Original Article Annals of Clinical Biochemistry 2015, Vol. 52(1) 61–66 ! The Author(s) 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0004563214547779 acb.sagepub.com
Reference ranges for serum total and monomeric prolactin for the current generation Abbott Architect assay SJ Whitehead1, MP Cornes1, C Ford1 and R Gama1,2
Abstract Background: Exclusion of macroprolactinaemia, a well-recognised interference, as the cause of hyperprolactinaemia is essential to avoid potential misdiagnosis and mismanagement of patients. We have derived gender-specific serum total and post-polyethylene glycol (PEG) precipitation monomeric reference ranges for the recently re-standardised Abbott Architect prolactin assay. Methods: Prolactin was measured in serum samples obtained from males (n ¼ 49) and females (n ¼ 52) using the current Abbott Architect immunoassay pre- and post-PEG precipitation. Gender-specific reference ranges were derived for total and monomeric (post-PEG) prolactin. Routine patients’ samples (n ¼ 175) with a serum total prolactin >700 mIU/L were screened for macroprolactinaemia to assess classification compared with our previous post-PEG precipitation percentage recovery-based approach. Results: Reference ranges for serum total prolactin were 58–419 mIU/L (male) and 63–561 mIU/L (female). Male and female monomeric prolactin reference ranges were 32–309 mIU/L and 39–422 mIU/L, respectively. Mean (SD) post-PEG percentage recovery of the IS 84/500 prolactin standard was 80 (2.3)%. Of 175 patients’ samples screened for macroprolactinaemia, 149 had monomeric prolactin concentrations (median monomeric prolactin ¼ 1035 mIU/L; median recovery ¼ 83%) above the gender-specific reference range. Monomeric prolactin concentrations (median monomeric prolactin ¼ 162 mIU/L; median recovery ¼ 20%) in the remaining 26 were within the reference ranges. One patient classified as macroprolactin positive and another classified as macroprolactin negative would not have been identified as such using the previous recovery-based approach. Conclusions: The use of post-PEG monomeric reference ranges not only identifies hyperprolactinaemia due solely to macroprolactinaemia but has the added advantage of identifying patients who have simultaneous true monomeric hyperprolactinaemia and elevated concentrations of macroprolactin.
Keywords Prolactin, macroprolactinaemia, monomeric prolactin, reference interval, immunoassay interference, Abbott Architect Accepted: 28th July 2014
1
Introduction Hyperprolactinaemia may manifest clinically with symptoms of hypogonadotrophic hypogonadism, infertility and galactorrhoea. The diagnosis is dependent upon the laboratory demonstration of hyperprolactinaemia in the appropriate clinical setting.
Department of Clinical Chemistry, New Cross Hospital, Wolverhampton, West Midlands, UK 2 Research Institute in Healthcare Sciences, Wolverhampton University, Wolverhampton, West Midlands, UK Corresponding author: SJ Whitehead, Department of Clinical Chemistry, New Cross Hospital, Wednesfield Road, Wolverhampton WV10 0QP, UK. Email: [email protected]
Downloaded from acb.sagepub.com at MCMASTER UNIV LIBRARY on December 18, 2014
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Prolactin is known to exist in a number of different molecular forms in the circulation.1–6 Monomeric prolactin (Mr ¼ 23 kDa) is the biologically active and most abundant form (typically 60–90%)5 found in healthy individuals and patients with true hyperprolactinaemia. However, prolactin may also be present in the serum in varying quantities as big-prolactin (typically 15–30%;5 Mr ¼ 60 kDa) and macroprolactin (typically 0–10%;5 a prolactin-IgG complex of Mr ¼ 150 kDa) which are thought to be biologically inactive. Despite its biological inactivity, macroprolactin remains immunoreactive and is detected to varying degrees by different immunoassay platforms.5–11 Depending upon the assay used, it has been reported that up to 26% of hyperprolactinaemia cases are due to macroprolactinaemia.5,6 Failure to identify macroprolactinaemia may lead to misdiagnosis and unnecessary intervention.6,11–16 Thus, when serum prolactin is raised, it is recommended that laboratories screen for macroprolactinaemia in order to differentiate between those patients with elevated concentrations of bioactive monomeric prolactin (true hyperprolactinaemia) and those whose hyperprolactinaemia is due to the presence of macroprolactin.12,13,17 Gel filtration chromatography (GFC), the gold standard for the measurement of serum monomeric prolactin,5 is slow, costly and labour intensive and therefore impractical for routine clinical use. While polyethylene glycol (PEG) precipitation4,18–21 is the method most commonly used in UK laboratories to screen for macroprolactinaemia (UK NEQAS [Edinburgh] for Prolactin scheme Survey of Practice 2012), it has limitations. Co-precipitation of monomeric prolactin can lead to significant under recovery of up to 25%.19,22 Furthermore, PEG itself is known to cause interference in some prolactin methods.22–25 Prior to changing analytical platforms, our laboratory screened samples with total serum prolactin >700 mIU/L for macroprolactinaemia on the basis of percentage recovery post-PEG precipitation as is the current conventional approach. A recovery of >60% was considered to indicate genuine hyperprolactinaemia and that significant macroprolactinaemia was not present, a recovery of 40–60% (classed as equivocal) indicated that macroprolactinaemia may be present (sample referred for GFC) and a recovery of 700 mIU/L were screened for macroprolactinaemia (median total prolactin ¼ 1434 mIU/L; interquartile range [IQR] ¼ 872–1617 mIU/L). The median postPEG monomeric prolactin concentration was 913 mIU/L (IQR ¼ 527–1036 mIU/L), and the median
Results
Table 2. Gender-specific reference ranges for serum total and monomeric post-PEG precipitation prolactin for the re-standardised Abbott Architect prolactin assay.
Both total and post-PEG prolactin results for the male sample population (Tables 1 and 2) were normally distributed, as confirmed by a one-sample Kolmogorov–Smirnov (KS) normality test (KS distance ¼ 0.1147 and P > 0.1 for both datasets). In contrast, the female total and post-PEG prolactin data distributions appeared positively skewed and nonGaussian (Tables 1 and 2), as confirmed by a KS normality test; KS distances of 0.1434 (P ¼ 0.0093) and 0.1616 (P ¼ 0.0017) for pre- and post-PEG datasets, respectively. All datasets were subsequently log transformed prior to reference range derivation (including males for consistency) and confirmed to be normally distributed (KS distances ¼ 0.06–0.08; P > 0.1). The 95% reference ranges (2.5th–97.5th percentiles) for serum total prolactin (pre-PEG) were 58–419 mIU/L and 63–561 mIU/L for males and females, respectively (Table 2). Male and female post-PEG monomeric prolactin reference ranges were 32–309 mIU/L and 39–422 mIU/L, respectively (Table 2). The observed differences between the male and female sample populations in the post-PEG percentage recoveries were not significant as determined using a Mann–Whitney test (P ¼ 0.1003).
Total prolactin (mIU/L) Post-PEG prolactin (mIU/L)
Male Female Male Female
Reference range
Manufacturer’s reference range
58–419 63–561 32–309 39–422
73–407 109–557 – –
Table 3. Comparison of macroprolactinaemia screening methods: percentage recovery versus monomeric post-PEG reference ranges.
>60% recovery 40–60% recovery 60% (Table 3).
Discussion Screening hyperprolactinaemic samples for macroprolactinaemia, a well-recognised cause of interference in prolactin assays, is important to prevent potential misdiagnosis and mismanagement of patients. Calculation of the percentage recovery post-PEG precipitation is the current conventional approach,18 with a >60% recovery indicating genuine hyperprolactinaemia, 40–60% recovery indicating that macroprolactinaemia may be present (i.e. an equivocal result requiring further investigation by GFC) and a 700 mIU/L are screened
Downloaded from acb.sagepub.com at MCMASTER UNIV LIBRARY on December 18, 2014
Whitehead et al.
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for macroprolactinaemia because values lower than this are thought less likely to be clinically significant. In conclusion, the use of post-PEG precipitation monomeric prolactin reference ranges not only simplifies result reporting and interpretation for the requesting clinician but also avoids potential misdiagnosis and mismanagement. Furthermore, the change in method has also provided a small cost saving by reducing the number of samples referred for GFC analysis. Acknowledgements The authors would like to thank the staff of Southend University Hospital Biochemistry Department for advice and donation of samples.
Declaration of conflicting interests None declared.
Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
Ethical approval Not needed.
Guarantor RG.
Contributorship SJW, MC and CF conceived the study. MC and SJW researched the literature, designed the studies, processed and analysed the data, and wrote the first draft. All authors reviewed and edited the manuscript, and approved the final version of the manuscript.
References 1. Suh HK and Frantz AG. Size heterogeneity of human prolactin in plasma and pituitary extracts. J Clin Endocrinol Metab 1974; 39: 928–935. 2. Fraser IS, Lun ZG, Zhou JP, et al. Detailed assessment of big big prolactin in women with hyperprolactinemia and normal ovarian function. J Clin Endocrinol Metab 1989; 69: 585–592. 3. Leite V, Cosby H, Sobrinho LG, et al. Characterization of big, big prolactin in patients with hyperprolactinaemia. Clin Endocrinol (Oxf) 1992; 37: 365–372. 4. Fahie-Wilson MN and Soule SG. Macroprolactinaemia: contribution to hyperprolactinaemia in a district general hospital and evaluation of a screening test based on precipitation with polyethylene glycol. Ann Clin Biochem 1997; 34: 252–258.
5. Fahie-Wilson MN, John R and Ellis AR. Macroprolactin; high molecular mass forms of circulating prolactin. Ann Clin Biochem 2005; 42: 175–192. 6. Gibney J, Smith TP and McKenna TJ. Clinical relevance of macroprolactin. Clin Endocrinol 2005; 62: 633–643. 7. Smith TP, Suliman AW, et al. Gross variability in the detection of big big prolactin (macroprolactin) by commercial immunoassays. J Clin Endocrinol Metab 2002; 87: 5410–5415. 8. John R, McDowell IFW, et al. Macroprolactin reactivities in prolactin assays: an issue for clinical laboratories and equipment manufacturers. Clin Chem 2000; 46: 884–885. 9. Schneider W, Marcovitz S, Al-Shammari S, et al. Reactivity of macroprolactin in common automated immunoassays. Clin Biochem 2001; 34: 469–473. 10. Cavaco B, Prazeres S, Santos MA, et al. Hyperprolactinemia due to big big prolactin is differently detected by commercially available immunoassays. J Endocrinol Invest 1999; 22: 203–208. 11. Fahie-Wilson MN. Detection of macroprolactin causing hyperprolactinemia in commercial assays for prolactin. Clin Chem 2000; 46: 2022–2023. 12. Suliman AM, Smith TP, et al. Frequent misdiagnosis and mismanagement of hyperprolactinaemic patients before the introduction of macroprolactin screening: application of a new strict definition of macroprolactinemia. Clin Chem 2003; 49: 1504–1509. 13. Fahie-Wilson M. In hyperprolactinaemia, testing for macroprolactin is essential. Clin Chem 2003; 49: 1434–1436. 14. Olukoga AO, Dornan TL and Kane JW. Three cases of macroprolactinaemia. J R Soc Med 1999; 92: 342–344. 15. Heaney AP, Laing I, Walton L, et al. Misleading hyperprolactinaemia in pregnancy. Lancet 1999; 353: 720. 16. Guay AT, Sabharwal P, et al. Delayed diagnosis of psychological erectile dysfunction because of the presence of macroprolactinemia. J Clin Endocrinol Metab 1996; 81: 2512–2514. 17. Jassam NF, Paterson A, et al. Macroprolactin on the Advia Centaur: experience with 409 patients over a three-year period. Ann Clin Biochem 2009; 46: 501–504. 18. Fahie-Wilson MN. Polyethylene glycol precipitation as a screening method for macroprolactinaemia. Clin Chem 1999; 45: 436–439. 19. Kavanagh L, McKenna TJ, Fahie-Wilson M, et al. Specificity and clinical utility of methods for the detection of macroprolactin. Clin Chem 2006; 52: 1366–1372. 20. Olukoga AO and Kane JW. Macroprolactinaemia: validation and application of the polyethylene glycol precipitation test and clinical characterization of the condition. Clin Endocrinol (Oxf) 1999; 51: 119–126. 21. Vieira JG, Tachibana TT, et al. Extensive experience and validation of polyethylene glycol precipitation as a screening method for macroprolactinemia. Clin Chem 1998; 44: 1758–1759. 22. Beltran L, Fahie-Wilson FN, McKenna TJ, et al. Serum total prolactin and monomeric prolactin reference intervals determined by precipitation with polyethylene
Downloaded from acb.sagepub.com at MCMASTER UNIV LIBRARY on December 18, 2014
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Annals of Clinical Biochemistry 52(1)
glycol: evaluation and validation on common immunoassay platforms. Clin Chem 2008; 54: 1673–1681. 23. Fahie-Wilson MN and Dearman G. The Beckman access prolactin assay and macroprolactin; prevalence and detection of hyperprolactinaemia due to macroprolactin. Clin Chem 2005; 51 Suppl: A231. 24. Sale JK and Fahie-Wilson MN. Macroprolactin and the DPC Immulite 2000 prolactin assay: characteristics of the reaction and detection by precipitation with polyethylene glycol [abstract from national meeting proceedings]. London: Association of Clinical Biochemists, 2002, p.78. 25. Craddock HS, Fahie-Wilson M and Heys AD. Macroprolactin detection by ultrafiltration screening
with the Abbott AxSYM assay [abstract from national meeting proceedings]. London: Association of Clinical Biochemists, 2000, p.148. 26. Smith TP and Fahie-Wilson FN. Reporting of post-PEG prolactin concentrations: time to change. Clin Chem 2008; 56: 484–490. 27. ARCHITECT prolactin assay (LN 7K76) kit insert. Abbott Ireland Diagnostics Division, Longford, Ireland. January 2010, Ref: 48-9177/R2. 28. ARCHITECT prolactin assay (LN 7K76) product information. Abbott Ireland Diagnostics Division, Longford, Ireland. January 2013, Ref: PI29JAN2013.
Downloaded from acb.sagepub.com at MCMASTER UNIV LIBRARY on December 18, 2014
Reference ranges for serum total and monomeric prolactin for the current generation Abbott Architect assay SJ Whitehead1, MP Cornes1, C Ford1 and R Gama1,2
Abstract Background: Exclusion of macroprolactinaemia, a well-recognised interference, as the cause of hyperprolactinaemia is essential to avoid potential misdiagnosis and mismanagement of patients. We have derived gender-specific serum total and post-polyethylene glycol (PEG) precipitation monomeric reference ranges for the recently re-standardised Abbott Architect prolactin assay. Methods: Prolactin was measured in serum samples obtained from males (n ¼ 49) and females (n ¼ 52) using the current Abbott Architect immunoassay pre- and post-PEG precipitation. Gender-specific reference ranges were derived for total and monomeric (post-PEG) prolactin. Routine patients’ samples (n ¼ 175) with a serum total prolactin >700 mIU/L were screened for macroprolactinaemia to assess classification compared with our previous post-PEG precipitation percentage recovery-based approach. Results: Reference ranges for serum total prolactin were 58–419 mIU/L (male) and 63–561 mIU/L (female). Male and female monomeric prolactin reference ranges were 32–309 mIU/L and 39–422 mIU/L, respectively. Mean (SD) post-PEG percentage recovery of the IS 84/500 prolactin standard was 80 (2.3)%. Of 175 patients’ samples screened for macroprolactinaemia, 149 had monomeric prolactin concentrations (median monomeric prolactin ¼ 1035 mIU/L; median recovery ¼ 83%) above the gender-specific reference range. Monomeric prolactin concentrations (median monomeric prolactin ¼ 162 mIU/L; median recovery ¼ 20%) in the remaining 26 were within the reference ranges. One patient classified as macroprolactin positive and another classified as macroprolactin negative would not have been identified as such using the previous recovery-based approach. Conclusions: The use of post-PEG monomeric reference ranges not only identifies hyperprolactinaemia due solely to macroprolactinaemia but has the added advantage of identifying patients who have simultaneous true monomeric hyperprolactinaemia and elevated concentrations of macroprolactin.
Keywords Prolactin, macroprolactinaemia, monomeric prolactin, reference interval, immunoassay interference, Abbott Architect Accepted: 28th July 2014
1
Introduction Hyperprolactinaemia may manifest clinically with symptoms of hypogonadotrophic hypogonadism, infertility and galactorrhoea. The diagnosis is dependent upon the laboratory demonstration of hyperprolactinaemia in the appropriate clinical setting.
Department of Clinical Chemistry, New Cross Hospital, Wolverhampton, West Midlands, UK 2 Research Institute in Healthcare Sciences, Wolverhampton University, Wolverhampton, West Midlands, UK Corresponding author: SJ Whitehead, Department of Clinical Chemistry, New Cross Hospital, Wednesfield Road, Wolverhampton WV10 0QP, UK. Email: [email protected]
Downloaded from acb.sagepub.com at MCMASTER UNIV LIBRARY on December 18, 2014
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Annals of Clinical Biochemistry 52(1)
Prolactin is known to exist in a number of different molecular forms in the circulation.1–6 Monomeric prolactin (Mr ¼ 23 kDa) is the biologically active and most abundant form (typically 60–90%)5 found in healthy individuals and patients with true hyperprolactinaemia. However, prolactin may also be present in the serum in varying quantities as big-prolactin (typically 15–30%;5 Mr ¼ 60 kDa) and macroprolactin (typically 0–10%;5 a prolactin-IgG complex of Mr ¼ 150 kDa) which are thought to be biologically inactive. Despite its biological inactivity, macroprolactin remains immunoreactive and is detected to varying degrees by different immunoassay platforms.5–11 Depending upon the assay used, it has been reported that up to 26% of hyperprolactinaemia cases are due to macroprolactinaemia.5,6 Failure to identify macroprolactinaemia may lead to misdiagnosis and unnecessary intervention.6,11–16 Thus, when serum prolactin is raised, it is recommended that laboratories screen for macroprolactinaemia in order to differentiate between those patients with elevated concentrations of bioactive monomeric prolactin (true hyperprolactinaemia) and those whose hyperprolactinaemia is due to the presence of macroprolactin.12,13,17 Gel filtration chromatography (GFC), the gold standard for the measurement of serum monomeric prolactin,5 is slow, costly and labour intensive and therefore impractical for routine clinical use. While polyethylene glycol (PEG) precipitation4,18–21 is the method most commonly used in UK laboratories to screen for macroprolactinaemia (UK NEQAS [Edinburgh] for Prolactin scheme Survey of Practice 2012), it has limitations. Co-precipitation of monomeric prolactin can lead to significant under recovery of up to 25%.19,22 Furthermore, PEG itself is known to cause interference in some prolactin methods.22–25 Prior to changing analytical platforms, our laboratory screened samples with total serum prolactin >700 mIU/L for macroprolactinaemia on the basis of percentage recovery post-PEG precipitation as is the current conventional approach. A recovery of >60% was considered to indicate genuine hyperprolactinaemia and that significant macroprolactinaemia was not present, a recovery of 40–60% (classed as equivocal) indicated that macroprolactinaemia may be present (sample referred for GFC) and a recovery of 700 mIU/L were screened for macroprolactinaemia (median total prolactin ¼ 1434 mIU/L; interquartile range [IQR] ¼ 872–1617 mIU/L). The median postPEG monomeric prolactin concentration was 913 mIU/L (IQR ¼ 527–1036 mIU/L), and the median
Results
Table 2. Gender-specific reference ranges for serum total and monomeric post-PEG precipitation prolactin for the re-standardised Abbott Architect prolactin assay.
Both total and post-PEG prolactin results for the male sample population (Tables 1 and 2) were normally distributed, as confirmed by a one-sample Kolmogorov–Smirnov (KS) normality test (KS distance ¼ 0.1147 and P > 0.1 for both datasets). In contrast, the female total and post-PEG prolactin data distributions appeared positively skewed and nonGaussian (Tables 1 and 2), as confirmed by a KS normality test; KS distances of 0.1434 (P ¼ 0.0093) and 0.1616 (P ¼ 0.0017) for pre- and post-PEG datasets, respectively. All datasets were subsequently log transformed prior to reference range derivation (including males for consistency) and confirmed to be normally distributed (KS distances ¼ 0.06–0.08; P > 0.1). The 95% reference ranges (2.5th–97.5th percentiles) for serum total prolactin (pre-PEG) were 58–419 mIU/L and 63–561 mIU/L for males and females, respectively (Table 2). Male and female post-PEG monomeric prolactin reference ranges were 32–309 mIU/L and 39–422 mIU/L, respectively (Table 2). The observed differences between the male and female sample populations in the post-PEG percentage recoveries were not significant as determined using a Mann–Whitney test (P ¼ 0.1003).
Total prolactin (mIU/L) Post-PEG prolactin (mIU/L)
Male Female Male Female
Reference range
Manufacturer’s reference range
58–419 63–561 32–309 39–422
73–407 109–557 – –
Table 3. Comparison of macroprolactinaemia screening methods: percentage recovery versus monomeric post-PEG reference ranges.
>60% recovery 40–60% recovery 60% (Table 3).
Discussion Screening hyperprolactinaemic samples for macroprolactinaemia, a well-recognised cause of interference in prolactin assays, is important to prevent potential misdiagnosis and mismanagement of patients. Calculation of the percentage recovery post-PEG precipitation is the current conventional approach,18 with a >60% recovery indicating genuine hyperprolactinaemia, 40–60% recovery indicating that macroprolactinaemia may be present (i.e. an equivocal result requiring further investigation by GFC) and a 700 mIU/L are screened
Downloaded from acb.sagepub.com at MCMASTER UNIV LIBRARY on December 18, 2014
Whitehead et al.
65
for macroprolactinaemia because values lower than this are thought less likely to be clinically significant. In conclusion, the use of post-PEG precipitation monomeric prolactin reference ranges not only simplifies result reporting and interpretation for the requesting clinician but also avoids potential misdiagnosis and mismanagement. Furthermore, the change in method has also provided a small cost saving by reducing the number of samples referred for GFC analysis. Acknowledgements The authors would like to thank the staff of Southend University Hospital Biochemistry Department for advice and donation of samples.
Declaration of conflicting interests None declared.
Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
Ethical approval Not needed.
Guarantor RG.
Contributorship SJW, MC and CF conceived the study. MC and SJW researched the literature, designed the studies, processed and analysed the data, and wrote the first draft. All authors reviewed and edited the manuscript, and approved the final version of the manuscript.
References 1. Suh HK and Frantz AG. Size heterogeneity of human prolactin in plasma and pituitary extracts. J Clin Endocrinol Metab 1974; 39: 928–935. 2. Fraser IS, Lun ZG, Zhou JP, et al. Detailed assessment of big big prolactin in women with hyperprolactinemia and normal ovarian function. J Clin Endocrinol Metab 1989; 69: 585–592. 3. Leite V, Cosby H, Sobrinho LG, et al. Characterization of big, big prolactin in patients with hyperprolactinaemia. Clin Endocrinol (Oxf) 1992; 37: 365–372. 4. Fahie-Wilson MN and Soule SG. Macroprolactinaemia: contribution to hyperprolactinaemia in a district general hospital and evaluation of a screening test based on precipitation with polyethylene glycol. Ann Clin Biochem 1997; 34: 252–258.
5. Fahie-Wilson MN, John R and Ellis AR. Macroprolactin; high molecular mass forms of circulating prolactin. Ann Clin Biochem 2005; 42: 175–192. 6. Gibney J, Smith TP and McKenna TJ. Clinical relevance of macroprolactin. Clin Endocrinol 2005; 62: 633–643. 7. Smith TP, Suliman AW, et al. Gross variability in the detection of big big prolactin (macroprolactin) by commercial immunoassays. J Clin Endocrinol Metab 2002; 87: 5410–5415. 8. John R, McDowell IFW, et al. Macroprolactin reactivities in prolactin assays: an issue for clinical laboratories and equipment manufacturers. Clin Chem 2000; 46: 884–885. 9. Schneider W, Marcovitz S, Al-Shammari S, et al. Reactivity of macroprolactin in common automated immunoassays. Clin Biochem 2001; 34: 469–473. 10. Cavaco B, Prazeres S, Santos MA, et al. Hyperprolactinemia due to big big prolactin is differently detected by commercially available immunoassays. J Endocrinol Invest 1999; 22: 203–208. 11. Fahie-Wilson MN. Detection of macroprolactin causing hyperprolactinemia in commercial assays for prolactin. Clin Chem 2000; 46: 2022–2023. 12. Suliman AM, Smith TP, et al. Frequent misdiagnosis and mismanagement of hyperprolactinaemic patients before the introduction of macroprolactin screening: application of a new strict definition of macroprolactinemia. Clin Chem 2003; 49: 1504–1509. 13. Fahie-Wilson M. In hyperprolactinaemia, testing for macroprolactin is essential. Clin Chem 2003; 49: 1434–1436. 14. Olukoga AO, Dornan TL and Kane JW. Three cases of macroprolactinaemia. J R Soc Med 1999; 92: 342–344. 15. Heaney AP, Laing I, Walton L, et al. Misleading hyperprolactinaemia in pregnancy. Lancet 1999; 353: 720. 16. Guay AT, Sabharwal P, et al. Delayed diagnosis of psychological erectile dysfunction because of the presence of macroprolactinemia. J Clin Endocrinol Metab 1996; 81: 2512–2514. 17. Jassam NF, Paterson A, et al. Macroprolactin on the Advia Centaur: experience with 409 patients over a three-year period. Ann Clin Biochem 2009; 46: 501–504. 18. Fahie-Wilson MN. Polyethylene glycol precipitation as a screening method for macroprolactinaemia. Clin Chem 1999; 45: 436–439. 19. Kavanagh L, McKenna TJ, Fahie-Wilson M, et al. Specificity and clinical utility of methods for the detection of macroprolactin. Clin Chem 2006; 52: 1366–1372. 20. Olukoga AO and Kane JW. Macroprolactinaemia: validation and application of the polyethylene glycol precipitation test and clinical characterization of the condition. Clin Endocrinol (Oxf) 1999; 51: 119–126. 21. Vieira JG, Tachibana TT, et al. Extensive experience and validation of polyethylene glycol precipitation as a screening method for macroprolactinemia. Clin Chem 1998; 44: 1758–1759. 22. Beltran L, Fahie-Wilson FN, McKenna TJ, et al. Serum total prolactin and monomeric prolactin reference intervals determined by precipitation with polyethylene
Downloaded from acb.sagepub.com at MCMASTER UNIV LIBRARY on December 18, 2014
66
Annals of Clinical Biochemistry 52(1)
glycol: evaluation and validation on common immunoassay platforms. Clin Chem 2008; 54: 1673–1681. 23. Fahie-Wilson MN and Dearman G. The Beckman access prolactin assay and macroprolactin; prevalence and detection of hyperprolactinaemia due to macroprolactin. Clin Chem 2005; 51 Suppl: A231. 24. Sale JK and Fahie-Wilson MN. Macroprolactin and the DPC Immulite 2000 prolactin assay: characteristics of the reaction and detection by precipitation with polyethylene glycol [abstract from national meeting proceedings]. London: Association of Clinical Biochemists, 2002, p.78. 25. Craddock HS, Fahie-Wilson M and Heys AD. Macroprolactin detection by ultrafiltration screening
with the Abbott AxSYM assay [abstract from national meeting proceedings]. London: Association of Clinical Biochemists, 2000, p.148. 26. Smith TP and Fahie-Wilson FN. Reporting of post-PEG prolactin concentrations: time to change. Clin Chem 2008; 56: 484–490. 27. ARCHITECT prolactin assay (LN 7K76) kit insert. Abbott Ireland Diagnostics Division, Longford, Ireland. January 2010, Ref: 48-9177/R2. 28. ARCHITECT prolactin assay (LN 7K76) product information. Abbott Ireland Diagnostics Division, Longford, Ireland. January 2013, Ref: PI29JAN2013.
Downloaded from acb.sagepub.com at MCMASTER UNIV LIBRARY on December 18, 2014
