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L J Rodriguez-Rigau

Publications and source records attributed to L J Rodriguez-Rigau.

40 records · Page 3Linked to original sources
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Bioassayable and immunoassayable prolactin responses to thyrotropin-releasing hormone: use of the Nb2 lymphoma cell bioassay.

The peak prolactin response to thyrotropin-releasing hormone (TRH) varies among patients. "Exaggerated" responses have been described and linked to ovulatory dysfunction. Herein we describe our initial observations on bioassayable prolactin (BA-PRL) versus immunoassayable prolactin (RIA-PRL) in women with normal baseline RIA-PRL concentrations but with varying peak RIA-PRL responses to TRH. Twenty-three women of reproductive age with baseline RIA-PRL of =25 ng/mL were administered 500 microg of TRH, and baseline and peak RIA-PRL concentrations were determined. Aliquots of the baseline sample and the sample representing the peak RIA-PRL were used for measuring BA-PRL by means of the Nb2 lymphoma cell bioassay. For each sample, BA/RIA-PRL ratios were determined. Positive correlations were found between peak RIA-PRL and baseline BA/RIA-PRL ratios (P<0.05) and also between baseline and peak BA/RIA-PRL ratios (P<0.001). Negative correlations were found between baseline RIA-PRL and both baseline and peak BA/RIA-PRL ratios (P<0.001 and P<0.05, respectively). We conclude that (1) the lactotroph response to TRH in women with normal RIA-PRL may, in part, be governed by the amount of biologically active prolactin at baseline and (2) the relative proportion of BA-PRL to RIA-PRL produced at baseline is maintained at peak response. Finally, in light of the greater availability of bioactive prolactin in women with exaggerated TRH responses, our findings support the use of bromocriptine in those patients with such responses and ovulatory dysfunction.

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Utilization of commercial laboratory results in management of hyperandrogenism in women.

OBJECTIVE: To compare results from testosterone radioimmunoassay kits commonly used by commercial laboratories as well as their reference ranges and to analyze the scientific literature for ranges of serum testosterone levels in normal women and those with hyperandrogenism. METHODS: We reviewed quality assurance reports of various testosterone ligand challenges from four groups of laboratories and summarized testosterone data from 17 published reports about normal women and 14 studies of hyperandrogenic women. RESULTS: A significant variability was demonstrated between the radioimmunoassay kits at all concentrations (for example, a sample with a mean testosterone level of 96.1 ng/dL was reported by some laboratories as containing 71.8 ng/dL and by others as 123.4 ng/dL). All laboratories provide essentially the same "reference range" (approximately 10 to 90 ng/dL) but do not report how the range was established. The scientific literature clearly shows a significant separation in serum testosterone levels between normal (that is, not hyperandrogenic) and hyperandrogenic women. Most hyperandrogenic women had testosterone levels >50 ng/dL, whereas most normal control subjects had levels <40 ng/dL. Thus, most of these women with hyperandrogenism would have been considered to have normal testosterone levels if the reference ranges of commercial laboratories were used. CONCLUSION: These data illustrate the difficulty that physicians face when they are required to use different commercial laboratories to measure serum testosterone levels. We propose that (1) reference ranges be established on a clinically defined population for each hormone and method used, (2) laboratory reports include information about method and reference range population, and (3) physicians be allowed to choose which laboratories are used for their patients' hormone determinations, for consistency of results.

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Serum testosterone levels and reference ranges in reproductive-age women.

OBJECTIVE: To determine the levels of serum testosterone and dehydroepiandrosterone sulfate (DHEAS) in women with no clinical signs of hyperandrogenism and no history of glucocorticoid or oral contraceptive use and to compare these levels with the reference ranges provided by commercial laboratories. METHODS: We undertook a cross-sectional retrospective study of 271 reproductive-age women encountered at an endocrinology clinic for complaints of potential thyroid problems. Serum testosterone and DHEAS levels were determined, and statistical analyses were performed. RESULTS: The serum testosterone level in women with no acne, hirsutism, or menstrual dysfunction was 14.1 +/- 0.9 ng/dL (mean +/- standard error of the mean) (95% confidence interval [CI] = 12.4 to 15.8). This group was considered our study reference population. In women with menstrual dysfunction but no acne or hirsutism, the mean testosterone level was significantly higher (17.9 +/- 1.1 ng/dL; 95% CI = 15.7 to 20.0; P<0.002); with mild hirsutism, it further increased (38.4 +/- 5.1 ng/dL; 95% CI = 27.4 to 49.4; P<0.005); and with moderate to severe hirsutism, it was still higher (49.0 +/- 2.3 ng/dL; 95% CI = 44.4 to 53.6; P<0.003). Serum DHEAS levels showed similar patterns. The upper limit (mean + 2 standard deviations) of testosterone in our study reference population was 28 ng/dL, a level that provided a sensitivity of 84% for detecting hyperandrogenemia. The detection of hyperandrogenemia is essentially impossible when the upper limit of the reference range for testosterone from commercial laboratories (95 ng/dL) is used. CONCLUSION: The testosterone levels reported herein and in the literature for hyperandrogenic women both are within the reference (normal) ranges provided by commercial laboratories. These observations demonstrate why diagnosis of hyperandrogenemia in hyperandrogenic women is difficult when commercial laboratories are used and why this condition is not detected in most affected women. Commercial laboratories should reevaluate the methods used for establishing their reference ranges for serum testosterone.

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