Showing papers on "Prolactin published in 1998"
TL;DR: It is shown that a new peptide, which shares no sequence similarity with known peptides and proteins, as an endogenous ligand is a potent prolactin-releasing factor for rat anterior pituitary cells and is named this peptide prolactIn-re releasing peptide.
Abstract: Hypothalamic peptide hormones regulate the secretion of most of the anterior pituitary hormones, that is, growth hormone, follicle-stimulating hormone, luteinizing hormone, thyroid-stimulating hormone and adrenocorticotropin. These peptides do not regulate the secretion of prolactin, at least in a specific manner, however. The peptides act through specific receptors, which are referred to as seven-transmembrane-domain receptors or G-protein-coupled receptors. Although prolactin is important in pregnancy and lactation in mammals, and is involved in the development of the mammary glands and the promotion of milk synthesis, a specific prolactin-releasing hormone has remained unknown. Here we identify a potent candidate for such a hormone. We first proposed that there may still be unknown peptide hormone factors that control pituitary function through seven-transmembrane-domain receptors. We isolated the complementary DNA encoding an 'orphan' receptor (that is, one for which the ligand is unknown). This receptor, hGR3, is specifically expressed in the human pituitary. We then searched for the hGR3 ligand in the hypothalamus and identified a new peptide, which shares no sequence similarity with known peptides and proteins, as an endogenous ligand. We show that this ligand is a potent prolactin-releasing factor for rat anterior pituitary cells; we have therefore named this peptide prolactin-releasing peptide.
566 citations
TL;DR: The results identify a major cause of CPHD in humans and suggest a direct or indirect role for PROP1 in the ontogenesis of pituitary gonadotropes, as well as somatotrope, lactotropes and caudomedial thyrotropes.
Abstract: Combined pituitary hormone deficiency (CPHD) in man denotes impaired production of growth hormone (GH) and one or more of the other five anterior pituitary hormones. Mutations of the pituitary transcription factor gene POU1F1 (the human homologue of mouse Pit1) are responsible for deficiencies of GH, prolactin and thyroid stimulating hormone (TSH) in Snell and Jackson dwarf mice and in man, while the production of adrenocorticotrophic hormone (ACTH), luteiniz-ing hormone (LH) and follicle stimulating hormone (FSH) is preserved. The Ames dwarf (df) mouse displays a similar phenotype, and appears to be epistatic to Snell and Jackson dwarfism. We have recently positionally cloned the putative Ames dwarf gene Prop1 (ref. 1)f which encodes a paired-like homeodomain protein that is expressed specifically in embryonic pituitary and is necessary for Pit1 expression. In this report we have identified four CPHD families with homozy-gosity or compound heterozygosity for inactivating mutations of PROP1. These mutations in the human PROP1 gene result in a gene product with reduced DNA-binding and transcriptional activation ability in comparison to the product of the murine df mutation. In contrast to individuals with POU1F1 mutations, those with PROP1 mutations cannot produce LH and FSH at a sufficient level and do not enter puberty spontaneously. Our results identify a major cause of CPHD in humans and suggest a direct or indirect role for PROP1 in the ontogenesis of pituitary gonadotropes, as well as somatotropes, lactotropes and caudomedial thyrotropes.
516 citations
TL;DR: The mammary gland is characterized by a unique dependence on hormonal signals for terminal differentiation, which is attained only after pregnancy as discussed by the authors, and it was introduced 200 million years ago with the appearance of mammals to provide nourishment to the newborn in the form of milk.
Abstract: On a phylogenetic scale of organ development the mammary gland is a recent acquisition. It was introduced 200 million years ago with the appearance of mammals to provide nourishment to the newborn in the form of milk. The mammary gland is characterized by a unique dependence on hormonal signals for terminal differentiation, which is attained only after pregnancy. At the time of birth, the anlage consists of a few rudimentary ducts in the vicinity of the nipple. Pronounced ductal outgrowth and branching commences at puberty, and in pregnancy an expanded lobulo-alveolar compartment develops. Functional differentiation of the secretory epithelium coincides with parturition and large amounts of milk are produced and secreted during lactation. After weaning of the young, the entire alveolar epithelial compartment is remodeled to resemble a virgin-like state. With each pregnancy, a new round of lobulo-alveolar development occurs. During the past 100 years, intensive efforts have been made to understand the endocrine control of mammopoiesis and lactogenesis. Classical research on endocrine ablated animals firmly established that ovarian steroids and pituitary peptide hormones are mandatory and sufficient for breast development and lactation. In 1900, Halban first established that mammary growth is controlled by the ovary (Halban 1900). He demonstrated that ovariectomy caused mammary regression, and that transplanted ovaries prevented the castration atrophy of mammary glands. Twenty-eight years later, Stricker and Grueter induced mammary development and milk secretion artificially in castrated virgin rabbits by injection of pituitary extract (Stricker and Grueter 1928). In 1933, Riddle, Bates, and Dykshorn purified the respective pituitary hormone (Riddle et al. 1933) and named it prolactin(PRL). In the last several years, the ability to delete genes from the mouse genome has allowed us to identify genetic components of mammary gland development. Molecular insight into the underlying genetic framework and signaling networks of the developing tissue has been gained through experimental manipulations of tissues from wild-type and knockout mice. Two distinct, yet braided, developmental concepts have unfolded. First, discrete signaling networks activated by systemic endocrine hormones induce mammopoiesis. Secondly, some of these signals are relayed through reciprocal interactions between the epithelium and the stroma. Table 1 contains those genes whose elimination from the mouse genome results in impaired mammary gland development. Among these genes are some of the ‘‘usual suspects’’ but also some previously unidentified players. Each mutation affects specific and distinct aspects of mammary development. These knockout mice not only confirmed the involvement of hormonal signaling but also provided tools to identify the tissue compartment that receives and executes these signals.
280 citations
TL;DR: The aim of this study was to establish the relationship between hyperprolactinaemia and body weight in patients with prolactin‐secreting pituitary tumours.
Abstract: Summary OBJECTIVE Hyperprolactinaemia in humans may be associated with a high prevalence of obesity but the nature of this link is poorly defined. The aim of this study was to establish the relationship between hyperprolactinaemia and body weight in patients with prolactin-secreting pituitary tumours. DESIGN We conducted a retrospective study of prolactinoma patients treated at the Endocrine Institute of the Tel Aviv Medical Center, Israel, during the period 1989‐1996. Patients with clinically nonfunctioning pituitary macroadenomas (NFA) served as the control group. Data on demographic parameters, body weight before and during treatment, clinical presentation including history of weight fluctuations, tumour size as measured by computed tomography or magnetic resonance imaging, modalities and response to treatment, and pituitary function before and during treatment were recorded from medical files. PATIENTS Forty-two patients with prolactinomas (PR) and 36 patients with clinically non-functioning macroadenomas (NFA) comprised the study population. RESULTS Mean weight was 93 6 3·4 kg and 78 6 2·7 kg in male patients with PR and NFA respectively (P o 0·0007). Recent weight gain (8 to 22 kg) was a presenting symptom in 13 PR patients, whereas only one NFA patient had this clinical presentation (P o 0·001). Seventeen PR patients lost weight (mean change π8·3 6 1·5 kg, range π2‐28 kg), during prolactin lowering therapy, 11 of whom had entirely normalized prolactin levels. Fourteen of the 18 patients who did not lose weight still had elevated prolactin levels (P o 0·01). Weight loss in patients with PR could not be attributed to altered pituitary function nor to compression of the third ventricle. In contrast to PR, no significant weight loss was observed in NFA patients. CONCLUSION Weight gain and elevated body weight are frequently associated with prolactinomas regardless of a mass effect on the hypothalamus or pituitary function. In this series, weight loss was recorded in 70% of prolactinomas patients and in 90% of male patients who normalized their prolactin levels. We propose the inclusion of hyperprolactinaemia in the differential diagnosis of endocrine obesity and weight gain.
208 citations
TL;DR: The results suggest that one action of E replacement therapy in postmenopausal women may be to decrease expression of the SERT gene.
200 citations
TL;DR: The hypothesis that galanin acts as a paracrine regulator of prolactin expression and as a growth factor to the lactotroph is supported by the generation of mice carrying a loss-of-function mutation of the endogenous galanIn gene.
Abstract: The neuropeptide galanin is predominantly expressed by the lactotrophs (the prolactin secreting cell type) in the rodent anterior pituitary and in the median eminence and paraventricular nucleus of the hypothalamus. Prolactin and galanin colocalize in the same secretory granule, the expression of both proteins is extremely sensitive to the estrogen status of the animal. The administration of estradiol-17β induces pituitary hyperplasia followed by adenoma formation and causes a 3,000-fold increase in the galanin mRNA content of the lactotroph. To further study the role of galanin in prolactin release and lactotroph growth we now report the generation of mice carrying a loss-of-function mutation of the endogenous galanin gene. There is no evidence of embryonic lethality and the mutant mice grow normally. The specific endocrine abnormalities identified to date, relate to the expression of prolactin. Pituitary prolactin message levels and protein content of adult female mutant mice are reduced by 30–40% compared with wild-type controls. Mutant females fail to lactate and pups die of starvation/dehydration unless fostered onto wild-type mothers. Prolactin secretion in mutant females is markedly reduced at 7 days postpartum compared with wild-type controls with an associated failure in mammary gland maturation. There is an almost complete abrogation of the proliferative response of the lactotroph to high doses of estrogen, with a failure to up-regulate prolactin release, STAT5 expression or to increase pituitary cell number. These data further support the hypothesis that galanin acts as a paracrine regulator of prolactin expression and as a growth factor to the lactotroph.
193 citations
TL;DR: Social subordination in female cynomolgus monkeys is stressful and brain dopaminergic activity is assessed, as reflected in the prolactin response to haloperidol, a dopamine2 (D2) receptor antagonist, which indicates that subordinate females have decreased D2 receptor function.
191 citations
TL;DR: It has been recently reported that subtle changes in the characteristics of the stressors or in their regularity can greatly influence adaptation, and these factors might explain failure to find adaptation of ACTH and prolactin in some works.
163 citations
TL;DR: Although cannabinoid receptors appear to play a major role in the ability of cannabinoids to influence hormone release, much remains to be learned concerning their function in the neuroendocrine regulation of hormone secretion.
163 citations
TL;DR: This is the first demonstration in humans that tear production is correlated with serum prolactin and sex hormone levels prior to and during the menopause.
Abstract: PurposeThe onset of dry eye is very common during menopause and may result from the loss of hormonal support. The purpose of this study was to assess the effect that changes in sex hormone and prolactin levels have on tear function in premenopausal and menopausal woman.MethodsWomen between the ages
162 citations
TL;DR: Postpartum women with current depression and those who developed depression within 6-10 weeks after delivery had significantly lower plasma prolactin levels and significantly greater progesterone levels than those who were not depressed, and there were significant correlations between age and plasma cortisol and prol actin levels.
TL;DR: The hypothesis is that recurrent infections over the life span play a significant role in producing aging changes in all systems outside the blood-brain barrier via release of toxic quantities of NO.
TL;DR: Orgasm induced transient increases in heart rate, blood pressure and noradrenaline plasma levels and none of the other endocrine variables were significantly affected by sexual arousal and orgasm.
01 Jun 1998-Comparative Biochemistry and Physiology Part C: Pharmacology, Toxicology and Endocrinology
TL;DR: In birds exposed to seasonal changes in daylength, the seasonally maximal concentrations of plasma Prolactin associated with the development of photorefractoriness can be explained, in part, by the saturation daylength for photoinduced prolactin release being reached in late spring/mid summer.
Journal Article•
TL;DR: Increases in testosterone and δ4-androstenedione levels and in free androgen index, along with a higher luteinizing hormone-follicle-stimulating hormone ratio in the luteal phase, were observed in women treated with VPA, although sex-hormone binding globulin levels were higher in CBZ and PB than in VPA-treated patients, the differences were not significant.
Abstract: Serum levels of sex-hormones, sex-hormone binding globulin, gonadotropin, and prolactin were evaluated during the follicular and the luteal phases in 65 women with epilepsy and in 20 healthy controls. Twenty-one patients were treated with sodium valproate (VPA), 21 with phenobarbital (PB), and 23 with carbamazepine (CBZ). VPA does not stimulate liver microsome enzymes, whereas PB and CBZ do. Patients on VPA therapy showed higher body weight and body mass index, but no significant differences in hirsutism score, or in ovary volume or polycystic ovary prevalence (at ultrasound examination). Estradiol levels were lower in all patient groups than in healthy controls in the follicular but not in the luteal phases. VPA affected luteal progesterone surge in 63.6% of cases. This effect was significantly lower in the CBZ and PB groups. Furthermore, increases in testosterone and delta 4-androstenedione levels and in free androgen index, along with a higher luteinizing hormone-follicle-stimulating hormone ratio in the luteal phase, were observed in women treated with VPA. Although sex-hormone binding globulin levels were higher in CBZ and PB than in VPA-treated patients, the differences were not significant because of the wide dispersion of the carrier protein levels. Inducer antiepileptic drugs decreased dehydroepiandrosterone sulfate levels, which remained unchanged during VPA treatment. No significant differences occurred in basal gonadotropin and prolactin levels.
TL;DR: Data are presented demonstrating that nicotine acts via a central mechanism to stimulate indirectly the release of ACTH from the anterior pituitary corticotropes, and the desensitization characteristics of the neuroendocrine responses to both acute and chronic nicotine exposure are indicative of an alteration in these NAchRs.
TL;DR: Data indicate that PRL acts at the endocrine, paracrine, and autocrine levels in regulating immune function, and the structure/ function relationships within the PRLr as they pertain to immunologically relevant signal transduction pathways.
Abstract: Prolactin (PRL) was originally identified as a neuroendocrine hormone of pituitary origin (Riddle & Braucher 1931, Riddle et al. 1933). While the primary function of this hormone was initially thought to lie solely within the breast, the functional pleiotropism of this peptide with regards to reproduction, osmoregulation, and behavior was subsequently recognized (Nicoll 1974). Several lines of evidence have now also demonstrated an immunoregulatory role for this peptide. Structural analysis of PRL has revealed it to be related to members of the cytokine/ hematopoietin family such as growth hormone (GH), erythropoietin, granulocyte–macrophage colony stimulating factor (GM-CSF) and the interleukins (IL) IL-2 to IL-7 (Bazan 1990). Synthesis of PRL is not limited to the hypophysis, as numerous extra-pituitary sites of PRL expression including the decidua, breast, and T lymphocytes have been detected (DiMattia et al. 1986, Montogomery et al. 1987, Clevenger et al. 1990, Gellersen et al. 1994, Ginsburg & Vonderhaar 1995, Mershon et al. 1995, Clevenger & Plank 1997). The receptor for PRL (PRLr) is present on T and B lymphocytes and macrophages (Pellegrini et al. 1992, Dardenne et al. 1994). Acting through its receptor, PRL modulates immune system function by stimulating both cell proliferation and survival. Taken together, these data indicate that PRL acts at the endocrine, paracrine, and autocrine levels in regulating immune function (Gala 1991, Prystowsky & Clevenger 1994, Kooijman et al. 1996, Yu-Lee 1997). This review initially focuses on the immunoregulatory functions of PRL in the immune system, and then focuses on the structure/ function relationships within the PRLr as they pertain to immunologically relevant signal transduction pathways.
TL;DR: PRL is a multifunctional hormone/cytokine that has been used as an evolutionary template for the generation of regulatory molecules involved in the establishment and maintenance of pregnancy.
Abstract: The establishment and maintenance of pregnancy requires significant modifications of the maternal environment. During pregnancy, changes arise in virtually every major organ system within the mother, permitting growth and development of the embryo/fetus within the protected confines of the maternal reproductive tract. These gestational-dependent adaptations are believed to be controlled, at least in part, through the elaboration of chemical signals by the uterus and placenta referred to as hormones/cytokines. Some uteroplacental signals have been coupled to the regulation of specific maternal responses, while a specific function is not known for other putative signaling molecules that have been identified. The subject of this review is the uteroplacental prolactin (PRL) family. PRL is a multifunctional hormone/cytokine that has been used as an evolutionary template for the generation of regulatory molecules involved in the establishment and maintenance of pregnancy. Several reviews on the PRL family have appeared over the past several years and are recommended [1-7].
TL;DR: It is demonstrated that PE are active in lactotroph cells of the pituitary, and the estrogenic effects of PE in PR1 cells were ER dependent, in that addition of the antiestrogen ICI-182,780 inhibited prolactin response.
TL;DR: The results indicate that the absence of PRL reduces pituitary LH release, attenuates median eminence dopaminergic activity, and affects the growth of seminal vesicles and ventral prostate.
Abstract: Mice with a targeted disruption (knock-out) of the PRL gene (PRL-KO) were used to study the physiological role of PRL in the control of male neuroendocrine functions related to reproduction. Compared with normal males, PRL-KO mice had significant reductions in median eminence dopamine content, plasma LH levels, LH and FSH secretion in vitro (per mg pituitary), and weights of seminal vesicles and ventral prostate. PRL was not detectable in incubation medium with pituitaries from PRL-KO mice. No alterations were detected in PRL-KO mice in median eminence norepinephrine, plasma testosterone levels, or testosterone release (per mg testis) in vitro with or without LH. No differences were detected in PRL-KO vs. normal male mice in the interval from housing with normal female mice until conception, rate of pregnancy, or the number of live pups per litter. Pituitary weight in PRL-KO mice was increased (1.78 +/- 0.22 vs. 3.35 +/- 0.20 mg; P < 0.001), presumably due to reduced feedback inhibition and hypertrophy and/or hyperplasia of nonfunctional lactotrophs. These results indicate that the absence of PRL reduces pituitary LH release, attenuates median eminence dopaminergic activity, and affects the growth of seminal vesicles and ventral prostate. Although it was previously shown that PRL can repair the reproductive defect in male pituitary dwarf mice, our current results imply that the PRL deficiency alone is not sufficient to cause male infertility, although there are obvious alterations in reproductive neuroendocrine function in PRL-KO males.
TL;DR: It is demonstrated that high estrogen levels do not accelerate murine SLE when the prolactin-stimulating property of estrogen is suppressed by bromocriptine and further investigation of hormonal interactions in autoimmunity will provide a better understanding of hormonal immunoregulation and, perhaps, lead to improved clinical application of hormonal Immunomodulation.
Abstract: Estrogen and prolactin have been shown to modulate autoimmunity in the NZB/NZW F1 (B/W) mouse model of systemic lupus erythematosus (SLE). However, estrogen stimulates prolactin secretion. The goal of this study was to examine differential effects of estrogen and prolactin in the female B/W mouse model of SLE. B/W females were manipulated to create combinations of low and high concentrations of serum estrogen and prolactin. Hyperprolactinemic mice with either low or high serum estrogen levels had accelerated development of albuminuria at 24 and 32 weeks of age compared to normal and hypoprolatinemic mice. High estrogen/high prolactin mice also had a higher percentage of anti-DNA antibodies compared to mice in the low estrogen/low prolactin and the high estrogen/low prolactin groups. IgG levels were not significantly different between groups. Mean survival was shortest in the high estrogen/high prolactin group (34+/-1.0 weeks) and longest in the high estrogen/low prolactin group (42+/-1.2 weeks; P < 0.05). High levels of serum estrogen were associated with depressed in vitro lymphoproliferation and IL-2 production. This study suggests that high prolactin levels in either high or low serum estrogen states are associated with accelerated autoimmunity in the B/W mouse. This study further demonstrates that high estrogen levels do not accelerate murine SLE when the prolactin-stimulating property of estrogen is suppressed by bromocriptine. Further investigation of hormonal interactions in autoimmunity will provide a better understanding of hormonal immunoregulation and, perhaps, lead to improved clinical application of hormonal immunomodulation.
TL;DR: To evaluate the changes in serum sex hormones of gonadal or adrenal origin, the gonadotropic hormones, and sex hormone‐binding globulin in men and women with chronic temporal lobe epilepsy, who are undergoing monotherapy with carbamazepine or receiving carbamazepsine in combination with other anticonvulsant drugs.
Abstract: Summary: Purpose: To evaluate the changes in serum sex hormones of gonadal or adrenal origin, the gonadotropic hormones, and sex hormone-binding globulin (SHBG) in men and women with chronic temporal lobe epilepsy (TLE), who are undergoing monotherapy with carbamazepine or receiving carbamazepine in combination with other anticonvulsant drugs.
Methods: Gonadal hormones (estradiol, testosterone, free testosterone, and inhibin B), adrenal hormones [cortisol, dehydroepiandrosterone sulfate (DHEAS), androstenedione, and 17a-hydroxyprogesterone], and gonadotropic hormones (luteinizing hormone [LH] and follicle-stimulating hormone [FSH]) were measured in 22 women and 26 men with TLE. The study also measured prolactin; human growth hormone and its major mediator, insulin-like growth factor–I; thyroid hormones (free thyroxine and free triiodothyronine); thyroid–stimulating hormone (TSH); and SHBG. The results were compared with those obtained from 60 healthy women and 106 healthy men.
Results: In the female patients, TSH, DHEAS, follicularphase LH, and luteal-phase estradiol were significantly lower than in the control groups, with prolactin and SHBG significantly higher. In the male patients, DHEAS, 17α-hydroxyprogesterone, free testosterone, inhibin B, and the testosterone LH ratio were significantly lower than in the control group, with LH, FSH, and SHBG significantly higher. Increased FSH in 31% of the men indicates an impairment of spermatogenesis; lowered inhibin B in 12% indicates an impaired Sertoli's cell function; and the decreased testosterone LH ratio in 50% indicates an impaired Leydig's cell function.
Conclusions: The case patients had endocrine disorders, mainly concerning the gonadotropic and gonadal functions in both sexes; the adrenal function, with lowered DHEAS levels in both sexes; and lowered 17α-hydroxyprogesterone levels in the men. SHBG levels were increased in patients taking anticonvulsant medications.
TL;DR: The findings do not support the hypothesis that T interferes with the expression of parental behavior by reducing PRL receptor binding activity at central sites.
TL;DR: The observed pattern of hormonal deviations in FMS patients is a CNS adjustment to chronic pain and stress, constitutes a specific entity of FMS, and is primarily evoked by activated CRH neurons.
Abstract: To study the hormonal perturbations in FMS patients we injected sixteen FMS patients and seventeen controls a cocktail of the hypothalamic releasing hormones: Corticotropin-releasing hormone (CRH), Thyrotropin-releasing hormone (TRH), Growth hormone-releasing hormone (GHRH), and Luteinizing hormone-releasing hormone (LHRH) and observed the hormonal secretion pattern of the pituitary together with the hormones of the peripheral endocrine glands. We found in FMS patients elevated basal values of ACTH and cortisol, lowered basal values of insulin-like growth factor I (IGF-I) and of triiodothyronine (T3), elevated basal values of follicle-stimulating hormone (FSH) and lowered basal values of estrogen. Following injection of the four releasing-hormones, we found in FMS patients an augmented response of ACTH, a blunted response of TSH, while the prolactin response was exaggerated. The effects of LHRH stimulation were investigated in six FMS patients and six controls and disclosed a significantly blunted response of LH in FMS. We explain the deviations of hormonal secretion in FMS patients as being caused by chronic stress, which, after being perceived and processed by the central nervous system (CNS), activates hypothalamic CRH neurons. CRH, on the one hand, activates the pituitary-adrenal axis, but also stimulates at the hypothalamic level somatostatin secretion which, in turn, causes inhibition of GH and TSH at the pituitary level. The suppression of gonadal function may also be attributed to elevated CRH by its ability to inhibit hypothalamic LHRH release, although it could act also directly on the ovary by inhibiting FSH-stimulated estrogen production. We conclude that the observed pattern of hormonal deviations in FMS patients is a CNS adjustment to chronic pain and stress, constitutes a specific entity of FMS, and is primarily evoked by activated CRH neurons.
01 Jun 1998-Comparative Biochemistry and Physiology Part C: Pharmacology, Toxicology and Endocrinology
TL;DR: The results support the view that the melatonin signal which encodes photoperiod, acts in the hypothalamus to regulate somePhotoperiodic responses (alpha-MSH and beta-endorphin-body weight axis, gonadotrophin-gonadal axis) but acts inThe pituitary gland to regulate other responses (prolactin-pelage axis).
TL;DR: A more rapid hormonal and clinical response was achieved with radiosurgery than with conventional pituitary irradiation treatment, and SRS and conventional methods showed similar responses.
Abstract: Purpose: To determine the impact of stereotactic radiosurgery (SRS) on the clinical course, hormonal status, and follow-up CT/MRI scan of pituitary macroadenomas. Methods and Materials: From July 1988 to March 1996, 24 pituitary macroadenomas had been treated using 6 MV linear accelerator based SRS. They consisted of 11 (45.8%) prolactinomas, 2 (8.3%) growth hormone (GH)-secreting tumors, 1 (4.2%) Cushing’s disease, 8 (33.3%) nonsecreting (nonfunctioning: NF) tumors, and 2 (8.3%) mixed prolactin-growth hormone (PRL-GH)-secreting tumors (M:F = 12:12; aged 21–61 years). Postoperative irradiation was performed in all cases except for the instance of Cushing’s disease. The prescribed dose to tumor center varied from 10 to 27 Gy (mean 21.1 Gy) using a collimator size of 0.5 to 2.5 cm. The follow-up duration ranged from 13 to 89 months (mean 49.2 months). Results from these patients were compared to our results using conventional radiation. Results: Visual acuity and field defect were improved or became normal in 19 (79.2%) cases. Four (16.7%) remained unchanged after the treatment. One (4.1%) progressed 6 years after SRS and subsequently had repeat surgery with conventional boost irradiation. Of the 13 (46.4%) prolactinomas, including two mixed PRL-GH secreting tumors, 11 (84.1%) revealed normal hormonal levels within 1 year after SRS. In contrast, it took 2 years to become normal after conventional radiation therapy. In four GH-secreting tumors including two mixed PRL-GH secreting tumors, SRS and conventional methods showed similar responses. On follow-up imagings of the 21 patients, the mass was completely resolved in 4 (16.7%), including 3 PRLs and one NF, decreased in 11 (45.8%), and unchanged in 5 (16.7%) with central necrosis or cysts. One (4.2%) progressed and was reoperated 6 years after treatment. The complications related to SRS were comparable to those from conventional method. Conclusion: Radiosurgery can be used effectively in patients with pituitary adenoma. In this study, a more rapid hormonal and clinical response was achieved with radiosurgery than with conventional pituitary irradiation treatment.
Journal Article•
TL;DR: Findings indicate hypoactivity of the HPA axis in patients with SS, and further studies are needed to definitively identify the locus of the defects and assess the significance of the pattern of the perturbations to the pathogenesis and expression of SS.
Abstract: OBJECTIVE: To examine the functional integrity of the hypothalamic-pituitary-adrenal (HPA) and thyroid axes in Sjogren's syndrome (SS) via the assessment of basal and stimulated adrenocorticotropin (ACTH), cortisol, thyroid stimulating hormone (TSH), and prolactin levels METHODS: Pituitary function of the HPA axis was assessed by determining the basal plasma levels of ACTH in the late afternoon, as well as the ACTH released to ovine corticotropin releasing hormone (oCRH) stimulation; adrenal function was assessed by measuring plasma cortisol levels in the late afternoon at baseline and after release of the endogenous ACTH during oCRH stimulation Basal and thyrotropin releasing hormone (TRH) stimulated levels of TSH and prolactin were also assessed Healthy volunteers were used as controls RESULTS: Patients with SS, compared to controls, were characterized by significantly lower ACTH levels (pg/ml), (51 +/- 05 vs 114 +/- 15, respectively; p < 005) and cortisol levels (microg/ml), (24 +/- 06 vs 59 +/- 12, respectively; p < 005) Furthermore, a blunted pituitary and adrenal response to oCRH compared to controls was observed: peak plasma ACTH and cortisol levels for patients with SS were 462 +/- 54 pg/ml and 157 +/- 16 microg/ml, respectively, and for controls 615 +/- 38 and 196 +/- 07, respectively (p < 005) Basal TSH levels were significantly elevated in patients (13 +/- 03 microIU/ml vs 09 +/- 005 microIU/ml; p < 005) CONCLUSION: The above findings indicate hypoactivity of the HPA axis in patients with SS Further studies are needed to definitively identify the locus of the defects and assess the significance of the pattern of the perturbations to the pathogenesis and expression of SS
TL;DR: It is suggested that protein-tyrosine phosphatases are novel targets for regulation by extracellular matrix and in mammary cells represent an additional control to the requirement of integrins for milk protein production.
TL;DR: 8-OH-DPAT stimulates oxytocin, ACTH, and corticosterone but not prolactin secretion via activation of5-HT1A receptors and blockade of 5-HT2A receptors may unmask 8-OH -DPAT simulation of renin secretion through non-5- HT1A receptor mechanisms.
01 Nov 1998
TL;DR: The basis for the observed differences in proliferative activities in tumors of the three study groups is not readily apparent but may reflect differences in the endocrine milieu or the effect of sex steroid hormone receptors, tumoral vascularity, or specific growth factors.
Abstract: Objective To explore the basis of the gender-based differences in endocrine and surgical findings in patients with prolactinoma (prolactin cell adenoma) as well as in their clinical outcome. Material and Methods In young or reproductive-age female patients, older women (beyond 40 years of age), and male patients, we systematically studied the following factors: operative and endocrine features (tumor size, invasiveness, preoperative serum prolactin level, and biochemical outcome), specific biologic variables (mitotic index, MIB-l labeling index, and p27 immunoreactivity), and hormone receptor status (estrogen and progesterone receptor proteins as well as dopamine D 2 receptor messenger RNA). Results Of the various factors assessed, the preoperative prolactin level and MIB-l labeling index were lower in young female patients in comparison with older female and particularly male patients. Hormone levels were also positively associated with mitotic activity as well as the MIB-l labeling index. Although invasion was infrequent in microadenomas of young female patients, no statistically significant differences in tumor size or invasiveness were noted among the three patient groups. Absence of differences in invasiveness may, in part, be explained by artifacts of case selection. Conclusion The basis for the observed differences in proliferative activities in tumors of the three study groups is not readily apparent but may reflect differences in the endocrine milieu or the effect of sex steroid hormone receptors, tumoral vascularity, or specific growth factors.