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Laboratory and Clinical Experience in 55 Patients with Macroprolactinemia Identified by a Simple Polyethylene Glycol Precipitation Method

Department of Endocrinology, Medical Center of Postgraduate Education, 01-809 Warsaw, Ceglowska 80, Poland

Address all correspondence to: Wojciech Jeske, M.D., Ph.D., Department of Endocrinology, Medical Center of Postgraduate Education, 01-809 Warsaw, Ceglowska 80, Poland. E-mail: . klinendo{at}cmkp.edu.pl

To the editor:

Referring to the article of Leslie et al. (1), we would like to address a few important issues.

Regarding the polyethylene glycol (PEG) method of large serum proteins’ precipitation as a preliminary step for detection of macroprolactin (BB-PRL), it is worthy to underline the necessity of the parallel assessment of both the total and the free PRL in the identical final dilution (preferable 1:10) prepared in "0" standard diluent. This notice should be taken into account because in cases with predominant BB-PRL, the results of direct measurement of PRL in undiluted serum and the recalculated results of estimation in diluted serum are often discordant (markedly higher are results recalculated, which probably is due to the interference of the endogenous a-PRL-IgG). The advised range of serum dilution has been stipulated to eliminate the possible influence of PEG on immunological reaction (we have tested that the presence in the assay tube of the diluted PEG, i.e. 2.5%, by all means does not influence the result).

Our second remark concerns the clinical implication of macroprolactinemia and confusing reports on the presence or absence of symptoms. To answer the question why the majority but not all of the patients with predominant BB-PRL are asymptomatic or present only scanty symptoms, it would be useful to correlate the clinical data with the amount of residual free PRL present in serum. It is reasonable to expect that two patients with the same total PRL concentration of 140 µg/liter, but in one of them BB-PRL shares 95% and in the other one only 70%, may differ in clinical presentation because in the former the level of residual free PRL is only 7 µg/liter, whereas in the latter it is 35 µg/liter, which is quite sufficient to induce symptoms characteristic for hyperprolactinemia.

Our third remark concerns the rare cases of coassociation of prolactinoma and macroprolactinemia. Leslie et al. (1) disregards his four patients with microadenoma, pointing out that the magnetic resonance imaging or computed tomography evidence of microadenoma in a patient with hyperprolactinemia does not necessarily mean that it is a PRL-secreting adenoma. He is right, but it is possible to evaluate further those cases and see whether the increased PRL secretion is autonomic or not. For this purpose, we can use the sulpiride or metoclopramide stimulation test. Lack of PRL response to one of these compounds is characteristic for the majority of PRL-secreting adenomas, whereas in cases of idiopathic hyperprolactinemia, we get a very marked PRL secretory response. The same applies to patients with macroprolactinemia, because in the majority of them, except those with the magnetic resonance imaging or computed tomography evidence of pituitary adenoma, there was a significant secretory response to the mentioned PRL stimulants (2). We claim therefore that the finding of predominance of macroprolactin in a patient with marked hyperprolactinemia by no means excludes the presence of prolactinoma. Such associations, although rare, were registered by us (2) and were also reported by other authors (3, 4).

Finally, thinking about the possible initiating factors responsible for self production of anti-PRL-IgG, we should carefully search for the drugs or food additives containing sulfhydryl groups. Interestingly, it has been recently suggested that the B-lactam antibiotics may also provide free sulfhydryl groups and therefore contribute in predisposed patients to autoimmune hyperinsulinemia or autoimmune hyperprolactinemia (5). This information however needs to be confirmed by further detailed analysis of the medical records of patients with macroprolactinemia.

Received November 29, 2001.

References

1. Leslie H, Courtney C, Bell P, Hadden DR, McCance DR, Ellis PK, Sheridan B, Atkinson AB 2001 Laboratory and clinical experience in 55 patients with macroprolactinemia identified by a simple polyethylene glycol precipitation method. J Clin Endocrinol Metab 86:2743–2746[Abstract/Free Full Text]
2. Jeske W, Zdunowski P, Bartoszewicz Z, Kondracka A, Gorzelak K, Zgliczynski W, Szczupacka I 2000 Large molecular weight prolactin in patients with hyperprolactinemia. Pol J Endocrinol 51:236–248
3. Hattori N, Ikekubo K, Moridera K, Hino M, Kurahachi H 1994 Correlation of the antibody titers with serum prolactin levels and their clinical course in patients with anti-prolactin autoantibody. Eur J Endocrinol 130:438–445[Abstract/Free Full Text]
4. Cavaco B, Leite V, Santos A, Arranhado E, Sobrinho G 1995 Some forms of big, big prolactin behave as a complex of monomeric prolactin with immunoglobulin G in patients with macroprolactinemia or prolactinoma. J Clin Endocrinol Metab 80:2342–2346[Abstract]
5. Cavaco B, Uchigata Y, Porto T, Amparo-Santos M, Sobrinho L, Leite V 2001 Hypoglycaemia due to insulin autoimmune syndrome: report of two cases with characterisation of HLA alleles and insulin autoantibodies. Eur J Endocrinol 145:311–316[Abstract]

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