Less is More – Possible Option in the Treatment of Depression

Depression is an illness of modern society, which affects population of different age. Etiological factors differ, and frustration factors as a cause of depression are multiplying. Each new episode presents diffi culties, both for patients and psychiatrists. Despite the increasing number of antidepressants we use in treatment, it is sometimes hard to notice an effi cient antidepressant in an optimal-effi cient dose. In resistant cases we apply combinations of psychopharmacs, and the choice of the same depends on the leading symptoms. We will present the case of a 67-year old patient where a depressive episode (in the terms of a reccurent major depressive disorder) lasts for one year. During this period she was treated as outpatient and inpatient with several antidepresants in combinations with other psychopharmacotherapeutical drugs. Despite regular treatment, mental state was worsening. Clinical presentation was indicating developing of dementia (behavior, cognition outges), which we excluded through diagnostic process. Psychopharmacological combinations (antidepresants, mood stabilizators, antypschotics, anxsiolotix) were not effi cant. Progression of simptoms leads to rehospitalisation. In further treatmen, we followed the principle «Less is more» which resulted with an expected and satisfactory outcome

PERSONALISED APPROACH IN TREATMENT OF A PREPSYCHOTIC ADOLESCENT

In clinical practice with adolescents we often come across with prepsychotic and psychotic disorders. When an adolescent patient has a positive hereditary burden for psychiatric illnesses in both parents, then the qualification of adolescent’s mental disorder seems closer to psychotic. We must have in mind that hereditary burden is only one of many etiological factors that contribute to mental decompensations in adolescent age, that can, but don’t have to be the prodrome of psychosis in the future. Whether is characterised as psychotic or not, the treatment of an adolescent in critical situation must be personalised, considering biological, social and individual factors of a patient. We believe that clinician’s experience in treating psychotic adolescent patients and personalised and integrative approach to a patient is of great importance. In this article we will present the therapeutical process of a 19-year old female adolescent, with psychotic symptoms, whose both parents are psychiatric patients. A personalised and integrative approach in treatment of this patient made possible the overcome of crisis, termination of high school education and an employment. These achievements, no matter what the future can bring to this patient, create better conditions for her functioning in life

THE INFLUENCE OF SIDE EFFECT OF ANTIPSYCHOTIC ON THE COURSE OF TREATMENT IN ADOLESCENT

The use of antipsychotics in treatment of children and adolescents requires good knowledge of psychopathology, psychofarmacotherapy, developmental processes and family relations. It is necessary to have parental consent for the use of a medication in this age, with previous explanation of therapeutic goals, limitations and possible side effects of antipsychotics. The number of antipsychotics registered for use in children and adolescents is quite limited. The combination of clinical experience of those working with psychotic adolescents and a good collaboration with parents, creates a therapeutic space where good results in treatment can be achieved. Side effects, though rarely, can bring in question the course of treatment and disorder follow up. In this work we will present a 14-year old girl adolescent with psychotic symptoms, in which case the course of treatment and discontinuance of therapy was caused by a side effect - an oculogyric crisis

Etiopathogenesis of metabolic syndrome in schizophrenia – recent findings

Uzrok polovice do dvije trećine smrtnih ishoda pacijenata sa shizofrenijom pripisuje se kardiovaskularnim bolestima. Smatra se da visoka učestalost metaboličkog sindroma najviše povećava rizik za nastanak kardiovaskularnih oboljenja u shizofreniji. Iako je metabolički sindrom jedan od vodećih uzroka morbiditeta i mortaliteta u pacijenata sa shizofrenijom, do prije petnaestak godina istraživanje etiologije metaboličkog sindroma u shizofreniji nije predstavljalo veći znanstveni interes. Novije spoznaje ukazuju na mogućnost da bi pojačano stanje upalnog odgovora u organizmu moglo predstavljati zajedničku etiopatogenetsku podlogu u nastanku metaboličkog sindroma i shizofrenije. Primjerice, značajno povišena koncentracija proupalnih citokina te C reaktivnog proteina uočena je u pacijenata sa shizofrenijom koji nisu uzimali antipsihotične lijekove ili su ih uzimali u vrlo malim dozama, a zamijećeno je i da uzimanje inhibitora ciklooksigeneze-2, uz antipsihotičnu terapiju, može ublažiti težinu kliničkih simptoma i kognitivnih deficita u oboljelih. U ovom preglednom radu iznesene su najnovije spoznaje o ulozi okolišnih i genetičkih čimbenika u etiopatogenezi metaboličkog sindroma u shizofreniji. Mnogi mehanizmi kojima bi okolišni čimbenici, poput nezdrave prehrane i pušenja, mogli pridonijeti nastanku metaboličkog sindroma u shizofreniji ne razlikuju se značajno u odnosu na opću populaciju. Ipak, uzimanje antipsihotičnih lijekova, posebice tzv. atipičnih antipsihotika, te njihova interakcija s okolišnim čimbenicima, kao i genetičkim čimbenicima podložnosti, dodatno pridonose heterogenosti etiopatogeneze metaboličkog sindroma u shizofreniji, ali i otežavaju adekvatan terapijski pristup. Budući da su dosadašnja istraživanja uglavnom bila usredotočena na moguću poveznicu antipsihotičnih lijekova i metaboličkih abnormalnosti u oboljelih, detaljnije su razmotrene značajke nezdrave prehrane i ovisnosti o pušenju te njihova moguća povezanost s metaboličkim sindromom.The etiology of one half to two-thirds of deaths among patients with schizophrenia could be attributed to cardiovascular diseases. It is believed that high prevalence of metabolic syndrome mostly contributes to the risk of cardiovascular diseases in schizophrenia. Although the metabolic syndrome is among the leading causes of morbidity and mortality among patients with schizophrenia, fifteen years ago studies investigating the etiology of the metabolic syndrome among patients with schizophrenia were not a part of scientific interest. Recent findings indicate the possibility that increased state of inflammatory response in the organism may underlie the etiopathogenesis of both schizophrenia and metabolic syndrome. For instance, significantly increased levels of proinflammatory cytokines and C reactive protein have been observed in schizophrenia patients with minimal or no exposure to antipsychotics and it has also been revealed that cyclooxygenase-2 inhibitor drugs add-on treatment to the antipsychotic therapy may lead to decrease in clinical symptom severity and alleviate cognitive deficits in the patient group. In this review we aim to provide an update on genetics and environmental factors in the etiopathogenesis of metabolic syndrome in schizophrenia. Numerous mechanisms by which the environmental factors such as unhealthy diet pattern and smoking could contribute to the etiology of the metabolic syndrome in schizophrenia do not differ significantly compared to a healthy population. However, treatment with antipsychotic medications, particularly with atypical antipsychotics, as well as interaction between antipsychotic drugs and environmental and genetic risk factors may additionally lead to heterogeneity of the etiopathogenesis of metabolic syndrome in schizophrenia as well as to complicate treatment approach. Since previous studies have been mostly focused on plausible associations between antipsychotic medications and metabolic abnormalities, we provided a more detailed characteristic of unhealthy diet among schizophrenia patients and its plausible relation to metabolic syndrome. Furthermore, more deeply have been discussed the possible associations between nicotine dependence and metabolic syndrome

Smoking, components of metabolic syndrome and clinical severity of schizophrenia

Cilj: Ispitali smo utječu li, i u kojoj mjeri, koncentracije lipida i glukoze u plazmi te vrijednosti indeksa tjelesne mase (engl. body mass index; BMI), na težinu kliničke slike shizofrenije u hrvatskih bolesnika, ovisno o njihovom pušačkom statusu. Ispitanici i metode: U istraživanju je sudjelovalo 263 kroničnih bolesnika (muškarci/žene: 139/124). Težina kliničke slike procijenjena je korištenjem ocjenske ljestvice PANSS-a (engl. Positive and Negative Syndrome Scale) u akutnoj fazi bolesti tijekom posljednje hospitalizacije. U pušače su klasificirani ispitanici koji puše najmanje jednu cigaretu dnevno u periodu duljem od godine dana, a u nepušače oni koji su popušili manje od 100 cigareta tijekom života. Rezultati: Koncentracije triglicerida, glukoze i vrijednosti BMI-a nisu pokazale povezanost s PANSS psihopatologijom, niti u bolesnika, niti u bolesnica, ovisno o pušačkom statusu (svi P > 0,05), a na težinu kliničke slike u bolesnica, utjecale su isključivo koncentracije kolesterola. Bolesnice pušači s višim koncentracijama LDL kolesterola (engl. low density lipoprotein cholesterol) imale su značajno niže vrijednosti općih i ukupnih simptoma (P = 0,023 i P = 0,015), dok su u bolesnica nepušača s višim koncentracijama HDL kolesterola (engl. high density lipoprotein cholesterol), uočene značajno niže vrijednosti pozitivnih i ukupnih PANSS simptoma (P = 0,041 i P = 0,002). Koncentracija LDL kolesterola opisuje približno 20% varijabilnosti općih simptoma i 23% varijabilnosti ukupnih simptoma u bolesnica pušača, a vrijednosti HDL kolesterola pridonose s otprilike 39% težini pozitivnih simptoma te s 69% težini ukupnih simptoma u bolesnica nepušača. Zaključak: Na temelju naših rezultata možemo zaključiti da na težinu kliničke slike shizofrenije utječu isključivo koncentracije kolesterola u bolesnica. Nadalje, koncentracije kolesterola opisuju mali do umjereno veliki udio varijabilnosti PANSS psihopatologije.Aim: We aimed to investigate whether, and to what extent, plasma glucose and lipid concentrations and body mass index (BMI) values, influence schizophrenia severity in Croatian patients, according to their smoking status. Patients and methods: Our study comprised 263 chronically ill patients (males/females: 139/124). Severity of schizophrenia was assessed via Positive and Negative Syndrome Scale (PANSS) psychopathology data during an acute illness state at the time of last hospital admission. Smokers were defined as individuals who smoked more than one cigarette each day for more than one year, and nonsmokers were defined as those who had smoked fewer than 100 cigarettes during their lifetime. Results: Plasma triglyceride and glucose levels and BMI values were not associated with PANSS psychopathology, neither among males, nor among females, according to their smoking status (all P > 0.05), whereas data of PANSS psychopathology among females were associated only with plasma cholesterol concentrations. Female smokers with higher LDL cholesterol (engl. low density lipoprotein cholesterol) concentrations had significantly lower general and total PANSS symptom values (P = 0.023 and P = 0.015), whereas among female nonsmokers with greater HDL cholesterol (engl. high density lipoprotein cholesterol) concentrations, significantly lower positive and total PANSS symptom values were observed (P = 0.041 and P = 0.002). The LDL cholesterol concentrations account for approximately 20% of the general symptom variability and 23% of the total symptom variability among female smokers; among nonsmoking females, HDL cholesterol concentrations contribute by approximately 39% to positive symptom severity and by approximately 69% to total symptom severity. Conclusion: According to our results, we can conclude that plasma cholesterol concentrations influence schizophrenia severity in female patients only. Furthermore, the contribution of cholesterol concentrations to PANSS psychopathology varies from small to moderate

The insertion/deletion polymorphism in the angiotensin-converting enzyme gene and nicotine dependence in schizophrenia patients

We investigated the relationship between the functional insertion/deletion (I/D) polymorphism in the angiotensin-converting enzyme (ACE) gene and the risk of nicotine dependence in Croatian schizophrenia patients. We also tested whether interactions between ACE-I/D polymorphism and smoking status affected the clinical psychopathology findings in patients as measured using Positive and Negative Symptom Scale (PANSS) scores. Polymerase chain reaction analysis was used to genotype 267 chronically ill schizophrenia patients (140 males/127 females).There were no significant differences in the distribution of ACE genotypes and alleles in male or female schizophrenia patients who were stratified based on their smoking status. However, there was a trend toward a difference in the ACE genotype distribution in female smokers vs. nonsmokers (χ2 = 5.13, p = 0.077) that was due mainly to the significant overrepresentation of ACE-ID heterozygous genotypes in female smokers compared to nonsmokers (62.3% vs. 42.0%, p = 0.025). ACE-ID heterozygous females had about a 2-fold higher smoking risk than ACE-II and ACE-DD homozygous carriers (OR = 2.29, 95% CI = 1.1–4.7, p = 0.026). We observed no contribution of the ACE genotype-smoking interaction to PANSS psychopathology. This is the first study to investigate the possible association between ACE-I/D polymorphism and nicotine dependence in schizophrenia. Our results suggest that the ACE-I/D polymorphism may be relevant in determining the risk of nicotine dependence in female patients with schizophrenia while the ACE genotype-smoking interaction does not contribute to the clinical expression of schizophrenia. Izvorni jezik: EN