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Yıl:2018; Cilt: 19; Sayı: 4>> Özet
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Anadolu Psikiyatri Dergisi; 2018;19(4):427-430
Kallmann Sendromunda psikoz: Olası genetik yatkınlık temelinde bir olgu bildirimi
SS Kırlıoğlu, YH Balcıoğlu, PÇ Aydın
Bakırköy Prof. Dr. Mazhar Osman Training and Research Hospital for Psychiatry, Neurology and Neurosurgery, Istanbul
Kallmann Sendromu (KS), gonadotropin salgılatıcı hormon (GnRH) üretimindeki veya salgılanmasındaki eksikliğe bağlı ortaya çıkan ve spontan pubertenin yokluğu ile koku duyusunda bozulmanın izlendiği sık görülmeyen bir hastalıktır. Etiyolojisinde çoklu genetik örüntüler yer almaktadır. KS ve psikozun ortak yatkınlaştırıcı genetik profilden köken aldığına zaman zaman dikkat çekilmiştir. Şizofreninin etiyopatogenezinde rol oynadığı öne sürülen bozuk KAL-X geninin GnRH nöronlarının migrasyonda bozulmaya ve sonuç olarak değişen şiddette olfaktör kusuruna ve normal cinsel gelişim sürecinde bozulmaya yol açtığı gösterilmiştir. Olgumuza 13 yaşındayken KS tanısı konmuş, halen aylık 250 mg testosteron propiyonat ve testosteron fenilpropiyonat intramuskuler uygulanan 19 yaşında bir erkektir. Hasta, kliniğimize iki yıl önce başlayan işitsel ve görsel varsanılar yakınmasıyla başvurmuştur. Hastamızda aynı zamanda kötülük görme sanrıları, sosyal izolasyon ve intihar düşünceleri de vardı. Ayrıntılı psikiyatrik muayene ve kliniğe yatışını izleyerek şizofreni tanısı konan hastanın tedavisine olanzapin 5 mg/gün ile başlanmış ve aşamalı olarak artırılarak 15 mg/güne yükseltilmiştir. Varsanıları, sanrıları ve intihar düşünceleri tedaviyle iyileşme göstermiştir. Bu yazıda söz konusu eş tanının altında yatan olası ortak etiyopatogenezin tartışılması amaçlanmıştır.
Psychosis in Kallmann Syndrome: A case illustration based on possible genetic liability
Kallmann Syndrome (KS) is an uncommon disorder caused by a deficient production or secretion of gonadotropinreleasing hormone (GnRH) and manifests with an absence of spontaneous puberty and impaired sense of smell. Multiple inheritance patterns have been recognized in the etiology. KS and psychosis have occasionally been considered to originate in similar predisposing genetic profile. Defective KAL-X gene which had previously been attributed in the etiopathogenesis of schizophrenia was asserted to lead to an impairment in the migration of GnRH neurons and olfactory deficits in various severity and disruption in sexual developmental, consequently. Our case is a 19-year-old male previously diagnosed with KS at his 13, who has been under the monthly intramuscular treatment of testosterone propionate and testosterone phenylpropionate at the dose of 250 mg. He was admitted to our clinic with auditory and visual hallucinations that started two years ago. Persecutory delusions, social isolation, and suicidal thoughts also existed. We diagnosed him schizophrenia with comorbid KS following the hospitalization and a detailed psychiatric examination. Olanzapine was initiated as 5 mg/day and potentiated to 15 mg/day. His delusions, hallucinations and suicidal thoughts had improved with the treatment. In this illustration, we purposed to discuss probable common etiopathogenesis underlying this comorbidity.

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