Sir George E. Clark Metabolic Unit, Royal Victoria Hospital, Belfast BT12 6BA, United Kingdom
Address correspondence to: A. B. Atkinson, M.D., Sir George E. Clark Metabolic Unit, Royal Victoria Hospital, Grosvenor Road, Belfast BT12 6BA, United Kingdom.
To the editor:
We appreciate the interest of Drs. Jeske, Zgliczynski, and Zdunowski in our study and wish to address the issues they have raised.
First, the method that we used for measuring serum PRL demonstrates linearity on dilution of serum samples containing macroprolactin and on dilution of the supernatant (1:2 to 1:8) after PEG precipitation. Discordance of results, therefore, does not apply to our study.
Second, we agree that while it would be interesting to correlate clinical status with the amount of residual "free" PRL, precipitation of macroprolactin in serum with PEG is neither "specific nor quantitative" (1), and, therefore, it would be inappropriate to use our results for such a purpose. Only results from gel filtration chromatography would allow such a relation to be studied.
Third, as we pointed out, the finding of a pituitary microadenoma in a patient with hyperprolactinemia may or may not be relevant. The natural history of such lesions are unclear, and indeed observation alone may be sufficient while the symptomatic patient may, as we indicated, warrant a trial of dopamine agonist therapy. Further assessment using the sulpiride or metoclopramide stimulation test was beyond the scope of our current study. Our four patients have now been followed for a mean of 3 yr since macroprolactinaemia was first noted, and none have developed either an increasing PRL or signs of optic compression.
Finally, because few of our study patients were on regular medication, initiation of macroprolactinemia by drugs was unlikely to have been of significance in our study population.
Received January 14, 2002.
References
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