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<title>Psychosomatics</title>
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<item rdf:about="http://psy.psychiatryonline.org/cgi/content/short/50/5/534?rss=1">
<title><![CDATA[Delusion of Oral Parasitosis and Thalamic Pain Syndrome [CASE REPORTS]]]></title>
<link>http://psy.psychiatryonline.org/cgi/content/short/50/5/534?rss=1</link>
<description><![CDATA[
<p> <b>BACKGROUND:</b> Delusional parasitosis is an uncommon psychiatric condition in which patients have the immutable conviction that small, living organisms, such as worms, insects, or larvae infest their skin or other organs. <b>Objective/METHOD:</b> The authors describe a case of an unusual association of delusional parasitosis and thalamic pain syndrome after left-posterior thalamic hemorrhage. The patient initially suffered from dysesthesia and burning pain typical of thalamic pain syndrome and subsequently developed delusional oral parasitosis ("worms" infesting her mouth). <b>RESULTS:</b> Sulpiride 100 mg/day administered in addition to amitriptyline gradually improved her delusions within 3 months. <b>DISCUSSION:</b> The authors speculate that this specific type of delusion can be elicited by the disruption of the somatosensory pathway and that the subsequent cortical sensory deafferentiation and reorganization arising from this disruption may contribute to the development of delusional parasitosis.</p>
]]></description>
<dc:creator><![CDATA[Hanihara, T., Takahashi, T., Washizuka, S., Ogihara, T., Kobayashi, M.]]></dc:creator>
<dc:date>Fri, 23 Oct 2009 10:47:50 PDT</dc:date>
<dc:subject><![CDATA[Somatoform Disorders]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.psy.50.5.534</dc:identifier>
<dc:title><![CDATA[Delusion of Oral Parasitosis and Thalamic Pain Syndrome [CASE REPORTS]]]></dc:title>
<dc:publisher>Acadamy of Psychosomatic Medicine</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>50</prism:volume>
<prism:endingPage>537</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>534</prism:startingPage>
<prism:section>CASE REPORTS</prism:section>
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<item rdf:about="http://psy.psychiatryonline.org/cgi/content/short/50/5/538?rss=1">
<title><![CDATA[Prolonged Psychosis Associated With Interferon Therapy in a Patient With Hepatitis C: Case Study and Literature Review [CASE REPORTS]]]></title>
<link>http://psy.psychiatryonline.org/cgi/content/short/50/5/538?rss=1</link>
<description><![CDATA[
<p><b>BACKGROUND:</b> Although rare, psychosis can emerge during interferon (IFN)-alpha therapy and persist after therapy is completed. <b>OBJECTIVE:</b> The authors report the case of a 30-year-old man with hepatitis C infection treated with IFN-alpha and ribavirin who developed acute psychosis with persecutory delusions and auditory hallucinations, resulting in a suicide attempt.<b>METHOD:</b> The patient was treated with amisulpride for 6 weeks and then with risperidone for 6 weeks. <b>RESULTS:</b> There was no improvement in symptoms until the patient was treated with quetiapine; he then had a marked recovery from the psychotic symptoms. The duration of the psychosis was 28 weeks. <b>CONCLUSION:</b> Hepatitis C can be successfully treated with IFN therapy, and the risk of IFN-induced psychosis is low, with psychotic symptoms resolving in most cases after completion of IFN therapy with or without antipsychotic treatment. In prolonged psychosis induced by IFN, quetiapine might also be of benefit. </p>
]]></description>
<dc:creator><![CDATA[Cheng, Y.-C., Chen, C.-C., Ho, A.-S., Chiu, N.-Y.]]></dc:creator>
<dc:date>Fri, 23 Oct 2009 10:47:50 PDT</dc:date>
<dc:subject><![CDATA[Delirium, Schizophrenia Spectrum Disorders, Syndromes Secondary to General Medical Disorders]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.psy.50.5.538</dc:identifier>
<dc:title><![CDATA[Prolonged Psychosis Associated With Interferon Therapy in a Patient With Hepatitis C: Case Study and Literature Review [CASE REPORTS]]]></dc:title>
<dc:publisher>Acadamy of Psychosomatic Medicine</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>50</prism:volume>
<prism:endingPage>542</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>538</prism:startingPage>
<prism:section>CASE REPORTS</prism:section>
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<item rdf:about="http://psy.psychiatryonline.org/cgi/content/short/50/5/543?rss=1">
<title><![CDATA[Neuropsychiatric Systemic Lupus Erythematosus Presenting as Bipolar I Disorder With Catatonic Features [CASE REPORTS]]]></title>
<link>http://psy.psychiatryonline.org/cgi/content/short/50/5/543?rss=1</link>
<description><![CDATA[
<p> <b>BACKGROUND:</b> The American College of Rheumatology has defined 19 neuropsychiatric syndromes associated with systemic lupus erythematosus (SLE) involving the central, peripheral, and autonomic nervous systems. Neuropsychiatric manifestations of lupus (NPSLE) have been shown to occur in up to 95% of pediatric patients with SLE. <b>OBJECTIVE:</b> The authors describe a 15-year-old African American young woman with a family history positive for bipolar I disorder and schizophrenia, who presented with symptoms consistent with an affective disorder. <b>METHOD:</b> The patient was diagnosed with Bipolar I disorder with catatonic features and required multiple hospitalizations for mood disturbance. Two years after her initial presentation, the patient was noted to have a malar rash and subsequently underwent a full rheumatologic work-up, which revealed cerebral vasculitis. <b>RESULTS:</b> NPSLE was diagnosed and, after treatment with steroids, the patient improved substantially and no longer required further psychiatric medication or therapy. <b>CONCLUSION:</b> Given the especially high prevalence of NPSLE in pediatric patients with lupus, it is important for clinicians to recognize that neuropsychiatric symptoms in an adolescent patient may indeed be the initial manifestations of SLE, as opposed to a primary affective disorder. </p>
]]></description>
<dc:creator><![CDATA[Alao, A. O., Chlebowski, S., Chung, C.]]></dc:creator>
<dc:date>Fri, 23 Oct 2009 10:47:50 PDT</dc:date>
<dc:subject><![CDATA[Bipolar Disorder, Syndromes Secondary to General Medical Disorders]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.psy.50.5.543</dc:identifier>
<dc:title><![CDATA[Neuropsychiatric Systemic Lupus Erythematosus Presenting as Bipolar I Disorder With Catatonic Features [CASE REPORTS]]]></dc:title>
<dc:publisher>Acadamy of Psychosomatic Medicine</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>50</prism:volume>
<prism:endingPage>547</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>543</prism:startingPage>
<prism:section>CASE REPORTS</prism:section>
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<item rdf:about="http://psy.psychiatryonline.org/cgi/content/short/50/4/413?rss=1">
<title><![CDATA[Bleeding the System: A Case of Feigned Enoxaparin Overdose [CASE REPORTS]]]></title>
<link>http://psy.psychiatryonline.org/cgi/content/short/50/4/413?rss=1</link>
<description><![CDATA[
<p><b>BACKGROUND:</b> Low-molecular-weight heparins (LMWHs) have become ubiquitously used as anticoagulants because of their comparative safety and ease of use; however they may be fatal if taken in overdose, and lack of familiarity with their pharmacology may hinder appropriate care. <b>OBJECTIVE:</b> The author reports a case of feigned LMWH overdose so as to alert practitioners to this diagnostic possibility. <b>METHOD:</b> This is a case report of a 49-year-old homeless man who reported a deliberate overdose of an injectable LMWH. The author reviews the mechanism of action and monitoring of LMWHs. <b>RESULTS:</b> On the basis of his unusual presentation and previously documented history and medical work-up, he was ultimately diagnosed with malingering. <b>DISCUSSION:</b> Feigned LMWH overdose is ideally suited to the purposes of malingering, since it represents a medical emergency that requires inpatient medical hospitalization and testing at outside laboratory facilities to verify the overdose.</p>
]]></description>
<dc:creator><![CDATA[Caplan, J. P.]]></dc:creator>
<dc:date>Mon, 17 Aug 2009 08:37:45 PDT</dc:date>
<dc:subject><![CDATA[Factitious Disorder]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.psy.50.4.413</dc:identifier>
<dc:title><![CDATA[Bleeding the System: A Case of Feigned Enoxaparin Overdose [CASE REPORTS]]]></dc:title>
<dc:publisher>Acadamy of Psychosomatic Medicine</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>50</prism:volume>
<prism:endingPage>415</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>413</prism:startingPage>
<prism:section>CASE REPORTS</prism:section>
</item>

<item rdf:about="http://psy.psychiatryonline.org/cgi/content/short/50/4/416?rss=1">
<title><![CDATA[Fatalities Associated With Clozapine-Related Constipation and Bowel Obstruction: A Literature Review and Two Case Reports [CASE REPORTS]]]></title>
<link>http://psy.psychiatryonline.org/cgi/content/short/50/4/416?rss=1</link>
<description><![CDATA[
<p><b>BACKGROUND:</b> Constipation is an exceedingly common side effect of treatment with clozapine. In rare cases, this side effect has resulted in fatal complications. <b>OBJECTIVE:</b> The authors review the literature on fatal complications of clozapine-related constipation and bowel obstruction. <b>METHOD:</b> The authors provide two new case reports of patients who died of similar causes. <b>RESULTS:</b> There were seven reports of deaths from clozapine-related bowel obstruction in the literature, with the most common mechanisms of death being severe impaction leading either to feculent vomiting or bowel necrosis. <b>DISCUSSION:</b> The discussion outlines potential mechanisms and management of clozapine-related constipation.</p>
]]></description>
<dc:creator><![CDATA[Hibbard, K. R., Propst, A., Frank, D. E., Wyse, J.]]></dc:creator>
<dc:date>Mon, 17 Aug 2009 08:37:45 PDT</dc:date>
<dc:subject><![CDATA[Atypical Neuroleptics]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.psy.50.4.416</dc:identifier>
<dc:title><![CDATA[Fatalities Associated With Clozapine-Related Constipation and Bowel Obstruction: A Literature Review and Two Case Reports [CASE REPORTS]]]></dc:title>
<dc:publisher>Acadamy of Psychosomatic Medicine</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>50</prism:volume>
<prism:endingPage>419</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>416</prism:startingPage>
<prism:section>CASE REPORTS</prism:section>
</item>

<item rdf:about="http://psy.psychiatryonline.org/cgi/content/short/50/4/420?rss=1">
<title><![CDATA[Vitamin D-Resistant Rickets Type II-A, Basal Ganglia Calcification, and Catatonia: A Casual or Causal Relationship? [CASE REPORTS]]]></title>
<link>http://psy.psychiatryonline.org/cgi/content/short/50/4/420?rss=1</link>
<description><![CDATA[
<p><b>BACKGROUND:</b> Vitamin D-resistant rickets type-IIA (VDRR-IIA) is a rare, congenital, metabolic disorder characterized by hypocalcemia, rickets, and alopecia. There are reports correlating calcium-metabolic disorders with basal ganglia calcification (BGC) and neuropsychiatric symptoms. <b>OBJECTIVE:</b> The authors document and discuss the relationships of these phenomena. <b>METHOD:</b> The authors describe a patient born with VDRR-IIA who subsequently developed BGC at age 15, and catatonic symptoms of progressive severity at age 16. <b>RESULTS:</b> There appeared to be a positive correlation between the severity of BGC and neuropsychiatric symptoms. <b>DISCUSSION:</b> This is the first time VDRR-IIA, BGC, and catatonia have been reported in a patient, and the authors discuss the relationship among the conditions.</p>
]]></description>
<dc:creator><![CDATA[Brunoni, A. R., Nakata, A. C.G., Tung, T. C., Busatto, G. F.]]></dc:creator>
<dc:date>Mon, 17 Aug 2009 08:37:45 PDT</dc:date>
<dc:subject><![CDATA[Schizophrenia Spectrum Disorders, Syndromes Secondary to General Medical Disorders]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.psy.50.4.420</dc:identifier>
<dc:title><![CDATA[Vitamin D-Resistant Rickets Type II-A, Basal Ganglia Calcification, and Catatonia: A Casual or Causal Relationship? [CASE REPORTS]]]></dc:title>
<dc:publisher>Acadamy of Psychosomatic Medicine</dc:publisher>
<prism:number>4</prism:number>
<prism:volume>50</prism:volume>
<prism:endingPage>424</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>420</prism:startingPage>
<prism:section>CASE REPORTS</prism:section>
</item>

<item rdf:about="http://psy.psychiatryonline.org/cgi/content/short/50/3/282?rss=1">
<title><![CDATA[Improvement of Paradoxical Vocal Cord Dysfunction With Integrated Psychiatric Care [CASE REPORTS]]]></title>
<link>http://psy.psychiatryonline.org/cgi/content/short/50/3/282?rss=1</link>
<description><![CDATA[
<p><b>BACKGROUND:</b> Paradoxical vocal cord dysfunction is associated with a high rate of psychiatric comorbidities, including mood, anxiety, somatoform, and personality disorders, and psychosocial distress. <b>OBJECTIVE:</b> The authors draw attention to this disorder because delayed diagnosis and misdiagnosis are common and can contribute to excessive morbidity. <b>METHOD:</b> The authors present a case of paradoxical vocal cord dysfunction. <b>RESULTS:</b> The condition improved dramatically with integrated psychopharmacologic and psychotherapeutic intervention. <b>CONCLUSION:</b> Integrated medication management and psychotherapy by a single psychiatrist-provider with relevant medical understanding can achieve a better alliance between patient and physician and, thus, improved outcomes.</p>
]]></description>
<dc:creator><![CDATA[Thurston, N. L., Fiedorowicz, J. G.]]></dc:creator>
<dc:date>Tue, 30 Jun 2009 11:04:36 PDT</dc:date>
<dc:subject><![CDATA[Somatoform Disorders, Syndromes Secondary to General Medical Disorders]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.psy.50.3.282</dc:identifier>
<dc:title><![CDATA[Improvement of Paradoxical Vocal Cord Dysfunction With Integrated Psychiatric Care [CASE REPORTS]]]></dc:title>
<dc:publisher>Acadamy of Psychosomatic Medicine</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>50</prism:volume>
<prism:endingPage>284</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>282</prism:startingPage>
<prism:section>CASE REPORTS</prism:section>
</item>

<item rdf:about="http://psy.psychiatryonline.org/cgi/content/short/50/3/285?rss=1">
<title><![CDATA[Recurring Episodes of Bell's Mania After Cerebrovascular Accident [CASE REPORTS]]]></title>
<link>http://psy.psychiatryonline.org/cgi/content/short/50/3/285?rss=1</link>
<description><![CDATA[
<p><b>BACKGROUND:</b> Bell&rsquo;s mania (mania with delirium) is an acute neurobehavioral syndrome of unknown etiology that is characterized by the rapid onset of grandiosity, psychomotor excitement, emotional lability, psychosis, and sleep disruption consistent with mania, coupled with alterations in sensorium, and disorientation characteristic of delirium. Catatonia is a common feature of the syndrome. <b>METHOD:</b> The authors describe a case of recurrent delirium/mania with prominent catatonic features after a cerebellar and pontine stroke, and subsequent successful treatment with lorazepam. <b>RESULTS:</b> Symptoms quickly resolved after antipsychotics were discontinued, with continuation of valproate and lorazapam treatment. <b>DISCUSSION:</b> Failure to recognize this patient&rsquo;s syndrome as a form of catatonia could have had severe, even life-threatening, consequences. The use of neuroleptic medications in cases of delirium/mania with catatonic signs may result in marked clinical deterioration, whereas high-dose lorazepam can ameliorate catatonic signs.</p>
]]></description>
<dc:creator><![CDATA[Bobo, W. V., Murphy, M. J., Heckers, S. H.]]></dc:creator>
<dc:date>Tue, 30 Jun 2009 11:04:36 PDT</dc:date>
<dc:subject><![CDATA[Other Mood Disorders, Stroke, Delirium, Syndromes Secondary to General Medical Disorders]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.psy.50.3.285</dc:identifier>
<dc:title><![CDATA[Recurring Episodes of Bell's Mania After Cerebrovascular Accident [CASE REPORTS]]]></dc:title>
<dc:publisher>Acadamy of Psychosomatic Medicine</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>50</prism:volume>
<prism:endingPage>288</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>285</prism:startingPage>
<prism:section>CASE REPORTS</prism:section>
</item>

<item rdf:about="http://psy.psychiatryonline.org/cgi/content/short/50/3/289?rss=1">
<title><![CDATA[Clonazepam Withdrawal-Induced Catatonia [CASE REPORTS]]]></title>
<link>http://psy.psychiatryonline.org/cgi/content/short/50/3/289?rss=1</link>
<description><![CDATA[
<p><b>BACKGROUND:</b> Catatonia is a often a complex syndrome. It has been divided into categories of simple and malignant, with the latter being a more severe form involving autonomic instability and/or fever and having a higher mortality rate. <b>OBJECTIVE:</b> There have been only two cases presented in the literature postulating benzodiazepine-withdrawal as a possible trigger for malignant catatonia. Here, the authors present a case of catatonia likely caused by abrupt benzodiazepine discontinuation; they also discuss neurobiological mechanisms relating to catatonia. <b>METHOD:</b> The authors report on a 60-year-old man with a history of depression and posttraumatic stress disorder who was brought to the emergency department with acute confusion, grimacing, stereotypy, refusal of food and water, muscle rigidity, mutism, and extreme negativism. He had recently and abruptly discontinued all psychotropic medication. <b>RESULTS:</b> After administration of lorazapam, the patient was re-started on clonazepam, after which there was a complete and sustained resolution of catatonic symptoms and autonomic instability. <b>CONCLUSION:</b> Catatonia may result from a wide variety of etiologies. Catatonia due to benzodiazepine-withdrawal is a rare but serious condition that may be difficult to distinguish from other causes of catatonia. The mechanism by which catatonia may be precipitated by benzodiazepine-withdrawal is unknown, but likely involves a rapid decrease in GABA transmission in the central nervous system.</p>
]]></description>
<dc:creator><![CDATA[Brown, M., Freeman, S.]]></dc:creator>
<dc:date>Tue, 30 Jun 2009 11:04:36 PDT</dc:date>
<dc:subject><![CDATA[Atypical Neuroleptics, Other Neuropsychiatric Disorders, Other Neuroscience]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.psy.50.3.289</dc:identifier>
<dc:title><![CDATA[Clonazepam Withdrawal-Induced Catatonia [CASE REPORTS]]]></dc:title>
<dc:publisher>Acadamy of Psychosomatic Medicine</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>50</prism:volume>
<prism:endingPage>292</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>289</prism:startingPage>
<prism:section>CASE REPORTS</prism:section>
</item>

<item rdf:about="http://psy.psychiatryonline.org/cgi/content/short/50/3/293?rss=1">
<title><![CDATA[Valacyclovir-Induced Psychosis and Manic Symptoms in an Adolescent Young Woman With Genital Herpes Simplex [CASE REPORTS]]]></title>
<link>http://psy.psychiatryonline.org/cgi/content/short/50/3/293?rss=1</link>
<description><![CDATA[
<p><b>BACKGROUND:</b> Genital herpes is a common and painful infection. Its prevalence within the United States is estimated to be 40 million to 60 million people. Three medications, acyclovir, valacyclovir, and famciclovir, have been shown to reduce the duration and severity of the disease. <b>OBJECTIVE:</b> The authors report on the first known case of valacyclovir-induced psychosis with symptoms of mania in a young woman with no previous psychiatric history. <b>METHOD:</b> The patient presented with irritable mood and grandiose delusions 72 hours after starting valacyclovir for genital herpes. Valacyclovir treatment was stopped, and risperidone was initiated. <b>RESULTS:</b> The symptoms continued after stopping the valacyclovir, but improved with risperidone.  <b>DISCUSSION:</b>There are reports of neuropsychiatric side effects with valacyclovir&rsquo;s structural analogs in elderly patients with renal dysfunction. Clinicians should be aware that valacyclovir may induce psychosis with manic presentation in young, healthy patients without a psychiatric history.</p>
]]></description>
<dc:creator><![CDATA[Aslam, S. P., Carroll, K. A., Naz, B., Alao, A. O.]]></dc:creator>
<dc:date>Tue, 30 Jun 2009 11:04:36 PDT</dc:date>
<dc:subject><![CDATA[Other Mood Disorders, Schizophrenia Spectrum Disorders, Syndromes Secondary to General Medical Disorders]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.psy.50.3.293</dc:identifier>
<dc:title><![CDATA[Valacyclovir-Induced Psychosis and Manic Symptoms in an Adolescent Young Woman With Genital Herpes Simplex [CASE REPORTS]]]></dc:title>
<dc:publisher>Acadamy of Psychosomatic Medicine</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>50</prism:volume>
<prism:endingPage>296</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>293</prism:startingPage>
<prism:section>CASE REPORTS</prism:section>
</item>

<item rdf:about="http://psy.psychiatryonline.org/cgi/content/short/50/3/297?rss=1">
<title><![CDATA[Citalopram-Induced Bleeding Due to Severe Thrombocytopenia [CASE REPORTS]]]></title>
<link>http://psy.psychiatryonline.org/cgi/content/short/50/3/297?rss=1</link>
<description><![CDATA[
<p><b>BACKGROUND:</b> In case reports and observational studies, serotonin reuptake-inhibitors (SSRIs) have been linked to an increased risk of bleeding, possibly due to platelet dysfunction as a consequence of serotonin-uptake blockade into platelets. <b>OBJECTIVE:</b> The authors propose that bleeding as a result of SSRI use may also be caused by other mechanisms. <b>METHOD:</b> Here, the authors report on a 32-year-old woman with hemorrhages resulting from severe drug-induced immune thrombocytopenia after 4 weeks of citalopram therapy. <b>RESULTS:</b> After withdrawal of citalopram and treatment with platelet concentrates and prednisolone, the patient recovered completely. <b>CONCLUSION:</b> As this case report shows, drug-induced immune thrombocytopenia may present another possible mechanism for bleeding in SSRI-treated patients.</p>
]]></description>
<dc:creator><![CDATA[Andersohn, F., Konzen, C., Bronder, E., Klimpel, A., Garbe, E.]]></dc:creator>
<dc:date>Tue, 30 Jun 2009 11:04:36 PDT</dc:date>
<dc:subject><![CDATA[Antidepressants]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.psy.50.3.297</dc:identifier>
<dc:title><![CDATA[Citalopram-Induced Bleeding Due to Severe Thrombocytopenia [CASE REPORTS]]]></dc:title>
<dc:publisher>Acadamy of Psychosomatic Medicine</dc:publisher>
<prism:number>3</prism:number>
<prism:volume>50</prism:volume>
<prism:endingPage>298</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>297</prism:startingPage>
<prism:section>CASE REPORTS</prism:section>
</item>

<item rdf:about="http://psy.psychiatryonline.org/cgi/content/short/50/2/155?rss=1">
<title><![CDATA[Postpartum Depression Co-Occurring With Lactation-Related Osteoporosis [CASE REPORTS]]]></title>
<link>http://psy.psychiatryonline.org/cgi/content/short/50/2/155?rss=1</link>
<description><![CDATA[
<p><b>BACKGROUND:</b> <I>Postpartum depression may present with somatic complaints. However, all somatic symptoms do not indicate a possible depression diagnosis. One of the clinical pictures related to physical complaints is osteoporosis in late pregnancy and lactation (PLO); this is a rare disorder, and its pathophysiology remains unknown.</I> <b>OBJECTIVE:</b> <I>The authors report here a case of PLO and depression in a 35-year-old primiparous patient with acute low back pain and postpartum depression 4 weeks after caesarean section.</I> <b>METHOD:</b> <I>Diagnosis was made by DXA scan and magnetic resonance imaging. Depression was assessed with the Edinburgh Postnatal Depression Scale.</I> <b>RESULTS:</b> <I>The patient achieved pain relief through treatment with calcium, vitamin D, calcitonin, weekly alendronate, and venlafaxine for depression.</I> <b>CONCLUSION:</b> <I>PLO and depression may have a common etiopathogenesis that needs further investigation.</I></p>
]]></description>
<dc:creator><![CDATA[Ozcelik, B., Ozcelik, A., Debre, M.]]></dc:creator>
<dc:date>Fri, 17 Apr 2009 11:44:01 PDT</dc:date>
<dc:subject><![CDATA[Depression, Syndromes Secondary to General Medical Disorders]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.psy.50.2.155</dc:identifier>
<dc:title><![CDATA[Postpartum Depression Co-Occurring With Lactation-Related Osteoporosis [CASE REPORTS]]]></dc:title>
<dc:publisher>Acadamy of Psychosomatic Medicine</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>50</prism:volume>
<prism:endingPage>158</prism:endingPage>
<prism:publicationDate>2009-03-01</prism:publicationDate>
<prism:startingPage>155</prism:startingPage>
<prism:section>CASE REPORTS</prism:section>
</item>

<item rdf:about="http://psy.psychiatryonline.org/cgi/content/short/50/2/159?rss=1">
<title><![CDATA[Quetiapine for Tamoxifen-Induced Insomnia in Women With Breast Cancer [CASE REPORTS]]]></title>
<link>http://psy.psychiatryonline.org/cgi/content/short/50/2/159?rss=1</link>
<description><![CDATA[
<p><b>BACKGROUND:</b> Insomnia is a frequent adverse effect reported by women taking tamoxifen, an estradiol receptor-antagonist, for breast cancer. <b>OBJECTIVE:</b> The authors report on six patients treated with quetiapine, an atypical antipsychotic, for tamoxifen-related insomnia without depression. <b>METHOD:</b> Quetiapine was started at 25 mg/day 1 hour before bedtime; dose adjustments upward were made in 25-mg increments, titrated to a maximum dose of 100 mg according to therapeutic response and tolerance. <b>RESULTS:</b> Five of the six women showed a prompt improvement of their insomnia; this effect was maintained after 6 weeks of treatment. <b>DISCUSSION:</b> Quetiapine might improve sleep alterations because of its high affinity for serotonergic receptors, enhancing central serotonergic neurotransmission, thus possibly decreasing excitatory glutamatergic transmission.</p>
]]></description>
<dc:creator><![CDATA[Pasquini, M., Speca, A., Biondi, M.]]></dc:creator>
<dc:date>Fri, 17 Apr 2009 11:44:01 PDT</dc:date>
<dc:subject><![CDATA[Atypical Neuroleptics, Sleep Disorders, Syndromes Secondary to General Medical Disorders]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.psy.50.2.159</dc:identifier>
<dc:title><![CDATA[Quetiapine for Tamoxifen-Induced Insomnia in Women With Breast Cancer [CASE REPORTS]]]></dc:title>
<dc:publisher>Acadamy of Psychosomatic Medicine</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>50</prism:volume>
<prism:endingPage>161</prism:endingPage>
<prism:publicationDate>2009-03-01</prism:publicationDate>
<prism:startingPage>159</prism:startingPage>
<prism:section>CASE REPORTS</prism:section>
</item>

<item rdf:about="http://psy.psychiatryonline.org/cgi/content/short/50/2/162?rss=1">
<title><![CDATA[Acute Tamoxifen-Induced Depression and Its Prevention With Venlafaxine [CASE REPORTS]]]></title>
<link>http://psy.psychiatryonline.org/cgi/content/short/50/2/162?rss=1</link>
<description><![CDATA[
<p><b>BACKGROUND:</b> Tamoxifen is a first-generation selective estrogen-receptor modulator that has been shown to decrease recurrence and prolong survival among premenopausal women with breast cancer; however, it also results in estrogen-insufficiency symptoms, the most common being hot flushes. <b>OBJECTIVE:</b> The authors present a case in which tamoxifen apparently produced acute depression symptoms in a 34-year-old breast cancer patient. <b>METHOD:</b> After two aborted periods of tamoxifen treatment, the patient was started on venlafaxine as a preventive measure before tamoxifen treatment was begun again. <b>RESULTS:</b> After 2 months of treatment with venlafaxine, tamoxifen was initiated for a third time, with no recurrence of her previous mood symptoms. <b>CONCLUSION:</b> Treatment of depression may result in better compliance with tamoxifen regimens and, thus, more favorable outcomes.</p>
]]></description>
<dc:creator><![CDATA[Bourque, F., Karama, S., Looper, K., Cohen, V.]]></dc:creator>
<dc:date>Fri, 17 Apr 2009 11:44:01 PDT</dc:date>
<dc:subject><![CDATA[Depression, Syndromes Secondary to General Medical Disorders, Antidepressants]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.psy.50.2.162</dc:identifier>
<dc:title><![CDATA[Acute Tamoxifen-Induced Depression and Its Prevention With Venlafaxine [CASE REPORTS]]]></dc:title>
<dc:publisher>Acadamy of Psychosomatic Medicine</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>50</prism:volume>
<prism:endingPage>165</prism:endingPage>
<prism:publicationDate>2009-03-01</prism:publicationDate>
<prism:startingPage>162</prism:startingPage>
<prism:section>CASE REPORTS</prism:section>
</item>

<item rdf:about="http://psy.psychiatryonline.org/cgi/content/short/50/2/166?rss=1">
<title><![CDATA[Caregiver Status: A Potential Risk Factor for Extreme Self-Neglect [CASE REPORTS]]]></title>
<link>http://psy.psychiatryonline.org/cgi/content/short/50/2/166?rss=1</link>
<description><![CDATA[
<p><b>BACKGROUND:</b> <I>Family caregivers are known to be at risk for physical illness and emotional distress caused by the extreme demands of the caregiving task.</I> <b>OBJECTIVE:</b> <I>The authors present the case of a middle-aged, well-educated woman with advanced endometrial cancer, the symptoms of which she had ignored over an extended period of time because of her family obligations.</I> <b>METHOD:</b> <I>The patient was treated with systemic chemotherapy and was evaluated for depression and subsequent delirium.</I> <b>RESULTS:</b> <I>The patient was informed about her poor prognosis and was transferred to a skilled nursing facility.</I> <b>DISCUSSION:</b> <I>The authors conclude that the caretaking responsibility, along with a low-grade depression, contributed to her delayed presentation and treatment.</I></p>
]]></description>
<dc:creator><![CDATA[Ortiz, N., Lamdan, R., Johnson, S., Korbage, A.]]></dc:creator>
<dc:date>Fri, 17 Apr 2009 11:44:01 PDT</dc:date>
<dc:subject><![CDATA[Other Patient Groups/Issues, Minority Issues, Patients' Families, Treatment Compliance, Depression]]></dc:subject>
<dc:identifier>info:doi/10.1176/appi.psy.50.2.166</dc:identifier>
<dc:title><![CDATA[Caregiver Status: A Potential Risk Factor for Extreme Self-Neglect [CASE REPORTS]]]></dc:title>
<dc:publisher>Acadamy of Psychosomatic Medicine</dc:publisher>
<prism:number>2</prism:number>
<prism:volume>50</prism:volume>
<prism:endingPage>168</prism:endingPage>
<prism:publicationDate>2009-03-01</prism:publicationDate>
<prism:startingPage>166</prism:startingPage>
<prism:section>CASE REPORTS</prism:section>
</item>

</rdf:RDF>