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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.ghpjournal.com//inpress?rss=yes"><title>General Hospital Psychiatry - Articles in Press</title><description>General Hospital Psychiatry RSS feed: Articles in Press. 
 General Hospital Psychiatry   explores the many linkages among psychiatry, medicine, and primary care. In emphasizing a biopsychosocial 
approach to illness and health, the journal provides a forum for professionals with clinical, academic, and research interests in psychiatry's 
role in the mainstream of medicine. The journal expands on traditional models of consultation-liaison, inpatient and outpatient services 
in the general hospital to address all aspects of ambulatory, inpatient, emergency, and community care. In response to the unpredictable 
nature of contemporary life, the journal explores the role of emergency psychiatry in addressing personal, social, political, and forensic 
responses to stress and trauma.  Studies of multisystem relationships between stress, illness, psychosocial factors, inter- and intra-personal 
relationships, family dynamics, ecological change, and institutional forces are especially relevant to the journal's objectives.  
 

 General Hospital Psychiatry  will publish original articles, case reports and brief communications on:  biopsychosocial approaches 
to medicine; liaison-consultation psychiatry; psychosomatic medicine; emergency and crisis psychiatry; the relationship of psychiatric 
services to general medical systems; and new directions in medical education that stress psychiatry's role in primary care, family practice, 
and continuing education.</description><link>http://www.ghpjournal.com//inpress?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2010 Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>General Hospital Psychiatry</prism:publicationName><prism:issn>0163-8343</prism:issn><prism:publicationDate>2010-07-23</prism:publicationDate><prism:copyright> © 2010 Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.ghpjournal.com/article/PIIS0163834310001088/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ghpjournal.com/article/PIIS0163834310001076/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ghpjournal.com/article/PIIS0163834310001052/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ghpjournal.com/article/PIIS0163834310001039/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ghpjournal.com/article/PIIS0163834310001015/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ghpjournal.com/article/PIIS0163834310001027/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ghpjournal.com/article/PIIS0163834310000988/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ghpjournal.com/article/PIIS016383431000099X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ghpjournal.com/article/PIIS0163834310000642/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ghpjournal.com/article/PIIS0163834310000629/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ghpjournal.com/article/PIIS0163834310000630/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ghpjournal.com/article/PIIS0163834310000046/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ghpjournal.com/article/PIIS016383431000054X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ghpjournal.com/article/PIIS0163834310000526/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ghpjournal.com/article/PIIS0163834310000551/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ghpjournal.com/article/PIIS0163834310000137/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ghpjournal.com/article/PIIS0163834310000058/abstract?rss=yes"/><rdf:li rdf:resource="http://www.ghpjournal.com/article/PIIS0163834309002850/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.ghpjournal.com/article/PIIS0163834310001088/abstract?rss=yes"><title>Comparison of patients with and without mental disorders treated for suicide attempts in the emergency departments of four general hospitals in Shenyang, China - Corrected Proof</title><link>http://www.ghpjournal.com/article/PIIS0163834310001088/abstract?rss=yes</link><description>Abstract: Objective: Compare the sociodemographic and psychological characteristics of suicide attempters admitted to emergency departments of general hospitals in China that do and do not meet diagnostic criteria for mental disorders.Methods: The Structured Clinical Interview for DSM-IV, the Suicide Ideation Scale, the Hamilton Depression Rating Scale and a quality of life measure were administered to 239 consecutive suicide attempters who were treated in the emergency departments of four randomly selected general hospitals in Shenyang.Results: Among the enrolled subjects, 166 (69.5%) met diagnostic criteria for a current mental disorder. Among these 166 subjects, 62.7% had mood disorders, 14.5% had anxiety disorders, 10.8% had psychotic disorders and 3.6% had substance use disorders. The 73 suicide attempters without a mental disorder were younger, had higher levels of impulsiveness and were more likely to have ideas about being rescued. Multivariate logistic regression analysis identified the following independent predictors of having a current psychiatric disorder in the suicide attempters: female gender (OR=3.67, 95% CI=1.23–10.91), more than 6 years of formal education (OR=1.19, 95% CI=1.04–1.36), a higher score on the suicide ideation scale (OR=1.01, 95% CI=1.00–1.03), a higher score on Hamilton depression rating scale (OR=1.26, 95% CI=1.16–1.37) and a lower score on the quality of life scale (OR=0.75, 95% CI=0.63–0.90).Conclusion: The prevalence of psychiatric disorders in suicide attempters in emergency departments of urban China is lower than that reported in most western countries. Suicide attempters with and without mental illnesses are distinct on a number of important dimensions. Mental health assessment and appropriate discharge planning for patients treated in emergency departments for suicide attempts are crucial components of comprehensive suicide prevention efforts.</description><dc:title>Comparison of patients with and without mental disorders treated for suicide attempts in the emergency departments of four general hospitals in Shenyang, China - Corrected Proof</dc:title><dc:creator>Bo Bi, Jianhua Tong, Li Liu, Shengnan Wei, Haiyan Li, Jinglin Hou, Shanyong Tan, Xu Chen, Wei Chen, Xiaoju Jia, Ying Liu, Guanghui Dong, Xiaoxia Qin, Michael R. Phillips</dc:creator><dc:identifier>10.1016/j.genhosppsych.2010.06.003</dc:identifier><dc:source>General Hospital Psychiatry (2010)</dc:source><dc:date>2010-07-23</dc:date><prism:publicationName>General Hospital Psychiatry</prism:publicationName><prism:publicationDate>2010-07-23</prism:publicationDate></item><item rdf:about="http://www.ghpjournal.com/article/PIIS0163834310001076/abstract?rss=yes"><title>Treatment-resistant depression prior to the diagnosis of cryptococcal meningitis: a case report - Corrected Proof</title><link>http://www.ghpjournal.com/article/PIIS0163834310001076/abstract?rss=yes</link><description>Abstract: Comorbidity of chronic infectious disorders is one of the common causes of treatment-resistant depression. Depression may alter some aspects of immunity that can contribute to the development of infection. Here we describe an elderly male with treatment-resistant depression. Ten months after antidepressants were administered, he was found to have cryptococcal meningitis. After successful treatment of the central nervous system infection, his depressive symptoms improved apparently. A possible interaction between depression and cellular immunity was discussed. Physicians should be cautious about the risk of opportunistic infection in patients with depression, especially in immunocompromised condition.</description><dc:title>Treatment-resistant depression prior to the diagnosis of cryptococcal meningitis: a case report - Corrected Proof</dc:title><dc:creator>Ker-Li Hsueh, Pao-Yen Lin</dc:creator><dc:identifier>10.1016/j.genhosppsych.2010.06.002</dc:identifier><dc:source>General Hospital Psychiatry (2010)</dc:source><dc:date>2010-07-20</dc:date><prism:publicationName>General Hospital Psychiatry</prism:publicationName><prism:publicationDate>2010-07-20</prism:publicationDate></item><item rdf:about="http://www.ghpjournal.com/article/PIIS0163834310001052/abstract?rss=yes"><title>Topiramate-induced confusion following a single ingestion of 400 mg - Corrected Proof</title><link>http://www.ghpjournal.com/article/PIIS0163834310001052/abstract?rss=yes</link><description>Abstract: Background: Topiramate is an anticonvulsant medication commonly used for a variety of neurological disorders including migraine prophylaxis. Broadened use of topiramate has brought an increased awareness of toxicity from this medication, particularly central nervous system side effects and metabolic acidosis.Objective: We describe a case of topiramate toxicity occurring in a 22-year-old female following the ingestion of two 200 mg tablets, which she was prescribed for the treatment of migraines.Results: During her outpatient cardiology evaluation for suspected postural orthostatic tachycardia syndrome (POTS), the patient experienced flushing and anxiety. Upon transfer to our hospital she was tachycardic, hypertensive, and confused. Her autonomic symptoms were consistent with her prior episodes of autonomic instability, while the confusion was new. Admission laboratory values revealed a metabolic acidosis with a mildly elevated anion gap. A blood topiramate level returned a value of 8.4 mg/L 15 h after the ingestion. Her symptoms cleared within 24 h following admission.Conclusion: Clinicians should consider topiramate toxicity in their differential diagnosis for patients with neurological diseases presenting with acute-onset confusion and metabolic acidosis.</description><dc:title>Topiramate-induced confusion following a single ingestion of 400 mg - Corrected Proof</dc:title><dc:creator>Matthew D. Pierson, Andrew J. Muzyk, Megan Lockamy, Xavier A. Preud'homme</dc:creator><dc:identifier>10.1016/j.genhosppsych.2010.05.004</dc:identifier><dc:source>General Hospital Psychiatry (2010)</dc:source><dc:date>2010-07-12</dc:date><prism:publicationName>General Hospital Psychiatry</prism:publicationName><prism:publicationDate>2010-07-12</prism:publicationDate><prism:section>CASE REPORT</prism:section></item><item rdf:about="http://www.ghpjournal.com/article/PIIS0163834310001039/abstract?rss=yes"><title>Depressive mood and quality of life in functional gastrointestinal disorders: differences between functional dyspepsia, irritable bowel syndrome and overlap syndrome - Corrected Proof</title><link>http://www.ghpjournal.com/article/PIIS0163834310001039/abstract?rss=yes</link><description>Abstract: Objective: To investigate the differences in depressive mood and quality of life in patients with between functional dyspepsia (FD), irritable bowel syndrome (IBS), and FD-IBS overlap as diagnosed based on Rome III criteria.Methods: The subjects completed a questionnaire based on Rome III criteria, the Beck Depressive Inventory (BDI) including Cognitive Depression Index (CDI) for depressive mood evaluation and the 36-item Short Form general health survey (SF-36) for quality of life assessment. Upper gastrointestinal endoscopy and colonoscopy were performed to exclude organic disease.Results: Of 279 subjects, 70 and 124 subjects were diagnosed as FD and IBS, respectively. FD-IBS overlap patients (n=42) and FD alone patients (n=28) showed higher BDI scores than normal subjects (n=127) (P&lt;.001 and P=.02, respectively), whereas that of IBS alone patients (n=82) did not show difference (P=.17). All the SF-36 subscores of the FD-IBS overlap patients were significantly lower than normal subjects (P&lt;.05).Conclusions: Depressive mood was significantly related to FD and FD-IBS overlap but not to IBS based on Rome III criteria. FD-IBS overlap patients have worse quality of life than FD-alone and IBS-alone patients.</description><dc:title>Depressive mood and quality of life in functional gastrointestinal disorders: differences between functional dyspepsia, irritable bowel syndrome and overlap syndrome - Corrected Proof</dc:title><dc:creator>Heon-Jeong Lee, Sun-Young Lee, Jeong Hwan Kim, In-Kyung Sung, Hyung Seok Park, Choon Jo Jin, Seung-Gul Kang, Hiejin Yoon, Hoon Jai Cheon</dc:creator><dc:identifier>10.1016/j.genhosppsych.2010.05.002</dc:identifier><dc:source>General Hospital Psychiatry (2010)</dc:source><dc:date>2010-06-25</dc:date><prism:publicationName>General Hospital Psychiatry</prism:publicationName><prism:publicationDate>2010-06-25</prism:publicationDate></item><item rdf:about="http://www.ghpjournal.com/article/PIIS0163834310001015/abstract?rss=yes"><title>Do the PHQ-8 and the PHQ-2 accurately screen for depressive disorders in a sample of pregnant women? - Corrected Proof</title><link>http://www.ghpjournal.com/article/PIIS0163834310001015/abstract?rss=yes</link><description>Abstract: Objective: The aim of this study was to assess the psychometric properties of the Patient Health Questionnaire (PHQ)-8, and the PHQ-2, a two-item version of the PHQ, respectively, in pregnancy. These screeners were compared to a structured diagnostic interview in a cohort of pregnant women attending prenatal care. Based upon studies documenting high sensitivity and specificity on the PHQ-8 and PHQ-2 in the general adult population, we hypothesized that both instruments would be effective in this population.Methods: Two hundred eighteen women, 13 of them depressed, were given the Composite International Diagnostic Interview and the PHQ-8 before 17 weeks of pregnancy. Receiver Operating Characteristic curves determined optimal thresholds and sensitivity and specificity were calculated using both dimensional and categorical approaches. Agreement between the PHQ-2 and PHQ-8 was measured using Cohen's kappa.Results: Optimal cutoffs for the PHQ-8 and PHQ-2 were 11 and 4, respectively. Using these cutoffs, the PHQ-8 had a sensitivity of 77% and a specificity of 62% while the PHQ-2 had a sensitivity of 62% and a specificity of 79%. The categorical method of scoring the PHQ-8 yielded a sensitivity of 54% and a specificity of 84%.Conclusions: In our sample, the PHQ-8 and PHQ-2 performed almost equally in detecting probable major depressive disorder in a sample of pregnant women. The categorical scoring method for the PHQ-8 had lower sensitivity but slightly higher specificity than the dimensional version. We found the PHQ-8 and PHQ-2 to have lower sensitivity and specificity in our pregnant population as compared to findings in nonpregnant populations; however, characteristics of our sample and choice of diagnostics instrument could explain these discrepant findings.</description><dc:title>Do the PHQ-8 and the PHQ-2 accurately screen for depressive disorders in a sample of pregnant women? - Corrected Proof</dc:title><dc:creator>Megan V. Smith, Nathan Gotman, Haiqun Lin, Kimberly A. Yonkers</dc:creator><dc:identifier>10.1016/j.genhosppsych.2010.04.011</dc:identifier><dc:source>General Hospital Psychiatry (2010)</dc:source><dc:date>2010-06-23</dc:date><prism:publicationName>General Hospital Psychiatry</prism:publicationName><prism:publicationDate>2010-06-23</prism:publicationDate></item><item rdf:about="http://www.ghpjournal.com/article/PIIS0163834310001027/abstract?rss=yes"><title>Desvenlafaxine as a possible cause of acquired hemophilia - Corrected Proof</title><link>http://www.ghpjournal.com/article/PIIS0163834310001027/abstract?rss=yes</link><description>Abstract: Objective: Acquired hemophilia A (AHA) is characterized by the depletion of Factor VIII mediated by specific autoantibodies. While the cause is unknown in 50% of the cases, an association with malignancy, peripartum period, autoimmune disease and the use of drugs has been described. We report a case of AHA possibly induced by desvenlafaxine.Case report: Mr. P, a 70-year-old Caucasian male with alcohol and opioid dependence in remission, was started on 50 mg of desvenlafaxine for a moderate depressive episode. After 10 weeks, he developed an ecchymosis of the right upper extremity, in the absence of past or family history of bleeding disorder. He had a prolonged activated partial thromboplastin time (74.5 s) not corrected on performing mixing study, decreased Factor VIII activity (&lt; 1%) and detectable Factor VIII inhibitor (30 Bethesda units) confirming a diagnosis of AHA. After all other causes were ruled out, desvenlafaxine was discontinued and the patient was infused with Factor VIIa followed by a 6-week prednisone taper with which he achieved remission.Discussion: While serotonin inhibitors are known to impair platelet aggregation leading to bleeding, abnormalities in the coagulation cascade have not been described so far. Desvenlafaxine appears to be the probable cause of AHA given the temporal association, remission after withdrawal of the drug and the lack of any other probable cause. New-onset abnormalities of the coagulation cascade such as AHA should be considered in the context of bleeding events with desvenlafaxine and perhaps other serotonin inhibitors, given the significant mortality rates when untreated.</description><dc:title>Desvenlafaxine as a possible cause of acquired hemophilia - Corrected Proof</dc:title><dc:creator>Deepika Shaligram, Tahani Alqassem, Elizabeth Koby</dc:creator><dc:identifier>10.1016/j.genhosppsych.2010.05.001</dc:identifier><dc:source>General Hospital Psychiatry (2010)</dc:source><dc:date>2010-06-23</dc:date><prism:publicationName>General Hospital Psychiatry</prism:publicationName><prism:publicationDate>2010-06-23</prism:publicationDate><prism:section>CASE REPORT</prism:section></item><item rdf:about="http://www.ghpjournal.com/article/PIIS0163834310000988/abstract?rss=yes"><title>Sleep disorders, nightmares, depression and anxiety in an elderly patient treated with low-dose metoprolol - Corrected Proof</title><link>http://www.ghpjournal.com/article/PIIS0163834310000988/abstract?rss=yes</link><description>Abstract: In the Netherlands, the prescription of beta-blockers to patients older than 70 years has increased sharply in recent years. The neuropsychiatric adverse reactions associated with the use of beta-blockers are relatively uncommon and they are mostly seen with poisoning or overdose. We describe an 81-year-old man who developed sleep disorders, nightmares, depression and anxiety as probable adverse effect of low-dose metoprolol (25 mg/day). This case illustrates not only the neuropsychiatric adverse reactions of beta-blockers, but also that diagnosis of these reactions can be easily missed in elderly patients.</description><dc:title>Sleep disorders, nightmares, depression and anxiety in an elderly patient treated with low-dose metoprolol - Corrected Proof</dc:title><dc:creator>Amir I.A. Ahmed, Patricia van Mierlo, Paul Jansen</dc:creator><dc:identifier>10.1016/j.genhosppsych.2010.04.008</dc:identifier><dc:source>General Hospital Psychiatry (2010)</dc:source><dc:date>2010-06-04</dc:date><prism:publicationName>General Hospital Psychiatry</prism:publicationName><prism:publicationDate>2010-06-04</prism:publicationDate><prism:section>CASE REPORT</prism:section></item><item rdf:about="http://www.ghpjournal.com/article/PIIS016383431000099X/abstract?rss=yes"><title>Duloxetine-related tardive dystonia and tardive dyskinesia: a case report - Corrected Proof</title><link>http://www.ghpjournal.com/article/PIIS016383431000099X/abstract?rss=yes</link><description>Abstract: Tardive dyskinesia and tardive dystonia are caused by dopamine receptor blocking agents, mostly antipsychotics and sometimes antidepressants or calcium channel blockers. Duloxetine-related tardive syndrome is rarely reported in the literature. We report one case of tardive dystonia and tardive dyskinesia occurring in a 58-year-old female with major depressive disorder, who developed distressing oral dyskinesia, mandibular dystonia with trismus and dystonia over left neck after treatment of duloxetine (30–60 mg per day) for 18 months. Despite discontinuation of duloxetine, she only obtained partial remission. Even though this association has been rarely reported, duloxetine may pose a potential risk of inducing tardive syndrome. Clinicians should cautiously detect early signs of movement abnormality when prescribing antidepressants.</description><dc:title>Duloxetine-related tardive dystonia and tardive dyskinesia: a case report - Corrected Proof</dc:title><dc:creator>Pei-Yi Chen, Pao-Yen Lin, Shin-Chiao Tien, Yung-Yee Chang, Yu Lee</dc:creator><dc:identifier>10.1016/j.genhosppsych.2010.04.009</dc:identifier><dc:source>General Hospital Psychiatry (2010)</dc:source><dc:date>2010-06-04</dc:date><prism:publicationName>General Hospital Psychiatry</prism:publicationName><prism:publicationDate>2010-06-04</prism:publicationDate><prism:section>CASE REPORT</prism:section></item><item rdf:about="http://www.ghpjournal.com/article/PIIS0163834310000642/abstract?rss=yes"><title>Multiple pulmonary thromboembolism and severe depression - Corrected Proof</title><link>http://www.ghpjournal.com/article/PIIS0163834310000642/abstract?rss=yes</link><description>Abstract: Introduction: Depression is known to have a bidirectional relationship with cardiovascular disease. Severe major depression associated with psychomotor retardation and immobility can be a risk factor for pulmonary embolism; the reverse pathway has not been reported.Case report: We report a case of a 61-year-old man diagnosed with multiple pulmonary thromboembolism finally attributed to a right pulmonary artery intraluminal sarcoma. One month after the onset of presenting symptoms, the patient suddenly developed an episode of severe, melancholic depression, which remitted in six weeks under treatment with venlafaxine 225 mg/day.Discussion: Pathophysiological mechanisms implicated in the development of depression in our patient might resemble those postulated for post-myocardial infarction depression; in line with the “vascular depression” hypothesis, cerebral damage in the limbic circuitry caused by transient hypoxia, an inflammatory response or both may have contributed.Conclusion: Multiple pulmonary thromboembolism seems to have a bidirectional relationship with major depression, in a similar way as myocardial infarction does.</description><dc:title>Multiple pulmonary thromboembolism and severe depression - Corrected Proof</dc:title><dc:creator>Panagiotis Ferentinos, Emmanouil Rizos, Christos Christodoulou, Paraskevi Nikolaidou, Despoina Chatzilia, Stelios Loukides, Spyros Papiris, Lefteris Lykouras</dc:creator><dc:identifier>10.1016/j.genhosppsych.2010.04.003</dc:identifier><dc:source>General Hospital Psychiatry (2010)</dc:source><dc:date>2010-05-12</dc:date><prism:publicationName>General Hospital Psychiatry</prism:publicationName><prism:publicationDate>2010-05-12</prism:publicationDate></item><item rdf:about="http://www.ghpjournal.com/article/PIIS0163834310000629/abstract?rss=yes"><title>Collaborative depression care: history, evolution and ways to enhance dissemination and sustainability - Corrected Proof</title><link>http://www.ghpjournal.com/article/PIIS0163834310000629/abstract?rss=yes</link><description>Abstract: Objective: To describe the history and evolution of the collaborative depression care model and new research aimed at enhancing dissemination.Method: Four keynote speakers from the 2009 NIMH Annual Mental Health Services Meeting collaborated in this article in order to describe the history and evolution of collaborative depression care, adaptation of collaborative care to new populations and medical settings, and optimal ways to enhance dissemination of this model.Results: Extensive evidence across 37 randomized trials has shown the effectiveness of collaborative care vs. usual primary care in enhancing quality of depression care and in improving depressive outcomes for up to 2 to 5 years. Collaborative care is currently being disseminated in large health care organizations such as the Veterans Administration and Kaiser Permanente, as well as in fee-for-services systems and federally funded clinic systems of care in multiple states. New adaptations of collaborative care are being tested in pediatric and ob-gyn populations as well as in populations of patients with multiple comorbid medical illnesses. New NIMH-funded research is also testing community-based participatory research approaches to collaborative care to attempt to decrease disparities of care in underserved minority populations.Conclusion: Collaborative depression care has extensive research supporting the effectiveness of this model. New research and demonstration projects have focused on adapting this model to new populations and medical settings and on studying ways to optimally disseminate this approach to care, including developing financial models to incentivize dissemination and partnerships with community populations to enhance sustainability and to decrease disparities in quality of mental health care.</description><dc:title>Collaborative depression care: history, evolution and ways to enhance dissemination and sustainability - Corrected Proof</dc:title><dc:creator>Wayne Katon, Jürgen Unützer, Kenneth Wells, Loretta Jones</dc:creator><dc:identifier>10.1016/j.genhosppsych.2010.04.001</dc:identifier><dc:source>General Hospital Psychiatry (2010)</dc:source><dc:date>2010-05-10</dc:date><prism:publicationName>General Hospital Psychiatry</prism:publicationName><prism:publicationDate>2010-05-10</prism:publicationDate></item><item rdf:about="http://www.ghpjournal.com/article/PIIS0163834310000630/abstract?rss=yes"><title>Urinary retention with a high dose of escitalopram - Corrected Proof</title><link>http://www.ghpjournal.com/article/PIIS0163834310000630/abstract?rss=yes</link><description>Selective serotonin reuptake inhibitors (SSRIs) are the first-line treatment for depressive disorders, having replaced tricyclic antidepressants (TCAs). One concern about TCAs is the prevalence of side effects, in particular, anticholinergic symptoms such as dry mouth, sedation and constipation . Urinary retention is another potential adverse effect of TCAs but is also rarely seen with SSRIs . The following is a case of an otherwise healthy man with major depression who developed acute urinary retention after taking a high dose of escitalopram, an SSRI, early in treatment.</description><dc:title>Urinary retention with a high dose of escitalopram - Corrected Proof</dc:title><dc:creator>Amir Garakani</dc:creator><dc:identifier>10.1016/j.genhosppsych.2010.04.002</dc:identifier><dc:source>General Hospital Psychiatry (2010)</dc:source><dc:date>2010-05-10</dc:date><prism:publicationName>General Hospital Psychiatry</prism:publicationName><prism:publicationDate>2010-05-10</prism:publicationDate></item><item rdf:about="http://www.ghpjournal.com/article/PIIS0163834310000046/abstract?rss=yes"><title>Reversible escitalopram-induced hypothyroidism - Corrected Proof</title><link>http://www.ghpjournal.com/article/PIIS0163834310000046/abstract?rss=yes</link><description>Abstract: Some drugs can cause alterations in the concentration of thyroid hormones in blood even without clinical signs of dysfunction or pathology of the thyroid gland. Apart from the well-known relationship between depression and hypothalamic-pituitary-thyroid (HPT) axis, and the impact of selective serotonin reuptake inhibitors (SSRIs) on thyroid indices, hypothyroidism is a very rare adverse effect of SSRI treatment. However, the case presented here demonstrates that escitalopram may have the potential to induce hypothyroidism without any significant clinical signs and symptoms. Therefore, the possibility of SSRI-induced asymptomatic hypothyroidism presented here may help clinicians in this regard.</description><dc:title>Reversible escitalopram-induced hypothyroidism - Corrected Proof</dc:title><dc:creator>Salih Saygin Eker, Cengiz Akkaya, Canan Ersoy, Asli Sarandol, Selcuk Kirli</dc:creator><dc:identifier>10.1016/j.genhosppsych.2010.01.003</dc:identifier><dc:source>General Hospital Psychiatry (2010)</dc:source><dc:date>2010-04-28</dc:date><prism:publicationName>General Hospital Psychiatry</prism:publicationName><prism:publicationDate>2010-04-28</prism:publicationDate></item><item rdf:about="http://www.ghpjournal.com/article/PIIS016383431000054X/abstract?rss=yes"><title>Drug interaction between carbapenems and extended-release divalproex sodium in a patient with schizoaffective disorder - Corrected Proof</title><link>http://www.ghpjournal.com/article/PIIS016383431000054X/abstract?rss=yes</link><description>Abstract: Background: Clinicians prescribing divalproex sodium (DVX) are well aware of its potential to cause a drug-drug interaction. One specific interaction occurs between the carbapenem antibiotics and DVX resulting in decreased valproic acid (VPA) levels immediately following the initiation of this antibiotic class.Objective/Method: We describe a case of a 46 year-old Caucasian male who had an undetectable VPA level following treatment with carbapenems.Results: On admission the patient's VPA level was 115 μg/ml; however, a routine VPA level on day 19 of his hospitalization returned a value of 16 μg/ml. At this point, he had received a total of 15 days of carbapenem antibiotics for treatment of lower leg cellulitis. His DVX dose was increased to a maximum of 6g daily, twice his home dose, but it did not produce a therapeutic VPA concentration. The patient was lost to follow-up before an outpatient VPA level was drawn.Conclusion: Our case report is the first to document this drug-drug interaction in a patient diagnosed with schizoaffective disorder, bipolar type.</description><dc:title>Drug interaction between carbapenems and extended-release divalproex sodium in a patient with schizoaffective disorder - Corrected Proof</dc:title><dc:creator>Andrew J. Muzyk, Christina L. Candeloro, Eric J. Christopher</dc:creator><dc:identifier>10.1016/j.genhosppsych.2010.03.004</dc:identifier><dc:source>General Hospital Psychiatry (2010)</dc:source><dc:date>2010-04-14</dc:date><prism:publicationName>General Hospital Psychiatry</prism:publicationName><prism:publicationDate>2010-04-14</prism:publicationDate><prism:section>CASE REPORT</prism:section></item><item rdf:about="http://www.ghpjournal.com/article/PIIS0163834310000526/abstract?rss=yes"><title>Anti-retroviral therapy-induced status epilepticus in “pseudo-HIV serodeconversion” - Corrected Proof</title><link>http://www.ghpjournal.com/article/PIIS0163834310000526/abstract?rss=yes</link><description>Abstract: Diligence in the interpretation of results is essential as information gained from the psychiatric patient's history might often be restricted. Nonobservance of established guidelines may lead to a wrong diagnosis, induce a false therapy and result in life-threatening situations. Communication errors between hospitals and doctors and uncritical acceptance of prior diagnoses add substantially to this problem. We present a patient with alcohol-related dementia who received anti-retroviral therapy that promoted a non-convulsive status epilepticus. HIV serodeconversion was considered after our laboratory result yielded a HIV-negative status. Critical review of previous diagnostic investigations revealed several errors in the diagnosis of HIV infection leading to a “pseudo-serodeconversion.” Finally, anti-retroviral therapy could be discontinued.</description><dc:title>Anti-retroviral therapy-induced status epilepticus in “pseudo-HIV serodeconversion” - Corrected Proof</dc:title><dc:creator>Thorleif Etgen, Bernhard Eberl, Thomas Freudenberger</dc:creator><dc:identifier>10.1016/j.genhosppsych.2010.03.002</dc:identifier><dc:source>General Hospital Psychiatry (2010)</dc:source><dc:date>2010-04-05</dc:date><prism:publicationName>General Hospital Psychiatry</prism:publicationName><prism:publicationDate>2010-04-05</prism:publicationDate><prism:section>CASE REPORT</prism:section></item><item rdf:about="http://www.ghpjournal.com/article/PIIS0163834310000551/abstract?rss=yes"><title>Angioneurotic edema with risperidone: a case report and review of literature - Corrected Proof</title><link>http://www.ghpjournal.com/article/PIIS0163834310000551/abstract?rss=yes</link><description>Angioedema as a rare adverse cutaneous reaction has been reported with antipsychotics like risperidone , clozapine , ziprasidone , droperidol  and chlorpromazine . Besides antipsychotics, it has also been reported to occur with the use of angiotensin-converting enzyme inhibitors, insulin, aspirin, nonsteroidal anti-inflammatory drugs, beta-lactam antibiotics and sulfonamides .</description><dc:title>Angioneurotic edema with risperidone: a case report and review of literature - Corrected Proof</dc:title><dc:creator>Ramachandran Naik Soumya, Sandeep Grover, Alakananda Dutt, Navendu Gaur</dc:creator><dc:identifier>10.1016/j.genhosppsych.2010.03.005</dc:identifier><dc:source>General Hospital Psychiatry (2010)</dc:source><dc:date>2010-04-05</dc:date><prism:publicationName>General Hospital Psychiatry</prism:publicationName><prism:publicationDate>2010-04-05</prism:publicationDate><prism:section>CASE REPORT</prism:section></item><item rdf:about="http://www.ghpjournal.com/article/PIIS0163834310000137/abstract?rss=yes"><title>A case of schizophrenia with dysphagia successfully treated by a multidimensional approach - Corrected Proof</title><link>http://www.ghpjournal.com/article/PIIS0163834310000137/abstract?rss=yes</link><description>Abstract: Dysphagia in patients with psychiatric illnesses contributes to morbidities and mortalities. It is, however, an overlooked problem in clinical practice. We report a patient of schizophrenia with dysphagia who was successfully treated using a multidimensional approach, which included medication adjustment, swallowing training and diet modification.</description><dc:title>A case of schizophrenia with dysphagia successfully treated by a multidimensional approach - Corrected Proof</dc:title><dc:creator>Kuo T. Tang, Ming H. Hsieh</dc:creator><dc:identifier>10.1016/j.genhosppsych.2010.01.012</dc:identifier><dc:source>General Hospital Psychiatry (2010)</dc:source><dc:date>2010-03-17</dc:date><prism:publicationName>General Hospital Psychiatry</prism:publicationName><prism:publicationDate>2010-03-17</prism:publicationDate></item><item rdf:about="http://www.ghpjournal.com/article/PIIS0163834310000058/abstract?rss=yes"><title>Risperidone induced stuttering - Corrected Proof</title><link>http://www.ghpjournal.com/article/PIIS0163834310000058/abstract?rss=yes</link><description>Abstract: Stuttering as a side effect of antipsychotics is rare.There are a few case reports of antipsychotic-induced stuttering, namely, chlorpromazine, levomepromazine, trifluoperazine, fluphenazine, olanzapine and clozapine.Risperidone is commonly used as an atypical antipsychotic. It is licensed for both acute and chronic psychosis and mania. There is only one documented case report mentioned on risperidone induced stuttering. One case report of risperidone-induced stuttering is now described. Stuttering is a rare side effect and requires a high index of suspicion for diagnosis.Further study and research to identify the neurophysiological and psychological processes behind adult onset stuttering and identification of the processes involved in risperidone induced stuttering would help our understanding further.</description><dc:title>Risperidone induced stuttering - Corrected Proof</dc:title><dc:creator>Devender Singh Yadav</dc:creator><dc:identifier>10.1016/j.genhosppsych.2010.01.004</dc:identifier><dc:source>General Hospital Psychiatry (2010)</dc:source><dc:date>2010-02-22</dc:date><prism:publicationName>General Hospital Psychiatry</prism:publicationName><prism:publicationDate>2010-02-22</prism:publicationDate></item><item rdf:about="http://www.ghpjournal.com/article/PIIS0163834309002850/abstract?rss=yes"><title>A case of methamphetamine use disorder treated with the antibiotic drug minocycline - Corrected Proof</title><link>http://www.ghpjournal.com/article/PIIS0163834309002850/abstract?rss=yes</link><description>Abstract: Methamphetamine (METH) use is one of the major public health concerns worldwide. Long-term use of METH induces not only dependence but also psychosis which is associated with METH-induced brain damage, including neuroinflammation produced by activated microglia. We report the case of a female patient whose psychotic symptoms in METH use disorder were successfully improved by anti-inflammatory drug minocycline therapy. Although the precise mechanism(s) underlying the efficacy of minocycline in METH use disorder are currently unclear, minocycline appears to be a good candidate for future investigation clinical trials for medication development in METH using populations.</description><dc:title>A case of methamphetamine use disorder treated with the antibiotic drug minocycline - Corrected Proof</dc:title><dc:creator>Yuko Tanibuchi, Minoru Shimagami, Goro Fukami, Yoshimoto Sekine, Masaomi Iyo, Kenji Hashimoto</dc:creator><dc:identifier>10.1016/j.genhosppsych.2009.12.005</dc:identifier><dc:source>General Hospital Psychiatry (2010)</dc:source><dc:date>2010-01-22</dc:date><prism:publicationName>General Hospital Psychiatry</prism:publicationName><prism:publicationDate>2010-01-22</prism:publicationDate></item></rdf:RDF>