Clozapine versus other antipsychotics during the first 18 weeks of treatment: A retrospective study on risk factor increase of blood dyscrasias

Fabrazzo, Michele; Prisco, Vincenzo; Sampogna, Gaia; Perris, Francesco; Catapano, Francesco; Monteleone, Alessio Maria; Maj, Mario

doi:10.1016/j.psychres.2017.06.068

Cited by 25 publications

(12 citation statements)

References 39 publications

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“…The epidermis function needs to be considered a natural source of vitamin D synthesis by the sun's ultraviolet light B (UVB) or other UVB sources. The accumulating evidence shows vitamin D as a key modulator of immune and inflammatory mechanisms [81][82][83]. However, it remains controversial the effectiveness of supplemented vitamin D as an adjunctive treatment in patients affected by Ps and depression or anxiety [84,85].…”

Section: Discussionmentioning

confidence: 99%

A systematic review on shared biological mechanisms of depression and anxiety in comorbidity with psoriasis, atopic dermatitis, and hidradenitis suppurativa

et al. 2021

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Background Mental disorders in comorbidity with chronic skin diseases may worsen disease outcome and patients’ quality of life. We hypothesized the comorbidity of depression, anxiety syndromes, or symptoms as attributable to biological mechanisms that the combined diseases share. Methods We conducted a systematic review based on the Preferred Reporting Items for Systematic Review and Meta-Analysis statement searching into PubMed, PsycInfo, and Scopus databases. We examined the literature regarding the comorbidity of psoriasis (Ps), atopic dermatitis (AD), or hidradenitis suppurativa with depression and/or anxiety in adults ≥18 years and the hypothetical shared underlying biological mechanisms. Results Sixteen studies were analyzed, mostly regarding Ps and AD. Brain-derived neurotrophic factor/tropomyosin receptor kinase B signaling and nuclear factor kappa-light-chain-enhancer of activated B cells/p38 mitogen-activated protein kinase pathways arose as shared mechanisms in Ps animal models with depression- and/or anxiety-like behaviors. Activated microglia and neuroinflammatory responses emerged in AD depressive models. As to genetic studies, atopic-dermatitis patients with comorbid anxiety traits carried the short variant of serotonin transporter and a polymorphism of the human translocator protein gene. A GA genotype of catechol-O-methyltransferase gene was instead associated with Ps. Reduced natural killer cell activity, IL-4, serotonin serum levels, and increased plasma cortisol and IgE levels were hypothesized in comorbid depressive AD patients. In Ps patients with comorbid depression, high serum concentrations of IL-6 and IL-18, as well as IL-17A, were presumed to act as shared inflammatory mechanisms. Conclusions Further studies should investigate mental disorders and chronic skin diseases concurrently across patients’ life course and identify their temporal relation and biological correlates. Future research should also identify biological characteristics of individuals at high risk of the comorbid disorders and associated complications.

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Section: Discussionmentioning

confidence: 99%

A systematic review on shared biological mechanisms of depression and anxiety in comorbidity with psoriasis, atopic dermatitis, and hidradenitis suppurativa

et al. 2021

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“…Blood dyscrasias, such as mild to moderate leukopenia decreased white blood cell count, mild neutropenia, anemia, eosinophilia and leukocytosis, are often seen with clozapine but, if cautiously monitored, in the majority of the cases this may be transient or benign. 127,128 The most severe and potentially life-threatening clozapine-related blood dyscrasias is neutropenia, which may eventually develop into clozapine-induced agranulocytosis or granulocytopenia. This occurs in roughly 0.8-2% of patients and requires mandatory hematological monitoring.…”

Section: Uncommon Adverse Effectsmentioning

confidence: 99%

Section: Clozapine Mechanism Of Action and Relationships With Adversementioning

confidence: 99%

Safety of antipsychotics for the treatment of schizophrenia: a focus on the adverse effects of clozapine

Berardis¹,

Rapini²,

Olivieri³

et al. 2018

Therapeutic Advances in Drug Safety

142

125

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Clozapine, a dibenzodiazepine developed in 1961, is a multireceptorial atypical antipsychotic approved for the treatment of resistant schizophrenia. Since its introduction, it has remained the drug of choice in treatment-resistant schizophrenia, despite a wide range of adverse effects, as it is a very effective drug in everyday clinical practice. However, clozapine is not considered as a top-of-the-line treatment because it may often be difficult for some patients to tolerate as some adverse effects can be particularly bothersome (i.e. sedation, weight gain, sialorrhea etc.) and it has some other potentially dangerous and life-threatening side effects (i.e. myocarditis, seizures, agranulocytosis or granulocytopenia, gastrointestinal hypomotility etc.). As poor treatment adherence in patients with resistant schizophrenia may increase the risk of a psychotic relapse, which may further lead to impaired social and cognitive functioning, psychiatric hospitalizations and increased treatment costs, clozapine adverse effects are a common reason for discontinuing this medication. Therefore, every effort should be made to monitor and minimize these adverse effects in order to improve their early detection and management. The aim of this paper is to briefly summarize and provide an update on major clozapine adverse effects, especially focusing on those that are severe and potentially life threatening, even if most of the latter are relatively uncommon.

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“…A more persistent form has been described mainly in case reports and especially with concomitant lithium use [ 38 ]. More recently, Fabrazzo et al reported leukocytosis in 37.8% of a clozapine-treated cohort of patients, with incidence rates of 11.1% and 26.7% for the transient and persistent types, respectively [ 22 ]. Male gender [ 27 , 28 , 29 , 30 , 32 , 38 ], and lithium co-administration represent the most important risk factors for leukocytosis [ 39 , 40 ].…”

Section: Discussionmentioning

confidence: 99%

“…An increased leukocyte count was observed with increasing daily doses, while subsequent dose reductions and the following withdrawal were associated with leukocyte count normalization in both cases, further supporting the causative role of clozapine in inducing leukocytosis [ 56 ]. Regarding the putative association between neutrophilia and the clinical outcome, Fabrazzo et al [ 22 ] found persistent neutrophilia associated with a loss of clozapine efficacy over time in their cohort. At present, the hypothesized association between leukocytosis and clinical worsening remains speculative at best, with the former representing a benign and transient phenomenon.…”

Section: Discussionmentioning

confidence: 99%

Leukocytosis Associated with Clozapine Treatment: A Case Series and Systematic Review of the Literature

et al. 2021

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Background and Objectives: Clozapine is the only antipsychotic approved for treatment-resistant schizophrenia. Despite its superior efficacy profile as compared with other antipsychotics, clozapine remains underutilized. Clozapine monitoring systems clearly describe the proposed management of clozapine-induced neutropenia; however, no specific mention is made of how to interpret neutrophilic leukocytosis, despite that being a relatively frequent finding. Prescribers unfamiliar with this molecule may misjudge its clinical significance, potentially leading to untimely treatment interruption. Here, we systematically review the literature on the risk of neutrophilic leukocytosis during clozapine treatment, and describe eight additional cases among our patient cohort. Materials and Methods: We performed a systematic review of the literature on PubMed and Embase using the PRISMA 2020 guidelines, and selected all original reports describing either (1) the prevalence of neutrophilic leukocytosis during clozapine treatment, or (2) the clinical significance of neutrophilic leukocytosis. We described eight additional cases of neutrophilic leukocytosis during clozapine treatment while attending an outpatient psychiatric clinic. Results: Our research ultimately yielded the selection of 13 articles included in this systematic review. The case series highlighted the presence of stable and clinically unremarkable neutrophilia during a follow-up ranging from one to ten years. Conclusions: Existing evidence indicates that leukocytosis associated with clozapine treatment can be considered as an asymptomatic and benign condition, suggesting that no change in clozapine treatment is needed upon its detection.

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Clozapine versus other antipsychotics during the first 18 weeks of treatment: A retrospective study on risk factor increase of blood dyscrasias

Cited by 25 publications

References 39 publications

A systematic review on shared biological mechanisms of depression and anxiety in comorbidity with psoriasis, atopic dermatitis, and hidradenitis suppurativa

A systematic review on shared biological mechanisms of depression and anxiety in comorbidity with psoriasis, atopic dermatitis, and hidradenitis suppurativa

Safety of antipsychotics for the treatment of schizophrenia: a focus on the adverse effects of clozapine

Leukocytosis Associated with Clozapine Treatment: A Case Series and Systematic Review of the Literature

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