic Drugs ◽  
Energy Homeostasis ◽  
Psychiatric Patients ◽  
Metabolic Disturbances ◽  
Drug Induced ◽  
Metabolic Side Effects ◽  
Early Weight Gain

Abstract Background Metabolic side effects induced by psychotropic drugs represent a major health issue in psychiatry. CREB-regulated transcription coactivator 1 (CRTC1) gene plays a major role in the regulation of energy homeostasis and epigenetic mechanisms may explain its association with obesity features previously described in psychiatric patients. This prospective study included 78 patients receiving psychotropic drugs that induce metabolic disturbances, with weight and other metabolic parameters monitored regularly. Methylation levels in 76 CRTC1 probes were assessed before and after 1 month of psychotropic treatment in blood samples. Results Significant methylation changes were observed in three CRTC1 CpG sites (i.e., cg07015183, cg12034943, and cg 17006757) in patients with early and important weight gain (i.e., equal or higher than 5% after 1 month; FDR p value = 0.02). Multivariable models showed that methylation decrease in cg12034943 was more important in patients with early weight gain (≥ 5%) than in those who did not gain weight (p = 0.01). Further analyses combining genetic and methylation data showed that cg12034943 was significantly associated with early weight gain in patients carrying the G allele of rs4808844A>G (p = 0.03), a SNP associated with this methylation site (p = 0.03). Conclusions These findings give new insights on psychotropic-induced weight gain and underline the need of future larger prospective epigenetic studies to better understand the complex pathways involved in psychotropic-induced metabolic side effects.

scholarly journals Characteristics of quinine- and quinidine-induced antibodies specific for platelet glycoproteins IIb and IIIa

Blood ◽  
1991 ◽  
Vol 77 (12) ◽  
pp. 2668-2676 ◽  
Author(s):  
GP Visentin ◽  
PJ Newman ◽  
RH Aster
Keyword(s):  
Immune Response ◽  
Platelet Membrane ◽  
The Other ◽  
Membrane Glycoprotein ◽  
Igg Antibodies ◽  
Drug Induced ◽  
Disulfide Bonding ◽  
Platelet Membrane Glycoprotein ◽  
Drug Dependent

Abstract Recent studies have shown that antibodies characteristic of quinine- and quinidine-induced thrombocytopenia sometimes recognize the platelet membrane glycoprotein (GP) complex IIb/IIIa in addition to their well known target, GPIb/IX. We have investigated the frequency with which drug-induced antibodies bind to GPIIb/IIIa and the nature of their target epitopes. In studies of sera from 13 patients sensitive to quinidine or quinine, we found that 10 contained IgG antibodies specific for both GPIb/IX and GPIIb/IIIa, two reacted with GPIb/IX alone, and one reacted with GPIIb/IIIa alone. In all cases, the presence of drug was required for binding of IgG to target GPs. By immunoabsorption, we found that each of five polyspecific sera contained at least two different antibodies, one reactive with GPb/IX and the other with GPIIb/IIIa. Further studies with eight drug- dependent antibodies (DDAb) specific for GPIIb/IIIa showed that three recognized the GPIIb/IIIa complex only, one recognized GPIIb alone, and three recognized GPIIIa alone. The eighth serum appeared to bind to both GPIIIa alone and to an epitope determined by the GPIIb/IIIa complex. The three antibodies specific for GPIIIa alone also reacted with GPIIIa deglycosylated with endo-H, and with the major (61 Kd) fragment obtained by chymotryptic digestion of GPIIIa but failed to react with reduced GPIIIa. These findings demonstrate that, in drug- induced, immunologic thrombocytopenia, the anti-platelet immune response is typically directed against epitopes on both GPIb/IX and GPIIb/IIIa. The three DDAb we studied that were specific for GPIIIa alone recognize epitopes resistant to chymotrypsin and endo-H treatment that are dependent on intrachain disulfide bonding.

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