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Aim. The aim of the present study was to summarise data regarding registration of generic medicinal products.

Data analysis. Introduction of equivalents of referencemedicinal products (also described as generic drugs) intomedicine has allowed patients to have broad access tonewest pharmacotherapy methods and significantly lowered treatment cost. Equivalents of reference medicinal products obtain marketing authorisations aftertheir bioequivalence to relevant reference products (alsodescribed as "innovative products") is proven in bioequivalence studies. Requirements for these studies areprecisely set by competent regulatory agencies.

Conclusions. Even though all generic medicinal prod-ucts currently on the market fulfil the requirements forquality and biological equivalence, some patients mayexperience transient symptoms of therapeutic equivalence disturbances. As this phenomenon is unpredict-able, assessment of patient clinical status is requiredduring first weeks after the switch from reference drugto generic. Dose adjustment may be necessary. However, sometimes deterioration of symptoms may also resultfrom natural progression of the disease.

During the last two decades, an increasing interest innon-medical use of pharmacological cognitive enhancement (PCE) has been noticed. Among PCE drugs, there arepsychostimulants, including methylphenidate, amphet-amines and modafinil. PCE is used by different groups ofpeople, mainly by students, but also surgeons, stock brokers, athletes, video game players, poker players. Effects of the aforementioned psychostimulants on cognitiveprocesses are consistently dependent on individual andsituational factors as well as the cognitive domain inquestion and applied analytical approach. Evidence fromseveral studies shows that methylphenidate, amphetamines and modafinil have limited pro-cognitive effects,especially when applied to subjects performing complextasks. Furthermore, they can deteriorate planning andcognitive flexibility. Adverse events produced by thesedrugs, mainly cardiovascular, psychiatric and neurologic,pose considerable safety risks on the consumers.

Sepsis-associated encephalopathy (SAE) is a centralnervous system disorder which develops in the course of an infection. About 1/3 of patients with an infection manifest qualitative consciousness disturbances possiblyrelated to SAE. This phenomenon is underdiagnosed inboth the general and specialised practices and in particular in the emergency medicine settings.This review paper is aimed at specifying the pathomechanisms, diagnostic procedures and differentialdiagnostics of SAE. The SAE diagnosis is possible in patients with qualitative or quantitative consciousness disturbances or a cognitive and executive functioning impairment who fulfil the sepsis diagnostic criteria. In differential diagnosis and monitoring of SAE patients the clinimetric methods are used: Richmond Agitation and Sedation Scale (RASS), Confusion Assessment Method for the Intensive Care Unit (CAM-ICU) and Sequential Organ Failure Assessment score (SOFA), along with neurophysiology (electroencephalography), neuroimaging (magnetic resonance imaging) and laboratory tests (C-reactive protein, procalcitonin, biomarkers of central nervous system and blood-brain barrier damage). The treatment of SAE patients is based on the infection control and homeostasis maintenance. During symptomatic treatment, benzodiazepines should be avoided, and dexmedetomidine seems to be beneficial. Potentially, the treatment with intravenous immunoglobulins may be favourable.

The etiopathogenesis of suicide is the subject of investigation from the point of view of psychology, philosophy, sociology and medicine. Suicide is a particularly important aspect in the course and treatment of affective disorders. Selected statistical data was taken from the websites of the World Health Organization WHO and the Police. The authors reviewed the psychiatric literature on the neurobiological aspects of suicidal behavior. We included English original papers, reviews, and search of reference lists, without the time limits of publication. To better present the biological mechanisms involved in the control of suicidal behavior, studies based on both clinical data and animal models were taken into account. Animal models play an important role in explaining the mechanisms of stress response and the developmentof depressive symptoms, allowing to track of the interaction of genetic and environmental factors. Genetic research (twin studies, studies of candidate genes andgenomewide association studies GWAS), neurochemical(neurotransmitter metabolites, receptors, transportersand protein expression in peripheral blood), neuropsychological (impulsivity and decision making strategies), neuroimaging (structural and functional imaging studies) and psychopharmacological results for the biologicalbasis of suicide were described.

Objectives. Central monoaminergic dysfunction with autonomic nervous system dysregulation are reportedin major depressive disorder (MDD). Salivary α-amylase (sAA) activity and salivary 3-methoxy-4-hydroxyphenylglycol (sMHPG) are adopted as markers of central noradrenergic activity with salivary 5-hydroxyindole acetic acid (s5-HIAA) being indicative of central serotonin turnover. No data is available on baseline sAA, s5-HIAA and sMHPG in MDD being interrelated to the specific psychopathological dimensions and item performance of the Hamilton Rating Scale for Depression(HAMD-17) in MDD.

Material and methods. The basal sMHPG and s5-HIAA concentrations and sAA activity as correlated with HAMD-17 psychometric assessment were studied in this exploratory study of 20 adult, treatment-naïve MDD patients.

Results. The negative correlations between sMHPG and HAMD-17 items 7 (work and activities) (r = –0.56, p = 0.01) and 4 (early insomnia) (r = –0.45, p = 0.049) were foundpost hoc. On exploration the correlations between sAA and items 7 (work and activities) (r = –0.47, p = 0.04) and 12 (gastrointestinal symptoms) (r = 0.49, p = 0.03) were also observed with no such observation with regard to s5-HIAA.

Conclusions. On exploratory analysis, in basal, non-stimulated conditions baseline sAA, sMHPG levelsin MDD were found to be correlated with HAMD-17 items representing clinical symptoms attributable to primary noradrenergic dysfunction at the early stage of major depression. Saliva is a promising source of monoaminergic biomarkers in MDD research. However, further systematic studies are needed to contribute consistent results to aid standardization, in particular with psychometric measures.