LETTERS TO THE EDITORS
Quetiapine in Postpartum Psychosis To the Editors: ostpartum psychosis (PP) is a rare psychiatric disorder with a prevalence of 1 to 2 per 1000 deliveries1 characterized by delusion, hallucinations, bizarre behavior, depression, mania, and mood liability that usually presents within the first 2 weeks postpartum.2 Postpartum psychosis increases the risk for suicide3 and infanticide4; for these reasons, the prevention, early detection, and treatment of the disorder are necessary and important. The onset of PP is rapid.5 The majority of cases begin within 2 weeks, but the symptoms often appear as early as 2 to 3 days after delivery. The early symptoms include insomnia, rapid mood fluctuations, and obsessive concerns regarding the newborn, but the presentation rapidly metamorphoses into a clinical state characterized by delusions of paranoia and grandiosity, hallucinations, disorganized behavior, and catatonic features.5,6 Cognitive changes in the form of confusion, disorientation, and perplexity are quite common.7 Symptoms of manic or mixed episodes are particularly common in early onset cases and usually precede the appearance of psychotic features.8 A few case reports suggest that PP may be treated with lithium or other anticonvulsants and typical antipsychotics.9,10 Little is known about the efficacy of atypical antipsychotics in PP.11 Clozapine has been reported to be effective in 1 case report,11 and olanzapine has been demonstrated to prevent PP and postpartum mood episodes in women with bipolar disorder.12 For the first time, here we present 2 different cases of PP, with different psychopathological presentations, both successfully treated with quetiapine. F.F. was 34 years old at the time of her first pregnancy, suffering from bipolar disorder, type I. The disease was first diagnosed at the age of 27 years, and she was successfully treated and stabilized with valproate (1000 mg/d) and quetiapine (200 mg/d). With the agreement of her psychiatrist, she decided not to take any medication during the pregnancy. The pregnancy went well; in the third trimester, the patient showed light depressive symptoms, which were treated with supportive psychotherapy. Two days after a noncomplicated vaginal delivery, the patient came
P
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back home and started breastfeeding. On the third day, she developed severe insomnia, religious delusions, disorganized speech, and word salad. The symptoms prevented her from taking care of her daughter’s basic needs. Since the clinical situation abruptly worsened after 24 hours, the patient was hospitalized. Quetiapine (up to 300 mg daily) was immediately prescribed. Given the critical conditions, the obstetrician added bromocriptine (5 mg daily) for lactation suppression. Psychotic symptoms progressively disappeared after 7 days, and the patient was discharged after 10 days. Quetiapine (300 mg daily) was continued as prophylactic and maintenance therapy. The patient had a second and a third child, 3 and 5 years after the first birth, respectively. Quetiapine (sustained released tablets 300 mg/d) was administered immediately after the births of her second and third child. Both postpartum periods occurred without any psychiatric complications. A.G. was 37 years old at the time of her first delivery, with a history of fibromyalgia and dysthymia. One week after the delivery, she developed symptoms of postpartum depression with anxiety, insomnia, fatigue, restlessness, and emotional liability. The anxiety worsened after her 1-month-old daughter developed severe infant sleep apnea, requiring immediate hospitalization and resuscitation. Two months after the delivery, the patient consulted her general practitioner (GP), complaining of paranoid delusions, excessive concerns about the baby’s health, and depersonalization. The GP prescribed risperidone (2 mg) and desvenlafaxine (50 mg), with no significant improvement after 2 weeks of treatment. Because infanticide delusions (‘‘an external voice telling her to kill the baby’’) and disorganized behavior appeared, the GP asked the patient to consult a psychiatrist, who immediately hospitalized the patient, stopping the previous therapy and starting quetiapine (up to 300 mg/d). Psychotic symptoms disappeared after 7 to 10 days. The quetiapine regimen was maintained for 3 months and then progressively decreased; escitalopram (10 mg) plus mirtazapine (30 mg) were introduced to treat the residual depression and anxiety symptoms. The literature about the immediate treatment of postpartum psychosis is scant, mostly because of the rarity of this condition and the lack of double-blind studies due to ethical limitations. The only studies available are retrospective studies or case reports. These studies indicate that lithium Journal of Clinical Psychopharmacology
and typical antipsychotics can be a good treatment9,10,13; similarly, sublingual 17-Aestradiol (3Y6 times a day) with a goal to reach the serum level of 400 pmol/L has been reported to be efficacious in a pilot study.14 On the other hand, a few naturalistic and open-label studies have been published, concerning the prevention of PP. In particular, lithium, with or without antidepressants, seems to be effective in preventing PP.15,16 More recently, olanzapine alone or in combination with other drugs seems also to represent a preventive drug for PP.12 On the other hand, 17-A-estradiol17 has no effect on the prevention of PP in women with histories of bipolar or schizoaffective disorder; similarly, valproic acid is no more effective than monitoring without drugs for the prevention of postpartum episodes of bipolar disorder.18 This is the first case report on the use of quetiapine in PP for immediate treatment and prevention. Quetiapine is an atypical antipsychotic medication indicated for the treatment of schizophrenia, short-term manic episodes, and depression associated with bipolar disorders, with 5-HT2A and D2 antagonist properties and low D2 affinities compared with other atypical antipsychotics.19 Remarkably, quetiapine also exerts partial agonist activity at 5-HT1A receptors, and this property, along with its antagonist action at 5-HT2A receptors and >2 adrenoreceptors, is believed to be the neurobiological mechanism accounting for quetiapine’s clinical antidepressant properties.19 For this dual action, along with its unique receptorial affinity, quetiapine may represent a first-choice treatment of PP, a condition characterized by the coexistence of depressive and psychotic symptoms. It has also been hypothesized that sleep loss resulting from the interaction of various putative causal factors may be the final common pathway in the development of PP in susceptible women; consequently, the improvement of insomnia induced by quetiapine could alleviate the symptoms of PP.20 Remarkably, as the first patient suggests, quetiapine may be also used for the prevention of PP in patients experiencing bipolar disorder, a clinical condition with increased risk for PP.1 Even if, for ethical reasons, double-blind, placebo-controlled studies are not allowed in PP, more clinical retrospective studies will be needed to assess the atypical antipsychotic in this lifethreatening psychiatric condition.
&
Volume 34, Number 6, December 2014
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Journal of Clinical Psychopharmacology
&
Volume 34, Number 6, December 2014
AUTHOR DISCLOSURE INFORMATION The present report did not receive any support from pharmaceutical companies. Dr Gobbi has been a speaker for Eli Lilly Canada and Merck Canada and has received grant/honoraria from GlaxoSmithKline, Merck & Co., AstraZeneca.
Gabriella Gobbi, MD, PhD Neurobiological Psychiatry Unit Department of Psychiatry McGill University Montreal, Quebec, Canada [email protected]
REFERENCES 1. Kendell R, Chalmers J, Platz C. Epidemiology of puerperal psychoses. Br J Psychiatry. 1987;150:662Y673. 2. Sit D, Rothschild AJ, Wisner KL. A review of postpartum psychosis. J Womens Health. 2006;15:352Y368. 3. Appleby L, Mortensen PB, Faragher EB. Suicide and other causes of mortality after post-partum psychiatric admission. Br J Psychiatry. 1998;173:209Y211. 4. Spinelli MG. Maternal infanticide associated with mental illness: prevention and promise of saved lives. Am J Psychiatry. 2004;161:1548Y1557. 5. Brockington IF, Hillier VF, Francis AF, et al. Definitions of mania: concordance and prediction of outcome. Am J Psychiatry. 1983;140:435Y439. 6. Dean C, Kendell RE. The symptomatology of puerperal illnesses. Br J Psychiatry. 1981;139:128Y133. 7. Wisner KL, Peindl K, Hanusa BH. Symptomatology of affective and psychotic illnesses related to childbearing. J Affect Disord. 1994;30:77Y87. 8. Protheroe C. Puerperal psychoses: a long-term study 1927Y1961. Br J Psychiatry. 1969;115:9Y30. 9. Doucet S, Jones I, Letourneau N, et al. Interventions for the prevention and treatment of postpartum psychosis: a systematic review. Arch Womens Ment Health. 2011;14:89Y98. 10. Sharma V. Treatment of postpartum psychosis: challenges and opportunities. Curr Drug Saf. 2008;3:76Y81. 11. Kornhuber J, Weller M. Postpartum psychosis and mastitis: a new indication for clozapine? Am J Psychiatry. 1991;148: 1751Y1752. 12. Sharma V, Smith A, Mazmanian D. Olanzapine in the prevention of postpartum psychosis and mood episodes in bipolar disorder. Bipolar Disord. 2006;8:400Y404.
* 2014 Lippincott Williams & Wilkins
13. Targum S, Davenport Y, Webster M. Postpartum mania in bipolar manic-depressive patients withdrawn from lithium carbonate. J Nerv Ment Dis. 1979;167:572Y574. 14. Ahokas A, Aito M, Rimon R. Positive treatment effect of estradiol in postpartum psychosis: a pilot study. J Clin Psychiatry. 2000;61:166Y169. 15. Austin MP. Puerperal affective psychosis: is there a case for lithium prophylaxis? Br J Psychiatry. 1992;161:692Y694. 16. Cohen LS, Sichel DA, Robertson LM, et al. Postpartum prophylaxis for women with bipolar disorder. Am J Psychiatry. 1995;152:1641Y1645. 17. Kumar C, McIvor RJ, Davies T, et al. Estrogen administration does not reduce the rate of recurrence of affective psychosis after childbirth. J Clin Psychiatry. 2003;64:112Y118. 18. Wisner KL, Hanusa BH, Piendl KS, et al. Prevention of postpartum episodes in women with bipolar disorder. Biol Psychiatry. 2004;56:592Y596. 19. Comai S, Tau M, Pavlovic Z, et al. The psychopharmacology of aggressive behavior: a translational approach: part 2: clinical studies using atypical antipsychotics, anticonvulsants, and lithium. J Clin Psychopharmacol. 2012;32:237Y260. 20. Sharma V, Mazmanian D. Sleep loss and postpartum psychosis. Bipolar Disord. 2003;5:98Y105.
Impact of Lithium Treatment on FGF-23 Serum Concentrations in Depressive Patients To the Editor: epression is a multifaceted disorder with diverse causes and has been associated with the risk to develop severe medical disorders.1 Indeed, depression increases the risk of cardiovascular disease by 1.5-fold to 2-fold, of stroke by 1.8-fold, of Alzheimer disease by 2.1-fold, of diabetes by 60%, and of cancer by 1.3-fold to 1.8fold.1 Fibroblast growth factors (FGFs) are best known for their regulatory roles in cell growth, differentiation, and morphogenesis in early stages of neural development and have been discussed as switch genes, biomarkers, and treatment targets for affective disorders recently.2,3 However, at least FGF23 has also been proposed as a cardiovascular risk marker,4 a central player of disordered mineral metabolism,5 and acts to
D
Letters to the Editors
decrease phosphate, 1,25-dihydroxyvitamin D, and parathyroid hormone levels.5 A close, bidirectional relationship exists between depression and cardiovascular disease.1 Indeed, major depression is associated with an increased risk of coronary artery disease, myocardial infarction, congestive heart failure, and isolated systolic hypertension leading to increased mortality and morbidity in patients.1 Moreover, a strong relationship has been described between severe coronary and aortic calcifications, intima thickness, osteoporosis, and depressive disorders.1 Fibroblast growth factor 23 lowers serum levels of 1,25(OH)2D3, which in turn up-regulates renal and intestinal phosphate and calcium transport.6Y9 In mice, it was shown recently that lithium treatment up-regulates FGF-23 formation, an effect paralleled by substantial decrease of serum 1,25(OH)2D3 and phosphate concentrations.10 The present study explores the effect of lithium treatment on serum FGF-23, 1,25(OH)2D3, calcium, and phosphate concentrations in depressed patients. A total of 95 acute depressive patients (age 48 T 14 years) were recruited for this study. Inclusion criteria consist of unipolar depression, age older than 18 years, indication for antidepressant pharmacotherapy, insufficient response to an adequate antidepressant pretreatment and clinical indication for lithium augmentation, hamilton depression rating score greater than 12, and written informed consent. Diagnosis was confirmed on the basis of the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders. Fibroblast growth factor 23 serum concentrations were measured first in medicated patients before lithium augmentation and then after 4 weeks of medication with lithium. Detailed clinical data of the patients have already been published.11 All patients reached a lithium serum level of more than 0.4 mmol/L. Serum FGF-23 concentrations were measured by enzyme-linked immunosorbent assay (Immutopics International, California; AVP EIA kit, Phoenix Europe, Karlsruhe, Germany). enzyme-linked immunosorbent assay kits were employed to determine serum concentrations of 1,25(OH)2D3 (IDS, Boldon, United Kingdom). Data are provided as mean T SEM; n represents the number of independent experiments. All data were tested for significance using unpaired Student t test. Only results with P G 0.05 were considered statistically significant. As illustrated in Figure 1, lithium treatment was followed by a marked increase of serum FGF-23 concentration. As shown in Figure 1, lithium treatment significantly decreased serum 1,25(OH)2D3 www.psychopharmacology.com
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
745
Quetiapine in Postpartum Psychosis To the Editors: ostpartum psychosis (PP) is a rare psychiatric disorder with a prevalence of 1 to 2 per 1000 deliveries1 characterized by delusion, hallucinations, bizarre behavior, depression, mania, and mood liability that usually presents within the first 2 weeks postpartum.2 Postpartum psychosis increases the risk for suicide3 and infanticide4; for these reasons, the prevention, early detection, and treatment of the disorder are necessary and important. The onset of PP is rapid.5 The majority of cases begin within 2 weeks, but the symptoms often appear as early as 2 to 3 days after delivery. The early symptoms include insomnia, rapid mood fluctuations, and obsessive concerns regarding the newborn, but the presentation rapidly metamorphoses into a clinical state characterized by delusions of paranoia and grandiosity, hallucinations, disorganized behavior, and catatonic features.5,6 Cognitive changes in the form of confusion, disorientation, and perplexity are quite common.7 Symptoms of manic or mixed episodes are particularly common in early onset cases and usually precede the appearance of psychotic features.8 A few case reports suggest that PP may be treated with lithium or other anticonvulsants and typical antipsychotics.9,10 Little is known about the efficacy of atypical antipsychotics in PP.11 Clozapine has been reported to be effective in 1 case report,11 and olanzapine has been demonstrated to prevent PP and postpartum mood episodes in women with bipolar disorder.12 For the first time, here we present 2 different cases of PP, with different psychopathological presentations, both successfully treated with quetiapine. F.F. was 34 years old at the time of her first pregnancy, suffering from bipolar disorder, type I. The disease was first diagnosed at the age of 27 years, and she was successfully treated and stabilized with valproate (1000 mg/d) and quetiapine (200 mg/d). With the agreement of her psychiatrist, she decided not to take any medication during the pregnancy. The pregnancy went well; in the third trimester, the patient showed light depressive symptoms, which were treated with supportive psychotherapy. Two days after a noncomplicated vaginal delivery, the patient came
P
744
www.psychopharmacology.com
back home and started breastfeeding. On the third day, she developed severe insomnia, religious delusions, disorganized speech, and word salad. The symptoms prevented her from taking care of her daughter’s basic needs. Since the clinical situation abruptly worsened after 24 hours, the patient was hospitalized. Quetiapine (up to 300 mg daily) was immediately prescribed. Given the critical conditions, the obstetrician added bromocriptine (5 mg daily) for lactation suppression. Psychotic symptoms progressively disappeared after 7 days, and the patient was discharged after 10 days. Quetiapine (300 mg daily) was continued as prophylactic and maintenance therapy. The patient had a second and a third child, 3 and 5 years after the first birth, respectively. Quetiapine (sustained released tablets 300 mg/d) was administered immediately after the births of her second and third child. Both postpartum periods occurred without any psychiatric complications. A.G. was 37 years old at the time of her first delivery, with a history of fibromyalgia and dysthymia. One week after the delivery, she developed symptoms of postpartum depression with anxiety, insomnia, fatigue, restlessness, and emotional liability. The anxiety worsened after her 1-month-old daughter developed severe infant sleep apnea, requiring immediate hospitalization and resuscitation. Two months after the delivery, the patient consulted her general practitioner (GP), complaining of paranoid delusions, excessive concerns about the baby’s health, and depersonalization. The GP prescribed risperidone (2 mg) and desvenlafaxine (50 mg), with no significant improvement after 2 weeks of treatment. Because infanticide delusions (‘‘an external voice telling her to kill the baby’’) and disorganized behavior appeared, the GP asked the patient to consult a psychiatrist, who immediately hospitalized the patient, stopping the previous therapy and starting quetiapine (up to 300 mg/d). Psychotic symptoms disappeared after 7 to 10 days. The quetiapine regimen was maintained for 3 months and then progressively decreased; escitalopram (10 mg) plus mirtazapine (30 mg) were introduced to treat the residual depression and anxiety symptoms. The literature about the immediate treatment of postpartum psychosis is scant, mostly because of the rarity of this condition and the lack of double-blind studies due to ethical limitations. The only studies available are retrospective studies or case reports. These studies indicate that lithium Journal of Clinical Psychopharmacology
and typical antipsychotics can be a good treatment9,10,13; similarly, sublingual 17-Aestradiol (3Y6 times a day) with a goal to reach the serum level of 400 pmol/L has been reported to be efficacious in a pilot study.14 On the other hand, a few naturalistic and open-label studies have been published, concerning the prevention of PP. In particular, lithium, with or without antidepressants, seems to be effective in preventing PP.15,16 More recently, olanzapine alone or in combination with other drugs seems also to represent a preventive drug for PP.12 On the other hand, 17-A-estradiol17 has no effect on the prevention of PP in women with histories of bipolar or schizoaffective disorder; similarly, valproic acid is no more effective than monitoring without drugs for the prevention of postpartum episodes of bipolar disorder.18 This is the first case report on the use of quetiapine in PP for immediate treatment and prevention. Quetiapine is an atypical antipsychotic medication indicated for the treatment of schizophrenia, short-term manic episodes, and depression associated with bipolar disorders, with 5-HT2A and D2 antagonist properties and low D2 affinities compared with other atypical antipsychotics.19 Remarkably, quetiapine also exerts partial agonist activity at 5-HT1A receptors, and this property, along with its antagonist action at 5-HT2A receptors and >2 adrenoreceptors, is believed to be the neurobiological mechanism accounting for quetiapine’s clinical antidepressant properties.19 For this dual action, along with its unique receptorial affinity, quetiapine may represent a first-choice treatment of PP, a condition characterized by the coexistence of depressive and psychotic symptoms. It has also been hypothesized that sleep loss resulting from the interaction of various putative causal factors may be the final common pathway in the development of PP in susceptible women; consequently, the improvement of insomnia induced by quetiapine could alleviate the symptoms of PP.20 Remarkably, as the first patient suggests, quetiapine may be also used for the prevention of PP in patients experiencing bipolar disorder, a clinical condition with increased risk for PP.1 Even if, for ethical reasons, double-blind, placebo-controlled studies are not allowed in PP, more clinical retrospective studies will be needed to assess the atypical antipsychotic in this lifethreatening psychiatric condition.
&
Volume 34, Number 6, December 2014
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Journal of Clinical Psychopharmacology
&
Volume 34, Number 6, December 2014
AUTHOR DISCLOSURE INFORMATION The present report did not receive any support from pharmaceutical companies. Dr Gobbi has been a speaker for Eli Lilly Canada and Merck Canada and has received grant/honoraria from GlaxoSmithKline, Merck & Co., AstraZeneca.
Gabriella Gobbi, MD, PhD Neurobiological Psychiatry Unit Department of Psychiatry McGill University Montreal, Quebec, Canada [email protected]
REFERENCES 1. Kendell R, Chalmers J, Platz C. Epidemiology of puerperal psychoses. Br J Psychiatry. 1987;150:662Y673. 2. Sit D, Rothschild AJ, Wisner KL. A review of postpartum psychosis. J Womens Health. 2006;15:352Y368. 3. Appleby L, Mortensen PB, Faragher EB. Suicide and other causes of mortality after post-partum psychiatric admission. Br J Psychiatry. 1998;173:209Y211. 4. Spinelli MG. Maternal infanticide associated with mental illness: prevention and promise of saved lives. Am J Psychiatry. 2004;161:1548Y1557. 5. Brockington IF, Hillier VF, Francis AF, et al. Definitions of mania: concordance and prediction of outcome. Am J Psychiatry. 1983;140:435Y439. 6. Dean C, Kendell RE. The symptomatology of puerperal illnesses. Br J Psychiatry. 1981;139:128Y133. 7. Wisner KL, Peindl K, Hanusa BH. Symptomatology of affective and psychotic illnesses related to childbearing. J Affect Disord. 1994;30:77Y87. 8. Protheroe C. Puerperal psychoses: a long-term study 1927Y1961. Br J Psychiatry. 1969;115:9Y30. 9. Doucet S, Jones I, Letourneau N, et al. Interventions for the prevention and treatment of postpartum psychosis: a systematic review. Arch Womens Ment Health. 2011;14:89Y98. 10. Sharma V. Treatment of postpartum psychosis: challenges and opportunities. Curr Drug Saf. 2008;3:76Y81. 11. Kornhuber J, Weller M. Postpartum psychosis and mastitis: a new indication for clozapine? Am J Psychiatry. 1991;148: 1751Y1752. 12. Sharma V, Smith A, Mazmanian D. Olanzapine in the prevention of postpartum psychosis and mood episodes in bipolar disorder. Bipolar Disord. 2006;8:400Y404.
* 2014 Lippincott Williams & Wilkins
13. Targum S, Davenport Y, Webster M. Postpartum mania in bipolar manic-depressive patients withdrawn from lithium carbonate. J Nerv Ment Dis. 1979;167:572Y574. 14. Ahokas A, Aito M, Rimon R. Positive treatment effect of estradiol in postpartum psychosis: a pilot study. J Clin Psychiatry. 2000;61:166Y169. 15. Austin MP. Puerperal affective psychosis: is there a case for lithium prophylaxis? Br J Psychiatry. 1992;161:692Y694. 16. Cohen LS, Sichel DA, Robertson LM, et al. Postpartum prophylaxis for women with bipolar disorder. Am J Psychiatry. 1995;152:1641Y1645. 17. Kumar C, McIvor RJ, Davies T, et al. Estrogen administration does not reduce the rate of recurrence of affective psychosis after childbirth. J Clin Psychiatry. 2003;64:112Y118. 18. Wisner KL, Hanusa BH, Piendl KS, et al. Prevention of postpartum episodes in women with bipolar disorder. Biol Psychiatry. 2004;56:592Y596. 19. Comai S, Tau M, Pavlovic Z, et al. The psychopharmacology of aggressive behavior: a translational approach: part 2: clinical studies using atypical antipsychotics, anticonvulsants, and lithium. J Clin Psychopharmacol. 2012;32:237Y260. 20. Sharma V, Mazmanian D. Sleep loss and postpartum psychosis. Bipolar Disord. 2003;5:98Y105.
Impact of Lithium Treatment on FGF-23 Serum Concentrations in Depressive Patients To the Editor: epression is a multifaceted disorder with diverse causes and has been associated with the risk to develop severe medical disorders.1 Indeed, depression increases the risk of cardiovascular disease by 1.5-fold to 2-fold, of stroke by 1.8-fold, of Alzheimer disease by 2.1-fold, of diabetes by 60%, and of cancer by 1.3-fold to 1.8fold.1 Fibroblast growth factors (FGFs) are best known for their regulatory roles in cell growth, differentiation, and morphogenesis in early stages of neural development and have been discussed as switch genes, biomarkers, and treatment targets for affective disorders recently.2,3 However, at least FGF23 has also been proposed as a cardiovascular risk marker,4 a central player of disordered mineral metabolism,5 and acts to
D
Letters to the Editors
decrease phosphate, 1,25-dihydroxyvitamin D, and parathyroid hormone levels.5 A close, bidirectional relationship exists between depression and cardiovascular disease.1 Indeed, major depression is associated with an increased risk of coronary artery disease, myocardial infarction, congestive heart failure, and isolated systolic hypertension leading to increased mortality and morbidity in patients.1 Moreover, a strong relationship has been described between severe coronary and aortic calcifications, intima thickness, osteoporosis, and depressive disorders.1 Fibroblast growth factor 23 lowers serum levels of 1,25(OH)2D3, which in turn up-regulates renal and intestinal phosphate and calcium transport.6Y9 In mice, it was shown recently that lithium treatment up-regulates FGF-23 formation, an effect paralleled by substantial decrease of serum 1,25(OH)2D3 and phosphate concentrations.10 The present study explores the effect of lithium treatment on serum FGF-23, 1,25(OH)2D3, calcium, and phosphate concentrations in depressed patients. A total of 95 acute depressive patients (age 48 T 14 years) were recruited for this study. Inclusion criteria consist of unipolar depression, age older than 18 years, indication for antidepressant pharmacotherapy, insufficient response to an adequate antidepressant pretreatment and clinical indication for lithium augmentation, hamilton depression rating score greater than 12, and written informed consent. Diagnosis was confirmed on the basis of the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders. Fibroblast growth factor 23 serum concentrations were measured first in medicated patients before lithium augmentation and then after 4 weeks of medication with lithium. Detailed clinical data of the patients have already been published.11 All patients reached a lithium serum level of more than 0.4 mmol/L. Serum FGF-23 concentrations were measured by enzyme-linked immunosorbent assay (Immutopics International, California; AVP EIA kit, Phoenix Europe, Karlsruhe, Germany). enzyme-linked immunosorbent assay kits were employed to determine serum concentrations of 1,25(OH)2D3 (IDS, Boldon, United Kingdom). Data are provided as mean T SEM; n represents the number of independent experiments. All data were tested for significance using unpaired Student t test. Only results with P G 0.05 were considered statistically significant. As illustrated in Figure 1, lithium treatment was followed by a marked increase of serum FGF-23 concentration. As shown in Figure 1, lithium treatment significantly decreased serum 1,25(OH)2D3 www.psychopharmacology.com
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
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