Clozapine Treatment for Cabergoline-Induced Psychosis in a Patient With a Giant Prolactinoma

Pérez‐Esparza, Rodrigo; Rojas-Guerrero, Carlos Alberto; Andino-Ríos, Gerson Geovany; Arias-Garro, Patricia; Ramı́rez-Bermúdez, Jesús; Portocarrero-Ortíz, Lesly

doi:10.1176/appi.neuropsych.16110313

Cited by 12 publications

(9 citation statements)

References 10 publications

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“…[4][5][6] However, Chang et al 7 in 2007 report 2 cases in which 0.5-mg cabergoline induced a worsening of psychotic symptoms in patients previously diagnosed with schizophrenia. Furthermore, Davie 8 in 2007 and Pérez-Esparza et al 9 in 2017 both describe cases of previously nonpsychotic patients who started cabergoline for a pituitary prolactinoma and developed psychiatric symptoms such as gambling, paranoid delusions, major depression, and auditory hallucinations. 9 The likely mechanism by which cabergoline induces psychotic features is thought to involve dopamine 2 receptor binding within the mesolimbic pathway.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, Davie 8 in 2007 and Pérez-Esparza et al 9 in 2017 both describe cases of previously nonpsychotic patients who started cabergoline for a pituitary prolactinoma and developed psychiatric symptoms such as gambling, paranoid delusions, major depression, and auditory hallucinations. 9 The likely mechanism by which cabergoline induces psychotic features is thought to involve dopamine 2 receptor binding within the mesolimbic pathway. Strong evidence suggests that dopamine is involved in the final common pathway responsible for positive symptoms of psychosis.…”

Section: Discussionmentioning

confidence: 99%

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A Case Report of Delusions in a Patient Receiving Cabergoline Therapy for Prolactinoma: Pathophysiology and Proposed Treatment With Aripiprazole

et al. 2023

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Cabergoline is a dopamine 2 receptor agonist used as first-line treatment of pituitary prolactinomas. Here, we describe the case of a 32-yearold woman with a pituitary prolactinoma who was treated with cabergoline for 1 year, during which time she developed delusions. We also discuss the use of aripiprazole to mitigate the psychotic symptoms, while maintaining the efficacy of cabergoline treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

A Case Report of Delusions in a Patient Receiving Cabergoline Therapy for Prolactinoma: Pathophysiology and Proposed Treatment With Aripiprazole

et al. 2023

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“…Clozapine was used in four of the patients presented [ 23 , 27 , 29 , 33 ]. Three of these patients were switched onto clozapine, which had a significant impact on prolactin levels [ 27 , 29 , 33 ].…”

Section: Reviewmentioning

confidence: 99%

The Effect of Antipsychotics on Prolactinoma Growth: A Radiological and Serological Analysis

Durrani,

Vasireddy,

Arshad

et al. 2023

Cureus

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Many antipsychotic (AP) medications work by reducing dopamine levels. As hyperdopaminergia is known to cause psychosis, antipsychotics work to relieve these symptoms by antagonizing dopamine receptors and lowering dopamine levels. Dopamine is also a known negative modulator of the prolactin pathway, which allows for drug agents like dopamine agonists (DAs) to be incredibly effective in managing tumors that secrete excess prolactin (prolactinomas). While the effects of DAs on prolactinoma size and growth have been studied for decades, the effects of APs on prolactinoma size remain to be seen. We hope to investigate the effects of APs on prolactinomas by conducting a thorough PubMed search, including patients with diagnosed prolactinoma on concurrent AP therapy. Our search led to 27 studies with a total of 32 patients. We identified themes regarding seven antipsychotics: risperidone, haloperidol, amisulpride, thioridazine, aripiprazole, olanzapine, and clozapine. Risperidone, haloperidol, amisulpride, and thioridazine caused a significant increase in prolactin in most cases where they were used, and prolactin decreased after their discontinuation. For example, risperidone discontinuation resulted in a decrease in prolactin levels by an average of 66%, while haloperidol, amisulpride, and thioridazine discontinuation lowered prolactin by an average of 82%, 72%, and 89.7%, respectively. However, there were some exceptions in regard to risperidone, haloperidol, and thioridazine, where prolactin levels were not as severely affected. Aripiprazole, olanzapine, and clozapine all had significant reductions in prolactin levels when patients were switched from another antipsychotic, such as risperidone or haloperidol. The average percent decrease in prolactin when switched to aripiprazole was 67.65%, while it was 54.16% and 68% for olanzapine and clozapine, respectively. The effect of individual antipsychotics on prolactinoma size was difficult to ascertain, as imaging was not obtained (or indicated) after every antipsychotic switch, and many patients were taking dopamine agonists concurrently. Therefore, it would be difficult to ascertain which factor affected size more. Also, some patients received surgery or radiotherapy, which completely negated our ability to make any assertions about the effects of certain pharmacological agents. Although it is difficult to ascertain the role that antipsychotic medications play in the formation of prolactinoma, we have found that the cessation of certain antipsychotic medications may lead to a reduction in prolactin levels and possibly the presence of a measurable prolactinoma.

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“…Several reports have described an induction of psychosis by most of the common dopamine agonists such as pergolide and bromocriptine in patients with PD, with dementia being a risk factor ( 24 ). In patients with prolactinomas, several case reports describing behavioral changes from low mood, irritability and verbal aggressiveness up to psychotic and manic symptoms and paranoid delusions have been published ( 25 , 26 , 27 , 28 ). This phenomenon seems to be more frequent in patients with previous personal or familial history of mental illness with DAs triggering the development of the psychiatric illness.…”

Section: The Psychiatrist’s Perspective: Neuropsychiatric Aspects Of mentioning

confidence: 99%

“…As psychosis is being treated with dopamine-receptor blockers (that in patients with prolactinomas may result in elevated serum prolactin, tumor growth or further uncontrolled hyperprolactinemia-related symptoms), clinicians are being confronted with the dilemma of treating patients while having to deal with severe possible side effects. According to the available literature, treatment options contain a discontinuation of the DA and/or adding clozapine for its low effect on prolactin and growth of the prolactinoma ( 26 ). Other approaches suggest administering aripiprazole, as it is a partial dopamine agonist especially at low doses and seems to reduce prolactin levels in patients with and without hyperprolactinemia ( 27 , 29 ) whereas other studies propose quetiapine ( 30 ) or the combination of clozapine and quinagolide ( 31 ).…”

Section: The Psychiatrist’s Perspective: Neuropsychiatric Aspects Of mentioning

confidence: 99%

Neuropsychiatric and metabolic aspects of dopaminergic therapy: perspectives from an endocrinologist and a psychiatrist

Athanasoulia-Kaspar¹,

Popp²,

Stalla³

2018

Endocrine Connections

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The dopaminergic treatment represents the primary treatment in prolactinomas, which are the most common pituitary adenomas and account for about 40% of all pituitary tumours with an annual incidence of six to ten cases per million population. The dopaminergic treatment includes ergot and non-ergot derivatives with high affinity for the dopamine receptors D1 or/and D2. Through the activation of the dopaminergic pathway on pituitary lactotrophs, the dopamine agonists inhibit the prolactin synthesis and secretion, therefore normalizing the prolactin levels and restoring eugonadism, but they also lead to tumour shrinkage. Treatment with dopamine agonists has been associated – apart from the common side effects such as gastrointestinal symptoms, dizziness and hypotension – with neuropsychiatric side effects such as impulse control disorders (e.g. pathological gambling, compulsive shopping, hypersexuality and binge eating) and also with behavioral changes from low mood, irritability and verbal aggressiveness up to psychotic and manic symptoms and paranoid delusions not only in patients with prolactinomas but also in patients with Parkinson’s disease and restless leg syndrome. They usually have de novo onset after initiation of the dopaminergic treatment and have been mainly reported in patients with Parkinson’s disease, who are being treated with higher doses of dopamine agonists. Moreover, dopamine and prolactin seem to play an essential role in the metabolic pathway. Patients with hyperprolactinemia tend to have increased body weight and an altered metabolic profile with hyperinsulinemia and increased prevalence of diabetes mellitus in comparison to healthy individuals and patients with non-functioning pituitary adenomas. Treatment with dopamine agonists in these patients in short-term studies seems to lead to weight loss and amelioration of the metabolic changes. Together these observations provide evidence that dopamine and prolactin have a crucial role both in the regard and metabolic system, findings that merit further investigation in long-term studies.

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Clozapine Treatment for Cabergoline-Induced Psychosis in a Patient With a Giant Prolactinoma

Cited by 12 publications

References 10 publications

A Case Report of Delusions in a Patient Receiving Cabergoline Therapy for Prolactinoma: Pathophysiology and Proposed Treatment With Aripiprazole

A Case Report of Delusions in a Patient Receiving Cabergoline Therapy for Prolactinoma: Pathophysiology and Proposed Treatment With Aripiprazole

The Effect of Antipsychotics on Prolactinoma Growth: A Radiological and Serological Analysis

Neuropsychiatric and metabolic aspects of dopaminergic therapy: perspectives from an endocrinologist and a psychiatrist

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