[ ISSN : 2576-5477 ]
Quetiapine; Edema; Adverse Effects
It is known that edema is a rare side effect of quetiapine. Until now only nine cases of peripheral edema related to quetiapine have been reported in the literature. We have determined five cases of pretibial edema associated with quetiapine during two years period of time. The common feature of these cases reported here are comorbid medical disorders, such as venous insufficiency, bladder tumor, chronic obstructive pulmonary disease, diabetes mellitus with excessive elevation of blood sugar. Although treatment protocol of edema and those comorbid medical diseases have been applied separately, at the end of these treatments it is seen that PTE has not been resolved. In all cases reported here that when the dose of quetiapine is reduced, it is observed that PTE is reduced or disappeared. This result brings to mind that there could be a relation between edema and quetiapine.
Peripheral edema could be occurred due to various reasons such as liver cirrhosis, kidney diseases, congestive heart failure, systemic diseases such as cancer, protein deficiency, prolonged immobilization, non-steroidal anti-inflammatory drugs, steroids, and the use of some antihypertensive drugs [1,2]. Moreover, edema due to antipsychotic use is a rare side effect [3- 9]. Although sedation, headache, weight increase, dry mouth and dizziness are among the most common side effects of quetiapine [10], there have been only a few case reports of edema related to quetiapine [8,11-16]. The etiology of this adverse effect has not been explored yet. It is recommended that new studies and case reports would be improved for our understanding of the causes of edema related with quetiapine. In this report, it is presented that five cases of Pre-Tibial Edema (PTE) due to quetiapine usage and associated literatures.
A 57-year-old male patient was admitted to our clinic with a diagnosis of Bipolar Disorder1(BD) - depressive episode, with rapid cycling according to the DSM-IV-TR. He had discontinued his drug regimen 10 days ago, in admission. Valproic acid 1000 mg/day, quetiapine XR 400 mg/day and clonazepam 1 mg/day was administered. Valproic acid dose was titrated to a dose of 1750 mg/ day in two weeks because of 60 µg/ml valproic acid blood level. Bilateral 3+ PTE was found on the 37th day of admission. Complete blood count, thyroid function tests, liver function tests, electrolytes, albumin, total protein, and renal function tests were within normal limits. There was no history of any physical disease. Minimal pericardial effusion and venous insufficiency (varicosis) were found as a result of medical evaluations. Oxerutin 1000 mg/day for venous insufficiency, Ibuprofen 1200 mg/day for pericardial effusion was started with the recommendation of cardiologist. Pericardial effusion did not improve following Ibuprofen; therefore Ibuprofen was discontinued during followup. The edema did not resolve despite treatment of venous insufficiency. By the cardiologist, edema was thought to be related with psychotropic drugs. So the quetiapine was gradually decreased and discontinued. PTE disappeared on the 21st day after quetiapine discontinuation.
A 62-year-old male patient was admitted to our clinic with a diagnosis of BD- manic episode according to the criteria of DSM-IV-TR. The patient had no known previous manic or depressive episode. Organic etiology was investigated because of late onset of BD. Magnetic Resonance Imaging and Electroencephalography was normal. He had a history of alcohol use for 30 years and had quit alcohol 2 years ago but had started to use alcohol again in the last 2 months. The patient was admitted to the clinic for insomnia, excessive spending, making new business plans, seeing himself as the chosen one, abusive speeches, and hearing voices giving orders. B12 vitamin as cyanocobalamin ampoule 1000 mcg/day intramuscular was administered for 3 days as the Vit. B12 level was 173 ng/ml. Quetiapine 150 mg/day, lorazepam 1 mg/day if needed was administered. Zuclopenthixol acuphase ampoule 50 mg intramuscular was administered to the patient when he became agitated. Valproic acid 250 mg/day was started on the 25th day and was titrated to a dose of 1500 mg/day on the 41st day of admission. The blood valproic acid level was 69 µg/ml. The quetiapine dose was slowly increased to a dose of 800 mg/day on the 31st day of admission. Bilateral 3+ PTE was found on the 33rd day of admission. Complete blood count, thyroid function tests, liver function tests, electrolytes, albumin, total protein, and renal function tests were within normal limits. Doppler ultrasonography was normal. The patient had symptoms of coughing and sputum production. The diagnosis was Chronic Obstructive Pulmonary Disease (COPD). Acetyl cysteine suspension 600 mg/day and ceftriaxone 2 gm/day intramuscular were recommended. A low salt diet and furosemide ampoule 20 mg/day were recommended as the PTE continued. The edema did not resolve despite furosemide and treatment of COPD. The quetiapine dose was gradually decreased and discontinued. PTE disappeared on the 12th day after quetiapine discontinuation.
A 50-year-old female patient was admitted to the clinic due to BD-1, depressive episode according to the DSM-IV-TR and was using Valproic acid 1500 mg/day, Lamotrigine 100 mg/day and Quetiapine 200 mg/day. She has been using quetiapine for 3 months. She had a history of hypothyroidism, Hypertension (HT), and Diabetes Mellitus (DM) and was using Levothyroxine sodium 0.15 mg/day, calcium dobesilate1000 mg/day, gliclazide 30 mg/day, perindopril arginine 5 mg/day and zinco 50 mg/day. Her physical examination revealed bilateral 2+ PTE. Oxerutin 1000 mg/day, 50 g diclofenac diethyl ammonium emulgel, and chondroitin polysulfate cream treatment were started by cardiovascular surgeon after venous insufficiency was revealed by venous Doppler ultrasonography. Acetylsalicylic acid 100 mg/day and furosemide 40 mg twice a week were recommended for PTE. Proteinuria and 1+ hematuria were found on urinalysis. Blood albumin levels were found to be low (total protein: 6 g/dL, albumin: 3.4 g/dL). Abdominal ultrasonography revealed a 26x17 mm bladder mass. The mass was considered to be a malignancy. The edema did not resolve despite furosemide and treatment of venous insufficiency. The quetiapine dose was reduced to a dose of 100 mg/day. The PTE decreased on the 14th day of reducing the dose of quetiapine.
A 65-year old male was an inpatient being treated for BD-manic episode due to Cerebrovascular Event (CVE). The patient had a history of three CVE’s in the last nine years with the last one about three months ago and history of an epileptic episode after CVE. Irritability, aggression, insomnia, increased speech, movement acceleration, and increased shopping and sexual desire had developed 1 to 2 days after the third CVE. At the time of admission, he was using quetiapine 125 mg/day for one month, clopidogrel hydrogen sulphate 75 mg/day, levatiracetam 1000 mg/day. The levatiracetam was gradually decreased and discontinued. On the 7th day of admission, Valproic acid was started because of its mood stabilizer and antiepileptic effects. The dose was gradually increased to a dose of 1250 mg/day in twenty days and the blood level was 94 µg/ml. For the presence of manic symptoms, dose of quetiapine was increased.
PTE was noticed just after increasing the dose of quetiapine to 300 mg/day, on the 6th day of admission. Complete blood count, thyroid function tests, liver function tests, electrolytes, albumin, total protein, and renal function tests were within normal limits. Chronic venous insufficiency and left carotid artery stenosis were found. Triperten glycoside, containing horse chestnut extract, 100 mg/day and chondroitin polysulfide cream twice a day were started for chronic venous insufficiency. PTE increased from bilateral 2+ to 3+ when the quetiapine dose was increased from 300 mg/day to 400 mg/day. 3+ PTE continued, although he was treated for venous insufficiency. Considering that the PTE could be related to quetiapine, the dose of quetiapine was gradually decreased to 225 mg/day and the PTE significantly decreased on the 13th day of decreasing quetiapine. Minimal PTE continued.
A 46-year-old female patient was admitted to the clinic due to mild mental retardation and psychotic depression. Quetiapine 300 mg/day and escitalopram 10 mg/day (increasing to 20 mg/day) were started. She had a history of Diabetes Mellitus (DM) and was treated with gliclazide 30 mg/day and metformin HCl 1700 mg/day. PTE was found on the 32nd day of the admission. The patient was found to have put on 10 kg of weight in the first month of her admission. The glucose level was 97 mg/dl at admission and 252 mg/dl at the end of the month. Metformin HCl was increased to 2550 mg/day due to the elevation in the blood sugar. Blood sugar regulation was provided. Furosemide 40 mg/day was started. Despite furosemide treatment, edema continued with the same intensity. Considering that edema could be due to quetiapine, so the quetiapine dose was decreased to 200 mg/day and a significant decrease was found in the PTE on the 7th day.
Although in all cases defined medical cure protocol for edema is given to patients, edema has not been resolved. But after the reduction dose of quetiapine, it is observed that the edema is decreased. This result brings to mind an idea that there is a relationship between quetiapine and edema.
Medical disorders are found in our cases after PTE, such as venous insufficiency in cases 1,3,4, bladder tumor in case 3, chronic obstructive pulmonary disease in case 2, excessive elevation of blood sugar of the patient with DM in case 5. Despite furosemid and the treatment of these medical conditions, there are any changes in edema. There upon it is thought that edema could be related with drugs. After discontinuation of quetiapine, PTE is disappeared within 21 days in case 1 and 12 days in case 2. It is preferred to decrease the dose of quetiapine in cases 3,4 and 5, because of beneficial effects for psychiatric status. The PTE is reduced within 7-14 days in all these three cases. The reduction of the edema by decreasing the dose of quetiapine made us think about the relationship between quetiapine and edema. In case 3, bladder tumor and venous insufficiency are detected. Edema associated with malignancy and venous insufficiency cannot be ruled out. However, there were any changes with the additional treatments for PTE. Decreasing the dose of quetiapine from 200 mg/day to 100 mg/day resulted with the reduction of the edema from 2+ to trace within 2 weeks, in case 3. No precise mechanism has been identified for atypical antipsychotic associated edema; however, several possibilities have been suggested. They may produce edema by increasing vascular permeability, which is similar to the pathophysiology involved in edema due to inflammation and cell injury [17]. In the presence of an underlying medical condition which leads to an inflammatory process in the veins, such as DM [18], CVE [19], COPD [20] and bladder tumor [21], quetiapine may have facilitated the emergence of edema. In our all cases, edema did not resolve with the treatment of medical disorders. The PTE reduced or disappeared only the reduction of the dose or discontinuation of quetiapine, in all cases reported above. In the literature, it is suggested that pedal edema associated with atypical antipsychotic medications does not require any additional treatment; either reduction of the dosage or switching to a different medication is usually sufficient. In our all cases, there is a similar condition [8].
Most of our cases had combined drug use for a medical condition and the psychiatric disorder. Each case was using a different combination of drugs for his/her medical conditions, making it impossible to discuss these drugs in relation to the edema. The disappearance of the edema after the quetiapine was decreased or discontinued indicates that the edema could be related to quetiapine. Most of the cases about this relation reported in the literature those were being treated with combined drugs due to medical conditions or psychiatric disorders [13,15]. McSkimming et. al. reported that the combination of valproate and quetiapine may lead to susceptibility to edema development in their case report [13]. It is reported that the effect and side effects of quetiapine are more dependent on the real plasma concentration of the active drug rather than the recommended dose and that the plasma concentration of quetiapine increases 77% when used together with valproate, thus, increasing the risk of side effects [22].We could not evaluate the plasma level of the active drug of quetiapine, in all cases.
The age range of our cases were 46 to 65 years. Most of the cases reported in the literature were similarly in over 40 years of age group [11-14]. Advanced age is suggested as an important factor in decreasing the hepatic activity of CYP3A4, an enzyme metabolizing quetiapine, and leading to a higher plasma quetiapine concentration in the literature [22]. Advanced age in our patients may have contributed to the edema.
Many mechanisms could play a role in the development of edema due to quetiapine. Quetiapine antagonizes alpha-1 adrenergic receptors, causes peripheral vasodilation and increased capillary hydrostatic pressure, and eventually causes fluid to pass into the interstitial area. It also blocks 5-HT2 receptors, increases intracellular cyclic adenosine monophosphate levels and causes relaxation of smooth muscles [23]. It inhibits muscarinic-1, histaminergic-1 and 5-HT2 receptors and inhibits the increase of inositol triphosphate, which plays a role in the mobilization of intracellular calcium stores necessary for smooth muscle contradiction. It is thought to be able to cause smooth muscle relaxation, vasodilatation and edema in this way [15]. Another alternative explanation for drug-related edema is an allergic reaction. Edema related to the elevation of Ig E, C3, C4 has been suggested as the most probably explanation in a case where ziprasidone-related edema was reported [24]. The sudden start of edema in cases developing edema due to quetiapine in the case series reported by Koleva et al. was thought to indicate a possible allergic mechanism [14]. It was suggested that an Immunoglobulin E (IgE)-mediated allergic reaction can cause relaxation in smooth muscles and lead to quetiapine-related edema [14,16]. Ig E levels were unfortunately not evaluated in our cases.
It is suggested that clinicians should be aware of the relation between edema and quetiapine. Cases reported here have advanced age and comorbid medical conditions. Despite the treatment of comorbid medical conditions in the reported cases above, edema didn’t resolve and it resolved with the reduction of the dose or cessation of the quetiapine. Performing a detailed physical examination, taking drug interactions into account and investigating whether another medical disease has been added to the background are recommended in cases using quetiapine that develop PTE. In addition, although comorbid medical conditions, the edema that may be associated quetiapine should be kept in mind. On the contrary to the above written explanations, it could be thought that the addition of any new unexplored medical conditions might have been facilitated the emergence of edema. In future studies, these possibilities should be taken in to consideration. We hope this article will help physicians to be aware of this potential vascular complication earlier.
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In Japan, there is a recognized need for further research into stigma in the workplace toward persons with mental illness. Toward that end, I will discuss here two studies that we have conducted with the aim of (I) elucidating the stigma experienced in the workplace by persons with mental illness, and (II) elucidating employers’ attitudes toward persons with mental illness.
Hatsumi Yoshii*
International literature has detected high levels of academic stress in students of universities and colleges, which manifests itself with clinical symptoms [1] and constitutes an obstacle to the activation of adaptive, functional and coping responses
Giulia Savarese*, Luna Carpinelli, Oreste Fasano, Monica Mollo, Nadia Pecoraro and Antonio Iannaccone
T he scientific literature has highlighted how the incoming and outgoing transitions through the university represent stressful moments for students. Generally, an adaptation of one’s self it’s needed
Giulia Savarese*, Luna Carpinelli, Oreste Fasano, Monica Mollo, Nadia Pecoraro, Pierpaolo Cavallo
War, quarrel, and some conflict were devastating. In some family for reasons of emotion, influence by other people, ideology, honor, politics, geography or the simple environment, elder brother can find themselves on opposing sides of a war and force them to be in facing battlefield. If we searching the reason for the quarrel between incent brothers, there may be the negligible reason. In straightforward, reasons for the quarrel were not very big.
Ashok Pandey*
Background: In Canada, industrial wind operations are important parts of the country’s long-term energy strategy and Wind Turbines (WTs) are represented as environmentally friendly projects; however, suspected health-related effects of exposure to WT noise have attracted much public attention. Sleep disturbance and degraded Health-Related Quality of Life (HRQoL) have been among the most common complaints reported by residents living close to wind farms.
Objective: The objective of this study was to evaluate the association between changes in sleep quality and HRQoL among residents living close to wind farms.
Methods: Pre- and post-natural experiments were conducted with two data collection periods, before and after WTs became operational; sleep quality was measured by using the Pittsburgh Sleep Quality Index (PSQI), and HRQoL was measured using the 12-item Short Form (SF-12) Health Survey of 50 participants.
Results: Changes in the SF-12 mental component summary (ΔMCS) were correlated inversely with the changes in PSQI score (ΔPSQI, Spearman’s correlation r_S= -0.595). The median values for ΔMCS were significantly associated with ΔPSQI (p=0.039) after controlling for age, sex, distance and attitude to WTs, in a quantile regression analysis.
Conclusion: Changes in sleep quality reported by residents living nearby WTs were a significant independent predictor of the degraded mental health domain of HRQoL.
Leila Jalali*, Ashok Chaurasia, Philip Bigelow, Shannon Majowicz and Stephen McColl
Acute psychiatric illness is associated with alterations of serum thyroid hormone levels including normal or high T3 levels and elevated T4 levels with normal or high TSH that have no clinical signs or symptoms and resolve within 2 weeks. This phenomenon is called euthyroid hyperthyroxinemia. We present a case of primary hyperparathyroidism contributing to a patient’s depression with psychosis that developed euthyroid hyperthyroxinemia. We also review the literature to present current thoughts about pathophysiology and treatment.
Joseph Wolfgang Mathews and Nicoleta Dorinela Sora*
One-third of people living with dementia also experience depression. Treating symptoms of depression may be a protective factor and reduce cognitive decline in dementia. People suffering from depression experience sad mood, reduced energy, poor concentration, loss of interest, diminished activity and they are at risk for death by suicide. Screening instruments include the Cornell Scale for Depression in Dementia (CSDD) and the Geriatric Depression Scale (GDS). Typical treatments include antidepressant medications, which may have limited efficacy; and Electroconvulsive Therapy (ECT), which may heighten memory loss. Psychotherapeutic approaches, including cognitive–behavioral therapy, interpersonal therapy and supportive counseling can be helpful. Lifestyle modifications addressing healthy diet, exercise and the inclusion of enjoyable activities can promote improved quality of life. Providing needed education and support to caregivers, who often experience depression, anxiety and sleep disorders themselves is critical. This paper provides health professionals with an overview of approaches for recognizing and responding to co-occurring dementia and depression.
Sherri Melrose*
This study investigated potential correlation between the inflammatory marker, Calprotectin, and a S.O.S questionnaire from forty-nine Autistic children. Symptom and behavioral questionnaires were completed contemporaneously with stool sample collection. Mixed Model data analysis showed strong correlation between some questionnaire parameters and Calprotectin. ‘Need for a fixed routine’ was highly significantly correlated with Calprotectin (????<0.00009) with Multivariate Coefficient of 3.227, whilst paradoxically ‘constipation’ indicated significant change (????<0.02) with negative Multivariate Coefficient (-1.584). The negative ‘constipation’ appears to associate with the positive ‘need for a fixed routine’ indicating possibility of reciprocal, independent prediction of gastrointestinal inflammation. Results suggest that ‘need for a fixed routine’ and ‘constipation’ be included in a screening questionnaire as independent predictors of bowel dysfunction in these children.
Ioná Bramati-Castellarin¹*, Vinood Patel¹ and Ian P Drysdale²
Background: Improved real world functioning is the ultimate goal of cognitive rehabilitation (which was developed for an acquired brain injury population), however, cognitive remediation for psychiatric populations focuses primarily on cognitive interventions (e.g., computerized cognitive training) and utilizes cognitive test results as outcomes. A broader range of neuropsychological interventions and outcome measures, incorporating real-world measures of functioning, is recommended for cognitive remediation program evaluation.
Objective: To determine the feasibility and explore the effectiveness of a holistic cognitive remediation program administered by clinical neuropsychologists for a community-based mixed psychiatric treatment seeking sample.
Method: Twenty-five adults of mixed psychiatric aetiology were referred for a 10-week intervention (including four hours of weekly individual and group-based sessions). A broad array of outcomes was assessed post-intervention. Functional status, self-reported cognitive symptoms and quality of life was assessed at 11.3 months follow-up.
Results: Eighteen of the referred participants (72%) completed the intervention. Completers showed: a high rate of functional cognitive goal attainment; increased employment rates; improved symptoms of psychological distress and quality of life; reduced self-report of cognitive difficulties; and improved auditory attention span and verbal memory. Self-report of reduced cognitive difficulties and improved quality of life was maintained approximately one year later. The majority of participants reported very high levels of satisfaction with the program.
Conclusions: This intervention was acceptable to participants and associated with high satisfaction rates and gains in cognitive, psychological and functional outcomes. Findings suggest there are multiple benefits to adopting an intervention program that is holistic, individualized to the goals of the patient and facilitated by trained neuropsychologists.
Jamie Berry¹,²*, Donel Martin¹, Karen Wallace¹, Anthony Miller², Travis Wearne² and Melanie Porter²
We are witnessing a rapidly growing type of Mobile Health. Mobile devices have allowed the control of activity levels in people, their habits and even their mobility through GPS. Vital signs, moods, sleep disorders, heart rates, or skin temperature can also be monitored. Literature specializing in psychosocial therapies addresses the usefulness of mobile phones in patients in general, with greater production from psychology and to a lesser extent from social work. We highlight the research developed in the USA and identify opportunities and limitations in terms of data privacy, access to and use of mobile phones; to reach isolated or poor populations or to facilitate access to social and health services. We conclude with possible orientations, hypotheses and goals for prospective investigation works.
Yolanda García Vázquez*