Alkol Kullanım Bozukluğu
Özet
Alkol kullanım bozukluğu (AKB); insanlık tarihi kadar eski, tekrarlayıcı alkol alımlarının olduğu, kontrol kaybı, aşerme ve depreşmelerle seyreden süreğen bir psikiyatrik bozukluktur. Vücutta akut ve kronik sistemik değişimlere neden olan etanol, karaciğerde ADH ve ALDH enzimleri aracılığıyla metabolize edilir. DSM-5 ve ICD-11 sistemleri, tanı koyarken kategorik yerine boyutsal yaklaşımı benimseyerek alkol bağımlılığı ve kötüye kullanımı tanılarını AKB çatısı altında birleştirmiştir. Etyolojisinde genetik, psikososyal ve çevresel etkenlerin kümülatif rolü büyüktür; kalıtımsal faktörler riski 4-5 kat artırmakta olup genom çalışmalarında bağımlılıkla ilişkili kromozomlar saptanmıştır. AKB, gidişat ve şiddet açısından heterojen bir yapıya sahip olduğundan Cloninger, Babor ve Lesch gibi araştırmacılar tarafından çeşitli klinik tiplere sınıflandırılmıştır. Sağaltım süreci akut ve kronik durumlar olarak ikiye ayrılır. Akut zehirlenme ve otonomik hiperaktivasyon içeren yoksunluk sendromunda solunum desteği, hidrasyon, Wernicke Ensefalopatisini önlemek adına hayati öneme sahip B1 vitamini replasmanı ve semptomları yatıştırmada üstün olan benzodiazepinler (diazepam) kullanılır. Kronik süreçte nüksleri ve alkol isteğini önlemek için disülfiram, naltrekson, nalmefen ve akamprosat gibi farmakolojik ajanların yanı sıra bilişsel davranışçı terapiler, Adsız Alkolikler (AA) gibi dayanışma grupları ve aile destek programları uygulanmaktadır.
Alcohol use disorder (AUD) is a chronic psychiatric disorder as ancient as human history, characterized by recurrent alcohol consumption, loss of control, craving, and relapses. Causing acute and chronic systemic changes in the body, ethanol is primarily metabolized in the liver via ADH and ALDH enzymes. DSM-5 and ICD-11 systems emphasize a dimensional rather than a categorical approach, merging the diagnoses of alcohol abuse and dependence under the single umbrella of AUD. In its etiology, the cumulative effect of genetic, psychosocial, and environmental factors plays a significant role; hereditary factors increase the risk 4 to 5 times, and genome studies have identified specific chromosomes associated with dependence. Being a heterogeneous disorder in terms of clinical course and severity, AUD has been classified into various clinical typologies by researchers such as Cloninger, Babor, and Lesch. The management process is examined in two categories as acute and chronic conditions. In the treatment of acute intoxication and alcohol withdrawal syndrome—which carries risks of seizures and autonomic hyperactivity—airway maintenance, hydration, vital vitamin B1 replacement to prevent Wernicke's Encephalopathy, and benzodiazepines (primarily diazepam) for managing irritability are utilized. In the chronic phase, pharmacological agents like disulfiram, naltrexone, nalmefen, and acamprosate are implemented to reduce craving and relapses, synergized by cognitive behavioral therapies, self-help groups like Alcoholics Anonymous (AA), and family support programs.
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