Hyperprolactinaemia and Nonpuerperal Lactation Associated with Clomipramine

Fowlie, Samuel; Burton, Jodie M.

doi:10.1177/003693308703200210

Cited by 12 publications

(6 citation statements)

References 1 publication

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“…Amisulpride is a substituted benzamide derivative, which is not FDA approved in the US but is used in European countries. It has few extrapyramidal symptoms (EPS) but significant prolactin elevation, similar to that of conventional antipsychotics and often clinically relevant (Fric and Laux, 2003). It is hypothesized that amisulpride may have a selectively higher occupancy of D 2 /D 3 receptors at the pituitary level than at the central regions, because of its poor brain barrier permeability (Bressan et al, 2004).…”

Section: Antipsychoticsmentioning

confidence: 99%

Hyperprolactinemia associated with psychotropics—a review

Madhusoodanan¹,

Parida

Jimenez

2010

Human Psychopharmacology

112

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Section: Antipsychoticsmentioning

confidence: 99%

Hyperprolactinemia associated with psychotropics—a review

Madhusoodanan¹,

Parida

Jimenez

2010

Human Psychopharmacology

112

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“…[5] Drugs that increase prolactin output include some antidepressants (clomipramine, fluoxetine), opioids and cocaine (mild elevations), antihypertensives (particularly verapamil, also used in the treatment of anxiety disorders, and a-methyldopa), and antiretroviral drugs. [4,[6][7][8][9][10][11] Psychotropic drugs unlikely to induce hyperprolactinaemia include benzodiazepines, buspirone, lithium and antimanic anticonvulsants including carbamazepine and divalproex sodium. [4,[12][13][14][15][16] Renal failure may also increase elevations of circulating prolactin induced by drugs.…”

Section: Hyperprolactinaemiamentioning

confidence: 99%

Adverse Endocrine and Metabolic Effects of Psychotropic Drugs

et al. 2009

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The article critically reviews selected, clinically significant, adverse endocrine and metabolic effects associated with psychotropic drug treatments, including hyperprolactinaemia, hyponatraemia, diabetes insipidus, hypothyroidism, hyperparathyroidism, sexual dysfunction and virilization, weight loss, weight gain and metabolic syndrome (type 2 diabetes mellitus, dyslipidaemia and hypertension). Such effects are prevalent and complex, but can be managed clinically when recognized. They encourage continued critical assessment of benefits versus risks of psychotropic drugs and underscore the importance of close coordination of psychiatric and general medical care to improve long-term health of psychiatric patients. Options for management of hyperprolactinaemia include lowering doses, switching to agents such as aripiprazole, clozapine or quetiapine, managing associated osteoporosis, carefully considering the use of dopamine receptor agonists and ruling out stress, oral contraceptive use and hypothyroidism as contributing factors. Disorders of water homeostasis may include syndrome of inappropriate antidiuretic hormone (SIADH), managed by water restriction or slow replacement by hypertonic saline along with drug discontinuation. Safe management of diabetes insipidus, commonly associated with lithium, involves switching mood stabilizer and consideration of potassium-sparing diuretics. Clinical hypothyroidism may be a more useful marker than absolute cut-offs of hormone values, and may be associated with quetiapine, antidepressant and lithium use, and managed by thyroxine replacement. Hyper-parathyroidism requires comprehensive medical evaluation for occult tumours. Hypocalcaemia, along with multiple other psychiatric and medical causes, may result in decreased bone density and require evaluation and management. Strategies for reducing sexual dysfunction with psychotropics remain largely unsatisfactory. Finally, management strategies for obesity and metabolic syndrome are reviewed in light of the recent expert guidelines, including risk assessment and treatments, such as monoamine transport inhibitors, anticonvulsants and cannabinoid receptor antagonists, as well as lifestyle changes.

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“…There are several case reports of TCA-emergent hyponatremia or syndrome of inappropriate antidiuretic hormone secretion (SIADH; Adlakha et al, 1991;Liskin et al, 1984;Madhusoodanan and Osnos, 1981;Parker, 1984). There are also case reports of galactorrhea with imipramine (Klein et al, 1964), and clomipramine (Anand, 1985;Fowlie and Burton, 1987), suggesting that an increase in prolactin levels, due to increased serotonergic turnover, may underly such phenomenon (Hanna et al, 1991). Amitriptyline or imipramine however, do not appear to increase prolactin levels (Meltzer et al, 1977;Sonntag et al, 1996;Steiger and Holsboer, 1997).…”

Section: Side-effect Profilementioning

confidence: 99%

Monoaminergic‐based Pharmacotherapy for Depression

Papakostas¹,

Fava²

2005

Biology of Depression

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Although recent advances in neuropharmacology, neuroendocrinology, molecular biology, and pharmacogenetics have been instrumental in bringing about potential treatments for depression which are fundamentally unrelated to their predecessors, including substance P antagonists, glutaminergic agents, and corticotropinreleasing factor (CRF) antagonists, nevertheless it was agents that influenced the function of monoamine receptors and transporters that were discovered initially by serendipity and then developed as treatments for depression. The development of such compounds also served as a framework for the understanding of depression as a medical illness affecting brain functioning. As a result of these efforts, our field has gained further understanding of the role of monoamines in depression. In previous chapters, the relevance of monoamines in the underlying pathophysiology of depression was reviewed. In the following chapter we will focus on describing the contemporary role of monoaminergic agents in the treatment of depression. 6.

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Hyperprolactinaemia and Nonpuerperal Lactation Associated with Clomipramine

Abstract: Clomipramine in therapeutic dose was associated with nonpuerperal lactation and an elevated plasma prolactin. Both features resolved within weeks of discontinuing the drug.

Cited by 12 publications

References 1 publication

Hyperprolactinemia associated with psychotropics—a review

Hyperprolactinemia associated with psychotropics—a review

Adverse Endocrine and Metabolic Effects of Psychotropic Drugs

Monoaminergic‐based Pharmacotherapy for Depression

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