Taha Can Tuman

Plasma omentin levels in drug-free patients with schizophrenia.

Aims: We aimed to investigate plasma omentin concentrations in non-obese, drug-free patients with schizophrenia in comparison with healthy volunteers. Method: Thirty-two patients with schizophrenia and 33 control subjects were recruited. Plasma omentin levels were determined by enzyme-linked immunosorbent assay. Results: Plasma levels of omentin (ng/ml) were found to be markedly lower in patients with schizophrenia (median = 7.7, 25th percentile = 6.3, 75th percentile = 604.9) than in controls (median = 486, 25th percentile = 326, 75th percentile = 794.2, p < 0.01). No significant difference was found between drug-free (n = 23) and drug-naive (n = 9) patients with respect to plasma omentin levels. Omentin concentrations correlated negatively with severity of illness, suggesting that patients with more severe pathology had lower fasting levels of omentin (n = 32; r = -0.387; p = 0.029). Conclusion: The present results suggest that plasma omentin levels are decreased in physically healthy, non-obese, antipsychotic-free patients with schizophrenia when compared with physically and mentally healthy individuals. To our knowledge, this is the first study that demonstrated the association between omentin and schizophrenia.

A rare side effect of escitalopram: bilateral peripheral edema

Escitalopram, S-isomer of sitalopram is well tolerated, rapid onset efficacy and used in the tratment of depression and other psychiatric disorders in elderly1-3. Escitalopram is highly serotonin specific and has minimal effect on the reuptake of other neurotransmitters4. Insomnia, headache, tremor, nausea, flushing, sweating, diarrhea, sexual dysfunction have been reported to be adverse drug reaction during escitalopram therapy3,5,6. In elderly patients, edema is an important health problem. Heart failure, renal failure, malabsorpsion, liver failure, allergic reactions, local inflammation and infections, burns, lymphatic obstruction increased capillary permeability, venous obstruction and drugs can cause peripheral edema7. Antihypertensive medications, nonsteroidal anti-inflammatory agents, calcium channel blockers, corticosteroids, hormones, antibiotics, beta blockers and direct vasodilators are drugs that often cause peripheral edema7,8. Edema has been reported rarely with psychiatric medications. Premarketing trials have reported peripheral edema as an infrequent adverse event which occured less than 1/1009. To the best of our knowladge, there are two case reports that edema associated with escitalopram. First, bilateral ankle edema in 69 year-old female patient after one month therapy with escitalopram 30 mg per day, resolved within first week after discontinuation of the drug10. In second case, bilateral pedal edema associated with escitalopram 10 mg per day developed 9th day of the treatment and resolved within 10 days after discontinuation of the drug11. Here, we report a case of bilateral leg edema on the 7th day of the treatment with escitalopram 10 mg/day and resolved within 12 days after discontinuation of the drug.

Tardive Dyskinesia Associated with Bupropion

Present report describes a 46 year old male patient with a diagnosis of major depression who developed tardive dyskinesia during bupropion therapy. Our patient had no history of neuroleptic use and his laboratory and neurologic examinations were normal. He had no family history of neurologic diseases. Although bupropion induced dyskinesia has been previously reported in the literature, it is rare and our case is the first case regarding tardive dyskinesia.

A new diagnostic tool for masked hypertension: impaired sleep quality

Introduction The aim of this study was to evaluate the relationship between masked hypertension and impaired sleep quality. Additionally, we evaluated the diagnostic role and prevalence of poor sleep quality among patients with newly diagnosed masked hypertension. Material and methods A total of 112 individuals, 72 patients with newly diagnosed masked hypertension and 40 normotensive healthy volunteers, were included in this study. All patients underwent evaluation comprising 12-lead electrocardiography, transthoracic echocardiography, 24-hour Holter ECG, and basic laboratory tests. Additionally, all participants completed questionnaires, including the Pittsburgh Sleep Quality Index (PSQI). Results The total PSQI score was significantly higher in the masked hypertension group than in the normotensive healthy volunteers (4.13 ±2.43 vs. 2.33 ±1.67, p < 0.001). A PSQI score > 5 was found in 45.8% (n = 33) of patients in the masked hypertension group and 15% (n = 6) of patients in the normotensive group (p < 0.001). The non-dipper pattern was found in 17.5% of the healthy volunteer group and 59.94% (n = 41) of the masked hypertension group (p < 0.001). When we compared the dipping pattern of the masked hypertension groups, there was a significant difference in PSQI score between the dipper and non-dipper groups (4.87 ±3.21 vs. 3.58 ±2.33, p < 0.001). Multiple logistic regression analyses showed that masked hypertension, LV mass, and LV mass index score were independent predictors of poor PSQI. Conclusions This study demonstrates impaired sleep quality in subjects with masked hypertension, particularly those with a non-dipper pattern. Additionally, this study indicates that impaired sleep quality may help diagnose masked hypertension, particularly in the non-dipper group.

Psikotik belirtilerin eşlik ettiği Huntington hastalığında olanzapin kullanımı

Huntington’s disease is an autosomal dominant neurodegenerative disease. The disease begins between the ages of 30-50, including motor symptoms, psychiatric symptoms and is characterized by progressive dementia. Common psychiatric disorders of Huntington’s disease include mood and anxiety disorders, behavior and personality changes. Psychosis is relatively rare. Here, a patient is present, who has Huntington’s disease, which is associated with psychotic symptoms. 61-year-old male patient who were followed for Huntington disease for 25 years was admitted for complaints of thinking of poisoning and refuse to eat something. Patient was started on olanzapine at dose of 5 mg/day. In follow up psychotic symptoms disappeared. Emerging psychotic symptoms in Huntington disease is created a need for antipsychotic treatment. Atypical antipsychotic agents should be preferred in the treatment and as in the case olanzapine may be used as a treatment option should be kept in mind to control both involuntary movements and psychotic symptoms in Huntington’s disease with psychotic features. J Clin Exp Invest 2014; 5 (2): 326-328Huntington hastaligi otozomal dominant gecisli, norodejeneratif bir hastaliktir. Hastalik 30-50 yaslar arasinda baslayan motor belirtiler olmak uzere, psikiyatrik belirtiler ve ilerleyici demans ile karakterizedir. Huntington hastaliginda gorulen psikiyatrik bozukluklar siklikla duygu durum ve anksiyete bozukluklari, davranis ve kisilik degisiklikleridir. Psikoz ise nisbeten nadir gorulur. Bu sunumda psikotik belirtilerle seyreden bir Huntington olgusu sunulacaktir. 25 yildir Huntington hastaligi nedeniyle takip edilen 61 yasinda erkek hasta zehirlendigini dusunme ve yemek yemeyi reddetme sikayetleri ile basvurdu. Hastaya olanzapin 5 mg/gun tedavisi baslandi. Izlemlerde psikotik belirtileri ortadan kalkti. Huntington hastaliginda ortaya cikan psikotik belirtiler, antipsikotik tedavi ihtiyaci olusturmaktadir. Tedavide atipik antipsikotikler tercih edilmeli ve bu olguda oldugu gibi olanzapin, psikotik belirtilerin eslik ettigi Huntington olgularinda psikozu ve istemsiz hareketleri kontrol altina almada tedavi secenegi olarak akilda tutulmalidir.