Breastfeeding in the systemic lupus erythematosus patient

Sir,

We read with great interest the previous letter by Francis et al. ‘Breastfeeding in the systemic lupus erythematosus patient’, ¹ concerning one of the most delicate topics regarding autoimmune patients. In fact, systemic lupus erythematosus (SLE) predominantly affects women of childbearing age, therefore it is to be expected that we will face the challenge of managing patients in the pregnancy and postpartum period any time in clinical practice. ² Recognizing the value of debate, we congratulate the authors on this issue and further express our opinion based on recent publications, in order to supplement the knowledge surrounding this sensitive subject.

The benefits of breastfeeding are not debatable. Decisive imprinting events might be modulated during the first months of life with potential long-term health effects for the newborn. ³ On the other hand, the assets might not be so widespread, especially focusing on breastfeeding mothers with SLE. The sexual dimorphic prevalence of autoimmunity represents one of the most alluring observations among the mosaic of autoimmunity, and sex hormones are believed to be a mainstay of this asymmetry. ⁴ The greater prevalence of autoimmunity among fertile women, disease onset/relapses during pregnancy and postpartum are some of the points that support this theory. ⁵ In the past two decades, growing evidence has demonstrated crucial interactions between neurological and endocrine systems, in order to promote immunological homeostasis. Prolactin has a recognized immune-stimulatory effect, mainly inhibiting the negative selection of autoreactive B lymphocytes. The prolactin receptor is a member of the type 1 cytokine/hematopoietic receptor super family and is widely expressed through the immune system, including monocytes, lymphocytes, macrophages, natural killer cells, granulocytes and thymic epithelial cells. The binding of prolactin to its receptor activates downstream signaling pathways that will manipulate immune cell proliferation, differentiation, secretion and survival. In accordance, hyperprolactinemia has been found in several autoimmune diseases, frequently influencing disease development and perpetuation. Exacerbation of SLE during pregnancy and especially during the postpartum period has been well documented. During lactation, plasma levels of prolactin are markedly increased. Suckling stimulates the nerve endings in the nipple–areolar complex and strongly promotes hormone release, with serum values ranging widely from 9 ng/dl to 74 ng/dl, depending on the frequency of feeding. ⁶ Needless to say, recent studies support a significant association between prolactin levels and the clinical and serological activity of the disease.^7,8 In animal models, prolactin was capable of inducing the development of a lupus-like phenotype in non-prone mice and exacerbated the disease in a lupus murine experimental study. ⁹ Likewise, hyperprolactinemia was correlated with neurological, hematological, renal involvement, serositis, low complement, high anti-dsDNA antibodies and lupus anticoagulant in SLE patients.^2,10–13 For instance, treatment with bromocriptine in postpartum patients showed benefits related to the protection against disease flairs and allowed lower steroid and immunosuppressant doses. ¹⁴

Breastfeeding promotion should not be standardized. In light of the above-mentioned body of evidence, SLE patients might benefit from avoiding breastfeeding practices. Certainly, we consider that the advantages and disadvantages have to be carefully evaluated, and the recommendations need to be personalized in accordance with each patient’s condition.