ÖzetRomatoid artrit (RA) nüfusun yaklaşık %0,3-1,5'inde görülen etiyolojisi bilinmeyen, eklemlerden iç organlara kadar vücudun farklı bölgelerinde tutulumla karakterli kronik otoimmün bir hastalıktır. Plöropulmoner tutulum ikinci sıklıkla görülen tutulum olup en başta gelen mortalite nedenidir. Plöropulmoner tutulum RA tanısı almadan önce ortaya çıkarsa, ayırıcı tanıda düşünülmeyip gözden kaçabilir. Başlangıç semptomu olarak plevral efüzyon, solunum sıkıntısı ve son altı aydır devam eden göğüs ağrısı şikâyetleri ile gelen ve takibinde RA tanısı alan olguyu literatür bilgileri ışığında sunmayı amaçladık. Anahtar sözcükler: Romatoid artrit, plevral efüzyon, plörit AbstractRheumatoid arthritis (RA) is a chronic autoimmune disease with unknown aetiology which effects a variety from joints to internal organs and other sites of organism. It's seen in 0.3-1.5% of population. Pleuropulmonary involvement which is the second frequent involvement is the major cause of mortality. If the pleuropulmonary involvement exists before the diagnosis of rheumatoid arthritis, it may be overlooked. We aimed to present a case with pleural effusion, respiratory distress and chest pain lasting for 6 months as initial symptoms and diagnosed as rheumatoid arthritis in follow up on the light of literature data.

PSYCHIATRIST.COM Method. The data derived from a retrospective study investigating demographic characteristics, diagnosis, and medication of all inpatients between August 1, 2002, and August 31, 2004, who were admitted to the Department of Child and Adolescent Psychiatry of Innsbruck Medical University. Seventy inpatients were prescribed drugs for the time after discharge. Data about further drug intake, consultations (psychiatrist or general practitioner), and weight gain were evaluated by follow-up interviews. Twenty-two of the 70 could not be contacted or were not willing to give any further information, and 48 patients were included in the study. Their mean ± SD age was 15.8 ± 1.7 years (range, 10-18 years), 23 (48%) were male, and 25 (52%) were female. According to DSM-IV criteria, 8 (17%) were diagnosed with schizophrenia, 22 (46%) with mood disorders (including adjustment disorders), 11 (23%) with disruptive behavior disorders, and 7 (15%) had other diagnoses (misuse of psychoactive substances, mental retardation, personality disorders, and development disorders). They were treated with antipsychotics (48%, N = 23; risperidone, olanzapine, clozapine, quetiapine, amisulpride, and ziprasidone) and antidepressants (52%, N = 25; citalopram, mirtazapine, fluoxetine, sertraline, escitalopram, trazodone, and venlafaxine).The effects of age, gender, time since discharge (≤ 6 months, 46%; > 6 months, 54%), weight gain (< 5 kg versus ≥ 5 kg), and pharmacologic treatment (antidepressant versus antipsychotic) on adherence were investigated by means of logistic regression with backward variable selection. The same method was applied to analyze the effects of the above-mentioned variables on weight gain. Odds ratios were calculated to quantify the effect of the potential risk factors. The logistic regression was supplemented by bivariate analyses of the associations between adherence and the individual potential risk factors using Fisher exact test.Results. Forty-six of 48 patients took part in follow-up consultations. Twenty-two patients continued the drug intake at the point of the interview, 12 had discontinued the drug intake after consulting their psychiatrist or general practitioner, and 12 had discontinued without consulting. These 12 patients were classified as noncompliant.When considering the effects of age, gender, time since discharge, weight gain, and pharmacologic treatment on adherence one by one, 2 variables were found to significantly increase the probability of nonadherence, namely, antidepressive treatment (p = .017) and diagnostic group (mood disorders versus all other diagnoses, p < .001). However, when investigating the potential risk factors jointly by logistic regression, only the effect of the diagnostic group remained significant (odds ratio = 26.4, p = .003, logistic regression), whereas the significance of antidepressive treatment disappeared (odds ratio = 4.33, p = .122, logistic regression). Obviously, the difference in adherence rate between patients with and without antidepressive treatm...

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Two Cases of Somnambulism Induced by QuetiapineSir: Somnambulism reflects an impairment in the normal mechanisms of arousal from sleep in which motor behaviors initiated during deep, non-rapid eye movement or slow-wave sleep are activated without full consciousness. Somnambulism, a previously unreported side effect of quetiapine, is described in 2 cases. Both cases described here involved individuals with attention-deficit/hyperactivity disorder (ADHD). The possible significance of this will be discussed.Case 1. Mr. A, a 52-year-old white man with no history of somnambulism, was undergoing treatment for DSM-IV panic disorder and schizoaffective disorder. He reported attention problems and hyperactivity since childhood and restless legs syndrome for 35 years. He was admitted to the medical unit in February 2006 to rule out myocardial infarction after falling off his porch while sleepwalking.The patient reported that somnambulism had begun 18 months previously, after his quetiapine dose was increased to 200 mg at bedtime. This dose was later titrated to a maximum of 1000 mg during the month prior to admission. At that time, mirtazapine 30 mg at bedtime was added. This combination further aggravated the patient's somnambulism, which occurred almost nightly. The patient was witnessed by his roommate to wander in a confused state, manipulate various belongings, open the refrigerator and eat, and visit the bathroom. He was easily redirected back to bed, but did not appear to awaken.A polysomnogram done when Mr. A was taking 800 mg of quetiapine showed no significant respiratory obstruction. Electroencephalogram (EEG) showed no epileptiform activity. Leg electromyogram findings were significant for frequent leg jerks. Quetiapine treatment was discontinued, and methylphenidate and clonazepam were started. Quetiapine 25 mg nightly was reinitiated later. No recurrence of somnambulism was reported at 8-month follow-up.Case 2. Mr. B, an 18-year-old white man with DSM-IV diagnoses of ADHD and pervasive developmental disorder, sought consultation for episodes of somnambulism and nocturnal combativeness. At the time of presentation in June 2003, he was receiving quetiapine 400 mg nightly and dextroamphetamine sulfate 35 mg daily in divided doses.The patient gave a history of starting quetiapine 8 months previously for onset of command auditory hallucinations. Shortly thereafter, he began to have nightmares associated with shouting, jumping from bed, property destruction, and assaults on family members. Mr. B awakened in the mornings with a headache but had no recollection of the events of the night before.Neurologic examination findings were unremarkable, and results of a 24-hour EEG study were normal. The patient's quetiapine dose was reduced to 350 mg nightly, resulting in the return of auditory hallucinations. Dextroamphetamine sulfate was then tapered over a period of 4 months and discontinued with good result and resolution of hallucinations. The patient continued to have nocturnal outbursts, though these were less frequen...