yes, I too have a low fT3, and 16% of CFS/ME patients have a low T3 syndrome in a recent study. High prolactinemia could be linked to low fT3 if TRH is high but pituitary not responsive to it...
And hypopituitarism is one of the hypothesis underlying CFS/ME pathogenesis
The way public health here is, they won't test your T3 and T4 unless your TSH shows abnormal. I went back today to get T3 and T4 specifically tested, but because my TSH was in normal range last time (barely), they only did a T4 test. I don't understand the logic of this, as the T3 value would've been helpful because T4 is useless if it's not converting.
Anyway... my TSH has gone up since last time. Maybe it's because I increased iodine in my diet after the last test. I realized that in the past 2 months of intense supplementation in recovery of my last auto-immune attack, I was not including enough food based iodine in my diet. I started taking a kelp extract with food 3 weeks ago as well as upping my calcium intake in the form of egg shells (can't do dairy, fibrous greens or calcium pills), and now TSH has risen.
TSH 1.53 (0.32-5.04)
T4 13.3 (10.6-19.7)
I don't know if this helps shed any light on the prolactin thing, or anything else.
I'm losing head hair a lot faster now, in the male baldness pattern. I'm assuming this is due to DHEA and/or pregnenolone. It could also be low iron. My hemoglobin is finally rising but it's still below normal. I get another iron IV in a couple weeks. Also hair loss is common after prednisone treatment... once the high cortisol drops the hair falls out. I just want it to stop because it's going to really start affecting my appearance.
Prolactin is as much an immune hormone as it is a reproductive one according to this article.
Prolactin (PRL) has a bioactive function acting as a hormone and a cytokine. It interferes with immune system modulation, mainly inhibiting the negative selection of autoreactive B lymphocytes. Likewise, hyperprolactinemia has been described in relation to the pathogenesis and activity of several autoimmune disorders.
Dopamine is an effective inhibitor of PRL secretion due to either a direct influence on the hypophysis or stimulation of postsynaptic dopamine receptors in the hypothalamus, arousing the release of the PRL inhibitory factor. Hence, dopamine agonists have proven to offer clinical benefits among autoimmune patients and represent a promising therapy to be explored.