У клозапина только риски агранулоцитоза 1%, а в остальном как и остальные *пины, с такими же рисками как оланзапин и кветиапин.
Психические заболевания повышают процент смертности по сравнению со здоровой популяцией, независимо от того принимает пациент лекарства или нет, всё равно риски повышаются, для шизофрении, биполярных расстройств и т.д.
из статей вот тут можно почитать, приводится обзор что антипсихотики второго поколения имеют меньший процент смертности. (Только это совершенно не значит что при приеме галоперидола умирает 3 из 10 а на зипрексе 1 из 10). Всё же это лекарства есть и минусы в лечении, у *пинов со временем могут возникнуть метаболические побочные явления, да это может привести через 20-30 лет к каким то осложнениям со стороны печени (может и не привести). Но что же тогда не лечить больных…. Во всех случаях необходимо серьозно относится к лечению, периодически сдавать анализы, контролировать соматический статус.
Antipsychotics and mortality
The premise has often been stated that second-generation antipsychotics (SGAs) may increase cardiovascular risk as many are associated with weight gain and worsening of metabolic parameters, often to a significantly greater degree than first-generation antipsychotics (FGAs) (Lieberman et al., 2005; Kahn et al., 2008). Clozapine, olanzapine and quetiapine are often cited as the antipsychotics with the most adverse metabolic profile (Hennekens et al., 2005). At present, somewhat surprisingly, we could find no evidence to support this hypothesis of increased cardiovascular risk. In contrast, many current data sets that compare FGAs and SGAs find either increased (Dean and Thuras, 2009; Enger et al., 2004; Osborn et al., 2007) or unchanged (Tiihonen et al., 2009) cardiovascular morbidity and mortality with FGAs.
A 10-year follow up study in the USA in 1621 patients with a mean age of 49 years at first observation found FGAs were associated with a doubling of mortality compared with SGA (RR 2.00, 95% CI 1.13–3.53) and had numerically greater association with cardiovascular mortality than SGA (rates per 100,000/year; 519 and 1178, significance not stated) (Dean and Thuras, 2009). The UK GPRD study reported significantly lower CVD mortality in SMI patients taking SGAs than FGAs (Osborn et al., 2007) and Enger et al. reported a five-fold increased risk of myocardial infarction in patients taking FGAs (Enger et al., 2004). During a 10-year follow up, recent data have also shown that the risk of CVD mortality does not differ between risperidone and clozapine despite known differences in their metabolic risk profiles (Kelly et al., 2010).
Where previously commentators have associated increased CVD mortality rates to antipsychotics (De Hert et al., 2010; Weinmann et al., 2009), it is salient to note that often these studies evaluated essentially only FGA (Joukamaa et al., 2006). The FIN 11 study concluded that mortality rates were heterogeneous amongst antipsychotics and were able to show dissonance in mortality rates between the individual FGAs haloperidol and perphenazine (Tiihonen et al., 2009). Overall mortality rates in the haloperidol cohort were significantly greater than the perphenazine cohort and some SGAs (Tiihonen et al., 2009). This review cannot address the potential reasons for these findings but it may be salient to focus on the recent finding that in a first-episode cohort in Finland, the greatest SMR for circulatory disease mortality was measured in the cohort aged 20–24 years (Kiviniemi et al., 2010).
In 2010 there seems little doubt that antipsychotic treatments reduce mortality with significant mortality elevations reported in the first admitted Finnish cohort (2006) and the complete Finnish cohort (2009), in patients who did not take antipsychotic treatments, with worsening of outcomes according to length of non-adherence to medications (Tiihonen et al., 2006, 2009). Even in short-term clinical trials there are similar findings (Khan et al., 2007; Issac and Koch, 2010) where the US Food and Drug Administration and European Medicines Agency have published mortality rates for antipsychotics in comparison to placebo cohorts. Schizophrenia patients in the placebo cohorts have elevated mortality rates compared with antipsychotic cohorts. Poor adherence to medication has been shown to be predictive of suicide in both small case–control studies (Pompili et al., 2009) and a large cohort study from Finland (Tiihonen et al., 2006). Mortality rates in the large Finland study in first admission schizophrenia patients with a mean follow up of 3 years were increased at least five-fold in the cohort not receiving any medication (adjusted RR 37.4; 95% CI 5.1–276) for suicide (Tiihonen et al., 2006) and by at least six-fold (adjusted RR 12.3: 95% CI 6.0–24.1) for overall mortality. In the 11-year follow up study of all schizophrenia patients in Finland, long-term exposure (7–11 years) to antipsychotic treatment was associated with around a 20% lower mortality than no drug use (Tiihonen et al., 2009) with an inverse relation between length of treatment and mortality rate.
Polypharmacy has often been associated with increased mortality (Joukamaa et al., 2006) though only with conventionals. A recent Danish case–control study in over 27,000 schizophrenia patients over a 10-year follow up (1996–2005) reported an unchanged mortality rate for the risk of natural death when utilising antipsychotic polypharmacy with up to three antipsychotics (conventionals were prescribed in 64% of patients) (Baandrup et al., 2010). An association was, however, reported for increased mortality when using benzodiazepines with a long elimination half-life (OR 1.78) that may require further clarification. The current findings that SGA have as a minimum similar associations with CVD mortality with FGA do require further study and importantly may require far longer follow up than currently reported.
исходник с пабмеда тут http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2951589/?tool=pmcentrez