Original article
Association between Systemic Lupus Erythematosus, Rheumatoid Arthritis, Hyperprolactinemia and Thyroid Autoantibodies

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Background

Hyperprolactinemia (hyperPRL) has been associated with autoimmune rheumatic disorders and the presence of thyroid autoantibodies (tAb). The interrelation between these variables was the focus of this prospective study.

Methods

The study assessed six groups of individuals: 26 with systemic lupus erythematosus (SLE), 20 with rheumatoid arthritis (RA), 28 with tAb (tAb+), 14 with untreated hyperprolactinemia (hyperPRL), 10 with treated hyperPRL, and a control group (n = 28). Prolactin (PRL), free thyroxin, TSH, antibodies against thyroglobulin (TgAb), thyroid microsomal antigen (MsAb) and/or thyroid peroxidase (TPOAb) were determined in all patients. Those with hyperPRL had macroprolactin investigated by the polyethylene glycol (PEG) precipitation method.

Results

PRL (ng/mL) levels in the SLE, RA, and tAb+ groups were, respectively, 21.3 ± 12.6, 11.5 ± 7.4, and 12.5 ± 8.6, and were significantly greater in the SLE group (p = 0.006) than in the controls (12.5 ± 6.5) and in the other groups. Five patients had hyperPRL: three with SLE, one with RA, and one with tAb+. Macroprolactinemia was detected in three of the untreated hyperprolactinemic patients and in the hyperprolactinemic patient of the tAb+ group. Positivity for any of the tAb was 15% in the SLE, 15% in the RA, 57.1% in the untreated hyperPRL, 10% in the hyperPRL on treatment, and 3.6% in the control group. The presence of antibodies was significantly more frequent in the untreated hyperPRL group than in the control group (p = 0.001).

Conclusions

The results indicate that the PRL level is higher in SLE patients and that in the presence of hyperPRL there is increased prevalence of antithyroid antibodies, evidencing the association of PRL and autoimmunity and pointing to the appropriateness of assessing and monitoring the progress of these markers in patients affected by these disorders.

Introduction

The role of prolactin (PRL) in the interrelation between the endocrine system and the immune system has a biphasic character; while at physiological levels PRL is trophic for the lymphocytes, its insufficiency or hypersecretion is immunosuppressive (1). PRL is produced by several hematopoietic cells and, acting through specific receptors expressed in the immune system cells, exerts a cytokine-like activity. This issue has been treated in several reviews 2, 3, 4, 5.

Autoimmune rheumatic disorders can be accompanied by increased PRL levels. Hyperprolactinemia (hyperPRL) in patients with systemic lupus erythematosus (SLE) was first reported by Lavalle et al. (6) and later described in rheumatoid arthritis (RA) (7).

The 150- to 170-kDa molecular form of PRL, known as big-big-prolactin or macroprolactin and which is associated with low biological activity of PRL, is present in a significant number of patients with hyperPRL (8). Recently, the presence of macroprolactin and antiPRL autoantibodies was reported in patients with SLE 9, 10.

Another situation in which PRL has a potential permissive factor is thyroid autoimmunity, with a greater prevalence of antithyroid antibodies (tAb) having already been observed in patients with hyperPRL (11).

Controversies over the extent of these findings have motivated the investigation of specific populations of patients with autoimmune rheumatic diseases, hyperPRL, and with markers of thyroid autoimmunity.

Section snippets

Patients and Methods

This study included 126 patients of both sexes and >18 years of age who visited the Rheumatology and the Endocrinology Divisions of a University Hospital in South Brazil. The admittance of cases and controls followed the order of medical appointment, after acceptance of participation was obtained. Five groups were used: group I: patients with a diagnosis of SLE by the criteria of the American College of Rheumatology (n = 26; 25 females and 1 male; 35.4 ± 11.7 years (mean ± SD); group II: with a

Results

The distribution of sex and age was similar in all groups. In five patients, all in group III, TSH level was slightly elevated, between 6.4 and 12.2 μUI/mL, in the presence of normal free T4, which, if confirmed, could characterize subclinical hypothyroidism. As all presented normal serum prolactin, between 7 and 10 ng/mL, they were kept in the series. HyperPRL was detected in three patients (12%) with SLE (values between 37.51 and 58 ng/mL), in one with RA (35 ng/mL), and in one with tAb+ (41

Discussion

The prevalence of hyperPRL in patients with SLE in most of the studied series ranges from 13 to 35% 10, 12, 13, 14, 15, 16, 17, 18. Our finding of a PRL level significantly higher in patients with SLE as compared to controls, and of 12% of patients with hyperPRL in this group, is compatible with literature reports.

In a recent study, Leaños-Miranda et al. (10), studying the prevalence of hyperPRL and macroprolactin in 259 patients with SLE, found 16.6% of hyperPRL and a predominance of

Acknowledgments

The authors thank Dra. Júlia Fernanda S. Pereira Lima for critical review of the manuscript.

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