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Letters to the Editor |
Department of Molecular and Clinical Endocrinology and Oncology "Federico II" University 80131 Napoli, Italy
As a matter of fact, the most relevant problem when evaluating the effectiveness of dopamine-agonist treatment in resistant hyperprolactinemic patients is the correct definition of therapy resistance. On this problem there is no consensus in the literature. In our paper (1), we defined the resistance to dopamine agonists as the absence of serum PRL level normalization, and/or tumor shrinkage after at least 3 months of treatment with bromocriptine at the dose of 15 mg, or quinagolide at the dose of 0.6 mg (2, 3, 4). These doses are considered rather elevated in the treatment of hyperprolactinemia. By contrast, we did not consider the percent PRL suppression achieved during these treatments, as the lack of PRL normalization has a clinical relevance, while the suppression below or above 50% of baseline does not. On the other hand, we agree with DelGrange and Donckier, authors of the letter above, that in most of the patients reported in our study (1) we could more often have a partial, rather than a complete, therapy resistance. Thus, increase in bromocriptine or quinagolide dose could likely allow patients to obtain normoprolactinemia. However, the effectiveness of any treatment is strictly related to tolerability and to patients’ compliance. In our study it was clearly shown that tolerability and compliance were better during cabergoline than during quinagolide or bromocriptine treatments. The efficacy of cabergoline in patients who did not normalize serum PRL levels during quinagolide treatment was rather surprising, taking into consideration that both drugs bind D2 receptor. We tried to explain these results with the evidence that cabergoline binds the receptor significantly longer than quinagolide (5, 6). Unfortunately, not all patients successfully respond to cabergoline treatment. The success rate is rather high in our hyperprolactinemic patients using the widely and currently available drug armamentarium. However, a low but not negligible number of patients (considering that approximately 30–40 new hyperprolactinemics come to our attention every year) still represent a challenge. In fact, in addition to the patients resistant to cabergoline reported in our paper (1), four other patients, presently treated with cabergoline, still have high PRL levels despite receiving doses ranging from 2.5–3 mg a week. This raises the question of the dose and frequency of administrations. In fact, in a few cases we improved the results by parceling out the weekly dose (unpublished data). One hypothesis to explain these effects is that the administration of cabergoline not in the classical schedule of once or twice a week could maintain a more constant suppression of PRL levels in poorly responsive patients.
Although the effectiveness of cabergoline treatment in bromocriptine and quinagolide resistant patients might be overestimated because of better compliance and tolerability, this aspect should not be underestimated because hyperprolactinemic patients have, theoretically, to be treated life-long (7). In this light, and also considering the rapid and notable tumor shrinking effect of cabergoline (unpublished data), the excellent compliance to cabergoline makes this drug the first option in the medical approach to hyperprolactinemia.
Footnotes
c Received May 6, 1997. Address correspondence to: Annamaria Colao, Department of Molecular and Clinical Endocrinology and Oncology, "Federico II" University of Naples, Via S. Pansini 5, Naples, Italy 80131.
References
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