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As lithium-related acne is often resistant to usual treatments, isotretinoin is frequently prescribed for this particular resistant acne. Several studies showed that BD patients treated with isotretinoin are at risk for clinically significant exacerbation of mood symptoms, including suicidal ideation. This exacerbation could arise in spite of a concurrent use of maintenance psychiatric medicines. Isotretinoin prescription in BD patients InBigby et al[ 28 ] described a BD patient taking lithium who became suicidal after six and a half weeks of isotretinoin treatment.

InCott et al[ 29 ] described a case report of a BD woman taking lithium who developed after 4 wk of isotretinoin treatment, signs of previous psychotic manic symptoms decompensations. The addition of an antipsychotic allowed the complete resolution of the episode. Ina retrospective chart review[ 30 ] of BD patients identified 10 patients treated with isotretinoin.

Nine of the ten patients experienced an exacerbation of mood symptoms: six mixed symptoms, two depressive symptoms and one hypomanic symptom. Three of them developed suicidal ideation.

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Symptoms began from 4 to 20 wk after initiation of therapy and resolved with discontinuation in all but 1 patient. Besides, seven of the nine patients were taking maintenance psychiatric medications for BD at the time of the apparent reaction. Isotretinoin prescription in non BD patients Barak et al[ 31 ] of soldiers with no prior history of psychiatric diagnosis treated with isotretinoin for severe acne reported that five of these patients developed manic psychosis within 8 mo of exposure.

This was accompanied by a suicide attempt for three of them. In three cases, they found a family history of BD in a first degree relative.

Bipolar Disorder Not Otherwise Specified (NOS)

A personal history of obsessive-compulsive disorder OCD was also found for three patients. InFornaro[ 32 ] described a year-old patient who developed OCD following isotretinoin treatment.

An unexpected mood switch was observed 1 mo after the introduction of an antidepressant fluvoxamine. This points out to the possible link between an iatrogenic induced OCD and an increasing risk for bipolar disorder.

Isotretinoin and psychosis Bremner et al[ 2 ] reported cases of hypervitaminosis A associated with psychotic symptoms.

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A few studies in the literature state a possible link between isotretinoin and psychosis[ 1633 ]. The neurobiological hypothesis for schizophrenia and psychotic symptoms is an increase in dopaminergic stimulation or sensitivity in the limbic system[ 34 ].

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In fact, Goodman[ 35 - 37 ] points out a link between site de rencontre bipolaire dysregulation and schizophrenia. He suggested that dysregulation by retinoids may be an important factor in the etiology of this pathology. The evidence of this association is based on three points, according to these studies. First, retinoid dysfunction produces congenital anomalies, the same found in schizophrenic patients. Additionally, schizophrenia and the retinoid cascade have been linked to the same gene loci.

Finally, RA regulates the transcriptional activation of the Dopamine D2 receptor and other schizophrenia candidates as serotonin and glutamate receptors [ 35 - 37 ]. A microarray study of schizophrenia in human brains published by Goodman[ 38 ] reported that two proteins aldehyde dehydrogenase 1A1 and albuminboth important for the transport and function of the vitamin A are altered in these patients.

Thus, RA, the final metabolic product of the retinoid cascade, would be insufficient in schizophrenia. Unavailability of RA impairs transcriptional regulation of retinoid target genes like the Dopamine D2 Receptor, which is a candidate gene in schizophrenia. The expression of dopamine receptors has indeed shown to be regulated by RA[ 3839 ]. So, Citver et al[ 40 ] proposed retinoid analogs as candidates for the treatment of schizophrenia, by altering the downstream expression of dopamine D2 receptors.

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Furthermore, mutations for the acid retinoic receptors demonstrated in mice could reduce expression of D1 and D2 receptors and do impair dopamine signaling[ 3841 ]. Literature studies have demonstrated two opposing views as to the role of isotretinoin from two differing clinical specialties. The psychiatric literature cf Bremner suggests a causal link between isotretinoin and depression.

The dermatological literature suggests that acne is an independent risk factor for depression and isotretinoin could be used to improve depression by treating acne and improving self-image. These differing views could be explained by a recruitment bias. Dermatologists may not have been aware of the occurrence of psychiatric disorders. There is strong evidence from the psychiatric literature that demonstrates an association of isotretinoin to depression, probable clinical exacerbation of bipolar mood disorder and possible links to psychosis.

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It is important that isotretinoin be prescribed only for severe acne, resistant to several course of antibiotics. The patients that may be susceptible to these side effects may not be able to be predicted.

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Close monitoring of these patients for neuropsychiatric side effects seems to be very important during isotretinoin therapy. For example, headache symptoms could constitute an alert symptom. The responsibility of lithium in the occurrence of acne may be established with the highest certainty possible.

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Then, the mental state of the patient has to be evaluated: is its pathology balanced under lithium In this case, it may be risky to stop lithium treatment, although there are many other pharmacological choices today such as anticonvulsants and atypical antipsychotics please find adequate references.

The optimal treatment may be discussed with both professionals and patient in order to choose the best option available. There is also a debate between nephrologists and psychiatrists regarding lithium and renal insufficiency. Plus Comment Choisir la "bonne personne"?

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Forty-eight received ketamine 0. The primary outcome was a reduction in depression severity assessed via the MADRS 24 hours after infusion.

Review of the Literature Ketamine Versus Placebo The objective of a single-setting, randomized, double-blind, crossover study by Zarate et al 17 was to determine whether ketamine can achieve a rapid antidepressant response in 18 subjects with treatment-resistant unipolar depression. Inclusion criteria consisted of men and women aged to years-old who were inpatients with a diagnosis of MDD recurrent without psychotic features and who failed at least 2 previous adequate antidepressant trials. Subjects were required to have a score of 18 or higher on the item Hamilton Depression Rating Scale at screening and before the first administration of either ketamine or placebo, be free of a comorbid substance use disorder for at least 3 months, have a negative urine toxicology screen, and have a 2-week medication free period before the start of the study. Exclusion criteria consisted of a DSM-IV diagnosis of bipolar disorder or a history of antidepressant or substance-induced mania or hypomania. The primary outcome measure was the changes in the Hamilton Depression Rating Scale scores from 60 minutes before infusion to 40, 80,and minutes after infusion.

Forty-seven subjects from the ketamine group and 25 from the midazolam group were included in the modified intention-to-treat analysis. Baseline characteristics were similar between the 2 groups. Subject's scores were studied at 1, 2, 3, and 7 days after infusion to evaluate durability of ketamine's effects.

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The positive effects of ketamine were lost starting around day 3 after infusion. At day 7, the positive effects on depression shown through the MADRS scale no longer showed significant differences between groups.

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Adverse effects lasting up to 4 hours and occurring more frequently in the ketamine group were dizziness, blurred vision, headache, nausea or vomiting, dry mouth, poor coordination, poor concentration, and restlessness. Murrough et al 21 were successful in creating a strong study design that maximized internal and external validity.

Study investigators did so by standardizing infusion and monitoring procedures, using blinding in the study and having an effective control that resulted in similar side effects at the time of and 24 hours after infusion.

Using a nonactive drug placebo would undermine the integrity of the study as ketamine produces behavioral effects that would not be present using nondrug placebo.

Limitations of this trial include not quite reaching power and lacking information on use of ketamine with other antidepressant or antipsychotic medications that may be used to manage MDD. Many patients with MDD may also have other concurrent mental illnesses, and many of these conditions were excluded from the study.

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Another study by Murrough et al 22 assessed cognitive functioning after a single dose of ketamine. This study was similar in sites and design to the previous study.

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The effects of time, treatment condition, and antidepressant response were analyzed using analysis of variance models and logistic regression. There were no changes in working memory or reasoning.

The study of Murrough et al 22 was well designed and had a fairly large sample size for this subject matter and strict inclusion and exclusion criteria.

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Another strength was the use of an active placebo to control for expectation bias. The authors used appropriate statistical analyses; however, they failed to state how many responders compared with nonresponders there were in the treatment group and neglected to take MADRS scores after infusion.

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Discussion Ketamine has shown promise in quickly reducing symptoms in patients with treatment-resistant depression and bipolar depression. Several small clinical trials have shown that a single subanesthetic dose of ketamine, 0. A meta-analysis by Romeo et al 24 analyzed ketamine's efficacy in depression at day 1, day 2, daysday 7, and day 14 compared with placebo in treatment-resistant depression.

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Ketamine demonstrated a statistically significant antidepressant effect compared with placebo from day 1 through day 7. Analyses were repeated to determine if there were any efficacy differences between unipolar and bipolar depression.

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When including only participants with unipolar depression, ketamine's efficacy was not affected from day 1 through day 7. Patients with bipolar depression, however, only saw efficacy through day 4. Ketamine offers many advantages to patients suffering from treatment-resistant depression and bipolar depression.