Posted by Maxime on April 7, 2005, at 16:44:42
In reply to Re: Got Milk? Lactating on Desipramine - SLS?? ED?? » Maxime, posted by ed_uk on April 7, 2005, at 15:35:19
Hi Ed. I appreciate your research. My doctor lowered my Synthroid on my last visit. I see him on Monday. You see he WON'T do the proper test. He just tests my TSH and free T4. I want him to test my Free T3. I also want the test that will show if I have a conversion problem. I still feel like have hypothroid symptoms (which present as psych symptoms) and Synthroid is T4 and need to be converted to T3 for my body to use it. Well some people can't convert it. So it would be better if I was taking something like Cytomel which is T3. He won't prescribe the Cytomel. Synthroid is so much easier to dose.
I can't force him to do these tests. I'm so f*cking frustrated. I think I will have my pdoc call him again or something.
I want to get to the bottom of this but no one will listen. And since so many of the symptoms of hypothyroidism mimic depression, my endo is no doubt assuming that "Ms. Psych Patient" problems are all in her head.
I saw my GP yesterday, and she said my endo had to look after these problems. Her nose is out of joint because last year I started to see an endo because she wasn't managing my thyroid problem. I was taking Dilantin and I told her it made the Synthroid less effective and she didn't believe me. I had read it on www.rxlist.com That's when my TSH went up to 25.
So that's my soap opera. Stay tuned.
xxxxxxx
Maxi> Hi Maxime,
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> >How could Desipramine make me lactate? Does it do anything to prolactin levels?
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> Tricyclic ADs have been known to induce lactation, it is thought that they can occasionally cause hyperprolactinemia in susceptible individuals. You are clearly susceptible to drug-induced hyperprolactinemia. The question is: why are you susceptible? It could be because your hypothyroidism is not being adequately treated.
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> >I am in tears right now....
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> Oh Maxime, please accept a gentle hug from me.
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> ((((Maxime))))
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> >Where do I go from here?
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> I think it would be useful to have your high prolactin investigated further. A prolactinoma is possible but very unlikely.
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> I have read that hypothyroidism can raise prolactin levels, perhaps you could encourage your doc to increase your thyroxine. Hypothyroidism can apparantly cause a condition called pituitary hyperplasia, which is associated excessive prolactin secretion. An adequate dose of thyroxine can treat the pituitary hyperplasia and decrease the prolactin level. Perhaps you would be able to take desipramine without lactating if your thyroxine dose was increased.
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> 'A 21-year-old woman complaining of 8-month amenorrhea associated to weight gain, galactorrhea and frequent headaches, presented for clinical evaluation; her laboratory tests were: TSH: 1192 mUI/ml (0.27-4.2); TT4: 1.0 microg/dl (4.4-11.4 l); TT3: 0.41 ng/ml (0.7-2.1); prolactin: 69.2 ng/ml (3-20) and a diagnosis of myxedema associated to galactorrhea was made. A hypothalamic-pituitary magnetic resonance imaging (MRI) showed a suprasellar and intrasellar mass lesion of 1.9 x 1.4 x 1.9 cm, determining compression and deviation of the optic chiasm. Due to the possibility of hyperplasia of the TSH-producing cells, treatment of hypothyroidism was initiated with levothyroxine. Two months later, upon normalization of thyroid hormones and TSH levels, a second MRI showed an anatomically normal pituitary gland. Regression of the pituitary mass after treatment with levothyroxine confirmed the hypothesis of pituitary hyperplasia secondary to primary hypothyroidism. Our findings support the importance of determining thyroid function tests during the investigation of pituitary masses and thus avoiding an unnecessary surgery.'
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> 'This study investigated the effect of levothyroxine treatment on serum prolactin (PRL) levels in women with subclinical hypothyroidism. Sixty-six women (mean age, 58.5 +/- 1.3 years) with confirmed subclinical hypothyroidism (mean thyrotropin [TSH], 11.7 +/- 0.8 mIU/L) were randomly assigned to receive levothyroxine or placebo for 48 weeks. Based on blinded TSH monitoring, physiologic levothyroxine replacement (85.5 +/- 4.3 microg/d; TSH, 3.1 +/- 0.3 mIU/L) was ascertained throughout the study. PRL levels were measured before and after administration of thyrotropin-releasing hormone (TRH) at baseline, after 24 and 48 weeks. Sixty-three of the 66 women completed the study. At baseline, basal PRL levels were elevated in 19% of the patients. None of the patients reported menstrual disturbances, infertility, or galactorrhea. In the levothyroxine group (n = 31) basal and peak PRL levels were significantly reduced after 24 and 48 weeks (p = 0.03 and p = 0.001). Mean changes in PRL levels differed significantly between the two treatment groups after 24 weeks (p = 0.03 and p = 0.01). The treatment effect was more pronounced in patients with PRL and TSH levels above the median at baseline (i.e., PRL > 16 ng/mL; TSH > 11 mIU/L). Based on this double-blinded, placebo-controlled study we demonstrate that in subclinical hypothyroidism PRL regulation is altered with elevated basal and stimulated PRL levels, and that physiologic levothyroxine treatment restores PRL concentrations.'
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> Some hypothyroid patients with galactorrea (lactation) may need high doses of T4..............
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> Galactorrhea was found in 5 patients with subclinical hypothyroidism. The galactorrhea consisted of the discharge of a few drops of milk only under pressure. Serum T4 was in the lower level of the normal range, but serum T3 was normal (T4: 6.3 +/- 1.2 micrograms/dl, T3: 113 +/- 7 ng/dl). Basal serum TSH and PRL were slightly increased only in 2 and 1 cases, respectively. The PRL (prolactin) responses to TRH stimulation were exaggerated in all cases, although the basal levels were normal. An enlarged pituitary gland was observed in 1 patient by means of CT scanning. All patients were treated by T4 replacement. ***In serial TRH tests during the T4 replacement therapy, the PRL response was still increased even when the TSH response was normalized. Galactorrhea disappeared when the patients were treated with an increased dose of T4 (150-200 micrograms/day).*** Recurrence of galactorrhea was not observed even though replacement dose of T4 was later decreased to 100 micrograms/day in 4 cases. In patients with galactorrhea of unknown origin, subclinical hypothyroidism should NOT be ruled out EVEN WHEN THEIR T4, T3, TSH and PRL are in the normal range. The TRH stimulation test IS NECESSARY to detect an exaggerated PRL response as the cause of the galactorrhea. To differentiate this from pituitary microadenoma, observation of the effects of T4 replacement therapy on galactorrhea is essential.
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> Have you ever had a TRH stimulation test Maxi??????????
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> Administration of thyroid hormones may produce *transient increases* in prolactin..........
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> Following the administration of gradually increasing doses of thyroid hormones, plasma PRL showed paradoxical and transient increases, while plasma TSH decreased steadily. The elevated basal PRL level and the enhanced response to sulpiride turned to be within the normal range when the patients became euthyroid by treatment.'
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> If increasing your thyroxine dose was not effective in normalising your prolactin level, treatment with a dopamine agonist could be helpful. A precise diagnosis is important. A CT or MRI of the pituitary gland might be useful.
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> Bromocriptine, quinagolide and cabergoline are dopamine agonists which are used to lower prolactin, they are used to treat prolactinomas.
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> Pramipexole is a dopamine agonist which is most commonly used to treat Parkinson's disease. It is also used to treat depression, including bipolar depression. It might be effective in reducing your prolactin level. Treatment with pramipexole might also allow you to tolerate desipramine if pramipexole was not an effective treatment for your depression on its own. I would be a bit concerned that pramipexole might induce hypomanic symptoms, it does seem to be useful in bipolar II disorder though.........
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> Pramipexole for bipolar II depression: a placebo-controlled proof of concept study.
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> BACKGROUND: The original serotonergic and noradrenergic hypotheses do not fully account for the neurobiology of depression or mechanism of action of effective antidepressants. Research implicates a potential role of the dopaminergic system in the pathophysiology of bipolar disorder. The current study was undertaken as a proof of the concept that dopamine agonists will be effective in patients with bipolar II depression. METHODS: In a double-blind, placebo-controlled study, 21 patients with DSM-IV bipolar II disorder, depressive phase on therapeutic levels of lithium or valproate were randomly assigned to treatment with pramipexole (n = 10) or placebo (n = 11) for 6 weeks. Primary efficacy was assessed by the Montgomery-Asberg Depression Rating Scale. RESULTS: All subjects except for one in each group completed the study. The analysis of variance for total Montgomery-Asberg Depression Rating Scale scores showed a significant treatment effect. A therapeutic response (>50% decrease in Montgomery-Asberg Depression Rating Scale from baseline) occurred in 60% of patients taking pramipexole and 9% taking placebo (p =.02). One subject on pramipexole and two on placebo developed hypomanic symptoms. CONCLUSIONS: The dopamine agonist pramipexole was found to have significant antidepressant effects in patients with bipolar II depression.
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> I don't know whether pramipexole is available in Canada, I would expect that it is. Other dopamine agonist will be available. Ropinirole is quite similar to pramipexole. It would be great if you could encourage your doc to increase your thyroxine dose.
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> Ed xxxxxxxxxxxxx
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> PS. I know very LITTLE about endocrinology. Everything I have said may be a load of rubbish. I just did a bit of research and came up with this!
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poster:Maxime
thread:481196
URL: http://www.dr-bob.org/babble/20050404/msgs/481273.html