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Introduction: In congenital adrenal hyperplasia (CAH), obesity, hyperinsulinemia and leptin levels are increased., Objective: To identify the frequency of cardiometabolic risk factors (CRF) in children and adolescents with CAH and to explore the relationship with leptin levels., Method: Cross-sectional study of 40 patients who underwent anthropometric measurements and had fasting glucose, insulin, triglycerides, 17-hidroxyprogesterone, leptin, HDL and LDL-cholesterol assessed. The patients were classified according to the number of CRFs, and leptin levels were analyzed with the Kruskal-Wallis test. Pearson's correlation was applied between leptin, body mass index (BMI) z-score and body fat percentage., Results: Fifty percent of the patients had obesity and overweight, 59% had hypertriglyceridemia, 40%, hypoalphalipoproteinemia, 27.5%, high LDL-cholesterol and 22.5% insulin resistance. There was positive correlation between leptin and body fat percentage (r = 0.64), BMI z-score (r = 0.55) and the number of CRFs (r = 0.65). In the obesity-adjusted multivariate analysis, leptin levels were associated with the number of CRFs., Conclusion: CAH had a high frequency of CRFs and leptin appeared to be associated with a more adverse cardiometabolic profile in subjects with obesity and overweight., (Copyright: © 2018 SecretarÍa de Salud.)

Background: Intranasal administration (Int adm) has been well-studied and offers the possibility to deliver larger molecular weight biologics, such as proteins, viral vectors, nanoparticles, and naked plasmids to the brain and treat a variety of diseases in the central nervous system. The predominant challenge in this field is finding efficient vectors that are capable of crossing the blood-brain barrier (BBB)., Objectives: Here, we investigated whether a naked plasmid (pIRES-hrGFP-1a), could cross the BBB, reach brain cells and express green fluorescent protein (GFP) after int-adm and propose it as candidate for future gene therapy studies., Material and Methods: Thirty-six mice were divided into 2 groups. Eighteen animals were assigned to each cluster. Mice from experimental groups received 25 μg of pIRES-hrGFP-1a. The control groups received 25 μl of PBS. Plasmids were given intranasally by applying little drops in both nostrils. Twenty-four hours later, the mice were sacrificed, and their brains were removed. Later, PCR, RT-PCR, and immunohistochemical techniques were performed., Results: pIRES-hrGFP-1a crossed the BBB and was mainly detected in the olfactory nerves (20%) and hypothalamus (16%). In contrast, GFP/18S-expressing mRNAs were detected mostly in the olfactory bulbs (95%), frontal cortex (71%) and amygdala (60%). GFP was detected in the olfactory bulb, hippocampus, frontal cortex and brainstem at 24 h., Conclusions: pIRES-hrGFP-1a could be considered a good candidate for gene therapy studies. In the future could be cloned some therapeutic genes in the pIRES-hrGFP-1a and could transcribe and translates deficient proteins that are required to restore a function., (Copyright © 2018 IMSS. Published by Elsevier Inc. All rights reserved.)

Objective: Patients with central precocious puberty (CPP) may have increased serum leptin levels; however, it is not well known whether this increase differs between patients with and without obesity. Our objectives were to describe the changes in serum leptin in girls with CPP in the first 12 months after diagnosis based on body mass index (BMI) and to explore whether serum leptin level at CPP diagnosis is related to BMI z-score (BMIz) after a 1-year follow-up., Methods: A prospective cohort study was performed. We included 42 girls with idiopathic CPP in Tanner stages II and III. Anthropometric measurements were performed, and serum leptin was measured at study initiation and after 12 months. Patients were stratified according to BMI category (30 with a BMI in the <94th percentile and 12 with a BMI in the >95th percentile). Study variables were compared. Correlations among leptin, BMIz, and body fat were assessed., Results: Leptin increased gradually during the first year of treatment. In girls with a BMI in the <94th percentile at diagnosis, body fat percentage increased gradually during the first year of follow-up., Conclusion: Girls with a BMI in the <94th percentile have a greater risk of weight increase. Leptin level >10.5 ng/dL at diagnosis is a risk factor for weight gain after 1 year., Abbreviations: BMI = body mass index BMIz = BMI z-score CPP = central precocious puberty GnRHa = gonadotropin-releasing hormone analogue.

Background: The aim of this paper is to investigated the contribution of adipose tissue thought the adipokines and kidney failure (KF), Methods: In male rats were fed with a standard lab diet (C) or a hypercaloric diet including 30% sucrose; obese group (Ob) and obese with kidney failure group (Ob/KF). We evaluated the changes of adipokines under conditions of obesity and KF, using 5/6 surgery to induce vascular injury. The anterior and media branches of the left kidney artery were tied together, leaving the posterior branch viable to enable the kidney to function. The right kidney was removed., Results: A 90% survival rate of the animals was achieved due to special care taken. Kidney function progressively decreased after surgery. Compared with the control group, in the other two groups (Ob and Ob/KF) the level of leptin increased and that of adiponectin decreased (p < 0.01). Post-surgery increases were observed in blood pressure, lipids, creatinine and insulin (p < 0.01)., Conclusion: This model is proposed for the study pathophysiological mechanisms that lead to obesity and complications of kidney or cardiovascular function.

Cholesterol is a precursor of steroid hormones and an essential component of the cell membrane; however, altered regulation of the synthesis, absorption and excretion of cholesterol predispose to cardiovascular diseases of atherosclerotic origin. Despite the recognition of historical events for 200 years starting with Chevreul naming "cholesterine"; later on, Lobstein coining the term atherosclerosis and Marchand introducing it, Anichkov identifying cholesterol in atheromatous plaque, and Brown and Goldstein discovering LDL receptor (r-LDL), as well as the emergence of different drugs such as fibrates, statins and cetrapibs during this decade promising to increase HDL, and the most recent, ezetimibe and anti-PCSK9 to inhibit the degradation of r-LDL, morbidity has not been reduced in cardiovascular disease. To date, the controversy continues regarding the best and appropriate medical therapy for hypercholesterolemia; likewise, there is the recommendation of a healthy dietary content regarding the amount of sugar as well as the type of fats, either saturated or polyunsaturated. Together, control of circulating cholesterol, amelioration of hypertension, regulation of diabetes, and dietary recommendations might prevent atherosclerosis., (Copyright © 2016 IMSS. Published by Elsevier Inc. All rights reserved.)

Introduction: The increment of lipocalin 2, also called neutrophil gelatinase-associated lipocalin, plasmatic levels is associated with cardiometabolic and nefrologic alterations. Nonetheless, there is much controversy about lipocalin 2 plasmatic concentrations among healthy individuals., Aim: The aim of this study was to quantify lipocalin 2 in plasma of healthy men and women and to assess a possible correlation with cardiometabolic risk factors., Methods: Fifty-three subjects (24 men and 29 women) were included. By means of an ELISA, a higher concentration of lipocalin 2 was observed in men than in women (91 ± 9 vs. 57 ± 7 ng/ml). Such difference was statistically significant (p < 0.0001)., Results: Lipocalin 2 levels were significantly correlated with body mass index, homeostasis model assessment index-insulin resistance index, triglycerides, high-density lipoprotein, and age., Conclusion: Lipocalin 2 plasmatic concentrations present a gender-specific profile in healthy subjects and its circulating levels appear to be age-dependent and associated with several cardiometabolic risk factors, including the triglycerides/high-density lipoprotein cholesterol ratio, which has proven to be a reliable marker for cardiometabolic risk among the global population.

Cholesterol is a precursor of steroid hormones and an essential component of the cell membrane, however, altered regulation of the synthesis, absorption and excretion of cholesterol predispose to cardiovascular diseases of atherosclerotic origin. Despite, the recognition of historical events for 200 years, starting with Michel Chevreul naming «cholesterol»; later on, Lobstein coining the term atherosclerosis and Marchand introducing it, Anichkov identifying cholesterol in atheromatous plaque, and Brown and Goldstein discovering LDL receptor; as well as the emerging of different drugs, such as fibrates, statins and cetrapibs this decade, promising to increase HDL and the most recent ezetimibe and anti-PCSK9 to inhibit the degradation of LDL receptor, however morbidity has not been reduced in cardiovascular disease., (Copyright © 2016. Published by Masson Doyma México S.A.)

Background: De-regulation of adipocytokines synthesis and secretion appears to be involved in the pathogenesis of different metabolic diseases., Aims: We assessed a possible association between plasmatic levels of lipocalin-2 (LCN2) and type 2 diabetes mellitus (T2DM), as well as among levels of LCN2 and those of adiponectin, ghrelin, leptin and resistin, in Mexican diabetic patients., Subjects and Methods: Fifty-three healthy individuals and fifty-three with long-term T2DM were included. Measurements from all patients for BMI, fasting glucose, insulin, lipids and adipocytokine profiles were obtained., Results: Comparison of data between the corresponding for diabetic subjects and those of healthy individuals showed significant differences in every anthropometric and metabolic parameter analyzed (P < 0.001). In diabetic subjects, lipocalin-2 and ghrelin plasmatic levels were statistically diminished (P < 0.001) in comparison with the levels registered in healthy subjects. In conclusion, in this study we found that LCN2 plasmatic levels are reduced in Mexican subjects with long-term diabetes and this reduction in circulating concentrations is similar to the one reported for anti-inflammatory adipocytokines, which suggests that lipocalin-2 is somehow involved in insulin resistance and cardiometabolic alterations through an uncharacterized mechanism generated by the inflammation process.

The autism spectrum disorder (ASD) was described in 1943 and is defined as a developmental disorder that affects social interaction and communication. It is usually identified in early stages of development from 18 months of age. Currently, autism is considered a neurological disorder with a spectrum covering cases of different degrees, which is associated with genetic factors, not genetic and environmental. Among the genetic factors, various syndromes have been described that are associated with this disorder. Also, the neurobiology of autism has been studied at the genetic, neurophysiological, neurochemical and neuropathological levels. Neuroimaging techniques have shown multiple structural abnormalities in these patients. There have also been changes in the serotonergic, GABAergic, catecholaminergic and cholinergic systems related to this disorder. This paper presents an update of the information presented in the genetic and neuroendocrine aspects of autism spectrum disorder., (Copyright © 2014 Hospital Infantil de México Federico Gómez. Publicado por Masson Doyma México S.A. All rights reserved.)

Anemia represents a global health problem that negatively impacts quality of life in elderly population; however, its impact on the geriatric syndrome of frailty is unclear. We examined the prevalence of anemia among elderly and sought a relationship between hemoglobin and the phenotype of frailty. Baseline hemoglobin quintiles and anemia were assessed in relation to frailty status in a prospective study with 1,933 older community-dwelling adults enrolled in the Study on Aging and Dementia in Mexico (SADEM). Logistic regression was used to model the relationship between frailty and Hb, adjusting for risk factors of frailty, sociodemographic data, cognitive decline, chronic diseases, and some risky habits. Prevalence of frailty was 8.3 %. Frailty risk was highest at the lowest hemoglobin quintile (<14.3 g/dL for men; <13.3 g/dL for women), and 160 (8.3 %) were anemic (<13 g/dL for men; <12 g/dL for women). The relationship between frailty and Hb levels, adjusted for age and sex, observed in the first and fifth quintiles, compared with the fourth quintile, were 1.53 (95 % confidence interval (CI), 1.46-1.60) and 1.05 (95 % CI, 1.01-1.15). After multivariate adjustment, the odds ratios (ORs) were 1.23 (95 % CI, 1.17-1.13) and 1.06 (95 % CI, 1.01-1.11). The association was not diminished by risk factors for frailty (body mass index (BMI), comorbidity, cognitive decline, smoking, alcohol consumption, etc.). In community-dwelling older adults, low hemoglobin concentrations and anemia were independently associated with increased frailty risk. This suggests that mild anemia and low Hb levels are independent, modifiable risk factors for frailty.

We compared and examined factors associated with ghrelin and uric acid in obese subjects (OB), obese plus type 2 diabetes mellitus (OBDM) and healthy controls (C). Methods. We analyzed blood count, renal function, liver enzymes, lipids, resistin, leptin, IL-6, uric acid and ghrelin in OB, OBDM and C. We included 76 subjects with different body mass index (BMI): 36 C (24 ± 3), 11 OB<40 (30-39.9), 20 OB>40 (40-60), and 9 OBDM (45.9 ± 9). Results. Metabolic profile was as follows: HOMA-IR 4.7 ± 3 and 5 ± 3 vs 2 ± 1 (p < 0.01), resistin 8.7 ± 2 and 9.4 ± 2 vs 5.4 ± 2 ng/mL (p < 0.001), leptin 6.2 ± 3.9 and 5.3 ± 2 vs 3.6 ± 1.8 ng/mL (p = 0.001) and IL-6 197.5 ± 78.9 and 223.6 ± 115 vs 7.4 ± 8.3 pg/mL (p = 0.001) in OB and OBDM vs C, respectively. Ghrelin was higher in OB<40 compared to C (1780 ± 197 vs 1465 ± 12 pg/mL, p < 0.05), and lower in OBDM (987.4 ± 114 pg/mL, p < 0.05). BMI showed a positive correlation with resistin (p < 0.001); leptin (p = 0.004), IL-6 (p = 0.001), uric acid (p = 0.0005) and negative with ghrelin (r = -0.431, p = 0.028). Resistin was directly correlated with leptin (p < 0.001) and inversely correlated with renal function (p = 0.03). Conclusion. Severe obesity and obesity-associated diabetes affected ghrelin and uric acid levels. This may well be associated with proinflammatory adipocytokines, insulin resistance, liver enzymes or renal function.

Perturbations in the levels of serotonin expression have a significant impact on behavior and have been implicated in the pathogenesis of several neuropsychiatric disorders including anxiety, mood and appetite. Fetal programming is a risk factor for the development of metabolic diseases during adulthood. Moreover, previous studies have shown that serotonin (5‑HT), dopamine and leptin are important in energy balance. In the present study, the impact of maternal malnutrition‑induced prenatal undernutrition (UN) was investigated in mice and the expression of 5‑HT1A, dopamine (D)1, D2 and Ob‑Rb receptors was analyzed in the hypothalamus during adulthood. The UN group showed a low birth weight compared with the control group. With regard to receptor expression, 5‑HT1A in the UN group was increased in the hypothalamus and D1 was reduced, whereas D2 showed an increase from postnatal day (P)14 in the arcuate nucleus. Ob‑Rb receptor expression was increased in the hypothalamus at P14 and P90. These observations indicated that maternal caloric restriction programs a postnatal body weight gain in offspring with an increased food intake in early postnatal life which continues into adulthood. In addition, UN in mice was found to be affected by Ob‑Rb, 5‑HT1A and D1/2 receptor expression, indicating that these observations may be associated with hyperphagia and obesity.

The hormonal therapy should begin only in order to control the symptoms of the climacteric in women; its use is not recommended to prevent other types of affections associated to the posmenopause, because, despite some other recognizable benefits have been described, many of them have not been demonstrated. Before beginning the treatment of hormonal therapy, it is recommended to analyze the risk factors for heart attack or other cardiovascular diseases, and also estimate risk for osteoporosis and breast cancer. Diverse presentations and ways of administration of the hormonal therapy have been used, with which outcome have been obtained that vary in connection with predominant symptoms. Recently, the introduction of the concept based on the combined use of an estrogen associated to selective estrogen receptor modulator (SERM), the tissue selective estrogen complex (TSEC), allows a better clinical profile for the patient. With this combination it is obtained endometrial protection and positive action about the changes that the menopause produces. The decision to continue the hormonal therapy should be individualized, based on the severity of the symptoms and recurrence, considering the risk-benefit foreseen with the woman in the clinic.

The human cervix is a tissue target of sex steroid hormones as estradiol (E2) which exerts its action through of the estrogen receptors alpha and beta (ER-α and ER-β). In this study we investigated the expression of ER-α and ER-β in human invasive cervical carcinomas using immunohistochemistry and RT-PCR analyses and compared with that observed in the corresponding normal tissue. The results show nuclear expression of ER-α mainly in the first third of normal cervical epithelium, however, decreased or absent expression were present in invasive cervical carcinoma, indicating that expression of ER-α is lost in cervical cancer. Nevertheless, by RT-PCR we were able to demonstrate mRNA expression of ER-α in invasive cervical tissues. These results suggest that loss of ER-α could be due to a mechanism of post-transcriptional and/or post-translational regulation of its gene during the progression to invasive carcinoma. On the other hand, ER-β was expressed in normal cervix with an expression pattern similar to ER-α. In addition to its nuclear localization, cytoplasmic immunoreaction of ER-β was present in the epithelium of invasive cervical carcinomas, suggesting an association between cytoplasmic ER-β expression and invasive phenotype in the cervical tumors. In summary, the results show that the cervical malignant cells tend to loss the ER-α but maintain the ER-β actively expressed. Loss of expression of ER-α in neoplastic tissue suggests that the estrogenic effects could be conducted through the ER-β in human neoplastic cervical tissue. More detailed studies are needed to confirm this suggestion and to determine the role of ER-β in cervical cancer.

There are several reports showing that hyperleptinemia positively correlates with atherogenic process including promotion of platelet aggregation, thrombosis, and production of inflammatory cytokines. Thereby endothelial dysfunction takes place and underlies metabolic and vascular alterations that contribute to the development of both cardiovascular disease and type 2 diabetes. It has been also proposed that endothelial dysfunction may antecede the development of insulin resistance and diabetes. Endothelial cells participate in vasoregulation by the modulation of nitric oxide production and prostaglandin; in addition these cells are major vector in angiogenesis and recruitment of leukocytes and adhesion molecules. Nevertheless mechanisms underlying vascular dysfunction remain to be fully elucidated. This experiment in vitro revealed that the addition of leptin to cultivated endothelial cells elicited a significant molecular expression of both COX 2 and ICAM-1: in addition, the response showed a positive relationship with leptin concentration and the time of incubation. Thus, it may be suggested that leptin acts directly on the endothelium by activating its specific receptor which in turn initiates the molecular response related with the production of factors involved in the inflammatory response. Alterations on prostaglandins and recruiting molecules of adhesion are relevant stages of the endothelial damage.

Background and Aims: DNA vaccination has a great potential to decrease infectious diseases worldwide, such as rabies. Here we showed the effects of a single anti-rabies DNA vaccination applied intranasally (IN) on plasmid survival time, neutralizing antibody (NA) titers, G-protein expression and Th1/Th2-related cytokines., Methods: Only one 50-μg dose of an anti-rabies DNA vaccine was IN administered to 160 Balb/c mice. Twenty mice were used for the neutralizing antibody study, 35 for the proliferation assay, 35 for Th1/Th2-related cytokines, 35 for glycoprotein expression by immunocytochemistry, and 35 for pGQH detection and G-protein mRNA expression., Results: Th1-type related cytokines from spleen cells (IFN-γ, TNF-α, and IL-2) were detected. Rabies NA titers were ≥0.6 IUs from day 30 onward in the IN DNA-vaccinated group. The plasmid was identified in brains and lungs from days 3-15. The mRNA transcript was amplified in brains and lungs from days 3-30, and G-protein expression was observed in spleens, brains and lungs on days 3, 8, and 15. In all cases, a gradual decrease was observed on days 30 and 45 and absent on day 60., Conclusions: We found that Th1-type related cytokines (IL-2, IFN-γ, and TNF-α) were stimulated during the first month after DNA vaccination, correlating with the proliferation assays. Also, it was associated with the plasmid survival time remaining in lungs and brains prior to its degradation., (Copyright © 2011 IMSS. All rights reserved.)

The metalloproteinases (MMP) 11 and 12 have been shown to be expressed in cervical cancer (CC). In order to extend our previous results, these MMPs were evaluated in cervical precursor lesions. One hundred seventeen cervical scrapes: thirty-six normal, thirty-six low grade squamous lesions (LSIL), thirty-six high grade (HSIL), nine CC; and, also ninety-nine paraffin-embedded cervical lesions: fifteen normal cervices, thirty eight LSIL, sixteen HSIL, and five CC were collected. The samples were analyzed for relative expression by real time RT-PCR or immunohistochemistry assay. We were able to identify a relative increased expression of MMP11 in 75% and 78% from LSIL and HSIL samples, respectively. While MMP12 expression was 64% and 75% in LSIL and HSIL, respectively. Positive samples for MMP11 expression were also positive for MMP12 expression and also increased according to illness progression. In the tissues, MMP11 or MMP12 expression was observed in the cytoplasm of the neoplastic cells, while in the normal epithelium was absent. The reaction was always stronger for MMP12 than MMP11. MMP11 expression was present in 77% and 66% of LSIL and HSIL, while MMP12 expression was 73% and 68%. There was a relationship between MMP11 or MMP12 expression and HPV infection. Our data are showing a relationship between diagnostic of precursor lesions and the MMP11 and 12 expressions, suggesting that their expression could be an early event in the neoplastic lesions of the cervix and could have clinical significance.

Background and Aims: Epidemiological associations between an adverse intrauterine environment and the induction of obesity in adult life led to the concept of fetal programming whereby an unfavorable prenatal environment induces adaptations that improve fetal survival or prepare the fetus in expectation of a particular range of postnatal environments. However, these adaptations (predictive adaptive responses) may later prove to be a disadvantage when the pre- and postnatal environments show discrepancies. We investigated the effect of maternal restricted diet on body weight and expression of hypothalamic Ob-Rb of the offspring., Methods: Balb C mice were mated after pregnancy and were randomly assigned to control (C) and undernutrition group (UN) groups. Control group was allowed food ad libitum and UN group had a 50% restriction of food intake during gestation. In the present study we assessed changes in hypothalamic Ob-Rb mRNA by RT-PCR in offspring from C and UN groups., Results: The offspring of UN at birth showed 17% less body weight compared with C, but at 90 days the UN had a greater body weight than C (p<0.01). The UN group also presented an increase in the expression of Ob-Rb at 90 postnatal days (p<0.01)., Conclusions: The results suggest that maternal caloric restriction programs a greater expression of Ob-Rb in the hypothalamus in offspring, as well as a body weight gain that persists into adulthood. In addition, changes in Ob-Rb expression suggest that Ob-Rb mRNA in the hypothalamus is sensitive to fetal undernutrition., (Copyright 2010 IMSS. Published by Elsevier Inc. All rights reserved.)

Background: Hypothyroidism is more frequent in woman and raises with age. It is not clear why do they have greater susceptibility, but it seems to be related with levels of estrogens and hormonal changes., Objective: To evaluate changes in symptoms of women with menopause and hypothyroidism after receiving hypothyroidism therapy and later hormonal therapy., Patients and Methods: Longitudinal, descriptive and comparative study. Two groups were formed: one with 27 patients with hypothyroidism diagnoses and menopause, and the other with 27 menopausal patients matched by age. Appraisal criterion of hormonal therapy efficacy was Greene scale. Levotiroxine was employed as hypothyroidism therapy, at doses required to get euthyroidism in each patient., Results: Basal climacteric symptoms' intensity was higher in patients with menopause and hypothyroidism, which decrease significantly (p < 0.05) after hypothyroidism therapy., Conclusions: Climacteric symptoms are more intense in patients with hypothyroidism, but they fall when euthyroidism is maintained. These changes in thyroid function can be associated to changes in estrogens concentrations, and therefore in direct relation to TRH neurohormone (thyroid releasing hormones).

The frequency of macroprolactinemia related to the presence of anti-PRL autoantibodies in the serum of 209 healthy women at different stages of pregnancy was studied. Measurements were taken of serum PRL concentrations before and after chromatographic separation (gel filtration and affinity with proteins A and G) and extraction of free PRL with polyethylene glycol (PEG). Sera from 8 of the 209 women (3.8%) were found to have a significantly high proportion of precipitated PRL by PEG (macroprolactinemia); in these patients, gel filtration showed that a substantial amount of big big PRL (molecular mass >100 kDa) was present (19.0--78.2% vs. 3.8-4.9%, P = 0.009 in normal pregnant women with a normal proportion of precipitated PRL by PEG). The presence of macroprolactinemia was attributable to anti-PRL autoantibodies in 5 of the 8 women. Comparison of serum levels of direct and free PRL between women with macroprolactinemia related to anti-PRL autoantibodies and women without macroprolactinemia showed significant differences (direct PRL: 270.2 +/- 86.9 vs. 203.4 +/- 69.0 microg/L, P = 0.04; and free PRL: 107.0 +/- 75.9 vs. 173.3 +/- 67.6 microg/L, P = 0.002). On the other hand, there was no difference between women with macroprolactinemia not related to anti-PRL autoantibodies and women with macroprolactinemia caused by anti-PRL autoantibodies, nor was there a difference between women with macroprolactinemia not related to anti-PRL autoantibodies and women without macroprolactinemia. There was a positive correlation between titers of the anti-PRL autoantibody and serum PRL levels (r = 0.82, P = 0.09). The presence of the anti-PRL autoantibody had no relation to the patient's age, stage of gestation, or number of previous pregnancies. We concluded that the frequency of macroprolactinemia was 3.8% among healthy, pregnant women, which was caused by a anti-PRL autoantibodies in 62.5% of the cases. The autoantibodies were found in the bloodstream, forming a PRL-IgG complex, in accordance with the following observations: 1) immunoreactive PRL on gel filtration was eluted in the fractions corresponding to the molecular mass of IgG (150 kDa); 2) a significantly high proportion of immunoreactive PRL was retained on an affinity gel for IgG (proteins A and G); and 3) a significantly high proportion of serum PRL bound to IgG was precipitated by protein A. There was a positive correlation between titers of anti-PRL autoantibodies and serum PRL levels. Serum levels of total PRL were higher, and serum levels of free PRL were lower, in pregnant women with anti-PRL autoantibodies than in pregnant women without macroprolactinemia.