ABSTRACT
BACKGROUND: Alcohol use disorder (AUD) is a psychiatric disorder characterized by excessive and uncontrolled drinking that causes distress and has damaging consequences for men and women of all ages. It is one of the four most disabling diseases and it affects approximately 14.6 million persons in Europe. OBJECTIVES: Objective of this study is to investigate changes in platelet serotonin concentration after four weeks of alcohol abstinence in regards to the genotype of the serotonin transporter. METHODS: A total of 154 patients with AUD were included in the study. Platelet serotonin concentrations were assessed by enzyme-linked immunosorbent assay. Genotype of serotonin transporter promoter polymorphism was determined by the polymerase chain reaction-based method. RESULTS: We did not establish a statistically significant main effect of serotonin transporter polymorphism on platelet serotonin concentration after four weeks of abstinence. CONCLUSION: Aforementioned finding is in line with previous research suggesting a complex relationship between serotonin transporter gene and platelet serotonin levels, and congruent with the well-established genotype interaction with numerous other factors, such as sex, ethnicity, education level, and stressful life events.
Subject(s)
Alcoholism , Serotonin Plasma Membrane Transport Proteins , Alcohol Abstinence , Alcoholism/genetics , Female , Genotype , Humans , Male , Serotonin/genetics , Serotonin Plasma Membrane Transport Proteins/geneticsABSTRACT
Lewy body dementia is a progressive neurodegenerative disease and is considered to be the second most common cause of dementia in the elderly. Because of the complexity of clinical presentation, it is often misdiagnosed and mistaken for other dementias, which may result in administering inappropriate therapy, and thus worsening of the patient condition. We reviewed a case of a 71-year-old patient whose clinical presentation gradually occurred with complex visual hallucinations, atypical extrapyramidal motor symptoms, fluctuating cognitive impairments with delirious episodes, and oscillating syncope. Depressive mood, impaired daily functioning and sensitivity to antipsychotics were also noted. Extensive diagnostic workup was performed with neuropsychological testing and use of single-photon emission computerized tomography. Considering the clinical presentation and diagnostic procedures performed, the diagnosis of Lewy body dementia was set and pharmacotherapy was revised. We discuss the importance of taking overall clinical presentation and diagnostic treatment in consideration and applying appropriate therapy to slow down the progression of the disease and exacerbation of the patient's psychological functions.
