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So this is my second practically-non-existent period in a row.

 

I've taken two pregnancy tests, and both were negative.  

 

I haven't started lactating yet though (I did this on Invega).  

 

I see my GP next week (sigh) to get a blood test (I'm going to ask them to check for pregnancy and prolactin).

 

I'm assuming my prolactin levels are elevated...though I didn't think that Saphris (25mg) and Latuda (80mg) were particularly bad for this.

 

Anyone?

 

I'll go back on bromocriptine if it is this, though my pdoc said I should find out the reason for the elevated prolactin, which I take to mean, don't automatically blame the meds.  

 

SIGH

 

I've been on Saphris for over a year and a half (I think; I don't think it's been longer...???) and Latuda since February this year.  So neither med is new.  

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From - http://www.drugs.com/pro/latuda.html

Hyperprolactinemia

As with other drugs that antagonize dopamine D2 receptors, Latuda elevates prolactin levels.

Hyperprolactinemia may suppress hypothalamic GnRH, resulting in reduced pituitary gonadotrophin secretion. This, in turn, may inhibit reproductive function by impairing gonadal steroidogenesis in both female and male patients. Galactorrhea, amenorrhea, gynecomastia, and impotence have been reported with prolactin-elevating compounds. Long-standing hyperprolactinemia, when associated with hypogonadism, may lead to decreased bone density in both female and male patients [see Adverse Reactions (6)].

Tissue culture experiments indicate that approximately one-third of human breast cancers are prolactin-dependent in vitro, a factor of potential importance if the prescription of these drugs is considered in a patient with previously detected breast cancer. As is common with compounds which increase prolactin release, an increase in mammary gland neoplasia was observed in a Latuda carcinogenicity study conducted in rats and mice [see Nonclinical Toxicology (13)]. Neither clinical studies nor epidemiologic studies conducted to date have shown an association between chronic administration of this class of drugs and tumorigenesis in humans, but the available evidence is too limited.

Bipolar Depression

Monotherapy

The median change from baseline to endpoint in prolactin levels, in the short-term, flexible-dosed, placebo-controlled monotherapy bipolar depression study, was +1.7 ng/mL and +3.5 ng/mL with Latuda 20 to 60 mg/day and 80 to 120 mg/day, respectively compared to +0.3 ng/mL with placebo-treated patients. The median change from baseline to endpoint for males was +1.5 ng/mL and for females was +3.1 ng/mL. Median changes for prolactin by dose range are shown in Table 13.

Table 13: Median Change in Prolactin (ng/mL) from Baseline in the Monotherapy Bipolar Depression Study

Latuda

Placebo 20 to 60 mg/day 80 to 120 mg/day

Patients were randomized to flexibly dosed Latuda 20 to 60 mg/day, Latuda 80 to 120 mg/day, or placebo

All Patients +0.3

(n=147) +1.7

(n=140) +3.5

(n=144)

Females 0.0

(n=82) +1.8

(n=78) +5.3

(n=88)

Males +0.4

(n=65) +1.2

(n=62) +1.9

(n=56)

The proportion of patients with prolactin elevations ≥ 5x upper limit of normal (ULN) was 0.4% for Latuda-treated patients versus 0.0% for placebo-treated patients. The proportion of female patients with prolactin elevations ≥ 5x ULN was 0.6% for Latuda-treated patients versus 0% for placebo-treated female patients. The proportion of male patients with prolactin elevations ≥ 5x ULN was 0% versus 0% for placebo-treated male patients.

In the uncontrolled, open-label, longer-term bipolar depression study, patients who were treated with Latuda as monotherapy in the short-term and continued in the longer-term study, had a median change in prolactin of -1.15 ng/mL at week 24 (n=130).

Adjunctive Therapy with Lithium or Valproate

The median change from baseline to endpoint in prolactin levels, in the short-term, flexible-dosed, placebo-controlled adjunctive therapy bipolar depression studies was +2.8 ng/mL with Latuda 20 to 120 mg/day compared to 0.0 ng/mL with placebo-treated patients. The median change from baseline to endpoint for males was +2.4 ng/mL and for females was +3.2 ng/mL. Median changes for prolactin across the dose range are shown in Table 14.

Table 14: Median Change in Prolactin (ng/mL) from Baseline in the Adjunctive Therapy Bipolar Depression Studies

Latuda

Placebo 20 to 120 mg/day

Patients were randomized to flexibly dosed Latuda 20 to 120 mg/day or placebo as adjunctive therapy with lithium or valproate.

All Patients 0.0

(n=301) +2.8

(n=321)

Females +0.4

(n=156) +3.2

(n=162)

Males -0.1

(n=145) +2.4

(n=159)

The proportion of patients with prolactin elevations ≥ 5x upper limit of normal (ULN) was 0.0% for Latuda-treated patients versus 0.0% for placebo-treated patients. The proportion of female patients with prolactin elevations ≥ 5x ULN was 0% for Latuda-treated patients versus 0% for placebo-treated female patients. The proportion of male patients with prolactin elevations ≥ 5x ULN was 0% versus 0% for placebo-treated male patients.

In the uncontrolled, open-label, longer-term bipolar depression study, patients who were treated with Latuda, as adjunctive therapy with either lithium or valproate, in the short-term and continued in the longer-term study, had a median change in prolactin of -2.9 ng/mL at week 24 (n=88).

And saphris. From - http://www.drugs.com/pro/saphris.html

Hyperprolactinemia

Like other drugs that antagonize dopamine D2 receptors, Saphris can elevate prolactin levels, and the elevation can persist during chronic administration. Hyperprolactinemia may suppress hypothalamic GnRH, resulting in reduced pituitary gonadotropin secretion. This, in turn, may inhibit reproductive function by impairing gonadal steroidogenesis in both female and male patients. Galactorrhea, amenorrhea, gynecomastia, and impotence have been reported in patients receiving prolactin-elevating compounds. Long-standing hyperprolactinemia when associated with hypogonadism may lead to decreased bone density in both female and male subjects. In Saphris clinical trials, the incidences of adverse events related to abnormal prolactin levels were 0.4% versus 0% for placebo [see Adverse Reactions (6.1)].

Tissue culture experiments indicate that approximately one-third of human breast cancers are prolactin-dependent in vitro, a factor of potential importance if the prescription of these drugs is considered in a patient with previously-detected breast cancer. Neither clinical studies nor epidemiologic studies conducted to date have shown an association between chronic administration of this class of drugs and tumorigenesis in humans, but the available evidence is too limited to be conclusive.

Sorry that's a lot of reading. I hope it helps, and i hope you don't start lactating again! I did on Invega too. Not fun.

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Thanks Cheese.  

 

So it seems like Latuda is the likelier culprit than Saphris.  I guess I just figured compared to Invega/Risperdal, Latuda wasn't bad.  Poop.  I really like my current med cocktail other than Pristiq.  I like Saphris and Latuda, I haven't had any psychosis more or less since February/March.  

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My first clue was my period. But I have itchy nipples and I'm worried if I scratch I'll get milk on my bra (probably not).

I feel like an unnatural woman. I've never been pregnant but this is my second episode of lactating. I go through all these biological urges about kids even though we don't want any (crazy being one, but not the only, reason) and it's like my body is mocking me...hahaha you'll never have a baby but you can lactate! Have part of the experience!

My boobs have betrayed me. All I can say is, I went up a cup size after Invega and I hope I get bigger boobs out of this too, because otherwise this is just scarring for no reason. I hate my body.

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OK, so I have some concerns and questions.

 

I emailed pdoc, and he said to dose Bromocriptine 2.5-7.5mg assuming my prolactin comes back high.  He wants me to exhaust all possible reasons for increased prolactin, which, fine, but even if it is a pituatary tumour (and it's not) - I'd still be put on bromocriptine.

 

Which impacts dopamine.

 

I was on bromocriptine (forget the dosage) when I was on Invega and had elevated prolactin.  It ended with a psychotic episode.  And psychosis or hallucinations can be a side effect of bromocriptine.  My pdoc was of the opinion that it was not the bromocriptine, but rather that the Invega simply stopped working.

 

I don't know.  He's an internationally-regarded psychopharmacologist, so presumably he understands this stuff, and I trust him.

 

But.  I am still really nervous about the bromocriptine.  I have had my best period in terms not being psychotic or having psychotic symptoms since Latuda got added to my Saphris in February.  I don't want to change that.  

 

I found this:

http://www.researchgate.net/publication/40455718_Effect_of_bromocriptine_on_antipsychotic_drug-induced_hyperprolactinemia_eight-week_randomized_single-blind_placebo-controlled_multicenter_study/links/0fcfd50b2db51ea4a4000000 

 

Quoting:

Changes in psychiatric symptomatology and
EPS side-effects
No significant interaction effects between time and
groups were found for the PANSS positive, negative,
general, and total scores, so that only the main effects
of time and group were considered in the final model
(Fig. 2). There were significantly decreasing time
trends for all of the PANSS scores (P < 0.001 from
trend tests), but no group differences were found.
Examination of the Simpson–Angus scale scores
indicated no significant time or group effects.
 
What does that mean?  Time or group effects?  What does that say about psychotic symptoms?  I'm not dumb, but I'm not understanding this.  
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I have an ob/gyn that thinks I have high prolactin due to meds, even though I've been tested, and he wants me on bromocriptine. I did lose a lot of weight, and am underweight - which is why I don't have a period. My pharmacist and I discussed bromocriptine and decided the risk outweighed the benefits for me, especially with hallucinations and such. So I don't take it.

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Yeah, San, I'm really nervous about that.  

 

I used to be on 30 mg Abilify, had EPS, dropped down to 20mg I think, ended up in the hospital for suicidal thoughts - looking back though, it was just bad intrusive thoughts, and now I know the difference - I'm wondering about adding Abilify to my Saphris instead of Latuda.  I THINK - though I haven't decided - that when my prolactin comes back as high I won't go on bromocriptine but wait until I see my pdoc in mid-January to talk to him.  

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Taking two AAPs together can also increase the likelihood of raised prolactin levels, I would imagine. Latuda is known to do this on it's own, too. It's incredibly potent at D2 receptors.

Abilify sounds like a good alternative to Latuda, as it's more of a dopamine stabilizer.

Edited by mjs190
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So it's just the receptionist telling me, I see the doctor on Tuesday...

Apparently my prolactin levels are normal. Despite the barely there periods and oh yeah, the lactation.

How is it possible to lactate with normal prolactin? Damn I really am a freak.

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Let us know how your appointment goes!

 

Normal prolactin levels are good. Very good. I'm not sure what else it could be, but swapping AP's could help. Definitely something to discuss with your treatment team. And have them keep an eye on your prolactin levels as well.

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I blogged about it a few days ago - despite me being on two AAPs now, my pdoc won't prescribe me 2 AAPs in the future, and I've been more stable on this med combination in terms of psychotic symptoms (Saphris 25mg and Latuda 80mg) so I feel completely fucked.  We'll see.  I have no idea what to do about meds.  

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