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Psychotropic drug

About: Psychotropic drug is a research topic. Over the lifetime, 2309 publications have been published within this topic receiving 54070 citations.


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TL;DR: A rare case of a 44-year-old man with fatal hyponatremia due to a combination of psychotropic polypharmacy and hypothyroidism, found unresponsive by his family in the month of January 2009 and brought to the emergency room.
Abstract: To the Editor: Hyponatremia is a very common electrolyte abnormality seen in hospitalized patients. Mild hyponatremia is generally asymptomatic, but severe hyponatremia can be fatal. Hyponatremia is a rare but well-known complication of selective serotonin reuptake inhibitors (SSRIs). Hypothyroidism is also independently known to cause hyponatremia. So far, fatal hyponatremia due to psychotropic polypharmacy has been reported only once.1 Here, we report a rare case of a 44-year-old man with fatal hyponatremia due to a combination of psychotropic polypharmacy and hypothyroidism. Case report. Mr A, a 44-year-old obese man (body mass index = 34.8 kg/m2), was found unresponsive by his family in the month of January 2009 and brought to the emergency room. His history consists of hypothyroidism, schizophrenia, and depression. History from the family members was significant for change in behavior in the 24 hours preceding presentation. Also, there was no history of excess water intake or a witnessed seizure episode. His medications taken at home included paroxetine 10 mg po once daily, quetiapine 100 mg po once daily, olanzapine 20 mg po once daily, and levothyroxine 300 μg po once daily. Other medications included gabapentin 800 mg po thrice daily, omeprazole 15 mg po once daily, clonazepam 1 mg po thrice daily, and valsartan 80 mg po once daily. Upon arrival, he was hypothermic with a temperature of 94.4°F, had no pulse, and was in asystole. He was aggressively resuscitated, and he regained normal sinus rhythm. Postresuscitation electrocardiogram showed ST segment depression in V1 and V2 with diffuse ST-T wave abnormality. He was started on a dopamine drip for hypotension and immediately taken to the cardiac catheterization laboratory due to the electrocardiographic changes and cardiac arrest, but no significant abnormalities were found in his coronary arteries. Meanwhile, his laboratory values were significant for serum sodium level of 107 mEq/L, serum chloride level of 71 mEq/L, and serum thyroid-stimulating hormone level of 63.03 UIU/mL. Other significant laboratory values included serum glucose level of 200 mg/dL, serum calcium level of 7.7 mg/dL, and serum lactic acid level of 6.2 mmol/L, as well as serum levels of cardiac enzyme creatine phosphokinase (5606 U/L) and the creatine kinase-MB fraction (72.2 ng/mL); MB index and serum troponin levels were within normal limits. Urine drug screen was positive for benzodiazepines, consistent with his clonazepam prescription, and his serum toxicology was negative. Serum osmolality and urine osmolality could not be obtained. His complete blood count and chest x-ray were within normal limits. Computed tomography scan of the brain revealed extensive hypoxic ischemic injury with extensive infarction and diffuse brain injury. Mr A was transferred to a medical intensive care unit, where he remained comatose and continued to be hypotensive. Due to the presence of severe hyponatremia, he was started on 3% hypertonic saline infusion with an aim to increase the serum sodium gradually to 120 mEq/L. He was also started on intravenous levothyroxine. Despite aggressive medical treatment, his hemodynamic status did not improve and he continued to be comatose, following which his family agreed to withdraw life support measures. Depression is a very commonly encountered illness in primary care practice. SSRIs are very widely prescribed drugs for the treatment of depression and are a known cause of hyponatremia. The incidence of hyponatremia in patients taking paroxetine is 3.5/1,000/year.2 Although about 50 case reports of SSRI-induced hyponatremia have appeared in the literature so far,3 fatal hyponatremia due to psychotropic drug polypharmacy has been reported only once.1 The risk of developing SSRI-associated hyponatremia appears to be increased with advanced age, female sex, previous history of hyponatremia, comorbid medical illness, or use of concomitant medications known to cause hyponatremia or alter secretion of antidiuretic hormone (ADH).4 The etiology of hyponatremia associated with SSRI use is highly controversial. Although there are some studies showing no elevation of ADH,5,6 the majority of the reports claim syndrome of inappropriate antidiuretic hormone secretion (SIADH) to be the cause of hyponatremia.4,7 Hyponatremia in these studies is seen soon after initiation of therapy with an SSRI, with the median time being 13 days according to previously published reports,2 and 75% of cases presented within 30 days after initiation of therapy.7 Delayed onset has also been reported, with 29% of patients presenting more than 3 months after beginning SSRI therapy.3,7 Quetiapine has also been reported to cause hyponatremia.8 The pathophysiology underlying hyponatremia in hypothyroidism is incompletely understood. Some studies claim that reduced cardiac output in hypothyroidism can lead to release of ADH via the carotid sinus baroreceptors,9–11 whereas other studies have claimed that the glomerular filtration rate and renal blood flow decrease in hypothyroidism and thereby can decrease free water excretion by diminishing water delivery to the diluting segments.12 Some reports cite indirect evidence that SIADH is the cause of water retention in hypothyroidism, thereby causing hyponatremia.13,14 However, more recent reports by Macaron and Famuyiwa15 proved that the ADH levels are appropriately suppressed and therefore do not contribute to the hyponatremia of hypothyroidism. This was further proved correct by failure of demeclocycline to correct the hyponatremia and low serum levels of ADH, leading to the conclusion that SIADH is not the cause of hyponatremia in such patients.15 It may be important to monitor sodium levels closely when a patient is started on SSRI treatment, especially in people with risk factors like advanced age, female sex, and comorbid illnesses and those on treatment with other medications known to cause hyponatremia. If the clinician considers the risk significant, baseline level of serum sodium should be obtained before the first dose.4 Follow-up levels of serum sodium should be obtained at least after the first 2 weeks of treatment4 or at 2–4 weeks after initiation of therapy.7 In case of mild hyponatremia, if the continuation of medication is required, close monitoring of levels of sodium is desired.4 Restriction of fluid intake is somewhat successful, although patient compliance is often poor.16 It is very important to consider the risks and benefits of continuing the treatment in such cases, and clinical judgment is required to make a decision. In almost all cases, the hyponatremia was reversed 2 days to 6 weeks after withdrawal of SSRIs depending on the serum sodium level at presentation.3,7 No guidelines are mentioned in the literature for the management of hyponatremia due to atypical antipsychotics. Also, no specific guidelines exist for routine monitoring of sodium in hypothyroidism. In our case, hyponatremia could be accounted for due to both psychotropic polypharmacy as well as hypothyroidism, eventually proving fatal. Although fatal hyponatremia due to SSRI use has been reported only once, to our knowledge fatal hyponatremia due to a combination of psychotropic polypharmacy and hypothyroidism has not been reported so far. It is highly prudent that serum sodium level should be routinely monitored closely in high-risk patients to avoid potentially fatal complications of a common and easily treatable medical condition.

4 citations

Journal ArticleDOI
TL;DR: In this article, the authors present an overview of new forms of psychotropic drug therapy that may be expected to play a role in psychiatric practice in the 1990s, and discuss those mental health problems most likely to undergo intensive study.
Abstract: The objective of this article is to present an overview of new forms of psychotropic drug therapy that may be expected to play a role in psychiatric practice in the 1990s. In predicting these future developments, three lines of approach have been followed. Firstly, progress in elucidating basic neuronal mechanisms is described. The radioligand receptor binding technique has proved to be an especially powerful tool in the search for novel psychoactive compounds. Secondly, those mental health problems most likely to undergo intensive study are discussed. It is likely that special attention will be devoted to organic mental disorders related to aging (dementia) or chronic exposure to toxic substances. In addition, research will be aimed at explaining and reducing the occurrence of auto-aggressive and hetero-aggressive behaviour. Thirdly, the types of newly designed agents and treatment strategies currently under investigation are outlined. In particular, the development of pharmacological agents that interfere with serotonergic molecular mechanisms has opened the way to improving existing psychotropic drugs, to inventing drugs that achieve known clinical effects via different mechanisms of action, and even to discovering entirely new categories of psychotropic drugs.

4 citations

Journal ArticleDOI
TL;DR: Investigation in a representative national sample of patients living in Residential Facilities (RFs) patterns of polypharmacy as well as related variables, association between diagnoses and therapeutic patterns, and the rate of adverse events found that specific actions are required to improve prescription patterns for severe patients in RFs.
Abstract: Aims — To investigate in a representative national sample (N=2,962) of patients living in Residential Facilities (RFs) patterns of polypharmacy as well as related variables, association between diagnoses and therapeutic patterns, and the rate of adverse events. Methods — Structured interviews focusing on each patient were conducted by trained research assistants with the manager and staff of each RF. Patients were rated with the HoNOS and the SOFAS, and comprehensive information about their sociodemographic and clinical status, and their pharmacological regimes were collected. Results — Conventional antipsychotics and second-generation antipsychotics were prescribed to 65% and 43% of the sample, respectively. Benzodiazepines were prescribed to two-thirds of the sample, while antidepressants were the least-used class of psychotropics. Polypharmacy was common: on average, each treated patient was taking 2.7 drugs (±1.1); antipsychotic polypharmacy was also common. Many prescriptions were loosely related to specific diagnoses. Antiparkinsonianian drugs were prescribed to approximately 1/4 of the sample. Mild or severe adverse events in the previous month were reported for 9.9% and 1.4% of the sample, respectively. About 15% of patients suffered from tardive dyskinesia. Conclusions — Psychotropic drug prescription patterns for severe patients living in RFs are only sometimes satisfactory and offer the opportunity of improvement. Specific actions are required to improve prescription patterns for severe patients in RFs.Declaration of Interest: in the past two years GdG has received two speaker fees from Janssen-Cilag and from Eli Lilly; GS has received one speaker fee from Solvay. RM, AP, SF and RT have received no fees or other financial support from pharmaceutical companies.

4 citations

Journal ArticleDOI
TL;DR: In this article, the authors present a biased and inaccurate account of the history of the treatment of mental illness and the role of social work in this treatment, and present a case against medication without reference to evidence that contravenes his position.
Abstract: In his article on social work and psychotropic medication (Social Service Review, December 1988), David Cohen spells out several roles for social workers in relation to the use of medication. Unfortunately, the merits of his recommendations that social work curricula include content on psychopharmacology and that social workers assume monitoring and advocacy roles on behalf of patients--recommendations with which I strongly concur-are eclipsed by a biased and inaccurate account of the history of the treatment of mental illness and the role of social work in this treatment. For every issue that he addresses, Cohen presents a case against medication without reference to evidence that contravenes his position. For example, in the political sphere, Cohen's rhetoric is intended to persuade the reader that drug treatment, like shock treatment before it, functions not to help relieve suffering but to enforce the social control needs of mental health professionals and to protect psychiatry's dominance of the mental health field. Historically, according to Cohen, social workers have played the role of subservient handmaiden to turf-building, pill-pushing psychiatrists, readily acquiescing to damaging pharmacologic treatments. Only the early social workers in the prepsychotropic era gave priority to patient needs; they "did something we seem to have forgotten to do: they listened to their clients."' Some of Cohen's sweeping generalizations are simply untrue. For instance, early trials of psychotropic medication did not involve merely "a few obscure chemicals tested in the back wards."2 In actual fact, prototypical trials of psychotropic medication were also conducted with patients in the community and in the active multimodal therapeutic milieux of major teaching institutions such as Harvard and Yale.3

4 citations

Journal ArticleDOI
TL;DR: The massive advertising of SGA focussed the doubtful reduction of extra-pyramidal side effects (EPS) overlooking the information about the cardiovascular risk induced by SGA.
Abstract: Thanks to their alleged better tolerability atypical or second-generation antipsychotic drugs (SGA) have gained a considerable fraction of the market at the expense of the classical antipsychotics. The massive advertising of SGA focussed the doubtful reduction of extra-pyramidal side effects (EPS) overlooking the information about the cardiovascular risk induced by SGA. This also led to extensive off-label use as the control of behavioural symptoms associated with dementia in elderly patients. Although the European Medicine Agency (EMEA) eventually warned physicians and patients of the risk associated with SGA use in this area, the regulatory system has some responsibility in this situation. No added therapeutic value is required for new drugs to be approved for the market. They are only evaluated for their own quality, efficacy and safety with no comparison with available alternative treatments. This implies that new drugs may, in fact, be potentially less effective or less safe than other drugs currently in use.

4 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202332
202268
202175
202058
201960
201876